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The objective of the present study was to determine the prevalence of postpartum dysgalactia syndrome (PDS) and associated clinical signs in farmed sows in the Republic of Macedonia (RM) in the first 12-24 h postpartum. A total of 202 sows of different parity and different genetic lines from 5 pig farms in RM were included in the study. The sows and their litters were clinically examined 12-24 hours after farrowing. Postpartum dysgalactia syndrome was detected in 23.3% of all clinically examined sows, while prevalence between farms ranged from 14.8% to 38.1%. Altered piglet’s behavior was the most frequent clinical pattern observed in 68.1% of the PDS–affected (PDSA) sows. Regarding the clinical signs in PDSA sows detected among farms, significant differences were observed in the altered piglet’s behavior (p

The aim of this study is to compare the results from the histopathology and the immunohistochemical method in the diagnostic of Porcine circovirus type 2 (PCV2) infection in pigs. The circovirus infection is a pig disease that is caused by a small, spherical, nonenveloped virus with a single stranded DNA genome which is spread throughout the pig industry worldwide. The circovirus is the etiological agent of a several pig diseases which today are thought to be the cause of the greatest economical loses in pig production. The most important of these diseases is the PMWS (post-weaning multisystemic wasting syndrome). In this article we have performed an investigation of four farms on which there had been a previous clinical diagnosis of the Post-weaning multisystemic wasting syndrome. The examination was performed on thirty pigs from these farms, from two to five months old, which had the most severe symptoms of the disease. Necropsy, histopathology and immunohistochemical diagnostic methods were performed. The most significant necropsy findings were the enlarged lymph nodes (especially the inguinal, mediasinal and the mesenteric lymph nodes). The main histopathological changes were located in the lymphatic organs presented by B and T lymphocyte depletion and increase in the number of the macrophages. PCV2 antigen and nucleic acid were detected in almost all of the examined tissues. The examination showed that the histopathological and immunohistochemical methods provide complementary results in diagnosing PCV2 in pigs.

Considering the preexisting influence of the process of natural aging on antioxidant enzymes activity and the level of lipid peroxidation, the age of the rats at which D-galactose (D-gal) treatment is started could strongly impact the development of D-gal induced senescence. To evaluate this, we subjected 1, 3 and 15 months old rats to D-gal treatment in parallel with having appropriate placebos (0.9 % saline). Our results showed elevated glutathione peroxidase (GPx) activity and no significant changes in superoxide dismutase (SOD), catalase (CAT) and glutathione reductase (GR) activity or malondialdehyde (MDA) levels in relation to natural aging. In mature and aged senescent livers we observed positive correlation between increased ratio R=SOD/(GPx+CAT) and increased MDA concentration. MDA levels seemed to correlate positively with the age of the animals at which D-gal treatment had started. In the case of 3 and 15 months old rats there was D-gal induced decrease in SOD and GR activity, but this effect of the treatment was not observed in 1 month old rats. Our results imply that the changes in the antioxidant enzyme activities are not only under the influence of the D-gal overload, but also depend on the developmental stage of the rats. According to our results, with regard to enzymatic antioxidant capacity and the level of lipid peroxidation, the best age for induction of senescence is somewhere after the third month.

To investigate early events possibly related to the development of heat shock, we examined whether inflammatory-(interleukin-6, tumor necrosis factor α and 15-keto-13,14-dihydro-PGF 2α ) and peroxidative-(8-iso-PGF 2α and malondialdehyde) markers are altered during acute heat exposure and aging. We also studied the relationships between inflammatory and peroxidative markers in these settings. In order to prevent these reactions developed as a consequence of the conditions mentioned above, we tested the effects of α-tocopherol. Our results demonstrated that 15-keto-13,14-dihydro-PGF 2α and malondialdehyde in the liver were altered during acute heat exposure in the young and middle-aged rats and could be predicted by changes in the levels of circulatory cytokines. Regardless of age, the supplementation with α-tocopherol prevented changes in the plasma cytokine levels and 15-keto-13,14-dihydro-PGF 2α and malondialdehyde levels in the liver, during acute heat exposure. This study notably emphasized the ability of α-tocopherol to prevent different heat induced mechanisms, involved in induction of inflammatory or peroxidative reactions.

