Animals ; Cochlea ; pathology ; Gene Deletion ; Hearing Loss ; etiology ; pathology ; KCNQ1 Potassium Channel ; genetics ; Mice

OBJECTIVESTo investigate incidence of perioperative cardiovascular events, to analyze related risk factors for the patients undergoing intraperitoneal surgery.

METHODSThe data of 1079 patients who underwent intraperitoneal surgery (exclude laparoscope surgery) from July 2007 to June 2008 was reviewed and analyzed.

RESULTSFor the patients undergoing intraperitoneal surgery, the incidence of major cardiovascular events was 3.99% (43/1079), all-cause mortality was 1.58% (17/1079). The independent risk factors of major cardiovascular events were age ≥ 60 years, history of coronary heart disease, cardiac insufficiency, arrhythmia, chronic obstructive pulmonary disease, estimated glomerular filtration rate (eGFR) < 60 ml/(min·1.73 m(2)), emergency surgery and duration of surgery > 2.82 h (OR = 2.68 to 5.19, P = 0.001 to 0.031).

CONCLUSIONSThe cardiac risk of intraperitoneal surgery is 3.99%. The risk of cardiac complications should be evaluated in elderly patients and those with ischaemic heart disease, chronic obstructive pulmonary disease, and renal disease, more specifically, when emergent or long duration major surgeries are needed.

Abdomen ; surgery ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Cardiovascular Diseases ; epidemiology ; mortality ; Female ; Humans ; Incidence ; Male ; Middle Aged ; Postoperative Complications ; epidemiology ; mortality ; Risk Factors ; Young Adult

OBJECTIVEWe investigated the in vivo effects of recombinant adenovirus-associated virus type-2 (AAV-2) mediated interleukin-10 (IL-10) gene transfer on the expression of matrix metalloproteinase (MMP)-2, 9, tissue inhibitor of metalloproteinase (TIMP)-1, collagen type I and type III in a rat acute myocardial infarction model.

METHODMale Sprague-Dawley (SD) rats were randomly divided into three groups (each n = 6): sham operation group, MI/AAV2 group, and MI/AAV2-IL-10 group (10(10) vg/ml x 0.1 ml injection at peri-infarct regions immediately post MI). Five days later, the expressions of MMP-2 and MMP-9 were measured by RT-PCR, Western blot and zymography. The expression of TIMP-1 was measured by RT-PCR and Western blot. Collagen type I and type III were assessed by RT-PCR and immunohistochemical stain.

RESULTSThe myocardial expressions of MMP-2, MMP-9 and collagen contents in MI/AAV2 group were significantly increased than those in sham operation group. Myocardial expressions of MMP-2, MMP-9 were significantly decreased and the expression of TIMP-1 significantly increased in the MI/AAV2-IL-10 group than those in MI/AAV2 group. Moreover, the expressions of collagen type I, collagen type III and the ratio of I/III collagen in border zones of infarcted myocardium were decreased by 47.6% (P < 0.01), 23.6% (P < 0.05), and 17.9% (P < 0.05) respectively, while the expression of TIMP-1 increased by 73.1%(P < 0.05) in MI/AAV2-IL-10 group compared to MI/AAV2 group.

CONCLUSIONIn vivo myocardial IL-10 transfer reduced myocardial MMP and collagen expression and increasing the TIMP expression.

Animals ; Extracellular Matrix ; metabolism ; Gene Expression ; Genetic Therapy ; Interleukin-10 ; genetics ; Male ; Matrix Metalloproteinase 2 ; metabolism ; Matrix Metalloproteinase 9 ; metabolism ; Myocardial Infarction ; genetics ; metabolism ; physiopathology ; Myocardium ; metabolism ; Rats ; Rats, Sprague-Dawley ; Tissue Inhibitor of Metalloproteinase-1 ; metabolism ; Transfection ; Ventricular Remodeling

OBJECTIVETo elucidate association between the mutation of nuclear factor of activated T cells 1 (NFATC1) gene in IPT-NFAT region and simple congenital heart disease (CHD) in children.

