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 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.

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.

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.

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.

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

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

The ocean is a huge resource of organisms and about 80% of the world species live in it. Marine organisms synthesize various structurally-unique and pharmacologically-active metabolites which differ from those derived from the land organisms and serve as lead compounds for drug development. More than 15 000 new compounds have been isolated and identified from marine animals, plants and microorganisms since decades ago, and drugs like cephalosporins, ziconotide (Prialt), cytarabine (AraC) and vidarabine (AraA) were developed using these compounds as precursors.

Objective To detect genetic causes of seizures and developmental retardation in 60 patients with abnormal head magnetic resonance imaging(MRI) ,and to analyze the clinical manifestations and head MRI manifestations in carriers of arylsulfatase A (ARSA) gene mutation.Methods The blood samples of children and genomic DNA were collected.Sixty cases of children with suspected metachromatic leukodystrophy were tested (MLD) by using the second generation sequencing technology.The genotype and phenotype and head MRI findings were analyzed.Results Of the 60 cases of children, 15 cases with gene mutations.There were 7 kinds of ARSA gene mutations, and 3 of them, c.1178C ＞ G, c.1055A ＞ G and c.883 G ＞ A were pathogenic.The others were single nucleotide polymorphism(SNP), which had no relationship with this disease.One of the patients carried only SNP, and 14 of them were carrying pathogenic mutation, c.1055A ＞ G (53.33％) ,c.1178C ＞ G (40.00％) were more common,and c.1055A ＞ G mutation was in 8 cases, of which 5 cases were late-onset type.One case of the 3 patients who were late infantile type was carrying c.1178C ＞ G mutation at the same time.All the eight cases had retardation.One case had hydrocephalus, and 5 cases had epilepsy.All of the 6 patients with c.1178C ＞ G were late-infantile type, and had retardation, including 4 cases of epilepsy, c.883G ＞ A mutation in 1 case,was late-infantile type,and the first symptom was binaural deafness and mental retardation.Three different types of mutations showed no significant difference in brain MRI.Conclusions There are 14 patients who were diagnosed as MLD.c.1178C ＞ G and c.883G ＞ A were late infantile type,and c.1055A ＞G was mostly late-onset type.The changes in head MRI caused by different types of ARSA gene mutations were of no significant differences in performance.

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.