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11.
Rahman Anisur Choudhury Parthankar Talukdar Nazimur Rahman 《Biological trace element research》2019,188(2):451-460
Biological Trace Element Research - This study investigated trace elements in the different organs of Eonycteris spelaea, a hill cave from the Bhuban Hills of Sonai Reserve Forest, Cachar, Assam... 相似文献
12.
Despite convincing physiological evidences for vasopressin (VP) autoregulation in the supraoptic (SON) and paraventricular (PVN) nuclei, the morphological demonstration of VP synapses has lagged behind. The present work investigates the possible existence of such synapses in the SON and PVN of the rat. Electron microscopy of sections immunostained with VP antibody (1:5,000) and conjugated with avidin-biotin demonstrated presynaptic terminals containing neurosecretory granule (NSG)-like bodies, 80-100 nm in diameter. The terminals formed axodendritic, axosomatic and axoaxonic synapses, though the postsynaptic elements remained largely unidentified. Other ultrastructural features of synaptic specialization were evident. The NSG-like bodies exhibited a varying and dynamic relationship to the presynaptic membrane, suggesting their involvement in synaptic mechanisms. 相似文献
13.
Malay Choudhury Takahiro Oku Shoji Yamada Masaharu Komatsu Keita Kudoh Takao Itakura Seiichi Ando 《Central European Journal of Biology》2011,6(4):545-557
Apolipoproteins such as apolipoprotein (apo) A-I, apoA-IV, and apoE are lipid binding proteins synthesized mainly in the liver
and the intestine and play an important role in the transfer of exogenous or endogenous lipids through the circulatory system.
To investigate the mechanism of lipid transport in fish, we have isolated some novel genes of the apoA-I family, apoIA-I (apoA-I isoform) 1–11, from Japanese eel by PCR amplification. Some of the isolated genes of apoIA-I corresponded to 28kDa-1 cDNAs which had already been deposited into the database and encoded an apolipoprotein with molecular
weight of 28 kDa in the LDL, whereas others seemed to be novel genes. The structural organization of all apoIA-Is consisted of four exons separated by three introns. ApoIA-I10 had a total length of 3232 bp, whereas other genes except for apoIA-I9 ranged from 1280 to 1441 bp. The sequences of apoIA-Is at the exon-intron junctions were mostly consistent with the consensus sequence (GT/AG) at exon-intron boundaries, whereas
the sequences of 3′ splice acceptor in intron 1 of apoIA-I1-7 were (AC) but not (AG). The deduced amino acid sequences of all apoIA-Is contained a putative signal peptide and a propeptide
of 17 and 5 amino acid residues, respectively. The mature proteins of apoIA-I1-3, 7, and 8 consisted of 237 amino acids, whereas
those of apoIA-I4-6 consisted of 239 amino acids. The mature apoIA-I10 sequence showed 65% identity to amino acid sequence
of apoIA-I11 which was associated with an apolipoprotein with molecular weight of 23 kDa in the VLDL. All these mature apoIA-I
sequences satisfied the common structural features depicted for the exchangeable apolipoproteins such as apoA-I, apoA-IV,
and apoE but apoIA-I11 lacked internal repeats 7, 8, and 9 when compared with other members of apoA-I family. Phylogenetic
analysis showed that these novel apoIA-Is isolated from Japanese eel were much closer to apoA-I than apoA-IV and apoE, suggesting
new members of the apoA-I family. 相似文献
14.