Background Oxidative stress and inflammation are involved in the pathogenesis of paracetamol-induced renal damage. This study examines the relationship between 8-iso-prostaglandin F2α (8-iso-PGF2α) and platelet activation as well as the relative contribution of the pro-inflammatory markers interleukin (IL)-1β and tumor necrosis factor-α (TNF-α) in enhanced 8-iso-PGF2α biosynthesis, as a complementary onset during analgesic nephropathy induced by chronic treatment with paracetamol. The protective effects of vitamin C on the aforementioned settings are also investigated. Methods Analgesic nephropathy was induced in Wistar rats. Renal function markers and the activity of antioxidant enzymes were determined spectrophotometrically. Immunoassays were used to measure the pro-inflammatory markers and the markers of lipid peroxidation and platelet activation. Results The chronic treatment with paracetamol led to renal dysfunction, represented by the elevation of plasma urea and creatinine and the decline in the enzymatic antioxidant status, but did not cause a significant increase in TNF-α and IL-1β. The paracetamol-induced lipid peroxidation and enhanced production of 8-iso-PGF2α was not sufficient to cause changes in platelet activation represented by the level of 11-dehydro thromboxane B2. Conclusions Our results suggest that oxidative stress cannot circumvent the need of stimulation by circulatory cytokines in order to induce inflammatory response and changes in platelet activation during analgesic nephropathy. Vitamin C proved to be beneficial in restoring the renal function markers to normal, increasing the renal enzymatic antioxidant potential, inhibiting lipid peroxidation, and lowering cytokine production and 11-dehydro thromboxane B2 excretion. The observed effects of vitamin C offer support for its potential use as protective treatment in cases of chronic paracetamol overdose.

Results. Starting from 2005 until 2009 a total of 559.476 cattle serum samples, from different villages across Macedonia, were collected and sent to the Faculty of Veterinary Medicine – Skopje, for testing for brucellosis. Seroprevalence in some epizootiological areas ranges from 0.1% up to 22.2%. According to the results, obtained with this study, the mean seroprevalence of cattle brucellosis in Macedonia for the last 5 years was estimated at 0.83% (ranging from 0.17% to 2.78%).

To investigate the impact of acute heat exposure on maintenance of redox homeostasis and antioxidant balance related to aging, we have determined the GSH levels in the liver and kidney, and the activity of antioxidant enzymes in the same organs from Wistar rats at two different ages, 35 days and 18 months. The animals were housed individually in a special heated chamber maintaining a constant temperature of 40±0.5 °C. The results showed that the level of endogenous GSH was significantly lower in aged than in young animals. In general, the activity of antioxidant enzymes in investigated tissues displayed an age-dependent decline. Indeed, we found unchanged CAT activity and decreased GPx activity with age. On the other hand acute heat exposure led to disproportion between peroxide metabolizing enzymes (CAT, GPx) and GR, thus promoting H 2 O 2 accumulation and prooxidative state in the liver of young animals. The results for the impact of l -2-oxothiazolidine-4-carboxylate in combined stress model suggested that in spite of restore levels of GSH, the restoration of oxido-reductive balance might have only been partial due to irreversible alterations in antioxidant enzymes set by acute heat exposure and aging. Interestingly, young animals appeared to be more sensitive to the supplementation of the l -2-oxothiazolidine-4-carboxylate, likely because of the more extensive increase of GSH observed in young l -2-oxothiazolidine-4-carboxylate treated animals.

To investigate the role of mitochondrial antioxidant capacity during increased susceptibility to heat accompanied by the aging, young and aged Wistar rats were exposed on heat for 60 min. After heat exposure, hepatic and brain mitochondria were isolated. Our results revealed changes in antioxidant enzyme activities in liver and brain mitochondria from young and to a greater extent in aged rats. Our measurements of MnSOD, GPx and GR activity indicate greater reactive oxygen species production from the mitochondria of aged heat exposed in comparison to young heat exposed rats. Also in the aged rats, the effect of α-tocopherol treatment in the prevention of oxidative stress occurred as a result of heat exposure, is less pronounced. Taken together, our data suggest that mitochondria in aged rats are more vulnerable and less able to prevent oxidative changes that occur in response to acute heat exposure.