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Sreejyothi Sankararaman Renjini Ammini Raj Vimal Swapna Mohanachandran Nair Sindhu Sankararaman Sankaranarayana Iyer 《Journal of biological physics》2021,47(2):103-115
Journal of Biological Physics - The paper delves into the plausibility of applying fractal, spectral, and nonlinear time series analyses for lung auscultation. The thirty-five sound signals of... 相似文献
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Muscular dystrophies (MDs) such as Duchenne muscular dystrophy (DMD), sarcoglycanopathy (Sgpy) and dysferlinopathy (Dysfy)
are recessive genetic neuromuscular diseases that display muscle degeneration. Although these MDs have comparable endpoints
of muscle pathology, the onset, severity and the course of these diseases are diverse. Different mechanisms downstream of
genetic mutations might underlie the disparity in these pathologies. We surmised that oxidative damage and altered antioxidant
function might contribute to these differences. The oxidant and antioxidant markers in the muscle biopsies from patients with
DMD (n = 15), Sgpy (n = 15) and Dysfy (n = 15) were compared to controls (n = 10). Protein oxidation and lipid peroxidation was evident in all MDs and correlated with the severity of pathology, with
DMD, the most severe dystrophic condition showing maximum damage, followed by Sgpy and Dysfy. Oxidative damage in DMD and
Sgpy was attributed to the depletion of glutathione (GSH) and lowered antioxidant activities while loss of GSH peroxidase
and GSH-S-transferase activities was observed in Dysfy. Lower GSH level in DMD was due to lowered activity of gamma-glutamyl
cysteine ligase, the rate limiting enzyme in GSH synthesis. Similar analysis in cardiotoxin (CTX) mouse model of MD showed
that the dystrophic muscle pathology correlated with GSH depletion and lipid peroxidation. Depletion of GSH prior to CTX exposure
in C2C12 myoblasts exacerbated oxidative damage and myotoxicity. We deduce that the pro and anti-oxidant mechanisms could
be correlated to the severity of MD and might influence the dystrophic pathology to a different extent in various MDs. On
a therapeutic note, this could help in evolving novel therapies that offer myoprotection in MD. 相似文献
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Renjini Ramadasan-Nair Narayanappa Gayathri Sudha Mishra Balaraju Sunitha Rajeswara Babu Mythri Atchayaram Nalini Yashwanth Subbannayya Hindalahalli Chandregowda Harsha Ullas Kolthur-Seetharam Muchukunte Mukunda Srinivas Bharath 《The Journal of biological chemistry》2014,289(1):485-509
Muscular dystrophies (MDs) and inflammatory myopathies (IMs) are debilitating skeletal muscle disorders characterized by common pathological events including myodegeneration and inflammation. However, an experimental model representing both muscle pathologies and displaying most of the distinctive markers has not been characterized. We investigated the cardiotoxin (CTX)-mediated transient acute mouse model of muscle degeneration and compared the cardinal features with human MDs and IMs. The CTX model displayed degeneration, apoptosis, inflammation, loss of sarcolemmal complexes, sarcolemmal disruption, and ultrastructural changes characteristic of human MDs and IMs. Cell death caused by CTX involved calcium influx and mitochondrial damage both in murine C2C12 muscle cells and in mice. Mitochondrial proteomic analysis at the initial phase of degeneration in the model detected lowered expression of 80 mitochondrial proteins including subunits of respiratory complexes, ATP machinery, fatty acid metabolism, and Krebs cycle, which further decreased in expression during the peak degenerative phase. The mass spectrometry (MS) data were supported by enzyme assays, Western blot, and histochemistry. The CTX model also displayed markers of oxidative stress and a lowered glutathione reduced/oxidized ratio (GSH/GSSG) similar to MDs, human myopathies, and neurogenic atrophies. MS analysis identified 6 unique oxidized proteins from Duchenne muscular dystrophy samples (n = 6) (versus controls; n = 6), including two mitochondrial proteins. Interestingly, these mitochondrial proteins were down-regulated in the CTX model thereby linking oxidative stress and mitochondrial dysfunction. We conclude that mitochondrial alterations and oxidative damage significantly contribute to CTX-mediated muscle pathology with implications for human muscle diseases. 相似文献
