查看更多>>摘要：The coronavirus disease 2019(COVID-19)outbreak has been brought under control through a nationwide effort,and now it has become a global pandemic and the situation seems grim.We summarized the measures taken in Wuhan and analyzed the effects to comprehensively describe the factors involved in controlling the COVID-19 in China.In China,several measures such as the lockdown of Wuhan,restriction of traffic and communities,increasing hospital beds,nationwide support from medical staff,epidemic prevention equipment and supplies,and establishment of makeshift shelter hospitals have been taken.The lockdown of Wuhan reduced the propagation of cases to other cities in Hubei province and throughout China,traffic and community restrictions reduced the flow of population and the spread of disease,increasing wards and beds and medical personnel reduced the incidence of severe cases and mortality,the establishment of the Fangcang shelter hospitals provided a good isolation and monitoring environment,and further reduced the spread and fatality of the disease.The fact that China was able to control the spread of COVID-19 within three months without a specific drug or vaccine suggests that these measures are more adequate and effective.
查看更多>>摘要：Tinnitus,acute or chronic,is one of the most common and refractory disorders.Acute tinnitus is a symptom that is a warning sign when compared with chronic tinnitus.Although hearing loss initiates acute tinnitus,the relationship between hearing loss and tinnitus is far from straightforward.Other factors beyond the auditory system may play important roles in the occurrence of acute tinnitus.To address this issue,we propose an integrated regulation theory of the possible physical causes of acute tinnitus,and summarize a classification system for acute tinnitus based on this regulation theory to help guide clinical treatment.
查看更多>>摘要：Tinnitus,acute or chronic,is one of the most common and refractory disorders.Acute tinnitus is a symptom that is a warning sign when compared with chronic tinnitus.Although hearing loss initiates acute tinnitus,the relationship between hearing loss and tinnitus is far from straightforward.Other factors beyond the auditory system may play important roles in the occurrence of acute tinnitus.To address this issue,we propose an integrated regulation theory of the possible physical causes of acute tinnitus,and summarize a classification system for acute tinnitus based on this regulation theory to help guide clinical treatment.
查看更多>>摘要：Insulin resistance is an essential characteristic of type 2 diabetes mellitus(T2DM),which can be induced by glucotoxicity and adipose chronic inflammation.Mesenchymal stem cells(MSCs)and their exosomes were reported to ameliorate T2DM and its complications by their immunoregulatory and healing abilities.Exosomes derived from MSCs contain abundant molecules to mediate crosstalk between cells and mimic biological function of MSCs.But the role of exosomes derived from human umbilical cord mesenchymal stem cells(hUC-MSCs)in insulin resistance of human adipocytes is unclear.In this study,exosomes were harvested from the conditioned medium of hUC-MSCs and added to insulin-resistant adipocytes.Insulin-stimulated glucose uptake was measured by glucose oxidase/peroxidase assay.The signal pathway involved in exosome-treated adipocytes was detected by RT-PCR and Western blotting.The biological characteristics and function were compared between hUC-MSCs and human adipose-derived mesenchymal stem cells(hAMSCs).The results showed that hAMSCs had better adipogenic ability than hUC-MSCs.After induction of mature adipocytes by adipogenesis of hAMSC,the model of insulin-resistant adipocytes was successfully established by TNF-a and high glucose intervention.After exosome treatment,the insulin-stimulated glucose uptake was significantly increased.In addition,the effect of exosomes could be stabilized for at least 48 h.Furthermore,the level of leptin was significantly decreased,and the mRNA expression of sirtuin-1 and insulin receptor substrate-1 was significantly upregulated after exosome treatment.In conclusion,exosomes significantly improve insulin sensitivity in insulin-resistant human adipocytes,and the mechanism involves the regulation of adipokines.
