A cumulative evidence indicates that consumption of tea catechin, flavan-3-ol derived from green tea leaves, lowers the risk of cardiovascular diseases. However, a precise mechanism for this cardiovascular action has not yet been fully understood. In the present study, we investigated the effects of different green tea catechins, such as epigallocatechin-3 gallate (EGCG), epigallocatechin (EGC), epicatechin-3 gallate (ECG), and epicatechin (EC), on angiotensin II (Ang II)-induced hypertrophy in primary cultured rat aortic vascular smooth muscle cell (VSMC). [$^3H$]-leucine incorporation was used to assess VSMC hypertrophy, protein kinase assay, and western blot analysis were used to assess mitogen-activated protein kinase (MAPK) activity, and RT-PCR was used to assess c-jun or c-fos transcription. Ang II increased [$^3H$]-leucine incorporation into VSMC. However, EGCG and ECG, but not EGC or EC, inhibited [$^3H$]-leucine incorporation increased by Ang II. Ang II increased phosphorylation of c-Jun, extracellular-signal regulated kinase (ERK) 1/2 and p38 MAPK in VSMC, however, EGCG and ECG , but not EGC or EC, attenuated c-Jun phosphorylation increased by Ang II. ERK 1/2 and p38 MAPK phosphorylation induced by Ang II were not affected by any catechins. Ang II increased c-jun and c-fos mRNA expression in VSMC, however, EGCG inhibited c-jun but not c-fos mRNA expression induced by Ang II. ECG, EGC and EC did not affect c-jun or c-fos mRNA expression induced by Ang II. Our findings indicate that the galloyl group in the position 3 of the catechin structure of EGCG or ECG is essential for inhibiting VSMC hypertrophy induced by Ang II via the specific inhibition of JNK signaling pathway, which may explain the beneficial effects of green tea catechin on the pathogenesis of cardiovascular diseases observed in several epidemiological studies.
Fatigue cracks of rib-to-deck (RD) joints have been frequently observed in the orthotropic steel decks (OSD) using conventional U-ribs (CU). Thickened edge U-rib (TEU) is proposed to enhance the fatigue strength of RD joints, and its effectiveness has been proved through fatigue tests. In-depth full-scale tests are further carried out to investigate both the fatigue strength and fractography of RD joints. Based on the test result, the mean fatigue strength of TEU specimens is 21% and 17% higher than that of CU specimens in terms of nominal and hot spot stress, respectively. Meanwhile, the development of fatigue cracks has been measured using the strain gauges installed along the welded joint. It is found that such the crack remains almost in semi-elliptical shape during the initiation and propagation. For the further application of TEUs, the design curve under the specific survival rate is required for the RD joints using TEUs. Since the fatigue strength of welded joints is highly scattered, the design curves derived by using the limited test data only are not reliable enough to be used as the reference. On this ground, an experiment-numerical hybrid approach is employed. Basing on the fatigue test, a probabilistic assessment model has been established to predict the fatigue strength of RD joints. In the model, the randomness in material properties, initial flaws and local geometries has been taken into consideration. The multiple-site initiation and coalescence of fatigue cracks are also considered to improve the accuracy. Validation of the model has been rigorously conducted using the test data. By extending the validated model, large-scale databases of fatigue life could be generated in a short period. Through the regression analysis on the generated database, design curves of the RD joint have been derived under the 95% survival rate. As the result, FAT 85 and FAT 110 curves with the power index m of 2.89 are recommended in the fatigue evaluation on the RD joint using TEUs in terms of nominal stress and hot spot stress respectively. Meanwhile, FAT 70 and FAT 90 curves with m of 2.92 are suggested in the evaluation on the RD joint using CUs in terms of nominal stress and hot spot stress, respectively.
