Objective To investigate the role of receptor for advanced glycation end - products nuclear factor - κB(RAGE - NF - κB)signaling pathway in the lipopolysaccharide - induced acute lung injury(ALI)in neo-natal rats. Methods Thirty - two SD rats were divided into 4 groups by complete randomization method(8 cases in each group).(1)Lipopolysaccharide(LPS)group was given intraperitoneal injection of 9 g/ L saline and 3 mg/ kg LPS 1 h later.(2)Bortezomib group was given intraperitoneal injection of Bortezomib(0. 2 mg/ kg)and 3 mg/ kg LPS 1 h later.(3)Anti - RAGE mAb group was given intraperitoneal injection of anti - RAGE mAb(15 mg/ kg)and 3 mg/ kg LPS 1 h later.(4)Control group was given 9 g/ L saline was given at each time point. All the rats were sacrificed and observed 24 h later. Levels of tumor necrosis factor(TNF) - α in the plasma and bronchoalveolar lavage fluid(BALF) were detected by enzyme linked immunosorbent assay. RAGE and NF - κB levels in tissue homogenates were detected by Western blot and mRNA levels were detected by reverse transcription - polymerase chain reaction. The pathological assessment of the lung tissues was performed by HE staining. Results (1)Among 4 groups,there were significantly differences in TNF - α in serum and BALF(F = 150. 70,P ﹤ 0. 001;F = 165. 83,P ﹤ 0. 001). Levels of TNF - α in LPS group were significantly higher than those of two pretreatment groups(all P ﹤ 0. 05).(2)Western blot figures il-lustrated that the concentrations of RAGE mRNA and NF - κB in anti - RAGE mAb group and bortezomib group were lower than those of the LPS group.(3)Reverse transcription - polymerase chain reaction analysis showed that there were significant differences in the expression of RAGE mRNA and NF - κB mRNA among 4 groups(F = 175. 14,P ﹤0. 05;F = 188. 65,P ﹤ 0. 05). Levels of RAGE mRNA and NF - κB mRNA in the LPS group were significantly higher than those of two pretreatment groups(all P ﹤ 0. 05).(4)Lung injury score differences among 4 groups were statistical-ly significant(F = 106. 01,P ﹤ 0. 001). Pathological changes in two pretreatment groups reduced compared to those of the LPS group(all P ﹤ 0. 05). Conclusions RAGE - NF - κB signaling pathway regulates the LPS - induced ALI in neonatal rats. Anti - RAGE mAb and Bortezomib both have a protective effect on LPS - induced ALI.

Objective To investigate the related risk factors in patients with atrial fibrillation in order to prevent and delay the occurrence of atrial fibrillation.Methods Five hundred and fifty-eight inpatients with atrial fibrillation were retrospectively analyzed from June 2005 to June 2008.They were divided into several groups according to the age and the characteristics of the elder patients with atrial fibrillation were analyzed.Results In the 558 cases with atrial fibrillation, there were 298 males (53.4%) and 260 females (46.6%) aged from 21 to 97 years.The average age was (72.8 ±10.1) years.There were 57 cases aged 21-59 years(10.2 %)and 501 cases aged 60-97 years(89.8 %).The total number of inpatients in our hospital was 11 869, and there were 4049 cases aged<60 years, 2527 cases aged 60-69 years, 3971 cases aged 70-79 years, 1244 cases aged 80-89 years and 78 cases aged>90 years.The proportions of the inpatients with atrial fibrillation in the above five age groups of inpatients were 1.4%(57 cases), 4.2%(107 cases), 6.6% (262 cases), 9.5%(118 cases)and 17.9% (14 cases), respectively.In 558 cases with atrial fibrillation, there were 230 cases (41.2%) with paroxysmal atrial fibrillation, 44 cases (7.9%) with persistent atrial fibrillation and 284 cases (50.9%) with permanent atrial fibrillation.The most common underlying disease was hypertension in the 558 cases, followed by coronary heart disease, heart failure, diabetes, rheumatic heart disease and so on.Conclusions The prevalence of atrial fibrillation is increased with aging.Hypertension, coronary heart disease, rheumatic heart disease, heart failure, hyperthyroidism,diabetes, chronic pulmonary disease and renal failure are all the risk factors for atrial fibrillation.

