bluuebunny/crossref_metadata_2025_split huggingface dataset:
Analysis of protein, starch and oil content of single intact kernels by near infrared reflectance spectroscopy (NIRS) in maize (Zea mays L.)
Authors: Jiang H. Y. , Zhu Y. J. , Wei L. M. , Dai J. R. , Song T. M. , Yan Y. L. , Chen S. J. 
Published: August 2007

AbstractMaize samples (n = 309) containing 3090 single intact kernels from a broad variety of breeding materials were scanned by Near Infrared Reflectance Spectroscopy (NIRS) to develop non‐destructive determination calibrations for crude protein, starch and oil content in kernels. Calibration equations of single kernels were developed by partial least square regression (PLS). Regression parameters between the chemical values, determined by reference methods, and the predicted values, determined by Near Infrared Reflectance Spectroscopy, were verified by cross validation and external validation. It was found that embryo position had a significant influence on the effect of calibrations. Reliable calibrations were developed for the prediction of protein and starch contents with the embryo upwards, whereas the oil content required the embryo to be downwards. The cross validation and external validation coefficients for protein were 0.91 and 0.94, for starch 0.90 and 0.89 and for oil 0.94 and 0.95, respectively. The data suggested that NIRS could be successfully used in breeding programmes, as an accurate and non‐destructive tool to predict protein, starch and oil contents at the level of single kernels.
Development of STS markers and QTL validation for common bacterial blight resistance in common bean
Authors: Liu S. , Yu K. , Park S. J. 
Published: August 2007

AbstractCommon bacterial blight (CBB) of common bean (Phaseolus vulgaris L.), is one of the major diseases that decrease yield and quality. A major quantitative trait locus (QTL) for CBB resistance from line XAN 159 was transferred into two bean lines, HR45 and HR67. Previous studies identified that two markers are linked to this QTL but the chromosome location was not consistent. To identify more tightly linked markers and to verify the chromosome location, 65 additional markers were mapped using 81 recombinant inbred lines (RILs) derived from a cross HR67 × OAC95‐4. The QTL was mapped to a 13 cM region on chromosome 1 and defined by eight molecular markers that explained 25–52% of the phenotypic variation. Six tightly linked amplified fragment length polymorphism markers (0.6–9.7 cM from the QTL peak) were converted into seven sequence tagged site markers, three of which were mapped to this QTL. Five tightly linked markers were used to screen 907 F2 plants derived from a cross HR45 × ‘OAC Rex’ and four of them were linked to each other within 4.2 cM. These markers may be useful in marker‐assisted selection and map‐based cloning of this major QTL.
Genetic linkage map construction and location of QTLs for fruit‐related traits in cucumber
Authors: Yuan X. J. , Li X. Z. , Pan J. S. , Wang G. , Jiang S. , Li X. H. , Deng S. L. , He H. L. , Si M. X. , Lai L. , Wu A. Z. , Zhu L. H. , Cai R. 
Published: August 2007

AbstractA 173‐point genetic linkage map of cucumber (Cucumis sativus L.), consisting of 116 SRAPs, 33 RAPDs, 11 SSRs, 9 SCARs, 3 ISSRs, and 1 STS, was constructed using 130 F2 progeny derived from a narrow cross between line S94 (Northern China open‐field type) and line S06 (greenhouse European type). The seven linkage groups spanned 1016 cM with a mean marker interval of 5.9 cM. Using the F2 population and its F3 derived families, a total of 38 QTLs were detected on five linkage groups with an LOD threshold of 3.0 for nine fruit‐related traits: fruit weight, length, and diameter, fruit flesh thickness, seed‐cavity diameter, fruit‐stalk length, fruit pedicel length, length/diameter and length/stalk ratio. Of the identified QTLs, fsl4.3 for fruit‐stalk length explained the largest portion of phenotypic variation (r2 = ∼30%). Several QTLs were detected in the same linkage region in different generations and different seasons. Additionally, several QTLs for various fruit traits were mapped to the same or neighbouring marker intervals, suggesting they are possible character associations for controlling cucumber fruit development.
Inheritance of compact dwarf plant type in pigeonpea (Cajanus cajan)
Authors: Dhanasekar P. , Pandey R. N. , Dhumal K. N. 
Published: August 2007

