活性鹌鹑蛋酒的研制及其在鸡尾酒调制中的运用

研究了以鹌鹑种蛋、糯米为主要原料,采用鹌鹑种蛋胚胎培育技术,糯米与活性鹌鹑蛋经发酵的工艺条件,并探讨了鹌鹑种蛋胚胎发育、发酵条件的优化以及活性鹌鹑蛋鸡尾酒的配方设计。

食疗食谱

白果乌鸡汤 材料:乌鸡一只(1000克—1500克即可)白果、莲子、江米各15克,胡椒3克。 作法:将乌鸡剖开洗净,把白果、莲子、江米、胡椒,装入鸡腹内,用慢火炖烂即可食用。

俳句汉译与联想引申

俳句汉译与联想引申西安外语学院贺明真俳句汉译，作为事物矛盾的两个方面，自然也是理解与表达，而理解则是俳句汉译的主要矛盾。译者理解不了原作的意境与妙趣，也就无法主作表达。日本俳句是一种语少意多的短诗，俳人力求“着里不多，而蓄意无尽”，以最经济的手段表现...

Targeting collagen expression in alcoholic liver disease

Alcoholic liver disease （ALD） is a leading cause of liver disease and liver-related deaths globally, particularly in developed nations. Liver fibrosis is a consequence of ALD and other chronic liver insults, which can progress to cirrhosis and hepatocellular carcinoma if left untreated. Liver fibrosis is characterized by accumulation of excess extracellular matrix components, including type I collagen, which disrupts liver microcirculation and leads to injury. To date, there is no therapy for the treatment of liver fibrosis; thus treatments that either prevent the accumulation of type I collagen or hasten its degradation are desirable. The focus of this review is to examine the regulation of type I collagen in fibrogenic cells of the liver and to discuss current advances in therapeutics to eliminate excessive collagen deposition.

Alcohol-induced protein hyperacetylation: Mechanisms and consequences

Although the clinical manifestations of alcoholic liver disease are well-described, little is known about the molecular basis of liver injury. Recent studies have indicated that ethanol exposure induces global protein hyperacetylationo This reversible, post- translational modification on the E-amino groups of lysine residues has been shown to modulate multiple, diverse cellular processes ranging from transcriptional activation to microtubule stability. Thus, alcohol- induced protein hyperacetylation likely leads to major physiological consequences that contribute to alcohol-induced hepatotoxicity. Lysine acetylation is controlled by the activities of two opposing enzymes, histone acetyltransferases and histone deacetylases. Currently, efforts are aimed at determining which enzymes are responsible for the increased acetylation of specific substrates. However, the greater challenge will be to determine the physiological ramifications of protein hyperacetylation and how they might contribute to the progression of liver disease. In this review, we will first list and discuss the proteins known to be hyperacetylated in the presence of ethanol. We will then describe what is known about the mechanisms leading to increased protein acetylation and how hyperacetylation may perturb hepatic function.

Fibronectin: Functional character and role in alcoholic liver disease

Fibronectins are adhesive glycoproteins that can be found in tissue matrices and circulating in various fluids of the body. The variable composition of fibronectin molecules facilitates a diversity of interactions with cell surface receptors that suggest a role for these proteins beyond the structural considerations of the extracellular matrix. These interactions implicate fibronectin in the regulation of mechanisms that also determine cell behavior and activity. The two major forms, plasma fibronectin (pFn) and cellular fibronectin (cFn), exist as balanced amounts under normal physiological conditions. However, during injury and/or disease, tissue and circulating levels of cFn become disproportionately elevated. The accumulating cFn, in addition to being a consequence of prolonged tissue damage, may in factstimulate cellular events that promote further damage. In this review, we summarize what is known regarding such interactions between fibronectin and cells that may influence the biological response to injury. We elaborate on the effects of cFn in the liver, specifically under a condition of chronic alcohol-induced injury. Studies have revealed that chronic alcohol consumption stimulates excess production of cFn by sinusoidal endothelial cells and hepatic stellate cells while impairing its clearance by other cell types resulting in the build up of this glycoprotein throughout the liver and its consequent increased availability to influence cellular activity that could promote the development of alcoholic liver disease. We describe recent findings by our laboratory that support a plausible role for cFn in the promotion of liver injury under a condition of chronic alcohol abuse and the implications of cFn stimulation on the pathogenesis of alcoholic liver disease. These findings suggest an effect of cFn in regulating cell behavior in the alcohol-injured liver that is worth further characterizing not only to gain a more comprehensive understanding of the role this reactive glycoprotein plays in the progression of injury but also for the insight further studies could provide towards the development of novel therapies for alcoholic liver disease.

