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 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.

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.