Sangita Choudhury Soochan Bae Qingen Ke Ji Yoo Lee Sylvia S. Singh René St-Arnaud Federica del Monte Peter M. Kang 《PloS one》2014,9(9)
Aim
Altered vitamin D signaling is associated with cardiac dysfunction, but the pathogenic mechanism is not clearly understood. We examine the mechanism and the role of vitamin D signaling in the development of cardiac dysfunction.Methods and Results
We analyzed 1α-hydroxylase (1α-OHase) knockout (1α-OHase−/−) mice, which lack 1α-OH enzymes that convert the inactive form to hormonally active form of vitamin D. 1α-OHase−/− mice showed modest cardiac hypertrophy at baseline. Induction of pressure overload by transverse aortic constriction (TAC) demonstrated exaggerated cardiac dysfunction in 1α-OHase−/− mice compared to their WT littermates with a significant increase in fibrosis and expression of inflammatory cytokines. Analysis of calcium (Ca2+) transient demonstrated profound Ca2+ handling abnormalities in 1α-OHase−/− mouse cardiomyocytes (CMs), and treatment with paricalcitol (PC), an activated vitamin D3 analog, significantly attenuated defective Ca2+ handling in 1α-OHase−/− CMs. We further delineated the effect of vitamin D deficiency condition to TAC by first correcting the vitamin D deficiency in 1α-OHase−/− mice, followed then by either a daily maintenance dose of vitamin D or vehicle (to achieve vitamin D deficiency) at the time of sham or TAC. In mice treated with vitamin D, there was a significant attenuation of TAC-induced cardiac hypertrophy, interstitial fibrosis, inflammatory markers, Ca2+ handling abnormalities and cardiac function compared to the vehicle treated animals.Conclusions
Our results provide insight into the mechanism of cardiac dysfunction, which is associated with severely defective Ca2+ handling and defective vitamin D signaling in 1α-OHase−/− mice. 相似文献15.
N.A. Chowdhury M. Moniruzzaman N. Nahar N. Choudhury 《World journal of microbiology & biotechnology》1991,7(6):603-606
A locally isolated strain of Micromonospora sp. when grown on different natural cellulosic substrates gave the highest activity of carboxymethylcellulase (34 U/ml) and Avicelase (0.9 U/ml) on rice straw. Sugar cane bagasse was also a good substrate for growth and cellulase production. With commercial cellulosic substrates, highest carboxymethylcellulase (90 U/ml) and Avicelase (2.8 U/ml) activities were when the organism grew on xylan. Saccharification of sugar cane bagasse and rice straw by enzyme preparations of the organism grown on the respective substrates released 5.6 and 5.8 mg reducing sugar/ml. With all enzyme preparations, bagasse was more easily saccharified than rice straw.The authors are with the Atomic Energy Research Establishment, GPO Box 3787, Dhaka 1000, Bangladesh; N.A. Chowdhury, M. Moniruzzaman, and N. Choudhury in the Institute of Food and Radiation Biology, and N. Nahar in the Institute of Nuclear Science and Technology. 相似文献
16.
Partial sequences of the 28S rDNA (ribosomal gene) were obtained from a total of 11 populations of 5 species (in 3 genera) of North American corallobothriine proteocephalideans. These included Corallobothrium fimbriatum (3 populations), Corallobothrium parafimbriatum (1 population), Corallotaenia minutia (1 population), Megathylacoides giganteum (2 populations), and Megathylacoides lamothei (4 populations). These sequences were used in a phylogenetic analysis to test the monophyly of Corallobothriinae and to investigate the interrelationships of the North American species. The results indicate that Corallobothriinae, as conventionally understood, is not monophyletic and that only the North American corallobothriines, parasites of ictalurid catfishes, form a monophyletic group. Corallobothrium parafimbriatum is sister taxon to a clade that includes Corallotaenia intermedia and C. minutia and not to its congener C. fimbriatum. Also, M. giganteum from Mexico appears to be more closely related to M. lamothei than to its conspecific in Canada. This and the amount of sequence divergence indicate possible cryptic speciation in its endemic host, the Lerma catfish, Ictalurus dugesi. 相似文献
17.
Venkatesan BA Mahimainathan L Ghosh-Choudhury N Gorin Y Bhandari B Valente AJ Abboud HE Choudhury GG 《Cellular signalling》2006,18(4):508-518
Monocyte chemotactic protein-1 (MCP-1) recruits activated phagocytes to the site of tissue injury. Interferon-gamma (IFN-gamma) present in the microenvironment of glomerulus acts on mesangial cells to induce local production of MCP-1. The mechanism by which IFN-gamma stimulates expression of MCP-1 is not clear. We therefore examined the role of PI 3 kinase signaling in regulating the IFN-gamma-induced MCP-1 expression in mesangial cells. Blocking PI 3 kinase activity with Ly294002 attenuated IFN-gamma-induced MCP-1 protein and mRNA expression. IFN-gamma increased Akt kinase activity in a PI 3 kinase-dependent manner. Expression of dominant negative Akt kinase inhibited serine phosphorylation of STAT1alpha, without any effect on its tyrosine phosphorylation, and decreased IFN-gamma-induced expression of MCP-1. These data for the first time indicate a role for PI 3 kinase-dependent Akt kinase in MCP-1 expression. We have recently shown that along with Akt, PKCepsilon is a downstream target of PI 3 kinase in IFN-gamma signaling. Similar to dominant negative Akt kinase, dominant negative PKCepsilon also inhibited serine phosphorylation of STAT1alpha without any effect on tyrosine phosphorylation. Dominant negative PKCepsilon also abrogated MAPK activity, resulting in decrease in IFN-gamma-induced MCP-1 expression. Furthermore, Akt and PKCepsilon are present together in a signaling complex. IFN-gamma had no effect on this complex formation, but did increase PKCepsilon-associated Akt kinase activity. PKCepsilon did not regulate IFN-gamma-induced Akt kinase. Finally, expression of dominant negative Akt kinase blocked IFN-gamma-stimulated MAPK activation. These data provide the first evidence that PI 3 kinase-dependent Akt and PKCepsilon activation independently regulate MAPK activity and serine phosphorylation of STAT1alpha to increase expression of MCP-1. 相似文献
18.
