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Biomedical subjects

A Banerjee

Publications and source records attributed to A Banerjee.

At least 181 records · Page 10Linked to original sources
PubMed1998

Patterns of injury associated with automobile airbag use.

The wide use of automobile airbags has undoubtedly reduced the mortality and the incidence of serious injuries from motor vehicle accidents. However, automobile airbags appear to be associated with a variety of injuries including fatal injuries, ocular injuries, upper limb and chest injuries. Further improvements in airbag design together with education of the general public in their use should help reduce airbag-related injuries.

Accidents, Traffic↗
PubMed1998

Myocardial gene reprogramming associated with a cardiac cross-resistant state induced by LPS preconditioning.

Lipopolysaccharide (LPS) preconditioning induces cardiac resistance to subsequent LPS or ischemia. This study tested the hypothesis that resistance to LPS and resistance to ischemia are two manifestations of cardiac cross-resistance which may involve reprogramming of cardiac gene expression. Rats were preconditioned with a single dose of LPS (0.5 mg/kg ip). Cardiac resistance to LPS was examined with a subsequent LPS challenge. Cardiac resistance to ischemia was determined by subjecting hearts to ischemia-reperfusion. Total RNA was extracted from myocardium for Northern analysis of mRNAs encoding protooncoproteins, antioxidant enzymes, and contractile protein isoforms. Rats preconditioned with LPS 1-7 days earlier acquired cardiac resistance to endotoxemic depression. This resistance temporally correlated with resistance to ischemia. Pretreatment with cycloheximide (0.5 mg/kg ip) abolished resistance to both LPS and ischemia. LPS preconditioning induced the expression of c-jun and c-fos mRNAs. LPS also transiently increased mRNAs encoding catalase and Mn-containing superoxide dismutase. The expression of both alpha- and beta-myosin heavy chain mRNAs was upregulated, whereas the expression of cardiac alpha-actin mRNA was suppressed. We conclude that 1) LPS induces sustained cardiac resistance to both LPS and ischemia, 2) resistance to ischemia and resistance to LPS seem to be two mechanistically indistinct components of cardiac cross-resistance, and 3) the cardiac cross-resistance is associated with reprogramming of myocardial gene expression.

Analysis of Variance↗
PubMed1998

Acute and chronic hypokalemia sensitize the isolated heart to hypoxic injury.

We examined the effects of acute and/or chronic hypokalemia on responses to 30 min of hypoxia and recovery in the isolated, perfused heart model. We found that both acute hypokalemia and chronic hypokalemia impaired contractility [expressed as maximum slope of pressure increase over time (dP/dt): 501 +/- 49 and 529 +/- 48 vs. 1,302 +/- 118 mmHg/s, P < 0.01] and recovery of ATP concentrations (determined with 31P NMR spectroscopy: 30 +/- 6 and 40 +/- 10 vs. 67 +/- 5% initial, P < 0.05) at 30 min of recovery. Moreover, the combination of acute hypokalemia and chronic hypokalemia had additive effects (dP/dt 166 +/- 15 mmHg/s and ATP 21 +/- 7% initial, both P < 0.01). We also measured cytosolic calcium with surface fluorescence spectroscopy after indo 1 loading. Acute hypokalemia and acute hypokalemia + chronic hypokalemia increased cytosolic calcium (averaged throughout the cardiac cycle) during and after hypoxia (390- to 460-nm ratio at 30 min of recovery: 0.46 +/- 0.07 and 0.65 +/- 0.07 vs. 0.18 +/- 0.03, P < 0.01), whereas control and chronic hypokalemia hearts had only small changes with hypoxia and recovery. Finally, when we examined mitochondria isolated from hearts perfused under experimental conditions, we found that chronic hypokalemia-alone mitochondria and chronic hypokalemia + acute hypokalemia mitochondria had marked impairment of state 3 respiration compared with control hearts (52 +/- 13 and 50 +/- 9 vs. 128 +/- 10 natm.min-1.mg protein-1 with succinate as substrate, P < 0.01), whereas acute hypokalemia mitochondria demonstrated only subtle changes. These data suggest that both acute hypokalemia and chronic hypokalemia impair cardiac responses to hypoxia. The mechanism may involve impairment of calcium metabolism, but cytosolic calcium alterations do not explain all of the metabolic and functional effects of acute hypokalemia and chronic hypokalemia in the setting of hypoxia.

