Persius/hicric huggingface dataset:
National Multiple Sclerosis Society
The National Multiple Sclerosis Society, a United States-based non-profit organization, and its network of chapters nationwide promote research, educate, advocate on issues relating to multiple sclerosis, and organize a wide range of programs, including support for the newly diagnosed and those living with MS.
Founded in 1946, the National Multiple Sclerosis Society supports more MS research, offers more services for people with MS, provides more professional education programs, and furthers more MS advocacy efforts than any other MS organization in the world.
It does this through the extensive research it supports to find the cause, cure and improved treatments of the disease; the comprehensive services it provides to people with MS and their families; the professional education programs it offers to assist health care providers better serve their MS patients; and through its advocacy efforts on state and federal levels to encourage public policies supportive of the needs of people with multiple sclerosis.

# Research
The MS society participates in research by funding projects. Currently they have launched a new research campaign called The Promise 2010, which consists in four specific areas:
- Nervous system repair and protection
- Pediatric MS Centers (management and care, and ultimately, research)
- The Sonya Slifka Longitudinal MS Study
- The MS pathological description (The Lesion Project)

# Resources
In March of 2007, the MS Society launched a new website to help increase awareness of this disease and how to help. MS interrupts the flow of information from the brain to the body and stops people from moving, and the National MS Society exists to make sure it doesnt.
One special feature on the new site is an interactive "Make Your Mark" tool where visitors can design their own marks against MS to be displayed on a "Wall". There is also video, a send-to-friend feature, easy ways to volunteer and join walk or bike events, and 25 user-generated stories.
There is also free MS button artwork available to increase awareness of how everyone can help bring about an end to multiple sclerosis.
The MS Society also has several resources available for research
- Two banks of tissue for MS research:
Human Brain and Spinal Fluid Resource Center in Los Angeles, California
The Rocky Mountain MS Center in Colorado
- Human Brain and Spinal Fluid Resource Center in Los Angeles, California
- The Rocky Mountain MS Center in Colorado
- One bank of DNA samples:
The Multiple Sclerosis DNA Bank at the University of California, San Francisco
- The Multiple Sclerosis DNA Bank at the University of California, San Francisco
- A database of medical tests at:
Sonya Slifka Longitudinal Multiple Sclerosis Study
- Sonya Slifka Longitudinal Multiple Sclerosis Study
Nelfinavir warnings and precautions

# Warnings and Precautions
ALERT: Find out about medicines that should not be taken with VIRACEPT. This statement is included on the product's bottle label.
Drug Interactions
See Table 3 for a listing of drugs that are contraindicated for use with VIRACEPT due to potentially life-threatening adverse events or potential loss of therapeutic effect . Please refer to Table 6 for established and other potentially significant drug-drug interactions .
Hepatic Impairment
VIRACEPT should not be used in patients with either moderate or severe hepatic impairment (Child-Pugh B or C, score greater than or equal to 7) .
Phenylketonurics
Viracept Oral Powder contains phenylalanine, a component of aspartame. Each gram of VIRACEPT powder contains 11.2 mg phenylalanine. Phenylalanine can be harmful to patients with phenylketonuria.
Diabetes Mellitus/Hyperglycemia
New onset diabetes mellitus, exacerbation of pre-existing diabetes mellitus and hyperglycemia have been reported during post-marketing surveillance in HIV-infected patients receiving protease inhibitor therapy. Some patients required either initiation or dose adjustments of insulin or oral hypoglycemic agents for treatment of these events. In some cases diabetic ketoacidosis has occurred. In those patients who discontinued protease inhibitor therapy, hyperglycemia persisted in some cases. Because these events have been reported voluntarily during clinical practice, estimates of frequency cannot be made and a causal relationship between protease inhibitor therapy and these events has not been established.
Hemophilia
There have been reports of increased bleeding, including spontaneous skin hematomas and hemarthrosis, in patients with hemophilia type A and B treated with protease inhibitors. In some patients, additional factor VIII was given. In more than half of the reported cases, treatment with protease inhibitors was continued or reintroduced. A causal relationship has not been established.
Fat Redistribution
Redistribution/accumulation of body fat including central obesity, dorsocervical fat enlargement ("buffalo hump"), peripheral wasting, facial wasting, breast enlargement, and "cushingoid appearance" have been observed in patients receiving antiretroviral therapy. The mechanism and long-term consequences of these events are currently unknown. A causal relationship has not been established.
Immune Reconstitution Syndrome
Immune reconstitution syndrome has been reported in patients treated with combination antiretroviral therapy, including VIRACEPT. During the initial phase of combination antiretroviral treatment, patients whose immune system responds may develop an inflammatory response to indolent or residual opportunistic infections , which may necessitate further evaluation and treatment.
Autoimmune disorders (such as Graves' disease, polymyositis, and Guillain-Barre syndrome) have also been reported to occur in the setting of immune reconstitution; however, the time to onset is more variable, and can occur many months after initiation of treatment.
Niacin/Simvastatin clinical studies

