The distinctive short-term response of late-pregnant prolific ewes to propylene glycol or glycerol drenching.

Pregnancy toxemia is the most frequent metabolic disorder of ewes in late pregnancy. Although propylene glycol (PG) and glycerol (GLY) are common glucogenic supplements for treating pregnancy toxemia in ewes, the relative benefit of these 2 supplements is not entirely clear. Therefore, the objectives of the present study were to determine the changes during 24 h in key blood metabolites and insulin in response to PG or GLY drenching in prolific ewes. To this end, 36 multiparous late-pregnant Afec-Assaf ewes (∼132.4 d pregnant) bearing 2 to 4 fetuses, divided into 2 blocks (18 ewes in each block), with a blood ß-hydroxybutyrate (BHB) concentration of 0.5 to 1.6 mmol/L were included. Ewes were divided into 3 groups (12 ewes each; 6 ewes in each experimental day), according to their BHB levels, expected litter size, body weight, and body condition score, and were drenched with the following: (1) control group (CTL), 55 mL of water; (2) PG, 106 mL of PG (100% PG, 448 calories); or (3) GLY, 108 mL of Koforin 80 (80% GL; 448 calories). Blood samples were taken before drenching and every hour after drenching for 24 h. Plasma concentration of glucose, BHB, nonesterified fatty acids, lactate, glycerol, and insulin were determined. Because there were no effects of treatments after 12 h in the first block, the data were analyzed for 12 h after drenching rather than 24 h. The plasma glucose concentration during the first 5 h after drenching was the highest in the GLY, BHB concentration was the lowest in the PG, and the nonesterified fatty acid levels were lower in the PG compared with the CTL ewes during the first 5 h after drenching. However, glucose concentration was higher in the PG ewes at 9, 11, and 12 h after drenching than in CTL or GLY ewes. The mean lactate concentration in plasma for 12 h was 2.5- and 1.9-fold higher in the PG compared with the CTL and GLY ewes, respectively, and except at 11 h after drenching, it was significantly higher at each time point. The insulin concentration was higher in the GLY than in both other groups at 2 to 5 h after drenching. These results suggest that during the first few hours after drenching the effect of PG was more effective in reducing the BHB concentration, whereas the GLY effect was more effective in enhancing glucose concentration. The increased concentration in lactate following PG treatment suggests that the PG contribution to gluconeogenesis is mediated through its metabolism to lactate. In contrast, the lack of an effect on lactate, and the faster increase in blood glucose in response to GLY suggest that GLY has a more advanced entry point to gluconeogenesis, which influences the immediate response in enhancing the glucose blood concentration.

Open Probe fast GC-MS - combining ambient sampling ultra-fast separation and in-vacuum ionization for real-time analysis.

An Open Probe inlet was combined with a low thermal mass ultra-fast gas chromatograph (GC), in-vacuum electron ionization ion source and a mass spectrometer (MS) of GC-MS for obtaining real-time analysis with separation. The Open Probe enables ambient sampling via sample vaporization in an oven that is open to room air, and the ultra-fast GC provides ~30-s separation, while if no separation is required, it can act as a transfer line with 2 to 3-s sample transfer time. Sample analysis is as simple as touching the sample, pushing the sample holder into the Open Probe oven and obtaining the results in 30 s. The Open Probe fast GC was mounted on a standard Agilent 7890 GC that was coupled with an Agilent 5977A MS. Open Probe fast GC-MS provides real-time analysis combined with GC separation and library identification, and it uses the low-cost MS of GC-MS. The operation of Open Probe fast GC-MS is demonstrated in the 30-s separation and 50-s full analysis cycle time of tetrahydrocannabinol and cannabinol in Cannabis flower, sub 1-min analysis of trace trinitrotoluene transferred from a finger onto a glass surface, vitamin E in canola oil, sterols in olive oil, polybrominated flame retardants in plastics, alprazolam in Xanax drug pill and free fatty acids and cholesterol in human blood. The extrapolated limit of detection for pyrene is <1 fg, but the concentration is too high and the software noise calculation is untrustworthy. The broad range of compounds amenable for analysis is demonstrated in the analysis of reserpine. The possible use with alternate standard GC-MS and Open Probe fast GC-MS is demonstrated in the analysis of heroin in its street drug powder. The use of Open Probe with the fast GC acting as a transfer line is demonstrated in <10-s analysis without separation of ibuprofen and estradiol. Copyright © 2017 John Wiley & Sons, Ltd.

Effect of nutritional composition of meals on exercise tests in patients with ischaemic heart disease.