查看更多>>摘要：Insulin resistance is an essential characteristic of type 2 diabetes mellitus(T2DM),which can be induced by glucotoxicity and adipose chronic inflammation.Mesenchymal stem cells(MSCs)and their exosomes were reported to ameliorate T2DM and its complications by their immunoregulatory and healing abilities.Exosomes derived from MSCs contain abundant molecules to mediate crosstalk between cells and mimic biological function of MSCs.But the role of exosomes derived from human umbilical cord mesenchymal stem cells(hUC-MSCs)in insulin resistance of human adipocytes is unclear.In this study,exosomes were harvested from the conditioned medium of hUC-MSCs and added to insulin-resistant adipocytes.Insulin-stimulated glucose uptake was measured by glucose oxidase/peroxidase assay.The signal pathway involved in exosome-treated adipocytes was detected by RT-PCR and Western blotting.The biological characteristics and function were compared between hUC-MSCs and human adipose-derived mesenchymal stem cells(hAMSCs).The results showed that hAMSCs had better adipogenic ability than hUC-MSCs.After induction of mature adipocytes by adipogenesis of hAMSC,the model of insulin-resistant adipocytes was successfully established by TNF-a and high glucose intervention.After exosome treatment,the insulin-stimulated glucose uptake was significantly increased.In addition,the effect of exosomes could be stabilized for at least 48 h.Furthermore,the level of leptin was significantly decreased,and the mRNA expression of sirtuin-1 and insulin receptor substrate-1 was significantly upregulated after exosome treatment.In conclusion,exosomes significantly improve insulin sensitivity in insulin-resistant human adipocytes,and the mechanism involves the regulation of adipokines.
查看更多>>摘要：Fibulin-1(FBLN-1),an elastin-associated extracellular matrix protein,has been found in blood and may play a role in the pathophysiological processes leading to cardiovascular disease(CVD).We aimed to investigate the relationship between fibulin-1 levels and the risk of CVD by evaluating vascular age derived from the Framingham Heart Study and brachial-ankle Pulse Wave Velocity(baPWV)in patients with asymptomatic hyperuricemia(AHU).In total,66 patients with AHU and 66 gender-and age-matched healthy individuals were enrolled.The plasma fibulin-1 levels were measured by immunochemistry.Patients with AHU presented significantly higher vascular age[median(interquartile range):54(22)vs.48(14)years,P=0.01]and baPWV[mean±SD:1373±223 vs.1291±177 cm/s,P=0.02]than the healthy subjects;however,no significant difference was observed in the plasma fibulin-1 level between the patients with AHU and healthy subjects[median(interquartile range):4018(3838)vs.3099(3405)ng/mL,P=0.31].A correlation between fibulin-1 levels and baPWV was observed only in patients with AHU(r=0.29,P=0.02);and there was also a suggestively statistically significant correlation between fibulin-1 levels and vascular age(r=0.22,P=0.08).However,these associations were rendered insignificant after adjustments for potential confounders.In healthy subjects,no correlation was observed between fibulin-1 levels and CVD risk.This study reveals that plasma fibulin-1 levels may reflect the CVD risk in patients with AHU,but the relationship is not robust.
查看更多>>摘要：Fibulin-1(FBLN-1),an elastin-associated extracellular matrix protein,has been found in blood and may play a role in the pathophysiological processes leading to cardiovascular disease(CVD).We aimed to investigate the relationship between fibulin-1 levels and the risk of CVD by evaluating vascular age derived from the Framingham Heart Study and brachial-ankle Pulse Wave Velocity(baPWV)in patients with asymptomatic hyperuricemia(AHU).In total,66 patients with AHU and 66 gender-and age-matched healthy individuals were enrolled.The plasma fibulin-1 levels were measured by immunochemistry.Patients with AHU presented significantly higher vascular age[median(interquartile range):54(22)vs.48(14)years,P=0.01]and baPWV[mean±SD:1373±223 vs.1291±177 cm/s,P=0.02]than the healthy subjects;however,no significant difference was observed in the plasma fibulin-1 level between the patients with AHU and healthy subjects[median(interquartile range):4018(3838)vs.3099(3405)ng/mL,P=0.31].A correlation between fibulin-1 levels and baPWV was observed only in patients with AHU(r=0.29,P=0.02);and there was also a suggestively statistically significant correlation between fibulin-1 levels and vascular age(r=0.22,P=0.08).However,these associations were rendered insignificant after adjustments for potential confounders.In healthy subjects,no correlation was observed between fibulin-1 levels and CVD risk.This study reveals that plasma fibulin-1 levels may reflect the CVD risk in patients with AHU,but the relationship is not robust.
