Objective To investigate the role of islet B cell dysfunction in the pathogenesis of type 2 diabetes mellitus. Methods FBG and fasting plasma insulin of 49 healthy subjects and 125 first-degree relatives of type 2 diabetes mellitus were determined. HOMA model was used to calculate HOMAIR as an index of insulin resistance and HOMAB as an index of B cell function of pancreatic islet.The insulin sensitivity index(ISI) and early-stage secretion index of islet ?cell(△I_ 30 /△G_ 30 )were calculated. Results The HOMAB and △I_ 30 /△G_ 30 of the group of normal first-degree relatives were higher (P

Hypertension is one of the most common cardiovascular diseases in clinic.TCM mostly treats it from the aspects of liver,kidney,spleen,and qi and blood,and often receives good clinical efficacy.But its modern scientific connotation still needs to be further elucidated.In recent years,it has been found that the intestinal flora is obviously related to the host's blood pressure and closely related to the function of dispersing liver-qi in TCM,so the"liver-intestine-bacteria"axis may become a new way to regulate hypertension.Based on the theory of"connection between liver and large intestine",this article discussed the correlation between liver-intestine-bacteria-hypertension with intestinal flora as the starting point,in order to provide some theoretical reference for the treatment of hypertension from liver.

Objective To explore the effect of let?7 miRNA silencing on Kaposi′s sarcoma? associated herpesvirus ( KSHV) lytic replication and the underling mechanism. Methods The pEGFP?C2?let?7 sponge vector was transfected into BCBL?1 and 293T cells with Lipofectamine 2000 to silence the expression of let?7 miRNAs. Quantitative real?time PCR ( qRT?PCR) was used to quantify the expression of let?7 miRNAs, the transcriptional levels of mitogen?activated protein kinase kinase kinase kinase 4 ( MAP4K4) , cyclooxygenase?2 ( COX?2) and matrix metalloproteinase 13 ( MMP?13) , and the DNA copy numbers of KSHV open reading frame 50 ( ORF50) and open reading frame 72 ( ORF72) . Western blot was used to detect the total and phosphorylated protein levels of MAP4K4, COX?2, extracellular regulated protein kinases (ERK1/2), c?Jun N?terminal kinase (JNK) and p38 MAPK. Results The expression of let?7 miRNAs was dramatically decreased in the let?7 sponge transfected BCBL?1 and 293T cells compared with that in the vector?transfected cells ( P<0.05 for all) . The gene copy number and mRNA transcriptional level of KSHV ORF50 were significantly increased in the let?7 sponge transfected BCBL?1 cells compared with that in the vector?transfected cells ( 1. 00 ± 0. 10 vs. 2. 33 ± 0. 18 and 1. 08 ± 0. 48 vs 3. 22 ± 0. 27, respectively, P<0.001 for both) . The gene copy number and mRNA transcriptional level of KSHV ORF72 were also significantly increased in let?7 sponge transfected BCBL?1 cells compared with those in the vector?transfected cells(1.07±0.49 vs 1.67±0.45 and 1.01±0.19 vs 1.54±0.11, respectively, P<0.05 for both). Furthermore, the mRNA transcriptional levels of MAP4K4, COX?2 and MMP?13 were significantly increased in the let?7 sponge transfected BCBL?1 cells compared with those in the vector?transfected cells (1.00±0.05 vs 5.73±0.96, 1.00±0.05 vs 2.68±0.19, 1.00±0.02 vs 2.69±0.25, respectively, P<0.001 for all). Let?7 miRNAs silencing also increased the protein expression levels of MAP4K4, COX?2 and phospho?ERK1/2, while the phospho?JNK and phospho?p38 were not changed in the BCBL?1 and 293T cells. Conclusions Let?7 silencing may activate the replication of KSHV, possibly through up?regulating MAP4K4 and its downstream molecules COX?2, MMP?13, and phosphorylation of ERK1/2, finally results in the progression of Kaposi sarcoma.

Objective To explore the effect of let?7 miRNA silencing on Kaposi′s sarcoma? associated herpesvirus ( KSHV) lytic replication and the underling mechanism. Methods The pEGFP?C2?let?7 sponge vector was transfected into BCBL?1 and 293T cells with Lipofectamine 2000 to silence the expression of let?7 miRNAs. Quantitative real?time PCR ( qRT?PCR) was used to quantify the expression of let?7 miRNAs, the transcriptional levels of mitogen?activated protein kinase kinase kinase kinase 4 ( MAP4K4) , cyclooxygenase?2 ( COX?2) and matrix metalloproteinase 13 ( MMP?13) , and the DNA copy numbers of KSHV open reading frame 50 ( ORF50) and open reading frame 72 ( ORF72) . Western blot was used to detect the total and phosphorylated protein levels of MAP4K4, COX?2, extracellular regulated protein kinases (ERK1/2), c?Jun N?terminal kinase (JNK) and p38 MAPK. Results The expression of let?7 miRNAs was dramatically decreased in the let?7 sponge transfected BCBL?1 and 293T cells compared with that in the vector?transfected cells ( P<0.05 for all) . The gene copy number and mRNA transcriptional level of KSHV ORF50 were significantly increased in the let?7 sponge transfected BCBL?1 cells compared with that in the vector?transfected cells ( 1. 00 ± 0. 10 vs. 2. 33 ± 0. 18 and 1. 08 ± 0. 48 vs 3. 22 ± 0. 27, respectively, P<0.001 for both) . The gene copy number and mRNA transcriptional level of KSHV ORF72 were also significantly increased in let?7 sponge transfected BCBL?1 cells compared with those in the vector?transfected cells(1.07±0.49 vs 1.67±0.45 and 1.01±0.19 vs 1.54±0.11, respectively, P<0.05 for both). Furthermore, the mRNA transcriptional levels of MAP4K4, COX?2 and MMP?13 were significantly increased in the let?7 sponge transfected BCBL?1 cells compared with those in the vector?transfected cells (1.00±0.05 vs 5.73±0.96, 1.00±0.05 vs 2.68±0.19, 1.00±0.02 vs 2.69±0.25, respectively, P<0.001 for all). Let?7 miRNAs silencing also increased the protein expression levels of MAP4K4, COX?2 and phospho?ERK1/2, while the phospho?JNK and phospho?p38 were not changed in the BCBL?1 and 293T cells. Conclusions Let?7 silencing may activate the replication of KSHV, possibly through up?regulating MAP4K4 and its downstream molecules COX?2, MMP?13, and phosphorylation of ERK1/2, finally results in the progression of Kaposi sarcoma.

Intestinal flora and bile acid metabolism regulate and influence each other,and an imbalance in the"intestinal flora-bile acid"pathway is closely related to atherosclerosis.Based on TCM theory and clinical practice,it is found that"earth congestion and wood depression"is the key mechanism of atherosclerosis,but its biological connotation needs to be further elucidated.Combined with the results of modern research,it is believed that intestinal flora imbalance is an important foundation of"earth congestion",and bile acid metabolism abnormality is an important manifestation of"wood depression".In the process of atherosclerosis,the imbalance of the"intestinal flora-bile acid"pathway is closely related to the"earth congestion and wood depression"pathogenesis of TCM in atherosclerosis.Exploring the biological connotation of the pathogenesis of"earth congestion and wood depression"of atherosclerosis from the"intestinal flora-bile acids"pathway is of far-reaching significance for clarifying the scientific connotation of TCM theory and guiding the TCM prevention and treatment of atherosclerosis.