Objective To discuss the relationship of hypertension with ageing and comorbidities in 6426 inpatients. Methods The data of 6426 inpatients with hypertension from May 2005 to May 2009 were analyzed retrospectively. All inpatients were divided into four groups: the young-aged group from 18 to 44 yrs (n= 312, 4. 8%), the middle-aged group from 45 to 59 yrs (n= 1529,23.8%), the elderly group from 60 to 79 yrs (n=3847, 59.9%) and the old old group from 80 to 99 yrs (n=738, 11.5%). The percentages of hypertension patients in the same age group over the same period were calculated and the comorbidities were observed respectively. Results Of 6426 hypertensive cases, there were 3438 males (53.5%) and 2988 females (46.5%), ranging from 18 to 99 yrs with the average age of (66.3± 12. 1) yrs. There were 25 504 inpatients over 18 years old including 11 208 in the youth group, 5389 in the middle-aged group, 7596 in the elderly group and 1311 in the old old group. The proportions of hypertension inpatients to total in-patients in the four age groups were 2.8%, 28. 4%, 50.7% and 56.3% respectively. In the youth and middle-aged groups, numbers of males with hypertension were more than of females, however there was no significant difference in gender in the elderly and the old old groups. Within 6426 inpatients with hypertension, 2069 (32.2 %) had diabetes mellitus, 1508 (23.5%) had hyperlipidemia, 105 (1.6 % )had sleep apnea syndrome, 1061 (16.5%) had coronary artery disease, 904 (14.1%) had heart failure, 2353 (36.6%) had stroke and 678 (10. 6%) had kidney failure. Conclusions The prevalence of hypertension increases with ageing significantly. The correlated risk factors for hypertension include diabetes mellitus, hyperlipidemia and sleep apnea syndrome, being a clustering phenomenon, especially for elder patients. These risk factors also deteriorate the damage on heart,brain, kidney and other target organs, which might ultimately result in serious cardio-cerebral vascular events. Therefore, besides control of blood pressure, we should strengthen the complex treatment on hypertension to prevent and delay the occur of complicating diseases.

AIM: To evaluate the relationship between damages of visual field and retinal nerve fiber layer (RNFL) thickness in primary open angle glaucoma (POAG)with highly myopia. POAG with highly myopia group (21 eyes of 17 cases), POAG with non-highly myopia group (17 eyes of 16 cases), highly myopia without POAG group (25 eyes of 20 cases) and normal control group (19 eyes of 17 cases).automated perimeter and thickness of RNFL was measured by optical coherent tomography(OCT). Main outcome mean deviation (MD), pattern standard deviation (PSD) and mean sensitivity at superior, inferior, nasal and temporal sectors in total deviation probability plots. Thickness of RNFL at superior, inferior, nasal and temporal sector.total deviation probability plots of the early POAG with highly myopia than that of POAG without highly myopia,and the early visual field defects of glaucoma in pattern deviation probability plots of this group. MD of POAG with highly myopia was more than those of others (P＜0.05).The differences of MD, PSD and mean sensitivity between POAG with highly myopia and others were significant(P＜0.05).Mean sensitivities in each sector of POAG without highly myopia were similar to those of highly myopia(P＞0.05). The thickness of RNFL of POAG with highly myopia was thinner than that of others and the thickness of RNFL of normality was thicker than that of others. The relationship between mean sensitivity and the thickness of RNFL in each quadrant was significant(P＜0.05).judgment of the visual field changes in POAG with highly myopia. The relationship between RNFL thickness by OCT and visual field damage may provide clinically relevant information in diagnosis of POAG with highly myopia. Field; optical coherent tomography

In order to investigate the relationship between sex dysplasia and sex-determining region Y (SRY) gene, 8 patients with sexual abnormality were analyzed by cytogenetic and molecular genetic methods. Fluorescence in situ hybridization (FISH) using PY3.4, X alpha satellite, and SRY probes was performed in each case to analyze the sex chromosome translocation and gene translocation. SRY gene was amplified by polymerase chain reaction (PCR) and its mutation was detected by direct sequencing. The results showed that among 8 patients, 5 were positive for SRY and the remaining negative for SRY. In the patients positive for SRY genes, 3 presented testes and the left 2 streak ovaries. In the patients negative for SRY, only one case presented testes, while 2 ovaries. Direct sequencing demonstrated that all SRY genes were normal in the patients positive for SRY genes. FISH technique demonstrated that SRY genes translocated from Ypter to Xpter in 2 46,XX phenotypic males positive for SRY genes. It was concluded that SRY gene is strongly involved in male sex determination, while a sequence of other genes may be taken into account in sexual development.
Genes, sry/*genetics ; Gonadal Dysgenesis, 46,XX/genetics ; Gonadal Dysgenesis, 46,XY/genetics ; Sex Chromosome Disorders/*genetics ; Sex-Determining Region Y Protein/*genetics

