Objective To investigate the effect of two different shift orders on night nurses in physical and psychological health. Methods One hundred night shift nurses of two different shift order in two hospitals were investigated by questionnaires. General information and moods, including sleepy, tiredness, irritation and vigor were collected. Results It revealed that the sleepy, tiredness, vigor in Night Shift Followed Middle Shift Group (MS-NS), is better than in Middle Shift Followed Night Shift Group (NS-MS) (P<0. 05). Conclusions The MS-NS order is easy to be accepted by night nurses. The effect of MS-NS order in the physical and psychol ogical functions is comparatively smaller. The MS-NS order is comparatively suitable.

Objective To observe the association between adiponectin and small dense low-density lipoprotein (sLDL-c) in coronary artery disease (CAD) patients.Furthermore,we sought to determine the association between single nucleotide polymorphisms (SNP) rs1501299 ( + 276G/T ), rs266729 (-11365C/G) and the incidence of CAD.Methods Consecutive subjects with chest discomfort were examined by coronary angiography and divided into non-CAD [ n =250,147 male,mean age (60.26 ±7.52) years] and CAD [n =267,153 male,mean age (60.79 ±9.63) years] groups.Blood samples were collected from all participants following an overnight fasting for at least 12 hours.Plasma adiponectin levels were measured by competitive enzyme-linked immunosorbent assay (ELISA).The serum levels of sLDL-C and oxidized low-density lipoprotein (ox-LDL) were determined by ELISA.Genotypes in rs1501299 and rs266729 of the adiponeetin were determined by polymerase chain reaetion ( PCR ).Results 1.The adiponectin levels were significantly lower [ ( 306.17 ± 74.52 ) mg/L vs.( 321.78 ± 86.28 ) mg/L ],whereas sLDL-C and ox-LDL levels were significantly higher [ ( 276.30 ± 45.55 ) ng/L vs.( 249.00 ±32.02) ng/L and (545.06 ± 115.46 ) μg/L vs.(497.74 ± 106.09 ) μg/L,P ＜ 0.05 ] in CAD group than non-CAD group.2.Adiponectin level was negatively associated with sLDL-C,whereas sLDL-C positively correlated with ox-LDL in all subjects.3.Genotype distribution and allele frequencies of rs1501299 and rs266729 were similar between CAD and non-CAD subjects and not related to the serum levels of adiponectin, sLDL-C and ox-LDL.Conclusions Reduced adiponectin and increased sLDL-C were independent risk factors for coronary artery disease.Genetic polymorphisms in rs1501299 and rs266729 were not linked with coronary artery disease.

BACKGROUND: In orthodontics, micro-implant anchorage in the infrazygomatic crest that cannot damage the tooth root can achieve an unobstructed overall movement of the upper dentition. However, little is reported on the stress and strain of the tooth and alveolar bone during the distal movement of the upper dentition. OBJECTIVE: To set up a three-dimensional finite element model to perform a biomechanical analysis of micro-implant anchorage in the infrazygomatic crest for the distal displacement of the upper dentition at different heights. METHODS: Cone-beam CT data from a female patient admitted for orthodontic treatment was saved in Dicom format, and imported into Mimics 16.01 software. Then, a three-dimensional model of the right maxilla and tooth dentition was made by automatically and manually selecting boundaries. The model was imported into Geomagic8.0 for removal of noise dots and smooth processing, and then it was imported into the Mimics16.01 software and meshed for the surface/body through 3 Matics software. Afterwards, three-dimensional models maxillary denture, archwires and traction hooks and implants were established by ProE5.0, and all the models were imported into ANSYS13.0 and assembled and analyzed for stress and strain analysis. RESULTS AND CONCLUSION: We successfully established the three-dimensional finite element model for biomechanical analysis of micro-implant anchorage in the infrazygomatic crest for the distal displacement of the upper dentition at different heights, and this model conformed to the anatomic features. With the increase of the height of traction hooks (1, 4, 7, 10 mm), the vertical stress of the maxillary teeth increased gradually, and had no correlation with the change of the horizontal stress. With the increase of the height of traction hooks, at the sagittal axis, the strain at midpoints of middle incisors, canine teeth, and first molars decreased gradually and the strain at the root of middle incisors and canine teeth also decreased gradually, but there was no change in the strain at the root of first molars. With the increase of the height of traction hooks, at the vertical axis, the strain at the midpoints and tooth root of middle incisors increased, while the strain of canine crown increased gradually and that of the canine root decreased; the strain at the midpoint of first molars changed a little, and the strain of the tooth root decreased gradually. The dentition rotated from clockwise to counterclockwise. To conclude, the three-dimensional finite element model made in the study is consistent with the anatomic structure, which provides a basis for biomechanical analysis of micro-implant anchorage in the infrazygomatic crest for the distal displacement of the upper dentition. The upper dentition impedance center located in the position of 4 to 7 mm of the arch wire can be used as the microimplant support site in the infrazygomatic crest.