AbstractA compact dwarf plant type TDT2004‐1 isolated from the progeny of a cross involving Cajanus cajan (cv. ‘C‐11’) and C. cajanifolia was investigated for its inheritance. Pigeonpea genotype TDT2004‐1 is semi‐determinate in growth habit; short (approximately 37 cm) with reduced internodal length (1.2 cm), a compact canopy and a high harvest index (40%), while genotype TT44‐4 is indeterminate in growth habit; tall (132 cm) with normal internodal length (2.3 cm), an open canopy and a low harvest index (28.9%). The inheritance study involving cross TT44‐4 × TDT2004‐1 showed that the compact dwarf plant type was governed by a single recessive gene. TDT2004‐1 could be utilized for improving the harvest index and also for restructuring the plant canopy in pigeonpea.
Mechanisms of Regulation of Litter Size in Pigs on the Genome Level
Authors: Distl O 
Published: August 2007

ContentsImprovement in litter size has become of great interest in pig industry as good fecundity is directly related to a sow's productive life. Genetic regulation of litter size is complex and the main component traits so far defined are ovulation rate, embryonic survival, uterus capacity, foetal survival and pre‐weaning losses. Improvements using concepts of the quantitative genetics let expect only slow genetic progress due to its low heritability of approximately 0.09 for number of piglets born alive. Marker assisted selection allows to dissect litter size in its component traits and using molecular genetic markers for the components of litter size traits promises more progress and advantages in optimum balancing of the different physiological mechanisms influencing litter size. In this review, efforts being made to unravel the genetic determinants of litter size are accounted and discussed. For litter size traits, more than 50 quantitative trait loci (QTL) were mapped and in more than 12 candidate genes associations confirmed. The number of useful candidate genes is much larger as shown by expression profiles and in addition, much more QTL can be assumed. These functional genomic approaches, both QTL mapping and candidate gene analysis, have to be merged for a better understanding of a wider application across different pig breeds and lines. Newly developed tools based on microarray techniques comprising DNA variants or expressed tags of many genes or even the whole genome appear useful for in depth understanding of the genetics of litter size in pigs.
Epigallocatechin gallate attenuates experimental non‐alcoholic steatohepatitis induced by high fat diet
Authors: Kuzu Nalan , Bahcecioglu Ibrahim Halil , Dagli Adile Ferda , Ozercan Ibrahim Hanifi , Ustündag Bilal , Sahin Kazim 
Published: August 2007

AbstractBackground and Aim:  In the present study, we examined the preventive role of epigallocatechin gallate (EGCG) in an experimental non‐alcoholic steatohepatitis model induced by a high fat diet.Methods:  The study included 21 male Sprague‐Dawley rats, which were equally divided into three groups. The first group was fed on a standard rat diet, the second group on a high fat diet (HFD), and the third group on a HFD + EGCG. The study concluded after 6 weeks. Histopathological examination was performed. Plasma and tissue MDA levels, glucose, insulin, alanine aminotransferase (ALT), aspartate aminotransferase, gamma glutamyltransferase, alkaline phosphatase, triglyceride, and cholesterol levels were studied. Insulin resistance was calculated by the homeostasis model of insulin resistance method.Results:  Steatosis, inflammation, ballooning degeneration, and necrosis increased significantly in the HFD group, compared to the control group (P < 0.01). Steatosis and inflammation decreased in the HFD + EGCG group, in comparison to the HFD group (P < 0.05, for each). There was a significant decline in ALT (P < 0.01), triglyceride (P < 0.01), insulin (P < 0.05), and glucose (P < 0.05) levels in the HFD + EGCG group, when compared to the HFD group. Plasma and liver MDA levels in the HFD + EGCG group were lower than those of the HFD group; the difference was significant (P < 0.01 for each). Glutathione levels in the HFD + EGCG group was significantly higher those in the HFD group. CYP 2E1 and α‐smooth muscle actin expression decreased in the HFD + EGCG group, in comparison to the HFD group (P < 0.01, P < 0.05, respectively).Conclusion:  EGCG reduces the development of experimental non‐alcoholic steatohepatitis induced by a high fat diet. It seems to exercise this effect through its effect on lipid metabolism and antioxidant characteristics.
RASSF1A expression inhibits the growth of hepatocellular carcinoma from Qidong County
Authors: Xue Wan‐Jiang , Li Chun , Zhou Xiao‐Jun , Guan Hong‐Geng , Qin Lei , Li Peng , Wang Zhi‐Wei , Qian Hai‐Xin 
Published: August 2007