# Overdosage

## Modifications of Lipid Profiles

### SIMCOR
In a double-blind, randomized, multicenter, multi-national, active-controlled, 24-week study, the lipid effects of SIMCOR were compared to simvastatin 20 mg and 80 mg in 641 patients with type II hyperlipidemia or mixed dyslipidemia. Following a lipid qualification phase, patients were eligible to enter one of two treatment groups. In Group A, patients on simvastatin 20 mg monotherapy with elevated non-HDL levels and LDL-C levels at goal, per the NCEP guidelines, were randomized to one of three treatment arms: SIMCOR 1000/20 mg, SIMCOR 2000/20 mg, or simvastatin 20 mg. In Group B, patients on simvastatin 40 mg monotherapy, with elevated non-HDL levels per the NCEP guidelines regardless of attainment of LDL-C goals, were randomized to one of three treatment arms: SIMCOR 1000/40 mg, SIMCOR 2000/40 mg, or simvastatin 80 mg. Therapy was initiated at the 500 mg dose of SIMCOR and increased by 500 mg every four weeks. Thus patients were titrated to the 1000 mg dose of SIMCOR after four weeks and to the 2000 mg dose of SIMCOR after 12 weeks. All patients randomized to simvastatin monotherapy received 50 mg immediate-release niacin daily in an attempt to keep the study from becoming unblinded due to flushing in the SIMCOR groups. Patients were instructed to take one 325 mg aspirin 30 minutes prior to taking the double-blind medication to help minimize flushing effects.
In Group A, the primary efficacy analysis was a comparison of the mean percent change in non-HDL levels between the SIMCOR 2000/20 mg and simvastatin 20 mg groups, and if statistically significant, then a comparison was conducted between the SIMCOR 1000/20 mg and simvastatin 20 mg groups. In Group B, the primary efficacy analysis was a determination of whether the mean percent change in non-HDL in the SIMCOR 2000/40 mg group was non-inferior to the mean percent change in the simvastatin 80 mg group, and if so, whether the mean percent change in non-HDL in the SIMCOR 1000/40 mg group was non-inferior to the mean percent change in the simvastatin 80 mg group.
In Group A, the non-HDL-C lowering with SIMCOR 2000/20 and SIMCOR 1000/20 was statistically significantly greater than that achieved with simvastatin 20 mg after 24 weeks (p<0.05; Table 6). The completion rate after 24 weeks was 72% for the SIMCOR arms and 88% for the simvastatin 20 mg arm. In Group B, the non-HDL-C lowering with SIMCOR 2000/40 and SIMCOR 1000/40 was non-inferior to that achieved with simvastatin 80 mg after 24 weeks (Table 7). The completion rate after 24 weeks was 78% for the SIMCOR arms and 80% for the simvastatin 80 mg arm.
SIMCOR was not superior to simvastatin in lowering LDL-C in either Group A or Group B. However, SIMCOR was superior to simvastatin in both groups in lowering TG and raising HDL (Tables 8 and 9).
Niacin/lovastatin adverse reactions

# Adverse Reactions

## Overview
In controlled clinical studies, 40/214 (19%) of patients randomized to ADVICOR discontinued therapy prior to study completion. Of the 214 patients enrolled 18 (8%) discontinued due to flushing. In the same controlled studies, 9/94 (10%) of patients randomized to lovastatin and 19/92 (21%) of patients randomized to NIASPAN also discontinued treatment prior to study completion secondary to adverse events. flushing episodes (i.e., warmth, redness, itching and/or tingling) were the most common treatment-emergent adverse events, and occurred in 53% to 83% of patients treated with ADVICOR. Spontaneous reports with NIASPAN and clinical studies with ADVICOR suggest that flushing may also be accompanied by symptoms of dizziness or syncope, tachycardia, palpitations, shortness of breath, sweating, burning sensation/skin burning sensation, chills, and/or edema.