The present study was conducted to evaluate and compare the effects of various animal and plant protein sources on piglet' performance, digestibility of amino acids and gut morphology in weaned pigs until 28 days after weaning. The plant protein sources used were soybean meal (SBM), fermented soy protein (FSP), rice protein concentrate (RPC); and animal protein sources tested were, whey protein concentrate (WPC) and fishmeal (FM). Iso-proteinous (21%) diets were formulated and lysine (1.55%) content was similar in all the diets. The level of each protein source added was 6% by replacing SBM to the same extent from the control diet containing 15% SBM. The ADG was higher (p<0.05) in the groups fed animal proteins as compared with plant proteins at all the levels of measurement, except during 15-28 days. The highest ADG was noted in WPC and FM fed diets and lowest in SBM fed diet. The feed intake was higher in animal protein fed groups than plant proteins at all phases, but the feed:gain ratio was not affected by protein sources except during overall (0 to 14 day) measurement which was improved (p<0.05) in animal protein fed diets compared to plant protein sources. The digestibilities of gross energy, dry matter and crude protein were higher in animal protein fed groups than for plant protein fed sources. The apparent ileal digestibilities of essential amino acids like Leu, Thr, and Met were significantly (p<0.05) higher in animal proteins fed animals as compared with plant protein fed animals. But the apparent fecal digestibilities of essential amino acids like Arg and Ile were significantly higher (p<0.05) in plant protein diets than animal protein sources. The villous structure studied by scanning electron microscope were prominent, straight finger-like, although shortened and densely located in FM fed group as compared with others. The lactic acid bacteria and C. perfringens counts were higher in caecal contents of pigs fed plant proteins than the animal proteins. Overall, it could be concluded that animal protein sources in the present study showed better effects on growth performance, nutrient digestibility and gut morphology than plant protein sources.
A total of 1,200 LinNan Chinese color-feathered chicks were used to study the effects of methionine source [DL-2-hydroxy-4-methylthio-butanoic acid (HMTBa) or DL-methionine (DLM)] and dietary crude protein (CP) level on growth performance, carcass traits, and whole-body nitrogen and fat retention. The trial was designed as a $2{\times}2$ factorial arrangement, including two CP levels (adequate and low) and two methionine sources (HMTBa and DL-methionine). Diets were formulated for three phases, starter (0-21 d), grower (21-42 d), and finisher (42-63 d). Chicks fed HMTBa had higher daily gain and improved feed efficiency than DLM during the grower phase (p<0.05). A significant two-way interaction was observed for growth performance during the finisher phase and overall (0-63 d). Growth performance was greater for chicks fed HMTBa than DLM on adequate-CP diets (p<0.05), but this was not observed at low-CP level (p>0.05). Chicks fed low-CP diets grew slower, used feed less efficiently during the grower, finisher phase and overall. On d 42, regardless of dietary CP levels, birds fed HMTBa had higher carcass weights, breast and thigh weights than DLM-fed birds (p<0.04). Birds fed low-CP diet had lighter carcass weights and less breast muscle, thigh muscle, and dressing percentage at the end of starter, grower and finisher phases (p<0.05). Whole body composition analyses found that birds fed HMTBa tended to contain more protein and less fat compared to those chicks fed DLM at the end of the starter phase (p<0.10). Low-CP diets increased CP concentration in the whole body at the end of the finisher phase (p = 0.05). HMTBa supplementation increased whole-body N retention rate during the finisher phase and overall (p<0.01), and low-CP diets reduced N intake and whole-body fat retention during the finisher phase and overall (p<0.05). In summary, HMTBa was better than DLM on an equimolar basis for growth performance, carcass traits, and N retention in Chinese color-feathered chicks. Low-CP diets lowered growth performance as well as carcass traits in color-feathered birds, probably due to imbalanced AA profiles.
Yang, Zhi Hong;Gu, Li Juan;Zhang, Dong Liang;Li, Zheng;Li, Jing Jie;Lee, Mi-Ra;Wang, Chun Yan;Wang, Zhen;Cho, Jeong-Hee;Sung, Chang-Keun
Asian-Australasian Journal of Animal Sciences
/
v.25
no.5
/
pp.708-716
/
2012
In order to investigate and evaluate the effects of red deer antlers on hair growth in the full-thickness wound healing model, Sprague-Dawley rats were given incision wounds through the full thickness of their dorsal skin and deer antler was applied for 40 days. At specified intervals thereafter (4, 8, 16, 32 and 40 days), the animals were sacrificed and the wound site skins were excised, processed, and sectioned. At post-injury days 16, 32 and 40, longer and more active new hair appeared around the healing wound of antler-treated skin. Histological studies showed that the antler extract markedly increases the depth, size, and number of hair follicles. Expression of IGF-I (insulin-like growth factor) mRNA was detected by RT-PCR and real time RT-PCR. The result showed that the expression of IGF-I (days 16, 32, and 40) was obviously up-regulated in antler-treated skins compared to control skins. Similar results were seen in the ELISA analysis to quantify the IGF-I expression. These results support the notion that wound healing can cause hair growth by enhancing the expression of IGF-I. Deer antler extract appears to have the potential to promote hair growth and could be used in hair growth products.
