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Wound healing is a well-known therapeutic challenge in animal and human medicine. This study aimed to investigate the effect of topical application of Nigella sativa (black cumin, NS) and Hypericum perforatum (St. John’s Wort, HP) on wound healing in streptozotocin (STZ) induced diabetic mice. For this aim, 25 male BALB/c mice were divided into five groups: i. Hypericum perforatum (HP), ii. Nigella sativa (NS), iii. Standard saline solution 0.9% NaCl (NSS), iv. Natural extra virgin olive oil (OL), and v. Fusidic acid-Centella asiatica cream (FM). A single dose (200 mg/kg) of STZ was intraperitoneally administered to induce type-1 diabetes. After diabetes was induced, six symmetrical excision wounds were performed on the dorsal areas of mice using a dermal biopsy punch. Wound areas were photographed every three days for 21 days, and the images were analyzed using software to achieve the daily wound closure rate in pixel values. On day one and day 21, wound tissues were dissected, total protein and hydroxyproline levels were measured by ELISA. Statistically significant differences were found in hydroxyproline change rates between the NS group with HP, NSS, and FM groups (P

Adrenomedullin, which is produced by the vascular endothelial and smooth muscle cells and cardiomyocytes, is considered to be a local factor controlling vascular tone, cardiac contractility, and renal sodium excretion. Hypertension is the most common cause of cardiovascular disorders and diseases. Exercise has beneficial effects on hypertension, but pathophysiological factors involved in exercise‐mediated amelioration of hypertension are yet to be elucidated. We hypothesized that adrenomedullin produced through exercise could play an essential role in the protection from hypertension. For this study rats were subjected to swimming training for six weeks (1‐h per day and five times each week). Meanwhile, hypertension was induced by the oral administration of L‐NAME (60 mg/kg). Here, we show that L‐NAME administration per se leads to a significant increase in mean arterial blood pressure. Notably, the 6‐week swimming exercise causes a protective effect from the development of hypertension. In addition, the rats rescued from hypertension have high mRNA levels of renal adrenomedullin while they have low levels of adrenomedullin mRNA in the aorta. The obtained data indicate that a 6‐week exercise intervention rescues rats from high blood pressure by leading to changes in adrenomedullin levels in the aorta and kidney. The increased expression of adrenomedullin in the aorta might have been a result that compensates for the hypertensive effect of L‐NAME. On the other hand, exercise probably exerts its protective effects on hypertension by increasing adrenomedullin in the kidney. A more extended exercise period may give more apparent results regarding the level of adrenomedullin in different organs.

—The antidiabetic drug empagliflozin is reported to have many cardioprotective effects. However, no studies have investigated the protective effects of empagliflozin (EMPA) in isoprenaline (ISO)-induced cardiac oxidative damage-a model mimicking the harmful effects of excess catecholamines on the heart. Therefore, in this study, we aimed to reveal the protective effect of EMPA in isoproterenol ISO-induced myocardial infarction in rats. We induced myocardial infarction by subcutaneously injecting ISO (100 mg/kg). To determine the protective effects of EMPA on the myocardial damage, we administered two different doses (10 and 20 mg/kg) by gavage for 14 days. Here we have shown that a 20 mg/kg dose of EMPA completely rescues rats from myocardial infarction by normalizing the following: elevated ST-segment, increased heart rate, decreased R amplitude, prolongation of the QT interval, and shortened RR interval. In addition, EMPA (20 mg/kg) ameliorates ISO-induced changes in serum cTnI, CK, ischemia-modified albumin (IMA), LDH, AST, ALT levels, and heart index. It improves serum lipid profile by decreasing cholesterol, triglycerides, LDL, and VLDL levels, and by increasing HDL levels. Moreover, EMPA (20 mg/kg) alleviates increased myocardial oxidative stress and inflammation by decreasing MDA, TNF-α, and IL-6 levels and increasing SOD and GPx levels. Furthermore, 20 mg/kg EMPA leads to reductions in DNA damage and apoptosis by downregulating of 8-OHdG and caspase-3 expressions. Collectively, EMPA exerts its protective effects on myocardial damage by improving oxidative stress, apoptosis, lipid profile and oxidative DNA damage in ISO-induced experimental myocardial infarction in rats.

