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Cumulative lipid profile burden is designed to dynamically measure lipid accumulation, and its effect on hypertension has been poorly studied. Our main purpose was to investigate the effect of cumulative lipid profile burden on the incidence of essential hypertension (EH) and. Secondly, to investigate whether there is a mediating role of cumulative lipid burden in the pathogenesis of the effects of diet and obesity on EH. A total of 1 295 participants were included in the study, which began in 2017. The average follow-up time was 2.98 years. A total of 240 EH patients occurred during the follow-up period. Compared with respective reference groups, the HR (95% CI) of the highest quartile in cumulative TC, TG and HDL burden were 1.747 (1.145 - 2.664), 1.502 (1.038 - 2.173), 0.615 (0.413 - 0.917) for incidence of EH. Participants with EH consumed more red meat and refined grains, and red meat was positively associated with cumulative TC burden . BMI and Waist-To-Height Ratio (WHtR) increased the incidence of EH, and obesity was positively correlated with cumulative TC burden. cumulative TC burden play a partially mediating role in the influence of obesity on EH (βindirect=0.0085, 95%CI: 0.0035, 0.1520). The cumulation TG, TC burden increased the risk of EH, while the cumulation HDL reduced the risk of EH. cumulative TG burden play a partially mediating role in the influence of obesity on EH. Diet was not found to influence hypertension through cumulative lipid profile burden.

To study the effects of aerobic exercise combined withFifty-five male Wistar rats were subjected to adaptive feeding for 4 days and weight-free swimming training for 3 days, 20 min/d. After eliminating 5 rats that were not suitable for swimming training, the others were randomly divided into 5 groups according to their weight: regular diet + quiet control group (RDC), high fat diet + quiet control group (HDC), high-fat diet +Compared with group RDC, Lee's index, serum free fatty acids (FFA), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C), myocardial FFA and intercellular adhesion molecule-1 (ICAM-1) increased significantly (Aerobic exercise and/or目的: 研究有氧运动联合黑果枸杞对高脂膳食大鼠心肌脂代谢某些指标的影响。方法: 55只雄性Wistar大鼠经过适应性饲养4 d后进行20 min/d的无负重游泳训练,连续3 d,筛选淘汰5只不适应游泳训练的大鼠后,按体重以数字随机分组法分为5组:普通膳食+安静组(RDC组)、高脂膳食+安静组(HDC组)、高脂膳食+黑果枸杞+安静组(HDLC组)、高脂膳食+有氧运动组(HDM组)、高脂膳食+黑果枸杞+有氧运动组(HDLM),每组10只。HDM组和HDLM组进行6周每周6次60 min/d的无负重游泳训练。RDC组大鼠以普通饲料常规喂养;其余各组以高脂饲料喂养;HDLC组和HDLM组大鼠灌胃黑果枸杞,灌胃剂量为4.48 g/(kg·d),灌胃体积为5 ml/kg,其余各组灌胃等量蒸馏水。6周后,测定大鼠Lee’s指数,取血、心肌检测相关生化指标。结果: 与RDC组比较,HDC组Lee’s指数,血清FFA、TNF-α、IL-6、TC、TG、LDL-C,心肌FFA、ICAM-1显著升高(

Considering the influence of the cutter head plane on manufacturing of spiral bevel gear, the method of 3D model for spiral bevel gear is built based on Program Pro/E. The relationship between the geometric parameters (such as addendum circle, dedendum circle and base circle) and the basic parameters (such as modulus and the number of teeth) of spiral bevel gear is established by using the inner program. The parametric solid model of spiral bevel gear can be obtained automatically by rotation, sweep, blend, and pattern after inputting the basic parameters. This method is significant to improve the accuracy of design and manufacturing of spiral bevel gear.

