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.

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.

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 Meibomain gland is a specially differentiated sebaceous gland lying in the tarsus of upper and lower eyelid.The morphological changes of the gland is associated with a variety of ocular surface diseases.Studying the relationship of morphological and functional change of meibomain gland with ocular surface is of great significance.Objective This study was to observe the change of morphology,structure and function of meibomain gland over aging and investigate the assocation of meibomain gland abnormality with ocular surface.Methods A prospectively cases-observational study was performed.Ninety-three eyes of 93 patients with age-related cataract aged 45 and older were enrolled in Shanxi Eye Hospital from March to September 2016 under the informed consent.The patients were divided into 45 to 59-year group and ≥60-year group according to age or meibomian gland loss ≥ 1/3 group and meibomian gland loss ＜ 1/3 group.The ocular anterior segment,lid margin,meibomian gland orifices and lipids traits were examined by slit-lamp microscope.The ocular surface symptoms were assessed and scored by Ocular Surface Disease Index (OSDI) scale.The break-up time of tear film (BUT),tear meniscus height,meibomian gland dropout degree,conjunctival hyperemia and corneal fluorescence staining scores were measured using ocular surface analyzer.Results No dry eye symptom was complained in all the subjects,and their OSDI scores were ＜12.No abnormal changes at the lid margin and the muco-cutaneous junction were observed.No abnormality of the meibomian gland orifices,the lipids traits and drainage was observed under the slit-lamp microscope.BUT was shortened in 42 eyes (45.16％);tear meniscus height was lowed in 52 eyes (55.91％);meibomian gland loss range was ≥1/3 in 58 eyes (62.27％).The meibomian gland loss scores were 1.65±0.79 in the 45 to 59-year group and 1.86±0.72 in the ≥60-year group,showing an insignificant difference between them (t =1.301,P =0.197).But when coming to the correlation analysis,a positive correlation was found between meibomian gland loss scores and age (rs =0.323,P=0.002),and no correlations were seen between age and BUT or tear meniscus height (rs =0.154,P =0.141;rs=-0.024,P =0.821).In addition,meibomian gland loss scores showed a negative correlation with mean BUT (rs =-0.251,P =0.015).The eye number of BUT abnormality in the meibomian gland loss ≥ 1/3 group was more than that in meibomian gland loss ＜1/3 group (P =0.018).Conclusions Meibomian gland loss is more serious over aging in middle aged and elderly population,and serious meibomian gland loss increases the risk of tear film instability.The early meibomain gland dysfunction-like signs occur prior to symptoms,which should raise concern in clinical work.

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.