Crosstalk between liver and skeletal muscle is vital for glucose homeostasis. Hepatokines, liver-derived proteins that play an important role in regulating muscle metabolism, are important to this communication. Here we identify apolipoprotein J (ApoJ) as a novel hepatokine targeting muscle glucose metabolism and insulin sensitivity through a low-density lipoprotein receptor-related protein-2 (LRP2)-dependent mechanism, coupled with the insulin receptor (IR) signaling cascade. In muscle, LRP2 is necessary for insulin-dependent IR internalization, an initial trigger for insulin signaling, that is crucial in regulating downstream signaling and glucose uptake. Of physiologic significance, deletion of hepatic ApoJ or muscle LRP2 causes insulin resistance and glucose intolerance. In patients with polycystic ovary syndrome and insulin resistance, pioglitazone-induced improvement of insulin action is associated with an increase in muscle ApoJ and LRP2 expression. Thus, the ApoJ-LRP2 axis is a novel endocrine circuit that is central to the maintenance of normal glucose homeostasis and insulin sensitivity.

SALMANOGLU, BERRIN/0000-0003-4344-5782; Meral, Ogunc/0000-0001-8813-4991 WOS: 000484847800005 Natural products and anti-inflammatory agents including cyclooxygenase-2 (COX-2) inhibitors which is a type of nonsteroidal anti-inflammatory drugs (NSAIDs) are highly considerable interest for the prevention of carcinogenesis. The objective of this study is to evaluate the oxidative status of colitis-associated cancer induced by azoxymethane (AOM)/dextran sulfate sodium (DSS), and the effects of COX-2 inhibitor in mice. Totally 40 mice were randomized and divided to four groups. All animals except control and Cox-2 inhibitor alone group received AOM/DSS to establish colitis-associated cancer model as reported elsewhere. COX-2 preferential inhibitor meloxicam was used to minimize side effects such as gastrointestinal hemorrhage. Meloxicam were used (5mg/kg, intraperitoneal) three times a week with meloxicam alone and AOM/DSS + meloxicam group. Superoxide dismutase (SOD), Glutathione peroxidase (GPx), Malondialdehyde (MDA) and Advanced Oxidation Protein Products (AOPP) which all of them are oxidative stress markers were measured by spectrophotometrically. The combination treatment of Meloxicam and AOM/DSS significantly increased (P

Leptin regulates both feeding and glycaemia primarily through its receptors expressed on agouti-related peptide (AgRP) and pro-opiomelanocortin-expressing (POMC) neurons; however, it is unknown whether activity of these neuronal populations mediates the regulation of these processes. To determine this, we injected Cre-dependent designer receptors exclusively activated by designer drugs (DREADD) viruses into the hypothalamus of normoglycaemic and diabetic AgRP-ires-cre and POMC-cre mice to chemogenetically activate or inhibit these neuronal populations. Despite robust changes in food intake, activation or inhibition of AgRP neurons did not affect glycaemia, while activation caused significant (P = 0.014) impairment in insulin sensitivity. Stimulation of AgRP neurons in diabetic mice reversed leptin’s ability to inhibit feeding but did not counter leptin’s ability to lower blood glucose levels. Notably, the inhibition of POMC neurons stimulated feeding while decreasing glucose levels in normoglycaemic mice. The findings suggest that leptin’s effects on feeding by AgRP neurons are mediated by changes in neuronal firing, while the control of glucose balance by these cells is independent of chemogenetic activation or inhibition. The firing-dependent glucose lowering mechanism within POMC neurons is a potential target for the development of novel anti-diabetic medicines.

