The brain is the body's control center, so when a disease affects it, the outcomes are devastating. Alzheimer's and Parkinson's disease, and multiple sclerosis are brain diseases that cause a large number of human deaths worldwide. Curcumin has demonstrated beneficial effects on brain health through several mechanisms such as antioxidant, amyloid β-binding, anti-inflammatory, tau inhibition, metal chelation, neurogenesis activity, and synaptogenesis promotion. The therapeutic limitation of curcumin is its bioavailability, and to address this problem, new nanoformulations are being developed. The present review aims to summarize the general bioactivity of curcumin in neurological disorders, how functional molecules are extracted, and the different types of nanoformulations available.

Green or red cabbage or their aqueous extracts based croquettes were formulated and compared with control croquettes over one‐month frozen storage, involving baking and frying procedures. Maximum ash (p < .05) was quantified in red cabbage croquettes, 3.99 ± 0.24% (Baked) and 4.27 ± 0.09% (Fried) while minimal fat was found in green and red cabbage croquettes, predominantly via baking; 3.07 ± 0.25% and 3.15 ± 0.30%, respectively. Antioxidant activity was maximally reported (p < .05) in red cabbage based treatments, though, it reduced with the progression in storage. Total polyphenols in baked and fried cabbage croquettes were in the range from 70.59 ± 3.25 to 121.61 ± 5.85 and 71.17 ± 3.06 to 125.82 ± 6.09 mg gallic acid equivalent (GAE) per 100 g F.W., respectively, and demonstrated linear relationship with antioxidant potential. Among treated samples, maximum score for overall acceptability was attained by green cabbage based croquettes among fried (7.71 ± 1.35) and baked (7.27 ± 0.49) samples. Thus, cabbage based croquettes showed high nutritional and antioxidant potential without affecting product acceptability.

BACKGROUND: The burden of inflammatory bowel disease (IBD) is rising globally, with substantial variation in levels and trends of disease in different countries and regions. Understanding these geographical differences is crucial for formulating effective strategies for preventing and treating IBD. We report the prevalence, mortality, and overall burden of IBD in 195 countries and territories between 1990 and 2017, based on data from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017. METHODS: We modelled mortality due to IBD using a standard Cause of Death Ensemble model including data mainly from vital registrations. To estimate the non-fatal burden, we used data presented in primary studies, hospital discharges, and claims data, and used DisMod-MR 2.1, a Bayesian meta-regression tool, to ensure consistency between measures. Mortality, prevalence, years of life lost (YLLs) due to premature death, years lived with disability (YLDs), and disability-adjusted life-years (DALYs) were estimated. All of the estimates were reported as numbers and rates per 100 000 population, with 95% uncertainty intervals (UI). FINDINGS: In 2017, there were 6·8 million (95% UI 6·4-7·3) cases of IBD globally. The age-standardised prevalence rate increased from 79·5 (75·9-83·5) per 100 000 population in 1990 to 84·3 (79·2-89·9) per 100 000 population in 2017. The age-standardised death rate decreased from 0·61 (0·55-0·69) per 100 000 population in 1990 to 0·51 (0·42-0·54) per 100 000 population in 2017. At the GBD regional level, the highest age-standardised prevalence rate in 2017 occurred in high-income North America (422·0 [398·7-446·1] per 100 000) and the lowest age-standardised prevalence rates were observed in the Caribbean (6·7 [6·3-7·2] per 100 000 population). High Socio-demographic Index (SDI) locations had the highest age-standardised prevalence rate, while low SDI regions had the lowest age-standardised prevalence rate. At the national level, the USA had the highest age-standardised prevalence rate (464·5 [438·6-490·9] per 100 000 population), followed by the UK (449·6 [420·6-481·6] per 100 000). Vanuatu had the highest age-standardised death rate in 2017 (1·8 [0·8-3·2] per 100 000 population) and Singapore had the lowest (0·08 [0·06-0·14] per 100 000 population). The total YLDs attributed to IBD almost doubled over the study period, from 0·56 million (0·39-0·77) in 1990 to 1·02 million (0·71-1·38) in 2017. The age-standardised rate of DALYs decreased from 26·5 (21·0-33·0) per 100 000 population in 1990 to 23·2 (19·1-27·8) per 100 000 population in 2017. INTERPRETATION: The prevalence of IBD increased substantially in many regions from 1990 to 2017, which might pose a substantial social and economic burden on governments and health systems in the coming years. Our findings can be useful for policy makers developing strategies to tackle IBD, including the education of specialised personnel to address the burden of this complex disease. FUNDING: Bill & Melinda Gates Foundation.

