Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence and incidence of left ventricular (LV) dysfunction was examined in patients infected with the human immunodeficiency virus (HIV). Sixty-nine randomly selected patients diagnosed with HIV infection who were followed in HIV clinics were prospectively evaluated by 2-dimensional echocardiography. Mean follow-up duration was 11 months. Additionally, 39 consecutive HIV-infected patients referred to the Cardiomyopathy Service and found to have LV dysfunction by 2-dimensional echocardiography were also studied. Of the 39 referred patients, 34 (87%) were referred for recent onset, unexplained, congestive heart failure. During this time, the HIV clinic population comprised 1,819 alive and actively followed patients; the 39 cardiomyopathy referrals therefore constituted a crude rate of 2.1% for this population. Of the 69 prospectively studied patients without clinical heart disease, a 14.5% prevalence of global LV hypokinesia and an incidence of 18%/patient-year were found. During a maximal 18-month follow-up period, 4 prospective patients (5.8%) developed symptoms of congestive heart failure. A greater proportion of prospective and referred patients with LV dysfunction had CD4 counts < 100/mm3 (62 and 79%, respectively) than did that of those without LV dysfunction (35%). In conclusion, the high rate of unexpected LV dysfunction in this HIV-infected population suggests that early cardiac contractile abnormalities may involve a significant number of patients, most of whom have low CD4 counts. A subgroup of these patients appears to progress to symptomatic congestive heart failure.
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PMID:Prevalence and incidence of left ventricular dysfunction in patients with human immunodeficiency virus infection. 846 88

Projection disease incidence, prevalence, and net morbidity is often needed when individuals are likely to die, either disease free or after the disease has developed. Examples of this include remission of cancer or heart disease in elderly people who can die from these or other causes and occurrence of a particular acquired immune deficiency syndrome illness in human immunodeficiency virus type 1 (HIV-1) disease. Death is not an ancillary event but, rather, indicates either and end to disease morbidity or an end to risk to ever develop the disease. Thus, time to disease survival analyses that censor disease-free individuals at death can produce misleading results. The paper describes several useful quantifications of disease and death for this setting. A paradigm that utilizes Kaplan-Meier functions to estimate these quantities is introduced. The approach anchors on a four-stage disease/death model: stage A, living without disease; stage B, dead without ever developing disease; stage C, developed the disease and living; and stage D, dead after developing the disease. An application is made to projecting cytomegalovirus disease in a cohort of HIV-1-infected users of zidovudine and Pneumocystis prophylaxis from the Multicenter AIDS Cohort Study (MACS) during 1989-1993. At 3 years after a CD4+ count below 100/microliters, a man had an 18.7%, 46.3%, 5.3% or 29.9% chance, respectively, to be in stage A, B, C, or D. This man, on average, had 0.28 years of cytomegalovirus morbidity during these 3 years.
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PMID:Projecting disease when death is likely. 861 Jul 8

We report on two patients with velo-cardio-facial syndrome (VCFS) and juvenile rheumatoid arthritis (JRA). The first, a 9-year-old girl, presented with microcephaly, characteristic face, congenital heart disease, and velopharyngeal insufficiency. Fluorescence in situ hybridization (FISH) study showed deletion of D22S75 (N25), confirming the diagnosis of VCFS. At age 7, she developed joint pain, and polyarticular JRA was diagnosed. Awareness of this case led to the subsequent diagnosis of VCFS (also confirmed by FISH) in another, unrelated 12-year-old girl with characteristic face, hypernasal speech, and obesity. JRA was first diagnosed in this case at age 5 years, and she subsequently developed severe polyarticular disease. Neither patient had clinical or laboratory evidence of immunodeficiency. This observation represents the first report of the association of JRA with VCFS and raises the question of whether this is a coincidental association or a rare complication of this condition.
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PMID:Juvenile rheumatoid arthritis in velo-cardio-facial syndrome: coincidence or unusual complication? 928 62

