Administration, Cutaneous ; Adolescent ; Antihypertensive Agents ; administration & dosage ; therapeutic use ; Child ; Clonidine ; administration & dosage ; therapeutic use ; Double-Blind Method ; Female ; Humans ; Male ; Tic Disorders ; drug therapy

Anticonvulsants ; adverse effects ; Humans ; Seizures ; chemically induced

Diabetes mellitus is a well documented risk factor for erectile dysfunction. Significant pathological changes observed in the cavernous tissues of ED patient with diabetes include generation of endothelial and smooth muscle cell, increase in thickness of collangen bundles, changes in vascular and neurotransmitters.
Diabetes Complications ; Diabetes Mellitus ; pathology ; Endothelium ; pathology ; Erectile Dysfunction ; etiology ; pathology ; Humans ; Male ; Muscle, Smooth ; pathology ; Neurotransmitter Agents ; Risk Factors

OBJECTIVETo investigate cell apoptosis, mitochondrial membrane potential, cytochrome C and mechanisms of mitochondria in lymphocyte apoptosis of sepsis.

METHODSIn the research, female C57BL/6 mice whose body weight ranged from 17 to 25 grams were utilized and assigned randomly to two groups: sham operated group (Control), cecal ligation and puncture group (CLP). The present study was undertaken by using the mice splenic lymphocyte to investigate cell apoptosis, mitochondrial membrane potential, cytochrome C. The apoptosis alteration was evaluated by Annexin V-FITC/PI double staining with flow cytometry. The alteration of mitochondrial membrane potential was investigated by Rhodamine-123 staining of cells. Cytochrome C of mitochondria and cytosol was investigated by Western blot methods. Statistical analysis was performed using SPSS 11.5 for Windows software. Experiment data was indicated with mean ± standard.

RESULTSThe splenic lymphocyte apoptosis was significantly accelerated in the CLP group when compared with that in control group (17.3% ± 2.2% vs. 3.5% ± 0.5%, P < 0.05). The Rhodamine-123 fluorescent intensity in splenic lymphocyte apoptosis was reduced in CLP group (76.2% ± 1.6%). Comparison between sham group (99.6% ± 0.4%) and CLP group had statistical significance (P < 0.05). Apoptosis could induce mitochondrial cytochrome C release into cytoplasm. In the CLP group, elevation of cytochrome C in cytosol was concurrently in accordance with decline in mitochondrial cytochrome C content.

CONCLUSIONThese data suggest that mitochondria and mitochondria signal pathway play an important role in lymphocyte apoptosis of sepsis.

Animals ; Apoptosis ; Cells, Cultured ; Cytochromes c ; metabolism ; Disease Models, Animal ; Female ; Lymphocytes ; metabolism ; pathology ; Mice ; Mice, Inbred C57BL ; Mitochondria ; metabolism ; physiology ; Sepsis ; metabolism ; pathology

Objective To detect the argyrophilic proteins in nucleolar organizer regions(Ag-NORs) that express rDNA and rRNA proliferation of T lymphocytes before chemotherapy and after complete remission(CR) in children with primary acute leukemia(AL).Methods The argyrophilic granules area of NOR/nuclear area(I.S%) of T lymphocytes was detected by image analysis system in peripheral blood of 42 patients before chemotherapy and after CR and 30 normal children.Results I.S% in the patients before chemotherapy(5.06%?1.36%) were significantly lower than those in the healthy donors(7.51%?1.06%)(t=8.238 P0.05).Conclusion These results suggest that decrease of Ag-NORs expresses the evidence for tumour induced suppression of immune function of T cells in children with AL prior to treatment.

OBJECTIVETo evaluate the effects of aminoguanidine on methylglyoxal-mediated oxygen-glucose deprivation (OGD) injury in the cultured human brain microvascular endothelial cells (HBMEC).

