Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acemannan, a complex carbohydrate shown to stimulate interleukin-1, tumor necrosis factor alpha and prostaglandin E2 production by macrophages, has also demonstrated antiviral activity in vitro against human immunodeficiency virus, Newcastle disease virus and influenza virus. A pilot study was undertaken to determine acemannan's effect in 49 feline immunodeficiency virus (FIV) infected cats with clinical signs of disease (Stage 3, 4 or 5), 23 of which had severe lymphopenia. Cats received acemannan either by intravenous (Group 1) or subcutaneous (Group 2) injection once weekly for 12 weeks, or by daily oral (Group 3) administration for 12 weeks. Upon entry into the study, cats were randomly assigned to one of the three groups. Laboratory analyses were performed at the beginning of the study and at Weeks 6 and 12. Cats were allowed to continue with a predetermined maintenance regimen of acemannan after completing the 12-week study. Thirteen cats died during the course of treatment. Upon necropsy, the most frequent histopathologic findings were neoplastic, kidney and pancreatic disease. Friedman's two-way ANOVA test showed no significant differences in efficacy among groups administered acemannan by the different routes. Therefore, groups were combined and a signed-ranks test was used to determine changes over time. A significant increase was seen in lymphocyte counts (P < 0.001). Neutrophil counts decreased significantly (P = 0.007), as did incidence of sepsis (P = 0.008). When cats entering with lymphopenia were analyzed separately, a much greater increase in lymphocyte counts was noted (235%) compared with non-lymphopenic cats (42%). A survival rate of 75% was found for all three groups. Thirty-six of 49 animals are alive 5-19 months post-entry. These results suggest that acemannan therapy may be of significant benefit in FIV-infected cats exhibiting clinical signs of disease.
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PMID:Pilot study of the effect of acemannan in cats infected with feline immunodeficiency virus. 133 96

The purpose of this study is to determine which of two educational approaches have the greater effect on the AIDS/human immunodeficiency virus (HIV) knowledge and attitudes of women participating in the Women, Infants, and Children (WIC) Program. A modified version of the Centers for Disease Control's (CDC) 1989 Health Risk Survey was administered to 217 women, who were then randomly assigned to either a control group receiving the usual written material, a nurse-educated group, or a videotape-educated group. The questionnaires were repeated immediately after and 2 months after the intervention. Chi square, Kruskall-Wallis ANOVA, and a repeated measures ANOVA were used for data analysis. Ninety-five percent of the subjects were black and the mean age was 25.8 years (+/- 5.9). The control group had significantly lower (p < or = 0.003) AIDS knowledge scores at both posttests, with the lowest knowledge level at 2 months. The videotape group had a greater (p < or = 0.048) intent to reduce risky behaviors at the initial posttest. Tolerance towards AIDS patients was significantly (p < or = 0.025) greater in the videotape and nurse groups. Both videotape and nurse education programs increased knowledge and influenced attitudes and behavioral intent. The more efficient videotape program had similar effects as the nurse program, and may be more generalizable to other populations.
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PMID:An experimental evaluation of an AIDS educational intervention for WIC mothers. 751 56

Recent studies have suggested that the neuronal damage during human immunodeficiency virus encephalitis (HIVE) might be mediated by increased intracellular calcium. Since in vitro studies have shown that calcium-binding proteins protect neurons from calcium-mediated toxicity, we hypothesized that calbindin-expressing neurons might be resistant to HIV1-mediated damage. We compared patterns of calbindin immunoreactivity in the cortex and subcortex of autopsied AIDS cases with and without HIVE. Calbindin-immunoreactive neurons in the neocortex were significantly reduced in HIVE (one-way ANOVA, p < 0.001), while these neurons in the basal ganglia and hippocampus were unaffected. The loss of calbindin-immunolabeled neurons in the neocortex was correlated with viral burden (r = -0.45, p < 0.001). Differential loss of calbindin-immunoreactive neurons in HIVE suggests that neuronal damage in different regions of the CNS may be mediated by different pathogenic mechanisms.
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PMID:Differential vulnerability of calbindin-immunoreactive neurons in HIV encephalitis. 774 34