Acute Disease↗
PubMed1998

Increased levels of myocardial IkappaB-alpha protein promote tolerance to endotoxin.

Endotoxin [lipopolysaccharide (LPS)] causes tumor necrosis factor-alpha (TNF-alpha)-mediated myocardial contractile depression. Tolerance to the cardiac toxicity of LPS can be induced by a prior exposure to LPS or by pretreatment with glucocorticoids. The mechanisms by which the myocardium acquires tolerance to LPS remain unknown. LPS causes phosphorylation and degradation of inhibitory kappaB-alpha (IkappaB-alpha), releasing nuclear factor-kappaB (NF-kappaB) to activate TNF-alpha gene transcription. We hypothesized that LPS induces supranormal synthesis of myocardial IkappaB-alpha protein and thus renders the myocardium tolerant to subsequent LPS. Rats were challenged with LPS after pretreatment with LPS, dexamethasone, or saline. In saline-pretreated rats, LPS caused a rapid decrease in myocardial IkappaB-alpha protein levels, activation of NF-kappaB, and increased TNF-alpha production. These events were followed by myocardial contractile depression. After the initial decrease in myocardial IkappaB-alpha, IkappaB-alpha protein levels rebounded to a level greater than control levels by 24 h. Dexamethasone pretreatment similarly increased myocardial IkappaB-alpha protein levels. In rats pretreated with either LPS or dexamethasone, myocardial IkappaB-alpha protein levels remained similar to control levels after LPS challenge. The preserved level of myocardial IkappaB-alpha protein was associated with diminished NF-kappaB activation, attenuated myocardial TNF-alpha production, and improved cardiac contractility. We conclude that LPS and dexamethasone upregulate myocardial IkappaB-alpha protein expression and that an increased level of myocardial IkappaB-alpha protein may promote cardiac tolerance to LPS by inhibition of NF-kappaB intranuclear translocation and myocardial TNF-alpha production.

Animals↗
PubMed1998

Mechanisms of pH preservation during global ischemia in preconditioned rat heart: roles for PKC and NHE.

Ischemic preconditioning (PC) attenuates cardiac acidosis during global ischemia. This adaptation to ischemia is detectable before other better known indexes of PC are manifested. Clarification of the endogenous mechanisms may provide insights into how protein kinase C (PKC) signaling might be linked to altered intracellular biochemistry. 31P NMR studies of isolated, buffer-perfused rat heart were performed to determine whether functionally cardioprotective PC by cyclic ischemia (CI) and alpha1-adrenergic stimuli [phenylephrine (PE)] attenuated acidosis during ischemia and, if so, whether this 1) involves a PKC-dependent pathway and is due to 2) decreased glycolytic proton production, 3) an increase in proton buffering, or 4) proton extrusion. At the end of 20 min of global ischemia, both CI-PC (pH = 6.86 +/- 0.14) and PE-PC (pH = 6.90 +/- 0.13) attenuated end-ischemic acidosis (control pH = 6.54 +/- 0.1). PKC blockade with chelerythrine (Chel) prevented the attenuation of ischemic acidosis by PC stimuli (end-ischemic pH: CI + Chel, 6.43 +/- 0.06; PE + Chel, 6.17 +/- 0.17). End-ischemic lactate accumulation was decreased in CI-PC hearts (7.54 +/- 0.5 vs. control, 14.61 +/- 2.1 micromol/g wet wt) but not in those preconditioned through the alpha1-adrenergic receptor (12.25 +/- 0.9 micromol/g wet wt). Physiologically relevant buffers were not increased in the preconditioned groups. Blockade of the Na+/H+ exchanger [NHE; with 5-(N-ethyl-N-isopropyl) amiloride (EIPA) or HOE-694] eliminated the attenuation of ischemic acidosis seen with PC stimuli (pH: CI + EIPA, 6.5 +/- 0.1; PE + EIPA, 6.46 +/- 0.2; PE + HOE-694, 6.26 +/- 0.15; not significantly different from control). We conclude that CI and alpha1-adrenergic PC stimuli attenuate ischemic acidosis, and this may involve the cardiac amiloride-sensitive NHE. The signaling pathways of both these two stimuli appear to involve PKC.

