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Biomedical subjects

J Puri

Publications and source records attributed to J Puri.

At least 19 recordsLinked to original sources
PubMed2002

Catheter associated urinary tract infections in neurology and neurosurgical units.

OBJECTIVE: Catheter associated bacteriuria is the most common infection acquired in hospitals. The objective of the study was (1) to study the incidence of bacteriuria following indwelling urethral catheterization in patients with short-term vs long-term catheterization (2) to define the antibiotic resistance pattern among these isolates so that the study can provide guidelines for choosing an effective antibiotic against infections in catheterized patients. METHODS: This is a prospective study carried out over a period of 18 months in Neurology/Neurosurgical patients who had indwelling catheters for > or =48 h. RESULTS: In this study, 68 out of 800 (8.5%) adult inpatients acquired urinary tract infection following indwelling bladder catheterizations. The risk was significantly higher for female, elderly patients, critically ill and patients on prolonged catheterization. Among the bacterial pathogens, Escherichia coli was the commonest organism isolated (32.9%) followed by Pseudomonas sp. (15.1%) and Staphylococcus aureus (12.3%). Candida sp. comprised 13.7% of all isolates. Among Gram negative bacterial pathogens maximum number of isolates were sensitive to Amikacin (sensitivity of 42%). All Gram positive organisms were however sensitive to Vancomycin. CONCLUSIONS: Our results provide guidelines for choosing salvage therapy against hospital resistant strains causing infection in catheterized patients. However, antibiotics seem to prevent urinary tract infections but primarily in patients catherized for short duration, i.e. 3-14 days and not in patients with long-term catheterization.

Aged↗
PubMed1998

Bacteriology of burns.

A retrospective study was undertaken at University College of Medical Sciences and Guru Teg Bahadur Hospital, Delhi, to examine the bacterial isolates from the Burns unit and to determine the antibiograms of the isolates to commonly used antimicrobial agents. A total of 600 pus samples from as many patients received, over a period of 5 years (June 1993-June 1997) yielded 920) isolates. Pseudomonas spp. was the most common (36%) followed by Staphylococcus aureus (19%), Klebsiella spp. (15.54%), Proteus spp. (11.19%), Enterococcus faecalis (8.5%), Escherichia coli (5.10%), Acinetobacter spp. (1.1%), Salmonella senftenberg (0.8%) and other (3%). Pseudomonas spp. was the most susceptible to ceftazidime (83% susceptible) and cefoperazone (82% susceptible), whereas the drugs most effective in other Gram-negative organisms were amikacin, netilmicin and ciproflox. Vancomycin was effective in 100% of Gram-positive organisms. The infection of burn wounds with multiple organisms, with the superadded problem of drug resistance, necessitate the institution of a drug policy by the hospitals for burn patients.

Anti-Bacterial Agents↗
PubMed1997

Modulation of the immune response in multiple sclerosis: production of monoclonal antibodies specific to HLA/myelin basic protein.

Monoclonal Abs to the complex formed between human MHC class II molecules (DR7 and DRw11) and myelin basic protein (MBP) were produced. The specificity of these Abs was established by both FACS analysis and complement-mediated cytotoxicity of MBP- or OVA-pulsed human APC of the same or of different DR restriction. These Abs bound to and lysed only MBP-pulsed human APC of the same DR restriction (DR7 or DRw11) but not to APC of different DR restriction or pulsed with a different Ag (OVA). The physiologic role of these Abs was further investigated. They blocked the in vitro proliferative response to MBP-specific T cell clones isolated from multiple sclerosis patients in an antigen-specific and DR-restricted manner. However, the Abs did not affect the response of MBP-specific T cell clones of other DR restriction nor did they interfere with the response to other Ags (purified protein derivative or copolymer 1) presented on APC with the same DR restriction. These Abs may be useful for treating multiple sclerosis in which reactivity to MBP is implicated. Moreover, this approach may be extended to other autoantigens and their counterpart autoimmune diseases.

Animals↗
PubMed1996

Frequency, microbial spectrum and outcome of spontaneous bacterial peritonitis in north India.

