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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study aimed at evaluating proximal renal tubule function in patients with nephrolithiasis and chronic pyelonephritis, and in patients with infectious diseases treated with gentamicin. The study involved 2 groups of patients: group A--17 patients with nephrolithiasis and chronic pyelonephritis and group B--30 patients with other infectious diseases (pneumonia, biliary tract infections) but with normal glomerular filtration rate. Patients from both groups were treated with gentamicin in a daily dose of 2-3 mg/kg for 7-10 days. Serum and urine creatinine levels were assayed in all patients prior to, 2-3, 7, 10 days, and after the treatment. Patients assigned to group B were divided into two subgroups: B1 included 15 patients with normal beta 2-microglobulinuria, and B2 15 patients with increased renal loss of beta 2-microglobulin and decreased tubular reabsorption of this protein. Significant increase in beta 2-microglobulinuria was seen on the third day of therapy, the decrease in the tubular reabsorption and glomerular filtration rate were noted in all patients on the seventh day of gentamicin administration. Beta 2-microglobulinuria was significantly higher in patients from groups A and B2 in comparison with group B1 in which no dysfunction of the proximal renal tubule was present before gentamicin therapy. A degree of beta 2-microglobulinuria is an early and sensitive indicator of gentamicin nephrotoxicity. The risk of nephrotixic symptoms is particularly obvious in patients with deteriorated function of renal proximal tubuli before the treatment with gentamicin.
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PMID:[Evaluation of selected indicators of the renal proximal tubule function in patients treated with gentamicin]. 149 34

To investigate the role of CD8+ T lymphocytes in recovery from influenza pneumonia, we used transgenic mice either homozygous (-/-) or heterozygous (+/-) for beta 2-microglobulin (beta 2-M) gene disruption. These mice lack major histocompatibility complex-restricted class I (CD8+) T cells. We found that after challenge with a nonlethal influenza virus, the beta 2-M (-/-) mice had significantly delayed pulmonary viral clearance. Furthermore, after challenge with a more virulent influenza virus, the beta 2-M (-/-) mice had a significantly higher mortality rate than did control mice. Thus, CD8+ T cells are important in recovery from virulent influenza infections, but other host defense mechanisms can clear the respiratory tract of more benign infections.
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PMID:Transgenic mice lacking class I major histocompatibility complex-restricted T cells have delayed viral clearance and increased mortality after influenza virus challenge. 155 85

AIDS is one of the most perplexing diseases to confront modern medicine today. AIDS will rank just behind accidents, heart disease and cancer as a major cause of potential life lost in the USA by 1991. Over half million AIDS cases are predicted by 1993 in the United States alone. There has been a great improvement in the understanding and treatment of opportunistic infections in AIDS. The most important concept is prophylactic treatment of the most common infectious complications as the immune system deteriorates. The major advance has been the prophylactic treatment of Pneumocystic Carinii Pneumonia (PCP) with either aerosolized Pentamidine or low dose Bactrim. Some experts advocate a low dose antibiotic prophylaxis for latent toxoplasma and cryptococcal infection in those patients whose immune systems are deteriorating. Prophylaxis would be instituted as the T4 helper lymphocyte count decreases. Finally, any patient found to be lately infected with either tuberculosis or syphilis, while HIV positive, must be thoroughly treated for these infections prior to any immunocompromise. The minimum follow-up of HIV positive individuals should include T4 lymphocyte counts and perhaps P24 antigen levels as well as beta 2-microglobulin levels. As these parameters worsen, patients should be directed to explore safe available treatments such as Antabuse, Naltrexone and Dextran sulfate. Any healthy patient with T4 helper counts under 400 should be directed to AIDS treatment evaluation units for enrolment in research protocols. At present over 100 drugs are being tested for the treatment of AIDS. However, researchers predict that no more than one or two drugs will be discovered over the next three years that will be helpful in the treatment of AIDS. If ever there was a more powerful argument to institute a new way of evaluating research drugs, it is this prediction. Due to the epidemic proportions of this disease, it seems reasonable to test epidemic proportions of this disease, it seems reasonable to test drugs shown to have some effect in groups of three of four drugs per patient. It is well demonstrated that AZT (Zidovudine) loses its anti-retroviral effect at about twelve to eighteen months. Drug resistance is seen in the treatment of a similar infectious agent, M. tuberculosis. Acute infection of MTB necessitates the use of three antibacterial agents. In AIDS infection, it seems logical to test two or three anti-retrovirals combined with one immunostimulant.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acquired immunodeficiency syndrome: molecular biology and its therapeutic intervention (review). 251 41

