text:
Rebecca Walker

Rebecca Walker (born Rebecca Leventhal; November 17, 1969) is an American writer, feminist, and activist. Walker has been regarded as one of the prominent voices of Third Wave Feminism, and the coiner of the term "third wave", since publishing a 1992 article on feminism in Ms. magazine called "Becoming the Third Wave", in which she proclaimed: "I am the Third Wave."

Walker's writing, teaching, and speeches focus on race, gender, politics, power, and culture. In her activism work, she helped co-found the Third Wave Fund that morphed into the Third Wave Foundation, an organization that supports young women of color, queer, intersex, and trans individuals by providing tools and resources they need to be leaders in their communities through activism and philanthropy.

Walker does extensive writing and speaking about gender, racial, economic, and social justice at universities around the United States and internationally.

In 1994, Time named Walker as one of the 50 future leaders of America. Her work has appeared in publications including The Washington Post, The Huffington Post, Salon, Glamour, and Essence and has been featured on CNN and MTV.

Early life and education
Born Rebecca Leventhal in 1969 in Jackson, Mississippi, she is the daughter of Alice Walker, an African-American writer whose work includes The Color Purple, and Melvyn R. Leventhal, a Jewish American civil rights lawyer. Her parents married in New York before going to Mississippi to work in civil rights. After her parents divorced in 1976, Walker spent her childhood alternating every two years between her father's home in the largely Jewish Riverdale section of the Bronx in New York City and her mother's largely African-American environment in San Francisco. Walker attended The Urban School of San Francisco.

When she was 15, she decided to change her surname from Leventhal to Walker, her mother's surname. After high school, she studied at Yale University, where she graduated cum laude in 1992. Walker identifies as Jewish, white and Black; her 2000 memoir is titled Black, White, and Jewish: Autobiography of a Shifting Self.

The Third Wave Fund
After graduating from Yale University, she and Shannon Liss (now Shannon Liss-Riordan) co-founded the Third Wave Fund, a non-profit organization aimed at encouraging young women to get involved in activism and leadership roles. The organization's initial mission, based on Walker's article, was to "fill a void in young women's leadership and to mobilize young people to become more involved socially and politically in their communities." In its first year, the organization initiated a campaign that registered more than 20,000 new voters across the United States. The organization now provides grants to individuals and projects that support young women. The fund was adapted as The Third Wave Foundation in 1997 and continues to support young activists. In the wake of the November 2016 presidential election in the United States, the organization received more than four times the normal number of requests for emergency grants.

Teaching
Walker views teaching as a way to give people the strength to speak the truth, to change perspectives, and to empower people with the ability to change the world. She lectures on writing memoirs, multi-generational feminism, diversity in the media, multi-racial identity, contemporary visual arts and emerging cultures.

Speaking
Walker concentrates on speaking about multicultural identity (including her own), enlightened masculinity, and inter-generational and third-wave feminism at high schools, universities and conferences around the world. She has spoken at Harvard, Exeter, Head Royce, Oberlin, Smith, MIT, Xavier, Stanford, and Louisiana State University. She has also addressed organizations and corporations such as The National Council of Teachers of English, the Walker Art Center, the American Association of University Women, the National Women's Studies Association, Out and Equal, the National Organization for Women, and Hewitt Associates. In the United States, she has been featured on various popular media outlets such as Good Morning America, The Oprah Winfrey Show, and Charlie Rose.

Major works
Walker's first major work was the book To be Real: Telling the Truth and Changing the Face of Feminism (1996), which consisted of articles that she compiled and edited. The book reevaluated the feminist movement of the time. Reviewer Emilie Fale, an Assistant Professor of Communication at Ithaca College, described it: "The twenty-three contributors in To Be Real offer varied perspectives and experiences that challenge our stereotypes of feminist beliefs as they negotiate the troubled waters of gender roles, identity politics and "power feminism". As a collection of "personal testimonies", this work shows how third-wave activists use personal narratives to describe their experiences with social and gender injustice. Contributors include feminist writers such as bell hooks and Naomi Wolf. According to Walker's website, this book has been taught in Gender Studies programs around the world.

In her memoir Black, White and Jewish: Autobiography of a Shifting Self (2000), Walker explores her early years in Mississippi as the child of parents who were active in the later years of the Civil Rights Movement. She also touches on living with two parents with very active careers, which she believes led to their separation. She discusses encountering racial prejudice and the difficulties of being mixed-race in a society with rigid cultural barriers. She also discusses developing her sexuality and identity as a bisexual woman.

Her 2007 memoir Baby Love: Choosing Motherhood After A Lifetime of Ambivalence explores her life with a stepson and biological son against a framework of feminism. Walker was criticized for her stigmatizing views on biological parenthood being superior to adoptive parenthood and adoptive parents boycotted her work.

Walker was a contributing editor to Ms. magazine for many years. Her writing has been published in a range of magazines, such as Harper's, Essence, Glamour, Interview, Buddhadharma, Vibe, Child, and Mademoiselle magazines. She has appeared on CNN and MTV, and has been covered in The New York Times, Chicago Times, Esquire, Shambhala Sun, among other publications. Walker has taught workshops on writing at international conferences and MFA programs. She also works as a private publishing consultant.

Her first novel, Adé: A Love Story, was published in 2013. It features a biracial college student, Farida, who falls in love with Adé, a black Kenyan man. The couple's plan to marry is interrupted when Farida gets malaria and the two must struggle through a civil war in Kenya. The novel was generally well received by critics and laypeople alike.

Personal life
Walker identifies as bisexual. She dated neo-soul musician Meshell Ndegeocello, whose son she helped raise even after their relationship ended.

She has a son (b. 2004) with her former partner Choyin Rangdrol, a Buddhist teacher.

Once estranged from her mother Alice Walker, she has reconciled with her, and the two have since appeared at literary events together.

Film
In the 1998 film Primary Colors, Walker played the character March. The movie is a roman à clef about Bill Clinton's 1992 presidential campaign.

In March 2014, the film rights for her novel Adé: A Love Story (2013) were reported to have been optioned, with Madonna to serve as director.

Awards

 * Women of Distinction Award from the American Association of University Women,
 * "Feminist of the Year" award from the Fund for the Feminist Majority,
 * "Paz y Justicia" award from the Vanguard Public Foundation,
 * "Intrepid Award" from the National Organization for Women,
 * "Champion of Choice" award from the California Abortion Rights Action League,
 * "Women Who Could Be President Award" from the League of Women Voters.

Walker has also received an honorary Doctorate from the North Carolina School of the Arts.

Walker is featured in The Advocate′s "Forty Under 40" issue of June/July 2009 as one of the most influential "out" media professionals.

In 2016, she was selected as one of BBC's 100 Women.

title: Rebecca Walker


text:
Acute lymphoblastic leukemia

Acute lymphoblastic leukemia (ALL) is a cancer of the lymphoid line of blood cells characterized by the development of large numbers of immature lymphocytes. Symptoms may include feeling tired, pale skin color, fever, easy bleeding or bruising, enlarged lymph nodes, or bone pain. As an acute leukemia, ALL progresses rapidly and is typically fatal within weeks or months if left untreated.

In most cases, the cause is unknown. Genetic risk factors may include Down syndrome, Li–Fraumeni syndrome, or neurofibromatosis type 1. Environmental risk factors may include significant radiation exposure or prior chemotherapy. Evidence regarding electromagnetic fields or pesticides is unclear. Some hypothesize that an abnormal immune response to a common infection may be a trigger. The underlying mechanism involves multiple genetic mutations that results in rapid cell division. The excessive immature lymphocytes in the bone marrow interfere with the production of new red blood cells, white blood cells, and platelets. Diagnosis is typically Acute lymphoblastic leukemia based on blood tests and bone marrow examination.

Acute lymphoblastic leukemia is typically treated initially with chemotherapy aimed at bringing about remission. This is then followed by further chemotherapy typically over a number of years. Treatment usually also includes intrathecal chemotherapy since systemic chemotherapy can have limited penetration into the central nervous system and the central nervous system is a common site for relapse of acute lymphoblastic leukemia.

Treatment can also include radiation therapy if spread to the brain has occurred. Stem cell transplantation may be used if the disease recurs following standard treatment. Additional treatments such as Chimeric antigen receptor T cell immunotherapy are being used and further studied.

Acute lymphoblastic leukemia affected about 876,000 people globally in 2015 and resulted in about 111,000 deaths. It occurs most commonly in children, particularly those between the ages of two and five. In the United States it is the most common cause of cancer and death from cancer among children. Acute lymphoblastic leukemia is notable for being the first disseminated cancer to be cured. Survival for children increased from under 10% in the 1960s to 90% in 2015. Survival rates remain lower for babies (50%) and adults (35%).

Signs and symptoms
Initial symptoms can be nonspecific, particularly in children. Over 50% of children with leukemia had one or more of five features: a liver one can feel (64%), a spleen one can feel (61%), pale complexion (54%), fever (53%), and bruising (52%). Additionally, recurrent infections, feeling tired, arm or leg pain, and enlarged lymph nodes can be prominent features. The B symptoms, such as fever, night sweats, and weight loss, are often present as well.

Central nervous system (CNS) symptoms such as cranial neuropathies due to meningeal infiltration are identified in less than 10% of adults and less than 5% of children, particularly mature B-cell ALL (Burkitt leukemia) at presentation.

The signs and symptoms of acute lymphoblastic leukemia are variable and include:
 * Generalized weakness and feeling tired
 * Anemia
 * Dizziness
 * Headache, vomiting, lethargy, neck stiffness, or cranial nerve palsies (CNS involvement)
 * Frequent or unexplained fever and infection
 * Weight loss and/or loss of appetite
 * Excessive and unexplained bruising
 * Bone pain, joint pain (caused by the spread of "blast" cells to the surface of the bone or into the joint from the marrow cavity)
 * Breathlessness
 * Enlarged lymph nodes, liver, and/or spleen
 * Pitting edema (swelling) in the lower limbs and/or abdomen
 * Petechiae, which are tiny red spots or lines in the skin due to low platelet levels
 * Testicular enlargement
 * Mediastinal mass

Cause

The cancerous cell in ALL is the lymphoblast. Normal lymphoblasts develop into mature, infection-fighting B-cells or T-cells, also called lymphocytes. Signals in the body control the number of lymphocytes so neither too few nor too many are made. In ALL, both the normal development of some lymphocytes and the control over the number of lymphoid cells become defective.

