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Biomedical subjects

Sanjay Mehta

Publications and source records attributed to Sanjay Mehta.

At least 19 recordsLinked to original sources
PubMed2006

Methicillin-resistant Staphylococcus aureus survival on hospital fomites.

We examined the duration of survival of 2 strains of methicillin-resistant Staphylococcus aureus (MRSA) on 3 types of hospital fomites. MRSA survived for 11 days on a plastic patient chart, more than 12 days on a laminated tabletop, and 9 days on a cloth curtain. Irregular surfaces may help harbor organisms in the environment. In addition to contact precautions, MRSA containment during an outbreak should include concurrent environmental decontamination.

Bedding and Linens↗
PubMed2006

Impact of rapid in situ hybridization testing on coagulase-negative staphylococci positive blood cultures.

OBJECTIVES: To evaluate the impact of the rapid differentiation of Staphylococcus aureus from coagulase-negative staphylococci (CoNS) in blood cultures using peptide nucleic acid fluorescence in situ hybridization (PNA FISH) on vancomycin usage, length of patient hospital stay and hospital costs. DESIGN: This was a retrospective, cost-effective analysis of PNA FISH in its initial 3 month implementation period in 2004 in a 650 bed academic medical centre. Blood cultures with Gram-positive cocci in clusters (GPCC) that were negative for S. aureus using the PNA FISH assay were compared with an untested control group in the same period that had similar illness severity and location. We evaluated the effectiveness of the early identification of CoNS by ruling out S. aureus in conjunction with an antimicrobial team (AMT) on antimicrobial therapy, patient length of stay and hospital costs. RESULTS: A total of 139 blood cultures positive with GPCC had PNA FISH results while 84 in the control group did not. Evaluable criteria were met in 53 patients in the PNA FISH group and 34 in the control group. When comparing the results obtained from using the PNA FISH assay with those for the control group, there was a significant reduction in median length of hospital stay from 6 to 4 days (P < 0.05, CI 0.95-1.87) and a trend towards less vancomycin usage with a decrease in associated hospital costs of approximately Dollars 4000 per patient. CONCLUSIONS: The PNA FISH assay is rapid, accurate and reliable and in association with an AMT could decrease hospital length of stay in patients with CoNS bacteraemia in non-intensive care unit settings and prevent excessive vancomycin usage.

Adult↗
PubMed2006

Thrombotic arteriopathy and anticoagulation in pulmonary hypertension.

The role of thrombotic arteriopathy in the pathophysiology of idiopathic pulmonary arterial hypertension (IPAH) and the use of anticoagulants in the treatment of IPAH are currently controversial issues. This article reviews the evidence for a role of vascular thrombosis in the pathophysiology of IPAH. There is sufficient biological rationale to support the notion that thrombotic arteriopathy is an important pathophysiologic feature of pulmonary arterial hypertension (PAH) and that its progression materially contributes to disease progression. To date, the data from observational studies suggest that anticoagulation with warfarin is an effective intervention in patients with IPAH. Its efficacy in other causes of PAH remains speculative.

Anticoagulants↗
PubMed2006

The utility of implantable loop recorders for diagnosing unexplained syncope in 100 consecutive patients: five-year, single-center experience.

