Alcohol ingestion before burn injury decreases splanchnic blood flow and oxygen delivery

Recent studies from our laboratory have shown that alcohol and burn injury impair intestinal barrier and immune functions. Although multiple factors can contribute to impaired intestinal barrier function, such an alteration could result from a decrease in intestinal blood flow (BF) and oxygen delivery (DO2). Therefore, in this study, we tested the hypothesis that alcohol ingestion before burn injury reduces splanchnic blood flow and oxygen delivery. Rats (250 g) were gavaged with alcohol to achieve a blood ethanol level in the range of 100 mg/dl before burn or sham injury (25% total body surface area). Day 1 after injury, animals were anesthetized with methoxyflurane. Blood pressure, cardiac output (CO), +/-dP/dt, organ BF (in ml.min(-1).100 g(-1)), and DO2 (in mg.ml(-1).100 g(-1)) were determined. CO and organ BF were determined using a radioactive microsphere technique. Our results indicate that blood pressure, CO, and +dP/dt were decreased in rats receiving a combined insult of alcohol and burn injury compared with rats receiving either burn injury or alcohol alone. This is accompanied by a decrease in BF and DO2 to the liver and intestine. No significant change in BF to the coronary arteries (heart), brain, lung, skin, and muscles was observed after alcohol and burn injury. In conclusion, the results presented here suggest that alcohol ingestion before burn injury reduces splanchnic BF and DO2. Such decreases in BF and DO2 may cause hypoxic insult to the intestine and liver. Although a hypoxic insult to the liver would result in a release of proinflammatory mediators, a similar insult to the intestine will likely perturb both intestinal immune cell and barrier functions, as observed in our previous study.     

Changes in the mucosa of the duodenum and stomach as a result of experimental duodenal ulcers and vagotomy

By means of the transmissive and scanning electron microscopy methods and radioautography, structure of mucous membrane of the stomach and duodenum has been studied under experimentally induced duodenal ulcers before and after vagotomy during various time. The vagotomy results in accelerated healing of the ulcer defect. This is connected with an increased proliferative activity in the crypta cells, however, this is accompanied with deceleration of their differentiation. Under the duodenal ulcers the amount of chief and parietal cells increases in the gastric mucous membrane, this depends on gastrostasis produced by stenosis of the pylorus. At vagotomy the amount of the chief and parietal cells in the fundal glands of the mucous membrane decreases; this is accompanied with a lowered secretory activity.     

Action of neurotensin on size, composition, and growth of pancreas and stomach in the rat

Since the gastrointestinal peptide neurotensin has a stimulatory effect on the secretion of the exocrine pancreas and an inhibitory effect on secretion and motility of the stomach, we investigated whether chronic parenteral administration of neurotensin would affect pancreatic and gastric growth. We therefore infused synthetic neurotensin subcutaneously (dose, 43 and 282 pmol X kg-1 X min-1) in 20 Wistar rats for 2 weeks using Alzet osmotic minipumps and compared pancreatic weight, DNA, RNA, protein, lipase, amylase, pancreatic polypeptide and insulin with these parameters in 10 control rats from the same litter with subcutaneously implanted plastic cylinders approximately the size of the minipumps. In another experiment, synthetic neurotensin (836 pmol X kg-1) was injected intraperitoneally three times a day for 3 days in 12 rats. Thereafter, we measured pancreatic DNA and in vitro incorporation of [3H]thymidine into pancreatic DNA. These effects were compared with the actions of caerulein and normal saline. Long term infusion of the high neurotensin dose induced an increase of pancreatic weight (control: 0.87 g, neurotensin: 1.02 g) and of DNA (control: 2.5 micrograms; neurotensin: 3.5 micrograms) and pancreatic polypeptide (control: 2.4 ng; neurotensin: 7.4 ng) contents, whereas pancreatic protein, RNA, amylase and lipase contents were not stimulated. In relation to DNA, these parameters even were significantly depressed. Insulin remained unchanged. Intraperitoneal injection of neurotensin induced an increase of pancreatic DNA content and stimulated [3H]thymidine incorporation into DNA (control: 11 000 dpm/g; neurotensin: 15 800 dpm/g pancreas). Moreover, long-term neurotensin infusion with the high dose led to a rise in protein concentration and an increase in the thickness of the gastric antrum; antral DNA concentration was insignificantly stimulated. Parenteral neurotensin in the doses and at the times administered, led therefore, to hyperplasia of the pancreas and induced growth of the gastric antrum. It is concluded that neurotensin can act as a trophic factor on pancreas and gastric antrum of the rat. It remains to be determined whether this represents a physiological effect of neurotensin.     

TGF-β binding in human Wharton’s jelly

Our previous study reported that TGF-β may be isolated from human Wharton’s jelly (WJ) in a form of soluble, high molecular complex(es). We decided to study the effect of extracellular matrix degradation and reduction of disulphide bridges reduction on the release of TGF-β from WJ. The WJ prepared from the umbilical cords of newborns delivered at term by healthy mothers was homogenised and treated with hyaluronidase, collagenase, heparinase, chondroitinase and β-mercaptoethanol, the resulting extracts were then submitted to TGF-β immunoassay and SDS/PAGE followed by Western immunoblotting. The effect of metalloproteinase activation on TGF-β was also studied. Pre-treatment of WJ homogenates with hyaluronidase or collagenase markedly increased the extractability of TGF-β, but did not dissociate the complexes. In contrast, the action of β-mercaptoethanol resulted in the release of free TGF-β; but activation of metalloproteinases resulted in the disappearance of this factor. We conclude that TGF-β1 is bound through disulphide bonds to an extracellular matrix component of WJ. The large amount of collagen fibrils and hyaluronate molecules which surround the cells scattered in WJ may prevent the access of extracting solution to TGF-β causing a low extractability of this factor. Although hyaluronate and collagen do not bind TGF-β directly, they may present a barrier that prevents the diffusion of TGF-β in WJ and results in its concentration around the cells thereby facilitating its interaction with membrane receptors and subsequent stimulation of cell division and synthesis of extracellular matrix components.     

