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Biomedical subjects

S Sethi

Publications and source records attributed to S Sethi.

At least 19 recordsLinked to original sources
PubMed2001

Generalized anxiety disorder in the elderly.

Anxiety disorders, especially GAD, are among the most prevalent psychiatric illnesses in the elderly. Unfortunately, research relative to late-onset anxiety syndromes and longitudinal studies of early-onset anxiety syndromes are sparse. Nonetheless, clinicians can properly assess and treat older adults with anxiety disorders and improve their quality of life. Additional research is needed to better elucidate the various presentations of GAD in the elderly and in developing safe, effective, nonpharmacologic and pharmacologic treatment approaches.

Aged↗
PubMed2001

Use of porcine acellular dermal matrix as a dermal substitute in rats.

OBJECTIVE: To examine porcine acellular dermal matrix (ADM) as a xenogenic dermal substitute in a rat model. SUMMARY BACKGROUND DATA: Acellular dermal matrix has been used in the treatment of full-thickness skin injuries as an allogenic dermal substitute providing a stable wound base in human and animal studies. METHODS: Xenogenic and allogenic ADMs were produced by treating porcine or rat skin with Dispase and Triton X-100. Full-thickness skin defects (225 mm2) were created on the dorsum of rats (n = 29), porcine or rat ADMs were implanted in them, and these were overlain with ultrathin split-thickness skin grafts (STSGs). In two adjacent wounds, 0.005- or 0.017-inch-thick autografts were implanted. In other experiments, the antimicrobial agent used during ADM processing (azide or a mixture of antibiotics) and the orientation of the implanted ADM (papillary or reticular side of ADM facing the STSG) were studied. Grafts were evaluated grossly and histologically for 30 days after surgery. RESULTS: Significant wound contraction was seen at 14, 20, and 30 days after surgery in wounds receiving xenogenic ADM, allogenic ADM, and thin STSGs. Contraction of wounds containing xenogenic ADM was significantly greater than that of wounds containing allogenic ADM at 30 days after surgery. Graft take was poor in wounds containing xenogenic ADM and moderately good in those containing allogenic ADM. Wound healing was not significantly affected by the antimicrobial agent used during ADM preparation or by the ADM orientation. CONCLUSION: Dispase-Triton-treated allogenic ADM was useful as a dermal substitute in full-thickness skin defects, but healing with xenogenic ADM was poor.

Animals↗
PubMed2001

Bacterial infection in chronic obstructive pulmonary disease in 2000: a state-of-the-art review.

Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death in the United States. The precise role of bacterial infection in the course and pathogenesis of COPD has been a source of controversy for decades. Chronic bacterial colonization of the lower airways contributes to airway inflammation; more research is needed to test the hypothesis that this bacterial colonization accelerates the progressive decline in lung function seen in COPD (the vicious circle hypothesis). The course of COPD is characterized by intermittent exacerbations of the disease. Studies of samples obtained by bronchoscopy with the protected specimen brush, analysis of the human immune response with appropriate immunoassays, and antibiotic trials reveal that approximately half of exacerbations are caused by bacteria. Nontypeable Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pneumoniae are the most common causes of exacerbations, while Chlamydia pneumoniae causes a small proportion. The role of Haemophilus parainfluenzae and gram-negative bacilli remains to be established. Recent progress in studies of the molecular mechanisms of pathogenesis of infection in the human respiratory tract and in vaccine development guided by such studies promises to lead to novel ways to treat and prevent bacterial infections in COPD.

Adult↗
PubMed2001

Acute exacerbations of chronic bronchitis: what role for the new fluoroquinolones?

Acute exacerbations of chronic bronchitis (AECB) are a major cause of morbidity and mortality. Bacterial pathogens are implicated in about half the episodes of AECB. Empirical antibacterials have a significant benefit in AECB; however, several recent developments have considerably complicated antibacterial choice for this condition. New fluoroquinolone antibacterials introduced in the last decade are theoretically well suited for the treatment of AECB, as the in vitro antimicrobial spectrum of these drugs includes all the major pathogens involved. The pharmacokinetic and pharmacodynamic properties of the new fluoroquinolones are superior to many other antibacterials used to treat AECB. In trials, clinical success with the new fluoroquinolones was equivalent and bacteriological success was occasionally superior to nonfluoroquinolone comparators. However, these clinical trials did not assess several potentially important end-points for which the theoretical superiority of the fluoroquinolones may translate into differences in outcome. Rare but serious adverse effects with some of the new fluoroquinolones have shaken the confidence of prescribing physicians in this class of drugs. Emergence of the resistance of Streptococcus pneumoniae to fluoroquinolones has raised concerns about indiscriminate and widespread use of the new agents for trivial infections. Patients with AECB are a heterogeneous population who should be stratified in order to appropriately choose empirical antibacterial therapy. Highly efficacious antibacterial therapy, such as the new fluoroquinolones, is appropriate as a first-line choice for patients who have risk factors for a poor outcome or are in intensive care units. Such selected use of the new fluoroquinolones balances individual benefit with societal concerns of the use of these agents for AECB.

