Ischemia-reperfusion after neonatal asphyxia is a key factor in renal injury,which often leads to apoptosis of tubular epithelial cells.Apoptosis is an important form of injury for renal tubular epithelial cells after asphyxia.Smac/DIABLO is released to the cytosol in response to diverse apoptotic stimuli while mitochondrial targeting signal peptide is removed.In the cytosol,Smac/DIABLO interacts and antagonizes inhibitors of apoptosis proteins,thus allowing the activation of caspases and apoptosis.And thus it increases the ischemia-reperfusion renal injury,leading to acute renal failure.

Hypoglycemia is a common metabolic disorder of neonates.Severe and prolonged neonatal symptomatichypoglycemia can cause cerebral lesions.Operational threshold is asscioated with delayed neurological development in infants at risk.Treatment should be based on diffenrent approaches guided by asymptomatic hypoglycemia and symptomatic hypoglycemia.Magnetic resonance diffusion weighted imaging and brain stem auditory evoked potentials in diagnosis hypocemic brain damage is more sensitive and specific,especially in the early period.With the current neonatal hypoglycemia the gradual deepening of understanding,and further put forward a neonatal hypoglycemia diagnosis and treatment strategy.The threshold of 2.6 mmol/L is recommended currently in guidelines.Key to preventing complications from glucose deficiency is to identify infants at risk,promote early and frequent feedings,normalize glucose homeostasis,measure glucose concentrations early and frequently in infants at risk,and treat promptly when glucose deficiency is marked and symptomatic.

Ischemia-reperfusion after neonatal asphyxia is a key factor in renal injury,which often can lead to apoptosis of tubular epithelial cells.Apoptosis is an important form of injury for renal tubular epithelial cells after asphyxia.Large number of cancer genes involve in regulation of renal ischemia-reperfusion injury in the process of apoptosis.Bcl-2 protein which are expression products of Bcl-2 oncogene act on the mitochondrial pathway in apoptosis.Furthermore they can inhibit the caspase cascade of apoptosis via the cells "cross-talk",which contribute to attenuate renal ischemia-reperfusion injury and improve renal function.

Melatonin is a bioactive substance primarily secreted by the pineal gland.Increasing evidences indicate that melatonin is effective in reducing breast cancer development.Melatonin exerts its anticarcinogenic actions through a variety of mechanisms.Melatonin suppresses estrogen receptor gene,modulates several estrogen dependent signal transductions,inhibits cell proliferation and impairs the metastatic capacity and so on.It has been suggested that enhanced endogenous melatonin secretion or melatonin treatment is beneficial for breast cancer patients.This review describes the mechanisms of melatonin on breast cancer and its possible application.

OBJECTIVE: To study the protection effects of echshinone acid (EA) on the primary cultured rat cardiomyocytes subjected to anoxia-reoxygenation (A/R) injury. METHODS: The primary cultured neonatal rat cardiomyocytes were pretreated with EA (0.5, 5 and 50 μmol · L-1), EA (5 μmol · L-1) and L-NAME (0.1 mmol · L-1), or PD98059 (50 μmol · L-1) respectively for 1 h, and then subjected to A/R injury after 24 h. The cell viability, activities of SOD and GSH-Px, MDA contents, LDH activity in the medium and HSP70 protein expression were measured. RESULTS: Pretreatment with Ech decreased LDH activity and MDA contents, increased cell viability and SOD and GSH-Px activities in a concentration-dependent manner, and increased HSP70 protein expression. The heart protective effects of EA were partly abolished by L-NAME or PD98059. CONCLUSION: Pretreatment with EA for 1h before ischemia can induce delayed cardiomyocyte protective effects by activation of NO and MAPK signaling pathways and increasing expression of HSP70 in rat neonatal cardiomyocytes.