The severity of major surgery determines the extent of immunodeficiency which follows. The most pronounced immunodepression is found after severe blunt trauma; in polytraumatized patients the alterations of many measured parameters correlate with the injury severity score (ISS) i.e. with the severity of the injuries. Infection is also followed by many changes in the immune response. A score including serum concentrations of IgA, beta 2-microglobulin and percentage of monocytes was found to be predictive for the first 3 days after trauma with regard to subsequent occurrence of infection. In the first post-trauma day the lymphocyte-monocyte ratio correlates with the probability of survival or death by infection. Pneumonia occurred in 47% and septicemia in 22% of 150 polytraumatized patients ventilated artificially for more than 24 hours. The first signs of these infections were already present during the first 5 days, i.e. in the period of the most severe immunodeficiency. The preliminary results of a pilot study with immunomodulation by thymopentin are encouraging and show a significant decrease in the frequency of infections.
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PMID:[Immunologic changes and infection in severely injured patients]. 265 71

Elevated plasma renin activity (PRA) has been documented in patients with established acute renal failure. To study the association of PRA and renal dysfunction, 53 patients who were at risk of developing acute renal failure had serial measurements of PRA, renal function, and urinary beta 2-microglobulin. Those entered for study had pneumonia, septicaemia, volume loss with hypotension, or major surgical procedures with complications. Patients were divided into groups of abnormal or normal renal function. Abnormal renal function was defined by an elevated plasma urea and/or creatinine level with a submaximal urine urea to plasma urea ratio. The mean values of PRA for the abnormal and normal renal function groups, respectively, were 29 and 5.2 ng/ml/h (p less than 0.0001) and for beta 2-microglobulin 16.2 and 6.4 micrograms/l X 10(3) (p less than 0.0005). A linear regression of the logs of PRA to beta 2-microglobulin for the total group of patients gave an r value of 0.526 (p less than 0.001). These data show an association of PRA to renal dysfunction and tubular injury/dysfunction in the prerenal phase of renal failure, suggesting an effect of the renin-angiotensin system at this phase. It is not possible, however, to conclude from our study that the renin-angiotensin system has a direct role in the development of established acute tubular necrosis, since only 3 patients fell within this category.
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PMID:Elevated plasma renin activity associated with renal dysfunction. 352 81

Immunoreactive thromboxane B2 (i-TXB2) was measured in daily urine samples from twelve patients after renal transplantation. In 21 of 30 rejection episodes, the increase in i-TXB2 preceded both the increase in serum beta 2-microglobulin (beta 2-MG) and the clinical diagnosis of rejection. In 26 of 30 rejection episodes, the increase in urine i-TXB2 preceded the increase in serum creatinine. The degree of change in i-TXB2 is greater than that of either serum beta 2-MG or creatinine. Urinary i-TXB2 was very high in one patient with deep venous thrombosis, but it did not rise in patients with urinary tract infection, pneumonia, or acute tubular necrosis. Thus, urinary i-TXB2 seems to be an early indicator of clinical renal allograft rejection.
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PMID:Urine i-TXB2 in renal allograft rejection. 611 99

Our aim was to investigate whether serum neopterin and beta 2-microglobulin have any value in the distinction between Pneumocystis carinii pneumonia (PCP) and pneumonia due to extracellular bacteria. Also, to study whether neopterin and beta 2-microglobulin would correlate with the clinical course of lung infections in human immunodeficiency virus (HIV)-positive and HIV-negative patients. Thirty HIV-positive subjects with PCP, 9 HIV-positive patients with bacterial pneumonia, and 16 HIV-negative patients with bacterial pneumonia were investigated. Thirty eight asymptomatic HIV-positive subjects and 48 healthy blood donors were used as controls. The HIV-positive patients with PCP and the HIV-positive subjects with bacterial pneumonia had significantly and similarly elevated levels of neopterin and beta 2-microglobulin in the acute stage. In the weeks before the acute stage of PCP, neopterin and beta 2-microglobulin had been increasing. After start of treatment, serum neopterin declined significantly, whilst serum beta 2-microglobulin remained elevated. The HIV-negative patients with bacterial pneumonia had significantly increased serum concentrations of both markers in the acute stage, and had decreasing serum concentrations in the weeks after treatment. We conclude that neither neopterin nor beta 2-microglobulin seem to be of value in distinction between PCP and bacterial pneumonia in HIV-positive subjects. In the HIV-positive patients, neopterin may correlate partly with the clinical activity of PCP, whilst serum beta 2-microglobulin may remain elevated after PCP, despite treatment and recovery. The elevated level may, in part, be due to repeated infections and progression to acquired immune deficiency syndrome (AIDS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in serum neopterin and serum beta 2-microglobulin in subjects with lung infections. 792

