The incidence of hypokalemia and periodic paralysis was retrospectively analyzed in 1225patients with hyperthyroidism. The results showed that 104 patients with hyperthyroidism (8.5%)had hypokalemia, and 82. 7% cases were women, with the potassium levels of 3.10 - 3.42 mmol/L. Periodic paralysis occurred in 60 patients (4. 9% ) and 96. 7% cases were men; 93.3% patients had the potassium levels less than 3. 0 mmol/L. Hypokalemia and periodic paralysis were alleviated after the control of hyperthyroidism.

Objective:To explore the effect of the interaction between B7H3 and fibronectin (FN) on the apoptosis of human chronic myeloid leukemia K562 cells.Methods:The expression of B7H3 molecules in K562 cells was detected using flow cytometry and B7H3 overexpressing cells were constructed. The interaction between B7H3 and FN was detected using the co-immunoprecipitation technology. After adding exogenous FN, cell experiments were performed to detect changes in adhesion and cell apoptosis. The changes in apoptosis-related proteins and PI3K/AKT signaling pathway were detected using Western blot.Results:The expression of B7H3 was low in K562, and the cell line K562 OE (overexpression) -B7H3 and the control cell line K562 NC (negative control) -B7H3 were obtained after lentivirus transfection. There is an interaction between B7H3 and FN ( P=0.036) , and this interaction promoted cell adhesion ( P<0.05) , inhibited cell apoptosis ( P<0.05) , and activated the PI3K/AKT signaling pathway ( P<0.05) . Conclusion:B7H3 interacts with FN to promote cell adhesion and may inhibit K562 cell apoptosis by activating the PI3K/AKT signaling pathway.

Objective:To investigate the effects of B7-H3 molecule on clear cell renal cell carcinoma (786-O) metastasis.Methods:Lentiviral transfection method was used to construct 786-O cells stably expressing low level of B7-H3 (shB7-H3 group) and a negative control cell line (shNC group). RT-qPCR, flow cytometry and Western blot were used to assess the efficiency of lentiviral transfection. CCK-8 method was used to detect the proliferation of 786-O cells in the two groups. Flow cytometry was performed to detect the changes in cell cycle. Cell scratch test and Transwell assay were used to detect the differences in cell migration and invasion. Western blot was used to detect the expression of marker proteins in the process of epithelial-mesenchymal transition (epithelial-mesenchymal transition, EMT). Changes in the expression of chemokines and their receptors were analyzed by flow cytometry and RT-qPCR. Effects of anti-CCL4 antibody on cell migration and invasion were analyzed by Transwell assay.Results:Flow cytometry showed that 786-O cells highly expressed B7-H3 molecules and the lentiviral transfection method successfully constructed the cell line with lower expression of B7-H3 (786-O-shB7-H3) and control cell line (786-O-shNC). B7-H3 molecule had no significant effect on the proliferation of 786-O cells. No significant difference in cell cycle was found between the two groups. Compared with 786-O-shNC cells, the migration and invasion ability of 786-O-shB7-H3 cells was suppressed. Moreover, the expression of EMT-related marker proteins (fibronectin and N-cadherin) was reduced and the expression of E-cadherin was increased in 786-O-shB7-H3 cells. The expression of CCL4 and its receptor CCR5 in the shB7-H3 group was lower than that in the shNC group. After intervention with anti-CCL4 antibody, the migration and invasion ability of 786-O-shNC cells was reduced, while that of 786-O-shB7-H3 cells had no significant change.Conclusions:Knocking down the expression of B7-H3 molecule had no significant effect on the proliferation of 786-O cells, but could affect the EMT process of 786-O cells and reduce tumor migration and invasion ability, thereby inhibiting tumor progression.