METHODSCultured HBMEC cells were pretreated with methylglyoxal before oxygen-glucose deprivation injury. Cell vitality was determined by MTT method, cell mortality was assessed by LDH release method, cell apoptosis was examined by Annexin V/PI formation method, and the advanced glycation end products (AGEs) were detected by Western-blot.

RESULTSMethylglyoxal induced HBMEC injury in a dose-dependent manner. At 2 mmol/L of methylglyoxal, the cell viability was 56.1% when methylglyoxal-pretreated cells exposed to oxygen-glucose deprivation, the cell inhibition rate was 90.0%. Aminoguanidine (1 mmol/L) inhibited methylglyoxal and OGD induced LDH release and Annexin V/PI formation. Furthermore, aminoguanidine (1 mmol/L) also decreased advanced glycation end products (AGEs) formation induced by methylglyoxal and oxygen-glucose deprivation.

CONCLUSIONAminoguanidine protected methylglyoxal mediated-oxygen-glucose deprivation injury in the cultured HBMEC, which may be associated with anti-glycation activity.

Apoptosis ; drug effects ; Cell Hypoxia ; drug effects ; Cell Survival ; drug effects ; Cells, Cultured ; Drug Antagonism ; Endothelial Cells ; drug effects ; metabolism ; pathology ; Endothelium, Vascular ; cytology ; Glycation End Products, Advanced ; metabolism ; Guanidines ; pharmacology ; Humans ; Pyruvaldehyde ; pharmacology

OBJECTIVESTo investigate the effect of diabetes mellitus on nNOS-containing nerve fibers in rats corpus cavernosum.

METHODSHealthy male Sprague-Deuley rats (n = 34) were divided into two groups randomly, the sixth (n = 17) and eighth groups (n = 17). Eleven of severteen rats wree intraperitoneal injection with streptozotocin (STZ) to induce experimented model of diabetes medilus in each group. The other were injected with citrate buffer as control. Injected with apmorphine at sixth and eight week, penile erection in diabetic and control groups were observed and noted. The expression of nNOS-positive containing nerver-fibers in corpous cavernosum were examined with streptavidin-peroxidase immunohistochemistry (SP method).

RESULTSThe erection rate of penile diabetic mellitus decreased compared to that in controls (P < 0.01). The erection rate of two diabetic groups were 37.5% and 14.3%, respectively, with significant difference (P < 0.05). The controls were all 100%. The significant changes of nNOS-containing never fibers were observed in the two diabetic groups. The numbers of nNOS-containing nerver fibers in the corpus cavernosum in the two diabetic groups were (37.00 +/- 6.76) and (28.00 +/- 5.29), respectively, with significant difference compared to each other (P < 0.05). In the two controls, the fibers were (83.00 +/- 3.22) and (81.00 +/- 3.61), respectively. The fibers in diabetic groups were less than those in controls (P < 0.01).

CONCLUSIONSThe erectile function of rats and the number of nNOS-positive containing nerve fibers is affected seriously by diabetes mellitus and it is positively correlated to the duration of diabetes mellitus. The decreasing of nNOS-positive containing nerve fibers may be one of the mechanisms of diabetic erectile dysfunction.

Animals ; Diabetes Complications ; Diabetes Mellitus ; enzymology ; pathology ; Disease Models, Animal ; Erectile Dysfunction ; enzymology ; etiology ; pathology ; Male ; Nerve Fibers ; enzymology ; Rats ; Rats, Sprague-Dawley