Acidosis↗
PubMed1998

Ischemic preconditioning triggers tyrosine kinase signaling: a potential role for MAPKAP kinase 2.

Myocardial adaptation to ischemia has been shown to activate protein tyrosine kinase, potentiating activation of phospholipase D, which leads to the stimulation of mitogen-activated protein (MAP) kinases and MAP kinase-activated protein (MAPKAP) kinase 2. The present study sought to further examine the signal transduction pathway for the MAPKAP kinase 2 activation during ischemic adaptation. Isolated perfused rat hearts were adapted to ischemic stress by repeated ischemia and reperfusion. Hearts were pretreated with genistein to block tyrosine kinase, whereas SB-203580 was used to inhibit p38 MAP kinases. Western blot analysis demonstrated that p38 MAP kinase is phosphorylated during ischemic stress adaptation. Phosphorylation of p38 MAP kinase was blocked by genistein, suggesting that activation of p38 MAP kinase during ischemic adaptation is mediated by a tyrosine kinase signaling pathway. MAPKAP kinase 2 was estimated by following in vitro phosphorylation with recombinant human heat shock protein 27 as specific substrate for MAPKAP kinase 2. Again, both genistein and SB-203580 blocked the activation of MAPKAP kinase 2 during myocardial adaptation to ischemia. Immunofluorescence microscopy with anti-p38-antibody revealed that p38 MAP kinase is primarily localized in perinuclear regions. p38 MAP kinase moves to the nucleus after ischemic stress adaptation. After ischemia and reperfusion, cytoplasmic striations in the myocytes become obvious, indicating translocation of p38 MAP kinase from nucleus to cytoplasm. Corroborating these results, myocardial adaptation to ischemia improved the left ventricular functions and reduced myocardial infarction that were reversed by blocking either tyrosine kinase or p38 MAP kinase. These results demonstrate that myocardial adaptation to ischemia triggers a tyrosine kinase-regulated signaling pathway, leading to the translocation and activation of p38 MAP kinase and implicating a role for MAPKAP kinase 2.

Adaptation, Biological↗
PubMed1998

Mitochondrial oxidative phosphorylation thermodynamic efficiencies reflect physiological organ roles.

Mitochondria cannot maximize energy production, efficiency, and the cellular ATP phosphorylation potential all at the same time. The theoretical and observed determinations of coupling of oxidative phosphorylation in mitochondria from rat liver, heart, and brain were compared using classical and nonequilibrium thermodynamic measures. Additionally, the optimal thermodynamic efficiency and flow ratios were determined for control of the two energy-converting complexes of the respiratory chain: complex I (NADH), which reflects the integrated cellular pathway, and complex II (FADH2), the predominantly tricarboxylic acid (TCA) cycle pathway. For all three organs, the cellular respiratory pathway was more tightly coupled than the TCA pathway and resulted in a greater optimal efficiency. Liver mitochondria are the most thermodynamically efficient at ATP production using oxidative phosphorylation. Heart and brain mitochondrial systems utilize more oxygen, but can produce ATP at a faster rate than liver systems. Per the theory of economic degrees of coupling, isolated rat liver mitochondrial systems are designed for the economic production of ATP for use in cellular processes. In the brain, the mitochondrial TCA cycle pathway promotes the maximal maintenance of the cellular energy state for cellular viability, whereas in the heart the TCA cycle pathway maximizes the production of ATP. The coupling of oxidative phosphorylation not only can be expected to change with substrate availability but may also reflect an ontogenetic response of mitochondria to fit specific organ roles in the rat.