BACKGROUND: Cirrhosis and other chronic liver diseases (collectively referred to as cirrhosis in this paper) are a major cause of morbidity and mortality globally, although the burden and underlying causes differ across locations and demographic groups. We report on results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017 on the burden of cirrhosis and its trends since 1990, by cause, sex, and age, for 195 countries and territories. METHODS: We used data from vital registrations, vital registration samples, and verbal autopsies to estimate mortality. We modelled prevalence of total, compensated, and decompensated cirrhosis on the basis of hospital and claims data. Disability-adjusted life-years (DALYs) were calculated as the sum of years of life lost due to premature death and years lived with disability. Estimates are presented as numbers and age-standardised or age-specific rates per 100 000 population, with 95% uncertainty intervals (UIs). All estimates are presented for five causes of cirrhosis: hepatitis B, hepatitis C, alcohol-related liver disease, non-alcoholic steatohepatitis (NASH), and other causes. We compared mortality, prevalence, and DALY estimates with those expected according to the Socio-demographic Index (SDI) as a proxy for the development status of regions and countries. FINDINGS: In 2017, cirrhosis caused more than 1·32 million (95% UI 1·27-1·45) deaths (440 000 [416 000-518 000; 33·3%] in females and 883 000 [838 000-967 000; 66·7%] in males) globally, compared with less than 899 000 (829 000-948 000) deaths in 1990. Deaths due to cirrhosis constituted 2·4% (2·3-2·6) of total deaths globally in 2017 compared with 1·9% (1·8-2·0) in 1990. Despite an increase in the number of deaths, the age-standardised death rate decreased from 21·0 (19·2-22·3) per 100 000 population in 1990 to 16·5 (15·8-18·1) per 100 000 population in 2017. Sub-Saharan Africa had the highest age-standardised death rate among GBD super-regions for all years of the study period (32·2 [25·8-38·6] deaths per 100 000 population in 2017), and the high-income super-region had the lowest (10·1 [9·8-10·5] deaths per 100 000 population in 2017). The age-standardised death rate decreased or remained constant from 1990 to 2017 in all GBD regions except eastern Europe and central Asia, where the age-standardised death rate increased, primarily due to increases in alcohol-related liver disease prevalence. At the national level, the age-standardised death rate of cirrhosis was lowest in Singapore in 2017 (3·7 [3·3-4·0] per 100 000 in 2017) and highest in Egypt in all years since 1990 (103·3 [64·4-133·4] per 100 000 in 2017). There were 10·6 million (10·3-10·9) prevalent cases of decompensated cirrhosis and 112 million (107-119) prevalent cases of compensated cirrhosis globally in 2017. There was a significant increase in age-standardised prevalence rate of decompensated cirrhosis between 1990 and 2017. Cirrhosis caused by NASH had a steady age-standardised death rate throughout the study period, whereas the other four causes showed declines in age-standardised death rate. The age-standardised prevalence of compensated and decompensated cirrhosis due to NASH increased more than for any other cause of cirrhosis (by 33·2% for compensated cirrhosis and 54·8% for decompensated cirrhosis) over the study period. From 1990 to 2017, the number of prevalent cases more than doubled for compensated cirrhosis due to NASH and more than tripled for decompensated cirrhosis due to NASH. In 2017, age-standardised death and DALY rates were lower among countries and territories with higher SDI. INTERPRETATION: Cirrhosis imposes a substantial health burden on many countries and this burden has increased at the global level since 1990, partly due to population growth and ageing. Although the age-standardised death and DALY rates of cirrhosis decreased from 1990 to 2017, numbers of deaths and DALYs and the proportion of all global deaths due to cirrhosis increased. Despite the availability of effective interventions for the prevention and treatment of hepatitis B and C, they were still the main causes of cirrhosis burden worldwide, particularly in low-income countries. The impact of hepatitis B and C is expected to be attenuated and overtaken by that of NASH in the near future. Cost-effective interventions are required to continue the prevention and treatment of viral hepatitis, and to achieve early diagnosis and prevention of cirrhosis due to alcohol-related liver disease and NASH. FUNDING: Bill & Melinda Gates Foundation.

The report describes how we have improved our understanding of the transmission of Hendra virus from flying foxes to horses. This information improves our ability to better manage the risk of transmission and spillover even with good vaccination rates of horses against Hendra virus. In areas where vaccination is poor then our findings are even more likely to prove lifesaving.

