Dietary silymarin, Silybum marianum extract ameliorates cadmium chloride toxicity in common carp, Cyprinus carpio

The present study evaluated the protective effects of silymarin extract (SIE) on cadmium chloride toxicity in common carp, Cyprinus carpio. Four experimental group were considered for the experiment including: SIE0 (control): non-SIE-supplemented fish, SIE1: fish supplemented with 400 mg SIE/kg diet, SIE2: fish supplemented with1400mg SIE/kg diet, SIE3: fish supplemented with 2400 mg SIE/kg diet). Fish were fed experimental diet for 60 days and then exposed to cadmium chloride (1.5 mg/l or 25% of LC50–96 h) and antioxidant defense components and the survival rate assayed. After 60 days feeding trial, total antioxidant capacity (TAC) levels significantly increased (P<0.01) in 1400–2400 mg SIE/kg diet treatments compared to those in control and 400 mg SIE/kg diet treatment. Malondialdehyde (MDA) (P>0.01) and acetylcholinesterase (AChE) levels (P>0.01) remained unchanged during the feeding period in all treatments. Hepatic catalase (CAT) in all SIE supplemented groups and superoxide dismutase (SOD) and glutathione peroxidase (GPx) in 1400–2400 mg SIE/kg diet treatments significantly elevated (P<0.01) in response to SIE. Plasma levels of hepatic metabolic enzymes [alanine transaminase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), creatine kinase (CK), lactate dehydrogenase (LDH) ] remained unchanged (P>0.01) in all experimental groups over feeding period. After exposure to cadmium chloride, TAC levels were significantly elevated (P<0.01) in all experimental groups. In control and 400 mg SIE/kg diet treatment, TAC showed lower levels (P<0.01) compared to other groups. MDA levels were significantly increased (P<0.01) in control and fish supplemented with 400 and 1400 mg SIE/kg diet. TAC in the fish of 2400 mg SIE/kg diet treatment remained unchanged (P>0.01), following the exposure. CAT (P<0.01), SOD (P<0.01) and GPx (P<0.01) were significantly elevated in response to cadmium chloride in all groups. However, the treatments, 1400 and 2400 mg SIE/kg diet, showed lower increases (P<0.01) of enzymes. AChE activity (P<0.01) in the liver were significantly decreased in control and fish fed 400 and 1400 mg SIE/kg diet. Exposure to cadmium significantly increased (P<0.01) the plasma levels of ALT, AST, ALP and LDH in control and those fed 400 and 1400 mg SIE/kg diet. The findings of the current study indicated that SIE at a rate of 1400–2400mg/kg diet might enhance antioxidant defense and protect hepatocytes against toxic effects of cadmium.

Gut Bacterial Communities of Lymantria xylina and Their Associations with Host Development and Diet

The gut microbiota of insects has a wide range of effects on host nutrition, physiology, and behavior. The structure of gut microbiota may also be shaped by their environment, causing them to adjust to their hosts; thus, the objective of this study was to examine variations in the morphological traits and gut microbiota of Lymantria xylina in response to natural and artificial diets using high-throughput sequencing. Regarding morphology, the head widths for larvae fed on a sterilized artificial diet were smaller than for larvae fed on a non-sterilized host-plant diet in the early instars. The gut microbiota diversity of L. xylina fed on different diets varied significantly, but did not change during different development periods. This seemed to indicate that vertical inheritance occurred in L. xylina mutualistic symbionts. Acinetobacter and Enterococcus were dominant in/on eggs. In the first instar larvae, Acinetobacter accounted for 33.52% of the sterilized artificial diet treatment, while Enterococcus (67.88%) was the predominant bacteria for the non-sterilized host-plant diet treatment. Gut microbe structures were adapted to both diets through vertical inheritance and self-regulation. This study clarified the impacts of microbial symbiosis on L. xylina and might provide new possibilities for improving the control of these bacteria.