Low-density lipoprotein receptor-related protein 1 (LRP1) is a member of LDL receptor family that plays a key role in systemic glucose and lipid homeostasis. LRP1 also regulates energy balance in the hypothalamus by mediating leptin’s anorexigenic action, although the underlying neurocircuitry involved is still unclear. Because GABAergic neurons are a major mediator of hypothalamic leptin action, we studied the role of GABAergic LRP1 in energy balance and leptin action using mice lacking LRP1 in Vgat- or AgRP-expressing neurons (Vgat-Cre; LRP1 loxP/loxP or AgRP-Cre; LRP1 loxP/loxP). Here, we show that LRP1 deficiency in GABAergic neurons results in severe obesity in male and female mice fed a normal-chow diet. This effect is most likely due to increased food intake and decreased energy expenditure and locomotor activity. Increased adiposity in GABAergic neuron-specific LRP1-deficient mice is accompanied by hyperleptinemia and hyperinsulinemia. Insulin resistance and glucose intolerance in these mice are occurred without change in body weight. Importantly, LRP1 in GABAergic neurons is not required for leptin action, as evidenced by normal leptin’s anorexigenic action and leptin-induced hypothalamic Stat3 phosphorylation. In contrast, LRP1 deficiency in AgRP neurons has no effect on adiposity and caloric intake. In conclusion, our data identify GABAergic neurons as a key neurocircuitry that underpins LRP1-dependent regulation of systemic energy balance and body-weight homeostasis. We further find that the GABAergic LRP1 signaling pathway modulates food intake and energy expenditure independently of leptin signaling and AgRP neurons.

Hypothalamic and extra-hypothalamic neuronal populations play important roles in the regulation of energy balance and glucose homeostasis. However, the underlying mechanisms of this control remain unclear. We have recently reported that inhibition of hypothalamic pro-opiomelanocortin (POMC) neuronal activity leads to a reduction in blood glucose levels of normoglycemic POMC-cre mice. This effect is independent of energy intake. Since hypothalamic POMC neurons project to the paraventricular nucleus of the hypothalamus (PVH) and regulate energy metabolism via melanocortin-4 receptor (MC4R), we hypothesized that changes in the activity of MC4R-expressing neurons in the PVH could alter glycemic levels. To address this, we stereotaxically injected designer receptors exclusively activated by designer drug (DREADD) viruses into the PVH of MC4R-cre mice to chemogenetically and selectively activate or inhibit these neurons. We continuously activated or inhibited these neurons by injecting clozapine-N-oxide (CNO) every 8 hours for 5 days and monitored daily blood glucose levels and energy intake. Interestingly, inhibition of MC4R-expressing neurons in the PVH leads to a significant reduction (∼ 30%) in blood glucose levels despite of increased food intake. On the other hand, blood glucose levels are significantly increased, but food intake is greatly decreased when MC4R-expressing neurons are activated. We further determined the peripheral insulin response via MC4R-expressing neurons in the PVH. We found that CNO-induced inhibition or activation of MC4R-expressing neurons did not affect serum insulin levels. These data suggest that MC4R-expressing neurons in the PVH can regulate blood glucose levels and food intake via divergent cellular mechanisms, which is independent of circulating insulin. Thus, the inhibition of MC4R-expressing neurons may be a promising target for novel antidiabetic medicines. Disclosure A.G. Uner: None. H. Lee: None. J. Han: None. R.M. Pereira: None. X. Sun: None. H. Kim: None. Y. Kim: None.

Insulin signaling is essential for the maintenance of glucose homeostasis. ROCK2 has been shown to participate in insulin signaling and glucose metabolism in cultured cell lines. However, the in vivo function of ROCK2 in muscle remains to be elucidated. To explore the physiological role of muscle ROCK2 in the regulation of whole-body glucose homeostasis and insulin sensitivity in vivo, mice lacking ROCK2 in skeletal muscle selectively (myogenic-Cre; ROCK2lox/lox) were studied. Here we show that muscle-specific ROCK1-deficient mice displayed insulin resistance, as revealed by the failure of blood glucose levels to decrease after insulin injection. However, glucose tolerance was normal in the absence of muscle-specific ROCK2. These effects were independent of changes in adiposity. To determine the mechanism(s) by which muscle-specific deletion of ROCK2 causes insulin resistance, we measured the ability of insulin to activate downstream distal pathways in skeletal muscle. Insulin-stimulated IRS-1 tyrosine phosphorylation in skeletal muscle was markedly reduced by ∼80% in myogenic-Cre; ROCK2lox/lox mice compared with control (ROCK2lox/lox) mice. Concurrently, impaired insulin-induced phosphorylation of Akt, AS160, GSK, and S6K was found when ROCK2 was specifically deleted in muscle. Of pathological significance, ROCK2 activity in skeletal muscle was markedly decreased in obese type 2 diabetic mice in response to insulin, along with an impairment of IRS-1 phosphorylation. These data suggest that ROCK2 deficiency results in systemic insulin resistance by impairing insulin signaling in skeletal muscle, at the level of IRS-1. Thus, our results identify ROCK2 as a novel regulator of glucose homeostasis and insulin sensitivity in vivo, which could lead to new treatment approaches for obesity and type 2 diabetes. Disclosure H. Kim: None. R.M. Pereira: None. A.G. Uner: None. H. Lee: None. Y. Kim: None.