Adsorption of Protein from Model Wine Solution by Different Bentonites

The adsorption of protein from model wine was investigated under different temperatures, pH values, contact times, and concentrations of ethanol, by certain bentonites. The results showed that ethanol molecules could broaden the protein molecules＇ channel to the interlayer of bentonite, and the maximum protein adsorption amount occurred under an ethanol concentration of 12% （by volume） and a pH value of 3.56. The increased single point Brunauer-Emmitt-Teller （BET） surface area （SBET） and adsorption pore volume （VAds） suggested a larger amount of active adsorption sites of the bentonite surface and a wider protein channel from the surface to the inner adsorption sites of bentonite, respectively. At the same time, higher methylene blue test （MBT） and swelling index （Sw） indicated that it was easy for the entrance of water and the absorbance of protein. Higher temperature was found favorable to eliminate more proteins and it took about 20 to 40min to arrive at the maximum adsorption.

Crosstalk between angiogenesis, cytokeratin-18, and insulin resistance in the progression of non-alcoholic steatohepatitis

AIM: To elucidate the possible crosstalk between angiogenesis, cytokeratin-18 (CK-18), and insulin resistance (IR) especially in patients with non-alcoholic steatohepatitis (NASH).METHODS: Twenty-eight patients with NASH and 11 with simple fatty liver disease (FL) were enrolled in this study and underwent clinicopathological examination. The measures of angiogenesis, CK-18, and IR employed were CD34-immunopositive vessels, CK-18immunopositive cells, and homeostasis model assessment of IR (HOMA-IR), respectively. The correlations of these factors with NASH were elucidated.RESULTS: Significant development of hepatic neovascularization was observed only in NASH, whereas almost no neovascularization could be observed in FL and healthy liver. The degree of angiogenesis was almost parallel to liver fibrosis development, and both parameters were positively correlated. Similarly, CK-18expression and HOMA-R were signifi cantly increased in NASH as compared with FL and healthy liver. Furthermore, CK-18 and HOMA-IR were also positively correlated with the degree of neovascularization. CONCLUSION: These results indicate that the crosstalk between angiogenesis, CK-18, and IR may play an important role in the onset and progression of NASH.

Histone modifications and alcohol-induced liver disease:Are altered nutrients the missing link?

Alcoholism is a major health problem in the United States and worldwide,and alcohol remains the single most significant cause of liver-related diseases and deaths.Alcohol is known to influence nutritional status at many levels including nutrient intake,absorption,utilization,and excretion,and can lead to many nutritional disturbances and deficiencies.Nutrients can dramatically affect gene expression and alcohol-induced nutrient imbalance may be a major contributor to pathogenic gene expression in alcohol-induced liver disease(ALD).There is growing interest regarding epigenetic changes,including histone modifications that regulate gene expression during disease pathogenesis.Notably,modifications of core histones in the nucleosome regulate chromatin structure and DNA methylation,and control gene transcription.This review highlights the role of nutrient disturbances brought about during alcohol metabolism and their impact on epigenetic histone modifications that may contribute to ALD.The review is focused on four critical metabolites,namely,acetate,S-adenosylmethionine,nicotinamide adenine dinucleotide and zinc that are particularly relevant to alcohol metabolism and ALD.

Effect of MS （Methylated Spirit） as a Disinfectant and Antisticking Agent on Hatchability of C/arias gariepinus Eggs and Survival of the Hatchlings

African catfish Clarias gariepinus brood stocks were bred by normal induced breeding method, After fertilization, the eggs were treated with 0.40%, 0.50% and 0.60% concentration levels of MS （methylated spirit） and a control treatment without MS （0%）. The objective was to remove the stickiness of the egg outer vitelline membrane to improve hatchability and survival of the hatchlings. Two batches of the treatments were carried out according to treatment duration of 5 s and l0 s. The eggs hatched normally with the highest hatching percentage of 62.31% in eggs treated with 0.40% MS concentration in 5 s treatment and 61.92% in the same concentration for 10 s. The control treatment of 0.00% MS treatment gave the lowest hatchability of 49.69% at 5 s and 45.71% at 10 s exposure time. Growth performance of the hatchlings improved in eggs treated than those not treated. Those treated had higher weight gain and percentage specific growth rates than those not treated. Percentage survival ranged from 75% to 90 % in both treated and untreated groups. MS can therefore be safely used in fish hatchery to prevent egg stickiness to improve hatchability and larval development.