Acute lymphoblastic leukemia emerges when a single lymphoblast gains many mutations to genes that affect blood cell development and proliferation. In childhood ALL, this process begins at conception with the inheritance of some of these genes. These genes, in turn, increase the risk that more mutations will occur in developing lymphoid cells. Certain genetic syndromes, like Down Syndrome, have the same effect. Environmental risk factors are also needed to help create enough genetic mutations to cause disease. Evidence for the role of the environment is seen in childhood ALL among twins, where only 10–15% of both genetically identical twins get ALL. Since they have the same genes, different environmental exposures explain why one twin gets ALL and the other does not.

Infant ALL is a rare variant that occurs in babies less than one year old. KMT2A (formerly MLL) gene rearrangements are most common and occur in the embryo or fetus before birth. These rearrangements result in increased expression of blood cell development genes by promoting gene transcription and through epigenetic changes. In contrast to childhood ALL, environmental factors are not thought to play a significant role. Aside from the KMT2A rearrangement, only one extra mutation is typically found. Environmental exposures are not needed to help create more mutations.

Genetics
Common inherited risk factors include mutations in ARID5B, CDKN2A/2B, CEBPE, IKZF1, GATA3, PIP4K2A and, more rarely, TP53. These genes play important roles in cellular development, proliferation, and differentiation. Individually, most of these mutations are low risk for ALL. Significant risk of disease occurs when a person inherits several of these mutations together.

The uneven distribution of genetic risk factors may help explain differences in disease rates among ethnic groups. For instance, the ARID5B mutation is less common in ethnic African populations.

Several genetic syndrome also carry increased risk of ALL. These include: Down syndrome, Fanconi anemia, Bloom syndrome, X-linked agammaglobulinemia, severe combined immunodeficiency, Shwachman–Diamond syndrome, Kostmann syndrome, neurofibromatosis type 1, ataxia-telangiectasia, paroxysmal nocturnal hemoglobinuria, and Li–Fraumeni syndrome. Fewer than 5% of cases are associated with a known genetic syndrome.

Rare mutations in ETV6 and PAX5 are associated with a familial form of ALL with autosomal dominant patterns of inheritance.

Environmental
The environmental exposures that contribute to emergence of ALL is contentious and a subject of ongoing debate.

High levels of radiation exposure from nuclear fallout is a known risk factor for developing leukemia. Evidence whether lesser radiation, as from x-ray imaging during pregnancy, increases risk of disease remains inconclusive. Studies that have identified an association between x-ray imaging during pregnancy and ALL found only a slightly increased risk. Exposure to strong electromagnetic radiation from power lines has also been associated with a slightly increased risk of ALL. This result is questioned as no causal mechanism linking electromagnetic radiation with cancer is known.

High birth weight (greater than 4000 g or 8.8 lbs) is also associated with a small increased risk. The mechanism connecting high birth weight to ALL is also not known.

Evidence suggests that secondary leukemia can develop in individuals treated with certain types of chemotherapy, such as epipodophyllotoxins and cyclophosphamide.

Infections
There is some evidence that a common infection, such as influenza, may indirectly promote the emergence of ALL. The delayed-infection hypothesis states that ALL results from an abnormal immune response to infection in a person with genetic risk factors. Delayed development of the immune system due to limited disease exposure may result in excessive production of lymphocytes and increased mutation rate during an illness. Several studies have identified lower rates of ALL among children with greater exposure to illness early in life. Very young children who attend daycare have lower rates of ALL. Evidence from many other studies looking at disease exposure and ALL is inconclusive. Some researchers have linked the hygiene hypothesis.

Mechanism
Several characteristic genetic changes lead to the creation of a leukemic lymphoblast. These changes include chromosomal translocations, intrachromosomal rearrangements, changes in the number of chromosomes in leukemic cells, and additional mutations in individual genes. Chromosomal translocations involve moving a large region of DNA from one chromosome to another. This move can result in placing a gene from one chromosome that promotes cell division to a more actively transcribed area on another chromosome. The result is a cell that divides more often. An example of this includes the translocation of C-MYC, a gene that encodes a transcription factor that leads to increased cell division, next to the immunoglobulin heavy- or light-chain gene enhancers, leading to increased C-MYC expression and increased cell division. Other large changes in chromosomal structure can result in the placement of two genes directly next to each other. The result is the combination of two usually separate proteins into a new fusion protein. This protein can have a new function that promotes the development of cancer. Examples of this include the ETV6–RUNX1 fusion gene that combines two factors that promote blood cell development and the BCR-ABL1 fusion gene of the Philadelphia chromosome. BCR–ABL1 encodes an always-activated tyrosine kinase that causes frequent cell division. These mutations produce a cell that divides more often, even in the absence of growth factors.

Other genetic changes in B-cell ALL include changes to the number of chromosomes within the leukemic cells. Gaining at least five additional chromosomes, called high hyperdiploidy, occurs more commonly. Less often, chromosomes are lost, called hypodiploidy, which is associated with a poorer prognosis. Additional common genetic changes in B-cell ALL involve non-inherited mutations to PAX5 and IKZF1. In T-cell ALL, LYL1, TAL1, TLX1, and TLX3 rearrangements can occur.

Acute lymphoblastic leukemia results when enough of these genetic changes are present in a single lymphoblast. In childhood ALL, for example, one fusion gene translocation is often found along with six to eight other ALL-related genetic changes. The initial leukemic lymphoblast copies itself into an excessive number of new lymphoblasts, none of which can develop into functioning lymphocytes. These lymphoblasts build up in the bone marrow and may spread to other sites in the body, such as lymph nodes, the mediastinum, the spleen, the testicles, and the brain, leading to the common symptoms of the disease.

Diagnosis
Diagnosing ALL begins with a thorough medical history, physical examination, complete blood count, and blood smears. While many symptoms of ALL can be found in common illnesses, persistent or unexplained symptoms raise suspicion of cancer. Because many features on the medical history and exam are not specific to ALL, further testing is often needed. A large number of white blood cells and lymphoblasts in the circulating blood can be suspicious for ALL because they indicate a rapid production of lymphoid cells in the marrow. The higher these numbers typically point to a worse prognosis. While white blood cell counts at initial presentation can vary significantly, circulating lymphoblast cells are seen on peripheral blood smears in the majority of cases.

A bone marrow biopsy provides conclusive proof of ALL, typically with >20% of all cells being leukemic lymphoblasts. A lumbar puncture (also known as a spinal tap) can determine whether the spinal column and brain have been invaded. Brain and spinal column involvement can be diagnosed either through confirmation of leukemic cells in the lumbar puncture or through clinical signs of CNS leukemia as described above. Laboratory tests that might show abnormalities include blood count, kidney function, electrolyte, and liver enzyme tests.

Pathological examination, cytogenetics (in particular the presence of Philadelphia chromosome), and immunophenotyping establish whether the leukemic cells are myeloblastic (neutrophils, eosinophils, or basophils) or lymphoblastic (B lymphocytes or T lymphocytes). Cytogenetic testing on the marrow samples can help classify disease and predict how aggressive the disease course will be. Different mutations have been associated with shorter or longer survival. Immunohistochemical testing may reveal TdT or CALLA antigens on the surface of leukemic cells. TdT is a protein expressed early in the development of pre-T and pre-B cells, whereas CALLA is an antigen found in 80% of ALL cases and also in the "blast crisis" of CML.

Medical imaging (such as ultrasound or CT scanning) can find invasion of other organs, commonly the lungs, liver, spleen, lymph nodes, brain, kidneys, and reproductive organs.

Immunophenotyping
In addition to cell morphology and cytogenetics, immunophenotyping, a laboratory technique used to identify proteins that are expressed on their cell surface, is a key component in the diagnosis of ALL. The preferred method of immunophenotyping is through flow cytometry. In the malignant lymphoblasts of ALL, expression of terminal deoxynucleotidyl transferase (TdT) on the cell surface can help differentiate malignant lymphocyte cells from reactive lymphocytes, white blood cells that are reacting normally to an infection in the body. On the other hand, myeloperoxidase (MPO), a marker for the myeloid lineage, is typically not expressed. Because precursor B cell and precursor T cells look the same, immunophenotyping can help differentiate the subtype of ALL and the level of maturity of the malignant white blood cells. The subtypes of ALL as determined by immunophenotype and according to the stages of maturation. An extensive panel of monoclonal antibodies to cell surface markers, particularly CD or cluster of differentiation markers, are used to classify cells by lineage. Below are immunological markers associated with B cell and T cell ALL.

Cytogenetics
Cytogenetic analysis has shown different proportions and frequencies of genetic abnormalities in cases of ALL from different age groups. This information is particularly valuable for classification and can in part explain the different prognoses of these groups. In regards to genetic analysis, cases can be stratified according to ploidy, a number of sets of chromosomes in the cell, and specific genetic abnormalities, such as translocations. Hyperdiploid cells are defined as cells with more than 50 chromosomes, while hypodiploid are defined as cells with less than 44 chromosomes. Hyperdiploid cases tend to carry a good prognosis while hypodiploid cases do not. For example, the most common specific abnormality in childhood B-ALL is the t(12;21) ETV6–RUNX1 translocation, in which the RUNX1 gene, encoding a protein involved in transcriptional control of hemopoiesis, has been translocated and repressed by the ETV6–RUNX1 fusion protein.

Below is a table with the frequencies of some cytogenetic translocations and molecular genetic abnormalities in ALL.

Classification
French-American-British

Historically, prior to 2008, ALL was classified morphologically using the French-American-British (FAB) system that heavily relied on morphological assessment. The FAB system takes into account information on size, cytoplasm, nucleoli, basophilia (color of cytoplasm), and vacuolation (bubble-like properties). While some clinicians still use the FAB scheme to describe tumor cell appearance, much of this classification has been abandoned because of its limited impact on treatment choice and prognostic value.

World Health Organization

In 2008, the World Health Organization classification of acute lymphoblastic leukemia was developed in an attempt to create a classification system that was more clinically relevant and could produce meaningful prognostic and treatment decisions. This system recognized differences in genetic, immunophenotype, molecular, and morphological features found through cytogenetic and molecular diagnostics tests. This subtyping helps determine the prognosis and the most appropriate treatment for each specific case of ALL.