AIM: To determine the prevalence, microbial spectrum and outcome of spontaneous bacterial peritonitis (SBP) and its variants in hospitalized cirrhotics. STUDY DESIGN: Prospective cohort study at a tertiary referral center in North India. METHODS: Over a four-month period, 70 consecutive adult patients with decompensated cirrhosis were screened for the presence of SBP or its variants. Ascitic fluid culture was done by direct inoculation of blood culture bottles at the bedside. Blood, urine and other fluids were cultured during hospital stay when clinically indicated. Ascitic fluid total leukocyte count and culture were repeated at any time during hospital stay if the patient showed clinical signs of deterioration. Patients with SBP and culture-negative neutrocytic ascites (CNNA) were treated empirically on the basis of ascitic fluid leukocyte count. RESULTS: Twenty-one of 70 (30%) patients with cirrhosis were diagnosed to have SBP or its variants CNNA and monomicrobial bacterascites (MBA). Ninety-five percent of the patients who developed this complication were in Child-Pugh class C. A causative organism was isolated in 62% of these patients. Gram-negative bucilli accounted for 6 of 10 patients with SBP whereas all cases of MBA were due to infection with Gram-positive cocei. A third of patients with SBP/CNNA had evidence of extra-abdominal focus of infection with the same organism. All episodes of SBP/CNNA were initially treated with either ciprofloxacin (12 patients) or a combination of third generation cephalosporin, cefotaxime and an aminoglycoside, gentamicin (n = 6). Fourteen patients (67%) recovered whereas 6 patients died during hospital stay. CONCLUSION: SBP is a common complication of decompensated liver disease in North India and is associated with significant in-hospital mortality. Ciprofloxacin is an effective drug for initial treatment of SBP/CNNA. Synchronous extra-peritoneal focus of infection is a frequent occurrence in these patients.

Adult↗
PubMed1996

Activity of third generation cephalosporins against Pseudomonas aeruginosa in high risk hospital units.

Ceftazidime and Cefoperazone are the two third generation cephalosporins with anti-pseudomonal activity. They have been frequently used in the I.C.U.s. in the developed countries but their use in the Indian hospitals has begun relatively recently. We studied the in-vitro susceptibility of 139 Pseudomonas aeruginosa isolates that were multiple drug resistant from the Resuscitation Unit/I.C.U. (61 strains), Burns Unit (48 strains), Surgical Post-operative unit (24 strains), Nephrology unit (6 strains) of our hospital to these two cephalosporine over a period of about 18 months. Antibiotic susceptibility was studied using Kirby Bauer's disc dibusion method. Out of a total of 139 strains of multiple drug resistant Pseudomonas aeruginosa tested, 17.9% were found resistant each to Ceftazidime and Cefoperazone separately and 10% were found resistant to both antibiotics.

Cephalosporins↗
PubMed1995

Role of body surface cultures in prediction of sepsis in a neonatal intensive care unit.

An analysis of surface cultures of 35 preterm infants of less than 33 weeks gestational age hospitalized in a neonatal intensive care unit was made. The babies had received neither antiseptic nor antibiotic therapy prior to collection of specimens. Surface cultures were collected on the 4th or 5th day of life from 16 skin or mucosal sites. At the onset of a febrile episode within 14 days of collection of surface swabs, a blood culture was done on 31 infants (four did not develop fever) and the results were compared with the surface cultures. Sepsis was diagnosed by positive blood culture in twenty neonates (57.1%). With this frequency of sepsis, the optimum sensitivity, specificity and positive predictive values of surface cultures were 60%, 27% and 60%, respectively. These values did not improve substantially for any anatomic site cultured or for any pathogen recovered. We conclude that surface cultures are of limited value in predicting the aetiology of sepsis in neonates.

Bacteria↗
PubMed1992

Differential turnover of enzymes involved in human monocyte eicosanoid metabolism. Selective inhibition of cyclooxygenase product formation by cycloheximide in the absence of effects on 5-lipoxygenase or phospholipase A2.

Human monocytes treated with cycloheximide (CHX) demonstrated a concentration- and time-dependent inhibition of prostaglandin E2 (PGE2) synthesis and release in response to stimulation with phorbol myristate acetate, ionomycin, serum-treated zymosan, or concanavalin A. The effect of CHX required preincubation and was largely reversible within 2 hr. Thromboxane A2 release was affected similarly but no comparable effects were observed on labeled arachidonic acid release or leukotriene B4 generation. The PGE2 response was also inhibited by CHX when monocytes were given exogenous arachidonic acid with or without stimulation. CHX pretreatment also comparably decreased the amount of immunoreactive cyclooxygenase in resting and stimulated monocytes. These data indicate that monocyte cyclooxygenase, in contrast to phospholipase A2 or 5-lipoxygenase and their regulatory proteins, turns over rapidly and may be a target for up- or down-regulation by pharmacologic or (potentially) physiologic agents which affect protein synthesis or degradation.

Arachidonate 5-Lipoxygenase↗
PubMed1992

Inhibition of release of arachidonic acid, superoxide, and IL-1 from human monocytes by monoclonal anti-HLA class II antibodies: effects at proximal and distal points of inositol phospholipid hydrolysis pathway.