Genome-wide differences in hepatitis C-vs alcoholism-associated hepatocellular carcinoma

AIM:To look at a comprehensive picture of etiology- dependent gene abnormalities in hepatocellular carcinoma in Western Europe. METHODS:With a liver-oriented microarray,transcript levels were compared in nodules and cirrhosis from a training set of patients with hepatocellular carcinoma (alcoholism,12;hepatitis C,10)and 5 controls.Loose or tight selection of informative transcripts with an abnormal abundance was statistically valid and the tightly selected transcripts were next quantified by qRTPCR in the nodules from our training set(12+10) and a test set(6+7). RESULTS:A selection of 475 transcripts pointed to significant gene over-representation on chromosome 8 (alcoholism)or-2(hepatitis C)and ontology indicated a predominant inflammatory response(alcoholism)or changes in cell cycle regulation,transcription factors and interferon responsiveness(hepatitis C).A stringent selection of 23 transcripts whose differences betweenetiologies were significant in nodules but not in cirrhotic tissue indicated that the above dysregulations take place in tumor but not in the surrounding cirrhosis.These 23 transcripts separated our test set according to etiologies. The inflammation-associated transcripts pointed to limited alterations of free iron metabolism in alcoholic vs hepatitis C tumors. CONCLUSION:Etiology-specific abnormalities(chromo- some preference;differences in transcriptomes and related functions)have been identified in hepatocellular carcinoma driven by alcoholism or hepatitis C.This may open novel avenues for differential therapies in this disease.

Impact of asialoglycoprotein receptor deficiency on the development of liver injury

The asialoglycoprotein （ASGP） receptor is a wellcharacterized hepatic receptor that is recycled via the common cellular process of receptor-mediated endocytosis （RME）. The RME process plays an integral part in the proper trafficking and routing of receptors and ligands in the healthy cell. Thus, the missorting or altered transport of proteins during RME is thought to play a role in several diseases associated with hepatocyte and liver dysfunction. Previously, we examined in detail alterations that occur in hepatocellular RME and associated receptor functions as a result of one particular liver injury, alcoholic liver disease （ALD）. The studies revealed profound ethanol- mediated impairments to the ASGP receptor and the RME process, indicating the importance of this receptor and the maintenance of proper endocytic events in normal tissue. To further clarify these observations, studies were performed utilizing knockout mice （lacking a functional ASGP receptor） to which were administered several liver toxicants. In addition to alcohol, we examined the effects following administration of anti- Fas （CD95） antibody, carbon tetrachloride （CCh） and lipopolysaccharide （LPS）/galactosamine. The results of these studies demonstrated that the knockout mice sustained enhanced liver injury in response to all of the treatments, as shown by increased indices of liver damage, such as enhancement of serum enzyme levels, histopathological scores, as well as hepatocellular death. Overall, the work completed to date suggests a possible link between hepatic receptors and liver injury. In particular, adequate function and content of the ASGP receptor may provide protection against various toxinmediated liver diseases.

Serum type Ⅳ collagen level is predictive for esophageal varices in patients with severe alcoholic disease

AIM： To determine factors predictive for esophagea varices in severe alcoholic disease （SAD）. METHODS： Abdominal ultrasonography （US） was performed on 444 patients suffering from alcoholism. Forty-four patients found to have splenomegaly and/ or withering of the right liver lobe were defined as those with SAD. SAD patients were examined by upper gastrointestinal （UGI） endoscopy for the presence of esophageal varices. The existence of esophageal varices was then related to clinical variables. RESULTS： Twenty-five patients （56.8%） had esophageal varices. A univariate analysis revealed a significant difference in age and type Ⅳ collagen levels between patients with and without esophageal varices. A logistic regression analysis identified type Ⅳ collagen as the only independent variable predictive for esophageal varices （P = 0.017）. The area under the curve （AUC） for type Ⅳ collagen as determined by the receiver operating characteristic （ROC） for predicting esophageal varices was 0.78. CONCLUSION： This study suggests that the level of type Ⅳ collagen has a high diagnostic accuracy for the detection of esophageal varices in SAD.