PURPOSE: Chloride channel-3 (ClC-3) is a member of the chloride channel family and plays a critical role in a variety of cellular activities. The aim of the present study is to explore the molecular mechanisms underlying the antitumor effect of silencing ClC-3 in breast cancer. METHODS: Human breast cancer cell lines MDA-MB-231 and MCF-7 were used in the experiments. Messenger RNA and protein expression were examined by quantitative real-time polymerase chain reaction and western blot analysis. Cell proliferation was measured by the bromodeoxyuridine method, and the cell cycle was evaluated using fluorescence-activated cell sorting. Protein interaction in cells was analyzed by co-immunoprecipitation. Tumor tissues were stained with hematoxylin-eosin and tumor burden was measured using the Metamorph software. RESULTS: Breast cancer tissues collected from patients showed an increase in ClC-3 expression. Knockdown of ClC-3 inhibited the secretion of insulin-like growth factor (IGF)-1, cell proliferation, and G1/S transition in breast cancer cells. In the mouse xenograft model of human breast carcinoma, tumor growth was significantly slower in animals injected with ClC-3-deficient cells compared with the growth of normal human breast cancer cells. In addition, silencing of ClC-3 attenuated the expression of proliferating cell nuclear antigen, Ki-67, cyclin D1, and cyclin E, as well as the activation of extracellular signal-regulated protein kinases (ERK) 1/2, both in vitro and in vivo. CONCLUSION: Together, our data suggest that upregulation of ClC-3 by IGF-1 contributes to cell proliferation and tumor growth in breast cancer, and ClC-3 deficiency suppresses cell proliferation and tumor growth via the IGF/IGF receptor/ERK pathway.
Animals ; Blotting, Western ; Breast Neoplasms* ; Breast* ; Bromodeoxyuridine ; Cell Cycle ; Cell Line ; Cell Proliferation ; Chloride Channels ; Cyclin D1 ; Cyclin E ; Cyclins ; Flow Cytometry ; Heterografts ; Humans ; Immunoprecipitation ; In Vitro Techniques* ; Insulin-Like Growth Factor I ; Methods ; Mice ; Proliferating Cell Nuclear Antigen ; Protein Kinases ; Real-Time Polymerase Chain Reaction ; RNA, Messenger ; Tumor Burden ; Up-Regulation

OBJECTIVE: To discuss the etiology, diagnosis, treatment, and prevention of pneumomediastinum or pneumothorax during the removal of bronchial foreign bodies in children. METHODS: We analyzed the clinical data of 10 cases of pneumomediastinum or pneumothorax during the removal of bronchial foreign bodies in children. RESULTS: Two patients died and the other 8 were cured. CONCLUSION Pneumomediastinum or pneumothorax is mainly caused by the intrapulmonary hyper-pressure and fracture of pulmonary bubbles. The prognosis of pneumomediastinum or pneumothorax is closely related to such factors as correct and punctual diagnosis and quick removal of the airway obstruction.
Bronchi ; Bronchoscopy ; adverse effects ; Child, Preschool ; Female ; Foreign Bodies ; surgery ; Humans ; Infant ; Male ; Mediastinal Emphysema ; etiology ; Pneumothorax ; etiology

Hematoporphyrin monomethyl ether (HMME) combined with He-Ne laser irradiation is a novel and promising photodynamic therapy (PDT)-induced apoptosis that can be applied in vitro on canine breast cancer cells. However, the exact pathway responsible for HMME-PDT in canine breast cancer cells remains unknown. CHMm cells morphology and apoptosis were analyzed using optical microscope, terminal deoxynucleotidyl transferase dUTP nick end labeling fluorescein staining and DNA ladder assays. Apoptotic pathway was further confirmed by Real-time-polymerase chain reaction and Western blotting assays. Our results showed that HMME-PDT induced significant changes in cell morphology, such as formation of cytoplasmic vacuoles and the gradual rounding of cells coupled with decreased size and detachment. DNA fragmentation and cell death was shown to occur in a time-dependent manner. Furthermore, HMME-PDT increased the activities of caspase-9 and caspase-3, and released cytochrome c from mitochondria into the cytoplasm. HMME-PDT also significantly increased both mRNA and protein levels of Bax and decreased P53 gene expression in a time-dependent manner, while the mRNA and protein expression of Bcl-2 were repressed. These alterations suggest that HMME-PDT induced CHMm cell apoptosis via the mitochondrial apoptosis pathway and had anti-canine breast cancer effects in vitro.
Apoptosis* ; Blotting, Western ; Breast Neoplasms* ; Breast* ; Caspase 3 ; Caspase 9 ; Cell Death ; Cytochromes c ; Cytoplasm ; DNA ; DNA Fragmentation ; DNA Nucleotidylexotransferase ; Ether* ; Fluorescein ; Genes, p53 ; Hematoporphyrins* ; In Vitro Techniques ; Mitochondria ; Photochemotherapy ; RNA, Messenger ; Vacuoles