The molecular regulation of palatogenesis continues to be an active area of investigation to provide a foundation for understanding the molecular etiology of cleft palate. Transforming growth factor (TGF) -β type III receptor (TβR-III) has been shown to be specifically expressed in the medial edge epithelium at critical stages of palatal shelf adherence during palatogenesis. The aim of this study was to examine TβR-III mRNA localization and expression levels in vivo and to determine the requirement for TβR-III expression during palatal fusion in vitro. TβR-III gene expression was analyzed by in situ hybridization in tissue specimens and real-time reverse transcriptase-polymerase chain reaction using specific cells in the palatal shelf isolated by laser capture microdissection. TβR-III was knocked down in embryonic day (E) 13 palatal shelves in organ culture. Palatal shelf organ cultures were treated with small interfering RNA (siRNA) at final concentrations of 300, 400, and 500 nM, respectively. The treatment with siRNA specific for TβR-III decreased the amount of protein by approximately 75%. The reduction in TβR-III resulted in a delay in the process of palatal fusion compared with control. The protein expression of phospho-Smad2 was decreased in the TβR-III siRNA group. In addition, palatal organ cultures treated with TβR-III siRNA + rhTGF-β3 completely fused by 72 hr in vitro. These results support our hypothesis that TβR-III has a critical role in the process of palatal fusion. Developmental Dynamics 236:791–801, 2007. © 2007 Wiley-Liss, Inc.

Transforming growth factor (TGF)-beta 3 is known to regulate the disappearance of murine medial edge epithelium (MEE) during palatal fusion. Our previous studies showed that SMAD2, a TGF-beta signaling mediator, was expressed and phosphorylated primarily in the MEE and that SMAD2 phosphorylation in the MEE was temporospatially regulated by TGF-beta 3. The goal of this study was to examine the requirement for SMAD2 to complete the developmental events necessary for palatal fusion. SMAD2 expression was inhibited with Smad2 siRNA transfection into palatal tissues in vitro. The results showed that Smad2 siRNA transfection resulted in the maintenance of MEE cells in the palatal midline. Western blot and immunofluorescence analyses confirmed that the endogenous SMAD2 and phospho-SMAD2 levels were reduced following siRNA transfection. The SMAD3 level was not altered by the Smad2 siRNA transfection. The persistence of the MEE and the decreased SMAD2/phospho-SMAD2 levels were coincident with increased MEE cell proliferation. Addition of exogenous TGF-beta 3 increased p-SMAD2 level but not the total SMAD2 level. Therefore, exogenous TGF-beta 3 was not able to induce p-SMAD2 enough to rescue the palatal phenotype in the Smad2 siRNA group. The results indicated that the endogenous SMAD2 level is crucial in the regulation of disappearance of MEE during palatal fusion.

During mammalian palatal fusion, the medial edge epithelial (MEE) cells must stop DNA synthesis prior to the initial contact of opposing palatal shelves and thereafter selectively disappear from the midline. Exogenous EGF has been shown to inhibit the cessation of DNA synthesis and induce cleft palate; however, the precise intracellular mechanism has not been determined. We hypothesized that EGF signaling acting via ERK1/2 would maintain MEE DNA synthesis and cell proliferation and consequently inhibit the process of palatal fusion. Palatal shelves from E13 mouse embryos were maintained in organ cultures and stimulated with EGF. EGF-treated palates failed to fuse with intact MEE and had significant ERK1/2 phosphorylation. Both EGF-induced ERK1/2 phosphorylation and BrdU-incorporation were localized in the nucleus of MEE cells. Subsequent inhibition assays using U0126, a specific inhibitor of ERK1/2 phosphorylation, were conducted. U0126 inhibited EGF-induced ERK1/2 phosphorylation in a dose-dependent manner and consequently MEE cells stopped proliferation. The threshold of ERK1/2 inactivation to stop MEE DNA synthesis coincides with the level required to rescue the EGF-induced cleft palate phenotype. These results indicate that EGF-induced inhibition of palatal fusion is dependent on nuclear ERK1/2 activation and that this mechanism must be tightly regulated during normal palatal fusion.

