Face ; blood supply ; Hemangioma ; therapy ; Humans ; Vascular Malformations ; therapy ; Vasculitis ; therapy

Face ; blood supply ; Hemangioma ; classification ; diagnosis ; therapy ; Humans ; Jaw ; blood supply ; Lymphatic Abnormalities ; classification ; diagnosis ; therapy ; Mouth ; blood supply ; Vascular Malformations ; classification ; diagnosis ; therapy

Objective To investigate the association between serum N-terminal pro brain natriuretic peptide(NT-ProBNP) and creatine kinase myocardial(CK-MB),cardiac troponin I(cTnI) in children who were diagnosed as viral myocarditis(VMC),and to explore the clinical significance.Methods Fifty children with VMC were selected as VMC group who were further divided into cTnI(+)group and cTnI(-)group.Fifteen healthy children were selected as healthy control group.The levels of myocardial enzyme of the 2 groups were tested by automatic biochemical analyzer and level of NT-proBNP was detected by specific NT-proBNP enzymelink immunosorbent assay(ELISA) kit.SPSS 13.0 software was used to analyze the data.Results 1.There were 23 cases with positive cTnI and 27 cases with negative cTnI.The levels of NT-proBNP in VMC group including cTnI positive and cTnI negative were significantly higher than those in healthy control group (P0.05).2.In the group with positive cTnI,the level of NT-proBNP was correlated with cTnI.The coefficient of determination was 0.17.3.In the group with negative cTnI,the level of NT-proBNP was correlated with CK-MB.The coefficient of determination was 0.34.NT-proBNP presented a increasing trend during interval of 25-100 U?L-1 and 175-255 U?L-1 of CK-MB.Conclusions The levels in the serum NT-proBNP in VMC children were higher than those in healthy children.Serum detection NT-proBNP may be applied as a new approach in diagnosis of VMC in children.

Leydig cells are the major source of androgens in males. Stem cells can be induced to differentiate into androgen-secreting Leydig like cells, whose functions are regulated by the hypothalamus and pituitary, so that they precisely secret the necessary hormones to maintain physiological function. Therefore, the establishment of an effective protocol to induce the differentiation of stem cells into androgen-secreting cells is very helpful for the treatment of hypogonadism caused by abnormalities of Leydig cells. This review outlines the recent findings concerning the differentiation of stem cells into androgen-secreting cells.
Androgens ; secretion ; Cell Differentiation ; physiology ; Humans ; Hypogonadism ; therapy ; Hypothalamus ; physiology ; Male ; Pituitary Gland ; physiology ; Stem Cells ; cytology ; secretion

OBJECTIVEEndothelial apoptosis plays an important role in the initiation of atherosclerosis. It would be useful to clarify whether activation of non-neuronal muscarinic receptor (NNMR) could prevent endothelial apoptosis and atherosclerosis. We investigated the effects of NNMR activation on regulating rat aortic endothelial cells (RAECs) apoptosis induced by homocysteine, an independent risk factor of atherosclerosis, and further studied its molecular mechanism.

METHODSRAECs were incubated using homocysteine at the concentration of 2.7 mmol/L for 36 h. RAECs were also pre-treated with carbachol or arecoline to examine their effects. RT-PCR was used to assess changes in the gene expression related to cell apoptosis.

RESULTSIncubation of RAECs with homocysteine at the concentration of 2.7 mmol/L resulted in morphologic changes, such as cellular shrinkage, membrane blebbing, chromatin condensation and margination. These could be attenuated by pretreatment with carbachol and arecoline at the concentration of 10 micromol/L for 12 h. Homocysteine induced apoptosis in RAECs and the molecular mechanisms were associated with the regulation of fas, fas-L and caspase-8 in the death receptor pathway, bcl-2, bcl-xL and bax in the mitochondrial pathway, caspase-12 in the endoplasmic reticulum pathway and caspase-3, caspase-6 and p53 as downstream effectors. Carbachol and arecoline attenuated the effects of homocysteine on genes in the death receptor pathway, in the mitochondrial pathway and in the downstream pathway. Atropine could reverse all of the effects of arecoline.

CONCLUSIONActivation of NNMR by carbacol and arecoline inhibits homocysteine-induced endothelial cell apoptosis mainly through regulation of death receptor pathway, mitochondrial pathway and downstream effectors.

