Adult ; Aged ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Carcinoma, Non-Small-Cell Lung ; diagnostic imaging ; drug therapy ; Female ; Fluorodeoxyglucose F18 ; Humans ; Lung Neoplasms ; diagnostic imaging ; drug therapy ; Male ; Middle Aged ; Positron-Emission Tomography ; Small Cell Lung Carcinoma ; diagnostic imaging ; drug therapy ; Tomography, X-Ray Computed

Objective To evaluate the value of gated ~(99)Tc~m-methoxyisobutylisonitrile (MIBI) myocardial perfusion imaging in detection of myocardial ischemia in hypertrophic cardiomyopathy.Methods Sixty-nine patients with clinically proven hypertrophic cardiomyopathy were divided into 2 groups using coronary angiogram as "gold standard":positive group(n=19,narrowing≥50%) and negative group (n=50,narrowing＜50%).Gated ~(99)Tc~m-MIBI myocardial perfusion imaging was performed and positive in all 69 patients (41 males,28 females,aged 35-75 years).Comparative analysis between the two groups was carried out using t-test.Results In the positive group,reversible and irreversible perfusion defects were detected in 9 and 10 patients,respectively.Left ventricular ejection fraction (LVEF) increased to (69.1±2.8)% in 8 patients and decreased to(42.8±2.1)% in 11 patients.In the negative group,reversible and irreversible perfusion defects were found in 37 and 13 patients,respectively.LVEF increased to(70.8±4.0)% in 38 patients and decreased to(48.9±2.7)% in 12 patients.The values of ischemic area,severity and extent of perfusion defect,and LVEF were significantly different between the two groups(t=9.28,16.51,2.65;P＜0.001,＜0.001,＜0.01,respectively).Conclusions Gated ~(99)Tc~m-MIBI myocardial perfusion imaging is valuable in assessing patients with hypertrophic cardiomyopathy.Detection for the presence or absence of coexisting coronary artery disease and myocardial ischemia has an important prognostic indication and management indication for these patients.

Objective To examine the levels of serum adipaneetin in patients with incipient chronic kidney disease (CKD, GFR≥ 60ml/min, and identify the relationship between serum adiponectin and albumin (ALB), urinary protein excretion amount, blood lipid and renal function. Methods Forty-two CKD patients and twenty normal healthy persons were involved in this study. These patients were divid- ed into two groups: nephrotic syndrome and non-nephrotic syndrome. The level of serum adiponectin, serum ALB, urinary protein excretion amount, blood lipid, renal function were measured and compared. Results The level of serum adiponectin in nephritic syndrome patients [(21.9±11.3) mg/L] and non-nephrotic syndrome patients [ ( 11.0±7.0) mg/L] was significantly higher than that in normal healthy per- sons[ (5.6±3.3) mg/L] ( P<0.01 ), and the level of serum adiponectin in nephritic syndrome patients was higher than that in non-ne- phrotic syndrome patients( P <0.01 ). Correlative analyses revealed a negatively correlation between serum adiponectin and serum total pro- tein(TP, ALB, BMI( r=-0.5680, r = -0.6241, r = -0.4083,respectively), and a positive correlation between serum adiponectin and urinary protein excretion amount ( r =0.4083). Stepwise regression analyses showed that serum adiponoctin was highly influenced by BMI, ALB and urinary protein excretion amount. Conclusion Serum adipanectin was markedly increased in incipient CKD, especially in patients with macroalbuminura. The effect of high level adiponectin in CKD was still not clear.

Objective To explore the roles of reactive oxygen species(ROS) and TGF-?1 in aldosterone-induced PAI-1 production.Methods Quiescent rat mesangial cells (MCs) were treated by aldosterone.The level of ROS in MCs induced by aldosterone was measured by confecal laser scanning microscopy and the TGF-?1 activity in the supematant of culture was measured by mink lung epithelial cell (Mvllu) proliferation inhibition MTT assay.Then,before the addition of aldosterone,MCs were pretreated with NAC or TGF-?1 neutralizing antibody to decrease cellular ROS or inhibit activity of TGF-?1 induced by aldosterone respectively.PAI-1 mRNA was examined by semi-quantification RT-PCR and PAI-1 protein by Western blotting.Results The intracellular ROS induced by aldosterone increased by 5-fold compared to that of control group,and the activity of TGF-?1 stimulated by aldosterone increased markedly.TGF-?1 neutralizing antibody and NAC effectively decreased aldosterone-induced PAI-1 mRNA expression by 30% and 32%,and PAI-1 protein expression by 21% and 11%,respectively.However,neither TGF-?1 neutralizing antibody nor NAC alone could regulate aldosterone-induced PAI-1 mRNA and protein expression to normal level in 24 hours.Conclusions ROS and TGF-?1 play important roles in up-regulation of aldosterone- induced PAI-1 in MCs.ROS and TGF-?1 are not the exclusive pathway of PAI-1 expression induced by aldosterone in MCs.