Animals↗
PubMed1998

TNF-alpha and myocardial depression in endotoxemic rats: temporal discordance of an obligatory relationship.

Exogenous tumor necrosis factor-alpha (TNF-alpha) induces delayed myocardial depression in vivo but promotes rapid myocardial depression in vitro. The temporal relationship between endogenous TNF-alpha and endotoxemic myocardial depression is unclear, and the role of TNF-alpha in this myocardial disorder remains controversial. Using a rat model of endotoxemia not complicated by shock, we sought to determine 1) the temporal relationship of changes in circulating and myocardial TNF-alpha with myocardial depression, 2) the influences of protein synthesis inhibition or immunosuppression on TNF-alpha production and myocardial depression, and 3) the influence of neutralization of TNF-alpha on myocardial depression. Rats were treated with lipopolysaccharide (LPS, 0.5 mg/kg ip). Circulating and myocardial TNF-alpha increased at 1 and 2 h, whereas myocardial contractility was depressed at 4 and 6 h. Pretreatment with cycloheximide or dexamethasone abolished the increase in circulating and myocardial TNF-alpha and preserved myocardial contractile function. Similarly, treatment with TNF binding protein immediately after LPS prevented myocardial depression. We conclude that endogenous TNF-alpha mediates delayed myocardial depression in endotoxemic rats and that inhibition of TNF-alpha production or neutralization of TNF-alpha preserves myocardial contractile function in endotoxemia.

Analysis of Variance↗
PubMed1998

Autofluorescence and mineral content of carious dentine: scanning optical and backscattered electron microscopic studies.

The aim of this study was to investigate the extent of natural intrinsic fluorescence in carious human dentine and any correspondence of such autofluorescence (AF) to the mineral distribution within the lesion. Two investigative techniques were used, both employing the same sample set and fields in diamond-polished block surfaces of polymethylmethacrylate-embedded carious teeth. AF at emission wavelengths >515 nm, excited by 488-nm laser light, was assessed using a confocal laser scanning optical microscope (CLSM), the recordings made under standard operating conditions. The relative mineral content was assessed using digital backscattered scanning electron microscopy (20 kV BSE-SEM). The AF intensity correlated with the level of demineralisation as seen by BSE, but the depth of the lesion as seen by CLSM was significantly greater implying that the AF is not directly related to the mineral component.

Bromides↗
PubMed1998

Reversal of cerebral vasospasm using an intrathecally administered nitric oxide donor.

OBJECT: Intrathecal bolus administration of (Z)-1-[N-(2-aminoethyl)-N-(2-ammonioethyl)aminio]diazen++ +-1-ium-1,2-diolate (DETA/NO), a long half-life diazeniumdiolate-class nitric oxide (NO) donor, was evaluated for safety and efficacy in the treatment of delayed cerebral vasospasm in a canine model of subarachnoid hemorrhage (SAH). METHODS: The baseline basilar artery (BA) diameter of 25 dogs was measured with the aid of angiography on Day 0. Vasospasm was then induced by intracisternal injection of autologous arterial blood on Days 0 and 2. Repeated arteriography on Day 7 revealed an average BA diameter of 58% of baseline. Each dog was then randomized to one of four groups: a pathology control group (SAH only, four animals); a treatment control group (SAH plus 2 micromol of the inactive drug carrier DETA, eight animals); a low-dose treatment group (SAH plus 0.2 micromol DETA/NO, six animals); or a high-dose treatment group (SAH plus 2 micromol DETA/NO, six animals). The drugs were administered in a 2-ml intrathecal bolus via the cisterna magna. Arterial caliber was monitored by angiography over the subsequent 4 hours. A 2-micromol dose of the drug was then given and serial arteriography continued for an additional hour to screen for tachyphylaxis. Intracranial pressure and respiratory and hemodynamic parameters were continuously monitored. Histopathological analyses of the animals' brains were performed after the dogs were killed on Day 8. The drug DETA/NO produced reversal of vasospasm in a dose-dependent fashion that roughly followed a double exponential time course. Doses of 2 micromol DETA/NO resulted in restoration of the angiographically monitored BA diameter to the prevasospasm size at 1.5 hours posttreatment, and this was sustained at 88% of baseline at 4 hours (p < 0.01, independent samples t-test). By contrast, the treatment control group remained on average at 54% of baseline diameter. The low-dose treatment group achieved only partial and more transitory relaxation. Histopathological analyses showed findings consistent with chronic SAH but did not demonstrate any toxicity associated with the NO donor. No adverse physiological changes were seen. CONCLUSIONS: This study indicates that long-acting NO donors are potentially useful as agents to restore circulation in patients suffering from cerebral vasospasm.