A Study on Assessment and Management of Diabetic Gastropathy

To assess and manage Diabetic gastropathy. Diabetic gastropathy is least concern in developing countries but many patients receiving oral anti diabetics leads to serious gastric problems. This study involves identification of gastric problems and improves compliance, medication adherence among population and also determine the severity of gastric problems due to oral hypoglycemic drugs. In our study, women are more effected (54%) than men (46%). Most effected age group is 40-60 years age with 58% Mild (male-20.9%, female-22.27%) and moderate (male-37.9%, females-39.7%) conditions are the most effected in terms of severity. This is due to poor glycemic control and not using proper medication, diet. Treatment should be focused on improving gastric symptoms by controlling gastric emptying. Prevention of gastric symptoms by following some dietary changes, nutritional and physiological support is effective to patients.

Newborn Screening and Treatment of Phenylketonuria: Projected Health Outcomes and Cost-Effectiveness

The objective of this study was to evaluate the cost-effectiveness of newborn screening and treatment for phenylketonuria (PKU) in the context of new data on adherence to recommended diet treatment and a newly available drug treatment (sapropterin dihydrochloride). A computer simulation model was developed to project outcomes for a hypothetical cohort of newborns with PKU. Four strategies were compared: (1) clinical identification (CI) with diet treatment; (2) newborn screening (NBS) with diet treatment; (3) CI with diet and medication (sapropterin dihydrochloride); and (4) NBS with diet and medication. Data sources included published literature, primary data, and expert opinion. From a societal perspective, newborn screening with diet treatment had an incremental cost-effectiveness ratio of $6400/QALY compared to clinical identification with diet treatment. Adding medication to NBS with diet treatment resulted in an incremental cost-effectiveness ratio of more than $16,000,000/QALY. Uncertainty analyses did not substantially alter the cost-effectiveness results. Newborn screening for PKU with diet treatment yields a cost-effectiveness ratio lower than many other recommended childhood prevention programs even if adherence is lower than previously assumed. Adding medication yields cost-effectiveness results unlikely to be considered favorable. Future research should consider conditions under which sapropterin dihydrochloride would be more economically attractive.

118 Increased Growth and Carcass Attributes in Improvest®-treated Gilts Do Not Require Additional Dietary Lysine

Numerous studies have shown that gilts treated with Improvest® have greater carcass weights and increased ADG compared with untreated gilts. To develop the optimum nutritional program for Improvest-treated gilts, a randomized 5×2 factorial design of dietary lysine levels (90, 100, 110, 120, and 130% of NRC recommendations) with or without Improvest was performed. Gilts were housed in 120 pens (4 pigs/pen) at 8 weeks of age (day 0). Gilts and feed were weighed immediately prior to each dietary phase change (days 0, 21, 42, 70, 91, and 105). Improvest was administered at 9 and 19 weeks of age (4 weeks pre-harvest). There was no diet × treatment × day (P &gt; 0.78) nor diet × treatment (P &gt; 0.11) interactions for any variables. Gilts had similar BWT, ADG, and ADFI until after the 2nd dose of Improvest, when Improvest-treated gilts were heavier (123.62 vs. 121.59 ± 0.68 and 138.16 vs. 133.97 ± 0.71 kg, days 91 and 105; P &lt; 0.01), had increased ADG (1.19 vs. 1.09 ± 0.01 and 1.03 vs. 0.88 ± 0.02 kg/day days 91 and 105; P &lt; 0.01) and consumed more feed (2.99 vs. 2.84 ± 0.03 and 3.19 vs. 2.68 ± 0.04 kg/pig/day; days 91 and 105; P &lt; 0.01) compared with untreated gilts. Carcass evaluation was conducted on 120 pigs (2 pigs/60 pens). No significant structures were present on ovaries of Improvest-treated gilts. Improvest-treated gilts were heavier (market and HCW; P ≤ 0.02) than controls. Improvest-treated gilts tended (P ≤ 0.08) to have heavier bone-in butt and bone-in ham weights. Belly weights were heavier (kg and %HCW; P ≤ 0.05) in Improvest-treated vs control gilts and were thicker (P = 0.01) but were similar (P &gt; 0.3) in length and width. While IV was similar (P &gt; 0.2) in belly fat, loin intramuscular fat was increased (P &lt; 0.01) from Improvest-treated gilts. Without additional dietary amino acids, Improvest-treated gilts delivered greater gain after the 2nd dose, yielding significantly heavier carcasses and primal cuts, including bellies which were larger as a percentage of HCW, and increased loin intramuscular fat.