Objective: This study compared the meat quality, muscle fiber characteristics, and fatty acids between Jinjiang yellow cattle (JJ) and F1 Simmental${\times}$Jinjiang yellow cattle (SJ) which were offered the same diet. Methods: Six JJ and six SJ individuals were reared and fattened from 10 to 26 months of age. After feeding, the highrib (HR), ribeye (RB), and tenderloin (TL) samples were taken from the carcass for meat quality evaluations. Results: The results showed that growth performance of SJ was higher than that of JJ (higher live weight and average daily gain), and the hot carcass weight of SJ was higher than that of JJ (p<0.05). pH of JJ was higher than that of SJ in TL (p<0.05); the color of $a^{\ast}$ of SJ was higher than that of JJ in TL and RB (p<0.05); the cooking loss of SJ was significantly lower than that of JJ in TL and RB (p<0.05); the shear force value was significantly lower in SJ compared to JJ (p<0.05); the muscle fiber diameter was higher and the fiber density was lower in SJ compared to JJ in HR and TL (p<0.05); compared to SJ, the muscles of JJ had higher saturated fatty acid (SFA) composition; the sum of monounsaturated fatty acid and polyunsaturated fatty acid (PUFA) were lower in the muscle of JJ; the mRNA expressions of myosin heavy chain-I (MyHC-I) and MyHC-IIa were higher in SJ compared to JJ in muscle of HR and RB; the mRNA expressions of MyHC-IIx and MyHC-IIb were lower in SJ compared to JJ in HR and RB (p<0.05). Conclusion: Meat quality and fatty acid profile differed between SJ and JJ; the muscle of SJ had higher $a^{\ast}$ and SFA; SJ had lower cooking loss, shear force and PUFA compared to the muscle of JJ. In addition, the type and development characteristics of the muscle fiber had some difference between SJ and JJ; these might be factors which caused the differences in meat quality and fatty acid profile between SJ and JJ.
Background: The study aimed to describe the age distribution of breast cancer diagnosis among Chinese females for comparison with the United States and the European Union, and provide evidence for the screening target population in China. Materials and Methods: Median age was estimated from hospital databases from 7 tertiary hospitals in China. Population-based data in China, United States and European Union was extracted from the National Central Cancer Registry, SEER program and GLOBOCAN 2008, respectively. Age-standardized distribution of breast cancer at diagnosis in the 3 areas was estimated based on the World Standard Population 2000. Results: The median age of breast cancer at diagnosis was around 50 in China, nearly 10 years earlier than United States and European Union. The diagnosis age in China did not vary between subgroups of calendar year, region and pathological characteristics. With adjustment for population structure, median age of breast cancer at diagnosis was 50~54 in China, but 55~59 in United States and European Union. Conclusions: The median diagnosis age of female breast cancer is much earlier in China than in the United States and the European Union pointing to racial differences in genetics and lifestyle. Screening programs should start at an earlier age for Chinese women and age disparities between Chinese and Western women warrant further studies.
Background: Due to the strong inhibitory effects of $PPAR{\gamma}$ gene on the growth of cancer cells, the role of Pro12Ala polymorphism in $PPAR{\gamma}$ gene has been extensively investigated in cancer recently. However, the results were inconsistent according to cancer type. The aim of this study was to comprehensively evaluate the $PPAR{\gamma}$ Pro12Ala polymorphism and gastric cancer susceptibility. Materials and Methods: Search strategies were conducted in Pubmed, Medline (Ovid), Chinese biomedical database (CBM), China national knowledge infrastructure (CNKI), VIP, and Wanfang database, covering all publications, with the last search up to November 01, 2014. The strength of association between $PPAR{\gamma}$ Pro12Ala polymorphism and gastric cancer risk was assessed by OR with 95%CI. Results: A total of 546 cases and 827 controls in 5 case-control studies were included in this meta-analysis. The results indicated that the variant G allele carriers (CG+GG) had a 2.31 times higher risk for gastric cancer when compared with the homozygote CC (odds ratio (OR)=2.31, 95% confidence interval (CI)=1.67-3.21 for CG+GG vs. CC). In the subgroup analysis by ethnicity, significantly elevated risks were both found in Asians (OR=2.56, 95% CI=1.42-4.64) and Caucasians (OR=2.20, 95% CI=1.48-3.25). Similarly, in the subgroup analysis by H. pylori status, a significantly increased risk was identified in H. pylori (+) populations (OR=3.68, 95%CI=2.07-6.52), but not in H. pylori(-) populations (OR=1.17, 95%CI=0.58-2.39). Conclusions: This pooled analysis suggested that the $PPAR{\gamma}$ Pro12Ala polymorphism could be an independent predictive risk factor for gastric cancer especially in H. pylori infected populations in Asians and Caucasians. Nevertheless, prospectively designed cohort studies are needed to further investigate gene-gene and gene-environment interactions to confirm the combined effects of $PPAR{\gamma}$ Pro12Ala polymorphisms and H. pylori infection on gastric cancer risk.
