Probing the effects of dietary selenised glucose on the selenium concentration, quality, and antioxidant activity of eggs and production performances of laying hens.

Selenised glucose (SeGlu) is a newly invented organic selenium compound being synthesised through the selenisation reaction of glucose with NaHSe. We hypothesised that glucose could be used as a carrier for the stable low-valent organoselenium to enhance the selenium concentrations of eggs. To probe the effects of SeGlu on production performances of laying hens, egg selenium concentration, egg quality, and antioxidant indexes, 360 Hy-Line Brown laying hens were randomly assigned to three treatment groups fed with a basal diet alone or the diet supplemented with 5 or 10 mg/kg of Se from SeGlu. The results showed that SeGlu treatment not only enhanced (P < 0.001) the Se concentration in albumen and yolks, glutathione peroxidase activity, and total antioxidant capacity of eggs but also increased (P = 0.032) the Haugh unit of eggs being stored for 2 weeks, while the production performances and egg qualities of fresh eggs were not affected. Moreover, SeGlu supplementation linearly (P < 0.001) increased the scavenging ability of superoxide radicals in eggs. Briefly, SeGlu can enhance the selenium deposition and antioxidant activity of eggs, thereby meeting the nutritional requirement for Se-deficient humans.

Thiamine modulates intestinal morphological structure and microbiota under subacute ruminal acidosis induced by a high-concentrate diet in Saanen goats.

Ruminant animals are generally fed with starch-rich grain as the main energy source, and the incidence of metabolic diseases such as subacute ruminal acidosis (SARA) is high due to the intensive farming. Thiamin has been reported to alleviate SARA caused by high-concentrate diets, but the exact mechanism is not well understood. The goal of this study was to examine the role of thiamine in intestinal inflammation and microbiota caused by high-concentrate diets. The SARA model was induced by low neutral detergent fibre/starch ration to study the effects of thiamine on intestinal tissue structure and microbiota. 18 mid-lactation (148 ± 3 d in milk; milk yield = 0.71 ± 0.0300 kg/d) Saanen goats (BW = 36.5 ± 1.99 kg; body condition score = 2.73 ± 0.16, where 1 = emaciated and 6 = obese) in parities 1 or 2 were selected. The goats were randomly divided into three groups with six replicates: (1) control diet (C; concentrate:forage 30:70), (2) high-concentrate diet (H; concentrate:forage 70:30), and (3) high-concentrate diet with 200 mg of thiamine/kg of DM intake (H + T;concentrate:forage 70:30). The experimental period was lasted for 56 d. The small and large intestine, expression of inflammatory factor genes, tight junction protein genes, total antioxidant capacity, and intestinal microbiota were measured. The results showed that SARA was observed in treatment H, whereas rumen fluid pH was improved in treatment H + T. Treatment H + T also significantly repaired the intestinal tissue structure damaged by SARA, improved the total antioxidant capacity of the small intestinal mucosa, reduced mRNA expression of inflammatory factors in the small intestine tissue, and increased the mRNA expression of tight junction genes in small intestine tissue. The high-concentrate diet reduced the diversity of intestinal microbiota. When thiamine is added to the high-concentrate diet, the relative abundance of intestinal Firmicutes and beneficial bacteria represented by Lactobacilli were upregulated, and the relative abundance of Proteus, a marker of intestinal dysbacteriosis, returned to normal. In conclusion, thiamine supplementation could alleviate the damage to the intestinal tissue structure and microbial environment caused by SARA condition in dairy goats fed a high-concentrate diet.

Transcriptome analysis of hepatic gene expression and DNA methylation in methionine- and betaine-supplemented geese (Anser cygnoides domesticus).

Dietary methionine (Met) restriction produces a coordinated series of transcriptional responses in the liver that limits growth performance and amino acid metabolism. Methyl donor supplementation with betaine (Bet) may protect against this disturbance and affect the molecular basis of gene regulation. However, a lack of genetic information remains an obstacle to understand the mechanisms underlying the relationship between Met and Bet supplementation and its effects on genetic mechanisms. The goal of this study was to identify the effects of dietary supplementation of Met and Bet on growth performance, transcriptomic gene expression, and epigenetic mechanisms in geese on a Met-deficient diet. One hundred and fifty 21-day-old healthy male Yangzhou geese of similar body weight were randomly distributed into 3 groups with 5 replicates per treatment and 10 geese per replicate: Met-deficient diet (Control), Control+1.2 g/kg of Met (Met), and Control+0.6 g/kg of Bet (Bet). All geese had free access to the diet and water throughout rearing. Our results indicated that supplementation of 1.2 g/kg of Met in Met-deficient feed increased growth performance and plasma homocysteine (HCY) levels, indicating increased transsulfuration flux in the liver. Supplementation of 0.6 g/kg Bet had no apparent sparing effect on Met needs for growth performance in growing geese. The expression of many genes critical for Met metabolism is increased in Met supplementation group. In the Bet-supplemented group, genes involved in energy production and conversion were up-regulated. Dietary supplementation with Bet and Met also altered DNA methylation. We observed changes in the methylation of the LOC106032502 promoter and corresponding changes in mRNA expression. In conclusion, Met and Bet supplementation in geese affects the transcriptional regulatory network and alters the hepatic DNA methylation of LOC106032502.