The duration and intensity of exercise are significant factors in oxidative, morphological, and functional changes of the gastrointestinal tract. This study aimed to investigate the effects of both exhaustive swimming and probiotic VSL#3 on rats that had been previously trained with moderate swimming. The rats were divided into four groups labeled: control (C), probiotic (P), exercise (E), and probiotic–exercise (PE). Groups P and PE were fed with probiotic mixture VSL#3. Groups E and PE had a 5-week moderate swimming program (1 h/day for 5 days/week), followed by a 1-week exhaustive swimming program (trained like in moderate program but 3 times with 150 min resting sessions, for 5 days/week). At the end of the program, the rats were euthanized. Malondialdehyde, superoxide dismutase, catalase, and reduced glutathione levels were measured in tissue samples from the gastrocnemius muscle, heart, liver, kidney, and colon. In vitro contractile activity and histomorphology of the colon were also determined. Exercise and/or probiotic decreased the oxidative stress and also increased the level of one or more of the antioxidant enzymes in some of the organs. Probiotics had more pronounced effects on colon morphology than exercise but unexpectedly this effect was non-trophic. In the colon, the thickness of the tunica muscularis and the number of goblet cells were not affected; however, probiotic administration decreased the crypt depth and tunica mucosa thickness. Exercise increased the Emax value of acetylcholine (ACh), while decreased its sensitivity. These findings suggest that exhaustive swimming does not cause oxidative stress and that probiotic consumption improves oxidative balance in trained rats. The probiotic intake does not alter the effect of exercise on the contractile activity of the colon. Colon mucosal changes induced by probiotics are independent of exercise.

Crosstalk between liver and skeletal muscle is vital for glucose homeostasis. Hepatokines, liver-derived proteins that play an important role in regulating muscle metabolism, are important to this communication. Here we identify apolipoprotein J (ApoJ) as a novel hepatokine targeting muscle glucose metabolism and insulin sensitivity through a low-density lipoprotein receptor-related protein-2 (LRP2)-dependent mechanism, coupled with the insulin receptor (IR) signaling cascade. In muscle, LRP2 is necessary for insulin-dependent IR internalization, an initial trigger for insulin signaling, that is crucial in regulating downstream signaling and glucose uptake. Of physiologic significance, deletion of hepatic ApoJ or muscle LRP2 causes insulin resistance and glucose intolerance. In patients with polycystic ovary syndrome and insulin resistance, pioglitazone-induced improvement of insulin action is associated with an increase in muscle ApoJ and LRP2 expression. Thus, the ApoJ-LRP2 axis is a novel endocrine circuit that is central to the maintenance of normal glucose homeostasis and insulin sensitivity., Hepatokines are proteins secreted by the liver that can regulate whole body metabolism. Here the authors identify apolipoprotein J as a hepatokine that regulates muscle glucose metabolism and insulin resistance through a low-density lipoprotein receptor-related protein−2 mediated mechanism in mice.