## Adverse Reactions Information
Because clinical studies are conducted under widely varying conditions, adverse reaction rates observed in clinical studies of a drug cannot be directly compared to rates in the clinical studies of another drug and may not reflect the rates observed in clinical practice. The adverse reaction information from clinical studies does, however provide a basis for identifying the adverse events that appear to be related to drug use and for approximating rates.
The data described in this section reflect the exposure to ADVICOR in two double-blind, controlled clinical studies of 400 patients. The population was 28 to 86 years-of-age, 54% male, 85% Caucasian, 9% Black, and 7% Other, and had mixed dyslipidemia.
In addition to flushing, other adverse events occurring in 5% or greater of patients treated with ADVICOR are shown in Table 10 below.
See also the full prescribing information for niacin extended release (Niaspan) and lovastatin products.
The following adverse events have also been reported with niacin, lovastatin, and/or other HMG-CoA reductase inhibitors, but not necessarily with ADVICOR, either during clinical studies or in routine patient management.
There have been rare postmarketing reports of cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion) associated with statin use. These cognitive issues have been reported for all statins. The reports are generally nonserious, and reversible upon statin discontinuation, with variable times to symptom onset (1 day to years) and symptom resolution (median of 3 weeks).

## Clinical Laboratory Abnormalities

### Chemistry
Elevations in serum transaminases (see WARNINGS - Liver Dysfunction), CPK and fasting glucose, and reductions in phosphorus. Niacin extended-release tablets have been associated with slight elevations in LDH, uric acid, total bilirubin, amylase and creatine kinase. Lovastatin and/or HMG-CoA reductase inhibitors have been associated with elevations in alkaline phosphatase, -glutamyl transpeptidase and bilirubin, and thyroid function abnormalities.

### Hematology
Niacin extended-release tablets have been associated with slight reductions in platelet counts and prolongation in PT (see WARNINGS).
Niacin/lovastatin contraindications

# Contraindications
ADVICOR is contraindicated in patients with a known hypersensitivity to niacin, lovastatin or any component of this medication, active liver disease or unexplained persistent elevations in serum transaminases (see WARNINGS), active peptic ulcer disease, or arterial bleeding.
Concomitant administration with strong CYP3A4 inhibitors (e.g.,itraconazole, ketoconazole, posaconazole, HIV protease inhibitors, boceprevir, telaprevir, erythromycin, clarithromycin, telithromycin and nefazodone) (see WARNINGS, Myopathy/Rhabdomyolysis).
Pregnancy and lactation - Atherosclerosis is a chronic process and the discontinuation of lipid-lowering drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hypercholesterolemia. Moreover, cholesterol and other products of the cholesterol biosynthesis pathway are essential components for fetal development, including synthesis of steroids and cell membranes. Because of the ability of inhibitors of HMG-CoA reductase, such as lovastatin, to decrease the synthesis of cholesterol and possibly other products of the cholesterol biosynthesis pathway, ADVICOR is contraindicated in women who are pregnant and in lactating mothers. ADVICOR may cause fetal harm when administered to pregnant women. ADVICOR should be administered to women of childbearing age only when such patients are highly unlikely to conceive. If the patient becomes pregnant while taking this drug, ADVICOR should be discontinued immediately and the patient should be apprised of the potential hazard to the fetus (see PRECAUTIONS, Pregnancy).
Nitric oxide synthase 2 (inducible)
Nitric oxide synthase, inducible is an enzyme that in humans is encoded by the NOS2 gene.
Nitric oxide is a reactive free radical which acts as a biologic mediator in several processes, including neurotransmission and antimicrobial and antitumoral activities. This gene encodes a nitric oxide synthase which is expressed in the liver and is inducible by a combination of lipopolysaccharide and certain cytokines. Three related pseudogenes are located within the Smith-Magenis syndrome region on chromosome 17. Alternative splicing of this gene results in two transcript variants encoding different isoforms.