Objective To explore the association between Toll-like receptor-8(TLR8) genetic polymorphisms and susceptibility to ischemic stroke (IS) in patients of different traditional Chinese medicine (TCM) pat-terns. Methods 311 IS patients of wind-phlegm stasis-obstruction pattern, 284 IS patients of qi-deficiency blood-stasis pattern and 605 controls were recruited. The real-time PCR technology was used to detect TLR8 gene expression levels. TLR8 rs3764880 single nucleotide polymorphism(SNPs) were genotyped using the Se-quenom Mass ARRAY platform. Levels of inflammatory cytokines were measured by using ELISA. Statistical analyses were carried out by using PLINK and SPSS 16. 0 software. Results TLR8 gene variant rs3764880 polymorphism was significantly associated with wind-phlegm stasis-obstruction pattern in IS males patients in the allele model (P<0. 05). In IS male patients of qi-deficiency blood-stasis pattern , level of IL-8 was high-er in the GG genotype carriers than the AA+AG genotype carriers (P<0. 05). The GG+AG genotype carri-ers had higher levels of TNF-α and IL-8 than the AA genotype carriers ( P <0. 05 ) . TLR8 gene variant rs3764880 polymorphism was significantly associated with the levels of TC (βb = -0. 03, Padj =0. 001) and LDL (βb= -0. 25, Padj =0. 018) in additive model in qi-deficiency blood-stasis pattern in Han Chinese IS male patients. Conclusion TLR8 gene rs3764880 polymorphism might be associated with the susceptibility to IS in patients of wind-phlegm stasis-obstruction and affect inflammatory reaction and lipid metabolism in Han Chinese males of qi-deficiency blood-stasis pattern.

The Gastroesophageal reflux disease(GERD)is related to the dynamic disorder of the digestive tract caused by the imbalance of the viscera and meridians.The spleen and stomach are the hub of the qi machinery,transforming the essence of water and valley into energy and regulating the Yin and Yang of all bodies.The sympathetic balance between Ren-Du and Qi is the motivity of the spleen and stomach.Interstitial cells of Cajal(ICC)are the hub of digestive motility,which can maintain mitochondrial energy metabolism through mitochondrial autophagy and improve the digestive motility.Therefore,in this paper,the molecular biological basis of GERD was discussed based on the"regulating pivot with pivot"theory that the pivots of viscera and meridians drive ICC mitochondrial energy balance.It also explains the feasibility of Qi-Shi-Sheng-Jiang-Gui-Yuan Decoction in treating GERD based on"regulating pivot with pivot",which is helpful to realize the microscopization and concretization of"regulating pivot with pivot"theory and realize the modernization of TCM theory.

Ulcerative colitis（UC）is a disease characterized by chronic persistent inflammation of the colorectal mucosa. Its complex pathological mechanism is related to immune inflammation and enhanced apoptotic activity. The Janus kinase（JAK）/signal transducer and activator of transcription（STAT）is an important regulatory pathway in the body's physiological function, which can regulate the release of intestinal pro-inflammatory factors and induce apoptosis, resulting in colon tissue damage. In the condition of UC, the biological activities and expression levels of JAK and STAT increased, and the tissue inflammatory response and apoptosis rate increased, which led to the destruction of intestinal mucosal tissues. At present, in the treatment of UC, glucocorticoids and immunosuppressants are mainly employed to reduce intestinal inflammation. Although they can block the progress of UC to some extent, the adverse reactions are severe. A large number of studies have shown that traditional Chinese medicine（TCM） has significant advantages in the prevention and treatment of UC and can significantly reduce the recurrence rate of this disease. In recent years, plenty of studies have been carried out to explore the role of TCM in the treatment of UC by regulating the JAK/STAT pathway. The results have shown that the JAK/STAT pathway is the key target pathway of TCM in the treatment of UC. Based on the etiology and pathogenesis of deficiency and excess, TCM regulates the JAK/STAT pathway by clearing heat, drying dampness, cooling and activating blood, invigorating the spleen, warming the kidney, and performing both tonification and elimination to maintain the balance between pro-inflammatory factors and anti-inflammatory factors, weaken colonic inflammatory response, inhibit apoptosis, and play a role in the treatment of UC. The present study analyzed the mechanism and effect of TCM in intervening in UC by targeting the JAK/STAT signaling pathway and summarized the molecular mechanisms of different cytokines such as interleukin-6（IL-6）, IL-10, IL-23, microRNA（miRNA）-146a, and suppressors of cytokine signaling 2/3（SOCS2/3） on many family subtypes of the JAK/STAT signaling pathway to facilitate the comprehensive understanding of researchers on the mechanism of TCM on the JAK/STAT pathway in UC, which is expected to provide a theoretical basis for the treatment of UC and further drug development.

Toxoplasma gondii is an obligatory intracellular parasite which infects a variety of warm-blooded animals and causes toxoplasmosis. Toxoplasmosis seriously endangers human health and animal husbandry production. As one of the effective gene editing tools, the clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated proteins (Cas) system has been widely used for knockout of genes in T. gondii. This review summarizes the applications of the CRISPR/Cas9 technology in vaccines against single- and double-gene deletion strains of T. gondii, so as to provide insights into development of toxoplasmosis vaccines.