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A single fatal dose of olanzapine
Majumder Shounak,Mandal Sanjay,Guha Gautam,Bandyopadhyay Dipanjan
Neurology India , 2009,
Abstract:
STUDY ON ENDOCRINOLOGICAL PROFILE OF HIV INFECTED MALE PATIENTS FROM EASTERN INDIA
Mandal Sanjay K,Paul Rudrajit,Bandyopadhyay Dipanjan,Basu Asish K
International Research Journal of Pharmacy , 2013, DOI: 10.7897/2230-8407.04347
Abstract: Human Immunodeficiency virus (HIV) infectionis associated with a variety of endocrine problems. Hypoadrenalism, hypothyroidism and hypogonadism are commonly found singly or in combination. Especially, male hypogonadism is very common in this population and may lead to weight loss, lethargy and other co morbidities. We undertook this cross sectional observational study to evaluate endocrine profile in HIV infected males in a sample Eastern Indian population. We also studied for any correlation of the endocrine dysfunctions with their immune status. We studied the blood hormone profiles along with blood CD4 counts. The bloods were drawn in fasting state and analysed using suitable high sensitivity assays. Standard statistical methods were used. We had 48 patients in our study. Among them, 33% had hypogonadism, 20% had hypothyroidism and 15 patients had diabetes. The hypogonadism was mainly hypogonadotropic. In other studies across the globe also, hypogonadism in HIV positive males is found to be significant. Our diabetic patients were not on protease inhibitors. We found some patients who had multiple endocrine dysfunctions. HIV infection is often associated with endocrine abnormalities. This aspect of the disease must be addressed during routine care of these patients. Hormone replacement must be individualized and may be needed for prolonged periods.
Interactions between Exosomes from Breast Cancer Cells and Primary Mammary Epithelial Cells Leads to Generation of Reactive Oxygen Species Which Induce DNA Damage Response, Stabilization of p53 and Autophagy in Epithelial Cells
Sujoy Dutta, Case Warshall, Chirosree Bandyopadhyay, Dipanjan Dutta, Bala Chandran
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0097580
Abstract: Exosomes are nanovesicles originating from multivesicular bodies and are released by all cell types. They contain proteins, lipids, microRNAs, mRNAs and DNA fragments, which act as mediators of intercellular communications by inducing phenotypic changes in recipient cells. Tumor-derived exosomes have been shown to play critical roles in different stages of tumor development and metastasis of almost all types of cancer. One of the ways by which exosomes affect tumorigenesis is to manipulate the tumor microenvironments to create tumor permissive “niches”. Whether breast cancer cell secreted exosomes manipulate epithelial cells of the mammary duct to facilitate tumor development is not known. To address whether and how breast cancer cell secreted exosomes manipulate ductal epithelial cells we studied the interactions between exosomes isolated from conditioned media of 3 different breast cancer cell lines (MDA-MB-231, T47DA18 and MCF7), representing three different types of breast carcinomas, and normal human primary mammary epithelial cells (HMECs). Our studies show that exosomes released by breast cancer cell lines are taken up by HMECs, resulting in the induction of reactive oxygen species (ROS) and autophagy. Inhibition of ROS by N-acetyl-L-cysteine (NAC) led to abrogation of autophagy. HMEC-exosome interactions also induced the phosphorylation of ATM, H2AX and Chk1 indicating the induction of DNA damage repair (DDR) responses. Under these conditions, phosphorylation of p53 at serine 15 was also observed. Both DDR responses and phosphorylation of p53 induced by HMEC-exosome interactions were also inhibited by NAC. Furthermore, exosome induced autophagic HMECs were found to release breast cancer cell growth promoting factors. Taken together, our results suggest novel mechanisms by which breast cancer cell secreted exosomes manipulate HMECs to create a tumor permissive microenvironment.
Non tuberculous mycobacteria and toxoplasma co-infection of the central nervous system in a patient with AIDS
Sardar, Partha;Bandyopadhyay, Dipanjan;Roy, Deeptarka;Guha, Pradipta;Guha, Goutam;Banerjee, Amit Kumar;
Brazilian Journal of Infectious Diseases , 2009, DOI: 10.1590/S1413-86702009000600011
Abstract: new-onset seizures are frequent manifestations in patients infected with human immunodeficiency virus (hiv). we describe the clinical and radiological findings in an 25yr old aids patient presenting with new onset seizures as the primary manifestation of cerebral toxoplasmosis and non tuberculous mycobacterial [ntm] co-infection. cranial computed tomography showed a subtle ventricular dilatation whereas magnetic resonance imaging disclosed prominent temporal horn. toxoplasma tachyzoites and rapidly growing mycobacteria were recovered from csf. seizures were complex partial in nature and refractory to antiepileptic therapy.
