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Mouse fetuses generated by in vitro embryo culture and embryo transfer exhibit impaired lung development, altered composition of pulmonary epithelial cells associated with downregulation of several genes involved in lung development and toll-like receptor (TLR) signaling pathway. The aims of the present study were to determine the expression of all TLRs and to examine if the expression of TLRs, along with genes involved in TLR signaling pathway, is altered in the lung tissue of mouse fetuses generated through embryo culture and embryo transfer. Two experimental (EGs) and one control (CG) group were included in the study. Embryos cultured at 5% CO2-95% air for 95 h or less than 24 h were transferred to pseudo-pregnant females to obtain fetuses comprising EGin vitro (n = 18) and EGin vivo (n = 18), respectively. Fetuses obtained from naturally ovulating females on day 18 of pregnancy served as the CG (n = 18). Western blot and immunohistochemistry were used to determine the expression of TLR proteins. The expression of transcripts encoding TLRs, and the genes involved in TLR signaling pathway (Lbp, Pik3r1, Pik3cb, Nfkbia, and Fos), was determined using qRT-PCR. While all TLRs were expressed by cells lining the bronchial/bronchiolar epithelium of lung tissues in all groups, some of the TLRs were expressed in a specific pattern. When compared to CG, the expression of transcripts encoding TLR-2, -3, -4, -5, -7, -8, -9, -12, -13, Lbp, Pik3r1, Pik3cb, Nfkbia, and Fos was significantly downregulated in both EGs. It appears that stress imposed on embryos at preimplantation stages of development is associated with downregulation of TLRs, along with some of the genes involved in TLR signaling pathway, in the lung tissue during the perinatal period. It remains to be determined if downregulation of TLRs, along with the genes involved in TLR signaling pathway, has any functional consequences in the adult lung tissue.

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 aim of the present study is to investigate the possible effects of acute blood loss (1% of body weight) on electrocardiogram (ECG) in male and female Swiss albino mice. Anesthesia was maintained with the ketamine-xylazine combination. The tail was cut using a scalpel blade and blood at a ratio of 1% body weight was collected in capillary tubes. ECG recording was done by using the standard lead II. P and T waves, intervals of PQ, QT, and RR, and QRS complex were measured after all ECG was recorded. The amplitude of P and QRS waves were significantly higher in males than that of females (P

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.

WOS: 000431511000003, PubMed ID: 29624513, Classical risk factors such as cholesterol and lipoproteins are currently not sufficient to explain all physiopathological processes of obesity-related vascular dysfunction as well as atherosclerosis and arteriosclerosis. Therefore, the discovery of potential markers involved in vascular dysfunction in the obese state is still needed. Disturbances in hemostatic factors may be involved in the developmental processes associated with obesity-related cardiovascular disorders. We hypothesized that alterations of several hemostatic factors in the obese state could correlate with the function and morphology of the aorta and it could play an important role in the development of vascular dysfunction. To test this, we fed mice with a high-fat diet for 18 weeks and investigated the relationships between selected hemostatic factors (in either plasma or in the liver), metabolic hormones and morphology, and ex-vivo function of the aorta. Here, we show that 18-week exposure to a high-fat diet results in a higher plasma fibrinogen and prolonged prothrombin time in diet-induced obese mice compared to the controls. In addition, liver levels or activities of FII, FX, activated protein C, AT-III, and protein S are significantly different in diet-induced obese mice as compared to the controls. Curiously, FII, FVIII, FX, activated protein C, PTT, and protein S are correlated with both the aorta histology (aortic thickness and diameter) and ex-vivo aortic function. Notably, ex-vivo studies revealed that diet-induced obese mice show a marked attenuation in the functions of the aorta. Taken together, aforementioned hemostatic factors may be considered as critical markers for obesity-related vascular dysfunction and they could play important roles in diagnosing of the dysfunction., Adnan Menderes University [VTF-12006, VTF-14027], A.G.U. and M.B. designed research; C.U., A.G.U., H.U., M.A.E., E.K., M.E., H.A., F.B., and L.T. performed research; C.U., A.G.U., M.B., and L.T. analyzed data; C.U. and A.G.U. wrote the paper with comments from all of the authors. This study was supported by the grants (VTF-12006 and VTF-14027 to AGU and MB, respectively) of Adnan Menderes University. We thank Dr Murat Boyacioglu, Dr Hande Sultan Yalinkilic, Dr Omer Sevim, and Biologist Necati Gunay for technical assistance. We also gratefully thank Ms. Tze-Min Lin for correcting the English grammar mistakes of the manuscript.