OBJECTIVECigarette smoke extract (CSE) can induce injuries of pulmonary II epithelial cells, activate nuclear factor-kappaB and increase tumor necrosis factor-alpha(TNF-alpha) secretion. This study aimed to investigate whether azithromycin can protect pulmonary II epithelial cells from injuries induced by CSE and relevant mechanisms.

METHODSPulmonary II epithelial cells (A549 cells) were cultured in vitro. After 48 hrs of culture the cells were randomly treated with serum-free DMEM only (blank control group), azithromycin + serum-free DMEM, CSE+ serum-free DMEM or CSE+azithromycin. Eight hours later the morphology of A549 cells, the activity of NF-kappaB and the levels of TNF-alpha were measured by inverted microscope, immunohistochemistry and ELISA.

RESULTSThe morphology and structure of A549 cells were changed, NF-kappaB activity increased (dark brown staining ) and TNF-alpha levels (0.307 +/- 0.036 pg/mL vs 0.234 +/- 0.028 pg/mL)increased in the CSE+ serum-free DMEM group compared with the blank control group (P < 0.01). CSE together with azithromycin treatment recovered partly the morphological injuries of A549 cells. It also attenuated NF-kappaB staining and decreased TNF-alpha levels from 0.307 +/- 0.036 pg/mL (CSE+serum-free DMEM group) to 0.269 +/- 0.009 pg/mL (P < 0.05).

CONCLUSIONSAzithromycin may inhibit NF-kappaB activity, decrease TNF-alpha secretion and thus lessen cytotoxicity of CSE to A549 cells.

Anti-Bacterial Agents ; pharmacology ; Azithromycin ; pharmacology ; Cells, Cultured ; Epithelial Cells ; drug effects ; Humans ; Immunohistochemistry ; Lung ; drug effects ; metabolism ; pathology ; NF-kappa B ; analysis ; Smoke ; adverse effects ; Tobacco ; adverse effects ; Tumor Necrosis Factor-alpha ; analysis

OBJECTIVETo evaluate the effect of Zhuanggu Jianxi Decoction (, ZGJXD) on interleukin-1 β (IL-1 β)-induced degeneration of chondrocytes (CDs) as well as the activation of caveolin-p38 mitogen-activated protein kinase (MAPK) signal pathway, investigating the possible molecular mechanism that ZGJXD treats osteoarthritis.

METHODSSerum pharmacology was applied in the present study, where ZGJXD was orally administrated to New Zealand rabbits and then ZGJXD containing serum (ZGJXD-S) was collected for following in vitro experiments. CDs were isolated aseptically from New Zealand rabbits and then cultured in vitro. Upon IL-1 β stimulation, the degeneration of CDs was verified by inverted microscope, toluidine blue stain and type II collagen immunocytochemistry. After IL-1 β-stimulated CDs were intervened with blank control serum, ZGJXD-S, together with or without SB203580 (a specific inhibitor of p38 MAPK) for 48 h, caveolin-1 protein expression and the phosphorylation level of p38 were determined by Western blotting, and the mRNA expression of IL-1 β, tumor necrosis factor α (TNF-α), matrix metalloproteinase 3 (MMP-3) and MMP-13 were examined by real-time polymerase chain reaction.

RESULTSIL-1 β stimulation induced degeneration of CDs, increased caveolin-1 expression and p38 phosphorylation, up-regulated the mRNA level of IL-1 β, TNF-α, MMP-3 and MMP-13. However, the IL-1 β-induced activation of caveolin-p38 signaling and alteration in the expression of p38 downstream target genes were suppressed by ZGJXD-S and/or SB203580 in CDs.

CONCLUSIONZGJXD can prevent CDs degeneration via inhibition of caveolin-p38 MAPK signal pathway, which might be one of the mechanisms that ZGJXD treats osteoarthritis.

Animals ; Base Sequence ; Blotting, Western ; Caveolins ; metabolism ; Chondrocytes ; drug effects ; enzymology ; metabolism ; DNA Primers ; Drugs, Chinese Herbal ; pharmacology ; Gene Expression Profiling ; Interleukin-1beta ; physiology ; MAP Kinase Signaling System ; Male ; RNA, Messenger ; genetics ; Rabbits ; p38 Mitogen-Activated Protein Kinases ; genetics ; metabolism

BACKGROUNDFew studies have given suggestions on appropriate initiation insulin dosage when combined with oral antidiabetic drugs (OADs). This research was to investigate appropriate initiation insulin doses for insulin-naive type 2 diabetes patients with different combinations and the relationship between insulin dosage and relevant factors.