Objectives: To explore the expression of astrocyte elevated gene-1 (AEG-1) in cervical cancer and analyze its correlation with microvascular density (MVD), nuclear factor kappaB (NF-kB p65) and vascular endothelial growth factor (VEGF). Materials and Methods: Immunohistochemical MaxVision method was adopted to detect the expression level of AEG-1, NF-kB p65 and VEGF in 45 samples of invading cervical cancer and 12 samples of cervicitis from The First Affiliated Hospital of Wenzhou Medical University. Tumor microvascular endothelial marker CD34 combined with Weidner was used to determine the MVD in cervical cancer tissue. The positive expression and staining conditions of AEG-1, NF-kB p65 and VEGF in cervical cancer tissues were observed under a light microscope. Correlations between expression of AEG-1 protein and those of NF-Kb p65 and VEGF, as well as MVD, were analyzed using Pearson correlation. Results: The expression levels of AEG-1 were $0.186{\pm}0.043$ in cervical cancer and $0.051{\pm}0.002$ in chronic cervicitis (p<0.01). Moreover, expression of AEG-1 was related to vascular invasion and lymphatic metastasis of cervical cancer (p<0.01), but not with age of the patients, differentiation degree, tumour size, pathological type and parametrial infiltration (p>0.05). Pearson correlation analysis showed that the expression of AEG-1 was linked with NF-kB p65 (r=0.501, p=0.000), VEGF (r=0.718, p=0.000) as well as MVD in cervical cancer tissue (r=0.815, p=0.000). Conclusions: AEG-1 is highly expressed in cervical cancer and promotes angiogenesis, which might be related to the fact that AEG-1 activating the signal pathway of NF-kB could up-regulate the level of VEGF expression.
SHP1 negatively regulates the Janus kinase 2/signal transducer and activator of transcription (JAK2/STAT) signaling pathway, which is constitutively activated in myeloproliferative neoplasms (MPNs) and leukemia. Promoter hypermethylation resulting in epigenetic inactivation of SHP1 has been reported in myelomas, leukemias and other cancers. However, whether SHP1 hypermethylation occurs in MPNs, especially in Chinese patients, has remained unclear. Here, we report that aberrant hypermethylation of SHP1 was observed in several leukemic cell lines and bone marrow mononuclear cells from MPN patients. About 51 of 118 (43.2%) MPN patients including 23 of 50 (46%) polycythaemia vera patients, 20 of 50 (40%) essential thrombocythaemia and 8 of 18 (44.4%) idiopathic myelofibrosis showed hypermethylation by methylation-specific polymerase chain reaction. However, SHP1 methylation was not measured in 20 healthy volunteers. Hypermethylation of SHP1 was found in MPN patients with both positive (34/81, 42%) and negative (17/37, 45.9%) JAK2V617F mutation. The levels of SHP1 mRNA were significantly lower in hypermethylated samples than unmethylated samples, suggesting SHP1 may be epigenetically inactivated in MPN patients. Furthermore, treatment with 5-aza-2'-deoxycytidine (AZA) in K562 cells showing hypermethylation of SHP1 led to progressive demethylation of SHP1, with consequently increased reexpression of SHP1. Meanwhile, phosphorylated JAK2 and STAT3 were progressively reduced. Finally, AZA increased the expression of SHP1 in primary MPN cells with hypermethylation of SHP1. Therefore, our data suggest that epigenetic inactivation of SHP1 contributes to the constitutive activation of JAK2/STAT signaling. Restoration of SHP1 expression by AZA may contribute to clinical treatment for MPN patients.
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