(-)-Carbovir (CBV) is a carbocyclic nucleoside analogue with in vitro activity against the human immunodeficiency virus. The sites and mechanism of absorption of (-)-CBV from the rat small intestine were studied in the anesthetized male Sprague-Dawley rat. (-)-CBV was perfused through either duodenal, jejunal, or ileal segments at three concentration levels ranging from 1 to 500 micrograms/mL. The fraction remaining to be absorbed at steady-state and the absorptive clearance were calculated for each experiment. The effect of solvent drag on the absorptive clearance was also investigated. Two-way ANOVA for the absorptive clearance per unit length was not significant for either (-)-CBV concentration or site of perfusion. The fraction remaining to be absorbed at steady-state was found to be 0.804 +/- 0.091 (n = 30). A strong correlation was found between the absorptive clearance and the net water absorptive flux. The mechanism of (-)-CBV absorption across the rat small intestine apparently consists of both passive diffusion and convection.
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PMID:Intestinal absorption of (-)-carbovir in the rat. 816 86

Recent data suggest that gp120, a human immunodeficiency virus-1 (HIV-1) coat glycoprotein that is secreted by HIV-infected cells, is neurotoxic, and that this toxicity is mediated, at least in part, by activation of N-methyl-D-aspartate-type excitatory amino acid receptors. To test this hypothesis in vivo, we examined the neurotoxicity of gp120 injected intrahippocampally, alone or co-injected with the selective excitatory amino acid agonist N-methyl-D-aspartate, in seven-day-old rats. Severity of injury in the lesioned hippocampus was assessed five days later, using three outcome measures: histopathology, hippocampal atrophy (derived from regional cross-sectional area measurements) and loss of [3H]glutamate receptor binding (based on in vitro autoradiography assays). To confirm that any observed effects were attributable to gp120 bioactivity, each group of experiments included controls that received equal amounts of heat-treated gp120. Gp120 (200 ng) elicited minimal focal pyramidal cell loss immediately adjacent to the injection track; there was no hippocampal atrophy or loss of [3H]glutamate binding. Co-injection of 50 ng gp120 with N-methyl-D-aspartate (5 nmol, threshold excitotoxic dose) increased the severity of hippocampal injury; hippocampal atrophy was greater in animals that received injections of 5 nmol N-methyl-D-aspartate in combination with 50 ng gp120 than in those that received either N-methyl-D-aspartate alone (5 nmol) or 5 nmol N-methyl-D-aspartate+50 ng heat-treated gp120 (mean+/-S.E.M. percentage reduction in injected hippocampal volume vs contralateral: N-methyl-D-aspartate, -19+/-3; N-methyl-D-aspartate+gp120, -26.8+/-2.1; N-methyl-D-aspartate+heat-treated gp120, -14.0+/-2.2; P<0.001, ANOVA). Treatment with the competitive N-methyl-D-aspartate antagonist 3-((RS)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (20mg/kg) markedly reduced the severity of injury elicited by the combination of gp120 with N-methyl-D-aspartate. These data support the hypothesis that locally secreted gp120 could exert neurotoxic effects, mediated by N-methyl-D-aspartate receptor activation, in vivo in the immature brain.
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PMID:gp120, a human immunodeficiency virus-1 coat protein, augments excitotoxic hippocampal injury in perinatal rats. 901 25

The serum magnesium concentrations are compared between the three clinical classification categories established in 1993 by the Centers for Disease Control (CDC) (infection) by the human immunodeficiency virus) in adults, and its relation with the CD4 lymphocyte count, albumin, and pre-albumin. The serum magnesium concentration is part of the broad analytical screening and it is determined by atomic absorption spectroscopy. The data obtained were analyzed by the statistical program SPSS. The comparisons of the serum magnesium concentrations between the three clinical categories of the CDC were evaluated by an analysis of variance (ANOVA test). Afterwards, and using a regression analysis, the relations between the different variables were evaluated. 35 patients affected by HIV-AIDS were studied, 22 belonging to category A, 3 to category B, and 10 to category C, 29.4% of the patients studied presented hypomagnesemia, with an average serum magnesium level of 17.6 +/- 10.3 mg/l. There is a quadratic relation between the serum magnesium level and the number of CD4 lymphocytes in HIV-AIDS patients studied. A larger number of cases would allow us to conclude whether hypomagnesemia is a factor belonging to the disease, as well showing the possible differences in the magnesium state between the three diagnostic groups studied. Future studies will be necessary to clarify the role of magnesium in the clinical progression of patients infected by HIV.
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PMID:[Magnesium deficiency in patients with HIV-AIDS]. 947 56