Studies on transforming growth factor β3 (TGF-β3) deficient mice have shown that TGF-β3 plays a critical role in palatogenesis. These null mutant mice have clefting of the secondary palate, caused by a defect in the process of fusion of the palatal shelves. A critical step in mammalian palatal fusion is removal of the medial edge epithelial cells from the midline seam and formation of continuous mesenchyme. To determine in more detail the role of TGF-β3 in palatogenesis, we cultured TGF-β3 null mutant and wild-type control palatal shelves in an organ culture system. The fate of the medial edge epithelial cells was studied in vitro using vital cell labeling and immunohistochemical techniques. Despite clear adherence, the null mutant palatal shelves did not fuse in vitro, but instead the medial edge epithelial cells survived at the midline position, and the basement membrane was resistant towards degradation. Supplementation of the culture medium with the mature form of TGF-β3 was able to fully correct the defective fusion in the null mutant specimens. Our results demonstrate that the reason for the defective palatal fusion in TGF-β3 (−/−) samples is not impaired adhesion. Our data define a specific role for TGF-β3 in the events that control transdifferentiation of the medial edge epithelial cells including degradation of the underlying basement membrane. Dev. Dyn. 209:255–260, 1997. © 1997 Wiley-Liss, Inc.

A generic, rapid and simple analytical method able to identify 255 veterinary drug residues and other contaminants in raw milk had been developed. The method was based on two-step simple precipitation and ultra performance liquid chromatography coupled with electrospray ionization and tandem mass spectrometry (UPLC-ESI-MS/MS) operating both in positive and negative multiple reaction mode (MRM). For most of the target analytes, the optimized pretreatment processes led to no significant interference on analysis from complicated sample matrix. For quantification, matrix-fortified calibration curves were performed to compensate for the matrix effect and loss in sample preparation. Competent linearity was found for over 90% of target compounds with linear regression coefficients (R) higher than 0.99. Detection limits ranged from 0.05 to 10μg/kg. Average recoveries spiked into raw milk were in the range from 63% to 141% with associated RSD values from 1% to 29% under the selected conditions. The method had been validated for its extraction sensitivity, linearity, recoveries and precision. The results clearly demonstrated the feasibility of the approach proposed. Application of this method, which improved efficiency and coverage of residues, would imply a drastic reduction of both effort and time in routine monitoring programs.

To observe the effect of electroacupuncture (EA) on the related hormones of the hypothalamus-pituitary-adrenal (HPA) axis in rats with cerebral ischemia-reperfusion injury (CI-RI).Ninety Wistar rats were randomly divided into normal control, sham-operation (sham), model, EA acupoint and EA non-acupoint groups. CI-RI model was established by using modified middle cerebral artery occlusion (MCAO) and reperfusion. These rats were further divided into 1 day (d), 3 d and 7 d subgroups, with 6 cases in each. EA (1 mA, 2 Hz/30 Hz) was applied to acupoint "Zusanli" (ST 36) and "Quchi" (LI 11), and non-acupoints (5 mm lateral to ST 36 and 5 mm apart from LI 11 on the radial side respectively) for 30 min, once daily for 1 d, 3 d and 7 d separately. Serum cortisole (CORT) content was assayed by enzyme linked immunosorbent assay (ELISA), and the expression of hypothalamic adrenocorticotropic releasing factor (CRF) mRNA and glucocorticoid receptor (GR) mRNA, and pituitary adrenocorticotrophic hormone (ACTH) mRNA was assayed by reverse transcription polymerase chain reaction (RT-PCR) method.Compared with normal and sham groups, serum CORT levels of model and EA non-acupoint groups on the 1st, 3rd and 7th day increased significantly (P0.05), while compared with model groups, serum CORT level of EA acupoint groups decreased apparently (P0.05). Compared with normal and sham groups, hypothalamic CRF mRNA and pituitary ACTH mRNA expression of model groups were upregulated significantly on the 1st, 3rd and 7th d after CI-RI (P0.01, P0.05), and hypothalamic GR mRNA expression of model groups were obviously downregulated (P0.01, P0.05). In comparison with model groups, hypothalamic CRF mRNA and pituitary ACTH mRNA expression of EA acupoint groups at the 3 time-points, and their expression of EA non-acupoint groups on the 1st and 3rd day were remarkably downregulated (P0.01, P0.05), and hypothalamic GR mRNA expression of EA acupoint groups was upregulated significantly at the 3 time-points (P0.01, P0.05). Comparison between EA acupoint and EA non-acupoint groups showed that the effect of EA acupoint groups was obviously superior to that of EA non-acupoint groups in downregulating CRF mRNA and ACTH mRNA expression and in upregulating GR mRNA expression at the 3 time-points (P0.01, P0.05).EA of meridian-acupoints can effectively downregulate serum CORT content, hypothalamic CRF mRNA and pituitary ACTH mRNA expression and upregulate hypothalamic GR mRNA expression in CI-RI rats, which may contribute to its effect in relieving CI-RI.