AbstractBackground and Aim:  The tumor‐suppressing role of Ras‐association domain family 1A (RASSF1A) has been described in several systems. In this study, we tested its tumor‐suppressing ability and the potential molecular mechanisms in hepatocellular carcinoma (HCC) from Qidong County.Methods:  Reverse transcription polymerase chain reaction and Northern blotting were employed to detect the expression of RASSF1A in HCC. After establishing stable RASSF1A (wild type or mutant) expressing ‘qi dong gan ai yan jiu suo’ ([Qidong Institute of Liver Cancer] QGY)‐7703 cell lines, we tested the effects of RASSF1A expression on cell growth by cell proliferation rate, cell colony formation, and cell cycle progression. We also tested the effects of RASSF1A expression on tumorigenesis in nude mice and on cellular sensitivity to mitomycin treatment.Results:  The RASSF1A transcript was not found in 75% (three of four) of HCC cell lines and 67% (32/48) of HCC primary biopsies. The stepwise regression analyses indicated that the loss of RASSF1A expression was more frequent in patients who were hepatitis B virus surface antigen positive (HBsAg+) compared to those who were HBsAg(−), both in tumor and corresponding non‐cancerous tissues. The wild‐type (wt)‐RASSF1A expression in the QGY‐7703 cell line resulted in fewer and smaller clones, decreased xenograft tumor volume and weight, and G1/S arrest in vitro and in vivo. The wt‐RASSF1A expression also decreased the cyclin D1 protein expression, which appeared to be at the level of post‐transcriptional control. In addition, the wt‐RASSF1A expression increased cell growth inhibition and the percentage of cells with sub‐G1 DNA content when the cells were treated with mitomycin.Conclusion:  RASSF1A is a tumor suppressor in HCC. The loss of RASSF1A expression may be related to HBsAg+ in hepatocarcinogenesis. Its inactivation may play an important role in the development of HCC.
Protein glutathionylation increases in the liver of patients with non‐alcoholic fatty liver disease
Authors: Piemonte Fiorella , Petrini Stefania , Gaeta Laura Maria , Tozzi Giulia , Bertini Enrico , Devito Rita , Boldrini Renata , Marcellini Matilde , Ciacco Enzo , Nobili Valerio 
Published: August 2007

AbstractBackground and Aim:  Oxidative stress is an important pathophysiological mechanism in non‐alcoholic steatohepatitis, where hepatocyte apoptosis is significantly increased correlating with disease severity. Protein glutathionylation occurs as a response to oxidative stress, where an increased concentration of oxidized glutathione modifies post‐translational proteins by thiol disulfide exchange. In this study, we analyzed the protein glutathionylation in non‐alcoholic fatty liver disease (NAFLD) and evaluated a potential association between glutathionylation, fibrosis, and vitamin E treatment.Methods:  Protein glutathionylation was studied in the livers of 36 children (mean age 12.5 years, range 4–16 years) subdivided into three groups according to their NAFLD activity score (NAS) by Western blot analysis and immunohistochemistry, using a specific monoclonal antibody. In addition, we identified the hepatocyte ultrastructures involved in glutathionylation by immunogold electron microscopy.Results:  Our findings showed that protein glutathionylation increases in the livers of patients with NAFLD and it is correlated with steatohepatitis and liver fibrosis. Its increase appears mainly in nuclei and cytosol of hepatocytes, and it is reversed by antioxidant therapy with reduced fibrosis.Conclusion:  Protein glutathionylation significantly increases in livers with NAFLD, strongly suggesting that oxidative injury plays a crucial role in this disease. Furthermore, the marked increase of protein glutathionylation, in correlation with collagen VI immunoreactivity, suggests a link between the redox status of hepatic protein thiols and fibrosis.
Hyperglycemia and hypertriglyceridemia may associate with the adenoma–carcinoma transition in colorectal epithelial cells
Authors: Tabuchi Masafumi , Kitayama Joji , Nagawa Hirokazu 
Published: August 2007

AbstractBackground and Aim:  Epidemiological studies have suggested the positive correlation between hyperlipidemia and/or hyperglycemia and colorectal cancer risk.Methods:  We retrospectively examined the association between fasting blood sugar (BS) or triglycerides (TG) and the presence of colorectal adenoma, carcinoma in situ and invasive cancer in 867 patients who received total colonoscopy by medical health check.Results:  An increased TG level, but not a BS level, was significantly associated with the increased risk of adenoma, although with non‐independent multivariate analysis. In contrast, an elevated BS level was identified as an independent risk factor for invasive cancer in 93 patients with carcinoma lesions with an odds ratio of 1.74 (P < 0.05).Conclusion:  Our data suggest that hypertriglyceridemia and hyperglycemia may correlate with the development of adenoma and invasive cancer, respectively. The effectiveness of strict BS control in patients with hypertriglyceridemia for the prevention of the invasive colorectal carcinoma deserves further studies.
Inhibition of hepatitis C virus infection and expression in vitro and in vivo by recombinant adenovirus expressing short hairpin RNA
Authors: Sakamoto Naoya , Tanabe Yoko , Yokota Takanori , Satoh Kenichi , Sekine‐Osajima Yuko , Nakagawa Mina , Itsui Yasuhiro , Tasaka Megumi , Sakurai Yuki , Cheng‐Hsin Chen , Yano Masahiko , Ohkoshi Shogo , Aoyagi Yutaka , Maekawa Shinya , Enomoto Nobuyuki , Kohara Michinori , Watanabe Mamoru 
Published: August 2007

