Mehmet Eray Alcigir

Expression of p53 protein, Jaagsiekte sheep retrovirus matrix protein, and surfactant protein in the lungs of sheep with pulmonary adenomatosis:

Ovine pulmonary adenocarcinoma (OPA) is a naturally occurring cancer in sheep that is caused by the Jaagsiekte sheep retrovirus (JSRV). Because the pathologic and epidemiologic features of OPA are similar to those of bronchoalveolar carcinoma in humans, OPA is considered a useful animal model for pulmonary carcinogenesis. In this study, 3,512 lungs from various breeds of sheep were collected and macroscopically examined. OPA was identified in 30 sheep, and samples of these animals were further examined by histologic, immunohistochemical (p53 protein, surfactant protein A [SP-A], proliferating cell nuclear antigen [PCNA], JSRV matrix protein [MA]), and PCR methods. Papillary or acinar adenocarcinomas were detected microscopically in the affected areas. Immunoreactivity for p53 PAb240 was detected in 13 sheep, whereas p53 DO-1 was not detected in any of the OPA animals. PCNA immunoreactivity was recorded in 27 animals. SP-A and JSRV MA protein was immunopositive in all 30. JSRV proviral DNA was detected by PCR analysis in all of the lung samples collected from OPA animals. In addition, the pulmonary SP-A levels were increased in tumor cells. The results of this study suggest that PCNA and p53 protein expression may be useful indicators in monitoring malignancy of pulmonary tumors.

Encephalitozoonosis infection in a traditional rabbit farm with neurological manifestations

Encephalitozoon cuniculi, a zoonotic and opportunistic pathogen, can cause latent infection, especially in lagomorphs. Nowadays, this member of the Eukaryotes has drawn significant attention in the fields of veterinary and public health. The purpose of this study was to determine the seroprevalence of infection in a New Zealand rabbit farm that has a clinical history of neurological manifestations including head tilt ataxia, aggressiveness, seizures, and circling and rotational movements around the body length axis, but the general conditions and food intake were normal. Blood samples were taken from 42 breeding rabbits and researched for E. cuniculi antibodies. Out of that, 25 (59%) animals resulted positive against the pathogen. The rabbit was found to be seropositive for E. cuniculi antibodies, but negative for Toxoplasma gondii and Listeria monocytogenes antibodies. Hematological and serum biochemical parameters were measured at reference intervals. No brain tissue impairment was observed the computed tomography (CT) scan. As a result of these histopathological findings, the brain cortex presented severe neuronal degeneration and partial myelin loss, with reactive diffuse gliosis against the parasite spores was observed to the histopathology. These results are possibly related to the early stage of infection because the parasitic infestation comprise long time spreading. E. cuniculi DNA was detected on brain tissues using polymerase chain reaction (PCR), and it partial DNA sequence was identified as E. cuniculi genotype I.

The Protective effect of P7C3 against DNA and neuron damage in rat pups with congenital hypothyroidism

Congenital hypothyroidism (CH) is defined as congenital thyroid hormone deficiency. The aim of this study was to examine the DNA and neuron damage in rat pups with CH and to evaluate the beneficial effects of 3.6-Dibromo-α-[(phenylamino) methyl]-9H-carbazole-9-ethanol (P7C3). Rat pups were assigned to four groups as Group 1: CH, Group 2: CH treated with P7C3, Group 3: CH treated with P7C3 and L-thyroxine, and Group 4: control group. Plasma 8-(OH)DG and neuron-specific enolase (NSE) concentrations were determined in all groups. For histopathological examinations haematoxylin-eosin staining was applied. Increased NSE concentrations were found in the CH group compared to the control group. The 8-(OH)DG concentrations were found to be higher in Group 2 and Group 3 than in the control group. Neuronal degenerations localized in the hippocampus and brain cortex were found in histopathological examinations in Group 1. The distribution of neuronal degeneration was less in Group 2 and Group 3 than Group 1 and lesser in Group 3 than in Group 2. DNA damage might have a role in CH pathogenesis. P7C3 compounds have a protective effect in CH.

Neuroprotective activity of cannabinoid receptor-2 against oxidative stress and apoptosis in rat pups having experimentally-induced congenital hypothyroidism

In this study, it was aimed to show the cannabinoid receptor‐2 (CB2) role, which is a part of neuroprotective endocannabinoidal system, against increasing nitric oxide synthetase (iNOS, eNOS) levels and the apoptotic activity (caspase‐3, caspase‐9, and DNA in situ fragmentation) within the postnatal critical period in pups of pregnant rats with artificially induced maternal thyroid hormone (TH) deficiency. Each of the three groups established comprised one male and two female rats, and they were coupled. Their pups were used. In the first two groups, the mothers were treated with 0.025% MMI during the critical period of the pregnancy. In the third group, as the control group, the mothers and pups were not treated. Euthanasia was applied to the pups in Group I on Day 10, and to the pups in Groups II and III on Day 21. In the biochemical analyses, total T4 levels of both mothers and pups in Group I and II were found to be lower than those of the control group. Histopathologically, karyopyknosis in migrating neurons and demyelinization were observed in both groups. Caspase‐3 and −9 expressions and TUNEL reactions showed parallelism to these findings. eNOS and iNOS activities were also increased in Groups I and II. CB2 receptor activity was observed in the fore and mid brain in Group I, and in the whole brain in Group II. In conclusion, apoptosis was triggered via oxidative stress in hypothyroid pups. Accordingly, neuroprotective activity of CB2 receptors were motivated spontaneously to resist to CNS lesions during the first 3 weeks of postnatal period.

Apoptosis in natural rabies virus infection in dogs

Abstract Introduction: In the present study apoptosis was investigated in the cornu ammonis and cerebellum of 10 dogs naturally infected with rabies virus. Diagnosis of rabies was based on the results of fluorescent antibody staining and experimental inoculation. Material and Methods: The paraffin tissue sections were stained with haematoxylin and eosin, avidin-biotin complex peroxidase (ABC-P), and terminal deoxynucleotidyl transferase biotin-dUTP nick end-labelling (TUNEL) methods. Results: Histopathological examination revealed encephalomyelitis of varying severity and the presence of Negri bodies. Dense rabies antigens were determined in the motor neurons with ABC-P method. On the other hand, Bcl-2 protein and Bax protein gave positive reaction in seven and five cases, respectively. TUNEL staining demonstrated very marked apoptotic changes in the nuclei of neurons localised deep in the substantia alba of the cerebellum. Similar changes were also determined in perivascular mononuclear cells and glia cells within the substantia alba. No apoptopic changes were found in the motor neurons of the cornu ammonis. Conclusion: The absence of apoptotic changes in the neurons was considered to be the consequence of the necrotic changes that developed in these neurons.