BACKGROUND:Individuals with different vertical facial types have different chin morphologies. For the individuals with different vertical facial types, what is the most beautiful chin morphology?
OBJECTIVE:To evaluate the effects of vertical facial types and chin morphology on facial profile attractiveness.
METHODS:Three beautiful females were selected, including one with high mandibular angle, one with average angle and one with low angle. Their facial profile photographs were taken. A series of new pictures were generated by the smal scale (2 mm per unit) modification of soft tissue chin in the sagittal direction and vertical direction. Raters consisting of 17 orthodontists and 35 laypersons were selected for aesthetic ratings, in order to evaluate the facial profile attractiveness of the individuals with different vertical facial types.
RESULTS AND CONCLUSION:There was no esthetic difference of vertical change in female with high angle;while slightly protrude chin was perceived to be more beautiful than retruded chin. For the female with average angle, lower chin was more attractive than higher chin;slightly protruded chin was beautiful than excessive protruded chin and retruded chin. For the individual with low angle, higher chin was preferred by raters;slightly protruded chin was more beautiful than excessive protruded chin and retruded chin.The results indicate that the effects of vertical facial types and chin morphology to facial profile attractiveness are different. In clinical orthodontic, vertical facial types should be taking into consideration to change the chin morphology of the patents, in order to obtain better profile attractiveness.

Objective To investigate the correlation of plasma N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP) level with echocardiographic indicators and P wave terminal force of lead V 1 (PtfV1) in the patients with hypertension and paroxysmal atrial fibrillation(PAF) .Methods Fifty‐six outpatients and inpatients with hypertension were divided into the PAF group (n=26) and the sinusrhythm group (n=30) .Thirty age‐matched and gender‐matched healthy volunteers were taken as the control group . The plasma NT‐proBNP level was determined .Left ventricular enddiastolic diameter (LVEDD) ,left atrial diameter(LAD) and left ventricular ejection fraction(LVEF) were examined by echocardiography .the 12‐lead electrocardiogram was routinely performed Pt‐fV1 was calculated .Results The plasma NT‐proBNP level in the PAF group was higher than that in the sinusrhythm group and the control group ,the difference was statistically significant (P<0 .05) .The plasma NT‐proBNP level in the PAF group was de‐creased significantly after successful cardioversion .The plasma NT‐proBNP level in the PAF group was positively correlated with LVEDD(r=0 .543 ,P<0 .05) and LAD (r=0 .606 ,P<0 .01) .The plasma NT‐proBNP level was negatively correlated with LVEF (r= -0 .750 ,P<0 .01) and positively correlated with the PtfV 1 absolute value (r= 0 .513 ,P< 0 .01) .Conclusion The plasma NT‐proBNP level can better reflect the heart structure and function in the patients with atrial fibrillation .Detecting the plasma NT‐proBNP level combined with echocardiographic indicators and PtfV 1 is conducive to comprehensively assess the heart function in the patients with hypertension and PAF .

AIMTo observe the differences of hemodynamics and nitric oxide synthase(NOS) activity of ventricular cardiac muscle in two septic shock models and explore the possible mechanism.

METHODSTwo rat models of septic shock[lipopolysaccharide(LPS)-induced and cecal ligation and puncture (CLP)-induced septic shock] were used. The hemodynamic parameters and nitric oxide synthase activity of ventricular cardiac muscle were measured.

RESULTSThe hemodynamic parameters in CLP-induced model were increased in the early stage and decreased in the late stage while in LPS-induced model the parameters showed the same change of the CLP late stage. Both LPS model and CLP model (late stage) showed significant increase in NOS activity, but there was no difference between the two models. After treatment of the NOS inhibitor N-nitro-L-arginine methyl ester (L-NAME), the parameters of CLP-late stage and LPS model increased significantly. The NOS activity reached the highest level in the CLP-middle stage. The production of nitrite/nitrate decreased significantly in LPS model and CLP model(late stage) after treatment of L-NAME, but the nitrite/nitrate produced by constitutive NOS in LPS model was higher than CLP model(late stage).