Incubation of human elutriator-purified monocytes with anti-HLA-DR or DQ antibody inhibited the release of arachidonic acid induced by serum-treated zymosan (STZ), a phagocytic stimulus that is known to induce inositol phospholipid hydrolysis and Ca2+ influx. However, only anti-HLA-DR antibody partially inhibited STZ-induced inositol phospholipid hydrolysis and concanavalin-A-induced Ca2+ influx. Incubation with anti-HLA-DR or -DQ antibody inhibited phorbol ester-induced AA release as well as superoxide production and IL-1 release. Inhibition of monocyte function by anti-class II antibodies was not accompanied by cAMP elevation. Furthermore, addition of exogenous db-cAMP and other agents (forskolin, cholera toxin, or 3-isobutyl-1-methyl-xanthine) that increase cAMP levels through different mechanisms, alone or in combination with anti-HLA antibodies, had no inhibitory effect on factor release. Our results demonstrate that perturbation of class II molecules down-modulates cell activation at more than one point of the signal transduction pathway with dominant inhibition distal to inositol phospholipid hydrolysis. They also suggest that the inhibition by anti-HLA class II antibody is probably not mediated via cAMP elevation.

Antibodies, Monoclonal↗
PubMed1992

Transduction of a signal for arachidonic acid metabolism by untriggered CSF-1 receptor induces an opposite effect to that induced by CSF-1 receptor and its ligand: separate regulation of phospholipase A2 and cyclooxygenase by CSF-1 receptor/CSF-1.

The mouse hematopoietic cell line, 32D, was transfected with c-fms, which encodes for the CSF-1 receptor, a tyrosine kinase (TK). In the absence of CSF-1, transfected cells show moderate levels of arachidonic acid (AA) release and produce a substantial amount of prostaglandin E2 (PGE2) in comparison with the original cell line. Exposure of transfected cells to CSF-1, while inducing a substantial increase in arachidonate release, nevertheless resulted in inhibition of PGE2 production. Addition of ST638, a tyrosine kinase inhibitor, to cells transfected with c-fms in the absence of CSF-1 inhibited PGE2 production within 10-60 min. Its addition to the same cells in the presence of CSF-1 induced an opposite effect, but required longer treatment (24 h). In either cell type, AA release was not affected by this agent. These data indicate that CSF-1 may regulate cyclooxygenase activity. The different effect of CSF-1 receptor on PGE2 production in the presence or absence of CSF-1 and the opposite effect of a tyrosine kinase inhibitor on PGE2 suggest that both the receptor alone or the receptor-ligand complex may transduce an active, but different, signal through tyrosine phosphorylation. CSF-1 receptor and CSF-1 may exert separate, but related, effects on phospholipase A2 and cyclooxygenase activity which, in concert, or along with other tyrosine kinases, regulate prostaglandin production.

Animals↗
PubMed1991

Immunomodulation of experimental allergic encephalomyelitis by antibodies to the antigen-Ia complex.

Autoimmune diseases occur when T lymphocytes become activated on recognizing self antigen linked to the autologous class II molecule of the major histocompatibility complex (MHC). The resulting complex of antigen MHC T-cell receptor could be a target for treatment of autoimmune diseases. Studies in which each component is blocked separately might be limited by interference in non-relevant immune responses that either use the same set of T-cell-receptor V gene segments or are linked to the same MHC. We report here an attack by a specific antibody on the unique antigenic site formed by the binding of two components of the trimolecular complex, the autoantigen bound to the self MHC. We tested its effect in experimental allergic encephalomyelitis, an acute neurological autoimmune disease which is widely regarded as a model for autoimmune disorders and which is mediated by CD4+ T cells recognizing myelin basic protein (BP), or its peptides, in association with self Ia. We made monoclonal antibodies which bound only the complex of BP and I-As. These antibodies blocked the proliferative response in vitro to the encephalitogenic determinant of BP and reduced the response to intact BP, without affecting the response to a nonrelevant antigen-purified protein derivative of tuberculin presented on syngeneic macrophages. They also inhibited experimental allergic encephalomyelitis in H-2s mice. Hence, antibodies directed specifically to the autoantigen-Ia complex, may offer a highly selective and effective treatment in autoimmune diseases.

Animals↗
PubMed1991

Down-regulation of surface FcRI and decrease in antibody-dependent cellular cytotoxicity of cultured monocytes. Reversal by monensin or cytochalasin-D.

