Objective To investigate the role of ?7nAChR in the pathogenesis of Alzheimer's disease(AD)through exploring the relationship between ?7nAChR and A?_(1-42) in AD brains.Methods The accumulation of ?7nAChR and the possible relationship between ?7nAChR and A?_(1-42) were observed in 3 clinically and pathologically confirmed AD brains by immunohistochemistry. 3 normal brains were set as controls.Results Respective staining of anti-?7nAChR and anti-A?_(1-42) showed that the abnormal accumulation of ?7nAChR existed in AD brains. The main location was at hippocampus and temporal cortex which was just in accordance with senile plaque consisted mainly of A?_(1-42). The major part of ?7nAChR was located extra-cellular and within senile plaque from the view of morphology. No accumulation of ?7nAChR existed in normal brains. Co-staining of anti-?7nAChR and anti-A?_(1-42) further showed that ?7nAChR and A?_(1-42) could accumulate together in senile plaque of AD brain. The average rate of positive co-staining in hippocampus, temporal lobe and frontal lobe is 57.8%, 51.0% and 21.8% respectively. The accumulation of ?7nAChR in hippocampus and temporal lobe seems much than that in the frontal lobe. Conclusion ?7nAChR may combine with A?_(1-42) in AD brains. It is suggested that the combination should destroy the ?7nAChR receptor, block the receptor or mediate the injury of cholinergic neurons with the result of recognition and memory impairment and that ?7nAChR might play an important role in the pathogenesis of Alzheimer's disease.

OBJECTIVEThe development of neonatology and the availability of pulmonary surfactant have been helpful in effective reduction of the mortality of very low birth weight infants at the expense of an increasing number of survivors with bronchopulmonary dysplasia (BPD) caused by lung immaturity. BPD is a common syndrome in newborns, especially in preterm infants, when treated with hyperoxia and mechanical ventilation. Unfortunately, there have been no effective measure for the prevention and treatment of BPD. The purpose of this study was to investigate the influence of recombinant human insulin-like growth factor-1 (rh-IGF-1) on cell apoptosis and Clara cell secretory protein (CCSP) expression during the lung injury induced by hyperoxia, so as to assess its effect on the inflammatory lung injury and its developmental repair.

METHODSEighty full term neonatal Wistar rats under the same condition were divided randomly into four groups on the second day after birth. Group I was air control, group II was exposed to hyperoxia, group III air + rh-IGF-1, and group IV was treated with hyperoxia + rh-IGF-1. The pups in the control group were kept in room air, while pups in hyperoxia group were kept in a Plexiglas chamber and exposed to over 85% oxygen. Pups in group III were under the same raising condition except for exposure to room air and treated with intraperitoneal injection of rh-IGF-1 (1 microg/Kg) everyday from the third day. Pups in group IV were treated with intraperitoneal injection of rh-IGF-1 (1 microg/Kg) everyday from the third day of exposure to hyperoxia. Lung tissue sections of the neonatal rats were stained with hematoxylin and eosin (HE) after 7 d of hyperoxia exposure, expression of CCSP was examined by immunohistochemical method, and apoptotic cell index of lung tissue was calculated by using TUNEL method.

RESULTSIt was observed from immunohistochemical examination that positive staining of CCSP was distributed mainly in distal and respiratory bronchioles. The percentage of Clara cells in distal and respiratory bronchioles epithelium decreased in hyperoxia group (32.17 +/- 3.19)% compared to that in air control group (68.32 +/- 2.04)%, P < 0.01. Statistically significant differences were found in intensity of positiveness of Clara cells between hyperoxia (29.45 +/- 5.56) and air control group (42.37 +/- 3.24), P < 0.01. TUNEL assay showed that most apoptotic cells were alveolar and bronchial epithelial cells. The apoptotic index increased significantly in the hyperoxia group (55.77 +/- 6.09)% compared to the air control group (16.41 +/- 4.01)%, (P < 0.01). The positive rate (52.98 +/- 2.68)% of Clara cells and the expression (41.22 +/- 6.36) of CCSP in hyperoxia + rh-IGF-1 group increased significantly when compared with hyperoxia group, and the differences between these two group were also statistically significant (P < 0.01). The apoptotic index increased significantly in the hyperoxia + rh-IGF-1 group (27.98 +/- 3.09)% compared to the hyperoxia group (P < 0.01).