Natural products and anti-inflammatory agents including cyclooxygenase-2 (COX-2) inhibitors which is a type of nonsteroidal anti-inflammatory drugs (NSAIDs) are highly considerable interest for the prevention of carcinogenesis. The objective of this study is to evaluate the oxidative status of colitis-associated cancer induced by azoxymethane (AOM)/dextran sulfate sodium (DSS), and the effects of COX-2 inhibitor in mice. Totally 40 mice were randomized and divided to four groups. All animals except control and Cox-2 inhibitor alone group received AOM/DSS to establish colitis-associated cancer model as reported elsewhere. COX-2 preferential inhibitor meloxicam was used to minimize side effects such as gastrointestinal hemorrhage. Meloxicam were used (5mg/kg, intraperitoneal) three times a week with meloxicam alone and AOM/DSS + meloxicam group. Superoxide dismutase (SOD), Glutathione peroxidase (GPx), Malondialdehyde (MDA) and Advanced Oxidation Protein Products (AOPP) which all of them are oxidative stress markers were measured by spectrophotometrically. The combination treatment of Meloxicam and AOM/DSS significantly increased (P< 0.05) SOD activities in mice. GPx activities were found significantly increased (P< 0.05) in Meloxicam and AOM/DSS combinations or alone. There were no differences between the control and treatment groups of MDA levels. AOPP levels of Meloxicam and AOM/DSS combination group were found higher than the other groups. Meloxicam and /or AOM/DSS treatment not caused lipid peroxidations, but increased the antioxidant enzymes and Advanced Oxidation Protein Products levels. Anti-inflamatuar ajanlar, selektif siklooksijenaz 2 inhibitörleri ve doğal moleküllerin karsinogenezin önlenmesinde kullanılması önemli araştırma ve ilgi alanını oluşturur. Bu çalışmanın amacı, farelerde azoksimetan (AOM)/dekstran sülfat sodyum (DSS) ile oluşturulan kolit ile ilişkili kanser modelinde oksidatif durum ve COX-2 inhibitörünün etkilerini araştırmaktır. Toplam 40 fare rastgele olarak dört gruba ayrıldı. Kontrol ve COX-2 inhibitörü alan gruplar hariç bütün gruplar daha önce bildirilen yönteme göre AOM/DSS uygulanarak kolit ile ilişkili kanser modeli oluşturuldu. Gastrointestinal hemoraji gibi yan etkileri minimize etmek için COX-2 seçici inhibitörü meloksikam kullanıldı. Meloksikam 5 mg/kg dozda haftada üç kez i.p. olarak uygulandı. Oksidatif stres belirteçleri süperoksit dismutaz (SOD), glutatyon peroksidaz (GPx), malondialdehit (MDA) ve ileri oksidasyon protein ürünleri (AOPP) spektrofotometrik olarak ölçüldü. Meloksikam ve AOM/DSS birlikte uygulaması farelerde SOD aktivitesine önemli düzeyde yükseltmiştir (P< 0.05). GPx aktivitesi meloksikam ve AOM/DSS tek ve kombine kullanımında önemli düzeyde artırmıştır (P< 0.05). MDA düzeyinde konrol grubu ile diğer gruplar arasında fark bulunmamıştır. AOPP seviyesi ise, meloksikam ve AOM/DSS kombine kullanıldığı grupta diğer gruplara göre daha yüksek bulundu. Meloksikam ve/veya AOM/DSS uygulaması lipid peroksidasyonuna neden olmazken, antioksidan enzim ve AOPP değerlerini yükselttiği görüldü.