# Interactions
Nitric oxide synthase 2A has been shown to interact with Caveolin 1 and Rac2.
Non-homologous end-joining factor 1
Non-homologous end-joining factor 1 (NHEJ1), also known as Cernunnos or XRCC4-like factor (XLF), is a protein that in humans is encoded by the NHEJ1 gene.  XLF was originally discovered as the protein mutated in five patients with growth retardation, microcephaly, and immunodeficiency.  The protein is required for the non-homologous end joining (NHEJ) pathway of DNA repair.  Patients with XLF mutations also have immunodeficiency due to a defect in V(D)J recombination, which uses NHEJ to generate diversity in the antibody repertoire of the immune system.  XLF interacts with DNA ligase IV and XRCC4 and is thought to be involved in the end-bridging or ligation steps of NHEJ.  The yeast (Saccharomyces cerevisiae) homolog of XLF is Nej1.

# Phenotypes
In contrast to the profound immunodeficiency phenotype of XLF deletion in humans, deletion of XLF alone has a mild phenotype in mice.   However, combining a deletion of XLF with deletion of the ATM kinase causes a synthetic defect in NHEJ, suggesting partial redundancy in the function of these two proteins in mice.

# Structure
XLF is structurally similar to XRCC4, existing as a constitutive dimer with an N-terminal globular head domain, an alpha-helical stalk, and an unstructured C-terminal region (CTR).

# Interactions
XLF has been shown to interact with XRCC4,  and with Ku protein, and it can also interact weakly with DNA. Co-crystal structures of XLF and XRCC4 suggest that the two proteins can form hetero-oligomers via head-to-head interaction of alternating XLF and XRCC4 subunits.  These XRCC4-XLF filaments have been proposed to bridge DNA prior to end ligation during NHEJ.  Formation of XRCC4-XLF oligomers can be disrupted by interaction of the C-terminal domain of XRCC4 with the BRCT domain of DNA ligase IV.

# Hematopoietic stem cell aging
Deficiency of NHEJ1 in mice leads to premature aging of hematopoietic stem cells as indicated by several lines of evidence including evidence that long-term repopulation is defective and worsens over time.  Using a human induced pluripotent stem cell model of NHEJ1 deficiency, it was shown that NHEJ1 has an important role in promoting survival of the primitive hematopoietic progenitors.  These NHEJ1 deficient cells possess a weak NHEJ1-mediated repair capacity that is apparently incapable of coping with DNA damages induced by physiological stress, normal metabolism, and ionizing radiation.
Oregon College of Oriental Medicine
The Oregon College of Oriental Medicine (OCOM), located in Portland, Oregon, United States, offers master's and postgraduate doctoral degrees in acupuncture and Oriental medicine. OCOM's programs are accredited by the Accreditation Commission for Acupuncture and Oriental Medicine and authorized by the Oregon Student Assistance Commission's Office of Degree Authorization  to award Master of Acupuncture and Oriental Medicine and Doctor of Acupuncture & Oriental Medicine degrees.
OCOM also operates an Intern Teaching Clinic and herbal dispensary, serving the Portland metropolitan area. More than 20,000 low cost acupuncture, Chinese herbal medicine, tuina, and shiatsu patient treatments are offered annually by the clinic, which also serves as a teaching facility for the college.
In July of 2005, OCOM became the first college to graduate a cohort of Doctors of Acupuncture and Oriental Medicine.
OCOM has an active research department, and has received substantial research grants from the National Institutes of Health/NCCAM.
Current OCOM research projects include a collaborative grant with the University of Arizona to study temporomandibular joint disorder.
Otosclerosis historical perspective
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# Overview
The renowned German composer Beethoven was theorized to suffer from otosclerosis, although this is controversial.
Howard Hughes the pioneering American aviator, engineer, industrialist, and film producer also suffered from otosclerosis. Frankie Valli, lead singer of The Four Seasons , suffered from it in the 1970s, forcing him to "sing from memory" in the latter part of the decade (surgery restored most of his hearing by 1980).
Ottawa Charter for Health Promotion

# Overview
The Ottawa Charter for Health Promotion is a 1986 document produced by the World Health Organization. It was launched at the first international conference for health promotion that was held in Ottawa, Canada.

# Context
The thirtieth World Health Assembly, held in 1977, had highlighted the importance of promoting health so that all the international citizens had an "economically productive" level of health by the year 2000. Further, a localised European taskforce developed a strategy for health promotion in the WHO European Region.

