Long-term treatment with an agonist of peroxisome proliferator-activated receptor (PPAR)-γ is associated with bone fractures in the clinical practice. However, the mechanisms underlying the fractures are not fully understood. This study was aimed to examine the effect of rosiglitazone (an agonist of PPAR-γ) of different doses on the proliferation, differentiation, and transforming growth factor beta 1 (TGF-β1)-induced expression of connective tissue growth factor (CTGF) in primary rat osteoblasts in vitro. Osteoblasts were isolated from newly born SD rats and treated with different doses of rosiglitazone (0-20 μmol/L). The proliferation and differentiation of osteoblasts were measured by MTT assay and NPP assay, respectively. The expression of CTGF was determined by RT-PCR and Western blotting. The results showed that most isolated osteoblasts displayed strong alkaline phosphatase (ALP) activity and treatment with different doses of rosiglitazone did not affect their proliferation, but significantly inhibited the differentiation of osteoblasts in a dose-dependent manner. Moreover, treatment with different doses of rosiglitazone significantly reduced the TGF-β1-induced CTGF mRNA transcription and protein expression in a dose-dependent manner in rat osteoblasts. It was concluded that the activation of PPAR-γ may inhibit the differentiation of osteoblasts by reducing the TGF-β1-induced CTGF expression in vitro.

Objectives To report a generalized atrophic benign epidermolysis bullosa family,identify the deficient protein and related pathogenic gene mutation. Methods The diagnosis was confirmed based on clinical manifestations and necessary examinations. Electron microscopy and immunofluorescent staining were used to detect the deficient protein. The pathogenic gene mutation was identified by PCR amplification of ge-nomic DNA with primers targeting the flanking introns, followed by direct automated sequencing. Results In the family, the affected individuals were homozygous for a novel 4-bp deletion in COL17A1, 3897delATCT, which resulted in a downstream premature termination codon. Conclusions 3897delATCT of COL17A1 is the pathogenic gene mutation in the patients and probably results in nonsense-mediated mRNA decay and abrogation of type XⅦ collagen synthesis, as documented in the literature.

Objective To investigate the effect of platelet-derived growth factor-D (PDGF-D) on the prostate cancer cells migration and its possible mechanism. Methods The expressions of PDGF-D in LNCaP and PC-3 cells were detected with western blot.PDGF-D siRNA was synthesized according to mRNA sequence of PDGF-D gene and was transfected into PC-3 cell.The cells were treated with PDGF-D and PDGF-D siRNA,the cell migration was examined by Boyden chamber migration assay.The expression changes of VEGF and MMP-9 mRNA were detected by RT-PCR. Results The results of western blot indicated that the PDGF-D protein expression level was lower in LNCaP cells (29.47 ± 1.68) than that in PC-3 cells (63.43 ±2.10),(P ＜ 0.05).PDGF-D siRNA could down-regulate the PDGF-D protein expression in the transfected group (35.19 ± 1.51).The exogenous PDGF-D could promote migration of LNCaP and PC-3cells,and up-regulate the expression of VEGF,MMP-9 mRNA in PC-3 cells (P ＜ 0.05,compared with control group).PDGF-D siRNA inhibited PC-3 cells' migration and decreased the level of VEGF,MMP-9mRNA expression (0.72 ± 0.09 vs 0.43 ± 0.18,0.65 ±0.07 vs 0.22 ± 0.08) (P ＜ 0.05). Conclusion PDGF-D is involved in the promotion of prostate cancer invasion and angiogenesis.

Objective Blood pressure variability (BPV) is an independent risk factor for the death of patients with maintenance hemodialysis (MHD).There is no study on the influencing factors of BPV at home in HD patients in China.The article aimed to investigate MHD patients'BPV at home and related influencing factors in order to provide theoretical basis for reducing home BPV (HBPV) clinically. Methods We chose 103 patients who were treated with MHD in the Renal Medicine Room of Nephrology Department in three upper first -class hospitals including Jiangsu Provincial People 's Hospital, the First Affiliated Hospital of Suzhou University and the Affiliated Hospi -tal of Jiangsu University from March 2017 to October 2017.We col-lected their 7 days'blood pressure monitoring at home and blood pressure before dialysis, average value and standard deviation in sys -tolic blood pressure monitoring at home, and took the coefficient of variation of systolic blood pressure as the expression of HBPV .The patients were divided into high BPV group (BPV≥5.8％) and low BPV group (BPV<5.8％) according to the average BPV.At the same time, we recorded indexes such as sex , age, dialysis age, primary disease, BMI, inter-dialytic weight gain (IDWG), left ven-tricular mass index(LVMI) and analyzed relative influencing factors by multiple linear regression . Results The age, IDWG and LV-MI were positive independent influencing factors of HBPV (R 2 =0.467,F=10.945,P<0.001).According to standardized regression co-efficient, the contribution of each variable to HBPV was as follows : PIBWG >Age>LVMI. Conclusion In clinical nursing, we should actively control the IDWG of patients , encourage patients to monitor their blood pressure at home , and increase their awareness of the importance of home BPV.Meanwhile, HBPV is an important index for predicting left ventricular hypertrophy and can be used as an objective tool to improve patients 'self-management ability.