AbstractBackground and Aim:  We have reported previously that synthetic small interfering RNA (siRNA) and DNA‐based siRNA expression vectors efficiently and specifically suppress hepatitis C virus (HCV) replication in vitro. In this study, we investigated the effects of the siRNA targeting HCV‐RNA in vivo.Methods:  We constructed recombinant retrovirus and adenovirus expressing short hairpin RNA (shRNA), and transfected into replicon‐expressing cells in vitro and transgenic mice in vivo.Results:  Retroviral transduction of Huh7 cells to express shRNA and subsequent transfection of an HCV replicon into the cells showed that the cells had acquired resistance to HCV replication. Infection of cells expressing the HCV replicon with an adenovirus expressing shRNA resulted in efficient vector delivery and expression of shRNA, leading to suppression of the replicon in the cells by ∼10−3. Intravenous delivery of the adenovirus expressing shRNA into transgenic mice that can be induced to express HCV structural proteins by the Cre/loxP switching system resulted in specific suppression of virus protein synthesis in the liver.Conclusion:  Taken together, our results support the feasibility of utilizing gene targeting therapy based on siRNA and/or shRNA expression to counteract HCV replication, which might prove valuable in the treatment of hepatitis C.
Functional and morphological alterations in small intestine mucosa of chronic alcoholics
Authors: Bhonchal Sonia , Nain Chander K , Prasad Kaushal K , Nada Ritambhara , Sharma Arun K , Sinha Saroj K , Singh Kartar 
Published: August 2007

AbstractBackground and Aim:  Alcohol‐related diseases constitute the third largest health problem after heart disease and cancer in the world. The objective was to study the effects of chronic alcohol intake on small bowel cellular functions with focus on brush border enzymes, membrane enzymes, cellular enzymes and their relationship with structural changes in small bowel mucosa of chronic alcoholics.Methods:  Duodenal biopsies were obtained by upper gastrointestinal endoscopy of chronic alcoholics having alcoholic liver disease (ALD) with and without cirrhosis. The biopsies were then processed for enzymatic assays to analyze the status of cellular functions. Light microscopy, transmission electron microscopy, and scanning electron microscopy were done to study the morphological alterations. Control group consisted of nonalcoholic gastroesophageal reflux disease patients reporting for routine endoscopy.Results:  The experimental group consisted of ALD patients which showed significant difference (P < 0.01) in cellular functions when compared with controls. The light microscopy showed partial villous atrophy, increase in lamina propria infiltrate, and intraepithelial lymphocytes as main findings in the alcoholic group. Ultrastructural evaluation revealed changes like widened intercellular junction, distorted microvilli, increased rough endoplasmic reticulum, and increased and dilated mitochondria. The enzyme parameters correlated positively with the mucosal morphology parameters indicating a direct relationship.Conclusion:  The study brought out the changes in small bowel of chronic alcoholics having ALD at both cellular and subcellular levels which correlated significantly.
Spontaneous bacterial peritonitis and bacterascites prevalence in asymptomatic cirrhotic outpatients undergoing large‐volume paracentesis
Authors: Castellote José , Girbau Ana , Maisterra Sandra , Charhi Nadia , Ballester Raquel , Xiol Xavier 
Published: August 2007