Anti-Infective Agents↗
PubMed2001

A case of fibrillary glomerulonephritis with linear immunoglobulin G staining of the glomerular capillary walls.

We report a case of crescentic glomerulonephritis that presented with extensive crescent formation and fibrinoid necrosis in the glomeruli. Immunofluorescence staining was strongly positive for linear and pseudolinear staining of the capillary walls for immunoglobulin G (IgG) in the absence of significant mesangial staining. Histologic examination and immunofluorescence staining suggested a diagnosis of anti-glomerular basement membrane disease. However, electron microscopy showed the presence of numerous fibrillary deposits in the subepithelial areas of the glomerular capillary walls, supporting the diagnosis of fibrillary glomerulonephritis. Test results for circulating anti-glomerular basement membrane antibodies were negative. We report this interesting case to illustrate the point that fibrillary glomerulonephritis should be considered in the differential diagnosis of crescentic glomerulonephritis with linear and pseudolinear IgG deposits within the capillary walls. In such cases, electron microscopy is critical in differentiating the cause of crescentic glomerulonephritis.

Acute Disease↗
PubMed2000

Modulation of polymorphonuclear leukocytes function by nitric oxide.

Recognition of the endothelium-derived relaxation factor as nitric oxide (NO) gave rise to an impression that NO was synthesised only by the endothelial lining of the vessel wall. Later it was found that NO is synthesized constitutively by the enzyme nitric oxide synthase (NOS) in various cells. However, inflammatory cytokines can induce NOS (known as inducible NOS [iNOS]) activity in all the somatic cells. Blood cells, such as eosinophils, platelets, neutrophils, monocytes, and macrophages, also synthesize NO. Among them, polymorphonuclear leukocytes (PMNs) constitute an important proportion and are also the major participants in a number of pathological conditions with suggestive involvement of NO. PMNs can synthesize NO at rates similar to endothelial cells, thus suggesting the importance of PMN-derived NO in various physiological and pathological conditions. Most of the studies so far focus on the peripheral PMNs, while studies on PMNs after emigration are limited, thus warranting systematic studies on PMNs from both sources. The role of the endothelial NOS (eNOS) and functions of NO derived from the endothelial cells has been studied extensively. However, understanding of the PMNs NOS and its regulatory role in their function is unraveling. The present review summarizes the modulatory role of NO on PMNs functions and points out the discrepancies relating to presence of NOS in PMNs. This information will be helpful in understanding the importance of NO in physiological and pathological conditions associated with PMNs.

Animals↗
PubMed2000

Mechanisms involved in the augmentation of arachidonic acid-induced free-radical generation from rat neutrophils following hypoxia-reoxygenation.

Polymorphonuclear leukocytes are known to play an important role in hypoxia/ischemia and reoxygenation injury. The present study was undertaken to investigate the involvement of protein kinase C, calmodulin, and cyclic adenosine monophosphate in the augmentation of the free-radical generation observed after hypoxia-reoxygenation (H-R). Free-radical generation from the rat polymorphonuclear leukocytes was measured as the arachidonic acid (1-5x10(-5) M)-induced luminol-dependent chemiluminescence response, which was augmented following H-R. The increase in free-radical generation after H-R was completely blocked by the pretreatment of cells with PKC inhibitor H(7), whereas indomethacin (a cyclo-oxygenase inhibitor) or forskolin (an adenylate cyclase activator) failed to modulate the H-R-dependent response. However, W(7)-a calcium/calmodulin (Ca(2+)/CaM) antagonist-partially reduced the augmented free-radical generation observed in the H-R cells. Results obtained thus suggest the possible involvement of protein kinase C and calcium in the augmentation of the free-radical generation response following H-R.

Adenylyl Cyclases↗
PubMed2000

Regulatory interactions of alphabeta and gammadelta T cells in glomerulonephritis.