METHODWe used polymerase chain reaction (PCR) and the sequencing reaction to detect the mutations on the patients and their parents and (or) siblings.

RESULTSPCR amplification of the exon 7 region showed that 2 bands are obtained in 58% of patients with CHD and in 74% of their healthy parents and (or) siblings. Sequencing of the 2 bands revealed that both are amplicons of the exon 7 region, and that the additional band harbors an additional 44 nucleotides segment in the intronic region. The homozygous form of this allele was only present in patients with ventricular septal defect (2/24), atrial septal defect (3/18) and bicuspid aortic valve (1/4) in which G to A transition at nucleotide 17 of the third 44 bps was found. Neither the unrelated non-CHD individuals nor the ones with other CHD showed positive presence for the homozygous form of this allele.

CONCLUSIONSThere is a differential amplification of a tandem repeat region in intron 7 of NFATC1 and homozygous form of this allele in patients with ventricular septal defect, atrial septal defect and bicuspid aortic valve. NFATC1 gene may be an a susceptibility marker for ventricular septal defect, atrial septal defect and bicuspid aortic valve.

Adolescent ; Adult ; Aged ; Base Sequence ; Child ; Child, Preschool ; Female ; Genetic Testing ; Heart Defects, Congenital ; genetics ; Humans ; Infant ; Male ; Middle Aged ; Molecular Sequence Data ; Mutation ; NFATC Transcription Factors ; genetics ; Pedigree ; Young Adult

OBJECTIVETo observe the effects of carboxymethyl chitosan calcium (CCC) on concentration of lead, calcium and zinc, and the liver antioxidative capacity in lead poisoned mice.

METHODSMice were randomly divided into 7 groups, including normal group, calcium carbonate group, lead-model group, and three experimental groups treated with CCC in three different doses, and the CaNa2EDTA positive control group. The lead poisoned mice model was established by giving water contained with lead acetate. CCC was administrated to mice i.g. once a day. Thirty days later, mice were killed and the concentrations of lead, calcium and zinc in blood, liver, brain and femur were determined by atomic absorption spectrophotometer. Maleic dialdehyde (MDA), total antioxidative capacity (T-AOC), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activities in liver were measured by using assay kit.

RESULTSCCC significantly reduced the concentration of lead in blood, brain, liver and femur from about 1.56 microg/g, 13.38 microg/g, 16.15 microg/g, 1011.62 microg/g to about 0.50 microg/g, 5.57microg/g, 5.64 microg/g, 457.86 microg/g, and markedly increased the concentration of calcium in femur in lead poisoned mice. CCC had no significant side-effects on concentration of zinc in lead poisoned mice. The antioxidative profile was favorably changed as manifested by decreasing the level of MDA, increasing the activities of SOD, GSH-Px and T-AOC in livers of the in lead poisoned mice.

CONCLUSIONCCC might significantly advance the excretion of lead, increase the concentration of calcium in femur and the antioxidative capacity in lead-loaded mice.

Animals ; Brain Chemistry ; Calcium ; metabolism ; Chitosan ; analogs & derivatives ; pharmacology ; Female ; Femur ; chemistry ; Lead ; metabolism ; Lead Poisoning ; metabolism ; Liver ; chemistry ; Mice ; Mice, Inbred Strains ; Zinc ; metabolism

OBJECTIVETo evaluate the efficacy of computer-aided design and computer-aided manufacturing (CAD/CAM) technique in reconstruction of zygomatic complex defect.

METHODSThree-dimensional computed tomography (3D-CT) and rapid prototyping (RP) techniques were applied to produce facsimile models in 13 patients with zygomatic complex defects resulted from trauma or tumor ablation. The zygomatic complex defect was reconstructed using a mirroring technique by CAD/CAM. Titanium mesh was prefabricated on individual facsimile models and combined with autologous bone graft and pedicled buccal fat pad flap for reconstruction.