BACKGROUND: Patients with ischaemic heart disease have to perform exercise tests repeatedly. It is not clear if a small meal eaten before the test might influence it and if the meal's composition is important. DESIGN AND METHOD: We performed a double blind, randomised, crossover study on 20 volunteers with documented ischaemic heart disease known to have positive exercise tests. Each had three symptom limited exercise tests done one hour after a 200 ml meal, rich in either fat, carbohydrate or protein. Each postprandial test was compared to a fasting exercise test performed just before the meal. RESULTS: Postprandial blood pressure, time to angina and to peak exercise and double product at onset of ST-depression were not significantly altered by any of the meals. Heart rate was slightly increased only after the fat meal. CONCLUSIONS: The nutritional composition of a small meal eaten an hour before an exercise test has no clinically important impact on the results of the test in patients with stable angina pectoris.

Mild sedation before transesophageal echo induces significant hemodynamic and respiratory depression.

AIMS: Midazolam is often used for conscious sedation before transesophageal echo (TEE) studies. It is not clear to what extent midazolam administration or the insertion of the TEE probe itself is responsible for the respiratory and hemodynamic depression during TEE examinations. We compared the performance of TEE with versus without midazolam to elucidate the effects of each. METHODS: Patients were given the choice of having midazolam prior to their TEE. Thirty-one patients preferred to have sedation (Sed+) and 31 others declined sedation (Sed-). Both groups had SaO(2) and blood pressure measured before the study, following sedation (in Sed+) and at the end of the TEE study. RESULTS: Increase in HR was greater in Sed+ than in Sed- (12 +/- 19% vs 6 +/- 11%, both P < 0.05). There was a greater decrease in saturation of O(2) in Sed+ than in Sed- (3 +/- 3% vs 2 +/- 3%, both P < 0.05). Systolic blood pressure (SBP) increased in Sed- by 6 +/- 11% (P< 0.05) but dropped in Sed+ immediately after sedation (16 +/- 8%, P < 0.000001). Diastolic blood pressure decreased in Sed+ after sedation by 11 +/- 9% (P < 0.05). CONCLUSIONS: Midazolam sedation before TEE examinations causes more prominent tachycardia and depression of SaO(2)than insertion of the TEE probe alone. It also causes a substantial drop in SBP. Midazolam should be offered only to hemodynamically stable patients without preceding respiratory depression.

Supplementation of urban home visitation with a series of group meetings for parents and infants: results of a "real-world" randomized, controlled trial.

OBJECTIVE: Home visitation has been shown to be effective in reducing rates of child maltreatment and in enhancing psychosocial outcomes in children and their parents. Even when available, however, it is underutilized by parents in some urban settings. We tested a supplemental 10-session group intervention for its ability to increase active participation in home visitation, enhance the quality of caregiving behavior of parents, and improve social developmental outcome in children. METHOD: A randomized controlled design was utilized, involving two separate cohorts of parents of 3- to 18-month old infants, totaling 148 parent-child dyads. The intervention focused on practical experience in promoting parent-infant attachment relationships. RESULTS: At 6 months follow-up, there was a substantial increase in the proportion of intervention group parents participating in home visitation, compared to parents in the control group (Fisher's exact p = .008). Parents in the intervention group exhibited a trend for improvement in their capacity to appropriately interpret infants' emotional cues (p = .08), independent of the effects of home visitation itself. Attrition in both the treatment and control groups was inversely associated with income and level of education. CONCLUSIONS: Group meetings may constitute an effective means of engaging stressed urban families in home visitation.

Tissue oxygen levels control astrocyte movement and differentiation in developing retina.

Astrocytes play a key role in the development of retinal vessels by detecting hypoxia in developing retina and secreting the hypoxia-induced angiogenic factor VEGF to induce vessel formation. The astrocytes which play this role are themselves spreading over the retina, just ahead of the growing vessels. To understand the mechanisms which keep astrocytes in this strategic 'just ahead' position we have studied the effects of hyperoxia and hypoxia on astrocyte differentiation and movement in situ in neonatal rat retina and in primary culture. Hyperoxia in situ inhibited the stellation of astrocytes, so that they persisted in a relatively unbranched form, which accumulated at the edge of their spreading population; hyperoxia permitted but did not accelerate migration. Conversely, hypoxia induced unstellated astrocytes to stellate within 6 h. If the hypoxia was abnormally severe, it caused the astrocytes to hyperstellate and slowed their spread. Astrocytes in primary culture did not change morphology or motility when challenged by hypoxia. When treated with medium conditioned by retina however, astrocytes became mobile and, if the medium was conditioned by hypoxic retina, became stellate. These results suggest that the oxygen released by retinal vessels maintains the mobility of astrocytes, via a diffusible factor released by other retinal cells. Conversely, naturally generated hypoxia of developing retina plays a triple role, inducing astrocytes to stellate, to end their migration and to produce VEGF, thereby inducing vessel formation. The induction of stellation is mediated by a diffusible factor released by other retinal cells. Thus hypoxia of the retina generated by neural maturation induces key events in both the differentiation of astrocytes and the formation of blood vessels.