A. M. Choudhury K. Y. Chu G. W. Kenner S. Moore K. L. Ramachandran R. Ramage 《Bioorganic chemistry》1979,8(4):471-483
The synthesis of fragments corresponding to the N-terminal region of porcine big gastrin is described. Radioimmunoassay using synthetic peptides supports the revised structure for the hormone. 相似文献
19.
Murai H Qi H Choudhury B Wild J Dharajiya N Vaidya S Kalita A Bacsi A Corry D Kurosky A Brasier A Boldogh I Sur S 《PloS one》2012,7(2):e30280
Background
A series of epidemiologic studies have identified the fungus Alternaria as a major risk factor for asthma. The airway epithelium plays a critical role in the pathogenesis of allergic asthma. These reports suggest that activated airway epithelial cells can produce cytokines such as IL-25, TSLP and IL-33 that induce Th2 phenotype. However the epithelium-derived products that mediate the pro-asthma effects of Alternaria are not well characterized. We hypothesized that exposure of the airway epithelium to Alternaria releasing cytokines that can induce Th2 differentiation.Methodology/Principal Finding
We used ELISA to measure human and mouse cytokines. Alternaria extract (ALT-E) induced rapid release of IL-18, but not IL-4, IL-9, IL-13, IL-25, IL-33, or TSLP from cultured normal human bronchial epithelial cells; and in the BAL fluids of naïve mice after challenge with ALT-E. Both microscopic and FACS indicated that this release was associated with necrosis of epithelial cells. ALT-E induced much greater IL-18 release compared to 19 major outdoor allergens. Culture of naïve CD4 cells with rmIL-18 induced Th2 differentiation in the absence of IL-4 and STAT6, and this effect was abrogated by disrupting NF- κB p50 or with a NEMO binding peptide inhibitor.Conclusion/Significance
Rapid and specific release of IL-18 from Alternaria-exposed damaged airway epithelial cells can directly initiate Th2 differentiation of naïve CD4+ T-cells via a unique NF-κB dependent pathway. 相似文献20.
We previously showed that P311, an intracellular protein involved in cell migration, is found in human wound myofibroblast precursors (proto-myofibroblasts) and myofibroblasts. Furthermore, by binding to the TGF-beta1 latency associated protein (LAP), P311 induced NIH 3T3 cells to transform into non-fibrogenic myofibroblasts characterized by lack of TGF-beta1 production. Here we demonstrate that P311-induced myofibroblasts migrate in an ameboid rather than a mesenchymal pattern. Ameboid migration is characterized by lack of focal adhesions and stress fibers, absence of integrins and MMPs clustering/activation and changes in small GTPases activity, all leading to increased cell motility. P311-induced ameboid migration depended on activation of the GTPase RalA and was reverted to mesenchymal-type migration by RalA RNA interference. Ameboid migration was conserved in cells plated on fibrin, the initial wound matrix, but was switched back to mesenchymal-type migration by collagen I, the main ECM component in late stages of wound healing. TGF-beta1, the major stimulus of collagen production during wound repair, also reversed the ameboid phenotype to mesenchymal. Our studies therefore suggest that, by inducing RalA activity, P311 promotes a motile proto-myofibroblast and myofibroblast phenotype specifically adapted to rapidly populate the initial wound matrix. 相似文献