Sleep disorders of acute thalamic stroke and its influence on plasma IL-17.

The aim of this study was to investigate the relationship between sleep disorders in acute thalamus stroke patients and plasma IL-17 levels and the mechanism through which inflammatory reactions develop in stroke. The study included two groups of patients: an experimental group consisting of 30 patients with thalamus stroke who received treatment at the Affiliated Hong Qi Hospital of Mu Dan Jiang Medical University during October 2015 to October 2016 and a control group consisting of 15 healthy volunteers. All the subjects included in the study were biochemically monitored for blood glucose, blood fats and IL-17 plasma levels. The sleep quality of all the subjects included in the study was evaluated [Epwort, Pittsburgh Sleep Quality Index (PSQI)] with 8-hour Polysonmography (PSG) monitoring. The experimental group was divided into 3 subgroups according to the part of the brain affected by stroke: anterior thalamus nucleus group, lateral thalamus nucleus group and medial thalamus nucleus group. The differences were analyzed between the experimental group and the control group in sleep quality scores, sleep structural changes, and plasma IL-17 levels. The differences in sleep structural scores were also analyzed according to different parts of the brain affected by stroke. The experimental group had a higher PSQI score compared with the control group, but this difference had no statistical significance (p>0.05). Compared with the control group, the N1 phase of the experimental group was longer while the N2 and N3 phases were shorter (p<0.05). There were no differences in sleep structure between the three regions of the brain affected by stroke (anterior thalamus nucleus group, lateral thalamus nucleus group and medial thalamus nucleus group) (p > 0.05). The plasma levels of IL-17 in the experimental group was higher compared to the control group (p<0.05). In the experimental group, the patients with hypersomnia had higher IL-17 levels than patients without hypersomnia (p<0.01). We can conclude that PSG can be used as an electrophysiology index for early detection of sleep disorders in thalamus stroke patients. Sleep disorders in patients with thalamus stroke persist a long time after the incident, therefore monitoring their sleep structure may become an important index to predict the prognosis of the disease. The increased level of IL-17 level in the experimental group shows its implication in appearance of sleep disorders of acute thalamus stroke through inflammatory mechanism.

Minimum alveolar anesthetic concentration of fluorinated alkanols in rats: relevance to theories of narcosis.

UNLABELLED: The Meyer-Overton hypothesis predicts that the potency of conventional inhaled anesthetics correlates inversely with lipophilicity: minimum alveolar anesthetic concentration (MAC) x the olive oil/gas partition coefficient equals a constant of approximately 1.82 +/- 0.56 atm (mean +/- SD), whereas MAC x the octanol/gas partition coefficient equals a constant of approximately 2.55 +/- 0.65 atm. MAC is the minimum alveolar concentration of anesthetic required to eliminate movement in response to a noxious stimulus in 50% of subjects. Although MAC x the olive oil/gas partition coefficient also equals a constant for normal alkanols from methanol through octanol, the constant (0.156 +/- 0.072 atm) is one-tenth that found for conventional anesthetics, whereas the product for MAC x the octanol/gas partition coefficient (1.72 +/- 1.19) is similar to that for conventional anesthetics. These normal alkanols also have much greater affinities for water (saline/gas partition coefficients equaling 708 [octanol] to 3780 [methanol]) than do conventional anesthetics. In the present study, we examined whether fluorination lowers alkanol saline/gas partition coefficients (i.e., decreases polarity) while sustaining or increasing lipid/gas partition coefficients, and whether alkanols with lower saline/gas partition coefficients had products of MAC x olive oil or octanol/gas partition coefficients that approached or exceeded those of conventional anesthetics. Fluorination decreased saline/gas partition coefficients to as low as 0.60 +/- 0.08 (CF3[CF2]6CH2OH) and, as hypothesized, increased the product of MAC x the olive oil or octanol/gas partition coefficients to values equaling or exceeding those found for conventional anesthetics. We conclude that the greater potency of many alkanols (greater than would be predicted from conventional inhaled anesthetics and the Meyer-Overton hypothesis) is associated with their greater polarity. IMPLICATIONS: Inhaled anesthetic potency correlates with lipophilicity, but potency of common alkanols is greater than their lipophilicity indicates, in part because alkanols have a greater hydrophilicity--i.e., a greater polarity.