Analysis of Variance↗
PubMed1998

Risk stratification by treadmill testing in acute myocardial infarction following thrombolytic therapy.

Survivors of acute myocardial infarction (AMI) should have risk stratification for assessment of their future risk of cardiovascular events. One of the important means of risk stratification is by treadmill test (TMT). Most of the algorithms for assessment were done in the prethrombolytic era. But in the post-thrombolytic era, risk stratification by TMT should be properly evaluated. Fifty males with confirmed AMI with age ranging from 38-62 years (mean 48 years) were tested with a symptom limited (Modified Bruce Protocol) TMT. The patients were followed up for a minimum of 6 months (range 6-10 months). Out of 50 patients, 38 reported for follow up. Among them 22 (Group A) had cardiac events and 16 (Group B) had no events. Among the patients (Group A), 6 had unstable angina, 7 had reinfarction, 2 had sudden death, 4 had coronary artery bypass grafting (CABG) and 3 had angioplasty. Comparison between the two groups, A and B in TMT parameters like ST segment depression > 2.5 mm (12 vs 9), no. of leads where ST depression occurred (66 vs 48) during exercise, mean work capacity (8.1 vs 7.9 mets), mean systolic blood pressure response were all statistically insignificant. Though TMT was believed to be a good prognostic indicator to assess further cardiac events after AMI, its efficacy in risk stratification after thrombolysis is yet to be determined. This study does not show its worth in post MI risk assessment.

Adult↗
PubMed1998

Safety in laboratories carrying out sputum smear microscopy: a dilemma for resource-poor countries.

Laboratory conditions and procedures for sputum smear microscopy (acid-fast bacilli) were assessed in 38 hospitals throughout Malawi. Of these, 17 (45%) had an area of less than 25 m2, eight (21%) had a separate room for tuberculosis work, and five (13%) had a safety cabinet. All laboratory personnel wore gloves, but in several hospitals there was no white coat, face mask, protective apron or soap for washing hands. Different disinfectants were used to clean work surfaces, only one laboratory decontaminated sputum specimens before disposal, and the laboratory cleaner was usually responsible for waste disposal. Laboratory conditions and safety procedures in Malawi are poor, indicating a need for education, training and supervision of staff.

Cytodiagnosis↗
PubMed1998

District sputum smear microscopy services in Malawi.

SETTING: Government hospitals and health centres in 23 districts in Malawi. OBJECTIVE: To determine 1) the number and smear-positivity rate of sputum samples submitted at health centres and hospitals, and 2) the time for sputum samples to get from health centres to smear examination. DESIGN: Prospective data collection on sputum specimens coming from health centres to hospital laboratories, and over the equivalent time period, retrospective data collection from laboratory sputum registers. RESULTS: Information was collected over a period of 5.6 months during 1997. Of 21 527 patients submitting sputum samples, 16995 (79%) were from within the hospital and 4532 (21%) were from health centres. Of 15 833 new TB suspects, 12 804 (81%) submitted sputum within the hospital and 3029 (19%) were from health centres. The overall smear-positivity rate was 11.9%: the proportion of new suspects who were smear-positive was significantly higher in health centres (14.1%) compared with hospital-based patients (11.4%, P < 0.05); 27% of all sputum specimens from health centres took 8 days or longer to get to smear examination. Sputum smears were positive from 1-30 days between submission and laboratory examination. CONCLUSION: Fewer sputum samples are submitted at health centres compared with hospitals, and there may be long delays between sputum submission and smear examination. The precise reasons are unclear, but health centre staff need training about the importance of timely case finding procedures.