Olive oil consumption and non-alcoholic fatty liver disease

The clinical implications of non-alcoholic fatty liver diseases(NAFLD)derive from their potential to progress to fibrosis and cirrhosis.Inappropriate dietary fat intake,excessive intake of soft drinks,insulin resistance and increased oxidative stress results in increased free fatty acid delivery to the liver and increased hepatic triglyceride(TG)accumulation.An olive oil-rich diet decreases accumulation of TGs in the liver,improves postprandial TGs,glucose and glucagonlike peptide-1 responses in insulin-resistant subjects, and upregulates glucose transporter-2 expression in the liver.The principal mechanisms include:decreased nuclear factor-kappaB activation,decreased lowdensity lipoprotein oxidation,and improved insulin resistance by reduced production of inflammatory cytokines(tumor necrosis factor,interleukin-6)and improvement of jun N-terminal kinase-mediated phosphorylation of insulin receptor substrate-1.The beneficial effect of the Mediterranean diet is derived from monounsaturated fatty acids,mainly from olive oil.In this review,we describe the dietary sources of the monounsaturated fatty acids,the composition of olive oil,dietary fats and their relationship to insulin resistance and postprandial lipid and glucose responses in non-alcoholic steatohepatitis,clinical and experimental studies that assess the relationship between olive oil and NAFLD,and the mechanism by which olive oil ameliorates fatty liver,and we discuss future perspectives.

Techniques Optimization of Combined Enzymatic Hydrolysis on Brewers＇ Spent Grain from Novozymes

Purpose： To extract protein, decrease the cellulose and facilitate the digestion and absorption of brewers＇ spent grain by animal. Topic： Discuss and optimize the hydrolysis conditions of the combined enzymatic hydrolysis by Novozymes. Method： The fresh brewers＇ spent grain was firstly dried, smashed and sifted. Then as indicators of the protein extraction rate in the enzyme solution and the content of cellulose in the index, the parameters of enzymatic hydrolysis, such as the solid-liquid ratio, reaction temperature, pH, enzyme dosage and reaction time, were investigated in detailed. After hydrolysis, the brewers＇ spent grain was put in the boiling water bath for inactivation for 15 minutes, and centrifuged, the supernatants were volume to 100 mL and the protein content was measured. After the precipitate was dried, the cellulose content was also measured. Achievements： The optimized conditions were with temperature of 50 ℃, pH 6.5, enzyme amount of 30 mg for Novozymes enzyme and 2.5 h for reaction time. Under these conditions, the protein extraction rate in the enzyme reaction reached 41.82%, and the cellulose content reached 13.90%, the degradation rate of cellulose was 18.86%.

Diagnostic and therapeutic implications of the association between ferritin level and severity of nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease(NAFLD),defined by excessive liver fat deposition related to the metabolic syndrome,is a leading cause of progressive liver disease,for which accurate non-invasive staging systems and effective treatments are still lacking.Evidence has shown that increased ferritin levels are associated with the metabolic insulin resistance syndrome,and higher hepatic iron and fat content.Hyperferritinemia and iron stores have been associated with the severity of liver damage in NAFLD,and iron depletion reduced insulin resistance and liver enzymes.Recently,Kowdley et al demonstrated in a multicenter study in 628 adult patients with NAFLD from the NAFLD-clinical research network database with central re-evaluation of liver histology and iron staining that the increased serum ferritin level is an independent predictor of liver damage in patients with NAFLD,and is useful to identify NAFLD patients at risk of non-alcoholic steatohepatitis and advanced fibrosis.These data indicate that incorporation of serum ferritin level may improve the performance of noninvasive scoring of liver damage in patients with NAFLD,and that iron depletion still represents an attractive therapeutic target to prevent the progression of liver damage in these patients.

Proteasome inhibitor treatment in alcoholic liver disease

Oxidative stress, generated by chronic ethanol consumption, is a major cause of hepatotoxicity and liver injury. Increased production of oxygen-derived free radicals due to ethanol metabolism by CYP2E1 is principally located in the cytoplasm and in the mitochondria, which does not only injure liver cells, but also other vital organs, such as the heart and the brain. Therefore, there is a need for better treatment to enhance the antioxidant response elements. To date, there is no established treatment to attenuate high levels of oxidative stress in the liver of alcoholic patients. To block this oxidative stress, proteasome inhibitor treatment has been found to significantly enhance the antioxidant response elements of hepatocytes exposed to ethanol. Recent studies have shown in an experimental model of alcoholic liver disease that proteasome inhibitor treatment at low dose has cytoprotective effects against ethanol-induced oxidative stress and liver steatosis. The beneficial effects of proteasome inhibitor treatment against oxidative stress occurred because antioxidant response elements （glutathione peroxidase 2, superoxide dismutase 2, glutathione synthetase, glutathione reductase, and GCLC） were upregulated when rats fed alcohol were treated with a low dose of PS-34Z （Bortezomib, Velcade）. This is an important finding because proteasome inhibitor treatment up-regulated reactive oxygen species removal and glutathione recycling enzymes, while ethanol feeding alone down-regulated these antioxidant elements. For the first time, it was shown that proteasome inhibition by a highly specific and reversible inhibitor is different from the chronic ethanol feeding-induced proteasome inhibition. As previously shown by our group, chronic ethanol feeding causes a complex dysfunction in the ubiquitin proteasome pathway, which affects the proteasome system, as well as the ubiquitination system. The beneficial effects of proteasome inhibitor treatment in alcoholic liver disease are related to proteasome inhibitor reversibility and the rebound of proteasome activity 72 h post PS-341 administration.