Risk factors associated with surgical infections are related to many events that modulate the immune system and affect the surgical procedure. The aim of this study was to determine the influence of low CD4+ lymphocyte counts in 24 patients with human immunodeficiency virus (HIV) undergoing abdominal surgery. Blood samples were obtained, and the lymphocyte population was evaluated perioperatively, as was the nutritional status of the patient. All the patients received selective antibiotic prophylaxis depending on the surgical procedure performed: (1) clean surgery: splenectomies (n = 8); (2) clean-contaminated: cholecystectomy and biliary tract surgery (n = 8); and (3) contaminated: appendectomy (n = 8). Depending on their CD4 count, two groups were formed: one with 200 to 500 cells/ml (n = 11) and the other with < 200 cells/ml (n = 13). When surgical infection was suspected, surgical drainage and microbiologic cultures were undertaken. For statistical evaluation of the groups ANOVA and the chi-square test were used; p < 0.05 was considered significant. Altogether 14 patients (58.3%) had a wound infection, and the mean (+/- SD) CD4 count in those patients was decreased (221.7 +/- 75.1) compared with that of the 10 patients in the uneventful group (386 +/- 81.2). Surgical infection rates were 50% for clean procedures, 62.5% for clean-contaminated procedures, and 62.5% for contaminated surgery. The group of patients with CD4 counts of < 200 cell/ml had an increased incidence of surgical infection, regardless of the type of surgery (p = 0.002). Thus the surgical infection rates with HIV patients undergoing abdominal surgery are dramatically increased. The CD4 and subsequently depressed neutrophil populations increase the risk of surgical infection during major procedures regardless of the type of surgery performed.
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PMID:Infective complications after abdominal surgery in patients infected with human immunodeficiency virus: role of CD4+ lymphocytes in prognosis. 967 46

Twenty children older than 2 y infected with human immunodeficiency virus (HIV) were examined by in vivo proton magnetic resonance spectroscopy (1H MRS) to study their cerebral metabolism and to identify metabolic profiles in relation with different stages of the disease. Patients were rated regarding their clinical and immunologic status according to the Centers for Disease Control classification and were divided into two groups: without encephalopathy (E-, n = 15) and with progressive encephalopathy (E+, n = 5). The acquisition was performed in the centrum semiovale using the short echo stimulated echo acquisition mode 20-ms sequence. The MRS profile was abnormal in all HIV-infected children compared with healthy age-matched controls (n = 7), even when magnetic resonance images were normal. A significant increase of the proportion of the lipid signals (ANOVA, p < 0.05) was found in all HIV-infected children. In addition, a significant decrease of the proportion of the N-acetylaspartate signal and a significant increase of the proportion of the myo-inositol signal (ANOVA, p < 0.05) characterized the E+ group. The principal component analysis performed on eight variables on 30 spectra confirms that the spectra of HIV-infected children differ from control spectra. The E+ group and the E- group are clearly separated on the map of subjects on the principal plane. The E- group lies in an intermediate position between the E+ group and the control group. The evolution of metabolic alterations in the brain of HIV-infected children can clearly be monitored by 1H MRS and associated with the occurrence of an encephalopathy.
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PMID:Localized proton magnetic resonance spectroscopy of the brain in children infected with human immunodeficiency virus with and without encephalopathy. 980 58