OBJECTIVETo explore the change of RAGE-NF-κB signaling pathway during the course of hyperoxia-induced lung injury in newborn rats, and the effect of glucocorticoid on this pathway.

METHODSTwenty-four Sprague-Dawley neonatal rats were randomly divided into three groups (n=8 each) : sham control (control group), hyperoxia-induced acute lung injury (model group) and glucocorticoid-treated acute lung injury (glucocorticoid group). Rats were sacrificed at 13 days after birth. RAGE and NF-κB expression levels in lung tissues were detected by reverse transcription polymerase chain reaction, Western blot and immunohistochemistry analysis. The levels of tumor necrosis factor α (TNF-α) and sRAGE in bronchoalveolar lavage fluid (BALF) and serum were measured using ELISA. Lung damage was evaluated by histological examinations.

RESULTSRAGE and NF-κB mRNA and protein expression levels in lung tissues were significantly increased in the model and glucocorticoid groups compared with the control group (P<0.05). Serum RAGE concentrations were significantly increased but RAGE concentrations in BALF were significantly reduced in the model and glucocorticoid groups compared with the control group (P<0.05). RAGE and NF-κB expression at both mRNA and protein levels in lung tissues was significantly lower in the glucocorticoid group than in the model group (P<0.05). RAGE concentrations were significantly lower in serum (P<0.05), but were higher in BALF (P<0.05) in the glucocorticoid group than in the model group.

CONCLUSIONSRAGE-NF-κB pathway plays an important role in hyperoxia-induced lung injury in neonatal rats, and glucocorticoid administration may play a protective role against the lung injury by down-regulating RAGE-NF-κB signaling pathway.

Animals ; Animals, Newborn ; Glucocorticoids ; pharmacology ; Hyperoxia ; complications ; Lung Injury ; prevention & control ; NF-kappa B ; analysis ; genetics ; physiology ; Rats ; Rats, Sprague-Dawley ; Receptor for Advanced Glycation End Products ; Receptors, Immunologic ; analysis ; genetics ; physiology ; Signal Transduction ; drug effects ; Tumor Necrosis Factor-alpha ; analysis

OBJECTIVETo study the histological change of microscrew-bone interface, detect the relative cytokine of gingival crevicular fluid, and explore the impossible mechanism of peri-implantitis.

METHODSFour male Beagles were collected. Randomly select one side of animals jaw as the experimental group to induce the peri-implantitis, and another side as the control group. Four microscrews were implanted on each side. In the 1st, 2nd, 3rd, 4th weeks after implantation, collect peri-implant sulcular fluid (PISF) and detect tumor necrosis factor-alpha (TNF-alpha) levels before sacrificed, and the harvest tissue were observed in histological ways.

RESULTSAccording to the extension of time after implantation, the experimental group showed visible progress of interface destruction: 1st week after implantation showed large numbers inflammatory cells collected at the neck but did not undermine the cortical bone; 2nd week after implantation, cortical bone were observed angular absorption; Bone resorption continued to develop and at the 4th week, bone resorption were enlarged to the second thread of microscrew and the interface was filled with a large number of collagen fibers.

CONCLUSIONThe destruction of interface began at the neck of microscrew, and the further development was along the interface in depth. Both microscrews with peri-implantitis and the healthy controls showed the presence of TNF-alpha. Inflammation accumulation might trigger the up-regulation of TNF-alpha level, and the onset of inflammation would enhance the up-trend.

Animals ; Bone and Bones ; Dental Implants ; Dogs ; Gingival Crevicular Fluid ; Male ; Peri-Implantitis ; Tumor Necrosis Factor-alpha