Animals ; Aorta ; cytology ; Apoptosis ; Apoptosis Regulatory Proteins ; metabolism ; Arecoline ; Carbachol ; Cell Cycle ; Endoplasmic Reticulum ; metabolism ; Endothelial Cells ; cytology ; drug effects ; Homocysteine ; adverse effects ; Mitochondria ; metabolism ; Rats ; Receptors, Muscarinic ; metabolism

China ; Oral Medicine ; education

Objective To determine how genetic polymorphisms in norepinephrine transporter (NET) gene influence the response of antidepressant treatment and how they interact with childhood trauma and recent life stress in a Chinese depressive patients.Methods 281 Chinese Han depressive patients received single antidepressant drugs for 6 weeks.Hamilton Depression Scale-17 (HAMD-17),the Childhood Trauma Questionnaire short term (CTQ-SF) and the Life Events Scale (LES) were used to evaluate severity of depressive symptoms and the occurrence of stressful life events respectively.Three single nucleotide polymorphisms (SNPs) in norepinephrine transporter were genotyped.Associations of single locus and haplotypes with antidepressant treatment response were analyzed using UNPHASED 3.0.13.The interaction of gene and life stress was analyzed by SPSS13.0 software.Results One NET SNP rs2242446 was significantly associated with antidepressant response in this Chinese male sample(0.4118vs0.2375,x2=7.046,P=0.0079,OR=0.445,95％ CI (0.243-0.815)),as was the haplotype CG(rs2242446 and rs5569;x2 =5.886,P=0.0153,OR=0.457,95％ CI (0.198-1.054)) and another haplotype CG-G(rs2242446,rs1532701 and rs5569;x2=5.360,P=0.0206,OR=0.530,95％ CI (0.202-1.386)) of NET in male samples.The NET SNPs rs5569 demonstrated interaction with childhood trauma to influence antidepressant response(β=-2.727,SE =1.195,P=0.023,OR=0.065,95％ CI (0.006-0.681)).Conclusion Antidepressant drug response was influenced by not only NET genetic polymorphisms in norepinephrine transporter gene but also interaction between the NET genetic polymorphisms and early life stress.

Plasma exchange is a commonly used blood purification method, h includes plasma exchange,double filtration plasmapheresis and immunoadsorption.Many nervous system diseases have the antibody. Guillian-Barre syndrome is caused by antibodies of the nervous system demyelinafing disease; Myasthenia grads is caused by the acetylcholinc receptor antibodies. CIDP also has autoimmune-mediated mechanism. Plasma exchange can be apphed effectively to remove antibodies, and to quickly improve the patient' s clinical symptoms and shorten the course of disease.

BACKGROUND: It has been proved that interleukin-18 (IL-18) involves in the development of acute cerebral infarction (ACI) and is positively correlated with the time of brain stroke onset, erythrocyte sedimentation rate (ESR), as well as neurological deficit and low-density value of brain CT.OBJECTIVE: To investigate the dynamic changes of serum IL-18 in the course of ACI.DESIGN: Verification analysis with patients as subjects and healthy volunteers as controls.SETTING: Department of neurology of a municipal hospital.PARTICIPANTS: Totally 46 inpatients (29 males and 17 females) with ACI were randomly selected from the Department of Neurology of People's Hospital, Maoming City, between December 2002 and January 2004.Meanwhile, 40 healthy controls (27 males and 13 females) were recruited from those who came to the hospital for routine physical examination. All the participants signed informed consent.METHODS: Fasting peripheral vein blood of 2 mL was collected from the patients on the 1st, 7rh, 14th and 21st days of ACI onset, and from healthy controls on the day of routine examination. The blood samples were centrifuged at 3 000 r/minute for 15 minutes at 4 ℃, and then the supernatant was collected for detecting IL-18 level by ELISA.MAIN OUTCOME MEASURES: The serum IL-18 level of patients on the 1st, 7th 14th and 21st days of ACI onset and that of healthy controls on the day of routine examination.RFSULTS: Totally 46 patients and 40 healthy controls were enrolled in this study and all data were statistically analyzed. The level of serum IL-18 was significantly higher in the patients with ACI than in normal controls on the 1st and 7th days of onset [(178±41) ng/L, (104±34) ng/L, (65±14) ng/L, P ＜ 0.01],but was similar on the 14th and 21st days [(88±36) ng/L, (72±33) ng/L,(65±14) ng/L, P＞ 0.05]. The level of serum IL-18 in ACI patients was significantly higher on the 1st day than on the 7th, 14th and 21 st days of the onset (P ＜ 0.05-0.01); moreover, it was also significantly higher on the 7th day than on the 21st day of the onset (P ＜ 0.05).CONCLUSION: The level of IL-18 increases obviously on the 1st day of ACI onset, and gradually decreases with the extended course of disease and time of treatment.