Multiorgan involvement due to cytomegalovirus infection in AIDS
Majumder, Shounak;Mandal, Sanjay K.;Bandyopadhyay, Dipanjan;Chowdhury, Subhasis Roy;Chakraborty, Partha P.;K., Mitra;
Brazilian Journal of Infectious Diseases , 2007, DOI: 10.1590/S1413-86702007000100039
Abstract: cytomegalovirus (cmv) infection is a relatively late complication of aids. like other viruses contributing to co-morbidity of hiv infection, cytomegalovirus has the propensity to cause multiorgan involvement. we report the case of a 34-year-old seropositive man who presented with bilateral lower limb weakness and symptomatic pallor. he was already on antiretroviral drugs for a month prior to presentation. detailed clinical examination and laboratory investigations revealed cytomegalovirus polyradiculoneuropathy associated with bone marrow dysplasia. dysplasia of haematopoeitic cell lines occurs in 30% to 70% of hiv infected patients, and is often indistinguishable from myelodysplastic syndrome. however, in our case, the bone marrow picture reverted back to normal with treatment of the cmv infection, pointing to a possible role of cmv as the causative agent of bone marrow dysplasia. moreover, cmv has been incriminated as a pathogen producing the immune reconstitution inflammatory syndrome. the onset of the disease in our case one month after initiation of haart strongly raises the possibility of this being a case of cmv related iris. this is the first reported case where iris has presented with cmv polyradiculoneuropathy and bone marrow dysplasia. we would like to highlight that in today's era of hiv care, clinicians should be aware of the possibility of multiorgan involvement by cmv, for appropriate management of this disease in the background of aids.
CIB1 Synergizes with EphrinA2 to Regulate Kaposi's Sarcoma-Associated Herpesvirus Macropinocytic Entry in Human Microvascular Dermal Endothelial Cells
Chirosree Bandyopadhyay,Mohanan Valiya-Veettil,Dipanjan Dutta,Sayan Chakraborty,Bala Chandran
PLOS Pathogens , 2014, DOI: doi/10.1371/journal.ppat.1003941
Abstract: KSHV envelope glycoproteins interact with cell surface heparan sulfate and integrins, and activate FAK, Src, PI3-K, c-Cbl, and Rho-GTPase signal molecules in human microvascular dermal endothelial (HMVEC-d) cells. c-Cbl mediates the translocation of virus bound α3β1 and αVβ3 integrins into lipid rafts (LRs), where KSHV interacts and activates EphrinA2 (EphA2). EphA2 associates with c-Cbl-myosin IIA and augmented KSHV-induced Src and PI3-K signals in LRs, leading to bleb formation and macropinocytosis of KSHV. To identify the factor(s) coordinating the EphA2-signal complex, the role of CIB1 (calcium and integrin binding protein-1) associated with integrin signaling was analyzed. CIB1 knockdown did not affect KSHV binding to HMVEC-d cells but significantly reduced its entry and gene expression. In contrast, CIB1 overexpression increased KSHV entry in 293 cells. Single virus particle infection and trafficking during HMVEC-d cell entry was examined by utilizing DiI (envelope) and BrdU (viral DNA) labeled virus. CIB1 was associated with KSHV in membrane blebs and in Rab5 positive macropinocytic vesicles. CIB1 knockdown abrogated virus induced blebs, macropinocytosis and virus association with the Rab5 macropinosome. Infection increased the association of CIB1 with LRs, and CIB1 was associated with EphA2 and KSHV entry associated signal molecules such as Src, PI3-K, and c-Cbl. CIB1 knockdown significantly reduced the infection induced EphA2, Src and Erk1/2 activation. Mass spectrometry revealed the simultaneous association of CIB1 and EphA2 with the actin cytoskeleton modulating myosin IIA and alpha-actinin 4 molecules, and CIB1 knockdown reduced EphA2's association with myosin IIA and alpha-actinin 4. Collectively, these studies revealed for the first time that CIB1 plays a role in virus entry and macropinocytosis, and suggested that KSHV utilizes CIB1 as one of the key molecule(s) to coordinate and sustain the EphA2 mediated signaling involved in its entry, and CIB1 is an attractive therapeutic target to block KSHV infection.