BACKGROUND: Several lines of evidence suggest that cellular immune mechanisms contribute to glomerulonephritis. METHODS: The roles of alphabeta and gammadelta T cells in the pathogenesis of glomerulonephritis were investigated in a model of nephrotoxic nephritis in mice deficient in either T-cell population [T-cell receptor (TCR)beta and TCRdelta knockout mice]. The model, induced by the injection of rabbit anti-mouse glomerular basement membrane antibody, is characterized by the development of proteinuria and glomerular damage over a 21-day observation period in wild-type mice. RESULTS: Mice deficient in either alphabeta or gammadelta T cells developed minimal proteinuria and glomerular lesions and had a significant reduction in macrophage accumulation compared with wild-type mice. In gammadelta T-cell-deficient mice, circulating levels and glomerular deposition of autologous IgG were comparable to wild-type levels, while alphabeta T-cell-deficient mice had no autologous IgG production. Autologous antibody production was not required for the development of glomerulonephritis since mice that lack IgG and B cells (micro-chain-/-) developed similar proteinuria to that observed in wild-type mice. CONCLUSIONS: These studies suggest a proinflammatory role for both alphabeta and gammadelta T cells in glomerular injury, independent of the humoral response. This is the first demonstration, to our knowledge, that both T-cell subsets contribute to the progression of a disease, and it suggests that complex regulatory interactions between alphabeta and gammadelta T cells play a role in glomerular injury.

Animals↗
PubMed2000

Three unusual siblings with Harlequin icthyosis in an Indian family.

Harlequin fetuses occurring as three siblings in an Indian family are described here. All three were preterm, low birth weight, and did not survive. There was no history of consanguinous marriage in the parents or in the family. Thus autosomal recessive inheritance appears to be a remote possibility, although not impossible or, as recently described, these recurrent harlequin fetuses could be the result of new dominant mutations with parental mosaicism.

Female↗
PubMed2000

Bacterial infection and the pathogenesis of COPD.

Bacterial infection of the lower respiratory tract can impact on the etiology, pathogenesis, and the clinical course of COPD in several ways. Several recent cohort studies suggest that lung growth is impaired by childhood lower respiratory tract infection, making these individuals more vulnerable to developing COPD on exposure to additional injurious agents. Impairment of mucociliary clearance and local immune defense in smokers allows bacterial pathogens to gain a foothold in the lower respiratory tract. These pathogens and their products can cause further impairment of mucociliary clearance due to enhanced mucus secretion, disruption of normal ciliary activity, and airway epithelial injury, and thus persist in the lower respiratory tract. This chronic colonization of the lower respiratory tract by bacterial pathogens could induce a chronic inflammatory response with lung damage. Nontypeable Haemophilus influenzae, usually regarded as an extracellular mucosal pathogen, has been demonstrated to cause intracellular infections of the upper and lower respiratory tract respiratory tissue. Increased incidence of chronic Chlamydia pneumoniae infection of the respiratory tract has been associated with COPD. These chronic infections of respiratory tissues could contribute to the pathogenesis of COPD by altering the host response to cigarette smoke or by inducing a chronic inflammatory response. Application of newer molecular and immunologic research techniques is helping us define precisely the role of bacterial infection in COPD.

Bacteria↗
PubMed2000

Infectious etiology of acute exacerbations of chronic bronchitis.

Infectious agents are a major cause of acute exacerbations of chronic bronchitis (AECB) and COPD. Several respiratory viruses are associated with 30% of exacerbations, with or without a superimposed bacterial infection. Atypical bacteria, mostly Chlamydia pneumoniae, have been implicated in < 10% of AECB. The role of bacterial pathogens when isolated from the respiratory tract during AECB has become better defined by application of several newer investigative techniques. Bacterial pathogens can be isolated in significant concentrations from distal airways in 50% of AECB. Specific immune responses to surface exposed antigens of the infecting pathogen have been shown to develop after an exacerbation. Emerging evidence from molecular epidemiology and measurement of airway inflammation further support the role of bacteria in AECB. When properly defined, 80% of AECB are likely to be infectious in origin.

Acute Disease↗
PubMed2000

The role of bacteria in exacerbations of COPD. A constructive view.

The role of infection in exacerbations of COPD remains controversial and incompletely understood. Although some investigators believe that bacteria are not important for patients with exacerbation, we disagree and believe that patients with at least two of the three cardinal symptoms of exacerbation should receive antibiotic therapy. With an open-minded view of the area, we review the data, showing that bacteriologic studies, pathologic investigations, and clinical trials all support roles for bacteria and antibiotic therapy in this disease. Still, many questions remain, and future studies will be needed to better define the mechanisms of bacterial invasion in the bronchitic patient and to develop effective vaccines to prevent exacerbations. In the meantime, we must rely on antibiotic therapy, and we will need prospective studies to corroborate preliminary findings showing that different patients may require different therapies; thus, patient subsetting may be vital in the selection of antibiotic therapy for exacerbations of COPD.