查看更多>>摘要：Osteoarthritis(OA)is a degenerative disease characterized by matrix degradation and cell death leading to a gradual loss of articular cartilage integrity.As a bacterial synthesis of quinine,pyrroloquinoline quinone(PQQ)is a strong redox cofactor with a variety of biological benefits,including antioxidant,anti-inflammation-induced mitochondrial metabolism regulation.This study was designed to investigate the effect of PQQ on TNF-α-induced mitochondrial damage in chondrocytes.Chondrocytes isolated from C57BL/6 mice were exposed to TNF-α 50 ng/mL,TNF-α 50 ng/mL+PQQ 10 pmol/L for 24 h.Then,morphological study,functional study and mechanism study were taken.The results revealed TNF-α-induced chondrocyte mitochondrion damage could be reduced by application of PQQ,evidenced by elevated number of mitochondria,well-kept mtDNA integrity,preserved ATP level,reestablished mitochondrial membrane potential,and prevented mitochondrial function.The present work strongly suggests that the mitochondrion is an important target for OA chondrocyte damage induced by TNF-α and the PQQ protection from this damage ameliorates mitochondrial dysfunction induced by TNF-α.PQQ might be a potential chemical for OA intervention.
查看更多>>摘要：Osteoarthritis(OA)is a degenerative disease characterized by matrix degradation and cell death leading to a gradual loss of articular cartilage integrity.As a bacterial synthesis of quinine,pyrroloquinoline quinone(PQQ)is a strong redox cofactor with a variety of biological benefits,including antioxidant,anti-inflammation-induced mitochondrial metabolism regulation.This study was designed to investigate the effect of PQQ on TNF-α-induced mitochondrial damage in chondrocytes.Chondrocytes isolated from C57BL/6 mice were exposed to TNF-α 50 ng/mL,TNF-α 50 ng/mL+PQQ 10 pmol/L for 24 h.Then,morphological study,functional study and mechanism study were taken.The results revealed TNF-α-induced chondrocyte mitochondrion damage could be reduced by application of PQQ,evidenced by elevated number of mitochondria,well-kept mtDNA integrity,preserved ATP level,reestablished mitochondrial membrane potential,and prevented mitochondrial function.The present work strongly suggests that the mitochondrion is an important target for OA chondrocyte damage induced by TNF-α and the PQQ protection from this damage ameliorates mitochondrial dysfunction induced by TNF-α.PQQ might be a potential chemical for OA intervention.
查看更多>>摘要：Microtubule-associated serine/threonine kinase(MASTL)functions to regulate chromosome condensation and mitotic progression.Therefore,aberrant MASTL expression is commonly implicated in various human cancers.This study analyzed MASTL expression in gastric cancer vs.adjacent normal tissue for elucidating the association with clinicopathological data from patients.This work was then extended to investigate the effects of MASTL knockdown on tumor cells in vitro.The level of MASTL expression in gastric cancer tissue was assessed from the UALCAN,GEPIA,and Oncomine online databases.Lentivirus carrying MASTL or negative control shRNA was infected into gastric cancer cells.RT-qPCR,Western blotting,cell viability,cell counting,flow cytometric apoptosis and cell cycle,and colony formation assays were performed.MASTL was upregulated in gastric cancer tissue compared to the adjacent normal tissue,and the MASTL expression was associated with advanced tumor stage,Helicobacter pylori infection and histological subtypes.On the other hand,knockdown of MASTL expression significantly reduced tumor cell viability and proliferation,and arrested cell cycle at G2/M stage but promoted tumor cells to undergo apoptosis.At protein level,knockdown of MASTL expression enhanced levels of cleaved PARP1,cleaved caspase-3,Bax and p-ERKl/2 expression,but downregulated expression levels of BCL-2 and p-NF-κB-p65 protein in AGS and MGC-803 cells.MASTL overexpression in gastric cancer tissue may be associated with gastric cancer development and progression,whereas knockdown of MASTL expression reduces tumor cell proliferation and induces apoptosis.Further study will evaluate MASTL as a potential target of gastric cancer therapeutic strategy.
NETL
NSTL
万方数据
维普