CONCLUSIONThe increase of the NOS activity may be the main reason to lead to the depression of the hemodynamic parameters. Inducible NOS may play the leading role in the LPS model while cNOS and iNOS have the same effect in the CLP model.

Animals ; Hemodynamics ; Lipopolysaccharides ; Male ; Myocytes, Cardiac ; metabolism ; Nitric Oxide Synthase ; metabolism ; Rats ; Rats, Sprague-Dawley ; Shock, Septic ; classification ; metabolism

OBJECTIVETo construct mouse enhanced green fluorecence protein (EGFP) -peroxisome proliferator-activated receptor (PPAR)gamma2, and to detect EGFP-PPARgamma2 expression in infected mouse bone marrow mesenchymal stem cells (BMSC).

METHODSCut the fragment of PPARgamma2 from the expression plasmid pcDNA flag PPARgamma2, then cloned the gene fragment into pEGFP-C1 and pEGFP-N1 vector. Subsequently, subclone the fragment EGFP-PPARgamma2 from pEGFP-C1-PPARgamma2 into the shuttle plasmid DC315. HEK293 cells were co-transfected with the constructed recombinant shuttle plasmid DC315-EGFP-PPARgamma2 and large adenovirus helper plasmid pBHGlox deltaE1, 3Cre in mediation of liposome. The obtained replication-defective recombinant adenovirus Ad-EGFP-PPARgamma2 was confirmed. Then it was propagated in HEK293 cells. After the BMSC were transfected for 72 h, adipogenic differentiation was demonstrated.

RESULTSHEK293 cells were transfected with the pEGFP-C1-PPARgamma2 or pEGFP-N1-PPARgamma2 in mediation of liposome. The former green fluorescence protein was better than the latter by fluorescence microscope. The recombinant plasmids were digested and identified. Western blot analysis showed the expression of EGFP-PPARgamma2 in vitro. EGFP-PPARgamma2 protein was detectable in the nucleus of BMSC.

CONCLUSIONThe recombinant adenovirus encoding EGFP-PPARgamma2 fusion protein was successfully constructed, which provided a basis for application of EGFP-PPARgamma2 gene to adenovirus-mediated gene therapy.

Adenoviridae ; Animals ; Bone Marrow Cells ; metabolism ; Genetic Vectors ; Green Fluorescent Proteins ; metabolism ; HEK293 Cells ; Humans ; Mesenchymal Stromal Cells ; metabolism ; Mice ; PPAR gamma ; metabolism ; Recombinant Proteins ; metabolism ; Transfection

OBJECTIVETo study the effect of necrostatin (Nec-1) on apoptosis induced by aluminum (Al), and approach the mechanism.

METHODSNeural cell death model was made by 4 mmol/L Al treated neuroblastoma cells (SH-SY5Y). Cell viabilities were detected at different concentrations of Al and/or Nec-1. Hoechst 33342/PI double staining was used to observe apoptosis and (or) necrosis that were quantified by flow cytometry using Annexin V/PI double staining. Apoptotic pathway was tested by activities of Caspase-3, Caspase-8 and Caspase-9. In addition, the expression of NF-kappa B and Cyt-c was measured by immunocytochemistry.

RESULTSCell viabilities were significantly decreased with the increasing concentrations of Al (P < 0.05), which could be significantly upregulated by 60 micromol/L Nec-1 (P < 0.05) and were correlated with the concentrations of Nec-1 (P < 0.05, P < 0.01). Apoptosis and necrosis were observed under fluorescent microscope and quantified by flow cytometry, which suggested an increasing trend of apoptotic and necrotic rates (P < 0.05, P < 0.01). Whereas, Nec-1 could not only decrease the necrotic rate but also apoptotic rate as well (P < 0.05, P < 0.01). Data of Nec-1 on caspases activities showed that Nec-1 could not affect Caspase-9 activity (P > 0.05) and Cty-c protein expression as well (P > 0.05). However, Nec-1 could reduce Caspase-8 activity significantly (P < 0.05, P < 0.01) and increase NF-kappa B protein expression (P < 0.05, P < 0.01) and finally decrease Caspase-3 activity (P < 0.05).

