[An investigation of a food poisoning incident caused by Amanita fuliginea].

Mistakenly picking and eating poisonous mushrooms can cause acute poisoning. In August 2020, Qingdao Hospital of Traditional Chinese Medicine handled a poisonous mushroom poisoning incident, conducted epidemiological investigation on all poisoned patients, collected suspicious food, clinical manifestations, clinical test results and treatment conditions, and identified the mushrooms as Amanita fuliginea poisoning after morphological identification. In this incident, 6 people ate grey goose paste, of which 4 were sick with a incubation period of 6~12 h. The clinical manifestations were gastrointestinal symptoms such as nausea, vomiting and diarrhea, liver and kidney damage. After symptomatic support treatment, hemoperfusion or continuous hemofiltration treatment, the patients were cured and discharged. It is suggested to strengthen the popular science education on poisonous mushroom poisoning and improve the ability of identification and clinical treatment of poisonous mushrooms in grass-roots medical institutions.

Effects of dietary supplementation of microencapsulated Enterococcus fecalis and the extract of Camellia oleifera seed on laying performance, egg quality, serum biochemical parameters, and cecal microflora diversity in laying hens.

The aim of this study was to investigate the effects of microencapsulted Enterococcus faecalis (MEF) and the extract of Camellia oleifera seed (ECOS) on laying performance, serum biochemical parameters, and cecal microflora diversity in laying hens. A total of 180 Hy-Line Brown laying hens, 26-wk-old, were randomly allocated to 6 treatments with 10 replicates and 3 hens per replicate. Dietary treatments were as follows: (A) control group, basal diet; (B) basal diet + 100 mg MEF/kg diet (1 × 1010 cfu/g MEF); (C) basal diet + 300 mg ECOS/kg diet; (D) basal diet + 100 mg MEF/kg diet + 300 mg ECOS/kg diet; (E) basal diet + 500 mg ECOS/kg diet; (F) basal diet + 100 mg MEF/kg diet + 500 mg ECOS/kg diet. The results showed that diets supplemented with MEF and ECOS had no significant effects on laying rate, average egg size, average daily feed intake, feed conversion ratio, eggshell thickness, albumen height, and yolk color (P > 0.05), but had significant effects on egg shape index, eggshell strength, and Haugh unit (P < 0.05) during whole feeding phases. Compared to the control group, the serum IgA and IgG levels of birds in Group F significantly increased (P < 0.05). The serum total cholesterol, low-density lipoprotein cholesterol, total triglyceride, and blood urea nitrogen levels of birds in Group D and Group F significantly reduced (P < 0.05), and the high-density lipoprotein cholesterol level of birds in Group D and Group F significantly increased (P < 0.05). At the phylum level, Firmicutes decreased (P < 0.05) and Bacteroidetes increased (P < 0.05) in the birds of Group D. Ruminococcus and Bacteroides were significantly affected by dietary treatments (P < 0.05), and Bacteroides in the birds of Group D significantly increased at the genus level. Therefore, diet supplemented with MEF and ECOS can significantly improve serum biochemical parameters and increase cecal microflora diversity.

Bacillus amyloliquefaciens supplementation alleviates immunological stress in lipopolysaccharide-challenged broilers at early age.

This study was conducted to investigate the effect of Bacillus amyloliquefaciens ( BA: ) on the immune function of broilers challenged with lipopolysaccharide ( LPS: ). 192 one-day-old male Arbor Acre broiler chickens were randomly distributed into four treatments: 1) broilers fed a basal diet; 2) broilers fed a basal diet supplemented with BA; 3) LPS-challenged broilers fed a basal diet; and 4) LPS-challenged broilers fed a basal diet supplemented with BA. Each treatment consisted of six replicates with eight broilers per replicate. Broilers were intraperitoneally injected with either 500 µg LPS per kg body weight or sterile saline at 16, 18 and 20 d of age. LPS decreased the average daily gain ( ADG: , P = 0.001) and average daily feed intake (P = 0.001). The decreased ADG (P = 0.009) and increased feed conversion ratio (P = 0.047) in LPS-challenged broilers were alleviated by BA. LPS increased the relative spleen weight (P = 0.001). Relative spleen (P = 0.014) and bursa (P = 0.024) weights in the LPS-challenged broilers were reduced by BA. LPS increased white blood cell ( WBC: ) numbers (P = 0.001). However, the WBC numbers (P = 0.042) and the ratio of lymphocytes to WBC (P = 0.020) in LPS-challenged broilers were decreased with BA treatment. LPS decreased plasma lysozyme activity (P = 0.001), but increased concentrations of plasma corticosterone (P = 0.012) and IL-2 (P = 0.020). In contrast, BA increased lysozyme activity in plasma (P = 0.040). LPS increased mRNA abundances of splenic toll-like receptor 4 (P = 0.046), interferon γ (P = 0.008), IL-1ß (P = 0.045) and IL-6, (P = 0.006). IL-2 (P = 0.014) and IL-6 (P = 0.074) mRNA abundances in LPS-challenged broilers were reduced by BA, although BA had an opposite effect for IL-10 mRNA expression in those broilers (P = 0.004). In conclusion, BA supplementation could partially alleviate the compromised growth performance and immune status of broilers under immune stress induced by LPS challenge at early age.

Vitamin B12 and homocysteine status during pregnancy in the metformin in gestational diabetes trial: responses to maternal metformin compared with insulin treatment.