AbstractBackground and Aim:  Spontaneous bacterial peritonitis and bacterascites prevalence in asymptomatic cirrhotic patients on large‐volume paracentesis is unknown. The aim of this study was to investigate spontaneous bacterial peritonitis and bacterascites prevalence in a prospective cohort of cirrhotic outpatients following large‐volume paracentesis with low risk of infection.Methods:  We prospectively studied all large‐volume paracenteses performed in cirrhotic outpatients for 1 year. Patients with fever, abdominal pain, peritonism or hepatic encephalopathy were excluded from the study. The ascitic fluid was analyzed by means of a reagent strip with a colorimetric scale from 0 to 4. A strip test of 0 or 1 was considered negative. In those cases with a reagent strip ≥2, conventional polymorphonuclear count was performed. Ascitic fluid culture was done into blood culture bottles in all cases.Results:  We performed 204 paracenteses in 40 patients. Nine cases were excluded. Culture‐negative neutrocytic ascites was diagnosed in one case (0.5%), while bacterascites was diagnosed in six out of 195 cases (3%), mainly by gram‐positive cocci.Conclusion:  The spontaneous bacterial peritonitis prevalence in outpatient cirrhotics with low risk of infection undergoing large‐volume paracentesis is very low. Moreover, the prevalence of bacterascites is low and without clinical consequences. The routine analysis of ascitic fluid may be unnecessary in this clinical setting. Nevertheless, the use of reagent strips is a reasonable alternative due to its accessibility and low cost.
Expression of somatostatin receptor subtype 3 in the gastric mucosa of dyspeptic patients in relation to Helicobacter pylori infection and a family history of gastric cancer
Authors: Stec‐Michalska Krystyna , Peczek Lukasz , Krakowiak Agnieszka , Michalski Blazej , Chojnacki Jan , Knopik‐Dabrowicz Alina , Klupinska Grazyna , Nawrot Barbara 
Published: August 2007

AbstractBackground and Aim:  The cytotoxic activity of Helicobacter pylori contributes significantly to the pathogenesis of gastric carcinoma. A preliminary study suggested that somatostatin receptor subtype 3 (SSTR3) might play a role in cell apoptosis and the growth of gastric cancer. The aim of the present study was to determine the influence of H. pylori infection and a family history of gastric cancer on the expression of SSTR3 in the gastric mucosa of non‐cancer patients with dyspepsia.Methods:  The expression of the SSTR3 gene in the gastric mucosa of the stomach antrum and corpus of 53 patients was determined by the use of quantitative reverse transcription–polymerase chain reaction.Results:  The SSTR3 mRNA level was lower in the H. pylori‐infected patients, as compared to the non‐infected patients, independently of a family history of gastric cancer and stomach topography. The greatest decrease of approximately 40% and 35% (P < 0.05) was observed for the antrum of the H. pylori‐positive patients without and with a family history of gastric cancer, respectively. In the corpus, these differences were much smaller, regardless of a family history of gastric cancer. Interestingly, for H. pylori‐negative patients, the density (at the mRNA level) of the SSTR3 receptor in the antrum was higher than in the corpus mucosa.Conclusions:  A decrease in the density of SSTR3 (especially in the antrum) in individuals with H. pylori infection and particularly with a family history of gastric cancer may point to an environmental and inherited predisposition in the development of distal gastric cancer.
Etiological spectrum of esophageal varices due to portal hypertension in Indian children: Is it different from the West?
Authors: Poddar Ujjal , Thapa Babu Ram , Rao KL Narsimha , Singh Kartar 
Published: August 2007

AbstractBackground and Aim:  Information about portal hypertension (PHT) in children is meagre. We therefore studied the spectrum and outcome of PHT in children (≤14 years of age) over a period of 9 years.Methods:  PHT was diagnosed on endoscopy (presence of varices) in 517 cases during the study period. The diagnosis of extrahepatic portal venous obstruction (EHPVO) and Budd–Chiari Syndrome (BCS) were made on the basis of ultrasound examination. Cirrhosis was diagnosed on the basis of clinical, biochemical, ultrasound, and liver biopsy (whenever feasible). Noncirrhotic portal fibrosis (NCPF) and congenital hepatic fibrosis (CHF) were diagnosed on liver biopsy. Endoscopic sclerotherapy (EST) was done in all the patients who presented with variceal bleeding and surgery was performed whenever indicated.Results:  Causes of PHT included EHPVO in 54%, cirrhosis in 39%, CHF in 3%, NCPF in 2%, and BCS in 2%. Of these, 279 (54%) patients presented with upper gastrointestinal bleeding and this group comprised of EHPVO in 85%, cirrhosis in 10%, CHF in 2.5%, NCPF in 2%, and BCS in 1%. Bleeding was the presenting feature in 85% of EHPVO cases and in 13% of cirrhosis cases. In EHPVO cases, variceal eradication was achieved in 95% of cases with a mean 5 ± 2.4 EST sessions. Surgery was required in 24 cases of EHPVO. Mortality due to bleeding was 1.7% in EHPVO and 30% in cirrhosis.Conclusions:  EHPVO and cirrhosis are the two major causes of PHT in children. However, predominant cause of variceal bleeding is EHPVO. EST is an effective method of treatment in EHPVO.