CONCLUSIONNec-1 could reduce cell apoptosis induced by Al, through Caspase-8 pathway, and up-regulate the expression of NF-kappa B protein.

Aluminum ; toxicity ; Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Caspase 8 ; metabolism ; Caspase 9 ; metabolism ; Cell Death ; drug effects ; Cell Line, Tumor ; Cell Survival ; drug effects ; Cytochromes c ; metabolism ; Humans ; Imidazoles ; pharmacology ; Indoles ; pharmacology ; NF-kappa B ; metabolism ; Neuroblastoma

NMDA-induced excitotoxicity cause severe neuronal damage including apoptosis and necrosis. The present study was aimed to evaluate the proportion of NMDA-induced apoptosis of rat cortical neurons and discover signal transduction mechanism. Caspase inhibitor and lactate dehydrogenase (LDH) assay were used to study the NMDA-induced apoptosis. To explore the involved signal pathways, the primary culture of rat cortical neurons were pretreated by the inhibitors of three MAPK pathways, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK. With 2 h of NMDA treatment, cellular apoptosis was measured by caspase-3 activity, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) and Annexin V staining. The results showed that: (1) Caspase-dependent apoptosis accounted for 22.49% in NMDA-induced neuronal death; (2) Pretreatment with p38 MAPK inhibitor SB203580 (10 μmol/L) significantly decreased NMDA-mediated caspase-3 activity by 30.43% (P < 0.05). However, ERK inhibitor PD98059 (20 μmol/L) or JNK inhibitor SP600125 (20 μmol/L) did not influence caspase-3 activity; (3) Pretreatment with SB203580 significantly reduced the number of NMDA-induced TUNEL-positive cells by 33.10% (P < 0.05). PD98059 (20 μmol/L) or SP600125 (20 μmol/L) did not show obvious effect; (4) Pretreatment with SB203580 (10 μmol/L) significantly reduced the number of NMDA-induced early apoptotic neurons by 55.56% (P < 0.05). Also, SP600125 (20 μmol/L) significantly decreased the amount of late apoptotic/dead cells by 67.59% (P < 0.05). There was no effect of PD98059 (20 μmol/L). These results indicate that: (1) NMDA induces neuronal apoptosis besides necrosis; (2) p38 MAPK, but not JNK and ERK, is involved in NMDA-induced neuronal apoptosis, and inhibition of the apoptotic signaling pathway contributes to neuroprotection; (3) JNK activation might contribute to NMDA-induced neuronal necrosis rather than apoptosis.
Animals ; Anthracenes ; pharmacology ; Apoptosis ; Caspase 3 ; metabolism ; Cells, Cultured ; Extracellular Signal-Regulated MAP Kinases ; antagonists & inhibitors ; Imidazoles ; pharmacology ; JNK Mitogen-Activated Protein Kinases ; antagonists & inhibitors ; MAP Kinase Signaling System ; N-Methylaspartate ; pharmacology ; Neurons ; cytology ; Primary Cell Culture ; Pyridines ; pharmacology ; Rats ; p38 Mitogen-Activated Protein Kinases ; antagonists & inhibitors

OBJECTIVETo determine the effect of tea polyphenol (TP) on the proliferation of human periodontal ligament fibroblasts (HPDLFs).

METHODSHPDLFs were primary cultured from tissue explants, and the cells of the 5th to 8th passages were used after immunohistochemical identification (with SABC method) of keratin and vimentin expressions. The cells were divided into 5 groups and treated with TP at 1, 0.5, 0.25, 0.125, and 0.0625 mg/ml, respectively, with another group without TP treatment as the blank control group. Cell counting and MTT colorimetric assay were performed to assess the cell proliferation, and flow cytometry was employed to determine the DNA content of the HPDLFs.

RESULTSDifferent concentrations of TP all significantly increased the proliferation and DNA synthesis of the HPDLFs (P<0.05), and TP treatment at 0.5 mg/ml for 6 h produced the optimal effect.