Anti-Bacterial Agents↗
PubMed2000

Airway inflammation and etiology of acute exacerbations of chronic bronchitis.

STUDY OBJECTIVES: The etiologic role of bacterial pathogens isolated from sputum culture in 40 to 50% of acute exacerbations of chronic bronchitis (AECB) is controversial. If bacterial pathogens cause these AECB, they should be associated with greater neutrophilic airway inflammation than pathogen-negative exacerbations. DESIGN: This hypothesis was tested by comparing levels of interleukin (IL)-8, tumor necrosis factor (TNF)-alpha, and neutrophil elastase (NE) in 81 sputum samples obtained from 45 patients with AECB. Four groups were compared. In the first three groups, nontypable Haemophilus influenzae (n = 20), Haemophilus parainfluenzae (n = 27), and Moraxella catarrhalis (n = 14) were isolated as sole pathogens, respectively. In the fourth group, only normal flora was isolated (n = 20). Paired samples, obtained from individual patients at different times, that differed in their culture results were also compared. SETTING: An outpatient research clinic at a Veterans Affairs Medical Center. PATIENTS: These patients were participating in a prospective, longitudinal study of the dynamics of bacterial infection in chronic bronchitis, for which they were seen in the study clinic on a monthly basis as well as when they were experiencing symptoms suggestive of AECB. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: H influenzae exacerbations were associated with significantly higher sputum IL-8, TNF-alpha, and NE. M catarrhalis exacerbations demonstrated significantly higher sputum TNF-alpha and NE when compared to pathogen-negative exacerbations. H parainfluenzae-associated exacerbations had an inflammatory profile similar to pathogen-negative exacerbations. Sputum elastase level distinguished bacterial from nonbacterial AECB and correlated with clinical severity of the AECB. CONCLUSIONS: Increased airway inflammation associated with isolation of H influenzae and M catarrhalis supports an etiologic role of these pathogens in AECB.

Acute Disease↗
PubMed2000

Evaluation of E test for susceptibility testing of Mycobacterium tuberculosis to primary anti tubercular drugs.

BACKGROUND & OBJECTIVES: Antimicrobial susceptibility tests for tuberculosis take weeks and delayed therapy can lead to an increase in disease incidence. The E test is a new concept for minimum inhibitory concentrations (MIC) determinations for antimicrobial agents that is based on a predefined antibiotic gradient on a plastic strip calibrated with a continuous logarithmic MIC scale covering 15 two-fold dilutions. The present study was undertaken to evaluate E test strips for susceptibility testing of Mycobacterium tuberculosis. METHODS: Twenty five clinical isolates of M. tuberculosis were tested for the four first line antitubercular drugs by E test and were compared with standard proportion method. The inoculum turbidity was adjusted to McFarland 3.0 standard and agar plates (Middle brook 7H11 agar) were inoculated and preincubated (37 degrees C in 7-10% CO2) for 24 h after which time, the E test strips were placed on the agar surface which were incubated under same conditions. The MIC was interpreted as the point at which the ellipse intersected the 'E test' strip as described in E test technical guide. RESULTS: Of the 25 strains, susceptibility as determined by both methods for isoniazid (INH), rifampin, ethambutol and streptomycin was found in 22 (88%), 20 (80%), 24 (96%) and 18 (72%) strains respectively. Agreement between E test and proportion method was 96 per cent for INH, 92 per cent for rifampin and 100 per cent for ethambutol and streptomycin each. However, sensitivity could be predicted after 7-10 days by E test and exact MIC could also be determined. INTERPRETATION & CONCLUSIONS: E test method was found to be rapid, accurate, reliable and easy to perform. It can be employed for routine susceptibility testing for antitubercular drugs.

Antitubercular Agents↗
PubMed2000

Evaluation of leukergy test as an indicator of infection in hip joint in children.

This new blood test (leukergy) for infection is based on the fact that white cells agglomerate in peripheral blood of patients with inflammatory diseases. We evaluated leukergy in 25 children with proven septic arthritis of hip. It was found to be the efficient and earliest indicator of septic arthritis than the erythrocyte sedimentation rate (ESR), total leucocyte count (TLC), polymorphs and C-reactive protein (CRP). It also correlated well with the clinical severity of infection and the prognosis of disease. Thus leukergy is a simple, rapid and inexpensive slide test which was found as the best indicator profile for the presence of septic arthritis.

Arthritis, Infectious↗