RESULTSThe measuring data of zygomatic complex defect between facsimile model and intraoperative findings was extremely consistent. The prefabrication of reconstructive titanium mesh was matched with zygomatic complex defect in the surgery. The postoperative 3D-CT image demonstrated the symmetry of reconstructed zygomatic complex. The functional recovery and facial contours were satisfactory in all cases.

CONCLUSIONThe application of CAD/CAM technique can simulate the surgery procedures accurately, which contributes to shorten the actual operative time. RP techniques can reconstruct the facial contours symmetry and recover the function of zygomatic complex defect.

Adolescent ; Adult ; Bone Substitutes ; Bone Transplantation ; Computer-Aided Design ; Female ; Humans ; Imaging, Three-Dimensional ; Male ; Prosthesis Design ; Reconstructive Surgical Procedures ; methods ; Surgical Flaps ; Titanium ; Tomography, X-Ray Computed ; Young Adult ; Zygoma ; surgery

OBJECTIVETo investigate the effect of chitosan on the capsule inside the expanded flap.

METHODSThe expanders were implanted in animals with the treatment of chitosan(experimental group, n = 15) or without (control group, n = 15). After taking out the expanders, the flap contraction rate was calculated. The samples were observed through HE, Masson dyeing and CD34 immunohistochemical study. The thickness of capsule inside the expanded flap was measured under microscope. The samples were also studied under electron microscope.

RESULTSThe thickness of capsule was 516.000 +/- 128.491 microm in the experimental group, and 833.000 +/- 227.379 microm in the control group (P < 0.05). The number of microvessels was 8.200 +/- 2.150 per visual in experimental group, and 7.900 +/- 1.729 per visual in control group (P > 0.05). Under the electron microscope, the rough endoplasmic reticulum (RER) in the capsule in experimental group decreased and enlarged with degranulation. The mitochondria emerged or disappeared. The number of ribosome was reduced. In the control group, the RER enlarged without degranulation, the mitochondria was intact. The number of ribosome was not reduced.

CONCLUSIONSThe chitosan can effectively reduce the contraction of expanded flap through collagen secretion of fibroblast, delaying the differentiation from fibroblast to fiber cell, inhibiting thansform from fibroblast to myofibroblast. It has no effect on the microvascular generation and expansion, so the flap blood supply will not be affected with thicker capsule.

Animals ; Chitosan ; administration & dosage ; pharmacology ; Female ; Graft Survival ; Male ; Rabbits ; Skin Transplantation ; methods ; Surgical Flaps ; Tissue Expansion

Objective:To observe the effect of warm joint needling plus rehabilitation techniques on the balance function and quality of life (QOL) of patients with spastic hemiplegia after ischemic cerebral stroke.Methods:Ninety patients with spastic hemiplegia after ischemic cerebral stroke were randomized into a rehabilitation group,a warm joint needling group and an observation group,with 30 cases in each group.The rehabilitation group was intervened by Bobath therapy,the warm joint needling group was treated with joint needling on the affected side plus warm needling,and the observation group was given the same rehabilitation treatment as the rehabilitation group together with the same warm joint needling as the warm joint needling group.The three groups were treated once another day,1 month as a treatment course for 6 months.Before the treatment,and respectively after 2-week,1-month,3-month,and 6-month treatment,the modified Ashworth scale (MAS) was used to measure the anti-spasm ability of the lower limb,the Berg balance scale (BBS) was adopted to evaluate the balance function,and the stroke-specific quality of life scale (SS-QOL)was employed to estimate the QOL.Results:After 3-month and 6-month treatment,the lower-limb MAS scores in the observation group were significantly better than those in the rehabilitation group and the warm joint needling group (all P＜0.05).After 1-month,3-month and 6-month treatment,the BBS scores in the observation group were significantly better than those in the rehabilitation group and the warm joint needling group (all P＜0.05).After 2-week,1-month,3-month and 6-month treatment,the SS-QOL scores in the observation group were markedly better than those in the rehabilitation group and the warm joint needling group (all P＜0.05).Conclusion:Warm joint needling plus rehabilitation can effectively improve the lower-limb spasticity state,balance function and QOL in patients with spastic hemiplegia after ischemic cerebral stroke.