The WHO subtypes related to ALL are:
 * B-lymphoblastic leukemia/lymphoma
 * Not otherwise specified (NOS)
 * with recurrent genetic abnormalities
 * with t(9;22)(q34.1;q11.2);BCR-ABL1
 * with t(v;11q23.3);KMT2A rearranged
 * with t(12;21)(p13.2;q22.1); ETV6-RUNX1
 * with t(5;14)(q31.1;q32.3) IL3-IGH
 * with t(1;19)(q23;p13.3);TCF3-PBX1
 * with hyperdiploidy
 * with hypodiploidy
 * T-lymphoblastic leukemia/lymphoma
 * Acute leukemias of ambiguous lineage
 * Acute undifferentiated leukemia
 * Mixed phenotype acute leukemia (MPAL) with t(9;22)(q34.1;q11.2); BCR–ABL1
 * MPAL with t(v;11q23.3); KMT2A rearranged
 * MPAL, B/myeloid, NOS
 * MPAL, T/myeloid, NOS

Treatment

The aim of treatment is to induce a lasting remission, defined as the absence of detectable cancer cells in the body (usually less than 5% blast cells in the bone marrow) or the absence of minimal residue disease.

Over the past several decades, there have been strides to increase the efficacy of treatment regimens, resulting in increased survival rates. Possible treatments for acute leukemia include chemotherapy, steroids, radiation therapy, intensive combined treatments (including bone marrow or stem cell transplants), targeted therapy, and/or growth factors.

Chemotherapy
Chemotherapy is the initial treatment of choice, and most people with ALL receive a combination of medications. There are no surgical options because of the body-wide distribution of the malignant cells. In general, cytotoxic chemotherapy for ALL combines multiple antileukemic drugs tailored to each person. Chemotherapy for ALL consists of three phases: remission induction, intensification, and maintenance therapy.

Adult chemotherapy regimens mimic those of childhood ALL; however, are linked with a higher risk of disease relapse with chemotherapy alone. Two subtypes of ALL (B-cell ALL and T-cell ALL) require special considerations when it comes to selecting an appropriate treatment regimen in adults with ALL. B-cell ALL is often associated with cytogenetic abnormalities (specifically, t(8;14), t (2;8), and t(8;22)), which require aggressive therapy consisting of brief, high-intensity regimens. T-cell ALL responds to cyclophosphamide-containing agents the most.

Recent updates on the treatment of adult acute lymphoblastic leukemia (ALL) include advancements in immunotherapy, particularly the use of monoclonal antibodies like blinatumomab and inotuzumab ozogamicin, which target specific cancer cells and are used alongside stem cell transplantation. Additionally, tyrosine kinase inhibitors (TKIs) such as imatinib and dasatinib are incorporated for Philadelphia chromosome-positive ALL, improving treatment outcomes.

Radiation therapy
Radiation therapy (or radiotherapy) is used on painful bony areas, in high disease burdens, or as part of the preparations for a bone marrow transplant (total body irradiation). In the past, physicians commonly utilized radiation in the form of whole-brain radiation for central nervous system prophylaxis, to prevent the occurrence and/or recurrence of leukemia in the brain. Recent studies showed that CNS chemotherapy provided results as favorable but with fewer developmental side effects. As a result, the use of whole-brain radiation has been more limited. Most specialists in adult leukemia have abandoned the use of radiation therapy for CNS prophylaxis, instead using intrathecal chemotherapy.

Biological therapy
Selection of biological targets on the basis of their combinatorial effects on the leukemic lymphoblasts can lead to clinical trials for improvement in the effects of ALL treatment. Tyrosine-kinase inhibitors (TKIs), such as imatinib, are often incorporated into the treatment plan for people with Bcr-Abl1+ (Ph+) ALL. However, this subtype of ALL is frequently resistant to the combination of chemotherapy and TKIs and allogeneic stem cell transplantation is often recommended upon relapse.

Blinatumomab is not only a promising add-on to chemotherapy in infant ALL, it is also a promising standalone therapy in children's.

Immunotherapy
Chimeric antigen receptors (CARs) have been developed as a promising immunotherapy for ALL. This technology uses a single chain variable fragment (scFv) designed to recognize the cell surface marker CD19 as a method of treating ALL.

CD19 is a molecule found on all B-cells and can be used as a means of distinguishing the potentially malignant B-cell population. In this therapy, mice are immunized with the CD19 antigen and produce anti-CD19 antibodies. Hybridomas developed from mouse spleen cells fused to a myeloma cell line can be developed as a source for the cDNA encoding the CD19 specific antibody. The cDNA is sequenced and the sequence encoding the variable heavy and variable light chains of these antibodies are cloned together using a small peptide linker. This resulting sequence encodes the scFv. This can be cloned into a transgene, encoding what will become the endodomain of the CAR. Varying arrangements of subunits serve as the endodomain, but they generally consist of the hinge region that attaches to the scFv, a transmembrane region, the intracellular region of a costimulatory molecule such as CD28, and the intracellular domain of CD3-zeta containing ITAM repeats. Other sequences frequently included are: 4-1bb and OX40. The final transgene sequence, containing the scFv and endodomain sequences is then inserted into immune effector cells that are obtained from the person and expanded in vitro. In trials these have been a type of T-cell capable of cytotoxicity.

Inserting the DNA into the effector cell can be accomplished by several methods. Most commonly, this is done using a lentivirus that encodes the transgene. Pseudotyped, self-inactivating lentiviruses are an effective method for the stable insertion of a desired transgene into the target cell. Other methods include electroporation and transfection, but these are limited in their efficacy as transgene expression diminishes over time.

The gene-modified effector cells are then transplanted back into the person. Typically this process is done in conjunction with a conditioning regimen such as cyclophosphamide, which has been shown to potentiate the effects of infused T-cells. This effect has been attributed to making an immunologic space within which the cells populate. The process as a whole result in an effector cell, typically a T-cell, that can recognize a tumor cell antigen in a manner that is independent of the major histocompatibility complex and which can initiate a cytotoxic response.

In 2017, tisagenlecleucel was approved by the FDA as a CAR-T therapy for people with acute B-cell lymphoblastic leukaemia who did not respond adequately to other treatments or have relapsed. In a 22-day process, the "drug" is customized for each person. T cells purified from each person are modified by a virus that inserts genes that encode a chimaeric antigen receptor into their DNA, one that recognizes leukemia cells.

Relapsed ALL
Typically, people who experience a relapse in their ALL after initial treatment have a poorer prognosis than those who remain in complete remission after induction therapy. It is unlikely that recurrent leukemia will respond favorably to the standard chemotherapy regimen that was initially implemented, and instead, these people should be trialed on reinduction chemotherapy followed by allogeneic bone marrow transplantation. These people in relapse may also receive blinatumomab, as it has shown to increase remission rates and overall survival rates, without increased toxic effects.

Low dose palliative radiation may also help reduce the burden of tumor inside or outside the central nervous system and alleviate some symptoms.

There has also been evidence and approval of use for dasatinib, a tyrosine kinase inhibitor. It has shown efficacy in cases of people with Ph1-positive and imatinib-resistant ALL, but more research needs to be done on long-term survival and time to relapse.

Side effects
Chemotherapies or stem cell transplantations may require a platelet transfusion to prevent bleeding. Moreover, patients undergoing a stem cell transplantation can develop a graft-versus-host disease (GvHD). It was evaluated whether mesenchymal stromal cells can be used to prevent a GvHD. The evidence is very uncertain about the therapeutic effect of mesenchymal stromal cells to treat graft-versus-host diseases after a stem cell transplantation on the all-cause mortality and complete disappear of chronic acute graft-versus-host diseases. Mesenchymal stromal cells may results in little to no difference in the all-cause mortality, relapse of malignant disease and incidence of acute and chronic graft-versus-host diseases if they are used for prophylactic reason.

Supportive therapy
Adding physical exercises to the standard treatment for adult patients with haematological malignancies like ALL may result in little to no difference in mortality, quality of life, and physical functioning. These exercises may result in a slight reduction in depression. Furthermore, aerobic physical exercises probably reduce fatigue. The evidence is very uncertain about the effect on anxiety and serious adverse events.

Gene therapy
Brexucabtagene autoleucel (Tecartus) was approved for the treatment of adults with relapsed or refractory B-cell precursor acute lymphoblastic leukemia in October 2021.

Each dose of brexucabtagene autoleucel is a customized treatment created using the recipient's own immune system to help fight the lymphoma. The recipient's T cells, a type of white blood cell, are collected and genetically modified to include a new gene that facilitates the targeting and killing of the lymphoma cells. These modified T cells are then infused back into the recipient.

Prognosis
Prior to the development of chemotherapy regimens and hematopoietic stem cell transplant, children were surviving a median length of 3 months, largely due to either infection or bleeding. Since the advent of chemotherapy, the prognosis for childhood leukemia has improved greatly and children with ALL are estimated to have a 95% probability of achieving a successful remission after 4 weeks of initiating treatment. People in pediatric care with ALL in developed countries have a greater than 80% five-year survival rate. It is estimated that 60–80% of adults undergoing induction chemotherapy achieve complete remission after 4 weeks, and those over the age of 70 have a cure rate of 5%.

However, there are differing prognoses for ALL among individuals depending on a variety of factors:
 * Gender: Females tend to fare better than males.
 * Ethnicity: Caucasians are more likely to develop acute leukemia than African-Americans, Asians, or Hispanics. However, they also tend to have a better prognosis than non-Caucasians.
 * Age at diagnosis: children 1–10 years of age are most likely to develop ALL and to be cured of it. Cases in older people are more likely to result from chromosomal abnormalities (e.g., the Philadelphia chromosome) that make treatment more difficult and prognoses poorer. Older people are also likely to have co-morbid medical conditions that make it even more difficult to tolerate ALL treatment.
 * White blood cell count at diagnosis of greater than 30,000 (B-ALL) or 100,000 (T-ALL) is associated with worse outcomes
 * Cancer spreading into the central nervous system (brain or spinal cord) has worse outcomes.
 * Morphological, immunological, and genetic subtypes
 * Person's response to initial treatment and longer length of time required (greater than 4 weeks) to reach complete remission
 * Early relapse of ALL
 * Minimal residual disease
 * Genetic disorders, such as Down syndrome, and other chromosomal abnormalities (aneuploidy and translocations)

Cytogenetics, the study of characteristic large changes in the chromosomes of cancer cells, is an important predictor of outcome. Some cytogenetic subtypes have a worse prognosis than others. These include:
 * Person with t(9,22) positive-ALL (30% of adult ALL cases) and other Bcr-abl-rearranged leukemias are more likely to have a poor prognosis, but survival rates may rise with treatment consisting of chemotherapy and Bcr-abl tyrosine kinase inhibitors.
 * A translocation between chromosomes 4 and 11 occurs in about 4% of cases and is most common in infants under 12 months.