Sendai virus pneumonia in beta 2-microglobulin-deficient [beta 2-m(-/-)] mice lacking CD8+ T cells is characterized by the development of CD4+ cytotoxic T lymphocytes that can be recovered directly from the respiratory tract. These CD4+ cytotoxic T lymphocytes are not found in beta 2-m (+/+) mice, though inflammatory CD4+ T cells from both beta 2-m (-/-) and beta 2-m (+/+) mice produce substantial amounts of tumor necrosis factor alpha. Blocking experiments with a monoclonal antibody that also inhibits tumor necrosis factor beta show that the secreted forms of these two cytokines are not responsible for virus-specific killing of class II major histocompatibility complex-compatible targets. Comparison of electron micrographs indicates that the CD4+ effectors from the beta 2-m (-/-) mice are potent inducers of apoptosis, while this is not the case for the beta 2-m (+/+) CD4+ set. These experiments further define the functional status of virus-specific CD4+ T cells responding in vivo in the presence or absence of CD8+ effectors.
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PMID:Divergence between cytotoxic effector function and tumor necrosis factor alpha production for inflammatory CD4+ T cells from mice with Sendai virus pneumonia. 839 84

Concentrations of beta 2-microglobulin (B2M) and angiotensin-converting enzyme (ACE) were measured in pleural fluid (Pf) and serum (S) of 364 patients with pleural effusions. Eleven patients had rheumatoid arthritis (RA), 36 verified tuberculosis (TB), 15 suspected TB, 120 cancer, 21 empyema, 34 pneumonia, 33 various defined diseases, 67 effusions of unknown aetiology and 27 congestive heart failure. The median concentrations of Pf-B2M and Pf-ACE were significantly higher in patients with RA than in patients with any other disease (p < 0.005). Tuberculous effusions contained higher Pf-ACE concentrations than any other type of non-rheumatoid effusion (p < 0.05). With sensitivities of 91%, the specificity of Pf-B2M and Pf-ACE for the diagnosis of RA was 86% and 55%, respectively. Local cellular immune events probably account for the abundance of B2M and ACE in rheumatoid and tuberculous pleural effusions. Pf-B2M and Pf-ACE determinations may aid in the differentiation of rheumatoid and tuberculous pleurisy from other types of pleural disease.
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PMID:Pleural fluid beta-2-microglobulin and angiotensin-converting enzyme concentrations in rheumatoid arthritis and tuberculosis. 888 98

Fifteen patients with stage II, IIIA, and IIIB non-small cell lung cancer (NSCLC) received subcutaneous (s.c.) recombinant, glycosylated, human interferon-beta 1a (Rebif; rHuIFN-beta 1a) on each day of conventionally fractionated radiation therapy (RT) given in 2.0 Gy fractions to 60 Gy in 6 weeks. The rHuIFN-beta 1a was generated in CHO cells by recombinant DNA technology and is identical to natural IFN-beta produced by fibroblasts in primary sequence and glycosylation. Cohorts of three patients each were treated with escalating doses of rHuIFN-beta 1a: 1.5, 3, 6, 12, and 24 MIU/m2 per treatment day. Acute toxicity was assessed according to modified WHO criteria; late toxicity was graded using RTOG late toxicity criteria. The maximum tolerated dose (MTD) of rHuIFN-beta 1a was defined as the dose level immediately below that in which dose-limiting toxicity occurred in > or = two of six patients. Immunomodulatory effects and antigenicity of rHuIFN-beta 1a were assessed by 2-5A synthetase, beta 2-microglobulin, and neopterin levels and by measurement of anti-rHuIFN-beta antibodies, respectively. Fourteen of fifteen patients experienced grades 1-3 acute (early) toxicity (< or = 90 days), which was primarily gastrointestinal: dysphagia/esophagitis (14/15), nausea/vomiting (12/15), anorexia (7/15), and liver transaminasemia (6/15). One of three patients treated with 24 MIU/m2 per treatment day (total rHuIFN-beta 1a dose 672 MIU) died of complications secondary to pneumonia, sepsis, adult respiratory distress syndrome (ARDS), and radiation pneumonitis. Twelve patients were evaluable for late toxicity (> 90 days). Maximum toxicity was grade 0 in five patients, grade 1 in four patients, and grade 5 in one patient (radiation pneumonitis). Clinical responses from the combination were 1/15 CR, 6/15 PR, 6/15 stable disease, and 1/15 progressive disease. The MTD of rHuIFN-beta 1a has been estimated at 12 MIU/m2 per treatment day when given daily during conventional RT to 60 Gy in 6 weeks. Biologic response by rHuIFN-beta 1a alone was reflected by significant and dose-related increases in 2-5A synthetase, beta 2-microglobulin, and neopterin. Radiation therapy alone had no effect on these immune response parameters and did not diminish their augmentation by rHuIFN-beta 1a. There was no association of biologic modulation with clinical response or survival.
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PMID:Recombinant human interferon-beta (rHuIFN-beta) and radiation therapy for inoperable non-small cell lung cancer. 893 64


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