OBJECTIVETo analyze the effect of hyperoxia on the proliferation and surfactant associated protein messenger RNA levels of type II alveolar epithelial cells (AECIIs) of premature rat, and to investigate the effect of amygdalin on the change resulted from hyperoxia in AECIIs isolated from premature rat lung in vitro.

METHODSThe lung tissue of 20-day fetal rat was digested by trypsin and collagenase. AECIIs and lung fibroblasts (LFs) were isolated and purified at different centrifugal force and different adherence, then cultured. The nature of the cultures was identified by cytokeratin staining, vimentin staining and transmission electron micrography. For establishing hyperoxia-exposed cell model, purified AECIIs were cultured for 24 hours after culture flasks were filled with 95% oxygen-5% CO2 at 3 L/min for 10 min, and then sealed. Oxygen concentrations were tested in CYS-1 digital oxygen monitor after 24 hours of exposure. A sample was discarded if its oxygen concentration was < 90%. Cell proliferating vitality was examined by MTT assay after treatment with amygdalin at various concentrations. DNA content, protein expression of proliferating cell nuclear antigen (PCNA) and mRNA levels of SPs of AECIIs were analyzed with flow cytometric assay, Western blot and reverse transcription polymerase chain reaction (RT-PCR) respectively after 24 hours of air or hyperoxia exposure in the presence or absence of 200 micromol/L amygdalin.

RESULTSExcellent yields of highly purified, culturable AECIIs could be obtained from 20-day fetal lungs. The expression of cytokeratin in AECIIs was positive and that of vimentin negative by immunocytochemistry. Those, however, in LFs were just opposite. Lamellar bodies in purified AECIIs were revealed by transmission electron micrography. The established hyperoxia-exposed cell model assured the oxygen concentrations of culture flasks more than 90%. Amygdalin at the concentration range from 50 micromol/L to 200 micromol/L stimulated the proliferation of AECIIs in a dose-dependent manner; however, at the concentration of 400 micromol/L inhibited the proliferation of AECII. Flow cytometric analysis showed that the apoptosis rate and G0/G1 phase percentage increased significantly (P < 0.01), S phase and G2/M phase percentage decreased significantly (P < 0.01), in hyperoxia group compared with that of air group. The apoptosis rate of air plus 200 micromol/L amygdalin group, compared with air group, was not significantly different (P > 0.05); however, G0/G1 phase percentage decreased markedly, S phase percentage increased significantly, G2/M phase percentage did not significantly change (P > 0.05). The apoptosis rate of hyperoxia plus 200 micromol/L amygdalin group was not significantly different (P > 0.05) from that of hyperoxia group, S phase and G2/M phase percentage increased significantly (P < 0.01), G0/G1 phase percentage decreased significantly (P < 0.01). Western blot analysis showed that the protein expression levels of PCNA in all group was significantly different, in turn, hyperoxia group < hyperoxia plus 200 micromol/L amygdalin < air group < air puls 200 micromol/L amygdalin (P < 0.01). SPs mRNA levels were significantly decreased in hyperoxia group, as compared with air group (P < 0.01). After amygdalin was added, SPs mRNA levels were elevated in air plus amygdalin group and hyperoxia plus amygdalin group, as compared with hyperoxia group (P < 0.01, P < 0.05, respectively), but compared with air group, SP mRNA levels were not significantly elevated (P > 0.05).