 * Hyperdiploidy (>50 chromosomes) and t(12;21) are good prognostic factors and also makeup 50% of pediatric ALL cases.

Unclassified ALL is considered to have an intermediate prognosis risk, somewhere in-between the good and poor risk categories.

Epidemiology
Acute lymphoblastic leukemia affected about 876,000 people and resulted in 111,000 deaths globally in 2015. It occurs in both children and adults with highest rates seen between the ages three and seven years. Around 75% of cases occur before the age of 6 with a secondary rise after the age of 40. It is estimated to affect 1 in 1500 children.

Accounting for the broad age profiles of those affected, ALL newly occurs in about 1.7 per 100,000 people per year. Acute lymphoblastic leukemia represents approximately 20% of adults and 80% of childhood leukemias, making it the most common childhood cancer. Although 80 to 90% of children will have a long term complete response with treatment, it remains the leading cause of cancer-related deaths among children. 85% of cases are of B-cell lineage and have an equal number of cases in both males and females. The remaining 15% of T-cell lineage have a male predominance.

Globally, ALL typically occurs more often in Caucasians, Hispanics, and Latin Americans than in Africans. In the US, ALL is more common in children from Caucasian (36 cases/million) and Hispanic (41 cases/million) descent when compared to those from African (15 cases/million) descent.

Pregnancy
Leukemia is rarely associated with pregnancy, affecting only about 1 in 10,000 pregnant women. The management of leukemia in a pregnant woman depends primarily on the type of leukemia. Acute leukemias normally require prompt, aggressive treatment, despite significant risks of pregnancy loss and birth defects, especially if chemotherapy is given during the developmentally sensitive first trimester.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: Acute lymphoblastic leukemia


text:
Joseph Saidu Momoh

Major General Joseph Saidu Momoh, OOR, OBE (January 26, 1937 – August 3, 2003) was a Sierra Leonean politician and military officer who served as the second President of Sierra Leone from November 1985 to 29 April 1992.

Momoh was a member of the Limba ethnic group and briefly began a career in civil service before joining the military in 1956. Following the rise to power of Siaka Stevens, Momoh was appointed force commander in 1971, promoted to major-general in 1983, and became the secretary general of the country's sole legal party, the All People's Congress in 1985.

Stevens' retired later that year, and was succeeded by Momoh after a presidential election with himself as the only candidate. He inherited a deteriorating economy, but made significant improvements in combatting corruption. In foreign policy, he enjoyed positive relations with the United States and the United Kingdom. In 1991, the Revolutionary United Front (RUF) rebel group incited the Sierra Leone Civil War with the goal of overthrowing him. Later that year, he introduced a new constitution allowing for a multiparty system. Despite this, he was overthrown in a coup d'état the following year led by Valentine Strasser, who cited his government's unpaid salaries and poor logistical supply to frontline soldiers fighting against the RUF as motives. He fled into exile in Guinea, where he died in 2003, one year after the end of the war.

Early life
Joseph Saidu Momoh was born on January 26, 1937, in Binkolo, Bombali District in the Northern Province of British Sierra Leone to Limba parents. In the early 1940s, his family moved to Freetown, ultimately settling in Wilberforce. His family were Christians.

From 1951 to 1955, he was educated at the West African Methodist Collegiate School. Momoh was very athletic and enjoyed playing tennis, basketball and volleyball. He played competitive football for the Young Stars FC at Makeni and Blackpool FC.

He completed his education at the Government Clerks School, Technical Institute.

Civil service
In 1956, Momoh worked as third grade clerk in Sierra Leone's civil service. He resigned from this position in 1958 in order to join the armed forces.

Military career
Momoh's military career began in 1958, when he enlisted in the Royal West African Frontier Force (RWAFF) as a private. He trained at the Regular Officers Training School in Ghana and the Nigerian Military Training Academy. He then travelled to the United Kingdom to train at the School of Infantry at Hythe and the Mons Officer Cadet School in Aldershot.

He was commissioned as second lieutenant in the Royal Sierra Leone Military Forces in 1963. He was elevated to the rank of major and given command at Moa Barracks, Kailahun.

In 1969, Momoh became lieutenant colonel and commanding officer of the First Battalion. A year later, he was promoted to the rank of Colonel.

He was appointed deputy force commander in 1971 by President Siaka Stevens, after a coup attempt by Brigadier John Amadu Bangura. Momoh succeeded Bangura as force commander in November 1971.

In 1974, he was appointed minister of state with cabinet status. He became major-general in 1983.

President of Sierra Leone
In 1985, Momoh became secretary-general and head of the All People's Congress (APC). The same year, he succeeded President Siaka Stevens by becoming the only candidate in a one-party election in the form of a referendum on 8 October 1985.

Momoh became the second President of Sierra Leone and he served from November 28, 1985, to April 29, 1992.

Momoh declared a state of economic emergency early in his rule, granting himself greater control over Sierra Leone's economy, but he was not regarded as a dictator. Instead, his people viewed him as far too weak and inattentive to the affairs of state, allowing his notoriously corrupt advisors to manipulate matters behind the scenes.

Momoh had inherited a disintegrating economy from his predecessor and he was unable to stop the trend. The country's currency decreased in value. Sierra Leone reached the point under President Momoh where it could not afford to import gasoline and fuel oil, and the country went without electricity for months at a time.

Momoh had also inherited a system that was rife with corruption and the instability which corruption led to. Momoh took huge strides to root out graft, cronyism, embezzlement, influence peddling and extortion from within Sierra Leone's government. International observers considered him mostly successful in these endeavors. This led to him forming a good relationship with British Prime Minister Margaret Thatcher and American President Ronald Reagan, who were encouraged by advisors to meet with Momoh and form a good partnership with him as a way of welcoming Sierra Leone out of the instability it had fallen into for so much of the 1970s and 1980s. Both leaders increased aid to Sierra Leone and increased governmental cooperation between their governments and that of Momoh's administration throughout 1987 and early 1988.

1987 treason trial
On 23 March 1987, police reported that a group of conspirators was plotting to assassinate Momoh and stage a coup d'état after they raided a house in Freetown and discovered a cache of weapons, including rocket launchers.

James Bambay Kamara, the Inspector General of the Sierra Leone Police, gave the order to arrest First Vice President Francis Minah, G.M.T. Kaikai, Jamil Sahid Mohamed and fifteen others.

Minah was a personal friend of Momoh and while he did not personally believe that Minah was involved in the plot, he did not want to oppose Inspector General Kamara. Momoh did not intervene on behalf of Minah.

The treason trial went on for five months until October 1987 when the jury delivered a guilty verdict. The former First Vice President and 17 others were convicted of treason and sentenced to death. Jamil Sahid Mohamed escaped to Lebanon where he remained in exile. They were executed on warrants signed by Momoh. A team of international oberservers from Norway, Sweden, Switzerland, Algeria and South Korea all concurred that the trial was justified, and was not politically motivated.

The 1991 Persian Gulf War
Under Momoh's leadership, Sierra Leone joined the coalition of nations that opposed Saddam Hussein's occupation of Kuwait.

The SCIPA Group
The SCIPA Group was an Israeli mineral company led by Nir Guaz that arrived in Sierra Leone in 1989. SCIPA bought its way into Momoh's favor by providing the government with loans and enabling Sierra Leone to enter into negotiations with the International Monetary Fund. On Christmas Eve 1989, Momoh had Guaz arrested, charged with economic sabotage and deported from Sierra Leone.

In September 1991, after the start of the Sierra Leone Civil War, Momoh ushered in a new constitution which dismantled the one-party state established in 1978 and instituted multiparty democracy. He also played a great part in dissolving tribalism. He was congratulated on this by British Prime Minister John Major and American President George H. W. Bush, who both declared these reforms as "important steps towards democratization" and "essential steps forward." Momoh said John Major had proven to be a "genuine friend of Sierra Leone" and he referred to George H.W. Bush as a "great leader of the world."

Military coup
Unfortunately, Momoh's efforts at reform came too late to rescue Sierra Leone from chaos. He was overthrown in a military coup staged by Valentine Strasser, a 25-year-old army captain, in April 1992.

In April 1992, a group of young soldiers marched to Freetown from the war front where they had been fighting the Revolutionary United Front (RUF) led by Foday Sankoh. Incensed by terrible working conditions, unpaid salaries and a lack of government support they staged a coup d'état.

On 29 April 1992, the soldiers, led by Captain Valentine Strasser announced the military coup on the radio.

Momoh fled to Guinea and sought political asylum.

Exile and death
Momoh was granted political asylum in neighboring Guinea by President Lansana Conté. He took up residence in a mansion in Nongo Tadi, Conakry. Momoh died on August 2, 2003, at the age of 66, Momoh spent the last years of his life as a guest of the military government in Guinea. Ironically, Foday Sankoh had died a few days earlier.

Honours
In 1971, Momoh was made an Officer of the Most Excellent Order of the British Empire. He was decorated as an Officer of the Order of the Rokel in 1974 by President Siaka Stevens.

 * 🇸🇱 Sierra Leone: Order of the Rokel (1974)
 * 🇬🇧 United Kingdom: Order of the British Empire (1971)

title: Joseph Saidu Momoh


text:
Loughgall F.C.

Loughgall Football Club is a semi-professional Northern Irish football club currently playing in the NIFL Premiership. The club has been managed by Dean Smith since 2016.

History
The club, founded in 1967, is situated in the village of Loughgall, near Armagh in County Armagh and they play their home games in the village at Lakeview Park. The club was accepted into the old Irish League B Division in 1991, having played largely at junior level prior. Alfie Wylie is their longest serving manager, being in charge from 1986 to 1999. In the 1996–97 season, the club would have a good season, notably defeating Cliftonville in the League Cup, winning the Bob Radcliffe cup and reaching the semi-final of the Irish Cup. In the space of four years, the Lakeview Park side would win four consecutive B Divisions however would not be granted election to the 1st Division, being overlooked for other, arguably bigger clubs further down the league table.