DOGAN, GOKSEL/0000-0002-4583-3140; CINAR KUL, Bengi/0000-0002-8955-0097, WOS: 000510017700006, PubMed: 31504752, In vitro culture under atmospheric oxygen puts embryos under oxidative stress and impairs preimplantation development. However, to what extent this process alters the redox balance in the perinatal period remains largely unknown. the aim of the present study was to examine if the redox balance is altered in the lung tissue of fetuses generated through transfer of mouse embryos exposed to atmospheric oxygen at different stages of development and to determine if this has any effect on lung morphogenesis and gene expression. Two experimental groups (EGs) were generated by transferring in vitro- and in vivo-derived blastocysts to pseudo-pregnant females. in vivo-developed fetuses served as control. Enzymatic/nonenzymatic antioxidants, malondialdehyde (MDA) levels, total antioxidant capacity, stage of lung development and gene expression were evaluated on day 18 of pregnancy. Weight of fetuses was significantly less in both experimental cohorts (ANOVA, P < 0.001 versus control), associated with delayed lung development, higher amounts of MDA (ANOVA, P < 0.001 versus control) and altered expression of several genes in oxidative stress/damage pathways. Evidence gathered in the present study indicates that pre-implantation stress caused by culture under atmospheric oxygen, even for a short period of time, leads to fetal growth restriction, impaired lung development and redox balance along with dysregulation of several genes in oxidative stress response. Absence of an EG in which in vitro embryo culture was performed at 5% oxygen and the use of genetically heterogeneous F2 fetuses are the limitations of the study. in any case, the long-term impact of such dramatic changes in the developmental programming of resulting fetuses warrants further investigations., Scientific and Technological Research Council of Turkey (TUB.ITAK)Turkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [112O259], This work was funded by the Scientific and Technological Research Council of Turkey (TUB.ITAK, Project no: 112O259).

SUMMARY A study was conducted to determine the effects of a dietary probiotic (a commonly used feed additive) and a posthatch holding time (0, 12, 24, and 36 h posthatching) on the growth performance, blood parameters, and intestinal microflora of male broiler chicks. The study used a 2 × 4 factorial arrangement of treatments. Eight experimental groups were formed by 2 levels of dietary probiotic supplementation [control and a dietary probiotic (Protexin), 0.5 kg/ ton] and 4 posthatch holding times (0, 12, 24, and 36 h). There were 4 replications for each treatment group, with each replication consisting of 20 birds. Depending on the time interval between arrival at the experimental site and feeding, holding chicks before free access to water and feed had a negative effect (P 0.05). A significant decrease in d 10 intestinal pH (P < 0.05) was noted in groups with probiotic supplementation (6.59 vs. 6.42). The number of lactobacilli in control chicks was significantly higher (7.96 vs. 7.13 and 7.28) than that in groups with a posthatch holding time before feeding on d 10 (P < 0.01). In brief, exposure to delayed feed access impaired early growth performance and microbiological measures in the gastrointestinal tract of fast-growing broiler chicks, and supplementing broiler chicks with a dietary probiotic was not an effective tool for ameliorating these negative effects.

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.