EphrinA2 Regulates Clathrin Mediated KSHV Endocytosis in Fibroblast Cells by Coordinating Integrin-Associated Signaling and c-Cbl Directed Polyubiquitination
Dipanjan Dutta,Sayan Chakraborty,Chirosree Bandyopadhyay,Mohanan Valiya Veettil,Mairaj Ahmed Ansari,Vivek Vikram Singh,Bala Chandran
PLOS Pathogens , 2013, DOI: 10.1371/journal.ppat.1003510
Abstract: Kaposi's sarcoma-associated herpesvirus (KSHV) interacts with human dermal endothelial cell surface tyrosine kinase EphrinA2 (EphA2) and integrins (α3β1 and αVβ3) in the lipid raft (LR) region, and EphA2 regulates macropinocytic virus entry by coordinating integrin-c-Cbl associated signaling. In contrast, KSHV enters human foreskin fibroblast (HFF) cells by LR-independent clathrin mediated endocytosis. The present studies conducted to identify the key molecules regulating KSHV entry in HFF cells showed that KSHV induces association with integrins (αVβ5, αVβ3 and α3β1) and EphA2 in non-LR regions early during infection and activates EphA2, which in turn associates with phosphorylated c-Cbl, myosin IIA, FAK, Src, and PI3-K, as well as clathrin and its adaptor AP2 and effector Epsin-15 proteins. EphA2 knockdown significantly reduced these signal inductions, virus internalization and gene expression. c-Cbl knockdown ablated the c-Cbl mediated K63 type polyubiquitination of EphA2 and clathrin association with EphA2 and KSHV. Mutations in EphA2's tyrosine kinase domain (TKD) or sterile alpha motif (SAM) abolished its interaction with c-Cbl. Mutations in tyrosine kinase binding (TKB) or RING finger (RF) domains of c-Cbl resulted in very poor association of c-Cbl with EphA2 and decreased EphA2 polyubiquitination. These studies demonstrated the contributions of these domains in EphA2 and c-Cbl association, EphA2 polyubiquitination and virus-EphA2 internalization. Collectively, these results revealed for the first time that EphA2 influences the tyrosine phosphorylation of clathrin, the role of EphA2 in clathrin mediated endocytosis of a virus, and c-Cbl mediated EphA2 polyubiquitination directing KSHV entry in HFF cells via coordinated signal induction and progression of endocytic events, all of which suggest that targeting EphA2 and c-Cbl could block KSHV entry and infection.
Glutamate Secretion and Metabotropic Glutamate Receptor 1 Expression during Kaposi's Sarcoma-Associated Herpesvirus Infection Promotes Cell Proliferation
Mohanan Valiya Veettil ,Dipanjan Dutta,Virginie Bottero,Chirosree Bandyopadhyay,Olsi Gjyshi,Neelam Sharma-Walia,Sujoy Dutta,Bala Chandran
PLOS Pathogens , 2014, DOI: doi/10.1371/journal.ppat.1004389
Abstract: Kaposi's sarcoma associated herpesvirus (KSHV) is etiologically associated with endothelial Kaposi's sarcoma (KS) and B-cell proliferative primary effusion lymphoma (PEL), common malignancies seen in immunocompromised HIV-1 infected patients. The progression of these cancers occurs by the proliferation of cells latently infected with KSHV, which is highly dependent on autocrine and paracrine factors secreted from the infected cells. Glutamate and glutamate receptors have emerged as key regulators of intracellular signaling pathways and cell proliferation. However, whether they play any role in the pathological changes associated with virus induced oncogenesis is not known. Here, we report the first systematic study of the role of glutamate and its metabotropic glutamate receptor 1 (mGluR1) in KSHV infected cell proliferation. Our studies show increased glutamate secretion and glutaminase expression during de novo KSHV infection of endothelial cells as well as in KSHV latently infected endothelial and B-cells. Increased mGluR1 expression was detected in KSHV infected KS and PEL tissue sections. Increased c-Myc and glutaminase expression in the infected cells was mediated by KSHV latency associated nuclear antigen 1 (LANA-1). In addition, mGluR1 expression regulating host RE-1 silencing transcription factor/neuron restrictive silencer factor (REST/NRSF) was retained in the cytoplasm of infected cells. KSHV latent protein Kaposin A was also involved in the over expression of mGluR1 by interacting with REST in the cytoplasm of infected cells and by regulating the phosphorylation of REST and interaction with β-TRCP for ubiquitination. Colocalization of Kaposin A with REST was also observed in KS and PEL tissue samples. KSHV infected cell proliferation was significantly inhibited by glutamate release inhibitor and mGluR1 antagonists. These studies demonstrated that elevated glutamate secretion and mGluR1 expression play a role in KSHV induced cell proliferation and suggest that targeting glutamate and mGluR1 is an attractive therapeutic strategy to effectively control the KSHV associated malignancies.
Observations that can unravel the coherent radio emission mechanism in pulsars
Dipanjan Mitra
Physics , 2013,
Abstract: Searching for the physical mechanism that can excite the coherent radio emission in pulsars is still an enigmatic problem. A wealth of high quality observations exist, which over the years have been instrumental in putting stringent constraints to pulsar emission models. In this article we will discuss the observational results that strongly suggests that pulsar radio emission is excited by coherent curvature radiation. We will also mention issues that remain to be resolved.
Modified NSGA-II for a Bi-Objective Job Sequencing Problem  [PDF]
Susmita Bandyopadhyay
Intelligent Information Management (IIM) , 2012, DOI: 10.4236/iim.2012.46036
Abstract: This paper proposes a better modified version of a well-known Multi-Objective Evolutionary Algorithm (MOEA) known as Non-dominated Sorting Genetic Algorithm-II (NSGA-II). The proposed algorithm contains a new mutation algorithm and has been applied on a bi-objective job sequencing problem. The objectives are the minimization of total weighted tardiness and the minimization of the deterioration cost. The results of the proposed algorithm have been compared with those of original NSGA-II. The comparison of the results shows that the modified NSGA-II performs better than the original NSGA-II.
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