Morphology and quantification of sheep pineal glands at pre-pubertal, pubertal and post-pubertal periods

Bolat, Durmus/0000-0001-7619-1913WOS: 000438337300008PubMed: 29774950The pineal gland is a neuroendocrine organ associated with photoperiodic regulation in mammals. The aim of this study was to evaluate the pineal gland at the pre-pubertal, pubertal and post-pubertal periods by means of morphology and stereology. The study examined at total of 24 ovine pineal glands collected from healthy female Akkaraman breed. Thick sections (40m) were cut and treated with synaptophysin. Following each thick section, six consecutive sections at a thickness of 5m were cut. Each thin section was stained with one of the following dyes: Crossman's modified triple dye, glial fibrillary acidic protein (GFAP), melatonin marker, periodic acid-Schiff, Von Kossa and AgNOR. The pineal gland volume was measured using Cavalieri's method. The optical fractionator was used to estimate the total number of pinealocytes. The percentage of parenchyma and connective tissue and degree of vascularization were estimated by the area fraction fractionator method. The pineal gland volumes in the pre-pubertal, pubertal and post-pubertal groups were 7.53 +/- 1.715mm(3), 11.20 +/- 1.336mm(3) and 17.75 +/- 1.188mm(3), respectively (p<.5). The number of pinealocytes in the pre-pubertal, pubertal and post-pubertal groups was 3,244,000 +/- 228,076, 4,438,000 +/- 243,610, 7,381,766 +/- 406,223, respectively (p<.05). The glands of the post-pubertal group contained the highest amount of connective tissue (11.49 +/- 2.103%; p<.5) and the largest GFAP staining area (p<.05). The melatonin staining density was the highest in the pubertal group. The density of lipofuscin staining was higher in the pubertal and post-pubertal groups.Turkiye Bilimsel ve Teknolojik Arastirma KurumuTurkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [TOVAG 1130578]Turkiye Bilimsel ve Teknolojik Arastirma Kurumu, Grant/Award Number: TOVAG 113057

Hepatic stellate cells increase in Toxoplasma gondii infection in mice

ATMACA, HASAN TARIK/0000-0001-8379-4114WOS: 000319162700003PubMed: 23642259Background: Toxoplasma gondii is a ubiquitous protozoan parasite that can infect humans and animals. The severity of toxoplasmosis varies according to the immune status of the individual, parasite strain, and host species. In mammalian species, it has been observed that severe lesions of acute toxoplasmosis form in visceral organs such as the liver, lung, and spleen. Some epidemiological studies have reported an association of T. gondii infection with liver cirrhosis. Methods: Acute infection was induced in fifteen 30-day-old normal Swiss albino mice. The mice were infected by intraperitoneal inoculation of 5000 T. gondii RH strain tachyzoites. The mice were sacrificed in groups of 5 at 2, 4, and 6 days after inoculation. Another group of 5 mice were used as the controls. Anti-glial fibrillary acidic protein (GFAP) and anti-T. gondii antibodies were used to compare GFAP-immunoreactive cells and anti-T. gondiiimmunopositive areas in the liver between the T. gondii-infected groups and the healthy controls, respectively. Results: There was a significant correlation between the numbers of GFAP-positive hepatic stellate cells (HSCs) when they were compared with T. gondii antigen immunostaining (p < 0.05). The amount of T. gondii immunostaining increased significantly with the increase in the number of HSCs. Conclusions: There is a significant relationship between the number of HSCs and T. gondii antigens, which may represent an active role of HSCs in liver pathology and the pathobiology of T. gondii-related hepatitis

Evaluation of oxidative stress, hematological and biochemical parameters during Toxoplasma gondii infection in gerbils

KABAKCI, Ruhi/0000-0001-9131-0933; ATMACA, HASAN TARIK/0000-0001-8379-4114WOS: 000357000800001The aim of the present study was to investigate the alterations of oxidative stress, hematological and biochemical parameters in experimental infection caused by Toxoplasma gondii in gerbil. A total of 16 gerbil, 8 of which were control and 8 was infection group, were used in the study. The gerbils were infected by intraperitoneal inoculation of 5000 T. gondii RH strain tachyzoites. In group of, the gerbil were sacrificed at 7th day after inoculation. At the end of this period, blood samples collected and erythrocyte malondialdehyde (MDA) concentrations, superoxide dismutase (SOD), catalase (CAT) activities, plasma aspartat aminotransferase (AST) and alanine aminotranspherase (ALT) activities, total protein, albumin, globulin were determined. Besides, hematological parameters were analysed in whole blood. Aspartat aminotransferase and ALT activities and MDA concentrations and neutrophil percentage and total leukocyte counts increased significantly in infected group when compared to control. In infected group, SOD activities, albumin concentrations and lymhocyte percentage decreased when compared to control. The results of this study suggest that oxidative stress, hematological and biochemical alterations may contribute to the pathogenesis of toxoplasmosis in gerbils

A splice site mutation in the TSEN2 causes a new syndrome with craniofacial and central nervous system malformations, and atypical hemolytic uremic syndrome

Recessive mutations in the genes encoding the four subunits of the tRNA splicing endonuclease complex (TSEN54, TSEN34, TSEN15, and TSEN2) cause various forms of pontocerebellar hypoplasia, a disorder characterized by hypoplasia of the cerebellum and the pons, microcephaly, dysmorphisms, and other variable clinical features. Here, we report an intronic recessive founder variant in the gene TSEN2 that results in abnormal splicing of the mRNA of this gene, in six individuals from four consanguineous families affected with microcephaly, multiple craniofacial malformations, radiological abnormalities of the central nervous system, and cognitive retardation of variable severity. Remarkably, unlike patients with previously described mutations in the components of the TSEN complex, all the individuals that we report developed atypical hemolytic uremic syndrome (aHUS) with thrombotic microangiopathy, microangiopathic hemolytic anemia, thrombocytopenia, proteinuria, severe hypertension, and end-stage kidney disease (ESKD) early in life. Bulk RNA sequencing of peripheral blood cells of four affected individuals revealed abnormal tRNA transcripts, indicating an alteration of the tRNA biogenesis. Morpholino-mediated skipping of exon 10 of tsen2 in zebrafish produced phenotypes similar to human patients. Thus, we have identified a novel syndrome accompanied by aHUS suggesting the existence of a link between tRNA biology and vascular endothelium homeostasis, which we propose to name with the acronym TRACK syndrome (TSEN2 Related Atypical hemolytic uremic syndrome, Craniofacial malformations, Kidney failure)