BACKGROUND Gallbladder polyps(GBPs)are known to be associated with obesity and metabolic diseases.However,to date,the relationship between GBPs and abnormal body fat distribution,such as fatty liver,visceral obesity,o...BACKGROUND Gallbladder polyps(GBPs)are known to be associated with obesity and metabolic diseases.However,to date,the relationship between GBPs and abnormal body fat distribution,such as fatty liver,visceral obesity,or sarcopenia,has not yet been established.AIM To evaluate whether GBPs are associated with fatty liver,visceral obesity,or sarcopenia.METHODS We retrospectively reviewed the medical records of subjects who underwent various laboratory tests,body composition measurement with a non-invasive body composition analyzer,and abdominal ultrasonography during health checkups.A total of 1405 subjects with GBPs were compared with 2810 age-and sex-matched controls.RESULTS The mean age of the subjects was 46.8±11.7 years,and 63.8%were male.According to multiple logistic regression analysis,the presence of fatty liver[odds ratio(OR)1.413;95%confidence interval(CI)1.218-1.638;P<0.001]was an independent risk factor for GBP,together with low levels of alanine aminotransferase(OR 0.993;95%CI 0.989-0.996;P<0.001).Additionally,fatty liver showed both independent(OR 1.629;95%CI,1.335-1.988;P<0.001)and dosedependent(moderate to severe fatty liver;OR 2.137;95%CI,1.662-2.749;P<0.001)relationship with large GBPs(≥5 mm).The presence of sarcopenia and high visceral fat area were not significantly associated with GBPs.CONCLUSION Fatty liver was found to be closely associated with GBPs irrespective of sarcopenia and visceral obesity.展开更多
We aimed to determine whether combination of LIM-kinase 2 inhibitor(LIMK2i)and phosphodiesterase type-5 inhibitor(PDE5i)could restore erectile function through suppressing cavernous fibrosis and improving caver nous a...We aimed to determine whether combination of LIM-kinase 2 inhibitor(LIMK2i)and phosphodiesterase type-5 inhibitor(PDE5i)could restore erectile function through suppressing cavernous fibrosis and improving caver nous apoptosis in a rat model of cavernous nerve crush injury(CNCI).Seventy 12-week-old Sprague-Dawley rats were equally distributed into five groups as follows:(1)sham surgery(Group S),(2)CNCI(Group I),(3)CNCI treated with daily intraperitoneal administration of 10.0 mg kg^-1 LIMK2i(Group I+L),(4)daily oral administration of 20.0 mg kg-1 udenafil,PDE5i(Group I+U),and(5)combined administration of 10.0 mg kg^-1 LIMK2i and 20.0 mg kg^-1 udenafil(Group I+L+U).Rats in Groups I+L,I+U,and I+L+U were treated with respective regimens for 2 weeks after CNCI.At 2 weeks after surgery,erectile response was assessed using electrostimulation.Penile tissues were processed for histological studies and western blot.Group I showed lower intracavernous pressure(ICP)/mean arterial pressure(MAP),lower area under the curve(AUC)/MAP,decreased immunohistochemical staining for alpha-smooth muscle(SM)actin,higher apoptotic index,lower SM/collagen ratio,increased phospho-LIMK2-positive fibroblasts,decreased protein kinase B/endothelial nitric oxide synthase(Akt/eNOS)phosphorylation,increased LIMK2/cofilin phosphorylation,and increased protein expression of fibronectin,compared to Group S.In all three treatment groups,erectile responses,protein expression of fibronectin,and SM/collagen ratio were improved.Group I+L+U showed greater improvement in erectile response than Group I+L.SM content and apoptotic index in Groups I+U and I+L+U were improved compared to those in Group I.However,Group I+L did not show a significant improvement in SM content or apoptotic index.The number of phospho-LIMK2-positive fibroblasts was normalized in Groups I+L and I+L+U,but not in Group I+U.Akt/eNOS phosphorylation was improved in Groups I+U and I+L+U,but not in Group I+L.LIMK2/cofilin phosphorylation was improved in Groups I+L and I+L+U,but not in Group I+U.Our data indicate that combined treatment of LIMK2i and PDE5i immediate after CN injury could improve erectile function by improving cavernous apoptosis or eNOS phosphorylation and suppressing cavernous fibrosis.Rectification of Akt/eNOS and LIMK2/cofilin pathways appears to be involved in their improvement.展开更多
