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( Sunit Jariwala ),( Ariel Benson ),( Payal Patel ),( Adam Friedman ),( Kameelah Broadway ) 대한피부과학회 2013 Annals of Dermatology Vol.25 No.1
Sweet`s syndrome (SS), or acute febrile neutrophilic dermatosis, is marked by fever, leukocytosis, and painful erythematous papules/plaques resulting from neutrophil migration and accumulation in the dermis. This condition has been associated with underlying hematologic as well as solid malignancies. We describe a unique case of SS in a patient with metastatic papillary follicular thyroid carcinoma and group A streptococcal pharyngitis. The distribution of the patient`s SS rash was similar to the rash of neutrophilic dermatosis (pustular vasculitis) of the dorsal hands. (Ann Dermatol 25(1) 84∼87, 2013)
Effect of Oroxylum indicum on intestinal motility in rodents
Joshi, Shrikant V.,Gandhi, Tejal R.,Vyas, Bhavin A.,Shah, Payal D.,Patel, Paras K.,Vyas, Heta G. 경희한의학연구센터 2012 Oriental Pharmacy and Experimental Medicine Vol.12 No.4
Oroxylum indicum is traditional herbal medicine in India, China and Japan used for its anti-diarrhoeal/anti-dysenteric activity, also found to be active against experimentally induced (DNBS induced) inflammatory bowel disease in rats with potential reduction in diarrhoea. It promotes us to evaluate effects of Oroxylum indicum on intestinal motility, both in vitro and in vivo, in rodents. Flavonoids rich fraction of O. indicum was obtained and the effect of extract on contraction of acetylcholine, barium chloride and electrical field stimulation was studied on isolated rabbit ileum. Anti-diarrhoeal activities were investigated using castor oil and magnesium sulphate-induced diarrhoeal models in mice. Effect on intestinal motility was studied using gastrointestinal motility and antienteropooling assay methods. Antimicrobial activity of extract was evaluated using disc diffusion assay method. Extract inhibited the contractions induced by acetylcholine, barium chloride and electrical field stimulation. Verapamil potentiates inhibitory effect of extract. Extract showed significant and dose-dependent antidiarrhoeal effect devoid of altering gastrointestinal motility in normal animals. It also inhibited the microbial growth in disc diffusion assay method. Extract normalized intestinal motility altered by inflammatory stimulus and possesses antidiarrhoeal activity. Alteration of intestinal motility may involve modification in L-type $Ca^{2+}$ channels.
Lee, Eunjung,Jung, Dae Young,Kim, Jong Hun,Patel, Payal R.,Hu, Xiaodi,Lee, Yongjin,Azuma, Yoshihiro,Wang, Hsun-Fan,Tsitsilianos, Nicholas,Shafiq, Umber,Kwon, Jung Yeon,Lee, Hyong Joo,Lee, Ki Won,Kim, The Federation of American Societies for Experimen 2015 The FASEB Journal Vol.29 No.8
<P>Insulin resistance is a major characteristic of obesity and type 2 diabetes, but the underlying mechanism is unclear. Recent studies have shown a metabolic role of capsaicin that may be mediated <I>via</I> the transient receptor potential vanilloid type-1 (TRPV1) channel. In this study, TRPV1 knockout (KO) and wild-type (WT) mice (as controls) were fed a high-fat diet (HFD), and metabolic studies were performed to measure insulin and leptin action. The TRPV1 KO mice became more obese than the WT mice after HFD, partly attributed to altered energy balance and leptin resistance in the KO mice. The hyperinsulinemic-euglycemic clamp experiment showed that the TRPV1 KO mice were more insulin resistant after HFD because of the ∼40% reduction in glucose metabolism in the white and brown adipose tissue, compared with that in the WT mice. Leptin treatment failed to suppress food intake, and leptin-mediated hypothalamic signal transducer and activator of transcription (STAT)-3 activity was blunted in the TRPV1 KO mice. We also found that the TRPV1 KO mice were more obese and insulin resistant than the WT mice at 9 mo of age. Taken together, these results indicate that lacking TRPV1 exacerbates the obesity and insulin resistance associated with an HFD and aging, and our findings further suggest that TRPV1 has a major role in regulating glucose metabolism and hypothalamic leptin’s effects in obesity.—Lee, E., Jung, D. Y., Kim, J. H., Patel, P. R., Hu, X., Lee, Y., Azuma, Y., Wang, H.-F., Tsitsilianos, N., Shafiq, U., Kwon, J. Y., Lee, H. J., Lee, K. W., Kim, J. K. Transient receptor potential vanilloid type-1 channel regulates diet-induced obesity, insulin resistance, and leptin resistance.</P>
IL-10 prevents aging-associated inflammation and insulin resistance in skeletal muscle
Dagdeviren, Sezin,Jung, Dae Young,Friedline, Randall H.,Noh, Hye Lim,Kim, Jong Hun,Patel, Payal R.,Tsitsilianos, Nicholas,Inashima, Kunikazu,Tran, Duy A.,Hu, Xiaodi,Loubato, Marilia M.,Craige, Siobhan The Federation of American Societies for Experimen 2017 The FASEB Journal Vol.31 No.2
