As an outward,voltage-dependent potassium channel,M type channel is crucial in the regulation of neuronal excitability;it is modulated by a variety of factors in vivo and its dysfunction often results in neuronal system diseases.Great efforts have been made to elucidate the mechanism underlying M channel modulation since its discovery decades ago.It is generally accepted that the Phospholipase C(PLC) signaling pathway plays a significant role in the M channel modulation.This review highlights the relationship between PLC signaling pathway and M channel modulation,as well as some recent progresses in the research of this field.

Receptor tyrosine kinase(RTK),a membrane receptor superfamily with intrinsic protein tyrosine kinase activity,has many members and complicated signal transduction pathways.Activation of RTKs can trigger a series of signal transduction pathways and play essential roles in modulating cell growth,proliferation,differentiation and metabolism through influencing gene transcription and expression.Activation of RTK can also rapidly modulate some cellular functions including the modulation of ion channels.Potassium channels play a critical role in stabilization of membrane potential and regulation of cellular excitability.This review highlights the rapid modulation of potassium channels by RTKs and reviews the recent progress in related research.

Aim To study the characteristics of KCNQ2/3 potassium channel expressed in CHO cells and its modulation by M_1 receptor.Methods KCNQ2 and KCNQ3 potassium channels and M_1 receptor were co-expressed in CHO cells.Whole cell patch-clamp techniques was used to observe the characteristics of KCNQ2/3 current,its modulation by the M_1 receptor,and the effects of the common potassium channel blockers.Results KCNQ2/3 current recorded in CHO cells was a slow-activation low-threshold non-inactivating,voltage-dependent outward potassium current.KCNQ2/3 current was elicited at about-60 mV,V_(1/2)(-26.8?1.2) mV and the deactivation current fitted two exponential function,with ?_(fast) of 101ms and ?_(slow) of 309 ms.The channel was not sensitive to common pharmacological blockers such as 4-AP,Ba~(2+) and TEA,but was inhibited significantly by linopirdine,with a IC_(50) of(6.5?0.83) ?mol?L~(-1).Acetylcholine suppressed the KCNQ2/3 current reversibly via M_1 receptor,with a IC_(50) of(0.7?0.05) ?mol?L~(-1).Conclusion KCNQ2 and KCNQ3 channels are the molecular basis of M-current observed in neuronal cells.KCNQ2/Q3 current expressed in CHO cells has similar characteristics as that seen in neuronal M-current.Linopirdine is a powerful blocker of KCNQ2/3 channel and acetylcholine inhibits the current by muscarinic M_1 receptor.This experiment has laid a solid basis for further study of M-current and KCNQ2/3 current,and is important for the study of neurological diseases relating to alteration of M-current,such as convulsion,epilepsy and Alzheimers disease.

Objective To explore the characteristics and data collection sources of featured literature databases in universities/colleges in Yunnan in order to provide evidence for building featured literature databases. Methods Key information about three types of featured literature databases was retrieved online, which included those being constructed jointly by some universities or colleges in Yunnan, owned by universities or colleges in Yunnan, and already in use in China Academic Library and Information System ( CALIS) , respectively. Comparison was performed among these featured literature databases in regard to data characteristics and collection sources. Results Among all the featured databases being constructed, 58.8% were based on literature on local resources, 17.6% on disciplines and specialties, and 11.8% on library literature. In-use featured databases in Yunnan were mainly based on local resources and disciplines, and the data were collected within their own organizations or through multi-sources. The featured databases in CALIS were of local resources, disciplines, and people, while their data were collected mainly within their own organizations, through other organizations and multi-sources. Conclusion Yunnan featured databases are of unique characteristics, but more should be done to define Yunnan style data, while it is necessary to collect data from a wider range of sources.

