Abstract Cachexia is one of the serious complications in patients with end-stage cancer.Progressive depletion of skeletal muscle is an important feature of cachexia.Previous studies have found that excessive activation of autophagy accelerates skeletal muscle wasting in cachexia,and glutamine released from excessive catabolism of muscle tissue can trigger the autophagy.Mammalian target of rapamycin complex 1(mTORC1) and AMP-activated protein kinase(AMPK) signaling regulate autophagy genesis;moreover,glutamine regulates the mTORC1 and AMPK signaling pathways.Therefore,it is deduced that higher level of glutamine may result in abnormal autophagy by regulating mTORC1 and AMPK in cancer cachexia,which contributes to the development of skeletal muscle wasting.Here,this review discusses the following three perspectives:firstly,autophagy hyperactivation is involved in skeletal muscle wasting in cancer cachexia.Secondly,how mTORC1 and AMPK signaling pathways regulate autophagy.Finally,glutamine is involved in skeletal muscle wasting in cancer cachexia by induced autophagy hyperactivation via regulating mTORC1/AMPK signaling.Our study will provide a scientific basis for the development of potential therapeutic strategies.

With the development of the health service in china,the old talent-training program for clinical medicine major was failed in meeting higher demands for talents of clinical medicine. To create the new talent-training program,therefore,has become the main content of teaching reform for medical col-leges and universities. Taking University of South China as an example,the paper analyzed the changing trend of talent-training program for five-year clinical medicine majors from talent-training goal,curriculum system,practical teaching and content of courses,which proposed some thoughts on the optimization of training program for clinical medicine majors.

Objective To evaluate the efficacy of intravenous recombinant human brain natriuretic peptide in acute anterior myocardial infarction complicated with heart failure.Methods Two hundred patients suffered from acute anterior myocardial infarction complicated with heart failure were randomly divided into two groups:rhBNP group ( n =100) and control group ( n =100 ).All patients were given conventional treatment,patients in rhBNP group were given rhBNP on the basis of conventional therapy.The clinical effectiveness including the improvement of cardiac function,cardiac ultrasound data,the incidence of hospital adverse cardiac events,and six month follow-up were compared between the two groups.Results The degree of decompensation and Killip class in rhBNP group were better than those of control group after treatment ( improved dyspnea:significantly improved:36 vs 27 ; improved:49 vs 46; no improvement:11 vs 20 ; deterioration:4 vs 7 ; Ridit value:0.4618 vs 0.5382,P =0.043) ( Killip class:significantly improved:26 vs 20; improved:56 vs 45; no improvement:14 vs 25 ; deterioration:4 vs 10; Ridit value:0.4553 vs 0.5447,P =0.017 ).After treatment for one week,The LVEF improvement in rhBNP group was more remarkable than that of control group ( [ 53.0 ± 5.2 ] ％vs.[ 50.0 ±:6.2 ] ％,P =0.014).The occurrence rate of angina ( 13.0％ vs.27.0％,P =0.013 ),heart failure ( 18.0％ vs.32.0％,P =0.022) and major adverse cardiac events(MACE) ( 17.0％ vs.30.0％,P =0.030) inrhBNP group was lower than that in control group.During 6 months follow-up period,event-free survival in rhBNP group was higher than that in control group ( 69.0％ vs.55.0％,P =0.041 ).Conclusion Transvenous injection of rhBNP combined with other routine treatment can improve cardiac function in patients with myocardial infarction in acute anterior myocardial infarction.It can also decrease adverse cardiac events during hospitalization and increase event-free survival in 6 months follow-up period.