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Padmanabhan RA Nirmala L Murali M Laloraya M 《Molecular endocrinology (Baltimore, Md.)》2011,25(9):1499-1512
Signaling via estrogen receptor (ER) occurs by interacting with many proteins. Nuclear interactome analysis of ERα in an embryo implantation model revealed the association of chicken tumor virus no. 10 regulator of kinase like (CrkL) with ERα, which was further validated by mammalian two-hybrid assay as well as coimmunoprecipitation and colocalization. Mutation in LPALL motif of CrkL disrupts the ERα-CrkL interaction and its transactivation potential, thereby suggesting that the interaction is mediated via its single ER binding motif, Leu-Pro-Ala-Leu-Leu (LXXLL) motif in the sarcoma homology (SH)2 domain. CrkL deletion constructs of SH2 domain target to the nucleus due to presence of nuclear localization signal. Interestingly, the SH2-SH3 (N terminal) construct shows an increased transactivation potential like CrkI. Weak interaction capability of mutated ERα-Y538F with CrkL validates that CrkL interacts with ERα via its YDLL motif at Tyr 541. In an attempt to understand the physiological relevance of this association, we investigated the impact on cell proliferation using a cancer model, because events associated in the process of pregnancy and cancer are analogous. Also, overexpression of CrkL is frequently associated with tumorigenesis. However, its significance in hormone-regulated cancers still remains obscure. Here, we demonstrate that association of ERα and CrkL directly enhances the tumorigenic potential of CrkL, thus pointing to its role in cell proliferation. In human endometrial cancers, we observed a strong association between ERα and CrkL levels. Thus, the molecular signaling set off by ERα and CrkL association may have a central role in pregnancy and cancer, two events which share parallels in growth, invasion, and immune tolerance. 相似文献
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Molecular Characterization of Vibrio cholerae O139 Bengal Isolated from Water and the Aquatic Plant Eichhornia crassipes in the River Ganga, Varanasi, India 下载免费PDF全文
R. Bhanumathi F. Sabeena Sree Renjini Isac B. N. Shukla D. V. Singh 《Applied microbiology》2003,69(4):2389-2394
A collection of ten strains of Vibrio cholerae O139, comprising six isolates from Eichhornia crassipes, two from water of the River Ganga, and one each from a well and a hand pump, were characterized. All the strains carried the CTX genetic element (ctxA, zot, and ace) except for the st gene and carried structural and regulatory genes for toxin-coregulated pilus (tcpA, tcpI, and toxR), adherence factor (ompU), and accessory colonization factor (acfB); all produced cholera toxin (CT). These strains were resistant to trimethoprim, sulfamethoxazole, streptomycin, and to the vibriostatic agent pteridine. Results obtained by ribotyping and enterobacterial repetitive intergenic consensus sequence-PCR fingerprint analysis indicate that multiple clones of toxigenic-pathogenic V. cholerae O139 were present in the aquatic environment. 相似文献
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Bhanumathi R Sabeena F Isac SR Shukla BN Singh DV 《Applied and environmental microbiology》2003,69(4):2389-2394
A collection of ten strains of Vibrio cholerae O139, comprising six isolates from Eichhornia crassipes, two from water of the River Ganga, and one each from a well and a hand pump, were characterized. All the strains carried the CTX genetic element (ctxA, zot, and ace) except for the st gene and carried structural and regulatory genes for toxin-coregulated pilus (tcpA, tcpI, and toxR), adherence factor (ompU), and accessory colonization factor (acfB); all produced cholera toxin (CT). These strains were resistant to trimethoprim, sulfamethoxazole, streptomycin, and to the vibriostatic agent pteridine. Results obtained by ribotyping and enterobacterial repetitive intergenic consensus sequence-PCR fingerprint analysis indicate that multiple clones of toxigenic-pathogenic V. cholerae O139 were present in the aquatic environment. 相似文献
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