Objective Hypothalamic agouti-related peptide (AgRP) and pro-opiomelanocortin (POMC) expressing neurons play critical roles in control of energy balance. Glutamatergic input via n-methyl-d-aspartate receptors (NMDARs) is pivotal for regulation of neuronal activity and is required in AgRP neurons for normal body weight homeostasis. NMDARs typically consist of the obligatory GluN1 subunit and different GluN2 subunits, the latter exerting crucial differential effects on channel activity and neuronal function. Currently, the role of specific GluN2 subunits in AgRP and POMC neurons on whole body energy and glucose balance is unknown. Methods We used the cre-lox system to genetically delete GluN2A or GluN2B only from AgRP or POMC neurons in mice. Mice were then subjected to metabolic analyses and assessment of AgRP and POMC neuronal function through morphological studies. Results We show that loss of GluN2B from AgRP neurons reduces body weight, fat mass, and food intake, whereas GluN2B in POMC neurons is not required for normal energy balance control. GluN2A subunits in either AgRP or POMC neurons are not required for regulation of body weight. Deletion of GluN2B reduces the number of AgRP neurons and decreases their dendritic length. In addition, loss of GluN2B in AgRP neurons of the morbidly obese and severely diabetic leptin-deficient Lepob/ob mice does not affect body weight and food intake but, remarkably, leads to full correction of hyperglycemia. Lepob/ob mice lacking GluN2B in AgRP neurons are also more sensitive to leptin's anti-obesity actions. Conclusions GluN2B-containing NMDA receptors in AgRP neurons play a critical role in central control of body weight homeostasis and blood glucose balance via mechanisms that likely involve regulation of AgRP neuronal survival and structure, and modulation of hypothalamic leptin action., Highlights • Glutamate action via GluN2B in AgRP neurons is required for normal body weight. • Genetic loss of GluN2B selectively in AgRP neurons reduces food intake. • Deletion of GluN2B from AgRP neurons prevents diabetes in ob/ob mice. • Glutamate action via GluN2B-NMDARs in AgRP neurons regulates neuronal survival and dendritic plasticity. • GluN2B-NMDARs in AgRP neurons are novel anti-obesity and anti-diabetes drug targets.

Day length-related alterations of several metabolic factors (glucose, leptin, insulin, and insulin-like growth factor-1 [IGF-1]), cytokines (interleukin-2 [IL-2], IL-4, IL-6, tumor necrosis factor-alpha [TNF-alpha], interferon-gamma [IFN-gamma], and lymphocyte subpopulations [CD2, CD3, CD4, CD8, CD19, natural killer (NK) cells) were evaluated in Arabian and Thoroughbred horses. Plasma glucose, leptin, IGF-1, insulin, and cytokines levels were measured on the longest day of the breeding season and on the shortest day of the nonbreeding season. Determination of lymphocyte subpopulations was performed by flow cytometry. Glucose and IL-2 levels, CD4:CD8 ratio, and NK cells showed variations that depended on the day length. Mean concentrations of plasma leptin were higher in Arabian horses than in Thoroughbred horses, whereas mean concentrations of IGF-1 and IL-2 were lower in Arabian horses. Day length-by-breed-by-gender interaction was found for insulin, IFN-gamma, and IL-4 levels. An interaction was also found between day length and gender for the expressions of CD2, CD3, CD8, and CD19. Correlations were detected between expression of CD8(+) cells and levels of TNF-alpha and IFN-gamma and between percentages of NK cells and levels of IGF-1, insulin, and glucose. Results suggested that day length and, therefore, season are important determinants or factors in modulating the immune system and could affect lymphocyte subpopulations depending on the sex of the horse. Additionally, it seems that a complex relationship in horses, as in humans and mice, exists between the immune and metabolic system, which changes according to day length, breed, and gender. (C) 2013 Elsevier Inc. All rights reserved.

A trial was conducted to investigate the effects of a dietary organic acid blend for a period of 35 days on the growth performance, intestinal histomorphology and microflora of male broiler chicks with delayed access to feed. One hundred and ninety two one day old broiler chicks (ROSS 308) were randomly distributed into 4 groups housed in four replicate pens with 12 birds in each. A 2 × 2 factorial design was implemented. Four experimental groups were formed by two levels of dietary organic acid blend supplementation (Control and Fysal Dry ® ) and two periods of delayed feed access (0 and 36 h). At 36 h after hatching body weight and body weight change of chicks were significantly (P < 0.001) lower than groups fed immediately after hatching. Delayed feed access had an adverse impact (P < 0.001) on the body weight and feed consumption of broiler chickens on days 14 and 28. Between the days 28 and 35 of the feeding period, these differences disappeared. The relative weight of gizzard (P < 0.05), pancreas (P < 0.01) on day 6 and intestine (P < 0.05) on day 10, and gizzard (P < 0.01) on day 10 were reduced in birds subjected to delayed feed access. Dietary organic acid blend inclusion increased villus length (P < 0.001), whereas delayed feed access decreased villus length (P < 0.05) and increased the incidence of epithelial degeneration and basal membrane separation of the propria mucosa of villus in the jejenum. A significant decrease in Enterobacteriaceae count (P < 0.01) was noted in organic acid blend supplemented groups on day 25. Pectoral muscle malondialdehyde levels were decreased (P < 0.01) with dietary organic acid blend supplementation at