METHODSThis was a randomized, open-label, treat to target study. The target was 20% decrease of both fasting plasma glucose (FPG) and 2 hours post-breakfast blood glucose (P2hBG). One hundred and forty-seven insulin-naive Chinese patients recruited were randomly assigned to 3 groups: group A, patients received insulin monotherapy; group B, received insulin plus metformin (0.5 g, tid) and group C, received insulin plus metformin (0.5 g, tid) and pioglitazone (15 mg, qd). Insulin doses were initiated with a dose of 0.3 U×kg(-1)×d(-1) and titrated according to FPG and P2hBG till reached the targets.

RESULTSBoth the time of getting 20% reduction of FPG and P2hBG showed significant differences among the three groups. The time was shortest in Group C. The insulin doses needed to achieve glucose reduction of 20% in three treatment groups were (0.40 ± 0.04) U×kg(-1)×d(-1) for Group A, (0.37 ± 0.04) U×kg(-1)×d(-1) for Group B, and (0.35 ± 0.03) U×kg(-1)×d(-1) for Group C, respectively. Multiple linear stepwise regression analysis showed that insulin doses correlated with body weight, FPG, diabetes duration, age and history of sulfonylurea treatment. The standardized regression coefficients were 0.871, 0.322, 0.089, 0.067 and 0.063 (with all P < 0.05).

CONCLUSIONSTo achieve blood glucose's reduction of 20% within safety context, initial insulin doses were recommended as the following: 0.40 U×kg(-1)×d(-1) for insulin mono-therapy, 0.37 U×kg(-1)×d(-1) for insulin plus metformin treatment, and 0.35 U×kg(-1)×d(-1) for insulin plus metformin and pioglitazone treatment in Chinese type 2 diabetes outpatients. Body weight is found the most closely related factor to the insulin dosage.

Adult ; Aged ; Blood Glucose ; analysis ; Body Weight ; drug effects ; Diabetes Mellitus, Type 2 ; blood ; drug therapy ; Drug Therapy, Combination ; Female ; Humans ; Hypoglycemic Agents ; administration & dosage ; Insulin ; administration & dosage ; adverse effects ; therapeutic use ; Linear Models ; Male ; Metformin ; administration & dosage ; adverse effects ; Middle Aged ; Outpatients ; Regression Analysis ; Thiazolidinediones ; administration & dosage ; adverse effects

Objective The purpose of the present study was to identify the relationship between the plasma level of adiponectin and in-stent restenosis of patients with coronary heart disease after coronary stenting. Method The study population comprised 119 individuals (92 men ) who underwent stent implantation, including 65 subjects without in-stent restenosis (group A ) and 54 patients with in-stent restenosis (group B). The level of plasma adiponectin was measured using ELISA. Coronary angiography was performed immediately before and after implanting stent and 9-12 months later. Results Baseline characteristics including drug use after PCI were similar between the groups. The rate of implanting bare metal stent is 8(12. 31% ) and 6(11.11% ), TAXUS drug-eluting stent is 11 (16. 92% ) and 10(18.52%) and CYPHER drug-eluting stent is 46 ( 70. 77% ) and 38 ( 70. 37% ) respectively ( all P > 0. 05 ). Plasma level of adiponectin in patient of group A was significantly higher than that in group B [ ( 15. 16±5.02 )mg/L vs. ( 10. 01±4. 93 ) mg/L, P < 0. 05 ]. The quantitative coronary angiography ( QCA ) showed that lesion length was similar between groups [ ( 15.82±: 6. 67 ) mm vs. ( 13.40±4. 20 )mm, P > 0. 05 ], minimum lumen diameter(MLD) and stenosis rate were also similar before and after implanting stent ( P > 0. 05 ) and acute gain was ( 1.48±0. 65 ) mm vs. ( 1.19±0. 37 ) mm ( P > 0. 05 ). MLD was higher in group A than that in group B [(2.55±0.53)mm vs. (0.57±0.60)mm, P<0.01] at 9-12 months follow up. Restenosis rate [(24.2±11.2)% vs. (81.0±19.1)%,P<0.01] and late lumen loss [(0.50±0.34)mm vs.( 1.60± 0. 54)mm, P < 0. 01 ] were lower in group A than in group B. Conclusions The lower plasma adiponectin level might be associated with in-stent restenosis after coronary stenting.