<P>Altered energy balance and insulin resistance are important characteristics of aging. Skeletal muscle is a major site of glucose disposal, and the role of aging-associated inflammation in skeletal muscle insulin resistance remains unclear. To investigate, we examined glucose metabolism in 18-mo-old transgenic mice with muscle-specific overexpression of IL-10 (M-IL10) and in wild-type mice during hyperinsulinemic-euglycemic clamping. Despite similar fat mass and energy balance, M-IL10 mice were protected from aging-associated insulin resistance with significant increases in glucose infusion rates, whole-body glucose turnover, and skeletal muscle glucose uptake (similar to 60%; P < 0.05), as compared to age-matched WT mice. This protective effect was associated with decreased muscle inflammation, but no changes in adipose tissue inflammation in aging M-IL10 mice. These results demonstrate the importance of skeletal muscle inflammation in aging-mediated insulin resistance, and our findings further implicate a potential therapeutic role of anti-inflammatory cytokine in the treatment of aging-mediated insulin resistance.</P>
Friedline, Randall H.,Ko, Hwi Jin,Jung, Dae Young,Lee, Yongjin,Bortell, Rita,Dagdeviren, Sezin,Patel, Payal R.,Hu, Xiaodi,Inashima, Kunikazu,Kearns, Caitlyn,Tsitsilianos, Nicholas,Shafiq, Umber,Shultz The Federation of American Societies for Experimen 2016 The FASEB Journal Vol.30 No.3
<P>Obesity is characterized by a dysregulated immune system, which may causally associate with insulin resistance and type 2 diabetes. Despite widespread use of nonobese diabetic (NOD) mice, NOD with severe combined immunodeficiency (scid) mutation (SCID) mice, and SCID bearing a null mutation in the IL-2 common chain receptor (NSG) mice as animal models of human diseases including type 1 diabetes, the underlying metabolic effects of a genetically altered immune system are poorly understood. For this, we performed a comprehensive metabolic characterization of these mice fed chow or after 6 wk of a high-fat diet. We found that NOD mice had similar to 50% less fat mass and were 2-fold more insulin sensitive, as measured by hyperinsulinemic-euglycemic clamp, than C57BL/6 wild-type mice. SCID mice were also more insulin sensitive with increased muscle glucose metabolism and resistant to diet-induced obesity due to increased energy expenditure (similar to 10%) and physical activity (similar to 40%) as measured by metabolic cages. NSG mice were completely protected from diet-induced obesity and insulin resistance with significant increases in glucose metabolism in peripheral organs. Our findings demonstrate an important role of genetic background, lymphocytes, and cytokine signaling in diet-induced obesity and insulin resistance.</P>
Dagdeviren, Sezin,Jung, Dae Young,Lee, Eunjung,Friedline, Randall H.,Noh, Hye Lim,Kim, Jong Hun,Patel, Payal R.,Tsitsilianos, Nicholas,Tsitsilianos, Andrew V.,Tran, Duy A.,Tsougranis, George H.,Kearns American Society for Microbiology 2016 Molecular and cellular biology Vol.36 No.23
<P>Skeletal muscle insulin resistance is a major characteristic of obesity and type 2 diabetes. Although obesity-mediated inflammation is causally associated with insulin resistance, the underlying mechanism is unclear. Here, we examined the effects of chronic obesity in mice with muscle-specific overexpression of interleukin-10 (M-IL10). After 16 weeks of a high-fat diet (HFD), M-IL10 mice became markedly obese but showed improved insulin action compared to that of wild-type mice, which was largely due to increased glucose metabolism and reduced inflammation in skeletal muscle. Since leptin regulates inflammation, the beneficial effects of interleukin-10 (IL-10) were further examined in leptin-deficient ob/ob mice. Muscle-specific overexpression of IL-10 in ob/ob mice (MCK-IL10(ob/ob)) did not affect spontaneous obesity, but MCK-IL10(ob/ob) mice showed increased glucose turnover compared to that in ob/ob mice. Last, mice with muscle-specific ablation of IL-10 receptor (M-IL10R(-/-)) were generated to determine whether IL-10 signaling in skeletal muscle is involved in IL-10 effects on glucose metabolism. After an HFD, M-IL10R(-/-) mice developed insulin resistance with reduced glucose metabolism compared to that in wild-type mice. Overall, these results demonstrate IL-10 effects to attenuate obesity-mediated inflammation and improve insulin sensitivity in skeletal muscle, and our findings implicate a potential therapeutic role of anti-inflammatory cytokines in treating insulin resistance and type 2 diabetes.</P>