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Biomedical subjects

A Bose

Publications and source records attributed to A Bose.

At least 19 recordsLinked to original sources
PubMed2002

Could a herpesvirus be the cause of Kawasaki disease?

Kawasaki disease (KD) is an acute vasculitis of early childhood, the cause of which remains unknown. Many lines of evidence suggest an infectious aetiology, which may-in association with host genetic factors-lead to the characteristic clinical presentation of this disease. Accumulating data including animal models and epidemiological and immunological studies, suggest that viruses have an important role in human vasculitic disease. Whereas many infectious agents including viruses have been postulated as possible causes of KD, no single agent has been shown definitely to be associated with this disease and the causative agent remains elusive. We hypothesise that a ubiquitous virus of the gamma herpesvirus family is the likely aetiological agent for KD in genetically susceptible individuals.

Animals↗
PubMed2002

Kawasaki disease: an evidence based approach to diagnosis, treatment, and proposals for future research.

This article proposes a clinical guideline for the diagnosis and treatment of Kawasaki disease in the UK based on the best available evidence to date, and highlights areas of practice where evidence is anecdotal or based on retrospective data. Future research as proposed by the London Kawasaki Disease Research Group is outlined, and clinicians are invited to prospectively enroll their suspected cases into this collaborative research project.

Adrenal Cortex Hormones↗
PubMed2001

PYK2 as a mediator of endothelin-1/G alpha 11 signaling to GLUT4 glucose transporters.

Endothelin-1 (ET-1) signaling through G alpha(q/11) stimulates translocation of intracellular GLUT4 glucose transporters to the plasma membrane of 3T3-L1 adipocytes by an unknown mechanism that requires protein tyrosine phosphorylation and ADP-ribosylation factor 6 (ARF6) but is independent of phosphatidylinositol 3 (PI3)-kinase. In contrast, insulin action on this process requires PI3-kinase but not ARF6. Here we report the identification of two proteins selectively tyrosine-phosphorylated in response to ET-1 but not insulin: the Ca(2+)-activated tyrosine kinase PYK2 and its physiological substrate, the adhesion scaffold protein paxillin. Endogenous paxillin as well as expressed Myc-tagged PYK2 or a Myc-tagged kinase-deficient PYK2 protein were acutely directed to F-actin-rich adhesion sites from the adipocyte cytoplasm in response to ET-1 but not insulin. CADTK-related non-kinase (CRNK) is a dominant negative form of PYK2 containing the C-terminal portion of the protein, which binds paxillin but lacks the PYK2 autophosphorylation site (Tyr(402)). CRNK expression in 3T3-L1 adipocytes inhibited ET-1-mediated F-actin polymerization and translocation of Myc-tagged GLUT4-enhanced green fluorescent protein (EGFP) to the plasma membrane without disrupting insulin action on these processes. These data reveal the tyrosine kinase PYK2 as a required signaling element in the regulation of GLUT4 recycling in 3T3-L1 adipocytes by ET-1, whereas insulin signaling is directed through a different pathway.

3T3 Cells↗
PubMed2001

Role of synaptic delay in organizing the behavior of networks of self-inhibiting neurons.

We consider a pair of mutually coupled inhibitory neurons in which each neuron is also self-inhibitory. We show that the size of the synaptic delay determines the existence and stability of solutions. For small delays, there is no synchronous solution, but a stable antiphase and a stable on-state solution. For long delays, only the synchronous solution is stable. For intermediate delays, either the antiphase or synchronous solutions are stable. In contrast to prior work, for stability of synchrony, we only require the existence of a single slow process.

Animals↗
PubMed2001

Phase precession and phase-locking of hippocampal pyramidal cells.

We propose that the activity patterns of CA3 hippocampal pyramidal cells in freely running rats can be described as a temporal phenomenon, where the timing of bursts is modulated by the animal's running speed. With this hypothesis, we explain why pyramidal cells fire in specific spatial locations, and how place cells phase-precess with respect to the EEG theta rhythm for rats running on linear tracks. We are also able to explain why wheel cells phase-lock with respect to the theta rhythm for rats running in a wheel. Using biophysically minimal models of neurons, we show how the same network of neurons displays these activity patterns. The different rhythms are the result of inhibition being used in different ways by the system. The inhibition is produced by anatomically and physiologically diverse types of interneurons, whose role in controlling the firing patterns of hippocampal cells we analyze. Each firing pattern is characterized by a different set of functional relationships between network elements. Our analysis suggests a way to understand these functional relationships and transitions between them.

Animals↗
PubMed2001

G(alpha)11 signaling through ARF6 regulates F-actin mobilization and GLUT4 glucose transporter translocation to the plasma membrane.