Community Health Centers↗
PubMed1997

Postischemic administration of succinate reverses the impairment of oxidative phosphorylation after cardiac ischemia and reperfusion injury.

BACKGROUND: Ischemia and reperfusion (IR) can lead to impaired myocardial mechanical function and inhibition of key metabolic enzyme systems after IR. In this study, we sought to identify the postischemic lesion in oxidative phosphorylation and hypothesized that selective substrate repletion would restore mitochondrial metabolic function during reperfusion. METHODS AND RESULTS: Isolated rat hearts were subjected to global ischemia (25 minutes; 37 degrees C) and reperfusion (40 minutes). Left ventricular developed pressure (LVDP) and the cytochrome a,a3 redox state (near infrared spectroscopy) were continuously monitored. Oxygen consumption was measured for the NADH (mitochondrial complex I) and FADH2 (complex II) pathways in both the resting and maximal ADP-stimulated states. Myocellular oxidative phosphorylation capacity was measured using an NADPH-linked assay specific for mitochondrial ATPase. The hearts were randomized to either succinate (200 micromol/L) or control for the first 5 minutes of reperfusion after ischemia. IR in the control group resulted in an impairment of NADH (complex I) oxidative phosphorylation capacity (1.4+/-0.4 versus control 3.9+/-0.6 nmol ATP/min/mg) and depressed LVDP (49+/-3% of baseline; P<.05). The oxidative phosphorylation capacity for the succinate-using FADH2 pathway remained intact (2.6+/-0.3 versus 2.4+/-0.4). Postischemic succinate administration enhanced LVDP recovery after IR (89+/-8% of baseline; P<.05). Diminished electron transport resulted in depletion of electrons from cytochrome a,a3 during ischemia and early reperfusion, which was reversed by providing succinate as substrate. CONCLUSIONS: Cardiac ischemia and reperfusion results in a defect at mitochondrial complex I but not complex II. Cytochrome a,a3 undergoes anomalous oxidation during ischemia. Postischemic administration of succinate infusion restores the cytochrome a,a3 redox state balance and myocardial function after IR.

Adenosine Triphosphate↗
PubMed1997

Borna disease virus P-protein is phosphorylated by protein kinase Cepsilon and casein kinase II.

Borna disease virus (BDV) is a newly classified nonsegmented negative-strand RNA virus (order of Mononegavirales) that persistently infects specific brain regions and circuits of warm-blooded animals to cause behavioral disturbances. Viruses within the order of Mononegavirales have phosphoproteins that typically serve as transcription factors and are modulated in functional activity through phosphorylation. To identify the kinases involved in BDV phosphoprotein (BDV-P) phosphorylation, in vitro phosphorylation assays were performed using recombinant phosphoprotein produced in Escherichia coli as substrate and cytoplasmic extracts from a rat glioma cell line (C6) or rat brain extracts as sources of kinase activity. These experiments revealed that BDV-P was phosphorylated predominantly by protein kinase C (PKC) and to a lesser extent by casein kinase II. Partial purification of the PKC from rat brain extract suggested that the BDV-P phosphorylating kinase is PKCepsilon. A role for PKC phosphorylation in vivo was confirmed by using the PKC-specific inhibitor GF109203X. Furthermore, peptide mapping studies indicated that BDV-P is phosphorylated at the same sites in vitro as it is in vivo. Mutational analysis identified Ser26 and Ser28 as sites for PKC phosphorylation and Ser70 and Ser86 as sites for casein kinase II phosphorylation. The anatomic distribution of PKCepsilon in the central nervous system may have implications for BDV neurotropism and pathogenesis.

Animals↗