Objective To investigate the effect of ulinastatin on postoperative cardiac troponin I ( cTnI) in patients underwent carotid endarterectomy ( CEA) under general anesthesia. Methods Forty patients with severe symptomatic carotid artery stenosis underwent unilateral CEA under general anesthesia from January 2011 to March 2012 were divided into either a ulinastatin group or a control group according to a random number table ( n=20 in each group) . Patients in the ulinastatin group received 500 000 U of ulinastatin via veins before induction of anesthesia. The patients in the control group were given the same amount of isotonic saline. The serum concentrations of cardiac troponin I ( cTnI ) were detected before surgery and at day 1,2,and 3 after procedure. Myocardial injury was defined as the cTnI peak concentration>0. 04μg/L . Results The levels of serum cTnI before procedure and at day 1,2,and 3 after procedure in the ulinastatin group were median (M) 0. 00 (0. 00-0. 03) μg/L,0. 07 (0. 00-1. 45) μg/L,0. 01 (0. 00-1. 21)μg/L,and 0. 05 (0. 00-0. 89)μg/L,respectively;those in the control group were 0. 00 (0. 00-0. 01)μg/L,0. 00 (0. 00-1. 42)μg/L,0. 00 (0. 00-1. 39)μg/L,and 0. 00 (0. 00-1. 24)μg/L, respectively. At day 1 after procedure,6 patients ( 30%) in the control group and 11 ( 55%) in the ulinastatin group occurred myocardial injury. There was no significant difference between the two groups (P<0. 05). In all the patients with the increased cTnI levels,the peak cTnI occurred at the first day after procedure,however,they did not reach the level ( >1. 5μg/L) of indicating patients occurring myocardial infarction. Conclusion Ulinastatin may not decrease the postoperative serum cTnI levels in CEA patients under general anesthesia. For whether to the CEA patients have myocardial protective effect,more samples are needed to be confirmed.

Child, Preschool ; Dexamethasone ; adverse effects ; Diaphragm ; drug effects ; Humans ; Infusions, Intravenous ; Male ; Spasm ; chemically induced

Carcinoma, Hepatocellular ; surgery ; Hepatectomy ; methods ; Humans ; Liver Neoplasms ; surgery

BACKGROUND: Exercise preconditioning can lighten exercise-induced muscle damage, thereby to avoid delayed onset muscle soreness. At present, experimental research is scarce that apply intedeukin-6 (IL-6), creatine kinase (CK) and creatine kinase isoenzyme (CK-MM) to evaluate skeletal muscle damage.OBJECTIVE: To observe the effects of exercise precondiUoning on muscle damage at different phases after eccentric exercise and changes of blood IL-6, CK and CK-MM.DESIGN, TIME AND SETTING: The randomized control animal expedmant was carded out in the Animal Laboratory of Chengdu Sports University between 2006 and 2007. MATERIALS: Eighty female adult SD rats, weighing (231.3+12.44) g, were adopted. Eighty rats were randomly divided into without exercise preconditioning group (n=40) and exercise preconditioning group (n=40). Each group was assigned into 5 subsets, termed before exercise, immediately after exercise, 24, 48, 72 hours after exercise, with 8 rats in each subset. METHODS: Except before exercise subset, other rats in the without exercise preconditioning group were forced to do treadmill exercise (19-21 m/min, -16° incline, 90 minutes). All rats of exercise preconditioning group were forced to do eccentric treadmill exercise for two weeks. After two weeks, treadmill test was made for rats except before exercise subset. MAIN OUTCOME MEASURES: Soleus muscle structure, blood IL-6, CK and CK-MM immediately, 24, 48, 72 hours after eccentric exercise.RESULTS: The soleus muscle was damaged after exercise, especially in without exercise preconditioning group at 24-48 hours after exercise. Blood IL-6 of without exercise preconditioning group increased significantly immediately after exercise and then gradually decreased, but again raised at 72 hours after exercise. In the exercise preconditioning group, blood IL-6 slightly reduced immediately after exercise and then gradually increased. Peak value appeared at 48 hours. After exercise, IL-6 of exercise preconditioning group was obviously lower than that of without exercise preconditioning group. Before exercise, serum CK and CK-MM of exercise preconditioning group were less than that of without exercise preconditioning group. After exercise, the CK and CK-MM were firstly raised and then reduced in two groups. Except 72 hours after exercise subset, the variation of CK and CK-MM of exercise preconditioning group was lower than that of without of exercise preconditioning group. CONCLUSION: Exercise preconditioning is redounded to lighten the ultrastructure injury of skeletal muscle induced by eccentric exercise and blood indices changes induced by exercise stress. The individual variation of CK and CK-MM is so tremendous that they fit the comparison of intrasubject variability.

Acute Disease ; Adult ; Humans ; Hydrogen Sulfide ; poisoning ; Male ; Poisoning ; pathology