OBJECTIVETo assess the effect of Guifu Dihuang Wan (GFDHW) in the treatment of yang deficiency and explore the underlying molecular mechanism.

METHODSSixty-two participants without diseases were randomized into control group (n=31) and experimental group (n=31) and were given lifestyle intervention additional GFDHW treatment for a month. NMR technology was used for metabonomics analysis.

RESULTSIntervention with GFDHW resulted in significantly decreased conversion scores of yang deficiency in the experimental group compared with the control group (P<0.005). The concentrations of lactate, valine, proline, arginine and 3-hydroxybutyrate were increased in the plasma of yang-deficient subjects after lifestyle intervention. GFDHW treatment with lifestyle intervention significantly increased the concentrations of lactate, valine, proline, arginine and 3-hydroxybutyrate and also the levels of alanine, glutamine, alpha glucose, isoleucine, betaine and propylene glycol.

CONCLUSIONGFDHW treatment improves yang deficiency possibly by increasing the concentrations of alanine, glutamine, alpha glucose, isoleucine, betaine and propylene glycol and promoting energy metabolism of the body.

OBJECTIVETo observe the effect of Yangxueqingnao particles on rat vascular smooth muscle cell (VSMC) proliferation induced by lysophosphatidic acid (LPA).

METHODSThe amount of (3)H-TdR ((3)H-thymidine) admixed in cultured rat VSMC was measured and mitogen-activated protein kinase (MAPK) activity and lipid peroxidation end product malondialdehyde (MDA) content of the VSMC were assayed.

RESULTS1x10(-9), 1x10(-8), 1x10(-7) mol/L LPA in a concentration dependent manner, induced the amount of (3)H-TdR admixed, MAP kinase activity, and MDA content of the cultured rat VSMC to increase. However, 5%, 10%, and 15% Yangxueqingnao serum preincubation resulted in a decrease of 23.0%, 42.0%, and 52.0% (P<0.01) respectively in the amount of (3)H-TdR admixed, a decline in VSMC MAP kinase activity of 13.9% (P<0.05), 29.6% (P<0.01), and 48.9% (P<0.01) respectively, and also, a decrease in MDA content of VSMC of 19.4%, 24.7%, and 43.2% (P<0.01) respectively, in the 1x10(-7) mol/L LPA-treated VSMC.

CONCLUSIONSLPA activates the proliferation and lipid peroxidation of VSMC in a concentration dependent manner. The LPA-induced VSMC proliferation is related to the activity of MAP kinases, enzymes involved in an intracellular signalling pathway. The results of the present study showed that Yangxueqingnao particles can effectively inhibit LPA-induced VSMC proliferation, MAP kinase activation, and reduce lipid peroxidative lesion.

Animals ; Cell Proliferation ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Extracellular Signal-Regulated MAP Kinases ; metabolism ; Lysophospholipids ; pharmacology ; Male ; Malondialdehyde ; metabolism ; Muscle, Smooth, Vascular ; cytology ; drug effects ; metabolism ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo identify the mutation of low density lipoprotein receptor(LDLR) gene in a large Chinese family with familial hypercholesterolemia(F H) and make a discussion on the pathogenesis of FH at the molecular level.

METHODSInvestigations were made on a patient with the clinical phenotype of homozygous FH and his parents for mutations of promoter and all 18 exons of LDLR gene. Screening was carried out using Touch down PCR and a g arose gel electrophoresis, combined with DNA sequence analysis. The results were compared with the normal sequences in GenBank and FH database (www.ucl.uk/fh) t o find the mutation. Then the mutation was identified in other members of the family. In addition, the authors screened the apolipoprotein B(100) (apoB(100)) gene f or known mutations (R3500Q) that cause familial defective apoB(100) (FDB) by PCR-RFLP.

RESULTSA novel homozygous IN III 5' GT --> AT mutation in the splice donor of LDLR intron 3 was detected in the homozygote propositus with FH. The mutation was also identified in four heterozygous carriers in his family. No mutations R3500Q of apoB(100)were observed.

CONCLUSIONA homozygous G --> A splice mutation in LDLR gene was first reported. The change of the splice donor in LDLR intron 3 may cause skipping of exon 3, which is responsible for FH. Perhaps it is a particular pathogenesis for Chinese people.

Adolescent ; Adult ; Alternative Splicing ; genetics ; Base Sequence ; Child ; China ; DNA ; chemistry ; genetics ; DNA Mutational Analysis ; Female ; Homozygote ; Humans ; Hyperlipoproteinemia Type II ; blood ; genetics ; pathology ; Lipids ; blood ; Male ; Middle Aged ; Mutation ; Pedigree ; Point Mutation ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Receptors, LDL ; genetics