CONCLUSIONSHyperoxia exposure can promote the pneumocyte apoptosis and inhibit the expression of CCSP. Rh-IGF-1 can remove the block of the formation of lung alveoli, increase the secretion of CCSP, mitigate inflammatory responses in airway and alleviate lung injury via pneumocyte apoptosis. Therefore, the results of this study provide a theoretic and experimental evidence for clinical application of rh-IGF-1 in prevention and treatment of BPD.

Alveolar Epithelial Cells ; metabolism ; Animals ; Apoptosis ; Epithelial Cells ; Humans ; Hyperoxia ; metabolism ; pathology ; Infant, Newborn ; Insulin-Like Growth Factor I ; genetics ; metabolism ; Lung ; Oxygen ; metabolism ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Uteroglobin ; metabolism

This study was aimed to establish a stable animal model of left ventricular hypertrophy (LVH) to provide theoretical and experimental basis for understanding the development of LVH. The abdominal aorta of male Wistar rats (80-100 g) was constricted to a diameter of 0.55 mm between the branches of the celiac and anterior mesenteric arteries. Echocardiography using a linear phased array probe was performed as well as pathological examination and plasma B-type natriuretic peptide (BNP) measurement at 3, 4 and 6 weeks after abdominal aortic constriction (AAC). The results showed that the acute mortality rate (within 24 h) of this modified rat model was 8%. Animals who underwent AAC demonstrated significantly increased interventricular septal (IVS), LV posterior wall (LVPWd), LV mass index (LVMI), cross-sectional area (CSA) of myocytes, and perivascular fibrosis; the ejection fraction (EF), fractional shortening (FS), and cardiac output (CO) were consistently lower at each time point after AAC. Notably, differences in these parameters between AAC group and sham group were significant by 3 weeks and reached peaks at 4th week. Following AAC, the plasma BNP was gradually elevated compared with the sham group at 3rd and 6th week. It was concluded that this modified AAC model can develop LVH, both stably and safely, by week four post-surgery; echocardiography is able to assess changes in chamber dimensions and systolic properties accurately in rats with LVH.

OBJECTIVETo observe the clinical effect of acupuncture for controlling the adverse response in gastroscopy.

METHODSNinety-seven cases of gastroscopy were randomly divided into an observation group of 52 cases and a control group of 45 cases. The observation group were treated by acupuncture at Hegu (LI 4), Neiguan (PC 6) and Zusanli (ST 36), in combined with oral administration of Lidocaine; the control group were treated by simple administration of Lidocaine. Changes of the adverse response, blood pressure and heart rate, and satisfactory degrees and the willing re-examination rate were investigated in the two groups. Results In the observation group, the nausea and vomiting, salivation, restlessness, breath holding and other adverse responses in gastroscopy were significantly decreased as compared with those in the control group (P < 0.01), and the blood pressure and heart rate were more stable than in the control group, and the satisfactory degree and willing re-examination rate were higher than the control group (P < 0.01).

CONCLUSIONAcupuncture can effectively control the adverse response in gastroscopy.

Acupuncture Therapy ; Adult ; Blood Pressure ; Female ; Gastroscopy ; Heart Rate ; Humans ; Male

OBJECTIVETo study the effects of prolonged 75% oxygen exposure on the expression of vascular endothelial growth factor (VEGF) and its receptors (VEGFR1 and VEGFR2) in the neonatal rat lungs and to elucidate the effects of prolonged exposure of high concentration of oxygen on lung vascular development and its relationship with bronchopulmonary dysplasia (BPD).

METHODSForty eight Sprague-Dawley rat pups were randomly exposed to air (control group) and 75% oxygen (experimental group) 12 hrs after birth. The rats were sacrificed 7, 14 and 21 days after exposure and their lungs were sampled. The lung sections were stained with hematoxylin and eosin for histological evaluation. Expression of VEGF, VEGFR1 and VEGFR2 protein and mRNA was detected by immunohistochemistry and RT-PCR.

RESULTSAfter being exposed to 75% oxygen for 21 days, lung tissues had pathological changes as 'new' BPD. Expressions of VEGF protein (10.9 + or - 2.7 vs 30.8 + or - 6.4), VEGFR1 protein (5.4 + or - 1.4 vs 15.6 + or - 3.4) and VEGFR2 protein (11.3 + or - 2.6 vs 21.7 + or - 4.5) on day 21 in the experimental group decreased significantly as compared with the control group (p<0.05). The expression of VEGF mRNA (1.6 vs 3.3), VEGFR1 mRNA (0.4 vs 6.6) and VEGFR2 mRNA (0.5 vs 4.9) on day 21 in the experimental group also decreased significantly as compared with the control group (p<0.05).