调亏灌溉对菘蓝水分利用及产量的影响

通过探究水分调亏对河西地区膜下滴灌菘蓝(Isatis indigotica)各项生理指标、产量和水分利用的影响, 为菘蓝高效节水种植提供理论指导。于2016年在河西走廊中部张掖市民乐县益民灌溉试验站进行菘蓝水分调亏研究, 在保持苗期和肉质根成熟期充分灌溉的情况下, 在菘蓝营养生长期和肉质根生长期分别进行轻度、中度和重度的水分亏缺处理, 并测定各项光合生理指标、产量和水分利用率。结果表明, 营养生长期和肉质根生长期的中度与重度水分亏缺显著降低了菘蓝叶片净光合速率、叶面积指数、株高及主根长, 并且随水分亏缺程度加重降幅增大; 而轻度水分亏缺与对照组的差异不显著。营养生长期和肉质根生长期轻度水分亏缺处理的菘蓝产量与水分利用效率最高, 分别达到8 239.56 kg·hm^-2和24.11 kg·hm^-2·mm^-1; 其它水分亏缺处理组产量和水分利用效率均有所降低, 与对照组之间差异显著(P<0.05), 重度水分亏缺处理各项指标均最低。因此, 最优的菘蓝水分调控处理为营养生长期和肉质根生长期的轻度水分调亏, 能够降低菘蓝耗水量, 提高水分利用效率且其产量不会降低。     

Free energy simulations of ligand binding to the aspartate transporter Glt(Ph)

Glutamate/Aspartate transporters cotransport three Na⁺ and one H⁺ ions with the substrate and countertransport one K⁺ ion. The binding sites for the substrate and two Na⁺ ions have been observed in the crystal structure of the archeal homolog Glt_Ph, while the binding site for the third Na⁺ ion has been proposed from computational studies and confirmed by experiments. Here we perform detailed free energy simulations of Glt_Ph, giving a comprehensive characterization of the substrate and ion binding sites, and calculating their binding free energies in various configurations. Our results show unequivocally that the substrate binds after the binding of two Na⁺ ions. They also shed light into Asp/Glu selectivity of Glt_Ph, which is not observed in eukaryotic glutamate transporters.     

Western Diet Triggers NLRP3-Dependent Innate Immune Reprogramming

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Prostaglandin synthesis by the cochlea of the guinea pig. Influence of aspirin, gentamicin, and acoustic stimulation

This study describes the synthesis of prostaglandins (PGs) by the vascular structures of the inner ear (lateral wall = stria vascularis and spiral ligament) in vitro. The main PGs produced were PGI2, PGF2 alpha and PGE2. PGI2 and PGF2 alpha were also found in the perilymph. A 350 mg/kg ip injection of aspirin decreased PG synthesis by the lateral wall and PG levels in perilymph. This effect was reversed after 3 days. Gentamicin (10(-9) to 10(-5) M) decreased significantly and reversibly PG synthesis in vitro, as did 100 mg/kg ip injection. Acoustic stimulation increased ex vivo PGI2 and PGE2 synthesis without modifying PG levels in perilymph. Results suggest that PGs could be one humoral mediator of the cochlear microcirculation homeostasis, and, possibly, of the circulatory disturbances reported after acoustic stimulation. The decreased PG synthesis after gentamicin treatment could account for the angiotoxic component observed in aminoglycoside ototoxicity.     

Wing size and shape variation of Phlebotomus papatasi (Diptera: Psychodidae) populations from the south and north slopes of the Atlas Mountains in Morocco

The wing shape and size morphology of populations of the medically important phlebotomine sand fly, Phlebotomus papatasi, were examined in two endemic (south of the Atlas Mountains) and nonendemic (north of the Atlas Mountains) foci of cutaneous leishmaniasis by using geometric morphometrics in Morocco. Although it is present in all of Morocco, P. papatasi is the main vector of Leishmania major in only southern part of the Atlas Mountains. There are four major mountain ranges that serve as geographical barriers for species distribution in the study area and at least four gaps were recognized among these barriers. We found statistically significant differences in wing shape morphology between southern and northern populations. Analysis clearly recognized two main groups of populations on both sides of the mountains. The graphical depiction of Principal Component Analysis (PCA) and Canonical Variates Analysis (CVA) confirmed our morphometric study suggesting that the difference in wing morphology between the populations indicates that the population of P. papatasi shows phenotypic plasticity in the study area. According to centroid size analyses, which were used as measures of wing size differences among different sites, the north population of P. papatasi had relatively larger wings than the south population.     

The role of stress proteins HSP70 and the adrenergic system in different resistance to myocardial infarction of August and Wistar genetic rat strains]

A lesser resistance against myocardial infarction (MI) in the Wistar rats as compared with the August rats was found to be combined with a greater stress-response and activation of the heart sympathetic regulation in the former rats. In the Wistar rats and not in August rats, an activation of hypothalamic noradrenaline (NA) system occurs as well as a greater "output" of the NA from sympathetic terminals in the myocardium. Accumulation of the HSP 70 stress-proteins in IM in the myocardium is nearly 2-2.5-fold lesser in the Wistar rats. Thereupon, different resistance against the IM in Wistar and August rats seems to be due to a genetically determine differences in intensity of the stress-response, activation of the heart sympathetic regulation in the IM, and production of the HSP 70 protective stress-proteins in the myocardium.