CONCLUSIONAECIIs of premature rats were isolated, purified and cultured successfully. Hyperoxia-exposed cell model was established in AECIIs of premature rat in this experiment. Amygdalin promotes the proliferation of premature rat AECII exposed to air or hyperoxia, the concentration of amygdalin with the best effect was 200 micromol/L. Hyperoxia inhibited the proliferation and decreased SPs mRNAs levels in AECIIs in vitro, which may contribute to hyperoxia-induced lung injury in premature rats. Amygdalin could inhibit the changes of SPs mRNAs levels and cell proliferation of AECIIs resulted from hyperoxia and may play partial protective role in hyperoxia-induced premature lung injury.

Amygdalin ; pharmacology ; Animals ; Animals, Newborn ; Cell Proliferation ; drug effects ; Cytoprotection ; Epithelial Cells ; drug effects ; metabolism ; pathology ; Hyperoxia ; metabolism ; pathology ; Proliferating Cell Nuclear Antigen ; analysis ; Pulmonary Alveoli ; drug effects ; metabolism ; pathology ; Pulmonary Surfactants ; analysis ; RNA, Messenger ; analysis ; Rats

OBJECTIVETo further investigate the protective effect of retinoic acid (RA) on hyperoxia induced lung injury and the role of RA as a modulator on mitogen-activated protein kinases (MAPKs).

METHODSEstablishment of hyperoxia (85%) induced lung injury model of premature Sprague-Dawley (SD) rats: 21 d gestational age SD rat's fetuses (term = 22 d) were delivered by hysterectomy. Within 12 - 24 h after birth, the premature rat pups were randomly divided into 4 groups: Group I, air-exposed control group; Group II, hyperoxia-exposed group; Group III, air plus RA-exposed group, Group IV, hyperoxia plus RA-exposed group. Group I and III were remained in room air, and group II and IV were placed in 85% oxygen. The pups in Group III and IV were injected with RA (500 microg/kg, every day) intraperitoneally. The entire lung tissues of premature rat pups were collected at 4 d, 7 d and 14 d. The mRNA levels of MMP-2 and MMP-9 were detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). MMP-2 and MMP-9 activities were measured by zymography. Western blot was used to detect phosphorylated and total nonphosphorylated form of ERKs, JNKs and p38.

RESULTSExposure to oxygen for 4 d, 7 d, and 14 d resulted in increased mRNA levels of MMP-2 and MMP-9 compared with air-exposed control group (P < 0.01 for all). The mean protein levels of active MMP-2 and pro/active MMP-9 after exposure to O2 were higher than air control groups on each experimental day (P < 0.01 or < 0.05). The phosphorylated ERK1/2, JNK1/2 and p38 proteins in hyperoxia-exposed group increased markedly compared with air-exposed control group (P < 0.01 for all). The pups treated with RA in the hyperoxic environment expressed significantly lower mRNA levels of MMP-2 and MMP-9 than the hyperoxic control pups on each experimental day (P < 0.05 for all). The levels of active MMP-2 and pro/active MMP-9 decreased to a different degree after RA treatment in hyperoxia exposure rat pups. In addition, RA treatment led to a decrease of p-JNK1/2 and p-38 (P < 0.01 for all) protein levels and a further elevation of p-ERK1/2 compared with hyperoxia-exposed group.

CONCLUSIONHyperoxia exposure elevated the expression of MMP-2 and MMP-9 markedly, which played a role in oxygen-induced lung injury. RA could have a protective effect on hyperoxia induced lung injury by decreasing active levels of JNK and p38, which subsequently reduce the expression and activation of MMP-2 and MMP-9.

Animals ; Animals, Newborn ; Disease Models, Animal ; Female ; Hyperoxia ; complications ; Lung ; drug effects ; metabolism ; Lung Injury ; etiology ; metabolism ; Male ; Matrix Metalloproteinase 2 ; metabolism ; Matrix Metalloproteinase 9 ; metabolism ; Mitogen-Activated Protein Kinases ; metabolism ; Rats ; Rats, Sprague-Dawley ; Tretinoin ; pharmacology