To investigate the mechanisms involved in regulation of antibody-dependent cellular cytotoxicity (ADCC) mediated by human monocytes, 51Cr-labeled sheep red blood cells (RBC) were used as target cells in vitro. Monocytes incubated overnight at 37 degrees C before addition of SRBC and antibody exhibited a significant decrease in ADCC activity compared with freshly isolated cells. This pattern was observed with monocytes from all donors tested, regardless of the media used for culture. Supernatants from monocyte cultures did not inhibit the cytotoxic ability of fresh monocytes and cycloheximide, a protein synthesis inhibitor, could not reverse ADCC suppression in cultured monocytes, indicating that the alteration in ADCC is probably not due to inhibitory molecules secreted or synthesized during incubation. A correlation between the decrease in the number of surface FcRI and loss in ADCC ability of cultured monocytes was found. One mechanism for the reduced FcRI expression of 1-day-old monocytes may be rapid internalization that exceeds the rate of reexpression, because cytochalasin-D or monensin, each of which inhibits receptor internalization, maintained FcR expression as well as ADCC ability of cultured monocytes. These data illustrate mechanisms whereby alteration in the number of receptors may underlie loss of receptor-mediated functions, or be involved in augmentation of their biologic activity. The findings that important monocyte functions change under conditions of storage or culture have relevance to in vitro testing of various immune functions of monocytes performed clinically to monitor or guide therapy.

Animals↗
PubMed1991

Calcium-dependent eicosanoid metabolism by concanavalin A-stimulated human monocytes in vitro. Synergism with phorbol ester indicates separate regulation of leukotriene B4 synthesis and release.

Human monocytes obtained by counter-current centrifugal elutriation released arachidonic acid when challenged in vitro with Con A, as well as with other soluble (PMA or ionomycin) or particulate stimuli (serum-treated zymosan). Cyclo-oxygenase metabolites were the principal eicosanoids detected in the supernatants of Con A-stimulated, [3H]arachidonate-labeled monocytes, 5-Lipoxygenase (5-LO) products, such as leukotriene B4 (LTB4), were conspicuously absent. Release of arachidonate and its metabolites in response to Con A was dependent on the presence of extracellular Ca2+, but not Mg2+. In contrast to serum-treated zymosan challenge, which resulted in increased inositol trisphosphate and LTB4 release, Con A-induced inositol phospholipid hydrolysis in monocytes was limited to phosphatidylinositol or phosphatidylinositol monophosphate. Despite an inability to augment LTB4 release, Con A or PMA induced a loss of 5-lipoxygenase from a cytosolic compartment that was similar to that achieved with a calcium ionophore (ionomycin), a potent stimulus for LTB4 generation. When cell-associated LTB4 was evaluated, evidence for increased LTB4 production was obtained in response to either stimulus (PMA greater than Con A). In combination, however, PMA and Con A treatment resulted in monocyte LTB4 release comparable with that observed with the calcium ionophore or STZ. LTB4 release in response to all stimuli tested was inhibited by MK-886, a drug that binds to 5-lipoxygenase-activating protein. These results indicate the following: 1) Phospholipase A2 activation and attendant arachidonic acid release induced by agents that increase intracellular Ca2+ and/or generate diacylglycerol results in increased synthesis and release of PG and increased synthesis of leukotrienes, but not necessarily leukotriene release. 2) 5-LO translocation, which may occur independently of increased intracellular Ca2+, may be necessary for LTB4 generation but is insufficient for its release. 3) 5-Lipoxygenase-activating protein activity is necessary for 5-LO activation and LTB4 release in response to all stimuli investigated here. 4) Phorbol ester, an activator of protein kinase C, may synergize with agents such as Con A (which by themselves induce a minimal intracellular Ca2+ rise), so as to result in the release of LTB4. Thus, Con A may represent a class of surface receptor-aggregating agents that initiates inflammatory changes or immunomodulation associated with liberation of PG and might predispose to release of other inflammatory mediators, such as leukotrienes, in the presence of additional signals including protein kinase activation.

Arachidonate 5-Lipoxygenase↗
PubMed1991

Selective inhibition of PGE2 production in cells transfected with c-fms encoded CSF-1 receptor genes by the tyrosine kinase inhibitor, ST638.