An improved sensitive method was developed and validated for the determination of histamine in food samples by using automated on-line pre-column derivatization coupled with high performance liquid chromatography and fluorescence detection (HPLC-FLD). o-Phthaldialdehyde (OPA) was adopted as derivatization reagent, and a "sandwich" (OPA+histamine+OPA) aspiration mode for the automated on-line pre-column derivatization was found to efficiently enhance the method sensitivity and precision. Histamine in food samples was efficiently extracted with a methanol-phosphate buffer solution (50:50, v/v) at 60 degrees C for 30 min, and purified with Waters Oasis MCX solid-phase extraction (SPE) cartridge. The limit of quantification for this method is 0.2 mg/kg, which is very sensitive for histamine determination. With the "sandwich" injection program, 3.7% of relative standard deviation (RSD) was achieved by five replicative determinations of a sample blank spiked with 0.25 mg/kg histamine standard. Histamine in food samples such as fumitory skipjack and mackerel was analyzed with relative recoveries over 95% at spiking level of 150 mg/kg, as well as canned tuna fish and cheese with relative recoveries up to 98% at spiking levels of 0.50 and 5.0 mg/kg, respectively. The proposed method was validated with a sample from the Food Analysis Performance Assessment Scheme (FAPAS) as a standard certified material; and the results (140+/-6 mg/kg) agreed well with the assigned value (139 mg/kg).

To compare therapeutic effects of acupuncture with pushing manipulation and routine acupuncture on finger flexion in the patient of poststroke.Eighty cases were randomly divided into a group of acupuncture with pushing manipulation and a routine acupuncture group. Hegu (LI 4), Houxi (SI 3), Waiguan (TE 5) were selected in the both groups. For the group of acupuncture with pushing manipulation (n=42), after arrival of qi acupuncture with pushing manipulation was given, the needle was inserted forcedly downwards, heavily thrust and lightly lifted with the thumb forward and the index-finger backward, and the needle was retained for 30 min. For the routine acupuncture group, after arrival of qi the needle was retained for 30 min. The therapeutic effects were assessed by modified Ashworth spastic rating and activity of metacarpophalangeal articulations after treatment of 30 days and 60 days in the two groups.The total effective rate of 81.0% in the group of acupuncture with pushing manipulation was significantly better than 57.9% in the routine acupuncture group (P0.05); there was a significant or a very significant difference between the two groups in changes of the spastic degree and the activity of metacarpophalangeal articulations after treatment (P0.05, P0.01).Acupuncture with pushing manipulation has a definite therapeutic effect on finger flexion in the patient of poststroke.

To compare therapeutic effects of abdominal electroacupuncture (EA) and western medicine on poststroke constipation.Eighty cases were randomly divided into an EA group and a medication group, 40 cases in each group. The EA group were treated with EA at Daheng (SP 15), Fujie (SP 14), Tianshu (ST 25), Shuidao (ST 28), etc., once a day, 30 min each session, and the medication group with oral administration of 10 mg Cisapride, thrice each day. Seven days constituted one course. After 2 courses, clinical therapeutic effects were evaluated by cumulative scores of symptoms.The total effective rate of 92.5% in the EA group was significantly better than 72.5% in the medication group (P0.05). After treatment, the cumulative scores of clinical symptoms significantly decreased in the two groups (P0.05) and the improving degrees of symptoms in the EA group was significantly better than that in the medication group (P0.05).Abdominal electroacupuncture has a definite therapeutic effect on poststroke constipation, accelerating gastrointestinal movement.