Differential ketogenic diet-induced shift in CSF lipid/carbohydrate metabolome of pediatric epilepsy patients with optimal vs. no anticonvulsant response: a pilot study

Background The low carbohydrate, high fat ketogenic diet can be an effective anticonvulsant treatment in some pediatric patients with pharmacoresistant epilepsy. Its mechanism(s) of action, however, remain uncertain. Direct sampling of cerebrospinal fluid before and during metabolic therapy may reveal key changes associated with differential clinical outcomes. We characterized the relationship between seizure responsiveness and changes in lipid and carbohydrate metabolites. Methods We performed metabolomic analysis of cerebrospinal fluid samples taken before and during ketogenic diet treatment in patients with optimal response (100% seizure remission) and patients with no response (no seizure improvement) to search for differential diet effects in hallmark metabolic compounds in these two groups. Optimal responders and non-responders were similar in age range and included males and females. Seizure types and the etiologies or syndromes of epilepsy varied but did not appear to differ systematically between responders and non-responders. Results Analysis showed a strong effect of ketogenic diet treatment on the cerebrospinal fluid metabolome. Longitudinal and between-subjects analyses revealed that many lipids and carbohydrates were changed significantly by ketogenic diet, with changes typically being of larger magnitude in responders. Notably, responders had more robust changes in glucose and the ketone bodies β-hydroxybutyrate and acetoacetate than non-responders; conversely, non-responders had significant increases in fructose and sorbose, which did not occur in responders. Conclusions The data suggest that a differential and stronger metabolic response to the ketogenic diet may predict a better anticonvulsant response, and such variability is likely due to inherent biological factors of individual patients. Strategies to boost the metabolic response may be beneficial.

Differential ketogenic diet-induced shift in CSF lipid/carbohydrate metabolome of pediatric epilepsy patients with optimal vs. no anticonvulsant response: a pilot study

Background: The low carbohydrate, high fat ketogenic diet can be an effective anticonvulsant treatment in some pediatric patients with pharmacoresistant epilepsy. Its mechanism(s) of action, however, remain uncertain. Direct sampling of cerebrospinal fluid before and during metabolic therapy may reveal key changes associated with differential clinical outcomes. We characterized the relationship between seizure responsiveness and changes in lipid and carbohydrate metabolites. Methods: We performed metabolomic analysis of cerebrospinal fluid samples taken before and during ketogenic diet treatment in patients with optimal response (100% seizure remission) and patients with no response (no seizure improvement) to search for differential diet effects in hallmark metabolic compounds in these two groups. Optimal responders and non-responders were similar in age range and included males and females. Seizure types and the etiologies or syndromes of epilepsy varied but did not appear to differ systematically between responders and non-responders. Results: Analysis showed a strong effect of ketogenic diet treatment on the cerebrospinal fluid metabolome. Longitudinal and between-subjects analyses revealed that many lipids and carbohydrates were changed significantly by ketogenic diet, with changes typically being of larger magnitude in responders. Notably, responders had more robust changes in glucose and the ketone bodies b-hydroxybutyrate and acetoacetate than non-responders; conversely, non-responders had significant increases in fructose and sorbose, which did not occur in responders. Conclusions: The data suggest that a differential and stronger metabolic response to the ketogenic diet may predict a better anticonvulsant response, and such variability is likely due to inherent biological factors of individual patients. Strategies to boost the metabolic response may be beneficial.