First Premiership foray, Championship era and Premiership return (2004-)
They achieved senior status in 2004 on promotion to the Irish Premier League, but reverted to intermediate status upon relegation in 2007. In 2007, under the management of Niall Currie, the club had their most successful season, winning the first division, Bob Radciffe, Mid Ulster Cup, Intermediate Cup and Carnegie League Cup. The villagers would win the league again in 2009–10 but would not be promoted. On 3 March 2018, Loughgall defeated Glenavon 2–1 to reach the semi-final of the Irish Cup for the first time since 1997.

In April 2023, the club would return to the NIFL Premiership for the first time since 2007, following a 3–1 win away to Dundela. In being promoted, the village of Loughgall would become the smallest settlement, with a population of 283, to have a top flight team in Europe. The club would start their season away to Newry City. The club would perform incredibly well in the top flight, securing a notable victory over champions Larne, and finishing well clear of the relegation zone. The villagers plaudits would see manager Dean Smith receive Manager of the Year from the NIFWA.

Managerial history

 * Noel Willis (1967–70)
 * George Willis (1970–76)
 * Sam Robinson (1977–81)
 * Raymond Nesbitt (1983–84)
 * Willie Forbes (1984–85)
 * Alfie Wylie (1986–99)
 * Alan Fraser (1999)
 * Ronnie Cromie (1999–01)
 * Jimmy Gardiner (2001–06)
 * Shane Reddish (2006–07)
 * Niall Currie (2007–Feb 2011)
 * Colin Malone (May 2011–Aug 2013)
 * Gary McKinstry (Aug 2013–Dec 2013)
 * Brian Adair (Dec 2013–Dec 2014)
 * Noel Mitchell (Jan 2015–May 2015)
 * Stephen Uprichard and Steven Hawe (May 2015–November 2016)
 * Dean Smith (November 2016-)

Senior honours
(Note: The NIFL Championship gained senior status in 2016, having previously been an intermediate competition.)
 * NIFL Championship: 1
 * 2022–23
 * Mid-Ulster Cup: 3
 * 2003–04, 2007–08, 2019–20

Intermediate honours

 * Irish League B Division/First Division /IFA Intermediate League/IFA Championship: 7
 * 1994–95, 1995–96, 1996–97, 1997–98, 2003–04, 2007–08, 2009–10
 * Irish Intermediate Cup: 2
 * 1997–98, 2007–08
 * IFA Intermediate League Cup: 1
 * 2007–08
 * Bob Radcliffe Cup: 12
 * 1978–79, 1996–97, 1998–99, 1999–00, 2001–02, 2002–03, 2003–04, 2007–08, 2008–09, 2009–10, 2012–13, 2014–15

title: Loughgall F.C.


text:
George Monckton-Arundell, 8th Viscount Galway

George Vere Arundel Monckton-Arundell, 8th Viscount Galway, (24 March 1882 – 27 March 1943) was a British politician. He served as the fifth Governor-General of New Zealand from 1935 to 1941.

Early life
George Vere Arundell Monckton-Arundell Galway was born on 24 March 1882. His parents were George Monckton-Arundell, 7th Viscount Galway and Vere Gosling. He had one sibling: Violet Frances Monckton-Arundell (wife of married Lt.-Col. Geoffrey Henry Julian FitzPatrick, son of Edward Skeffington-Smyth).

He received his education at a preparatory school in Berkshire before attending Eton College (1895–1900) and Christ Church College, University of Oxford (1900–1904). He read Modern History and graduated with Bachelor of Arts and took the Master of Arts subsequently (this degree at Oxford, Cambridge and Dublin is an elevation in rank and not a postgraduate qualification).

Lord Galway succeeded his father to the family's Irish peerage in 1931.

Military career
Monckton-Arundell was commissioned a second lieutenant in the Nottinghamshire (Sherwood Rangers) Yeomanry on 1 January 1900, and promoted to lieutenant on 11 June 1902. In 1904, he joined the First Life Guards, the senior regiment of the British Army that makes up the Household Cavalry, where he rose to the rank of colonel. During the First World War he was appointed as adjutant general and quartermaster general. He was of the Royal Artillery (1933–35). In 1933 he was appointed Colonel Commandant of the Honourable Artillery Company (HAC) until 1935, when he relinquished it on appointment as Governor-General of New Zealand. Upon retirement from his post as governor-general he returned as Colonel Commandant of the HAC until his death. He was also appointed Honorary Colonel of the 7th (Robin Hood) Battalion, Sherwood Foresters (later 42nd (The Robin Hoods, Sherwood Foresters) Anti-Aircraft Battalion, Royal Engineers) in 1933.

Political ambitions
In 1910, Monckton-Arundell attempted to follow his father into the House of Commons. He contested the Scarborough constituency in the January and December elections of 1910, but was unsuccessful both times.

Governor-General of New Zealand
Viscount Galway was Governor-General of New Zealand from 12 April 1935 to 3 February 1941. His military background made an impression with cabinet ministers of the time. His term was twice extended because of the Second World War. Viscount Galway and his wife received numerous gifts during his time as governor-general. Some were returned to New Zealand around the time of the sale of the family house Serlby Hall, and were donated to the Museum of New Zealand Te Papa Tongarewa in 1980.

Galway was a freemason. During his term as governor-general, he was also Grand Master of the Grand Lodge of New Zealand. In the 1937 Coronation Honours, he was appointed a member of the Privy Council.

Later years
Upon his return to England, Galway held the honorary post of Deputy Lord Lieutenant of Nottinghamshire under the 7th Duke of Portland.

Personal life
Viscount Galway married Lucia Margaret White, daughter of the 3rd Baron Annaly, in 1922. They had four children:

 * Mary Victoria Monckton (1924–2010), who married David Henry Fetherstonhaugh, son of Lt.-Col. Timothy Fetherstonhaugh, in 1947. They divorced in 1972 and she married Maj. Robert Patricius Chaworth-Musters, son of Col. John Neville Chaworth-Musters, in 1974.
 * Celia Ella Vere Monckton (1925–1997), who married Sir Joshua Rowley, 7th Baronet, son of Lt.-Col. Sir Charles Rowley, 6th Baronet, in 1959.
 * Isabel Cynthia Monckton (b. 1926), who married John King, Baron King of Wartnaby, son of Albert John King, in 1970.
 * Simon George Robert Monckton-Arundell (1929–1971), who married Lady Theresa Jane Fox-Strangways, daughter of Harry Fox-Strangways, 7th Earl of Ilchester, in 1953.

He died suddenly on 27 March 1943 in Blyth.


text:
Frank W. Mondell

Frank Wheeler Mondell (November 6, 1860 – August 6, 1939) was a United States representative of Wyoming.

Biography
Born in St. Louis, Missouri, he was educated in the public schools. For many years he was engaged in farming, stock-raising, and railroad construction. He settled in the Wyoming Territory in 1887, was mayor of Newcastle from 1888 to 1895, and served in Congress from 1895 to 1897 and once again from 1899 to 1923. He was majority leader in the Sixty-sixth and Sixty-seventh Congresses on the floor of the House and took a prominent part in framing the legislation passed by that body. He took an active part in all the Republican conventions from 1902 to 1924 when he was a chairman at the 1924 Republican National Convention. He died in 1939 in Washington, D.C.

title: Frank W. Mondell


text:
Category:Galois theory

In mathematics, Galois theory is a branch of abstract algebra.

At the most basic level, it uses permutation groups to describe how the various roots of a given polynomial equation are related to each other. This was the original point of view of Évariste Galois.

The modern approach to Galois theory, developed by Richard Dedekind, Leopold Kronecker and Emil Artin, among others, involves studying automorphisms of field extensions.

title: Category:Galois theory


text:
Talk:Gharu

I think this needs to be merged with the Chinese language articles, but I am definitely not qualified to do so. Making it a stub for now. (Is the invasion of Western culture thing factual, or NPOV?) --Ardonik 09:19, Jul 17, 2004 (UTC

This Article is Fake
The information inside is fake

title: Talk:Gharu


text:
Bartolomeo Montagna

Bartolomeo (or Bartolommeo) Montagna (,, ; 1450?– 11 October 1523) was an Italian Renaissance painter who mainly worked in Vicenza. He also produced works in Venice, Verona, and Padua. He is most famous for his many Madonnas and his works are known for their soft figures and depiction of eccentric marble architecture. He is considered to be heavily influenced by Giovanni Bellini, in whose workshop he might have worked around 1470. Benedetto Montagna, a productive engraver, was his son and pupil and active until about 1540. He was mentioned in Vasari's Lives as a student of Andrea Mantegna but this is widely contested by art historians.

Life
He was born Bartolomeo Cincani and later changed his name to Bartolomeo Montagna. The first known written record of his existence is from 1459 and list him as a minor. The first known documentation of him as an adult is in 1480 as a witness of a will. Differences in two documents regarding his father's property from 1467 and 1469 imply he became an adult between those two years. Because of the lack of formal documentation of his birth and confusion on the age of legal adulthood in Vicenza at that time, there is much debate as to his actual birthdate. Some scholars have agreed on close to 1450 while others place him closer to 1453-1454.

His family originated in Brescia, Italy and later moved to Biron around 1450 before settling in Vicenza sometime by 1460. His brother, Baldissera, was a goldsmith. For most of his life through his death he was a resident of Vicenza and lived in a house he purchased directly across from the Church of San Lorenzo in 1484. From 1469-1475 Montagna was in Venice before returning to Vicenza and starting his career as a painter. In 1509, he moved from Vicenza to Padua likely due to the war in Vicenza, and remained there until 1514.

The identity of his wife is unknown, but they had three sons. One of his sons, Benedetto Montagna, was also an artist famous for his engravings. His other two sons, Filippo and Paolo are mentioned in some contracts but absent from his will. Bartolomeo Montagna died on October 11, 1523. He left the majority of his possessions and his practice to his son, Benedetto.

Career
Because the birthdate of Montagna is unknown, there is also debate as to when exactly he began his career and how old he was at the time. Throughout his career, his works are characterized by a simple, laconic nature. His figures often appear solemn and plastic in form.

Early works (1480s–1499)
His first known documented commission was for two paintings for the Scuola Grande di San Marco in Venice. The paintings were contracted to depict the Deluge (flood myth) and another scene from Genesis, however their final status is unknown as they were destroyed in a fire in 1485. The next known record of Montagna's work is for an altarpiece in the hospital of Vicenza, of which the current whereabouts are also unknown.