Recent trends in the vital statistics of the United States continued in 1995, including decreases in the number of births, the birth rate, the age-adjusted death rate, and the infant mortality rate; life expectancy at birth increased to a level equal to the record high of 75.8 years in 1992. Marriages and divorces both decreased. An estimated 3,900,089 infants were born during 1995, a decline of 1% from 1994. The preliminary birth rate for 1995 was 14.8 live births per 1000 total population, a 3% decline, and the lowest recorded in nearly two decades. The fertility rate, which relates births to women in the childbearing ages, declined to 65.6 live births per 1000 women 15 to 44 years old, the lowest rate since 1986. According to preliminary data for 1995, fertility rates declined for all racial groups with the gap narrowing between black and white rates. The fertility rate for black women declined 7% to a historic low level (71.7); the preliminary rate for white women (64.5) dropped just 1%. Fertility rates continue to be highest for Hispanic, especially Mexican-American, women. Preliminary data for 1995 suggest a 2% decline in the rate for Hispanic women to 103.7. The birth rate for teenagers has now decreased for four consecutive years, from a high of 62.1 per 1000 women 15 to 19 years old in 1991 to 56.9 in 1995, an overall decline of 8%. The rate of childbearing by unmarried mothers dropped 4% from 1994 to 1995, from 46.9 births per 1000 unmarried women 15 to 44 years old to 44.9, the first decline in the rate in nearly two decades. The proportion of all births occurring to unmarried women dropped as well in 1995, to 32.0% from 32.6% in 1994. Smoking during pregnancy dropped steadily from 1989 (19.5%) to 1994 (14.6%), a decline of about 25%. Prenatal care utilization continued to improve in 1995 with 81.2% of all mothers receiving care in the first trimester compared with 78.9% in 1993. Preliminary data for 1995 suggests continued improvement to 81.2%. The percent of infants delivered by cesarean delivery declined slightly to 20.8% in 1995. The percent of low birth weight (LBW) infants continued to climb in 1994 rising to 7.3%, from 7.2% in 1993. The proportion of LBW improved slightly among black infants, declining from 13.3% to 13.2% between 1993 and 1994. Preliminary figures for 1995 suggest continued decline in LBW for black infants (13.0%). The multiple birth ratio rose to 25.7 per 1000 births for 1994, an increase of 2% over 1993 and 33% since 1980. Age-adjusted death rates in 1995 were lower for heart disease, malignant neoplasms, accidents, and homicide. Although the total number of human immunodeficiency virus (HIV) infection deaths increased slightly from 42,114 in 1994 to an estimated 42,506 in 1995, the age-adjusted death rate for HIV infection did not increase, which may indicate a leveling off of the steep upward trend in mortality from HIV infection since 1987. Nearly 15,000 children between the ages of 1-14 years died in the United States (US) in 1995. The death rate for children 1 to 4 years old in 1995 was 40.4 per 100,000 population aged 1 to 4 years, 6% lower than the rate of 42.9 in 1994. The 1995 death rate for 5- to 14-year-olds was 22.1, 2% lower than the rate of 22.5 in 1994. Since 1979, death rates have declined by 37% for children 1 to 4 years old, and by 30% for children 5 to 14 years old. For children 1 to 4 years old, the leading cause of death was injuries, which accounted for for an estimated 2277 deaths in 1995, 36% of all deaths in this age group. Injuries were the leading cause of death for 5- to 14-year-olds as well, accounting for an ever higher percentage (41%) of all deaths. In 1995, the preliminary infant mortality rate was 7.5 per 1000live births, 6% lower than 1994, and the lowest ever recorded in the US. The decline occurred for neonatal as well as postneonatal mortality rates, and among white and black infants alike.
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PMID:Annual summary of vital statistics--1995. 971 45

Chromosome 22q11 deletion syndrome is a relatively newly described syndrome that encompasses the majority of patients previously felt to have velo-cardio-facial syndrome, DiGeorge syndrome, and conotruncal anomaly face syndrome. The disorder is characterized by a deletion of band 11 on the long arm of chromosome 22 most often recognized by fluorescent in situ hybridization (FISH) techniques. Extensive laboratory investigations are currently ongoing to uncover the specific genes involved and their functions. Phenotypically, individuals present with congenital heart disease, palatal abnormalities, facial dysmorphism, and developmental delay, as well as variable degrees of immunodeficiency, hypocalcemia, and endocrine abnormalities. The primary care physician has an important role in caring for these patients and their families. We review the current state of knowledge regarding chromosome 22q11 deletion syndrome, with an emphasis on the clinical presentation and on prevention and treatment of the known complications associated with this multisystem disorder. Chromosome 22q11 deletion syndrome can be inherited in an autosomal dominant fashion or result from a de novo deletion or translocation. Hence, this syndrome may have significant reproductive risks to affected individuals and families.
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PMID:Chromosomes 22q11 deletion syndrome: an update and review for the primary pediatrician. 915 51