INTRODUCTION: The purpose of this study was to retrospectively review the 5-year experience of a university hospital with implantable loop recorders (ILR) for the diagnosis of recurrent, unexplained syncope or presyncope. METHODS: One hundred patients with syncope or presyncope of unknown etiology (negative tilt-table test, electrophysiology study and neurologic workup) underwent prolonged monitoring with an ILR from March 2000 to December 2004. All implants were performed using a first-generation (manual activation) or second-generation (manual plus automatic activation) ILR. RESULTS: One hundred patients (70 women, 30 men) with a mean age of 68 +/- 18 years received the ILR. Twenty-three patients had coronary artery disease; 2 patients had dilated cardiomyopathy. Ten patients received a first-generation ILR, and 90 patients received a second-generation ILR. After 9 +/- 8 months' follow up, ILR interrogation identified an arrhythmogenic etiology to the syncope/presyncope in 45 patients with 55 events. Eight patients had a diagnosis by ILR less than 2 months from the date of implantation. Twenty-six patients had documented symptomatic bradycardia (asystole, sinus pauses, atrial fibrillation with long pauses); 11 patients had episodes of sinus tachycardia with heart rates of 130 to 140 beats/minute; 2 patients had atrial tachycardia; 5 patients had multiple episodes of nonsustained ventricular tachycardia (NSVT); 1 patient had sustained ventricular tachycardia, and 4 patients had paroxysmal supraventricular tachycardia. All arrhythmias were treated successfully by pacemaker/ICD implantation, radiofrequency catheter ablation and/or medications. One patient had seizure activity, which was detected by ILR as high-frequency noise. Two patients failed to activate their device, as it was a first-generation device. CONCLUSION: Five-year experience with the ILR in 100 consecutive patients confirms the utility of this device in the diagnosis of recurrent, infrequent, unexplained syncope or presyncope. It helped diagnose 45% of patients with unexplained syncope with negative electrophysiologic and neurologic workup. Most of these patients had an arrhythmogenic etiology to their syncope. Medical therapy, device therapy, and/or catheter ablation helped successfully treat all patients with an arrhythmogenic etiology detected by ILR.

Adrenergic beta-Antagonists↗
PubMed2005

Albumin leak across human pulmonary microvascular vs. umbilical vein endothelial cells under septic conditions.

Human pulmonary microvascular endothelial cell (HPMVEC) injury is central to the pathophysiology of human lung injury. However, septic HPMVEC barrier dysfunction and the contribution of neutrophils have not been directly addressed in vitro. Instead, human EC responses are often extrapolated from studies of human umbilical vein EC (HUVEC). We hypothesized that HUVEC was not a good model for investigating HPMVEC barrier function under septic conditions. HPMVEC was isolated from lung tissue resected from lung cancer patients using magnetic bead-bound anti-PECAM-1 antibody. In confluent monolayers in 3-mum cell-culture inserts, we assessed trans-EC Evans-Blue (EB)-conjugated albumin leak under basal, unstimulated conditions and following stimulation with either lipopolysaccharide or a mixture of equal concentrations of TNF-alpha, IL-1beta and IFN-gamma (cytomix). Basal EB-albumin leak was significantly lower across HPMVEC than HUVEC (0.64 +/- 0.06% vs. 1.13 +/- 0.10%, respectively, P < 0.001). Lipopolysaccharide and cytomix increased leak across both HPMVEC and HUVEC in a dose-dependent manner, with a similar increase relative to basal leak in both cell types. The presence of neutrophils markedly and dose-dependently enhanced cytomix-induced EB-albumin leak across HPMVEC (P < 0.01), but had no effect on EB-albumin leak across HUVEC. Both cytomix and lipopolysaccharide-induced albumin leak was not associated with a loss of cell viability. In conclusion, HPMVEC barrier dysfunction under septic conditions is dramatically enhanced by neutrophil presence, and HUVEC is not a suitable model for studying HPMVEC septic barrier responses. The direct study of HPMVEC septic responses will lead to a better understanding of human lung injury.

Cell Culture Techniques↗
PubMed2005

The effects of nitric oxide in acute lung injury.

Acute lung injury (ALI) is a common clinical problem associated with significant morbidity and mortality. Ongoing clinical and basic research and a greater understanding of the pathophysiology of ALI have not been translated into new anti-inflammatory therapeutic options for patients with ALI, or into a significant improvement in the outcome of ALI. In both animal models and humans with ALI, there is increased endogenous production of nitric oxide (NO) due to enhanced expression and activity of inducible NO synthase (iNOS). This increased presence of iNOS and NO in ALI contributes importantly to the pathophysiology of ALI. However, inhibition of total NO production or selective inhibition of iNOS has not been effective in the treatment of ALI. We have recently suggested that there may be differential effects of NO derived from different cell populations in ALI. This concept of cell-source-specific effects of NO in ALI has potential therapeutic relevance, as targeted iNOS inhibition specifically to key individual cells may be an effective therapeutic approach in patients with ALI. In this paper, we will explore the potential role for endogenous iNOS-derived NO in ALI. We will review the evidence for increased iNOS expression and NO production, the effects of non-selective NOS inhibition, the effects of selective inhibition or deficiency of iNOS, and this concept of cell-source-specific effects of iNOS in both animal models and human ALI.