His first extant painting is from September 1487 (as inscribed on the back of the work) for a painting of The Virgin and Child with Saint Sebastian and Roch. A small work intended for private use, it depicts the figures in a marble enclosure with a Vicentine landscape in the background. This painting also shows Montagna's first known use of trachyte marble, a unique texture of marble, which is seen in most of his works. Around this time, he was also commissioned to do the high altarpiece of San Bartolomeo of Vicenza, of which the exact date is often debated. This shows influences from multiple works of Giovanni Bellini located Venice that are also undated. In 1490 he painted an altarpiece for the Certosa di Pavia showing the Virgin and Child Enthroned with Saint John the Baptist and Jerome. In 1491 he painted the altarpiece, the semi-dome, and other wall frescos for the oratory dedicated to St. Blaise at the church of Santi Nazaro e Celso in Verona. The semidome depicts St. Blaise with companions and the walls depict other scenes from the legends of St. Blaise. These works are noted for their realistic gaunt figures. From 1497-1499 he was paid monthly to work on an altarpiece for the Squarzi family. His final payment was in the form of a piece of property which he kept until 1503. This was located in a chapel in the Church of San Michele and entitled Madonna and Child Enthroned with Saints. The outlines of this painting are very bold compared to his other works and it features detailed drapery.

His early works are generally characterized by the use of trachyte marble architecture and a particular positioning of the Virgin's hand, showing the middle and ring-finger touching and widely separated from the index and pinky finger. They also are usually distinguished by their symmetry, organization, equally distributed light, and plastic-like quality to the figures.

Maturity (1499–1507)
An altarpiece in San Michele at Vicenza (Virgin and Child with Four Saints and Music-making Angels) from 1499 is considered by many art historians to be a turning point in Montagna's style. This development in his style is characterized by change in tone and use of warmer and richer colors. This particular painting depicts an outdoor scene and is a variation of a work by Giovanni Bellini. Around this time he also completed another Bellinesque altarpiece for San Bartolomeo in Vicenza, Madonna and Child with Saint Monica and Mary. In 1500 Montagna completed a Pieta in the Church of the Madonna del Monte. The painting depicts the Virgin Mary holding Christ's dead body and Mary Magdalen kissing his feet. They are flanked by St. John and St. Joseph. This features dull color and the use continuous lines as a compositional element, a growing trend in renaissance paintings. This painting is characterized by a less rigid form than Montagna's previous works. In the same year he also completed the Virgin and St. Joseph Adoring Christ in the Church of Orgiano. This depicts the infant Jesus sitting upright, flanked by the soft figures of the Virgin and St. Joseph.

Around this time the Bishop of Vicenza, Cardinal Battista Zeno, also commissioned Montagna to create a painting of the Virgin and Child with Eight Saints for the Cathedral of Vicenza. This work was lost after 1779 but is documented in multiple records. In 1504 Montagna travelled to Verona to complete frescos for the choir and vaults of the Cappella di San Biagio depicting many scenes of St. Blaise. Due to the success of this work, in 1507 he was commissioned to do the altarpiece for the Church of San Sebastiano in Verona, depicting the Virgin and Child Enthroned with St. Sebastian and St. Jerome. This work is characterized by brightly colored architecture, an oddly shaped throne, and elaborate outfits. After returning to Vicenza, Montagna completed a painting of Madonna between Saint Anthony and John the Evangelists for San Lorenzo. This is often considered the height of Montagna's paintings. Montagna's style at this time is noted for its eccentric qualities despite the trend of a more mellow style that was adopted by his peers. His paintings frequently featured bright colors, decorative architecture, detailed drapery, and sharp angles. Despite the bright colors and sharp angles, the human figures pictured in them were often fuller and softer.

Late works (1507–1522)
The last known dated painting of Montagna's is from 1507 although there are many paintings that have been dated by scholars after this time. Paintings from the last 15 years of his life are often considered a decline from the height of his career. His style was noticeably different in the years he spent in Padua (1509-1514), showing more landscapes, sunsets and warm colors incorporated with his signature architecture look. His style was more inconsistent, but often included fuller figures, deep shadows and less angular details. Examples of works Montagna's time in Padua featuring this style are the Exhumation of St. Anthony for the Scuola di San Antonio and the Virgin and Child with Four Saints in Saint Maria in Vanzo. In 1517 Montagna returned to Vicenza. In 1522 he was commissioned by the Scuola di San Giuseppe to paint an altarpiece for Cologna Veneta. This depicts the Virgin, Child, 3 shepherds, and St. Joseph and St. Sebastian.

Influences
There is no written record of Montagna's training as a painter but there are many speculations and debates about his influences. In the second edition of Vasari's Lives, Vasari mentions that Montagna learned to draw from Andrea Mantegna but does not specify if he did this as an actual pupil or if he just privately studied Mantegna's works. It is generally agreed on that Montagna was influenced by Giovanni Bellini, Antonello da Messina, and Alvise Vivarni. It is generally accepted that Bellini had the most prolific influence on Montagna's works, but to whether he was actually a pupil of any of these artists and in what order is highly debated. Montagna's use of intricate and angular drapery is linked to the works of Vivarni. His works inspired by Antonello are characterized by rounded forms whereas those inspired by Bellini feature thinner and sharper figures. His transition to use of brighter and richer colorings later in life are also attributed to Bellini's influence. A drawing with a previously mistranslated note was attributed to Montagna, but has now been identified as a gift from Bellini to Montagna. This still however does not confirm Bellini as Montagna's master as it was common among artists of the renaissance to gift each other drawings. Many of Montagna's paintings borrow compositions from these mentioned artists, a common practice in Italian renaissance painting.

List of works
Permanent collections that hold works by Bartolomeo Montagna

 * Madonna and Child (c. 1490-1510) - Rijksmuseum, Amsterdam
 * Madonna and Child (c. 1485-1523) - Walters Art Museum, Baltimore
 * Virgin Enthroned, with the Child Jesus and Saint Jerome and John the Baptist (c. 1490) - Museo della Certosa di Pavia
 * Madonna and Child; Madonna and Child - Musei Civici, Belluno
 * Virgin, Jesus and Several Saints; Virgin and Child; St Jerome; St Sebastian and St Roch - Accademia Carrara, Bergamo
 * Virgin Enthroned, with the Child Jesus and Two Saints (1515); Resurrected Christ and Mary Magdalene - Berlin State Museums, Berlin
 * Head and Hands of a Praying Madonna - Bremen
 * Saint Sebastian (pen and brown ink/paper) - Fitzwilliam Museum, Cambridge
 * Virgin and the Child Jesus on a Throne - Glasgow
 * The Virgin and Child with a Saint (c. 1483-1499) - Walker Art Gallery, Liverpool
 * Holy Family (c. 1500, oil/wood)- Courtauld Gallery, London
 * Holy Family (c. 1500, oil/wood)- Pavia Civic Museums, Pavia
 * Saint Zeno, Saint John the Baptist and a Female Martyr (c. 1495, oil/wood/canvas); The Virgin and Child (c. 1485-1487, tempera/wood);The Virgin and Child (c. 1504-1506, oil/wood/canvas) - National Gallery, London
 * Saint Jerome; Saint Paul - Museo Poldi Pezzoli, Milan
 * Virgin with the Child and Saints (1498, oil/canvas); Saint Jerome (c. 1500, oil/canvas) - Pinacoteca di Brera, Milan
 * Madonna Adoring the Child (oil/wood); Saint Justina of Padua (c. 1490-1500, fragment oil/wood) - Metropolitan Museum of Art, New York City
 * Saint Jerome in Penitence - National Gallery of Canada, Ottawa
 * Christ Carrying the Cross (c. 1503, oil/wood); The Incident in the Story of the Vestal Claudia (tempera/wood), The Marriage of Antiochus and Stratonice (c. 1490-1495, tempera/wood), The Virgin and Child (c. 1480-1489, tempera/wood) - Ashmolean Museum of Art and Archaeology - University of Oxford, Oxford
 * Ecce Homo (c. 1500, oil/wood); Three Children Playing Musical Instruments - Louvre, Paris
 * Adoration of the Child Jesus - Musée des Beaux-Arts, Strasbourg
 * Landscape with Castle (c. 1495-1505, oil/wood) - National Museum of Western Art, Tokyo
 * Jesus between Saint Roch and Saint Sebastian; Madonna with Saint Sebastian and Saint Jerome - Venice
 * Madonna and Child with Saint Joseph (c. 1520, tempera/canvas) - Museo Correr, Venice
 * Saint Peter Blessing with a Donor (c. 1505, oil/wood) - Gallerie dell'Accademia, Venice
 * Madonna and Child - Musei Civici, Verona
 * Maria Vergine col Bambino tra le sante Lucia e Maddalena (altar painting) - Vicenza Cathedral, Vicenza
 * Madonna with the Child and Saint John; Madonna and Child; Madonna with Four Saints (oil/wood); Nativity; Madonna with Saint John and Saint Jerome; Christ Bearing the Cross (oil/wood); Madonna; Holy Family; Madonna with the Child and Saint John as a Child; Madonna and Child with Saint Monica and Mary (c. 1482, oil/wood) - Musei Civici, Vicenza
 * Madonna and Child (c. 1490, oil/wood) - National Gallery of Art, Washington, D.C.
 * The Virgin and Child (tempera/panel) - Worcester Art Museum, Worcester, MA

title: Bartolomeo Montagna


text:
Lurgan Celtic F.C.

Lurgan Celtic Football Club is a Northern Irish intermediate football club based in Lurgan, County Armagh, that currently plays in the Mid-Ulster Football League Junior Division 1. The club was founded 1903 & reformed in 1970, and plays in a strip based on Scottish team Celtic. On 15 August 2019, Lurgan Celtic announced that its senior side would withdraw from the NIFL and implement new youth academy structures, with a view to restarting its senior teams for the 2020–21 season. Lurgan Celtic resumed senior football activities at the bottom of the Mid-Ulster Football League pyramid, upon the commencement of the 2020–21 season.

History
A club by the name of Lurgan Celtic was originally formed in 1903, with the obvious slant of aiming towards the Roman Catholic community of the town, adopting the name and colours of Glasgow Celtic, a popular club among the Irish Catholics population of Glasgow and the west of Scotland. At the time it was a bold move to try and break into the world of football. The Gaelic Athletic Association was in its early stages and was keen to promote Gaelic sports and football in particular, perceived as "foreign", was discouraged. A change in attitudes gradually took hold in the early 1970s and Lurgan Celtic was reborn to try its luck again in the local football scene, rising to become one of the strongest clubs in the Craigavon area. The club won several honours in Mid-Ulster Football League Divisions & Cup competitions in various age groups, including several senior honours in that league, during the 1970s, 1980s and 1990s.