CONCLUSIONTP has obviously effect in promoting the proliferation of HPDLFs.

Cell Proliferation ; drug effects ; Cells, Cultured ; DNA ; biosynthesis ; Fibroblasts ; cytology ; drug effects ; metabolism ; Flavonoids ; pharmacology ; Flow Cytometry ; Humans ; Immunohistochemistry ; Keratins ; biosynthesis ; Periodontal Ligament ; cytology ; Phenols ; pharmacology ; Polyphenols ; Tea ; chemistry ; Vimentin ; biosynthesis

OBJECTIVETo investigate the brain oxidative stress injury induced by nano-alumina particles in ICR mice.

METHODSSixty male ICR mice were randomly divided into 6 groups: control group, solvent control group, 100 mg/kg micro-alumina particles group, 3 groups exposed to nano-alumina particles at the doses of 50, 100 and 200 mg/kg. The mice were exposed by nasal drip for 30 days. Then levels of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-PX) in brain tissues of mice were detected.

RESULTSThere was no difference of SOD activity in mouse brain between control group [(17.32 +/- 6.23)U/gHb] and 50 mg/kg nano-alumina particles group [(17.89 +/- 1.82) U/gHb]. The SOD activity [(4.93 +/- 2.30)U/gHb] in 200 mg/kg nano-alumina particles group was significantly lower than that in control group (P < 0.05). The MDA levels in 3 nano-alumina particles groups were (0.76 +/- 0.13), (1.00 +/- 0.30) and (1.16 +/- 0.39)nmol/ml, respectively, which were significantly higher than that [( 0.24 +/- 0.09)nmol/ml] in control group (P < 0.05). The GSH levels in 3 nano-alumina particles groups were (0.72 +/- 0.08), (0.55 +/- 0.19) and (0.61 +/- 0.20)mg/gpro, respectively, which were significantly lower than that [(1.55 +/- 0.34)mg/gpro]] in control group (P < 0.05). The CAT activity in 50 and 100 mg/kg nano-alumina particles groups were (10.40 +/- 3.84) and (10.40 +/- 2.00)U/mgpro, respectively, which were significantly higher than that [(5.79 +/- 0.96) U/mgpro] in control group (P < 0.05). The CAT activity [(3.25 +/- 1.04)U/mgpro] in 200 mg/kg nano-alumina particles group was significantly lower than that in control group (P < 0.05 ).

CONCLUSIONNano-alumina particles can induce the oxidative stress damage in brain tissues of mice.

Aluminum Oxide ; toxicity ; Animals ; Cerebral Cortex ; metabolism ; Glutathione Peroxidase ; metabolism ; Male ; Malondialdehyde ; metabolism ; Mice ; Mice, Inbred ICR ; Nanoparticles ; toxicity ; Oxidative Stress ; Superoxide Dismutase ; metabolism

Silent information regulator 1 (SIRT1), an NAD(+)-dependent deacetylase, is involved in the regulation of gene transcription, energy metabolism and cell aging. Recent studies have showed that SIRT1 possesses neuroprotective effects, however, it is not very clear how SIRT1 exerts the neuroprotection in Alzheimer's disease (AD). In this review, we summarized the neuroprotective role of SIRT1 in AD and its possible molecular mechanisms, proposing a novel strategy for preventing and treating neurodegeneration.
Alzheimer Disease ; genetics ; physiopathology ; Animals ; Energy Metabolism ; physiology ; Humans ; Neuroprotective Agents ; Sirtuin 1 ; physiology ; Transcription, Genetic ; physiology

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Air Microbiology ; Bacteria/isolation & purification* ; Child ; Child, Preschool ; China/epidemiology* ; DNA, Bacterial/analysis* ; DNA, Ribosomal/analysis* ; Female ; Humans ; Infant ; Infant, Newborn ; Male ; Middle Aged ; Pneumonia, Bacterial/microbiology* ; Risk Assessment/methods* ; Young Adult