The action of insulin to recruit the intracellular GLUT4 glucose transporter to the plasma membrane of 3T3-L1 adipocytes is mimicked by endothelin 1, which signals through trimeric G(alpha)q or G(alpha)11 proteins. Here we report that murine G(alpha)11 is most abundant in fat and that expression of the constitutively active form of G(alpha)11 [G(alpha)11(Q209L)] in 3T3-L1 adipocytes causes recruitment of GLUT4 to the plasma membrane and stimulation of 2-deoxyglucose uptake. In contrast to the action of insulin on GLUT4, the effects of endothelin 1 and G(alpha)11 were not inhibited by the phosphatidylinositol 3-kinase inhibitor wortmannin at 100 nM. Signaling by insulin, endothelin 1, or G(alpha)11(Q209L) also mobilized cortical F-actin in cultured adipocytes. Importantly, GLUT4 translocation caused by all three agents was blocked upon disassembly of F-actin by latrunculin B, suggesting that the F-actin polymerization caused by these agents may be required for their effects on GLUT4. Remarkably, expression of a dominant inhibitory form of the actin-regulatory GTPase ARF6 [ARF6(T27N)] in cultured adipocytes selectively inhibited both F-actin formation and GLUT4 translocation in response to endothelin 1 but not insulin. These data indicate that ARF6 is a required downstream element in endothelin 1 signaling through G(alpha)11 to regulate cortical actin and GLUT4 translocation in cultured adipocytes, while insulin action involves different signaling pathways.

ADP-Ribosylation Factor 6↗
PubMed2001

Neural mechanisms for generating rate and temporal codes in model CA3 pyramidal cells.

The effect of synaptic inhibition on burst firing of a two-compartment model of a CA3 pyramidal cell is considered. We show that, depending on its timing, a short dose of fast decaying synaptic inhibition can either delay or advance the timing of firing of subsequent bursts. Moreover, increasing the strength of the inhibitory input is shown to modulate the burst profile from a full complex burst, to a burst with multiple spikes, to single spikes. We additionally show how slowly decaying inhibitory input can be used to synchronize a network of pyramidal cells. Implications for the phase precession phenomenon of hippocampal place cells and for the generation of temporal and rate codes are discussed.

Action Potentials↗
PubMed2001

Role of destructive operations in modern day obstetrics.

One hundred and forty-one cases of obstructed labour was referred to RG Kar Medical College and Hospital in the last one year. Out of 12,034 total hospital deliveries, incidence of obstructed labour was 1.17% whereas 36 cases (0.29%) accounted for intra-uterine foetal death (IUD). Of the IUD with obstructed labour, 69.4% were delivered by destructive operation and 30.6% by lower segment caesarean section (LSCS). Craniotomy was performed in 44.4% cases and evisceration in 25% of cases. About 68% of the patients were in the young age group belonging to 20-30 years and 36% of cases were primigravida. It ws found that cephalopelvic disproportion was the commonest cause of obstruction for which craniotomy was performed. Traumatic rupture uterus was encountered in one case. There was no maternal death following destructive operation.

Adult↗
PubMed2000

Encephalitogenic and immunogenic potential of the stress protein alphaB-crystallin in Biozzi ABH (H-2A(g7)) mice.

The stress protein alphaB-crystallin is an immunodominant antigen in multiple sclerosis (MS)-affected myelin for human T cells and is expressed at elevated levels in MS lesions. Using bovine alphaB-crystallin and synthetic peptides based on mouse alphaB-crystallin the ability of this stress protein to induce experimental allergic encephalomyelitis (EAE) was screened in Biozzi ABH (H-2A(g7)) mice. While whole alphaB-crystallin and the immunodominant T cell epitopes (49-64, 73-88, 153-168) failed to induce disease the subdominant or cryptic epitope (1-16) was weakly encephalitogenic. The lack of encephalitogenicity of whole protein and dominant epitopes may be due to the low constitutive expression of alphaB-crystallin in the CNS combined with a state of peripheral tolerance suggested by the constitutive expression of alphaB-crystallin in secondary lymphoid tissues in ABH mice. Further evidence for a role of alphaB-crystallin in the progression of chronic relapsing neurological disease is suggested by the development of T cell responses to alphaB-crystallin during MOG-induced relapsing EAE as myelin damage accumulates. Together our data indicate that normal tolerising mechanisms in ABH mice prevent the induction of EAE by alphaB-crystallin while the subdominant or cryptic epitope is able to circumvent these mechanisms and contribute to pathogenic myelin-directed autoimmunity following T cell activation.

Animals↗
PubMed2000

Familial arteriovenous malformations in siblings.

BACKGROUND: Familial arteriovenous malformations (AVMs) of the brain are rare. We present two sisters with the same parents who harbored AVMs that were successfully treated. METHODS: The elder sister presented with a unilateral migrainous type of headache overlying the right parietal area. The younger one suffered from exercise-induced headaches. Both were neurologically intact. Magnetic resonance imaging scans of the brain and cerebral angiography delineated the lesions. Both sisters underwent endovascular embolization followed by surgical resection. RESULTS: Postoperatively, aside from a left inferior quadrantanopsia in the elder sister, both were neurologically intact. CONCLUSIONS: We report the rare occurrence of familial AVMs in two siblings and review the literature of 14 reports. No genetic predisposition was found.

Adolescent↗