Hydrated sodium calcium aluminosilicate for reduction of aflatoxin in quails (Coturnix coturnix japonica)

Essiz, Dinc/0000-0002-4759-7858WOS: 000248379700002PubMed: 17724933The purpose of the present study was to evaluate the toxic effects of aflatoxin (AF) on growth performance and various processing parameters of quails and to determine the preventive efficacy of hydrated sodium calcium aluminosilicate (HSCAS). One hundred and eighty 1-d-old quails of both sexes were randomly divided into 4 experimental groups with 5 replicates and 45 birds following weighing.The experimental design consisted of four dietary treatments: 1) control with 0 mg AF/kg of diet and 0 % HSCAS; 2) 0.5 % HSCAS; 3) 2.5 mg AF/kg of diet; 4) 2.5 mg AF/kg of diet plus 0.5 % HSCAS.The chicks were housed in electrically heated battery cages and exposed to light for 24 h from hatching to 3 weeks of age. Quails consumed the diets and water od libitum. Body weight (BW) was significantly (p < 0.001) increased by addition of HSCAS to AF diet. The lowest BW gains in groups received AF alone was observed at all periods. The reduction in BW gain caused by 2.5 mg AF/kg of diet was significantly (p < 0.001) diminished by the addition of 0.5 % HSCAS to the diet. The addition of HSCAS to the AF diet significantly (p < 0.001) protected against decrease of feed intake at all periods with exception of the first period. None of the treatments altered significantly the feed conversion ratio (FCR).The relative weights of the liver, kidney and spleen were increased in the chickens consuming the AF alone diet. However, light microscopic examination demonstrated the addition of HSCAS to quail feed to partially decrease fat deposition caused by the toxin, and besides, electron microscopic examination of indicated a reorganization in the encloplasmic reticulum and increase in the number of ribosomes and polisomes. Furthermore, the decrease in the antibody titre induced by Newcastle vaccine, due to aflatoxins, was relatively prevented. No significant differences were observed for serum total protein, total cholesterol and glucose levels. The results of indicate that HSCAS is effective in preventing the deleterious effects of A

A new case of hairy elbows syndrome (hypertrichosis cubiti)

A new case of hairy elbows syndrome (hypertrichosiscubii): Hairy Elbows Syndrome (Hypertrichosis Cubiti; OMIM# 139600) is a rare syndrome, and characterized by the presence of long vellus hair localized on the extensor surfaces of the distal third of the arms and proximal third of the forearm bilaterally. Occasionally hypertrichosis of other body regions may accompany hairy elbows. About half of the reported patients have short stature. Aside from short stature other relatively rare abnormalities related with this syndrome were also described. Most of the reported cases were sporadic, but autosomal dominant as well as autosomal recessive inheritance patterns have also been postulated. In this report, we present a girl with Hairy Elbows syndrome who has both characteristic and uncommon findings of the syndrome. She has excessive hair on her elbows, along with short stature, microcephaly, joint hyperlaxity, thin-long-webbed neck, dysmorphic facial features and mental retardation

Calpain 10 gene single-nucleotide 44 polymorphism may have an influence on clinical and metabolic features in patients with polycystic ovary syndrome