In this study, we investigated the effect of ST638, a novel tyrosine kinase inhibitor, on TPA and ionomycin-stimulated PGE2 production after transfection of c-fms encoded CSF-1 receptor (CSF-1R) DNA (with or without transforming activity) into the myeloid progenitor cell line, 32D. ST638 inhibited prostaglandin E2 (PGE2) production induced after transfection of normal c-fms into 32D cell line, but failed to inhibit PGE2 production induced in 32D cells transformed with c-fms containing a point mutation at tyrosine 969 in the intracellular domain (substitution with phenylalanine) and at leucine 301 in the extracellular domain (substitution with serine). The selective effect on PGE2 production in normal c-fms-bearing cells by ST638 may indicate the presence of different induction pathways, one sensitive to ST638 and the other not. Alternatively, the phosphorylation site at tyr969 in c-fms may be a site of ST638 action, and upon its removal from the transforming c-fms, ST638 loses its inhibitory effect.

Arachidonic Acid↗
PubMed1991

Augmentation of monocyte-mediated antibody-dependent cellular cytotoxicity by protein synthesis inhibitors: evidence for an endogenous regulatory mechanism.

Protein synthesis inhibitors, cycloheximide and puromycin, were used in cytotoxic assays employing human peripheral blood monocytes as effectors and sheep erythrocytes as target cells. ADCC could be initiated and could also achieve its full lytic activity in the absence of new protein synthesis. Furthermore, an augmentation of ADCC was observed in the presence of protein synthesis inhibitors. This augmentation was due to an increase in the cytotoxic ability of effector cells rather than a change in the lytic susceptibility of the target. Enhanced cytotoxic potential could not be attributed to an increase in the expression of FcRI but could be due to increased availability of antibody for mediating ADCC as a result of reduced numbers of FcRII. Suppression of prostaglandin-E2 release by monocytes was noted in the presence of cycloheximide, possibly as a result of inhibition of synthesis of cyclooxygenase. However, prostaglandin-E2 and other arachidonic acid metabolites did not appear likely to play a role in negatively regulating human monocyte ADCC since neither cytotoxicity nor cycloheximide-induced augmentation was affected by the presence of exogenous prostaglandin-E2 or arachidonic acid. Cycloheximide was found to induce the secretion of superoxide anions by monocytes, but a role for reactive oxygen species in cycloheximide-induced augmentation of ADCC could not be established by experiments involving the use of catalase or superoxide dismutase. These results raise the possibility that a rapidly turning over protein which negatively regulates monocyte-mediated ADCC exists.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1991

Absence of modulation of monokine production via endogenous cyclooxygenase or 5-lipoxygenase metabolites: MK-886 (3-[1-(4-chlorobenzyl)-3-t-butyl-thio-5-isopropylindol-2-yl]-2,2- dimethylpropanoic acid), indomethacin, or arachidonate fail to alter immunoreactive interleukin-1 beta, or TNF-alpha production by human monocytes in vitro.

Human peripheral blood monocytes exposed to MK-886 (3-[1-(4-chlorobenzyl)-3-t-butyl-thio-5-isopropylindol-2-yl]-2,2- dimethylpropanoic acid) at doses which abolish formation of 5-lipoxygenase metabolites showed unaltered interleukin-1 beta (IL-1 beta) or tumor necrosis factor-alpha (TNF-alpha) levels in response to phorbol ester, concanavalin A, serum-treated zymosan, or lipopolysaccharide. Indomethacin (10 microM), alone or in combination with MK-886, also failed to modulate monokine production in response to any stimulus. Exogenous arachidonate (3-30 microM) which augmented the formation of PGE2 and LTB4 in the absence of stimulation, also had no effect on monokine production. LPS-induced IL-1 and TNF production occurred despite stimulation of PGE2 synthesis. The results make a role for endogenous prostaglandins and leukotrienes in the regulation of monocyte IL-1 beta and TNF-alpha production unlikely. These data also indicate that MK-886, a novel inhibitor of 5-lipoxygenase product formation, is a potentially useful leukotriene inhibitor which does not affect monokine production.

Analysis of Variance↗
PubMed1990

[Acute tonsillitis: clinical symptoms; bacteriologic culture and rapid test as deciding criteria for the use of antibiotics].

In order to prevent late sequelae from an untreated streptococcal pharyngitis all patients with streptococcal tonsillitis/pharyngitis have to be treated with antibiotics, preferably penicillin. A correct diagnosis by clinical criteria is only achievable in 72% of patients with streptococcal pharyngitis. Additional criteria such as diagnosis by culture are, therefore, mandatory. Time is a major disadvantage of traditional culture methods. Slide agglutination tests show an acceptable sensitivity of 92% and a specificity of 93%. Due to the possibility of false negative test results, with consequent withholding of adequate antimicrobial chemotherapy, these test results should be used only as a valuable guide. Decision to administer an antibiotic should still be based on clinical criteria.

Adolescent↗