AIM: The aim of the study is to compare the effects of metformin and insulin treatment for gestational diabetes mellitus (GDM) on vitamin B12 and homocysteine (Hcy) status. METHODS: Women with GDM, who met criteria for insulin treatment, were randomly assigned to metformin (n = 89) or insulin (n = 91) in the Adelaide cohort of the metformin in gestational diabetes (MiG) trial. Fasting serum total vitamin B12 (TB12), holotranscobalamin (HoloTC), a marker of functional B12 status and plasma Hcy concentrations were measured at 20-34 weeks (at randomization) and 36 weeks gestation, then at 6-8 weeks postpartum. RESULTS: Circulating TB12, HoloTC and Hcy were similar in both treatment groups at each time point. Women who were taking dietary folate supplements at randomization had higher serum TB12 and HoloTC at randomization than those not taking folate. Overall, serum TB12 fell more between randomization and 36 weeks gestation in the metformin group than in the insulin group (metformin: -19.7 ± 4.7 pmol/l, insulin: -6.4 ± 3.6 pmol/l, p = 0.004). The decrease in serum TB12 during treatment was greater with increasing treatment duration in metformin-treated (p < 0.001), but not in insulin-treated women. CONCLUSIONS: Total, but not bioavailable, vitamin B12 stores were depleted during pregnancy to a greater extent in metformin-treated than in insulin-treated women with GDM, but neither analyte differed between groups at any stage. This adds further evidence supporting metformin as a safe alternative treatment to insulin in GDM. Further investigation is needed to evaluate whether women treated with metformin for longer periods in pregnancy require additional B12 or other supplementation.

Inhibition of eukaryote protein kinases and of a cyclic nucleotide-binding phosphatase by prenylated xanthones.

A series of prenylated xanthones are variously potent inhibitors of the catalytic subunit (cAK) of rat liver cyclic AMP-dependent protein kinase (PKA), rat brain Ca2+ and phospholipid-dependent protein kinase C (PKC), chicken gizzard myosin light chain kinase (MLCK), wheat embryo Ca2+-dependent protein kinase (CDPK) and potato tuber cyclic nucleotide-binding phosphatase (Pase). The prenylated xanthones examined are mostly derivatives of alpha-mangostin in which the 3-hydroxyl and 6-hydroxyl are variously substituted with groups R or R', respectively, or derivatives of 3-isomangostin (mangostanol) in which the 9-hydroxyl is substituted with groups R' or the prenyl side chain is modified. The most potent inhibitors of cAK have non-protonatable and relatively small R' and R groups. Conversely, the most potent inhibitors of PKC and MLCK have bulkier and basic R' groups. Some prenylated xanthones are also potent inhibitors of CDPK. PKC and cAK are competitively inhibited by particular prenylated xanthones whereas the compounds that are the most potent inhibitors of MLCK and CDPK are non-competitive inhibitors. Prenylated xanthones having relatively small and non-protonatable R' and R groups inhibit a high-affinity cyclic nucleotide binding Pase in a non-competitive fashion.

Inhibition of eukaryote serine/threonine-specific protein kinases by piceatannol.

The protein tyrosine kinase (PTK) inhibitor piceatannol is also an inhibitor of the rat liver cyclic AMP-dependent protein kinase (PKA) catalytic subunit (cAK), rat brain Ca(2+)- and phospholipid-dependent protein kinase C (PKC), avian gizzard Ca(2+)-calmodulin-dependent myosin light chain kinae (MLCK), and of wheat embryo Ca(2+)-dependent protein kinase (CDPK) (IC50 values 3, 8, 12, and 19 microM, respectively). However, a number of piceatannol-related compounds with fewer or no phenolic hydroxy substituents are inactive or very poor inhibitors of these serine/threonine protein kinases. Similarly, the PTK inhibitor ellagic acid is a potent inhibitor of cAK and of PKC (IC50 values 2 and 8 microM, respectively), whereas the non-phenolic perylene is ineffective as a protein kinase inhibitor. Ellagic acid is a competitive inhibitor of both cAK and of PKC but piceatannol inhibits these enzymes in a fashion that is competitive and non-competitive, respectively. Interaction with calmodulin may contribute to the inhibition of MLCK and CDPK by piceatannol.

Inhibition of eukaryote protein kinases by isoquinoline and oxazine alkaloids.

The aporphine isoquinoline alkaloid apomorphine is a potent inhibitor of the catalytic subunit (cAK) of rat liver cyclic AMP-dependent protein kinase (PKA), myosin light chain kinase (MLCK), and Ca(2+)- and phospholipid-dependent protein kinase C (PKC) (IC50 values 1, 11, and 8 microM, respectively). However, a number of O-methylated analogues of apomorphine are inactive or poor inhibitors of cAK. The benzophenanthridine isoquinoline alkaloid sanguinarine is a potent inhibitor of cAK but is a relatively poor inhibitor of PKC (IC50 values 6 and 217 microM respectively). However a number of methylated analogues of sanguinarine are inactive as cAK inhibitors. The aporphine isoquinoline alkaloids (+)-boldine and bulbocapnine are non-competitive inhibitors of MLCK with respect to both peptide substrate and ATP. The inhibition of cAK, MLCK, and PKC by apomorphine and sanguinarine is competitive with respect to ATP as substrate. The oxazine alkaloids darrow red, nile blue A, and oxazine 170 are variously effective as inhibitors of cAK, MLCK, PKC, and CDPK (IC50 values 4-65 microM). Ca2+ binds to apomorphine and (+)-boldine which, together with nile blue A and oxazine 170, are potent inhibitors of calmodulin (CaM)-dependent MLCK (IC50 values 11, 12, 4, and 7 microM, respectively), and interact with dansyl-CaM.