ergun, mehmet ali/0000-0001-9696-0433WOS: 000264938300003PubMed: 19337008Aim: This study was designed in order to examine the relationship between Calpain 10 [single-nucleotide polymorphism (SNP) 19,43,44,63] gene polymorphisms and clinical and hormonal characteristics in women with polycystic ovary syndrome (PCOS). Materials and methods: One hundred and seven patients with PCOS and 114 healthy subjects were included in this study. Serum levels of sex steroids were measured for each individual. Insulin resistance (IR) was evaluated by the homeostasis model assessment (HOMA) and quantitative insulin-sensitivity check index (QUICKI) methods. Insulin and glucose responses to the oral glucose tolerance test (OGTT) were analyzed by calculating the areas under the curve for insulin (AUCI) and glucose by the trapezoidal methods. We used PCR and restriction fragment length polymorphism technique to examine Calpain 10 SNP 19, 43, 44, and 63 polymorphisms. Results: Allele distribution of Calpain 10 SNP 44 gene polymorphism was observed as significantly different between the groups. Calpain 10 SNP 44 TC genotype was found to be increased in PCOS subjects (69.15%) compared to the control subjects (50%). However, when compared to control subjects, patients with PCOS had similar Calpain 10 SNP 19, Calpain 10 SNP 43, and SNP 63 gene polymorphisms. When compared with normal Calpain 10 gene SNP 44 allele in PCOS subjects, subjects with PCOS having Calpain 10 gene SNP 44 allele polymorphism had higher free testosterone, androstenedione, DHEA-S, and fasting insulin levels. Also, PCOS women with Calpain 10 gene SNP 44 allele polymorphism had high Ferriman-Gallwey (F-G) score, acne, prevalence of menstrual disturbances, waist-hip ratio, HOMA-IR, AUCI levels and low QUICKI levels. Conclusion: The findings show that Calpain 10 gene SNP 44 allele polymorphism may have a role in PCOS pathogenesis. However, larger-scale studies are needed in this field

External confinement of brick masonry columns with open-grid basalt reinforced mortar

A large portion of existing unreinforced masonry buildings in earthquake regions is in urgent need of retrofitting. Masonry brick columns are frequently used as load-bearing elements in such buildings. In this paper, the efficiency of historical masonry column confinement externally with open-grid basalt fiber reinforced mortar, as a strengthening method, is investigated experimentally. A total of 5 masonry column specimens are produced with solid bricks, which have been collected from a historical building constructed around the 1930s, and a local mortar with sub-standard mechanical characteristics to simulate existing historical mortar. The columns with 900 mm height and cross-sectional dimensions of 360 mm x 360 mm are constructed in running bond. All column specimens are tested under concentric compressive loads and the outcomes of the column tests are evaluated in terms of strength, deformability and failure characteristics. A comparison is also made between the experimental results and theoretical predictions made using available analytical models

DNA-Dependent Protein Kinase Catalytic Subunit Is Not Required for Dysfunctional Telomere Fusion and Checkpoint Response in the Telomerase-Deficient Mouse

Telomeres are key structural elements for the protection and maintenance of linear chromosomes, and they function to prevent recognition of chromosomal ends as DNA double-stranded breaks. Loss of telomere capping function brought about by telomerase deficiency and gradual erosion of telomere ends or by experimental disruption of higher-order telomere structure culminates in the fusion of defective telomeres and/or the activation of DNA damage checkpoints. Previous work has implicated the nonhomologous end-joining (NHEJ) DNA repair pathway as a critical mediator of these biological processes. Here, employing the telomerase-deficient mouse model, we tested whether the NHEJ component DNA-dependent protein kinase catalytic subunit (DNA-PKcs) was required for fusion of eroded/dysfunctional telomere ends and the telomere checkpoint responses. In late-generation mTerc(−)(/)(−) DNA-PKcs(−)(/)(−) cells and tissues, chromosomal end-to-end fusions and anaphase bridges were readily evident. Notably, nullizygosity for DNA Ligase4 (Lig4)—an additional crucial NHEJ component—was also permissive for chromosome fusions in mTerc(−)(/)(−) cells, indicating that, in contrast to results seen with experimental disruption of telomere structure, telomere dysfunction in the context of gradual telomere erosion can engage additional DNA repair pathways. Furthermore, we found that DNA-PKcs deficiency does not reduce apoptosis, tissue atrophy, or p53 activation in late-generation mTerc(−)(/)(−) tissues but rather moderately exacerbates germ cell apoptosis and testicular degeneration. Thus, our studies indicate that the NHEJ components, DNA-PKcs and Lig4, are not required for fusion of critically shortened telomeric ends and that DNA-PKcs is not required for sensing and executing the telomere checkpoint response, findings consistent with the consensus view of the limited role of DNA-PKcs in DNA damage signaling in general