Summary: The objective of this study was to characterize seasonal variations in serum concentrations of melatonin, testosterone, and progesterone in Arabian horses under natural photoperiodic conditions. Peripheral blood samples were collected during breeding and non-breeding seasons from mares and stallions. Serum concentrations of melatonin, testosterone, and progesterone were determined by radioimmunoassay. Serum concentrations of melatonin were greater in the non-breeding season (42.41±1.59 and 37.68±1.55 pg/ml) when compared to breeding season (23.52±1.24 and 17.22±2.10 pg/ml) in both mares and stallions, respectively. Melatonin concentrations were low but not different between the luteal and follicular phases during breeding season in cyclic mares. Mares had greater concentrations of melatonin than stallions in both breeding and non-breeding season. Mean concentrations of testosterone were greater during breeding season (6.58±0.50 ng/ml) than non-breeding season (3.64±0.48 ng/ml) in stallions. There was a negative correlation (r=-0.658, p

Moderate exercise stimulates immune system whereas intensive exercise may display immune-suppressive effect associated with the disruption of intestinal barrier. With this study, we tested the effects of moderate and intensive swimming exercises on some cytokines and oxidant variables and zonulin, an intestinal barrier marker, in rats. We also tested possible ameliorative effects of probiotic VSL#3 in both moderate and intensive exercise regimens. Twenty eight rats were randomly divided into 4 equal groups: Control-C, Probiotic-P, Exercise-E, Probiotic+Exercise-PE. The rats in group E and PE underwent moderate swimming exercise for 5 weeks. Following this period, intensive swimming exercise was performed for 5 days. The rats in group C and group P were sedentary. Probiotic VSL#3 was given to group P and PE in the water. At the end of the experiments, serum zonulin, TNF-α, IL-6, IL-10, TGF-β, MDA, and protein carbonyl levels were determined. Evidences obtained from present study indicate that moderate swimming exercise improves barrier integrity of intestine and decreases oxidative stress. During the moderate swimming experiment, probiotic VSL#3 supplementation may also improve inflammatory response. On the other hand, intensive exercise does not led changes in the inflammatory response and oxidative stress, but beneficial responses of moderate exercise on the selected parameters probably disappear due to the intense exercise-induced mild stress.

A study was carried out to evaluate the effect of dietary probiotic supplementation and stocking density on the performance, relative carcass yield, gut microflora, and stress markers of broilers. One-day-old Ross 308 male broiler chickens (n = 480) were allocated to 4 experimental groups for 42 d. Each treatment had 8 replicates of 15 chicks each. Two groups were subjected to a high stocking density (HSD) of 20 birds/m(2) and the other 2 groups were kept at low stocking density (LSD) of 10 birds/m(2). A basal diet supplemented with probiotic 1 and 0.5 g/kg of diet (in starter and finisher diets, respectively) was fed to 2 treatments, one with HSD and the other with LSD, thereby making a 2x2 factorial arrangement. There was no interaction between stocking density (LSD and HSD) and dietary probiotic (supplemented and unsupplemented) for all the variables. Feed intake and weight gain were significantly low and feed conversion ratio was poor in broilers at HSD. Dietary probiotic significantly enhanced the feed intake and weight gain in starter phase only. Dietary probiotic supplementation had no effect (P > 0.05) on total aerobs, Salmonella sp., and Lactobacilli populations in the intestines of broilers. However, HSD reduced the Lactobacilli population only (P < 0.05). Relative breast yields were significantly higher in broilers reared at LSD than HSD. Thigh meat yield was higher in broilers in HSD group compared to LSD. Dietary probiotic did not affect the relative carcass yield and weight of lymphoid organs. Serum malondialdehyde, corticosterone, nitric oxide, and plasma heterophil: lymphocyte ratio were not affected either by stocking density or dietary probiotic supplementation. In conclusion, HSD negatively affected the performance and intestinal Lactobacilli population of broilers only, whereas probiotic supplementation enhanced the performance of broilers during the starter phase only. Total aerobes, Salmonella, Lactobacilli carcass yield, and stress indicators of broilers were not affected by the dietary supplementation of probiotic under the conditions of the present study.