Acute Disease↗
PubMed2005

Pulmonary oxidant stress in murine sepsis is due to inflammatory cell nitric oxide.

OBJECTIVE: Pulmonary oxidant stress is an important pathophysiologic feature of acute lung injury. It is unclear whether nitric oxide contributes to this oxidant stress. Thus, we examined the role of inducible nitric oxide synthase (iNOS) in pulmonary oxidant stress in murine sepsis and the differential contribution of different cellular sources of iNOS. DESIGN: Randomized, controlled animal study. SETTING: Research laboratory of an academic institution. SUBJECTS: Male iNOS+/+, iNOS-/- C57Bl/6 mice, and bone-marrow transplanted iNOS chimeric mice: +to- (wild-type iNOS+/+ donor bone-marrow transplanted into iNOS-/- recipient mice) and the reciprocal -to+ chimeras. INTERVENTIONS: Animals were randomized to sepsis (n = 264), induced by cecal ligation and perforation, vs. naive groups (n = 138). MEASUREMENTS AND MAIN RESULTS: In septic iNOS-/- vs. wild-type iNOS+/+ mice, sepsis-induced pulmonary oxidant stress (33 +/- 11 [mean +/- sem] vs. 365 +/- 48 pg 8-isoprostane/mg protein, p < .01) and nitrosative stress (0.0 +/- 0.0 vs. 0.9 +/- 0.4 micromol 3-nitrotyrosine/mmol para-tyrosine, p < .05) were abolished, despite similar septic increases in pulmonary myeloperoxidase activity in both (86 +/- 20 vs. 83 +/- 12 mU/mg protein, p = .78). In +to- iNOS chimeric mice (iNOS localized only to donor bone-marrow-derived inflammatory cells), cecal ligation and perforation resulted in significant pulmonary oxidant stress (368 +/- 81 pg 8-isoprostane/mg protein) and nitrosative stress (0.6 +/- 0.2 micromol 3-nitrotyrosine/mmol para-tyrosine), similar in degree to septic wild-type mice. In contrast, pulmonary oxidant and nitrosative stresses were absent in septic -to+ iNOS chimeras (iNOS localized only to recipient parenchymal cells), similar to iNOS-/- mice. CONCLUSIONS: In murine sepsis-induced acute lung injury, pulmonary oxidant stress is completely iNOS dependent and is associated with tyrosine nitration. Moreover, pulmonary oxidant stress and nitrosative stress were uniquely dependent on the presence of iNOS in inflammatory cells (e.g., macrophages and neutrophils), with no apparent contribution of iNOS in pulmonary parenchymal cells. iNOS inhibition targeted specifically to inflammatory cells may be an effective therapeutic approach in sepsis and acute lung injury.

Analysis of Variance↗
PubMed2005

Canadian Cardiovascular Society and Canadian Thoracic Society position statement on pulmonary arterial hypertension.

The Canadian Cardiovascular Society and the Canadian Thoracic Society requested a position statement on pulmonary arterial hypertension from leading Canadian experts. The present document is intended to act as an update for the clinician, to provide a template for the initial evaluation of patients, to enable the understanding of current therapeutic paradigms based on approved indications for Canada, to highlight new therapies on the horizon, and to state the positions of the Canadian Cardiovascular Society and the Canadian Thoracic Society on resource management for pulmonary arterial hypertension in Canada.

Humans↗
PubMed2005

Gastrointestinal infections in the immunocompromised host.