Nonimmobilizers and transitional compounds may produce convulsions by two mechanisms.

UNLABELLED: Some inhaled compounds cause convulsions. To better appreciate the physical basis for this property, we correlated the partial pressures that produced convulsions in rats with the lipophilicity (nonpolarity) and hydrophilicity (polarity) of 45 compounds: 3 n-alkanes, 18 n-haloalkanes, 3 halogenated aromatic compounds, 3 cycloalkanes and 3 halocycloalkanes, 13 halogenated ethers, and 2 noble gases (He and Ne). In most cases, convulsions were quantified by averaging the alveolar partial pressures just below the pressures that caused and slightly higher pressures that did cause clonic convulsions (ED50). The ED50 did not correlate with hydrophilicity (the saline/gas partition coefficient), nor was there an obvious correlation with molecular structure. For 80% of compounds (36 of 45), the ED50 correlated closely (r2 = 0.99) with lipophilicity (the olive oil/gas partition coefficient). Perhaps because they block the effect of GABA on GABA(A) receptors, five compounds were more potent than would be predicted from their lipophilicity. Conversely, four compounds may have been less potent than would be predicted because they (like conventional inhaled anesthetics) enhance the effect of GABA on GABA(A) receptors. IMPLICATIONS: Nonimmobilizers and transitional compounds may produce convulsions by two mechanisms. One correlates with lipophilicity (nonpolarity), and the other correlates with an action on GABA(A) receptors.

[Effects of different acupuncture manipulation on plasma estradiol, testosterone and cortisol in patients with kidney deficiency].

Observation was made on the effect of different acupuncture manipulation on plasma estradiol (E2), testosterone (T), E2/T and cortisol (C) in 78 patients with kidney deficiency. The results showed that the level of E2 and T in women was lowered by both reinforcing manipulation (RFM) and reducing manipulation (RDM). E2/T index was lowered by RDM but not by RFM, and there was significance (P < 0.05) between the RDM group and RDM group in E2/T, but no significance between the man's groups. The level of C was decreased by RDM but not by RFM. The results suggest that the different manipulation effects are different on the level of sex hormones in women and the C content in patients with kidney deficiency.

Hepatic triiodothyronine sulfation and its regulation by growth hormone and triiodothyronine in rats.

The regulatory mechanism of cytosolic sulfation of T3 has been studied in rat liver. Sulfation of T3 is sexually differentiated in adult rats of Sprague-Dawley (SD), Fisher 344, and ACI strains. In SD strain, the male animals showed 4 times higher sulfating activity than did the females. The specific activity was decreased by hypophysectomy of male adult rats, but was not affected in the females. Thus, the sex-difference was abolished in the hypophysectomized condition. Supplement of human GH intermittently twice daily for 7 days, to mimic the male secretory pattern, increased T3 sulfating activity in both sexes of hypophysectomized rats, whereas continuous infusion to mimic a female secretory pattern had no appreciable effect. Cytosolic sulfation of T3 was decreased by 25 to 30% by thyroidectomy or propylthiouracil treatment of male adult rats, and was restored by the supplementation of T3 (50 micrograms/kg daily for 7 days) to thyroidectomized rats. Administration of T3 in hypophysectomized rats almost completely restored the sulfating activity in the males and increased the activity in the females. Cytosolic T3 sulfation was inhibited by the addition of known inhibitors of phenol sulfotransferase, pentachlorophenol or 2,6-dichloro-4-nitrophenol. These results indicate a role of pituitary GH in hepatic sulfation of thyroid hormones in rats. The data obtained also raise the possibility that GH may modify the effect of thyroid hormones on the pituitary by a feed-back mechanism through changing the level of a sex-dominant phenol sulfotransferase(s) in rat livers. T3 was also sulfated in hepatic cytosols of mouse, hamster, rabbit, dog, monkey, and human.(ABSTRACT TRUNCATED AT 250 WORDS)