Measurement of serum IgG subclass levels in 3005 patients disclosed abnormally low IgG1 levels with normal levels of the other IgG subclasses and of IgM and IgA in 119 patients, predominantly adults. Not all patients were hypogammaglobulinemic due to nonrare increases of other isotypes, mostly IgM. A familial context of immunodeficiency was frequent, more often combined than selective IgG1 deficiency. A familial association with IgG2 deficiency was found also and IgG1 replaced IgG2 deficiency in 3 cases (and succeeded to or preceded more complex IgG defects in 3 cases, whereas IgG1 deficiency was consistently found at examinations repeated in the absence of therapy in 10 additional cases). Most but not all (83.2%) patients suffered infections, generally moderate, similar to those observed in other selective IgG subclass deficiencies (IgGSD), with predominantly sinorespiratory infections. Other clinical manifestations such as atopy, congenital cardiopathy, and autoimmune diseases were already known in IgGSD but the incidence of asthma was strikingly high (one-fifth of the cases).
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PMID:Selective IgG1 deficiency. 924 52

DiGeorge Syndrome is a congenital immunodeficiency characterized clinically by hypocalcemic tetany, congenital heart disease, unusual facies, and increased susceptibility to infection. Pathologically, the syndrome is marked by the abscence or hipoplasia of the thymus and parathyroid glands as well as cardiac or aortic arch abnormalities. Most patients show partial or complete T cell immunodeficiency and normal or near-normal B-cell immunity. A review is made on a clinical case of DiGeorge syndrome is presented. A 52 days old boy, was admitted through emergency. There was no familial evidence of alcoholism or immunodeficiency. He showed irritability due to hypocalcemia. The examination revealed facial and cardiovascular abnormalities and the immunological investigation revealed hypogammaglobulinemia, deficiency of the cell, CD4 and CD8 decreased and with inverted relation. Chest X ray showed cardiomegaly grade II, and no thymus was seen. The diagnosis of the complete DiGeorge syndrome was based on the abnormalities found.
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PMID:[Immunogenetic study in a case of DiGeorge syndrome]. 929 18

The most widely accepted etiological explanation for acquired immune deficiency syndrome (AIDS) currently invokes an infectious model involving the human immunodeficiency virus (HIV). Because this infectious model has failed to meet any conventional criteria for establishing microbial causation, this theory still relies on the high, though not perfect, statistical correlation linking presence of HIV antibodies with patients diagnosed with, and at risk for the syndrome. Many scientists and clinicians now doubt the HIV theory, though, and propose instead a multifactorial causation similar to that seen in cancer and heart disease. In order to discard the HIV model, however, it is necessary to explain the high statistical correlation mentioned above. Recent studies involving cellular mediated immunity and cytokine modulation may explain this statistical relationship without the need to invoke infectious causation, by suggesting certain functional characteristics and feedback loops in the immune system which the author calls selective compartmental dominance (SCD). SCD provides a model in which chronic dominance of the humoral immune compartment secondary to chronic high-dose antigenic challenge results in chronic suppression of the cellular immune compartment. This model predicts that even HIV-negative members of the risk groups are susceptible to AIDS, assigns no special causal role for HIV in AIDS, and suggests a rational course of nontoxic therapy that can potentially reverse cases in the earlier stages.
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PMID:Selective compartmental dominance: an explanation for a noninfectious, multifactorial etiology for acquired immune deficiency syndrome (AIDS), and a rationale for ozone therapy and other immune modulating therapies. 948 85

