Influence of environmental factors on birth weight variability of indigenous Serbian breeds of sheep

The present investigation was carried out to study the influence of environmental factors on the birth weight variability of two breeds of sheep. Animals used in this research were taken from the Pirot and Svrljig indigenous sheep breeds. The data were collected from 1999 to 2009 and were analyzed to determine the effect of the year and season, age of the lamb, weight of the lamb, birth type and sex on the birth weight of lambs. Both sheep breeds were managed in the same farm and under the same farm conditions. Statistical analysis was performed by using GLM procedure of SAS statistical package program. Results showed that young (2 to 3 years) and old (6 to 7 years) mothers gave birth to lighter lambs, while sheep in the middle age (4 to 5 years) gave birth to lambs with the heaviest body weight. However, the differences were respectively significant (P < 0.01). Birth weight of lambs also depended on weight of lamb, although differences in the average body weight of lambs were statistically significant (P < 0.05). Type of birth also had effect on the body weight of lambs at birth in both Pirot and Svrljig breeds (P < 0.05). Body weight of lambs at birth were almost the same for both sexes (3.39 and 3.36 kg for male and female in Pirot breed and 3.48 and 3.43 kg for male and female in Svrljig breed, respectively), though the difference was not statistically significant (P > 0.05). The values of birth weight observed for quite a number of years ranged from 3.27 to 3.52 kg in Pirot and 3.34 to 3.51 kg in Svrljig breed (P < 0.01). Lambs born in the spring-summer season has the heaviest body weight at birth. Conversely, the significant difference (P < 0.05) can only be interpreted as the factor of food source.Key words: Environmental factors, birth weight variability, indigenous sheep

Loss of Metal Ions, Disulfide Reduction and Mutations Related to Familial ALS Promote Formation of Amyloid-Like Aggregates from Superoxide Dismutase

Mutations in the gene encoding Cu-Zn superoxide dismutase (SOD1) are one of the causes of familial amyotrophic lateral sclerosis (FALS). Fibrillar inclusions containing SOD1 and SOD1 inclusions that bind the amyloid-specific dye thioflavin S have been found in neurons of transgenic mice expressing mutant SOD1. Therefore, the formation of amyloid fibrils from human SOD1 was investigated. When agitated at acidic pH in the presence of low concentrations of guanidine or acetonitrile, metalated SOD1 formed fibrillar material which bound both thioflavin T and Congo red and had circular dichroism and infrared spectra characteristic of amyloid. While metalated SOD1 did not form amyloid-like aggregates at neutral pH, either removing metals from SOD1 with its intramolecular disulfide bond intact or reducing the intramolecular disulfide bond of metalated SOD1 was sufficient to promote formation of these aggregates. SOD1 formed amyloid-like aggregates both with and without intermolecular disulfide bonds, depending on the incubation conditions, and a mutant SOD1 lacking free sulfhydryl groups (AS-SOD1) formed amyloid-like aggregates at neutral pH under reducing conditions. ALS mutations enhanced the ability of disulfide-reduced SOD1 to form amyloid-like aggregates, and apo-AS-SOD1 formed amyloid-like aggregates at pH 7 only when an ALS mutation was also present. These results indicate that some mutations related to ALS promote formation of amyloid-like aggregates by facilitating the loss of metals and/or by making the intramolecular disulfide bond more susceptible to reduction, thus allowing the conversion of SOD1 to a form that aggregates to form resembling amyloid. Furthermore, the occurrence of amyloid-like aggregates per se does not depend on forming intermolecular disulfide bonds, and multiple forms of such aggregates can be produced from SOD1

Ablation of kallikrein 7 (KLK7) in adipose tissue ameliorates metabolic consequences of high fat diet-induced obesity by counteracting adipose tissue inflammation in vivo

Vaspin is an adipokine which improves glucose metabolism and insulin sensitivity in obesity. Kallikrein 7 (KLK7) is the first known protease target inhibited by vaspin and a potential target for the treatment of metabolic disorders. Here, we tested the hypothesis that inhibition of KLK7 in adipose tissue may beneficially affect glucose metabolism and adipose tissue function. Therefore, we have inactivated the Klk7 gene in adipose tissue using conditional gene-targeting strategies in mice. Klk7-deficient mice (ATKlk7 −/−) exhibited less weight gain, predominant expansion of subcutaneous adipose tissue and improved whole body insulin sensitivity under a high fat diet (HFD). ATKlk7 −/− mice displayed higher energy expenditure and food intake, most likely due to altered adipokine secretion including lower circulating leptin. Pro-inflammatory cytokine expression was significantly reduced in combination with an increased percentage of alternatively activated (anti-inflammatory) M2 macrophages in epigonadal adipose tissue of ATKlk7 −/−. Taken together, by attenuating adipose tissue inflammation, altering adipokine secretion and epigonadal adipose tissue expansion, Klk7 deficiency in adipose tissue partially ameliorates the adverse effects of HFD-induced obesity. In summary, we provide first evidence for a previously unrecognized role of KLK7 in adipose tissue with effects on whole body energy expenditure and insulin sensitivity