Epigenetic regulation in alcoholic liver disease

Alcoholic liver disease （ALD） is characterized by steatosis or fat deposition in the liver and inflammation, which leads to cirrhosis and hepatocellular carcinoma. Induction of target genes without involving changes in DNA sequence seems to contribute greatly to liver injury. Chromatin modifications including alterations in histones and DNA, as well as post-transcriptional changes collectively referred to as epigenetic effects are altered by alcohol. Recent studies have pointed to a significant role for epigenetic mechanisms at the nucleosomal level influencing gene expression and disease outcome in ALD. Specifically, epigenetic alterations by alcohol include histone modifications such as changes in acetylation and phosphorylation, hypomethylation of DNA, and alterations in miRNAs. These modifications can be induced by alcoholnduced oxidative stress that results in altered recruitment of transcriptional machinery and abnormal gene expression. Delineating these mechanisms in initiation and progression of ALD is becoming a major area of interest. This review summarizes key epigenetic mechanisms that are dysregulated by alcohol in the liver. Alterations by alcohol in histone and DNA modifications, enzymes related to histone acetylation such as histone acetyltransferases, his-tone deacetylases and sirtuins, and methylation enzymes such as DNA methyltransferases are discussed. Chromatin modifications and miRNA alterations that result in immune cell dysfunction contributing to inflammatory cytokine production in ALD is reviewed. Finally, the role of alcohol-mediated oxidative stress in epigenetic regulation in ALD is described. A better understanding of these mechanisms is crucial for designing novel epigenetic based therapies to ameliorate ALD.

Vague relationship between alcohol consumption and metabolic syndrome in nonobese people

Fatty liver, including non-alcoholic fatty liver disease, is closely associated with metabolic syndrome (MS). Thus, the presence of fatty liver without MS in some conditions may be clinically important. Many studies have shown that compared with no or occasional alcohol intake, moderate alcohol consumption is associated with lower prevalence rates of hypertension and type 2 diabetes, and lower levels of circulating C-reactive protein, a valuable marker for MS and insulin resistance. Considering these findings, light to moderate alcohol consumption has theoretical benefits on fatty liver and MS. Fatty liver, including non-alcoholic fatty liver disease, may be more clinically important than MS, particularly in non-obese individuals, because fatty liver can develop before MS in several conditions, such as regular alcohol consumers. Furthermore, most of the currently used MS criteria are unable to detect "true MS" because of variations in multiple factors such as age, height, medications, and complications.

Effect of Feeding Different Levels of Dietary Protein and Addition of Baker＇s Yeast （Saccharomyces cerevisiae） on Productive Parameters of Awassi Lambs

Forty eight individually fed Awassi male lambs were used in factorial experiment to investigate their responses to feeding concentrate diets containing three levels of dietary crude protein （CP）, each was offered without or with baker＇s yeast （SC） at rate of 0.5% （on dry matter （DM） basis）. Concentrates were offered at rate of 3% of live body weight with free choice of barley straw. Results revealed that higher （P 〈 0.05） digestible dry matter （DDM） and digestible organic matter （DOM） intakes were achieved due to feeding medium level of CP and to the addition of SC. Addition of SC improved （P 〈 0.05） gain, lambs fed medium and high levels gained higher （P 〈 0.05） than those fed the low level of dietary CP. Feed conversion ratio （FCR） based on DM and organic matter （OM） intakes was not significantly affected by level of dietary CP or addition of yeast. Even though, less amount of N required per unit of gain was achieved with low and medium as compared to high levels. Higher DM, nitrogen free extract （NFE） and hemicellulose （P 〈 0.05）, OM, CP, crude fiber （CF） and cellulose （P 〈 0.01） digestibilities were achieved in lambs fed the medium level of CP, whereas, no significant effect was observed on ether extract （EE）, neutral detergent fiber （NDF） and acid detergent fiber （ADF） digestibilities. Results also revealed that digestibility of almost all nutrients was improved with different extent due to addition of SC. Effect of interaction between levels of dietary CP and addition of SC referred to the preferability of addition of SC with medium level of dietary protein.