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Aim To investigate the feasibility and mechanism of rhynchophylline in the treatment of in-rhynchophylline flammatory bowel disease (IBD) based on network pharmacology combined with in vivo and in vitro experiments. Methods The target of rhynchophylline-IBD intersection was obtained from the database, and GO and KEGG enrichment analysis were performed. The binding of key target proteins was screened by molecular docking. In vivo the IBD model of mice was induced by sodium dextran sulfate (DSS). After seven days of rhynchophylline intervention, the signs of mice in each group were observed and DAI scores were recorded. The levels of interleukin-1β (3 (IL-1 β), my-eloperoxidase (MPO) and other inflammatory factors in colon tissue of mice were detected by ELISA. The intestinal permeability of each group was detected. In vitro experiments were conducted to establish the inflammatory model of Caco2 cells induced by DSS, and to clarify the regulatory effect of leptosinine on key targets. Results A total of 70 rhynchophylline-IBD intersection targets were screened, and enrichment analysis showed that they were related to the inflammatory prooess, PI3K-Akt and Hippo signaling pathway s. Molecular docking results showed that was most stable in binding with JAK2 and JAK1. In vivo experiment results showed that compared with model group, body weight, colon length and weight of rhynchophylline group significantly increased (P < 0. 05). DAI score, IL-1β, MPO and other inflammatory factors in colon tissue and intestinal permeability significantly decreased (P < 0. 01). In vitro experiment results showed that compared with model group, rhynchophylline group significantly promoted the proliferation of Caco2 cells (P < 0. 05). The levels of IL-6 and NO were significantly reduced (P < 0. 05). Western blot results showed that rhynchophylline could decrease the expressions of JAK2 and JAK1 (P < 0. 05). Conclusion Rhynchophylline may play a role in the treatment of IBD by inhibiting the expression of JAK2 and JAK1 proteins and reducing inflammatory response in body.

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OBJECTIVE: Angle stable interlocking intramedullary nail (ASIN), a novel technique, has rarely been used for treatment of tibial plateau fractures (TPF). This retrospective study was designed to introduce this novel technique, ASIN, as well as to describe the initial experience and verify the effectiveness when ASIN was used for the management for TPF. METHODS: A cohort of 19 cases with closed TPF aged from 18-70 years with at least 23 months follow-up from November 2008 to September 2013 was analyzed retrospectively. All patients underwent the ASIN procedure, which was performed by the same group of surgeons. Perioperative and postoperative parameters like the measurement of radiographic pictures, surgical data, and clinical function were recorded including the changes in treatment. A modified Hohl-Luck radiological and functional score combined with the Hospital for Special Surgery (HSS) score were applied to evaluate the final results and to provide reliable data through the whole procedure when applying the ASIN procedure. RESULTS: The patients were followed up regularly for an average of 26.3 (range, 23-34) months. All patients achieved a bony union at an average of 15.1 weeks with no incidences of malunion, nonunion, or infection. Anatomical reduction of the articular surface was obtained in 16 patients. No secondary failure of fixation occurred. The mean postoperative knee flexion was 122.9°. The modified Hohl-Luck radiological and functional score was excellent and good, respectively, in 16 patients. The mean HSS score was 89.4. CONCLUSION: The angle stable interlocking intramedullary nail system turned out to be a viable alternative protocol in the treatment of tibia plateau fractures and provided satisfactory results, with good fracture reduction, biomechanical fixation, low rates of complications, and passable postoperative knee function.

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<p><b>OBJECTIVE</b>To observe the current changes of voltage-dependent potassium channel (Kv1.3 potassium channel) and calcium-activated potassium channel (IKCa1 potassium channel) in peripheral blood T-lymphocyte derived from hypertensive patients of Xinjiang Kazakh.</p><p><b>METHODS</b>Twenty randomly selected untreated Kazakh hypertensive patients and 20 Kazakh healthy subjects from Xinjiang were included in this study. T-lymphocytes were isolated from peripheral blood with magnetic cell sorting, the whole-cell currents of Kv1.3 and IKCa1 potassium channels were recorded with patch-clamp technique.</p><p><b>RESULTS</b>(1) The current density of Kv1.3 potassium channel was significantly higher in the hypertensive group [(280 ± 74) pA/pF (n = 39)] than that in the control group [(179 ± 51) pA/pF (n = 38), P < 0.01], while the membrane capacitance was similar between the two groups. (2) The current density of IKCa1 potassium channel was also significantly higher in the hypertensive group [(198 ± 44) pA/pF (n = 28)] than that in the control group [(124 ± 43) pA/pF (n = 26), P < 0.01], while the membrane capacitance was also similar between the two groups.</p><p><b>CONCLUSIONS</b>The T-lymphocytes Kv1.3 potassium channel and IKCa1 potassium channel current densities are higher in hypertensive patients in Xinjiang Kazakh suggesting a potential role of Kv1.3 and IKCa1 potassium channels activation in the pathophysiology of hypertension.</p>

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