CONCLUSIONSProlonged exposure of high concentration of oxygen may cause BPD possibly by inhibiting lung vascular development in neonatal rats.

Animals ; Animals, Newborn ; Bronchopulmonary Dysplasia ; etiology ; Female ; Humans ; Infant, Newborn ; Lung ; blood supply ; Male ; Oxygen ; toxicity ; RNA, Messenger ; analysis ; Rats ; Rats, Sprague-Dawley ; Vascular Endothelial Growth Factor A ; analysis ; genetics ; Vascular Endothelial Growth Factor Receptor-1 ; analysis ; genetics ; Vascular Endothelial Growth Factor Receptor-2 ; analysis ; genetics

Objective:To investigate the expression of Fas、FasL and the apoptosis of liver cancer cell line HepG2 transfected with LIGHT and IFN-? gene mediated by Cationic liposome.Methods:HepG2 cells were divided into two groups(the solo transfection of LIGHT gene and the combined transfection of LIGHT and IFN-? genes) and the control groups(no transfection).HepG2 cells were cellected at 12h,24h and 48h after transfection.The apoptosis of HepG2 cells and the expression of Fas and FasL of the HepG2 cells were investigated with flow cytometry.Results:After transfection,the apoptosis of HepG2 cells increased,and the apoptosis of combined transfection group was higher than the solo transfection of LIGHT(P

OBJECTIVETo explore the association of interleukin 8 (IL-8)-251T/A and 781 C/T single nucleotide polymorphisms (SNPs) with the susceptibility of infants and young children to respiratory syncytial virus (RSV) infection.

METHODThis study included 101 hospitalized patients under 2 years of age who suffered from RSV pneumonia, 108 hospitalized patients under 2 years of age with non-RSV pneumonia and 35 core families with a child hospitalized for RSV pneumonia. Genotypes of 2 SNP loci in all enrolled persons were defined by allele specific polymerase chain reaction (AS-PCR), and confirmed by gene sequencing. The allele's frequencies of SNPs were analyzed with case-control study and transmission disequilibrium test (TDT), linkage of 2 loci and haplotypes composed of the 2 loci were also studied.

RESULTS(1) The frequency of IL-8-251T in cases was dramatically high (OR = 2.08, P = 0.0002, case-control study; LRT = 14.31, P = 0.0008, TDT). (2) IL-8-251T and 781C was linkaged (D' = 0.607 +/- 0.03, r(2) = 0.2861, P = 0.0000). (3) Haplotype of TC was significantly high in cases (P = 0.01).

CONCLUSIONThese findings support that haplotype of TC composed of IL-8-251T and 781C is associated with the susceptibility to RSV, namely, some RSV predisposing genes are located in the gene fragment including TC haplotype or linked tightly with this gene fragment.

Case-Control Studies ; Child, Preschool ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Haplotypes ; Humans ; Infant ; Interleukin-8 ; genetics ; Linkage Disequilibrium ; Male ; Polymorphism, Single Nucleotide ; Respiratory Syncytial Virus Infections ; genetics ; Respiratory Syncytial Viruses ; Sequence Analysis, DNA

OBJECTIVETo study inhibitory efficacy of combined gene therapy for malignant gliomas transfected with antisense human telomerase reverse transcriptase (hTERT)/PTEN in vitro and in vivo.

METHODSTo construct two adenovirus recons which contained antisense hTERT and wild-type PTEN respectively with high performance homologous recombination system in bacteria. The two adenovirus recons were transfected into U251 human malignant glioma cells combinedly or respectively in vitro and in vivo. U251 cell proliferation in vitro was determined by MTT assay and flow cytometry, tumor growth in vivo was measured by the volume of glioma in nude mice. Telomerase activity was detected by telomeric repeat amplification protocol (TRAP) assay. Expression of hTERT and PTEN protein was detected by Western blotting methods.

RESULTSAfter transfection in vitro, the growth of U251 cells was inhibited significantly. The inhibitory effect was time-dependent. The strongest inhibition was observed in combined transfection group, at the 6th day, the survival rate was 37.6%, telomerase activity (only 28.8TPG) was inhibited significantly, hTERT protein expression was inhibited significantly too, which was 0.2106, but PTEN protein expression was increased significantly, which was 0.9630. In vivo, the growth of tumors was also effectively inhibited.