Irish Football League membership remained elusive during these years, partly due to the presence of Glenavon down the road at a time when the IFA was trying to reach out to new footballing towns. There was also a suggestion that it was the club's clearly Nationalist stance as they pushed for membership of what was considered a predominantly Unionist league that stood in their way. So strongly was this felt that the club joined forces with Belfast club Donegal Celtic, another club that took its name and kit from the Glasgow club, and threatened the League with legal action to gain membership. The restructuring of the league in the early part of the 21st century eventually resulted in both Celtic clubs gaining admission to the Irish Football League Second Division for the 2002–03 season.

In 2003 the club closed their town centre ground Grattan Park and relocated to share Oxford United's ground on the edge of Lurgan at Knockramer Park, which offered better facilities.

Promotion to the Intermediate League First Division was achieved in 2006–07, but in 2008 the club failed to meet the criteria for a place in the new IFA Championship, and found itself in the IFA Interim League for the 2008–09 season. They successfully made the necessary improvements to gain admission to the newly formed third tier, IFA Championship 2, for the 2009–10 season. After seven seasons of consolidation in Championship 2 with occasional flirts with relegation, Celtic surged to the 2014–15 NIFL Championship 2 title, achieving promotion to the national second tier, Championship 1.

On the back of their title success the previous season, Celtic pulled off one of the local game's biggest giant-killing acts of the 21st century. After reaching the quarter-finals for the first time ever in the 2015–16 Irish Cup, Celtic were drawn to face senior NIFL Premiership side and beaten Irish Cup finalists the previous year, Portadown away at Shamrock Park. Celtic stunned the Ports by taking a 2–0 lead after 54 minutes. However, Portadown came back into the match after 70 minutes with two goals of their own to level the score at 2–2. However, Lurgan Celtic had the last say, and scored a last-minute penalty to win 3–2 and cause a major upset by eliminating Portadown, and reaching the semi-finals of the cup for the first time in the club's history. The match was also notable as Portadown's final match under the management of Ronnie McFall. After the match, the Portadown manager resigned, ending his reign at the club after 29 years. In the Irish Cup semi-final they were defeated 3–0 by Linfield with Aaron Burns scoring a hat-trick.

Despite the achievement of reaching the Irish-Cup semi-finals, manager Colin Malone resigned at the end of the 2016-17 season and the club endured a period of instability. The appointment of Brendan Shannon as Celtic player-manager could not prevent a serious downturn in results, and Shannon left halfway through the 2017-18 season, to be succeeded by Frankie Wilson. By this point, relegation to the third tier had become an inevitability; Celtic finished the season 20 points adrift of 11th-placed Dergview.

Life in the NIFL Premier Intermediate League started with another managerial change, with former Glenavon, Spurs and Northern Ireland winger Gerard McMahon taking the reins at Knockramer Park. This, however, failed to stem the club's decline, as they finished second-bottom of the division, on 19 points.

A 17-year spell in the Northern Ireland Football League ended on 15 August 2019, as the club announced its intention to withdraw from the Premier Intermediate League, with a view to reforming youth structures and resuming senior football activities for the 2020–21 season. It was announced on 29 June 2020 that Lurgan Celtic's application to join the Mid-Ulster Football League was accepted, and the club will play in the MUFL Junior Division 3 for the 2020–21 season.

Intermediate honours

 * NIFL Championship 2 (tier 3): 1
 * 2014–15
 * Mid-Ulster Football League: 1
 * 1997–98
 * Northern Ireland Intermediate League: 1
 * 2000–01
 * Bob Radcliffe Cup: 2
 * 1997–98, 2011–12
 * Challenge Cup: 1
 * 1997/98
 * Premier Cup: 1
 * 1993/94
 * Alan Wilson Cup: 1
 * 1992/93
 * Bass Bowl: 1
 * 1995/96

Junior honours

 * Irish Junior Cup: 1
 * 1990–91
 * Mid-Ulster Shield: 1
 * 1971/72
 * Parley Jackson Cup: 1
 * 1987/88
 * Alexandra Cup: 2
 * 1991/92, 1992/93
 * Foster Cup: 1
 * 1970/71
 * 2nd Division Cup: 1
 * 1993/94
 * John Magee Cup: 1
 * 2022
 * Gerald Kennedy Cup 2
 * 2007, 2022
 * MUFL Division 1: 1
 * 1922/23
 * MUFL Division 3: 1
 * 1981/82
 * MUFL Division 4: 1
 * 1979/80
 * MUFL Division 5: 1
 * 1969/70

title: Lurgan Celtic F.C.


text:
Luc Montagnier

Luc Montagnier (, ; 18 August 1932 – 8 February 2022) was a French virologist and joint recipient, with Françoise Barré-Sinoussi and Harald zur Hausen, of the 2008 Nobel Prize in Physiology or Medicine for his discovery of the human immunodeficiency virus (HIV). He worked as a researcher at the Pasteur Institute in Paris and as a full-time professor at Shanghai Jiao Tong University in China.

In 2017, Montagnier was criticised by other academics for using his Nobel prize status to "spread dangerous health messages outside of his field of knowledge". During the COVID-19 pandemic, Montagnier promoted the conspiracy theory that SARS-CoV-2, the causative virus, was deliberately created and escaped from a laboratory. Such a claim has been rejected by other virologists.

Early life and education
Montagnier was born in Chabris in central France. Montagnier became interested in science as a teenager. He studied science at the University of Poitiers, France, and then became an assistant in the Faculty of Sciences at Sorbonne University, where he obtained a PhD.

Career
In 1960, Montagnier moved to Carshalton, UK as a postdoctoral fellow at the now defunct Virus Research Unit of the Medical Research Council (United Kingdom). In 1963, he moved to the Glasgow Institute of Virology. He developed a soft agar culture medium to culture viruses.

From 1965 until 1972 he was Laboratory Chief at the Institut Curie, then moved to the Institut Pasteur working on the effects of interferon on viruses.

Discovery of HIV
In 1982, Willy Rozenbaum, a clinician at the Hôpital Bichat hospital in Paris, asked Montagnier for assistance in establishing the cause of a mysterious new syndrome, AIDS (known at the time as "gay-related immune deficiency" or GRID). Rozenbaum had suggested at scientific meetings that the cause of the disease might be a retrovirus. Montagnier and members of his group at the Pasteur Institute, notably including Françoise Barré-Sinoussi and Jean-Claude Chermann, had extensive experience with retroviruses. Montagnier and his team examined samples taken from Rozenbaum's AIDS patients in 1983 and found the virus that would later become known as HIV in a lymph node biopsy. They named it "lymphadenopathy-associated virus", or LAV, since it was not then clear that it was the cause of AIDS, and published their findings in the journal Science on 20 May 1983.

A team led by Robert Gallo of the United States published similar findings in the same issue of Science and later confirmed the discovery of the virus and presented evidence that it caused AIDS. Gallo called the virus "human T-lymphotropic virus type III" (HTLV-III) because of perceived similarities with HTLV-I and -II, which had previously been discovered in his lab. Because of the timing of the discoveries, whether Montagnier's or Gallo's group was first to isolate HIV was for many years the subject of an acrimonious dispute. HIV isolates usually have a high degree of variability because the virus mutates rapidly. In comparison, the first two-human immunodeficiency virus type 1 (HIV-1) isolates, Lai/LAV (formerly LAV, isolated at the Pasteur Institute) and Lai/IIIB (formerly HTLV-IIIB, isolated from a pooled culture at the Laboratory of Tumor Cell Biology (LTCB) of the National Cancer Institute) were strikingly similar in sequence, suggesting that the two isolates were in fact the same, and likely from the same source.

In November 1990, the Office of Scientific Integrity at the National Institutes of Health attempted to clear up the matter by commissioning a group at Roche to analyze archival samples established at the Pasteur Institute and the Laboratory of Tumor Cell Biology (LTCB) of the National Cancer Institute between 1983 and 1985. The group, led by American epidemiologist Sheng-Yung Chang, examined archival specimens and concluded in Nature in 1993 that the American sample in fact originated from the French lab.

Chang determined that the French group's LAV was a virus from one patient that had contaminated a culture from another. On request, Montagnier's group had sent a sample of this culture to Gallo, not knowing it contained two viruses. It then contaminated the pooled culture on which Gallo was working.

Before the 1993 publication of Chang's results, Gallo's lab was accused and initially found guilty of "minor misconduct" by the Office of Scientific Integrity in 1991, and then by the newly created Office of Research Integrity in 1992 for the misappropriation of a sample of HIV produced at the Pasteur Institute. The subsequent publication in 1993 of Chang's investigation cleared Gallo's lab of the charges, although his reputation had already been tainted by the accusations.

Today it is agreed that Montagnier's group first isolated HIV, but Gallo's group is credited with discovering that the virus causes AIDS and with generating much of the science that made the discovery possible, including a technique previously developed by Gallo's lab for growing T cells in the laboratory. When Montagnier's group first published their discovery, they said HIV's role in causing AIDS "remains to be determined."

The question of whether the true discoverers of the virus were French or American was more than a matter of prestige. A US government patent for the AIDS test, filed by the United States Department of Health and Human Services and based on what was claimed to be Gallo's identification of the virus, was at stake. In 1987, both governments attempted to end the dispute by arranging to split the prestige of the discovery and the proceeds from the patent 50–50, naming Montagnier and Gallo co-discoverers. The two scientists continued to dispute each other's claims until 1987.

It was not until French President François Mitterrand and American President Ronald Reagan met in person that the major issues were ironed out. The scientists finally agreed to share credit for the discovery of HIV, and in 1986, both the French and the US names (LAV and HTLV-III) were dropped in favor of the new term human immunodeficiency virus (virus de l'immunodéficience humaine, abbreviated HIV or VIH) (Coffin, 1986). They concluded that the origin of the HIV-1 Lai/IIIB isolate discovered by Gallo was the same as that discovered by Montagnier (but not known by Montagnier to cause AIDS). This compromise allowed Montagnier and Gallo to end their feud and collaborate with each other again, writing a chronology that appeared in Nature that year.

On 29 November 2002 issue of Science, Gallo and Montagnier published a series of articles, one of which was co-written by both scientists, in which they acknowledged the pivotal roles that each had played in the discovery of HIV.