Objective To map the specific gene responsible for primary erythromelalgia and identify gene mutations in a Chinese family and one sporadic patient with primary erythromelalgia. Methods Geno-mic DNA was extracted from peripheral lymphocytes of the family members of the pedigree and the sporadic patient. Scanning the genes on chromosome 2q that had been identified was performed by using 6 microsatellite markers for the family members with primary erythromelalgia. Then linkage analysis and haplotype analysis were conducted. All exons of SCN9A gene were analyzed by PCR-DNA sequencing. The mutation identification was also confirmed by restriction fragment length polymorphism(RFLP). Results A maximum 2-point LOD score of 2.11 was found at a recombination fraction (? = 0.00) with markers D2S2370 and D2S2330. Recombination events were detected by markers D2S1353 and D2S2345 in this family by the haplotype analysis. There were two missense heterozygous point mutations in the 15th exon of SCN9A gene both in the family(T2573A) and the sporadic patient(T2543C), leading to the substitution of the amino acid leucine to histidine(L858H) and isoleucine to threonine(I848T), respectively. The above mutations were not found in 400 normal alleles. Conclusion It is proved that primary erythromelalgia is caused by mutations in SCN9A gene.

Long-term treatment with an agonist of peroxisome proliferator-activated receptor (PPAR)-γ is associated with bone fractures in the clinical practice. However, the mechanisms underlying the fractures are not fully understood. This study was aimed to examine the effect of rosiglitazone (an agonist of PPAR-γ) of different doses on the proliferation, differentiation, and transforming growth factor beta 1 (TGF-β1)-induced expression of connective tissue growth factor (CTGF) in primary rat osteoblasts in vitro. Osteoblasts were isolated from newly born SD rats and treated with different doses of rosiglitazone (0-20 μmol/L). The proliferation and differentiation of osteoblasts were measured by MTT assay and NPP assay, respectively. The expression of CTGF was determined by RT-PCR and Western blotting. The results showed that most isolated osteoblasts displayed strong alkaline phosphatase (ALP) activity and treatment with different doses of rosiglitazone did not affect their proliferation, but significantly inhibited the differentiation of osteoblasts in a dose-dependent manner. Moreover, treatment with different doses of rosiglitazone significantly reduced the TGF-β1-induced CTGF mRNA transcription and protein expression in a dose-dependent manner in rat osteoblasts. It was concluded that the activation of PPAR-γ may inhibit the differentiation of osteoblasts by reducing the TGF-β1-induced CTGF expression in vitro.
Animals ; Animals, Newborn ; Blotting, Western ; Cell Differentiation ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; Connective Tissue Growth Factor ; genetics ; metabolism ; Dose-Response Relationship, Drug ; Gene Expression ; drug effects ; Hypoglycemic Agents ; pharmacology ; Osteoblasts ; cytology ; drug effects ; metabolism ; PPAR gamma ; agonists ; metabolism ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; Thiazolidinediones ; pharmacology ; Transforming Growth Factor beta1 ; pharmacology

OBJECTIVETo evaluate the expression of recombinant plasmid pcDNA3.1/GBD of glucan binding protein of Streptococcus mutans in mammalian cells COS-7.

METHODSEukaryotic plasmid carrying encoding gene of GBD of Streptococcus mutans gbpA was constructed and the plasmid was introduced into COS-7 cells by Lipofectamine reagent. The transient expressed protein in COS-7 cells was detected by immunochemistry technique.

RESULTSThe positive expression was detected in plasma of the cells which were transfected with recombinant plasmid pcDNA3.1/GBD. The cells which were transfected with pcDNA3.1 were negative.

CONCLUSIONGBD can translate and express in COS-7 cells after transfected with recombinant plasmid pcDNA3.1/GBD. The expressed protein locates in the plasma and the protein is able to combine with anti-GbpA antibody. The expressed protein has the antigenicity and is a candidate gene vaccine.

