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RISS 인기검색어
- 검색키워드
- 저자 : Padmanabhan P Nair (검색결과 3 건)
- 무료
- 기관 내 무료
- 유료
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Dutta, Anand,Girotra, Mohit,Merchant, Nipun,Nair, Padmanabhan,Dutta, Sudhir Kumar Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.10
Background: Heat-shock protein70 (HSP70) are intracellular protein chaperones, with emerging evidence of their association with various diseases. We have previously reported significantly elevated plasma-HSP70 (pHSP70) in pancreatic cancer. Current methods of pHSP70 isolation are ELISA-based which lack specificity due to cross-reactivity by similarities in the amino-acid sequence in regions of the protein backbone resulting in overestimated HSP70 value. Materials and Methods: This study was undertaken to develop a methodology to capture all isoforms of pHSP70, while further defining their tyrosine and serine phosphorylation status. Results: The methodology included gel electrophoresis on centrifuged supernatant obtained from plasma incubated with HSP70 antibody-coupled beads. After blocking non-specific binding sites, blots were immunostained with monoclonal-antibody specific for human-HSP70, phosphoserine and phosphotyrosine. Conclusions: Our novel immunocapture approach has distinct advantages over the commercially available methods of pHSP70 quantification by allowing isolation of molecular aggregates of HSP70 with additional ability to precisely distinguish phosphorylation state of HSP70 molecules at serine and tyrosine residues.
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Dutta, Sudhir K.,Agrawal, Kireet,Girotra, Mohit,Fleisher, A. Steven,Motevalli, Mahnaz,Mah'moud, Mitchell A.,Nair, Padmanabhan P. Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.12
Introduction: Epidemiological studies suggest a protective role for ${\beta}$-carotene with several malignancies. Esophageal adenocarcinoma frequently arises from Barrett's esophagus (BE). We postulated that ${\beta}$-carotene therapy maybe protective in BE. Materials and Method: We conducted a prospective study in which 25 mg of ${\beta}$-carotene was administered daily for six-months to six patients. Each patient underwent upper endoscopy before and after therapy and multiple mucosal biopsies were obtained. Additionally, patients completed a gastroesophageal reflux disease (GERD) symptoms questionnaire before and after therapy and severity score was calculated. To study the effect of ${\beta}$-carotene at molecular level, tissue extracts of the esophageal mucosal biopsy were subjected to assessment of heat-shock protein 70 (HSP70). Results: A significant (p<0.05) reduction in mean GERD symptoms severity score from $7.0{\pm}2.4$ to $2.7{\pm}1.7$ following ${\beta}$-carotene therapy was noted. Measurement of Barrett's segment also revealed a significant reduction in mean length after therapy. In fact, two patients had complete disappearance of intestinal metaplasia. Furthermore, marked enhancement of HSP70 expression was demonstrated in biopsy specimens from Barrett's epithelium in four cases that were tested. Conclusions: Long-term ${\beta}$-carotene therapy realizes amelioration of GERD symptoms along with restitution of the histological and molecular changes in esophageal mucosa of patients with BE, associated with concurrent increase in mucosal HSP70 expression.
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Sudhir K Dutta,Sandeep Verma,Vardhmaan Jain,Balarama K Surapaneni,Rakesh Vinayek,Laila Phillips,Padmanabhan P Nair 대한소화기 기능성질환∙운동학회 2019 Journal of Neurogastroenterology and Motility (JNM Vol.25 No.3
2 decades evidence has emerged to suggest that inflammation-derived oxidative damage and cytokine induced toxicity may play asignificant role in the neuronal damage associated with Parkinson’s disease (PD). Presence of pro-inflammatory cytokines and T cellinfiltration has been observed in the brain parenchyma of patients with PD. Furthermore, evidence for inflammatory changes hasbeen reported in the enteric nervous system, the vagus nerve branches and glial cells. The presence of α-synuclein deposits in thepost-mortem brain biopsy in patients with PD has further substantiated the role of inflammation in PD. It has been suggested thatthe α-synuclein misfolding might begin in the gut and spread “prion like” via the vagus nerve into lower brainstem and ultimately tothe midbrain; this is known as the Braak hypothesis. It is noteworthy that the presence of gastrointestinal symptoms (constipation,dysphagia, and hypersalivation), altered gut microbiota and leaky gut have been observed in PD patients several years prior to theclinical onset of the disease. These clinical observations have been supported by in vitro studies in mice as well, demonstrating the roleof genetic (α-synuclein overexpression) and environmental (gut dysbiosis) factors in the pathogenesis of PD. The restoration of the gutmicrobiome in patients with PD may alter the clinical progression of PD and this alteration can be accomplished by carefully designedstudies using customized probiotics and fecal microbiota transplantation.
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