This case report aims to highlight the utility of the jaundice foal agglutination (JFA) test used in the prevention of neonatal foal death caused by equine neonatal isoerythrolysis. The colostrum and the serum of a Friesian mare with repeated neonatal foal deaths and the whole blood of her newborn foal were tested for 5 days with the JFA test to detect a probable incompatibility. For the first 2 days, the JFA test gave a significantly positive reaction, indicating the existence of antibodies in the colostrum of the mare against the foal's erythrocyte antigens. The foal was not allowed access to her mother's colostrum and was fed with the frozen colostrum of other mares. At day 5, JFA test results were negative, indicating the disappearance of maternal antibodies from the colostrum.

The aim of this study was to investigate the H-reflex in the forelimb and to compare the forelimb and hindlimb H-reflex results and Hmax/Mmax ratios in rabbit. For this purpose, we used 15 healthy adult female New Zealand albino rabbits. Left limbs of rabbits were used for stimulation and recording procedures using general anesthesia. Electrophysiological tests were performed using Nikolet Viking Quest (USA) 2-channel EMG equipment. The median and the tibial nerves were used to evaluate H-reflex and M-waves. Latencies of the H-reflex were almost the same in both limbs. However, M-wave latencies and amplitudes were significantly different, P-values being P < 0.001 and P = 0.001, respectively. Hmax/Mmax ratios of the forelimb (0.15 ± 0.075) and the hindlimb (0.15 ± 0.068) were similar in rabbits. One possible reason for our Hmax/Mmax ratio results may be related to interspecies differences in descending pathways from red nucleus and reticular formation to cervical and lumbar spinal segments.

Purpose: The current study aimed to reveal the therapeutic effects of a pulsed electromagnetic field and swimming exercises on rats with experimental sciatic nerve injury, which was induced with crush-type neuropathy model damage, using electrophysiological methods. Subjects: In the current study, the sample consisted of 28 adult male Wistar albino rats. Methods: The rats were randomized into four groups (n=7). Swimming exercise and PEMF (2 Hz and 0.3 MT) were applied one hour a day, five days a week, for four weeks. Electroneuromyographic (ENMG) measurements were taken on day 7. Results: When the data were evaluated, it was found that the 4 weeks of PEMF and swimming exercises led to an increase in motor conduction rates and a decrease in latency values, but the changes were not significant in comparison with the control and injury groups. The compound muscle action potential (CMAP) values of the left leg were lower in weeks 2, 3, and 4 in the swimming exercise group in comparison with the control group, although for the PEMF group, the CMAP values of the left leg reached the level observed in the control group beginning in week 3. Conclusion: PEMF and swimming exercise made positive contributions to nerve regeneration after week 1, and regeneration was enhanced. © 2014 The Society of Physical Therapy Science. Published by IPEC Inc.

A five-year-old female dog was presented with a four-week history of inappetence, weight loss, and skin and gait abnormalities. Physical examination revealed weakness, depression, incoordination of the posterior limbs, emaciation, skin and hair coat alterations, peripheral lymphadenopathy, pale mucous membranes and fever. Laboratory analysis of samples revealed abnormalities which included anaemia, neutrophilic leucocytosis, thrombocytopenia, low serum glucose and albumin concentrations, and increased serum alkaline phosphatase activity. The diagnosis was confirmed microscopically, by demonstrating the presence of Hepatozoon canis gametocytes within neutrophils in Giemsa-stained peripheral blood smears. Treatment consisting of toltrazuril and a trimethoprim-sulfamethoxazole combination was effective in relieving the clinical signs and clearing the blood of H. canis gametocytes. To the authors' knowledge, this is the first detailed clinical description of H. canis infection in a dog in Turkey.