To test the hypothesis that the human immunodeficiency virus-1-derived Tat protein may cause neuronal damage in the CNS, we evaluated the neurotoxicity of recombinant human immunodeficiency virus-1-derived Tat in vivo in seven-day-old rats. The intrinsic neurotoxicity of Tat (250 ng-1 microg) and the effects of direct intra-hippocampal co-infusion of Tat with N-methyl-D-aspartate were assessed. Extent of injury in the lesioned hippocampus was evaluated five days later, based on histopathology and morphometric measurements of hippocampal volume. To confirm that any observed neurotoxic effects were attributable to Tat bioactivity, all experiments included controls that received equal amounts of heat-treated (boiled) Tat. Intra-hippocampal injection of Tat, alone, elicited minimal focal tissue damage immediately adjacent to the injection track, and no hippocampal atrophy. Co-injection of Tat (500 ng) with N-methyl-D-aspartate (5 nmol, threshold excitotoxic dose) doubled the severity of hippocampal injury, quantified by comparison of bilateral hippocampal volumes, in comparison with animals that received heat-treated Tat or saline co-injections; in animals that received injections of N-methyl-D-aspartate (5 nmol) in combination with saline, heat-treated Tat, or Tat [mean(+/-S.E.M.) % volume loss values in the lesioned hippocampus were: 11(+/-3), 11(+/-3), and 26(+/-3), respectively (P<0.002, ANOVA)]. Co-injection of 100 ng Tat with 5 nmol N-methyl-D-aspartate exacerbated the severity of excitotoxic injury to a similar extent, whereas co-injection of 20 ng Tat had no effect on N-methyl-D-aspartate-mediated injury. Treatment with the N-methyl-D-aspartate antagonist 3-((RS)-2-carboxypiperazin4-yl)-propyl-1-phosphonic acid (20 mg/kg) markedly attenuated hippocampal injury resulting from co-injection of 100 ng Tat with N-methyl-D-aspartate [mean(+/-S.E.M.) % volume loss in lesioned hippocampus: 0.1(+/-2) in 3-((RS)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid-treated vs 19(+/-3) in controls, P<0.001, ANOVA]. Co-injection of Tat had no effect on N-methyl-D-aspartate-mediated striatal damage or on alpha-amino-3-hydroxy-5-methylisoxazole-4-pro hippocampal damage. These data support the hypothesis that locally released Tat could exert neurotoxic effects, mediated by N-methyl-D-aspartate receptor activation, in vivo in the immature brain.
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PMID:Tat, a human immunodeficiency virus-1-derived protein, augments excitotoxic hippocampal injury in neonatal rats. 1019 77

AIDS is known to cause a shift of cytokines in the periphery. However, predominant cytokines in skin of patients with HIV-associated skin diseases have not been clearly defined. We hypothesized that there are distinct cytokine profiles that distinguish among the different clinical manifestations of AIDS-related skin diseases. To test this hypothesis, lesional and non-lesional skin was biopsied from 53 HIV+ patients with Kaposi's sarcoma (KS), psoriasis, and pruritus due to eosinophilic folliculitis, and from HIV negative controls with psoriasis or KS prior to therapy. Immunohistochemistry was performed with antibodies to tumor necrosis factor (TNF)-alpha, interleukin (IL)-10, interferon (IFN)-gamma, and interferon-inducible protein (IP)-10. HIV positive individuals included 10 with psoriasis, 14 with pruritus, and 15 with Kaposi's sarcoma. HIV negative controls included 12 with psoriasis and two with KS. Semi-quantitative analysis of cytokine staining was confirmed by optical density using a digital imaging system on four representative skin sections from each disease. Optical density analyses were conducted using ANOVA and t-tests. We found that epidermis overlying HIV+ Kaposi's sarcoma was hyperproliferative and was highest in IP-10, IFN-gamma, and IL-10 (P=0.0001). HIV+ pruritus was significantly highest in TNF-alpha (P=0.0001) staining. HIV+ psoriasis represented an intermediate state for all four cytokines. Normal skin adjacent to lesions showed the same relative patterns, with lower intensities. Skin diseases seen frequently in the setting of HIV and immunodeficiency have relatively distinct levels and patterns of cytokine expression that may reflect immune dysfunction, reactivity to HIV and to opportunistic infections.
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PMID:Cytokine expression patterns distinguish HIV associated skin diseases. 1101 55


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