PURPOSE OF REVIEW: Infections of the gastrointestinal tract are an important cause of morbidity and mortality in immunocompromised patients. This review summarizes the most important articles published between July 2003 and June 2004 in the pathogenesis, diagnosis, and treatment of gastrointestinal infections in the immunocompromised host. RECENT FINDINGS: The articles summarized include multiple case reports of novel pathogens such as spirochetes infecting the gut and common pathogens with atypical presentations such as Mycobacterium tuberculosis presenting as colonic perforation. In addition, there are multiple retrospective reviews with insight into typical presentations and risk factors for certain diseases. Furthermore, there are multiple drug reviews and prevalence studies. The recurrent theme, however, is the frequent appearance of infections, such as Strongyloides stercoralis, commonly found in the developing world but now occurring much more commonly in all parts of the world because of AIDS and other disease- or therapeutic-induced immunosuppression. SUMMARY: As people continue to emigrate and travel internationally, it is increasingly important to know about pathogens and disease processes in other parts of the world. The case reports and studies that follow will help clinicians improve their diagnostic and therapeutic skills regarding gastrointestinal infections in the immunocompromised host.

Bacterial Infections↗
PubMed2005

Canadian Cardiovascular Society and Canadian Thoracic Society position statement on pulmonary arterial hypertension.

The Canadian Cardiovascular Society and the Canadian Thoracic Society requested a position statement on pulmonary arterial hypertension from leading Canadian experts. The present document is intended to act as an update for the clinician, to provide a template for the initial evaluation of patients, to enable understanding of current therapeutic paradigms based on approved indications for Canada, to highlight new therapies on the horizon, and to state the positions of the Canadian Cardiovascular Society and the Canadian Thoracic Society on resource management for pulmonary arterial hypertension in Canada.

Canada↗
PubMed2004

A painful shoulder.

Explore the source record for details and available documents.

Arthritis, Infectious↗
PubMed2004

Pulmonary neutrophil infiltration in murine sepsis: role of inducible nitric oxide synthase.

Nitric oxide (NO) derived from inducible NO synthase (iNOS) contributes to the pathophysiology of acute lung injury (ALI). The effect of iNOS on pulmonary neutrophil infiltration in ALI is not known. Thus, we assessed pulmonary microvascular neutrophil sequestration through intravital videomicroscopy and pulmonary neutrophil infiltration, reflected by myeloperoxidase activity and lavage neutrophil counts, after induction of sepsis by cecal ligation/perforation in wild-type (iNOS+/+) versus iNOS-/- mice. Pulmonary microvascular neutrophil sequestration was attenuated in septic iNOS-/- versus iNOS+/+ mice (15 +/- 1 vs. 20 +/- 1 leukocytes per field, p < 0.05), but lavage neutrophil counts were greater in iNOS-/- mice (5.7 +/- 1.5% vs. 0.7 +/- 0.1%, p < 0.05) between 6 and 18 hours after cecal ligation and perforation. When iNOS+/+ bone marrow was transplanted into bone marrow-depleted iNOS-/- mice (+ to - chimeras; iNOS limited to marrow-derived inflammatory cells), septic pulmonary microvascular neutrophil sequestration and lavage neutrophil counts were restored to levels seen in septic iNOS+/+ mice. In contrast, in - to + chimeras, pulmonary neutrophil trafficking was similar to iNOS-/- mice. In vitro cytokine-stimulated neutrophil transendothelial migration was significantly greater for iNOS-/- versus iNOS+/+ neutrophils (7.9 +/- 0.7% vs. 3.8 +/- 0.6%, p < 0.05) but was independent of endothelial iNOS. Thus, neutrophil iNOS-derived NO is an important autocrine modulator of pulmonary neutrophil infiltration in murine sepsis.

Acute Disease↗
PubMed2004

Excess nitric oxide decreases cytochrome P-450 2J4 content and P-450-dependent arachidonic acid metabolism in lungs of rats with acute pneumonia.