CONCLUSIONGrowth of malignant glioma cells is effectively inhibited after transfection with combined antisense hTERT and PTEN in vitro and in vivo.

Adenoviridae ; genetics ; Animals ; Apoptosis ; Blotting, Western ; Brain Neoplasms ; pathology ; therapy ; Cell Line, Tumor ; Cell Proliferation ; DNA, Antisense ; genetics ; metabolism ; Flow Cytometry ; Genetic Therapy ; methods ; Glioma ; pathology ; therapy ; Green Fluorescent Proteins ; genetics ; metabolism ; Humans ; Mice ; Mice, Nude ; Microscopy, Fluorescence ; PTEN Phosphohydrolase ; genetics ; Recombinant Fusion Proteins ; genetics ; metabolism ; Telomerase ; genetics ; metabolism ; Transfection ; Tumor Burden ; Xenograft Model Antitumor Assays

Objective To unveil the changes of endemic fluorosis in order to provide the scientific basis for making countermeasure. Methods Seven villages was selected as monitoring points in Qianan County of Jilin Province where drinking water was improved or was going tobe improved. Dental fluorosis was surveyed with Dean method and for urine fluoride content was tested using fluoride ion-selective electrode analysis in 8 - 12 years old children. Clinical skeletal fluorosis was detected in all residents of aged 16 and over in the beginning of the monitor and every 3 years. X-ray films were taken in those over 16 years old at the beginning of the monitor and every 5 years. Results Detectable rate of dental fluorosis was decreased compared with before(Weizi: 11.3% to 2.2%, Danzi: 16.3% to 12.1%, Houqi: 53.7% to 37.5%, Houju: 38.6% to 33.3%), and severity was declining, for example, in Dongnanjing, rate of being moderate was dropping from 11.3% to 7.8%, severe rate from 2.8% to 0;in Houqi: moderate rate from 16.7% to 0, severe rate from 1.9% to 0;in Houju, moderate rate from 1.4% to 0,severe rate from 1.4% to 0. However, detectable rate of dental fluorosis rose in Dabin from 61.7% to 70.0% and in Dongbin-donju from 52.7% to 71.1% due to increased fluorides in drinking water. Urine fluorides content in 8 - 12 years old children was decreased to normal level(1.5 mg/L) in most of monitoring spots, but in Dabin it still remained at a high level, being 4.03 and 4.57 mg/L before and after respectively. Detectable rate clinical skeletal fluorosis was between 11.1% - 25.7% among those aged 16 and over in 7 monitoring point in 1991 - 2006, however it increased year after year in Dabin (15.9%, 21.6% and 25.7% in 1991, 1993 and 1995). Positive X-ray rate for skeletal fluorosis was decreased from 54.9% to 24.0% in Dabin, from 40.7% to 23.5% in Dongbin-donju and from 28.6% to 20.4% in Dangnanjing. Conclusions Endemic fluorosis has been controlled attributed to improved drinking water and decreased fluorides content in drinking water. Combined methods are needed to decrease to the intake of fluorides to control the diseases.

Objective To investigate the diagnosis,operation and outcomes of congenital cystic lung lesions in children.Methods Fifty-two children with congenital cystic lung lesions were collected.The clinical data s were analyzed including manifestations,lesion characteristics,imaging,histopathology,diagnosis,surgical treatment methods and short-term pulmonary functions.Results There were 33 male and 19 female,aged from 1 day to 159 months,their median age was 3.67 months.Five cases were neonates.There were 42 cases of bronchogenic cyst,6 cases of pulmonary sequestration,3 cases of congenital lobar emphysema and 1 case of congenital cystic adenomatoid malformation.The cases commonly manifested by lung infections.Of 52 cases,61.5％ were diagnosed after the first onset of lung infection,21.1％ for repeated lung infections and 17.3％ with no symptom.Right lower lung was the most common lesion site and the cases accounted about for 36.5％.Multiple gas cysts were the most common imaging findings accounting about for 42.3％.The pathologic examination of all cases showed bronchogenic cysts.The missed diagnosis rate was 17.3％.The misdiagnosis rate was 24.9％,which of bronchogenic cyst cases was 19.2％.All cases received the lobectomy without death.Conclusions The preoperative diagnosis of congenital cystic lung lesions is mostly based on imaging findings.Clinical manifestations are useful for identifying early the lesions.The preoperative diagnosis may be easily missed or incorrectly done.Pathological findings contribute to make a definite diagnosis.The surgery effect is satisfactory and the outcome is good.