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RISS 인기검색어
- 검색키워드
- 저자 : ( Rakesh Vinayek ) (검색결과 2 건)
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( Paul Y. Kwo ),( Rakesh Vinayek ) 대한간학회 2011 Gut and Liver Vol.5 No.4
The current standard of care for hepatitis C infection is peginterferon/ ribavirin (PegIFN/RBV). We are entering the era where direct-acting antiviral agents (DAAs) will be added to PegIFN/RBV, leading to higher sustained response rates in genotype 1 infected individuals. Currently DAAs are directed toward specific proteins involved in hepatitis C replication with NS3/NS4A protease inhibitors furthest in development. Telaprevir and boceprevir are both NS3/NS4a inhibitors that significantly improve sustained response when added to PegIFN and RBV. The hepatitis C virus (HCV) polymerase inhibitors are another promising DAA class. These molecules are divided into nucleoside/nucleotide polymerase inhibitors and nonnucleotide/nucleoside polymerase inhibitors. Nucleoside/ nucleotide polymerase inhibitors have a high barrier to resistance and appear to be effective across a broad range of genotypes. Nonnucleoside polymerase inhibitors have a lower barrier of resistance and appear to be genotype specifi c. Preliminary data with these compounds are also promising. A third class, NS5A inhibitors, has also shown potent HCV RNA suppression in preliminary studies as monotherapy and with PegIFN and RBV. Combinations of these agents are also entering clinical trials and indeed a preliminary report has demonstrated that the combination of an NS3/4A protease inhibitor and NS5B polymerase inhibitor can effectively suppress virus in genotype 1 individuals. Future studies will concentrate on combinations of direct-acting antiviral agents without and with PegIFN and RBV. Clinicians will need to be familiar with managing side effects as well as resistance as we enter this new era. (Gut Liver 2011;5:406-417)
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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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