Child ; Female ; Hamartoma ; diagnosis ; pathology ; surgery ; Humans ; Tracheal Diseases ; diagnosis ; pathology ; surgery

Adult ; Cryptococcosis ; Cryptococcus neoformans ; Humans ; Lung Diseases, Fungal ; Male

OsRacD is a critical molecular switch involved in photoperiod fertility conversion of photoperiod sensitive genic male sterile rice.Taking OsRacD as bait,a new rice myosin heavy chain partial cDNA was isolated from the rice panicle by yeast two-hybrid,and designated OsMY1.The interaction between OsMY1 and OsRacD had been testified by yeast two-hybrid and pull down assay,it showed that OsMY1 could bind with OsRacD,suggested that OsMY1 maybe the target of OsRacD.The important evidence for further study on the functional relationship between OsMY1 and OsRacD in vivo are also provided.

In order to assess the feasibility of subcutaneous administration of Triptorelin with 6-week intervals for the suppression of pituitary-gonadal axis and changes of clinical signs in girls with idiopathic central precocious puberty (ICPP), 46 girls with ICPP were treated with GnRHa. Triptorelin (Decapeptyl, 3.75 mg) was administered subcutaneously (SC) at 6-weeks intervals or intramuscularly (IM) at 4-weeks intervals randomly for more than 12 months consecutively. During GnRHa therapy, clinical parameters and laboratory data, including height, weight, pubertal stage, bone age, uterine volume and ovarian size, serum levels of luteinizing hormone (LH), follicle stimulating hormone (FSH) and estradiol (E2), were monitored and analyzed. It was found that both treatment regimes led to regression of precocious puberty and reversal of secondary sexual characteristics. Breast developments regressed. Uterine volume was decreased after treatment, but there was no statistically significant difference. Mean ovarian volume did not change significantly during treatment. The height velocity was decreased significantly from 6.3+/-1.4 cm/year to 5.8+/-1.2 cm/year in group SC and 6.7+/-1.3 cm/year to 5.4+/-1.0 cm/year in group IM, respectively. The rate of bone maturation was reduced significantly during treatment. The ratio of deltaBA/deltaCA was 1.2+/-0.2 or 1.3+/-0.3 at the onset of therapy and decreased significantly after the treatment to 0.7+/-0.2 or 0.9+/-0.1, respectively. The predicted adult height was increased significantly and progressively during therapy. The levels of serum LH, FSH and E2 returned to the prepubertal condition. No significant side effects of therapy were noted. The most common side effect during SC treatment was that a non-irritating, 1 cm in diameter mass was palpated at the site of subcutaneous injection in the abdominal wall of patients, which disappeared after 6-12 weeks. Two girls had minimal withdrawal vaginal bleeding episodes after the first injection. It was concluded that both IM and SC triptorelin administrations were clinically effective. They induce profound suppression of hypothalamic-pituitary-gonadal axis while stabilizing height velocity, slowing bone maturation and increasing predicted adult height. These results suggest that subcutaneous injection of triptorelin in 6-weeks intervals at a dosage of 3.75 mg be a safe and acceptable regimen for ICPP

Catheter Ablation ; Child ; Child, Preschool ; Female ; Humans ; Hypertrophy ; Male ; Palatine Tonsil ; pathology ; surgery ; Snoring ; surgery ; Turbinates ; pathology ; surgery

Aged ; Anthracosis ; complications ; pathology ; Cardiomyopathy, Hypertrophic ; pathology ; Edema ; Humans ; Male ; Middle Aged ; Myocardium ; pathology ; Pulmonary Heart Disease ; etiology ; pathology

Anti-Bacterial Agents ; pharmacology ; Child ; Humans ; Macrolides ; pharmacology ; Microbial Sensitivity Tests ; Mycoplasma pneumoniae ; drug effects

Objective To analyze the clinical manifestations,diagnosis and treatment of cerebral amyloid angiopathy (CAA) associated intracerebral hemorrhage.Methods The clinical manifestations,treatment and prognosis of CAA associated intracerebral hemorrhage were analyzed in 4 patients who were identified as CAA-related hemorrhage (CAAH) by pathology.Results All of the 4 patients showed massive lobar intracranial hemorrhage,and underwent craniotomy evacuation of hematoma.One patient had postoperative hemorrhage,and 2 patients were treated with recombinant activated factor Ⅶ after operation.In the next 6 months,re-hemorrhage was found in 3 patients in whom one patient died due to massive hemorrhage.Conclusions CAAH has varied clinical manifestations with high risk of cerebral hemorrhage,and pathological diagnosis is necessary for a definite diagnosis.The very elderly patients with CAAH can benefit from the craniotomy evacuation of hematoma.Although surgery for massive hemorrhage has risks in very elderly patients,it is a better treatment to save their lives.