Animals ; Antigens, Surface ; biosynthesis ; genetics ; immunology ; Bacterial Proteins ; biosynthesis ; genetics ; immunology ; COS Cells ; Carrier Proteins ; biosynthesis ; genetics ; immunology ; Dental Caries ; prevention & control ; Eukaryotic Cells ; metabolism ; Gene Expression ; Genetic Vectors ; Humans ; Lectins ; Mammals ; Plasmids ; genetics ; immunology ; Recombinant Proteins ; Streptococcus mutans ; genetics ; metabolism ; Transfection ; Vaccines, DNA

Objective To understand the relationship between the concentration of air pollutants and daily emergency department visits for different diseases (circulatory system disease, digestive system disease, nervous system disease and respiratory system disease) in Guangzhou, Guangdong Province. Methods The daily average concentrations of sulfur dioxide (SO2), nitrogen dioxide (NO2, carbon monoxide (CO) and PM2.5 and the daily maximum 8-hour concentrations of O3, the daily average temperature, the relative humidity and cause -specific emergency department visits of the four major diseases from 2015 to 2017 were collected in Guangzhou. Semi-parametric generalized additive model was used to analyze the relationship between the concentration of pollutants and daily cause-specific emergency department visits. Results The daily average concentrations of SO2, NO2, CO, O3 and PM2.5 during the study period were 13.24 μg /m3, 45.96 μg /m3, 0.97 mg /m3, 123.77 μg /m3 and 36.22 μg /m3, respectively. For circulatory system disease，the independently significant associations of SO2 with emergency department visits in single-pollutant models (2.91%, 95% CI: 1.00%-4.85%), and multipollutant models (4.39%, 95% CI: 1.22%-7.67%) were observed. Conclusion The ambient SO2 increases the risk of emergency department visits due to circulatory diseases in Guangzhou. Comprehensive prevention and control measures should be taken to reduce the emission of SO2.

OBJECTIVEThis research reported the experience of early surgical treatment for infants with large atrial septal defects (ASD) or ventricular septal defects (VSD) complicated by pneumonia.

METHODSBetween January 2003 and January 2008, 39 infants with large ASD or VSD complicated by pneumonia were admitted to the Second Xiangya Hospital. Thirty-six patients underwent surgical repair within 7-10 days after pneumonia had been controlled. Mean age was 5.4+/-3.4 months and mean weight was 4.7+/-1.6 kg in the 36 patients. Three patients received conservative treatment due to uncontrolled lung infections.

RESULTSOf the 36 patients, 33 had successful surgery and 3 (8.3%) died of serious low cardiac output (n=1) or respiratory failure due to congenital tracheostenosis (n=2). The 33 survivors showed normal growth and development in a 6 month-5 year follow-up. Of the 3 patients receiving conservative treatment, 1 died of cardiopulmonary failure and 2 were discharged after the symptoms had been improved.

CONCLUSIONSWith increasing medical experience and technique, early surgical operation may be performed with good outcomes in infants with large ASD or VSD complicated by pneumonia.

Adolescent ; Child ; Child, Preschool ; Female ; Heart Septal Defects, Atrial ; complications ; surgery ; Heart Septal Defects, Ventricular ; complications ; surgery ; Humans ; Infant ; Male ; Pneumonia ; etiology ; Postoperative Complications ; etiology

OBJECTIVETo investigate the changes of p38MAPK expression in a rat model of Alzheimer disease (AD).

METHODSSeventy-two adult SD rats were randomized equally into 4 groups, and a single-dose injection of Abeta25-35 (dementia group), normal saline (saline group), SB203580 (inhibitor group), or DMSO (inhibitor control group) was administered into the lateral cerebral ventricle. Y-maze tast was performed to evaluate the behavioral changes of the rats after the injections, and on days 4, 7 and 14 after the injection, p38MAPK expression in the hippocampal CA1 area was measured by means of immunohistochemistry.

RESULTSOn days 7 and 14 following Abeta25-35 injection, the training times, error number and total reaction time were significantly higher in dementia group than in saline group (P<0.05), but all these indices were significantly lowered in the inhibitor group as compared with the dementia group (P<0.05). Immunohistochemistry revealed obvious p38 expression in the dementia group 4 days after Abeta25-35 injection, which increased significantly with the passage of time (P<0.01). The gray scale in the inhibitor group was significantly higher than that in the dementia group (P<0.01).

CONCLUSIONp38MAPK activation in the hippocampal CA1 area is an event that persists during the entire course of Abeta25-35-induced AD in rats, and the inhibitor SB203580 prevents p38MAPK expression and improves the learning and memory abilities of the rats.

Alzheimer Disease ; chemically induced ; enzymology ; metabolism ; Amyloid beta-Peptides ; administration & dosage ; toxicity ; Animals ; Hippocampus ; drug effects ; enzymology ; Immunohistochemistry ; Male ; Maze Learning ; drug effects ; Peptide Fragments ; administration & dosage ; toxicity ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; p38 Mitogen-Activated Protein Kinases ; biosynthesis