文摘BACKGROUND Gallbladder polyps(GBPs)are known to be associated with obesity and metabolic diseases.However,to date,the relationship between GBPs and abnormal body fat distribution,such as fatty liver,visceral obesity,or sarcopenia,has not yet been established.AIM To evaluate whether GBPs are associated with fatty liver,visceral obesity,or sarcopenia.METHODS We retrospectively reviewed the medical records of subjects who underwent various laboratory tests,body composition measurement with a non-invasive body composition analyzer,and abdominal ultrasonography during health checkups.A total of 1405 subjects with GBPs were compared with 2810 age-and sex-matched controls.RESULTS The mean age of the subjects was 46.8±11.7 years,and 63.8%were male.According to multiple logistic regression analysis,the presence of fatty liver[odds ratio(OR)1.413;95%confidence interval(CI)1.218-1.638;P<0.001]was an independent risk factor for GBP,together with low levels of alanine aminotransferase(OR 0.993;95%CI 0.989-0.996;P<0.001).Additionally,fatty liver showed both independent(OR 1.629;95%CI,1.335-1.988;P<0.001)and dosedependent(moderate to severe fatty liver;OR 2.137;95%CI,1.662-2.749;P<0.001)relationship with large GBPs(≥5 mm).The presence of sarcopenia and high visceral fat area were not significantly associated with GBPs.CONCLUSION Fatty liver was found to be closely associated with GBPs irrespective of sarcopenia and visceral obesity.
文摘We aimed to determine whether combination of LIM-kinase 2 inhibitor(LIMK2i)and phosphodiesterase type-5 inhibitor(PDE5i)could restore erectile function through suppressing cavernous fibrosis and improving caver nous apoptosis in a rat model of cavernous nerve crush injury(CNCI).Seventy 12-week-old Sprague-Dawley rats were equally distributed into five groups as follows:(1)sham surgery(Group S),(2)CNCI(Group I),(3)CNCI treated with daily intraperitoneal administration of 10.0 mg kg^-1 LIMK2i(Group I+L),(4)daily oral administration of 20.0 mg kg-1 udenafil,PDE5i(Group I+U),and(5)combined administration of 10.0 mg kg^-1 LIMK2i and 20.0 mg kg^-1 udenafil(Group I+L+U).Rats in Groups I+L,I+U,and I+L+U were treated with respective regimens for 2 weeks after CNCI.At 2 weeks after surgery,erectile response was assessed using electrostimulation.Penile tissues were processed for histological studies and western blot.Group I showed lower intracavernous pressure(ICP)/mean arterial pressure(MAP),lower area under the curve(AUC)/MAP,decreased immunohistochemical staining for alpha-smooth muscle(SM)actin,higher apoptotic index,lower SM/collagen ratio,increased phospho-LIMK2-positive fibroblasts,decreased protein kinase B/endothelial nitric oxide synthase(Akt/eNOS)phosphorylation,increased LIMK2/cofilin phosphorylation,and increased protein expression of fibronectin,compared to Group S.In all three treatment groups,erectile responses,protein expression of fibronectin,and SM/collagen ratio were improved.Group I+L+U showed greater improvement in erectile response than Group I+L.SM content and apoptotic index in Groups I+U and I+L+U were improved compared to those in Group I.However,Group I+L did not show a significant improvement in SM content or apoptotic index.The number of phospho-LIMK2-positive fibroblasts was normalized in Groups I+L and I+L+U,but not in Group I+U.Akt/eNOS phosphorylation was improved in Groups I+U and I+L+U,but not in Group I+L.LIMK2/cofilin phosphorylation was improved in Groups I+L and I+L+U,but not in Group I+U.Our data indicate that combined treatment of LIMK2i and PDE5i immediate after CN injury could improve erectile function by improving cavernous apoptosis or eNOS phosphorylation and suppressing cavernous fibrosis.Rectification of Akt/eNOS and LIMK2/cofilin pathways appears to be involved in their improvement.