Personal life and death
In 1961, Montagnier married Dorothea Ackerman, and they had three children. He died in Neuilly-sur-Seine on 8 February 2022, at the age of 89.

Awards and honors
The 2008 Nobel Prize in Physiology or Medicine was awarded to Montagnier and Françoise Barré-Sinoussi for the discovery of HIV. They shared the Prize with Harald zur Hausen, who discovered that human papilloma viruses can cause cervical cancer. Montagnier said he was "surprised" that Robert Gallo was not also recognized by the Nobel Committee: "It was important to prove that HIV was the cause of AIDS, and Gallo had a very important role in that. I'm very sorry for Robert Gallo." According to Maria Masucci, a member of the Nobel Assembly, "there was no doubt as to who made the fundamental discoveries."

Montagnier was the co-founder of the World Foundation for AIDS Research and Prevention and co-directed the Program for International Viral Collaboration. He was the founder and a former president of the Houston-based World Foundation for Medical Research and Prevention. He received more than 20 major awards, including the National Order of Merit (Commander, 1986) and the Légion d'honneur (Knight: 1984; Officer: 1990; Commander: 1993; Grand Officer: 2009), He was a recipient of the Lasker Award and the Scheele Award (1986), the Louis-Jeantet Prize for medicine (1986), the Gairdner Award (1987), the Golden Plate Award of the American Academy of Achievement (1987), King Faisal International Prize (1993) (known as the Arab Nobel Prize), and the Prince of Asturias Award (2000). He was also a member of the Académie Nationale de Médecine, and was awarded the honorary Doctor of Humane Letters (L.H.D.) from Whittier College in 2010.

Electromagnetic signals from DNA
In 2009, Montagnier published two controversial independent research studies, one of which was entitled "Electromagnetic Signals Are Produced by Aqueous Nanostructures Derived from Bacterial DNA Sequences". Jeff Reimers, of the University of Sydney, said that if its conclusions are true, "these would be the most significant experiments performed in the past 90 years, demanding re-evaluation of the whole conceptual framework of modern chemistry". The paper concluded that diluted DNA from pathogenic bacterial and viral species was able to emit "specific radio waves" and that "these radio waves [are] associated with 'nanostructures' in the solution that might be able to recreate the pathogen".

They were published in a new journal, of which he was chair of the editorial board, allegedly detecting electromagnetic signals from bacterial DNA (M. pirum and E. coli) in water that had been prepared using agitation and high dilutions, and similar research on electromagnetic detection of HIV RNA in the blood of AIDS patients treated by antiretroviral therapy.

COVID-19 pandemic
In 2020, Montagnier argued that SARS-CoV-2, the virus that causes COVID-19, was man-made in a laboratory and that it might have been the result of an attempt to create a vaccine for HIV/AIDS. His allegation came after the United States had launched a probe into whether the virus came from a laboratory. According to Montagnier, the "presence of elements of HIV and germ of malaria in the genome of coronavirus is highly suspect and the characteristics of the virus could not have arisen naturally." Montagnier's conclusions were rejected as hasty by the scientific community, considering the gene sequences were common among similar organisms; no evidence arose that SARS-CoV-2 was genetically engineered.

In a 2021 interview with the French media group "Hold Up", Montagnier claimed that the use of vaccinations for COVID was steering the evolution of new strains, and that the process of antibody-dependent enhancement (ADE) would cause vaccinated individuals to suffer more strongly. The former claim had no obvious basis in fact, while ADE had only ever been conclusively demonstrated for dengue virus infections, and not for COVID-19.

Homeopathy
On 28 June 2010, Montagnier spoke at the Lindau Nobel Laureate Meeting in Germany, "where 60 Nobel prize winners had gathered, along with 700 other scientists, to discuss the latest breakthroughs in medicine, chemistry and physics." He "stunned his colleagues ... when he presented a new method for detecting viral infections that bore close parallels to the basic tenets of homeopathy. Although fellow Nobel prize winners – who view homeopathy as quackery – were left openly shaking their heads, Montagnier's comments were rapidly embraced by homeopaths eager for greater credibility. Cristal Sumner, of the British Homeopathic Association, said Montagnier's work gave homeopathy 'a true scientific ethos'."

When asked by Canada's CBC Marketplace program if his work was indeed a theoretical basis for homeopathy as homeopaths had claimed, Montagnier replied that one "cannot extrapolate it to the products used in homeopathy".

Responses, criticisms, and interviews
The homeopathy paper met with harsh criticism for not being peer-reviewed, and its claims unsubstantiated by modern mainstream conventions of physics and chemistry. In response to Montagnier's statement that the generally unfavorable response is due to the "non-understanding or misunderstanding of the breakthrough findings", blogger Andy Lewis has written that he has found it difficult to assert what the paper "actually claims", saying: "The paper ... lacks any rigour. ... important experimental steps are described dismissively in a sentence and little attempt is made to describe the detail of the work". While homeopaths claim his research as support for homeopathy, many scientists have greeted it with scorn and harsh criticism.

In a 24 December 2010 Science magazine interview entitled "French Nobelist Escapes 'Intellectual Terror' to Pursue Radical Ideas in China", he was questioned about his research and plans. In the interview he stated that Jacques Benveniste, whose controversial homeopathic work had been discredited, was "a modern Galileo". When asked if he was not "worried that your colleagues will think you have drifted into pseudo-science", he replied: "No, because it's not pseudoscience. It's not quackery. These are real phenomena which deserve further study." He also mentioned that his applications for funding had been turned down and that he was leaving his home country to set up shop in China so he could escape what he called the "intellectual terror" which he claimed had prevented others from publishing their results. He stated that China's Shanghai Jiao Tong University is more "open minded" to his research. There he was chairman of the editorial board of a new journal which published his research.

Montagnier was also questioned on his beliefs about homeopathy, to which he replied: "I can't say that homeopathy is right in everything. What I can say now is that the high dilutions are right. High dilutions of something are not nothing. They are water structures which mimic the original molecules. We find that with DNA, we cannot work at the extremely high dilutions used in homeopathy; we cannot go further than a 10−18 dilution, or we lose the signal. But even at 10−18, you can calculate that there is not a single molecule of DNA left. And yet we detect a signal."

A 12 January 2011 New Scientist editorial described the controversial nature of the research, while also noting how many researchers "reacted with disbelief", with chemist and university president Gary Schuster comparing it to "pathological science". Evolutionary biologist PZ Myers also described the work as "pathological science". He described the paper as "one of the more unprofessional write-ups I've ever run across", and criticized the publication process as having an "unbelievable turnaround" time: "another suspicious sign are the dates. This paper was submitted on 3 January 2009, revised on 5 January 2009, and accepted on 6 January 2009", leading him to ask: "Who reviewed this, the author's mother? Maybe someone even closer. Guess who the chairman of the editorial board is: Luc Montagnier."

On 25 May 2012, he gave the keynote address at the 2012 conference for AutismOne, an anti-vaccination group. Similar to the controversy he aroused by extolling homeopathy, his latest group, Chronimed, claimed to have made a discovery for autistic children that was sharply criticized by computational biologist Steven Salzberg.

In 2017, 106 academic scientists wrote an open letter "calling [Montagnier] to order". The letter read: "We, academics of medicine, cannot accept that one of our peers is using his Nobel prize [status] to spread dangerous health messages outside of his field of knowledge."

For his defense of such anti-scientific views, Montagnier has been cited as an example of the phenomenon called Nobel disease.

title: Luc Montagnier


text:
Wikipedia:Articles for deletion/Self-harm to breasts and sexual organs

Self-harm to breasts and sexual organs was proposed for deletion. This page is an archive of the discussion about the proposed deletion. This page is no longer live. Further comments should be made on the article's talk page rather than here so that this page is preserved as an historic record. The result of the debate was CONSENSUS NOT REACHED

Reasoning: Clearly a superfulous article. It contributes nothing of fundamental value to Wikipedia. It's not an issue of content being unacceptable (I'm not disputing that the content has merit), but an issue of the manner in which it is presented. There are already pages able to deal with this and this is a page written by someone clearly excited by this practice, but allowing that excitement to spill over into the Wikipedia community. This is not the proper forum for this especially because there are other pages. I recommend it be deleted immeditially. -SocratesJedi 09:26, 17 Jul 2004 (UTC) Reasoning continues: As PlatinumX points out (and I should have initially pointed out) this site is already included in the various references to self harm, self-bondage and even partially by masochism. I recommend this particular page either be deleted or integrated into self harm or self-bondage.

This page is now preserved as an archive of the debate and, like other '/delete' pages is no longer 'live'. Subsequent comments on the issue, the deletion or on the decision-making process should be placed on the relevant 'live' pages. Please do not edit this page.
 * What other pages? Also, did you read the talk page? It suffers from original research, but the main author is at work bringing it up to scratch. Keep - David Gerard 09:29, 17 Jul 2004 (UTC)
 * Keep. Secretlondon 12:52, 17 Jul 2004 (UTC)
 * Keep. --G3pro July 17 2004
 * Keep. It's educational, it has the potential to become a great article, and it complements self harm well.  --Ardonik 18:30, Jul 17, 2004 (UTC)
 * Neutral. The content is good and informative, but I don't know if the topic is broad enough to not be merged into self harm. The original research needs to be pared out, but I'm sure there is information on the subject in medical journals.– PlatinumX 19:23, 17 Jul 2004 (UTC)
 * Merge applicable content with self harm. In the AMA medical encyclopedia and one of the paper encyclopedias I've seen, this type of self-mutilation is covered under such a heading. I feel it's important to try and avoid having a topic spread over too many overlapping articles, as it invites redundancy, circular references, and POV problems due to different wordings being employed with their respective connotations. Jeeves 21:04, 17 Jul 2004 (UTC)
 * Merge and redirect. Exploding Boy 07:50, Jul 18, 2004 (UTC)
 * Merge into self-harm Shimmin 21:03, 18 Jul 2004 (UTC)
 * At the very least, it needs a hardcore rewrite. I'm also wondering about the title: "Breasts and sexual organs" seems a bit redundant.  I think maybe merging any useful information with self harm is fine, no redirect. -Seth Mahoney
 * If it were to be rewritten a title of "Sexual Self Harm" then it might have merit, but isn't this already covered elsewhere? -SocratesJedi 20:21, 19 Jul 2004 (UTC)
 * Keep. --Gary D 22:46, 19 Jul 2004 (UTC)
 * Merge and redirect. -- Cyrius|✎ 02:19, 21 Jul 2004 (UTC)