Objective To collect the families with generalized epilepsy with febrile seizures plus(GEFS+) and analyze the clinical status and heredity features of Chinese GEFS+.Voltaged-gated sodium channel ?1 subunit(SCN1B) gene of 2 families were detected,and expect to find new mutation sites.Methods All participant in the study of 2 families members were informed of voluntary participate in this investigation,health examination and blood sampling.All 6 gene exons of proband,patients and healthy control group were sequenced.The sequencing result was compared and analyzed with the normal sequence of genomic exon fragment and exon fragment sequencing result of control group through internet(BLAST).Results 1.A new G/A heterozygous polymorphism (G181A)was found in the 181th basyl of SCN1B gene exon 3,and codon was changed from TCG to TCA,both encoding serine (Ser,S).It was synonymous mutation.2.A new G/A heterozygous polymophism(G15A)was found in the 15th basyl of SCN1B gene exon 3,and codon was changed from GAG to GAA,both encoding glutamic acid(Glu,E).It belonged to synonymous mutation.3.A new T/C heterozygous polymorphism (T37C)was found in the 37th basyl of SCN1B gene exon 6.The patients genetype were:5 cases with T/C heterozygote,3 cases with T/T homozygote,2 cases with C/C homozygote.Healthy control group were all T/T homozygote.Allele frequency distribution for T was 55.0%,and 45.0% for C.4.A new A/C heterozygous polymorphism (A81C)was found in the 81th basyl of SCN1B gene exon 6.The patients genetype were:5 cases with A/C heterozygote,3 cases with A/A homozygote,2 cases with C/C homozygote.Healthy control group were all A/A homozygote.Allele frequency distribution for A was 55.0%,and 45.0% for C.Conclusions Two new heterozygous polymorphism (G181A),(G15A) were found in SCN1B gene exon 3.Two new heterozygous polymorphism (T37C),(A81C) were found in SCN1B gene exon 6.These 4 polymorphism enriched single nucleotide polymorphism(SPN) database and provided candidate sites for the research of epilepsy susceptbility polymorphisms.

Generalized epilepsy with febrile seizures plus(GEFS+) is a new epilepsy syndrome proposed by International League Against Epilepsy.At present,the progress of genetic studies of GEFS+ focus on gene mapping based on family analysis,many researches indicate that GEFS+ is associated with voltaged-gated sodium channel(SCN) gene mutation.This paper intends to discuss the relationship beween GEFS+ and SCN1B,SCN2B,SCN1A,SCN2A genes,mutations in order to improve the cognition about GEFS+.

Breast Neoplasms ; metabolism ; pathology ; surgery ; Carcinoma, Lobular ; metabolism ; pathology ; secondary ; surgery ; Carrier Proteins ; metabolism ; Female ; Glycolipids ; metabolism ; Glycoproteins ; metabolism ; Humans ; Mastectomy, Modified Radical ; Middle Aged ; Rectal Neoplasms ; secondary

Objective To explore the function of fluorescent probe JC-1 in detecting the changes of mitochondrial membrane potential(△?m)in early apoptotic cells.Methods After 2-ME was used to induce MUTZ-1 cell apoptosis,cells were dyed with fluorescent probe JC-1,and then the changes of △?m in the early stage of apoptotic cells were analyzed by flow cytometry or detected under fluorescent microscope. Results The control cells with high △?m are those forming JC-1 aggregates in the inner membrane of mitochondria,thus showing orange-red fluorescence.2-ME caused decrease of △?m in MUTZ-1 cells,in which JC-1 maintains monomeric form,thus showing only green fluorescence.The decreases of △?m were in a time-dependent manner,which were significantly higher than those in control group(P

OBJECTIVETo study risk factors for periventricular-intraventricular hemorrhage (PVH-IVH) in premature infants treated with mechanical ventilation.

METHODSA total of 205 premature infants who were admitted to the neonatal intensive care unit (NICU) and treated with mechanical ventilation between January 2009 and December 2011 were enrolled. They were classified into PVH-IVH and non-PVH-IVH groups according to the results of head ultrasonography performed at 3 to 7 days after birth. Single factor and multivariate logistic regression analysis were used to identify risk factors for PVH-IVH.

RESULTSSingle factor analysis indicated 9 factors associated with the development of PVH-IVH, including a gestational age of <32 weeks, a birth weight of <1500 g, intrauterine distress, severe asphyxia, vaginal delivery, maternal perinatal infection, premature rupture of membranes (PROM) at ≥8 hours, mechanical ventilation duration of ≥7 days and ventilator-associated pneumonia (VAP) (P<0.05). Multivariate logistic regression analysis showed that a birth weight of <1500 g (OR=2.665), intrauterine distress (OR=2.177), severe asphyxia (OR=5.653), maternal perinatal infection (OR=4.365) and VAP (OR=2.299) were independent risk factors for the development of PVH-IVH (P<0.05).

CONCLUSIONSVery low birth weight, intrauterine distress, severe asphyxia, maternal perinatal infection and VAP are closely associated with an increased risk of PVH-IVH in premature infants treated with mechanical ventilation. These clinical risk factors should be given more attention in the prevention of PVH-IVH.

Cerebral Hemorrhage ; etiology ; Female ; Humans ; Infant, Newborn ; Infant, Premature ; Infant, Premature, Diseases ; etiology ; Intensive Care Units, Neonatal ; Logistic Models ; Male ; Pneumonia, Ventilator-Associated ; complications ; Prognosis ; Respiration, Artificial ; adverse effects ; Risk Factors