Background Rapamycin(RAPA)is a specific inhibitor of the mammalian target of rapamycin (mTOR).Researches showed that RAPA inhibits the proliferation of lens epithelium cells(LECs)and tumor cells and induces apoptosis of tumor cells.To investigate whether rapamycin has the inhibitory effect on retinal pigment epithelium(RPE)cells is very important for the prevention and management of proliferative vitreoretinopathy (PVR).Objective This study was to investigate the effects of RAPA on the proliferation and apoptosis of human RPE cells in vitro.Methods Human RPE cells(D407 strain)were cultured and passaged and then divided into regular culture group(blank control group),DMSO control group(0.1‰ DMSO +regular culture),and different concentrations RAPA-treatment groups(5,10,20,40,80,160,320 nmol/L).The proliferation(A490)of human RPE cells was detected using MTT,and the inhibitory rates of RAPA on the proliferation of RPE cells were calculated and compared among different groups at 12,24 and 48 hours.The apoptosis rates of the cells were analyzed among various groups by Hoechst staining after 12,24,48 hours.Results The inhibitory rates of RAPA on RPE cells were significantly different among various groups(F=484.451,P＜0.01)and evidently elevated in 20-320 nmol/L RAPA groups compared with DMSO control group(P ＜ 0.01).The inhibition of RAPA on the cells was considerably enhanced as the lapse of time(F=232.262,P＜0.01)with more dominant effects in 24 and 48 hours compared to 12 hours after addition of RAPA(P＜0.05-0.01).Compared with blank control group and DMSO control group,the apoptotic rates of the cells were evidently increased in 12,24,48 hours in 10 nmol/L RAPA group(all P＜0.05),and higher cellular apoptotic rates were found in 20-320 nmol/L RAPA groups(all P＜0.01).The alteration of cellular apoptotic rate showed a gradually incremental trend as the acting time of RAPA(F =625.584,P＜0.01).Karyorrhexis and mass-like density staining and chromatin substance were seen in RPE cells under the fluorescence microscope in ≥ 10 nmoL/L RAPA groups.Conclusions RAPA suppresses the proliferation and induces the apoptosis of human RPE cells in concentration-and time-dependent manner in vitro.

Objective To investigate the effects and mechanism of glucagon-like peptide-1 ( GLP-1 ) receptor agonist liraglutide on the proliferation and apoptosis of human pancreatic cancer cells. Methods The human pancreatic cancer cell line MIA PaCa-2 was incubated for 24 h with liraglutide at various concentrations (10-1 000 nmol/ L), or with 100 nmol/ L liraglutide for various durations (0-72 h). Cell proliferation was determined by Cell Counting Kit-8 (CCK-8) analysis. RT-PCR and Western blot were used to detect the mRNA and protein expression levels of related genes. Results GLP-1 receptor was expressed in the MIA PaCa-2 cells. Liraglutide suppressed cell proliferation, up-regulated the expression levels of pro-apoptotic protein Bax and down-regulated the expression levels of anti-apoptotic protein Bcl2 in human pancreatic cancer cells in a dose- and time-dependent manner. Meanwhile, liraglutide down-regulated the expression levels of insulin receptor (INSR) and insulin-like growth factor-1 receptor (IGF-1R), and the phosphorylation levels of their downstream signaling proteins Erk1 / 2 and Akt, in a dose- and time-dependent way. Conclusion Liraglutide inhibits proliferation and promotes apoptosis of human pancreatic cancer cells; the process may be mediated via suppressing the expression of INSR and IGF-1R and inhibiting activation of the downstream MEK/ Erk1 / 2 and PI3k/ Akt pathways.