Recently, we demonstrated that pulmonary CYP2J4 content, a prominent source of EETs and HETEs formation in rat lungs, is reduced in pneumonia. Therefore, the purpose of this study was to determine the role of iNOS-derived NO in reduced pulmonary CYP2J4 protein content and decreased CYP metabolites in pneumonia. Rats were randomized to control, control plus 1400W (iNOS inhibitor), pneumonia, and pneumonia plus 1400W groups. Pseudomonas organisms were injected into lungs of pneumonia rats. At 40 h after surgery, rats were treated with either saline or 1400W for 4 h before death. Venous plasma samples were obtained for measuring nitrites/nitrates (NOx). There was no significant effect of 1400W on blood pressure measured in control or pneumonia rats, whereas 1400W reduced the elevated plasma NOx levels in pneumonia rats by half. CYP primary metabolites of AA formed at significantly lower rates in pulmonary microsomes from pneumonia rats compared with control rats. Treatment of pneumonia rats with 1400W resulted in a significant increase in the rate of formation of pulmonary EETs and omega-terminal HETEs compared with untreated pneumonia rats. The reduction in CYP2J4 protein content in pneumonia lung microsomes was also partially prevented by 1400W. Therefore, excess NO from iNOS decreases the pulmonary production of EETs and omega-HETEs in acute pneumonia. Inhibition of iNOS restores CYP2J4 protein content and CYP activity in acute pneumonia, indicating an important NO-CYP interaction in pulmonary responses to infection. We speculate CYP2J4 and its AA metabolites are involved in the modulation of pulmonary function in health and disease.

Acute Disease↗
PubMed2003

Pulmonary cytochrome P-450 2J4 is reduced in a rat model of acute Pseudomonas pneumonia.

We previously reported that the levels of epoxyeicosatrienoic acids (EETs) and 20-hydroxyeicosatetraenoic acid (20-HETE) are depressed in microsomes prepared from lungs of rats with acute Pseudomonas pneumonia. We also showed a potential role for cytochrome P-450 (CYP) metabolites of arachidonic acid (AA) in contractile responses of both normal pulmonary arteries and pulmonary arteries from rats with pneumonia. The CYP2J subfamily enzymes (endogenous source of EETs and HETEs) are constitutively expressed in human and rat lungs where they are localized in vascular smooth muscle and endothelium. The purpose of this study was to determine if CYP2J proteins are modified in pneumonia. Pseudomonas organisms were injected via a tracheostomy in the lungs of rats. Later (44 h), lungs were frozen, and microsomes were prepared from pneumonia and control rat lung homogenates. Lung microsomal proteins were then immunoblotted with anti-CYP2B1/2B2, anti-CYP4A, anti-CYP2J9pep2 (which reacts with rat CYP2J3), anti-CYP2J6pep1 (which reacts with rat CYP2J4), anti-CYP2J2pep4, or anti-CYP2J2pep3 (both of which react with all known CYP2J isozymes). Western blotting revealed a prominent 55-kDa band with anti-CYP2J2pep3, anti-CYP2J2pep4, and anti-CYP2J6pep1 (but not anti-CYP2J9pep2) that was reduced in pneumonia compared with control lung microsomes. The CYP2B bands (51-52 kDa) were less prominent and not different between pneumonia and control lungs. CYP4A proteins (20-HETE sources) were not detected in rat lung microsomes. Therefore, rat lung contains a protein with immunological characteristics similar to CYP2J4, and this CYP is reduced after pneumonia. We speculate that CYP2J (but not CYP2B) enzymes and their AA metabolic products (EETs) are involved in the modulation of pulmonary vascular tone in pneumonia in rats.

Acute Disease↗
PubMed2003

Traumatic aortic transection with intraluminal aortic fat: transesophageal echocardiographic characteristics and implications.

Aortic transection can be a catastrophic complication of blunt chest trauma. Transesophageal echocardiography is a useful tool for assessing aortic pathology. Presented is a case of traumatic aortic transection in which periaortic fat was found within the aortic lumen. Transesophageal echocardiographic characteristics are reviewed and clinical implications discussed.

Accidents, Traffic↗