Expression and function of TLR2, TLR4, and Nod2 in primary canine colonic epithelial cells

The gut maintains a delicate balance between the downregulation of inflammatory reactions to commensal bacteria and the capacity to respond to pathogens with vigorous cellular and humoral immune responses. Intestinal epithelial cells, including colonic epithelial cells (CECs) possess many properties of cells of the innate immune system, in particular the ability to recognize and respond to microbial antigens. Recognition of microorganisms by CECs is based upon their recognition of signature molecules, called microbe-associated molecular patterns (MAMP), by pattern recognition receptors (PRR) including membrane toll-like receptors (TLR) and cytosolic Nod2, an intracellular counterpart of TLRs. The purpose of this study was to determine whether primary CECs from normal dogs express a functional TLR2, TLR4, and Nod2 and whether they are regulated by inflammatory mediators. We show that canine primary CECs express TLR2, TLR4, and Nod2 that can be modulated in response to their respective MAMPs, lipopolysaccharides (LPS) or peptidoglycans (PGN). Furthermore, we demonstrate that these receptors are functional as evidenced by the induction of cytokine gene expression in response to LPS or PGN.     

Increased excitability and metabolism in pilocarpine induced epileptic rats: Effect of Bacopa monnieri

We have evaluated the acetylcholine esterase and malate dehydrogenase activity in the muscle, epinephrine, norepinephrine, insulin and T3 content in the serum of epileptic rats. Acetylcholine esterase and malate dehydrogenase activity increased in the muscle and decreased in the heart of the epileptic rats compared to control. Insulin and T3 content were increased significantly in the serum of the epileptic rats. Our results suggest that repetitive seizures resulted in increased metabolism and excitability in epileptic rats. Bacopa monnieri and Bacoside-A treatment prevents the occurrence of seizures there by reducing the impairment on peripheral nervous system.     

Acute Effects of Pomegranate Extract on Postprandial Lipaemia, Vascular Function and Blood Pressure

We investigated whether a test drink enriched in pomegranate polyphenols, consumed with a high-fat meal, can reduce postprandial lipaemia and improve vascular function and blood pressure compared to placebo. Nineteen young, healthy men completed a randomized, controlled crossover trial. The active drink (containing a pomegranate extract) was consumed during a high-fat meal (ET-DUR) or 15 min before (ET-PRE), and the placebo drink (no pomegranate extract) was consumed during the high-fat meal (CONTROL). Postprandial lipaemia was assessed by venous plasma TAG 0–2 h, and capillary plasma TAG 0–4 h. Blood pressure and digital volume pulse, to measure reflection index (DVP-RI) and stiffness index (DVP-SI), were monitored at baseline, 2 and 4 h. There was no inhibition of postprandial lipaemia by the active drink compared to CONTROL. ET-PRE caused a greater increase in the venous plasma TAG at 2 h compared to CONTROL and ET-DUR (treatment effect P?=?0.001). The incremental area under the curve 0–4 h for capillary plasma TAG was not significantly different between treatments. Systolic blood pressure (SBP) increased in the ET-PRE and ET-DUR groups to a lesser extent than the CONTROL group (treatment effect P?=?0.041). There were no treatment effects for DVP-RI, DVP-SI or diastolic blood pressure. In conclusion, the consumption of a single drink containing ET-rich pomegranate extract did not decrease postprandial plasma TAG concentrations, but suppressed the postprandial increase in SBP following the high-fat meal.     

Effects of hydrochloric,acetic, butyric,and propionic acids on pathogenesis of ulcers in the nonglandular portion of the stomach of horses

OBJECTIVE: To identify the pathogenesis of gastric ulcers by comparing injury to the nonglandular gastric mucosa of horses caused by hydrochloric acid (HCl) or volatile fatty acids (VFAs). SAMPLE POPULATION: Gastric tissues from 30 horses. PROCEDURE: Nonglandular gastric mucosa was studied by use of Ussing chambers. Short-circuit current (Isc) and potential difference were measured and electrical resistance calculated for tissues after addition of HCl and VFAs to normal Ringer's solution (NRS). Tissues were examined histologically. RESULTS: Mucosa exposed to HCl in NRS (pH, 1.5) had a significant decrease in Isc, compared with Isc for mucosa exposed to NRS at pH 4.0 or 7.0. Also, exposure to 60mM acetic, propionic, and butyric acids (pH, 4.0 or 1.5) caused an immediate significant decrease in Isc. Recovery of sodium transport was detected only in samples exposed to acetic acid at pH 4.0. Recovery of sodium transport was not seen in other mucosal samples exposed to VFAs at pH < or = 4.0. CONCLUSIONS AND CLINICAL RELEVANCE: Acetic, butyric, and propionic acids and, to a lesser extent, HCl caused decreases in mucosal barrier function of the nonglandular portion of the equine stomach. Because of their lipid solubility at pH < or = 4.0, undissociated VFAs penetrate cells in the nonglandular gastric mucosa, which causes acidification of cellular contents, inhibition of sodium transport, and cellular swelling. Results indicate that HCl alone or in combination with VFAs at gastric pH < or = 4.0 may be important in the pathogenesis of gastric ulcers in the nonglandular portion of the stomach of horses.     

Origin of postcranial skeletal pneumaticity in dinosaurs

The sauropodomorph Thecodontosaurus caducus and theropod Coelophysis bauri are the earliest known dinosaurs with postcranial skeletal pneumaticity. In both taxa, postcranial pneumatic features are confined to the cervical vertebrae. This distribution of pneumaticity in the skeleton is most consistent with pneumatization by diverticula of cervical air sacs similar to those of birds. Other hypotheses, including pneumatization by diverticula of the lungs, larynx and trachea, or cranial air spaces, are less well‐supported.     

Canine hepatozoonosis: comparison of lesions and parasites in skeletal muscle of dogs experimentally or naturally infected with Hepatozoon americanum.

We report previously undescribed, early lesions in skeletal muscle of dogs experimentally infected with Hepatozoon americanum by ingestion of laboratory-reared, infected Amblyomma maculatum. The earliest muscle lesion was recognized at the first interval of examination 3 weeks following exposure. The lesion consisted of a large, modified host cell whose cytoplasm frequently contained a demonstrable parasite. In skeletal muscle, the cell was consistently located between muscle fibers or in loose connective tissue adjacent to those fibers. Evidence suggesting that the parasite arrives in muscle and other tissue within the host cell cytoplasm is presented. Mucopolysaccharide encystment of the host cell, absent at this early stage, was acquired gradually and approached maximal development 26 weeks post exposure. Completion of the asexual cycle as evidenced by the presence of parasites entering vascular lumens within granulomas and also by the presence of gamonts in peripheral blood leukocytes, occurred within 28-32 days postexposure. Progression of the parasite cycle from meront to passage of zoites into vessel lumens of granulomas can occur in 11 or fewer days. The density with which parasitic lesions occur in one named skeletal muscle compared to other named muscles, although somewhat variable, was not significantly different in either experimentally induced or natural infections. The distribution of developmental stages of the parasite/lesion in four experimental infections (969 lesions) is compared with those in eight dogs with natural infections (557 lesions).