We investigated the effects of transient receptor potential M8 (TRPM8) channel on the proliferation and motility of androgen-independent prostate cancer PC-3 cells. After being permanently transfected with an empty vector and cDNA encoding the TRPM8 protein, cells were analysed for cell cycle distribution and motility using flow cytometry and scratch assay. Immunocytochemistry and Ca2+ imaging analysis revealed the overexpression of functional TRPM8 channel on both endoplasmic reticulum and plasma membrane of PC-3-TRPM8 cells. Cell cycle distribution and scratch assay analysis revealed that TRPM8 induced cell cycle arrest at the G0/G1 stage (P < 0.05) and facilitated the cell apoptosis induced by starvation (P < 0.05). Furthermore, TRPM8 inhibited the migration of PC-3-TRPM8 cells (P < 0.01) through the inactivation of focal-adhesion kinase. It appears that TRPM8 was not essential for the survival of PC-3 cells; however, the overexpression of TRPM8 had negative effects on the proliferation and migration of PC-3 cells. Thus, TRPM8 and its agonists may serve as important targets for the treatment of prostate cancer.
Adenocarcinoma ; genetics ; metabolism ; pathology ; Apoptosis ; Calcium ; metabolism ; Cell Cycle ; Cell Line, Tumor ; Cell Movement ; physiology ; Cell Proliferation ; Cell Transformation, Neoplastic ; Cytosol ; metabolism ; DNA-Binding Proteins ; genetics ; metabolism ; Epithelial Cells ; metabolism ; pathology ; Focal Adhesion Protein-Tyrosine Kinases ; antagonists & inhibitors ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Prostatic Neoplasms ; genetics ; metabolism ; pathology ; Starvation ; pathology ; TRPM Cation Channels ; genetics ; metabolism ; Transcription Factors ; genetics ; metabolism ; Transfection

OBJECTIVETo evaluate the role of adiponectin in regulating tumor necrosis factor alpha (TNF alpha) production and preventing fulminant autoimmunological damage of hepatocytes following concanavalin A (Con A) injection into mice.

METHODSThree days after recombinant plasmids pAA-neo-mAd were injected into the mice via the tail veins, Con A was injected into the mice. Mice transfected with empty pAA-neo vector served as controls. The serum levels of alanine aminotransferase (ALT), TNF alpha and adiponectin were detected, and histological examination of livers was carried out at different time points after the Con A injection. All results were subjected to statistical analyses.

RESULTSHistological examinations showed that the damage in livers of mice with high serum adiponectin levels was milder than that of the controls. The serum levels of ALT and TNF alpha were both lower than those of the controls (P less than 0.01, respectively). Statistical analyses showed the serum levels of ALT was negatively related to the levels of adiponectin in the sera (r=-0.5034).

CONCLUSIONAdiponectin is effective in protecting hepatocytes from Con A-induced immunological injury. The mechanism of this protective effect may be caused by inhibiting the synthesis and/or release of TNF alpha.

Adiponectin ; blood ; pharmacology ; Alanine Transaminase ; blood ; Animals ; Concanavalin A ; adverse effects ; Female ; Immune System Diseases ; chemically induced ; pathology ; prevention & control ; Liver ; drug effects ; pathology ; Liver Diseases ; pathology ; prevention & control ; Mice ; Mice, Inbred BALB C ; Tumor Necrosis Factor-alpha ; blood

OBJECTIVETo study the expression of MMP-8 in human and rat tooth development.

METHODSImmunohistochemistry was used to detect the localization of MMP-8 protein while in situ hybridization was used to examine the expression of MMP-8 mRNA.

RESULTSThe expression of MMP-8 protein was localized in odontoblast and dentin matrix at the later bell stage in human tooth germ. The dentin was denser close to the pulp cavity. The expression of MMP-8 mRNA was found in very few polarized odontoblast at the early bell stage and all polarized odontoblast at the later bell stage in rat tooth germ.

CONCLUSIONThe results suggested that MMP-8 involved in dentin matrix rebuilding in the process of dentin formation in human and rat dental development.

Animals ; Animals, Newborn ; Dentin ; enzymology ; Embryo, Mammalian ; In Situ Hybridization ; Matrix Metalloproteinase 8 ; biosynthesis ; genetics ; Maxilla ; enzymology ; Odontogenesis ; RNA, Messenger ; biosynthesis ; genetics ; Rats ; Rats, Sprague-Dawley ; Tooth Germ ; embryology ; enzymology