Maternal smoking has been linked to an increased risk for orofacial clefts. N'-nitrosonornicotine (NNN) is one of the tobacco-specific nitrosamines that has been shown to be linked to the deleterious effects of tobacco and could be linked to the formation of cleft palate birth defects. The effect of NNN on palatal fusion was examined using an in vitro organ culture model of palatal development. The organ cultures were exposed to NNN (0.01, 0.1, 1, 10 and 100 mM) and the effects on palatal development characterized at defined points. Palatal fusion was evaluated at embryonic day 13 (E13)+72 h by characterizing the remaining medial edge epithelium (MEE) and determining the extent of fusion compared to controls. The NNN-treated group (1 mM) had more MEE remaining in the palatal midline than the untreated group at E13+72 h (P0.05). Changes in cell proliferation in the MEE resulting from NNN exposure were examined by BrdU incorporation in replicating DNA. Changes in the pattern of MEE cell death were examined by TUNEL. BrdU incorporation and TUNEL staining showed that the NNN (1 mM)-treated palates had more MEE cell proliferation and less apoptosis than the untreated-palates at E13+24 h (P0.05). The mechanism altered by NNN was further evaluated by characterizations of extracellular signal-regulated kinase (ERK) 1/2, p38 and c-jun amino-terminal kinase (JNK). NNN at 1 mM induced ERK1/2 phosphorylation, but reduced p38 phosphorylation (P0.05, P0.01, respectively) in the MEE. The results suggest that NNN inhibited palatal fusion by effects on cell proliferation and MEE cell death.

Transforming growth factor (TGF)-beta3 is an important contributor to the regulation of medial edge epithelium (MEE) disappearance during palatal fusion. SMAD2 phosphorylation in the MEE has been shown to be directly regulated by TGF-beta3. No phospho-SMAD2 was identified in the MEE in Tgf-beta3-null mutant mice (Tgf-beta3-/-), which was correlated with the persistence of the MEE and failure of palatal fusion. In the present study, the cleft palate phenotype in Tgf-beta3-/- mice was rescued by overexpression of a Smad2 transgene in Keratin 14-synthesizing MEE cells following mating Tgf-beta3 heterozygous mice with Keratin 14 promoter directed Smad2 transgenic mice (K14-Smad2). Success of the rescue could be attributed to the elevated phospho-SMAD2 level in the MEE, demonstrated by two indirect evidences. The rescued palatal fusion in Tgf-beta3-/-/K14-Smad2 mice, however, never proceeded to the junction of primary and secondary palates and the most posterior border of the soft palate, despite phospho-SMAD2 expression in these regions at the same level as in the middle portion of the secondary palate. The K14-Smad2 transgene was unable to restore all the functional outcomes of TGF-beta3. This may indicate an anterior-posterior patterning in the palatal shelves with respect to TGF-beta3 signaling and the mechanism of secondary palatal fusion.

Transforming growth factor (TGF) -beta3 is known to selectively regulate the disappearance of murine medial edge epithelium (MEE) during palatal fusion. Previous studies suggested that the selective function of TGF-beta3 in MEE was conducted by TGF-beta receptors. Further studies were needed to demonstrate that the TGF-beta signaling mediators were indeed expressed and phosphorylated in the MEE cells. SMAD2 and SMAD3 were both present in the MEE, whereas SMAD2 was the only one phosphorylated during palatal fusion. SMAD2 phosphorylation was temporospatially restricted to the MEE and correlated with the disappearance of the MEE. No phosphorylated SMAD2 was found in MEE in TGF-beta3(-/-) mice, although nonphosphorylated SMAD2 was present. The results suggest that TGF-beta3 is required for initiating and maintaining SMAD2 phosphorylation in MEE. Phospho-SMAD3 was not detectable in palate during normal palatal fusion. Previous results suggested TGF-beta-induced cessation of DNA synthesis in MEE cells during palatal fusion in vitro. The present results provide evidence that inhibition of MEE proliferation in vivo was controlled by endogenous TGF-beta3. The number of 5-bromo-2'-deoxyuridine (BrdU) -labeled MEE cells was significantly reduced in TGF-beta3(+/+) compared with TGF-beta3(-/-) mice when the MEE seam formed (t-test, P < 0.05). This finding suggests that TGF-beta3 is required for inhibiting MEE proliferation during palatal fusion. The inhibition of MEE proliferation may be mediated by TGF-beta3-dependent phosphorylation of SMAD2.