Neutrophils are the major cellular immune components in response to bacterial infections. Neutrophil enzymes are important in invasion, inflammation, and infection processes. In order to understand the basic effects of protein malnutrition on neutrophils we studied matrix metalloproteinases 8 and 9 (MMP-8 and MMP-9) production in severe quantitative and qualitative protein malnutrition in rats. Wistar rats (2 months old) were divided into four groups each with three subgroups and fed various protein-containing diets (24% protein, 20% gelatin-containing and N-free) for 7, 14, 21, and/or 28 days. Neutrophil enzyme expression was determined by Western blotting. Leukocytes decreased significantly due to malnutrition (p = 0.001) whilst the percentage of neutrophils increased (p = 0.02) in protein-deprived groups. Neutrophils of malnourished rats produced lower levels of MMP-8 at early stages of protein deprivation with an increase in the following weeks. MMP-9 production by neutrophils from N-free diet fed animals was highest after one week. Serum MMP-9 levels decreased in the qualitative but not in the quantitative protein malnutrition groups. Results suggest that neutrophils might be important in reuse of body cell proteins during fasting or malnutrition conditions and dietary manipulation might have profound effects on MMP-8 and -9 production in rats.

Objective: Moderate food restriction, such as a 20-40% reduction of the ad libitum intake without causing malnutrition, delays or prevents morphological and functional changes related to aging and overnutrition. This study was performed to evaluate the effects of moderate to severe food restriction (20%, 40%, and 60% of ad libitum intake) for 28 days on some bacterial groups in the cecum and certain biochemical variables in male Sprague Dawley rats. Materials and methods: One group was allowed free access to food (control), while the others were given food restricted to 20%, 40%, and 60% of the ad libitum consumption for 28 days. At the end of the experiment control and food-restricted animals were sacrificed and cecum weight, pH of cecal contents, and counts of total anaerobes, total aerobes, lactobacilli, and coliform bacteria in cecal contents were determined. Metabolic effects of food restriction were evaluated by analyzing some biochemical parameters in plasma and serum. Results : The effect of 60% restriction was severe; three animals died before the 28th day of experiment in this group. In general, biochemical variables did not change in 20% and 40% food-restricted groups. Although lactobacilli counts of the 20% and 40% restricted groups were significantly increased when compared with the 60% restricted group, none of the three groups were differed from the control group. Furthermore, the total aerobe bacteria counts of the 20% restricted group were significantly lower than those of the 60% restricted group. Conclusion: The results of this study suggest that restriction of food by 20% and 40% may affect cecal microbiota beneficially without causing considerable changes in the metabolism of the host, while 60% restriction causes dietary stress. Key words: food restriction, starvation, malnutrition, rat, cecal microbiota, biochemical variables

Objective : Protein deficiencies are common conditions around the world. They may affect organisms directly or indirectly by changing their normal microbiota. This study aimed to determine time-dependent effects of the quality and quantity of dietary proteins on intestinal microbiota. Materials and methods : Sixty young male Wistar rats were used in four experiments with durations of 1, 2, 3 or 4 weeks, respectively. In each experiment 15 animals were divided into 3 equal groups and given either a complete rat chow (controls) or semi-synthetic diets containing almost no protein (N-free) or 20% gelatin ad libitum . Total aerobes, Enterobacteriaceae, coliform, and lactobacilli colonies were counted in cecal contents. Results : Generally, total aerobic bacteria and lactobacilli were most affected by protein malnutrition in all experiments. Both types of protein malnutrition decreased the numbers of total aerobic bacteria in all experiments except for the gelatin-fed animals in experiment I. Mean lactobacilli counts also decreased in both malnutrition groups but the decrease in lactobacilli count was more severe in N-free groups than in gelatin-fed groups. Conclusion: These results suggest that the effects of dietary proteins on cecal bacteria are dependent on the type of bacteria and partly time-dependent. Key words: Dietary protein, malnutrition, cecum, microbiota, time, rat