# Action areas of the Ottawa Charter
Five action areas for health promotion were identified, these are:
- Developing personal skills through information and education skills - enabling people to learn (throughout life) to prepare themselves for all of its stages and to cope with chronic illness and injuries is essential. This has to be facilitated in school, home, work and community settings.
- Strengthening community action - community development draws on existing human and material resources to enhance self-help and social support, and to develop flexible systems for strengthening public participation in, and direction of, health matters. This requires full and continuous access to information and learning opportunities for health, as well as funding support
- Creating supportive environments - the protection of the natural and built environments and the conservation of natural resources must be addressed in any health promotion strategy. Work, leisure and living environments should be a source of health for people.
- Building healthy public policy - health promotion policy combines diverse but complementary approaches, including legislation, fiscal measures, taxation and organisational change. Health promotion policy requires the identification of obstacles to the adoption of healthy public policies in non-health sectors and the development of ways to remove them.
- Re-orientating health care services toward prevention of illness and promotion of health - the role of the health sector must move increasingly in a health promotion direction, beyond its responsibility for providing clinical and curative services. Reorienting health services also requires stronger attention to health research, as well as changes in professional education and training.
Also, three basic strategies for health promotion are to:
- Advocate: To create an environment of which a positive health choice can be made
- Enable: To encourage positive lifestyle changes by explaining the benefits of change
- Mediate: To try to mediate between two parties with opposing interests to come to a compromise for the promotion of health.

# Developments after Ottawa
- WHO: Jakarta Declaration in 1997
- WHO: Health for all targets in 1997
- WHO: Health 21 in 1999
- The UK: Our Healthier Nation
- The UK: National Plan
- WHO: Bangkok Charter in 2005
Parathyroid hormone-related protein
Parathyroid hormone-related protein (or PTHrP) is a protein member of the parathyroid hormone family. It is occasionally secreted by cancer cells (breast cancer, certain types of lung cancer including squamous cell lung carcinoma). However, it also has normal functions.

# Function
PTHrP acts as an endocrine, autocrine, paracrine, and intracrine hormone. It regulates endochondral bone development by maintaining the endochondral growth plate at a constant width. It also regulates epithelial-mesenchymal interactions during the formation of the mammary glands.

## Tooth eruption
PTHrP is critical in  intraosseous phase of tooth eruption where it acts as a signalling molecule to stimulate local bone resorption. Without PTHrP, the bony crypt surrounding the tooth follicle will not resorb, and therefore the tooth will not erupt. In the context of tooth eruption, PTHrP is secreted by the cells of the Reduced Enamel Epithelium.

## Mammary glands
It aids in normal mammary gland development. It is necessary for maintenance of the mammary bud. Loss of PTHrP or its receptor causes the mammary bud cell fate to change back into epidermis. In lactation, it may regulate in conjunction with the calcium sensing receptor the mobilization and transfer of calcium to the milk, as well as placental transfer of calcium.

## Humoral hypercalcemia of malignancy
PTHrP is related in function to the "normal" parathyroid hormone. When a tumor secretes PTHrP, this can lead to hypercalcemia. As this is sometimes the first sign of the malignancy, hypercalcemia caused by PTHrP is considered a paraneoplastic phenomenon. PTHR1 is responsible for most cases of humoral hypercalcemia of malignancy.
PTHrP shares the same N-terminal end as parathyroid hormone and therefore it can bind to the same receptor, the Type I PTH receptor (PTHR1). PTHrP can simulate most of the actions of PTH including increases in bone resorption and distal tubular calcium reabsorption, and inhibition of proximal tubular phosphate transport.
However, PTHrP is less likely than PTH to stimulate 1,25-dihydroxyvitamin D production. Therefore, PTHrP does not increase intestinal calcium absorption.

# Genetics
Four alternatively spliced transcript variants encoding two distinct isoforms have been observed. There is also evidence for alternative translation initiation from non-AUG (CUG and GUG) start sites, in-frame and downstream of the initiator AUG codon, to give rise to nuclear forms of this hormone.

# Discovery
The protein was first isolated in 1987 by T.J. Martin's team at the University of Melbourne. Miao et al. showed that disruption of the PTHrP gene in mice caused a lethal phenotype and distinct bone abnormalities, suggesting that PTHrP has a physiological function.

# Interactions
Parathyroid hormone-related protein has been shown to interact with KPNB1 and Arrestin beta 1.