The trithorax group gene moira encodes a brahma-associated putative chromatin-remodeling factor in Drosophila melanogaster.

The genes of the trithorax group (trxG) in Drosophila melanogaster are required to maintain the pattern of homeotic gene expression that is established early in embryogenesis by the transient expression of the segmentation genes. The precise role of each of the diverse trxG members and the functional relationships among them are not well understood. Here, we report on the isolation of the trxG gene moira (mor) and its molecular characterization. mor encodes a fruit fly homolog of the human and yeast chromatin-remodeling factors BAF170, BAF155, and SWI3. mor is widely expressed throughout development, and its 170-kDa protein product is present in many embryonic tissues. In vitro, MOR can bind to itself and it interacts with Brahma (BRM), an SWI2-SNF2 homolog, with which it is associated in embryonic nuclear extracts. The leucine zipper motif of MOR is likely to participate in self-oligomerization; the equally conserved SANT domain, for which no function is known, may be required for optimal binding to BRM. MOR thus joins BRM and Snf5-related 1 (SNR1), two known Drosophila SWI-SNF subunits that act as positive regulators of the homeotic genes. These observations provide a molecular explanation for the phenotypic and genetic relationships among several of the trxG genes by suggesting that they encode evolutionarily conserved components of a chromatin-remodeling complex.

Vascular endothelial growth factor acts as a survival factor for newly formed retinal vessels and has implications for retinopathy of prematurity.

Retinopathy of prematurity (ROP) is initiated by hyperoxia-induced obliteration of newly formed blood vessels in the retina of the premature newborn. We propose that vessel regression is a consequence of hyperoxia-induced withdrawal of a critical vascular survival factor. We show that regression of retinal capillaries in neonatal rats exposed to high oxygen, is preceded by a shut-off of vascular endothelial growth factor (VEGF) production by nearby neuroglial cells. Vessel regression occurs via selective apoptosis of endothelial cells. Intraocular injection of VEGF at the onset of experimental hyperoxia prevents apoptotic death of endothelial cells and rescues the retinal vasculature. These findings provide evidence for a specific angiogenic factor acting as a vascular survival factor in vivo. The system also provides a paradigm for vascular remodelling as an adaptive response to an increase in oxygen tension and suggests a novel approach to prevention of ROP.

Development of retinal vasculature is mediated by hypoxia-induced vascular endothelial growth factor (VEGF) expression by neuroglia.

We have studied the role of the hypoxia-inducible angiogenic growth factor vascular endothelial growth factor (VEGF) in the induction and control of vessel growth in the developing retina of rats and cats, using in situ hybridization techniques. VEGF is expressed successively in two layers of neural retina, the innermost (axon) layer and the inner nuclear layer (INL). In the axon layer, VEGF is expressed transiently by astrocytes as they spread across the layer, closely preceding the formation of superficial vessels. In the INL, VEGF is expressed transiently by somas at the middle of the layer (presumably Müller cells), closely preceding the formation of the deep layer of retinal vessels. We propose that hypoxia caused by the onset of neuronal activity is detected by strategically located populations of neuroglia, first astrocytes, then Müller cells. In response they secrete VEGF, inducing formation of the superficial and deep layers of retinal vessels, respectively. As the vessels become patent, they relieve the hypoxic stimulus, so vessel formation is matched to oxygen demand. This hypothesis was tested experimentally in three ways. Expression of the high affinity flk-1 receptor for VEGF was demonstrated in newly formed retinal vessels, confirming that the secreted VEGF acts on the vessels, in a paracrine fashion. Direct hypoxic regulation of VEGF expression by macroglia was demonstrated in primary cultures of astrocytes and in cells of a glioma line. Hypoxic regulation of VEGF expression in the intact developing retina was demonstrated by showing that oxygen-enriched atmospheres that inhibit vessel formation also suppress endogenous VEGF production.

Expression of a sodium proton antiporter (NhaA) in Escherichia coli is induced by Na+ and Li+ ions.

Regulation of expression of nhaA, the gene which encodes a Na+/H+ antiporter in Escherichia coli has been studied. Two promoters have been identified in the upstream sequence of the gene and the corresponding start point of transcription mapped by primer extension. Monitoring the beta-galactosidase activity of a chromosomal translation fusion of nhaA'-'lacZ show that at pH 7.5 the gene is induced, within 1 h, by 100 mM of either Li+ or Na+. Change of pH between 6.5 and 8.5 by itself does not increase expression of the gene but it markedly increases the sensitivity of the expression system to the ions. At pH 7.5 maximal induction is obtained by 100 mM NaCl, whereas at pH 8.6, 10 mM NaCl elicit similar response. The pattern of regulation of nhaA reflects its importance in adaptation to high salinity and alkaline pH in E. coli.