During the last decade there were extensive investigations in clinical and molecular andrology with emphasis on assisted reproduction, micromanipulation techniques of gametes, sperm/egg interaction, male contraception, diabetes mellitus, varicocele, andropause versus menopause, sexual dysfunction, associated hypertension/stress, prostatic carcinoma and molecular parameters of male reproduction. Sperm hyperactivation is a required step in capacitation sequence. Sperm motility is measured by videotape to evaluate the Straight Line Velocity (microm/s) (VSLI). Fertilization/embryonic development results from single sperm transfer (S-MIST) and multiple sperm transfer. Fertilization/embryo development is achieved by injection of immotile sperm into the perivitelline space. To assess sperm viability, a supravital stain suitable for use in combination with immunofluorescent assay, Hoeschst 33258, is used. The dye fluoresces with an intense blue when bound to DNA. To assess sperm plasma membrane integrity, a hypo-osmotic swelling test (HOST) is performed, using fluoresceinated D-mannose enriched albumin (FITC-DMA). The ability of sperm to swell under hypo-osmotic conditions indicates an intact membrane. A human protein, C-peptide, thought to be a useless byproduct of insulin may protect against devastating heart and nerve damage that diabetes causes. Human diabetics may benefit from the substance. Over 15 million Americans have diabetes, in which blood sugar levels rise out of control. There are two types of diabetics: Type I diabetics produce no insulin, the hormone that regulates blood sugar. Type II diabetics are unable to use their insulin properly. Diabetics are at great risk of heart disease and nerve damage, as arteries throughout the body leak and nerve-cell impulses fail. C-peptide is a byproduct of insulin production; it can be produced by the body or synthetically. Production of this protein is not induced by insulin, so diabetics who take insulin do not get C-peptide with it. Varicocele occurs unilaterally on the left side in 78% to 93% of men. Typically the presence of a varicocele is associated with an abnormal semen analysis (sperm density and morphology) and a decreased testicular volume on the affected side. Impaired sperm motility occurs in 89.5% of all varicocele patients. Varicocele ligation improves semen parameters in two thirds of patients. A few studies on andropause included sexual dysfunction, hormonal changes, medical/psychological correlates of impotence, ostenopenia/osteoporosis and bone loss; indices of bone remodeling, testosterone supplementation, androgen, negative feedback and hypothalamo-pituitary-testicular axis. Prostatic cancer is the second leading cause of cancer death for men between the ages of 60 and 80. Early detection involves a simple blood test for prostate specific antigen (PSA). Regular screening and early detection are essential. This is an important test because a high antigen count can be the only symptom. Since no screening is 100% accurate, physicians recommend both a PSA blood test and a physical examination. Although heredity plays a major role in whether a man will develop prostate cancer, men who lead healthy lives can dramatically reduce their chances of cancer: low-fat diet, eating plenty of fruits and vegetables and not smoking. Recent advances in molecular andrology include peptide hormone binding proteins; gonadotropin-releasing hormone (GnRH) agonists/antagonists analog; gonadotropins/their receptors; growth factors/reproduction; peptides as intratesticular regulators; molecular cloning of reproductive proteins/peptides. Gene cloning is applied for characterization/expression of genes coding. The interaction of gp120 with CD4 receptor plays a role in syncytium formation, apoptosis and CD4 cell deletion in human immunodeficiency virus (HIV) infection. The recombinant V3 peptide of fragment 307-330 of HIV-1 can induce sperm head agglutination. The generation process of react
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PMID:Recent advances in clinical/molecular andrology. 958 57

This study examined years of potential life lost (YPLL) before age 65 years to assess the relative impact of human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS) versus other leading causes of death on premature mortality in New York City, New York, between 1983 and 1994. Most causes of death showed substantial year-to-year variation in YPLL, with the exception of HIV/AIDS. The YPLL attributed to HIV/AIDS increased monotonically from 11,866 in 1983 to 167,317 in 1994, a nearly 15-fold increase. The rank order of the relative contribution of HIV/AIDS to total YPLL changed from the eighth leading cause of death to the leading cause. YPLL from heart disease, which ranked second in 1983, declined to fourth in 1994, homicide was unchanged, and chronic liver disease declined from fifth to ninth rank. The annual YPLL attributed to malignant neoplasms was similar to that for heart disease, but peaked in 1984, and the reduction over the subsequent decade was about 13%. Total YPLL was 78% greater among males than among females in 1983 and was nearly twice as high in 1994. Premature mortality decreased steadily for non-Hispanic whites, from 150,967 to 135,027 years for the years 1983-1994, while increasing 20% among blacks (from 179,176 to 215,826 years) and 48% among Hispanics (from 89,869 to 132,869 years). Among blacks and Hispanics, homicide contributed more years of YPLL than did either heart disease or malignant neoplasms in every year of observation. The HIV/AIDS epidemic and mortality associated with violence have become important public health challenges to the health and well-being of New Yorkers.
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PMID:Effect of HIV/AIDS versus other causes of death on premature mortality in New York City, 1983-1994. 958 14


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