This paper was aimed to study the effect of Qing-Chang Wen-Zhong (QCWZ) decoction on interferon gamma induced protein 10 (IP10) in colon tissues of rats with ulcerative colitis (UC).The UC model was induced using 4.5％ DSS added to distilled water for 7 days.At the same time,low-,medium-and high-dose of QCWZ decoction and mesalazine was given by gavage route daily.Then,the rats were killed and the colon tissues were taken.Expression level of interleukin-1 alpha (IL-1α),IL-1β,IL-6,tumor necrosis factor alpha (TNF-α) and interferon gamma (INF-γ) in colon were detected by Elisa assay.The expression and distribution of IP10 protein were detected by immunohistochemistry (IHC).The results showed that compared with the normal group,inflammatory factors (IL-1α,IL-1β,IL-6,TNF-α,INF-γ) and IP10 expression level in DSS-induced UC rats were significantly increased.After 7 days of intervention,inflammatory factors (IL-1α,IL-1β,IL-6,TNF-α,INF-γ) and IP10 decreased significantly (p＜0.01,p＜0.05).It was concluded that QCWZ decoction may down-regulate the expression of IP 10 and inflammatory factors (IL-1α,IL-1β,IL-6,TNF-α,INF-γ),and then inhibit intestinal inflammation and repair intestinal mucosal damage,so as to achieve the purpose of UC treatment.

Objective To investigate the prevalence of musculoskeletal disorders (MSD) in dentists and to analyze the risk factors of MSD to provide suggestions for preventing and reducing MSD in dentists. Methods Through stratified cluster random sampling, 373 dentists were selected from one Hospital of Stomatolagy and five general hospitals among Three-A hospitals in Wuhan as the research objects. The prevalence of MSD was surveyed using the Nordic musculoskeletal disorders standard questionnaire (NMQ) and Numerical Rating Scale (NRS) of pain measurement, and the risk factors of MSD was analyzed with binary Logistic regression. Results The total MSD annual prevalence rate of dentists was 93.3%, with a prevalence rate in neck, shoulder and back, waist and wrist at 78.3%, 70.0%, 56.0% and 36.2% respectively. Through Binary Logistic regression analysis, it was found that the risk factors associated with neck MSD were work fatigue（χ²=24.00，P=0.000）, neck hunching（χ²=23.55，P=0.000）, and shoulder side lift（χ²=24.52，P=0.000）. The risk factors associated with MSD in shoulder and back were work fatigue（χ²=34.64，P=0.000）, neck twisting（χ²=21.68，P=0.000） and wrist bending（χ²=45.87，P=0.000）. The risk factors associated with waist MSD were age（χ²=29.83，P=0.000）, majors（χ²=16.68，P=0.028）, work fatigue（χ²=21.08，P=0.000）, waist bending（χ²=22.88，P=0.000）. The risk factors associated with wrist MSD were gender（χ²=4.17，P=0.041）, majors（χ²=23.47，P=0.001）, working years（χ²=11.63，P=0.009）, physical activities（χ²=9.14，P=0.028）, number of patient visits per day（χ²=18.41，P=0.000）, bending and twisting（χ²=24.12，P=0.000）, wrist twisting（χ²=34.41，P=0.000）, and prevalence of microscope using（χ²=12.09，P=0.020）, while physical exercise was a protective factor for wrist MSD.The differences of the above-mentioned risk factors were statistically significant (P<0.05). Conclusion The prevalence of MSD in dentists is relatively high, and hospital management should strengthen organizational training to help dentists to realize the importance of adopting correct operating posture, a 5-minute breaks during work, prevent MSD at an early stage.

The mechanisms underlying autophagic defects in nonalcoholic steatohepatitis (NASH) remain largely unknown. We aimed to elucidate the roles of hepatic cyclooxygenase 1 (COX1) in autophagy and the pathogenesis of diet-induced steatohepatitis in mice. Human nonalcoholic fatty liver disease (NAFLD) liver samples were used to examine the protein expression of COX1 and the level of autophagy. Cox1^Δhepa mice and their wildtype littermates were generated and fed with 3 different NASH models. We found that hepatic COX1 expression was increased in patients with NASH and diet-induced NASH mice models accompanied by impaired autophagy. COX1 was required for basal autophagy in hepatocytes and liver specific COX1 deletion exacerbated steatohepatitis by inhibiting autophagy. Mechanistically, COX1 directly interacted with WD repeat domain, phosphoinositide interacting 2 (WIPI2), which was crucial for autophagosome maturation. Adeno-associated virus (AAV)-mediated rescue of WIPI2 reversed the impaired autophagic flux and improved NASH phenotypes in Cox1^Δhepa mice, indicating that COX1 deletion-mediated steatohepatitis was partially dependent on WIPI2-mediated autophagy. In conclusion, we demonstrated a novel role of COX1 in hepatic autophagy that protected against NASH by interacting with WIPI2. Targeting the COX1-WIPI2 axis may be a novel therapeutic strategy for NASH.