The fungal skin disease chytridiomycosis has caused the devastating decline and extinction of hundreds of amphibian species globally, yet the potential for evolving resistance, and the underlying pathophysiological mechanisms remain poorly understood. We exposed 406 naïve, captive-raised alpine tree frogs (Litoria verreauxii alpina) from multiple populations (one evolutionarily naïve to chytridiomycosis) to the aetiological agent Batrachochytrium dendrobatidis in two concurrent and controlled infection experiments. We investigated (A) survival outcomes and clinical pathogen burdens between populations and clutches, and (B) individual host tissue responses to chytridiomycosis. Here we present multiple interrelated datasets associated with these exposure experiments, including animal signalment, survival and pathogen burden of 355 animals from Experiment A, and the following datasets related to 61 animals from Experiment B: animal signalment and pathogen burden; raw RNA-Seq reads from skin, liver and spleen tissues; de novo assembled transcriptomes for each tissue type; raw gene expression data; annotation data for each gene; and raw metabolite expression data from skin and liver tissues. These data provide an extensive baseline for future analyses.

X-ray tomography can provide structural information of whole cells in close to their native state. Radiation-induced damage, however, imposes a practical limit to image resolution, and as such, a choice between damage, image contrast, and image resolution must be made. New coherent diffractive imaging techniques, such Fresnel Coherent Diffractive Imaging (FCDI), allows quantitative phase information with exceptional dose efficiency, high contrast, and nano-scale resolution. Here we present three-dimensional quantitative images of a whole eukaryotic cell by FCDI at a spatial resolution below 70 nm with sufficient phase contrast to distinguish major cellular components. From our data, we estimate that the minimum dose required for a similar resolution is close to that predicted by the Rose criterion, considerably below accepted estimates of the maximum dose a frozen-hydrated cell can tolerate. Based on the dose efficiency, contrast, and resolution achieved, we expect this technique will find immediate applications in tomographic cellular characterisation.

The effect of short term-heat stress and -vitamin E supplementation on carcass traits and muscle quality – vitamin E, nutritional value and retail colour of lambs was investigated. Forty-eight lambs (crossbred; 42 ± 2 kg body weight, 7 mo age) were randomly allocated by body weight to one of three groups (n = 16) and fed 3 different doses of Vitamin E and Se. The doses of Vitamin E and Se for control (CON), moderate (MOD), and supranutritional (SUP) diets were 28, 130, 228 mg/kg DM as α-tocopherol acetate and 0.16, 0.66, 1.16 mg Se as SelPlex™ kg/DM, respectively. Lambs were fed for 4 weeks followed by a week of exposure to heat treatment. After 4 weeks feeding in individual pens, including 1 week of adaptation, lambs were moved to metabolism cages for 1 week and allocated to one of 2 heat regimes (8 per feeding group): thermoneutral (TN) (18–21◦C and 40–50% relative humidity) or heat stress (HS) (28–40◦C and 30–40% relative humidity) conditions. Final body weight (P = 0.05, 44.1 vs 46.6 kg) and hot carcass weight (P = 0.01, 21.1 vs 22.5 kg) were significantly affected by diet such that lambs supplemented with SUP levels of antioxidants had a higher FBW and HCW as compared with lambs fed MOD and CON antioxidant diets, respectively. Vitamin E concentration in the longissimus lumborum (LL) muscle tended to be higher in lambs fed moderate or supranutritional levels of antioxidants compared with control lambs and values from all treatments were below the threshold (3.2 mg/kg muscle) for optimal maintenance of retail colour. Vitamin E supplementation also reduced lipid oxidation of aged meat, as assessed by thiobarbituric acid reactive substances (TBARS) formation after 72 h of display. One week of heat stress to lambs significantly increased muscle linoleic acid concentration, which in turn increased total n-6 concentration compared with the control group. Results demonstrate that 4 weeks of vitamin E supplementation or 1 week heat stress might not have been adequate to make significant changes in muscle vitamin E concentration and fatty acid composition, which in turn can influence retail colour stability of meat.

Phosphofructokinase-1 (PFK-1) is a key regulatory enzyme of postmortem glycolysis. PFK-1’s activity is regulated antemortem by a number of compounds including adenosine monophosphate (AMP) and fructose 2,6-bisphosphate (F-2,6-BP). However, PFK-1’s postmortem regulation by AMP and F-2,6-BP is still unclear. Therefore, a study was conducted where porcine longissimus lumborum samples were collected to determine PFK-1 activity as affected by various concentrations of AMP and F-2,6-BP at buffered pH. Both compounds increased PFK-1 activity. However, at physiological concentrations, 50 and 150 μM AMP increased PFK-1 activity compared to 1 and 2 μM F-2,6-BP. Thus, AMP may play a greater role in dictating the rate and extent of postmortem glycolysis and pH decline than F-2,6-BP.