To evaluate clinical response after external lumbar drainage (ELD) and ventriculoperitoneal shunting (VPS) in a cohort of patients with idiopathic normal pressure hydrocephalus associated with parkinsonism (iNPH-P), considering parkinsonism as clinical primary outcome.

Patients underwent long-term 72-h intracranial pressure-controlled CSF ELD. Clinical motor response before and after ELD was evaluated using changes in UPDRS-ME as outcome measure. A standardized cognitive assessment was also performed. iNPH-P patients who underwent VPS were clinically followed-up after surgery.

Fourteen iNPH-P patients (age 69.3 ± 11.6years) were studied. The time of evaluation after ELD removal was 3.5 ± 1.8days. Piperlongumine manufacturer We observed a significant motor improvement after the drainage in eight (57.1%) patients. Percent clinical motor response was 18.4 ± 6.7%. Twelve (85.7%) patients underwent VPS. Nine patients were examined after surgery at 31.6 ± 7months. Four (44.4%) patients presented a clinically detectable improvement in motor response after VPS. No significant changes in cognitive performances were detected.

A clinically detectable motor response on parkinsonian signs was observed in a consistent part of iNPH-P patients few days after ELD as well as over two and half years after VPS. Parkinsonism should be considered as outcome measure for the clinical management of patients with iNPH-P.

A clinically detectable motor response on parkinsonian signs was observed in a consistent part of iNPH-P patients few days after ELD as well as over two and half years after VPS. Parkinsonism should be considered as outcome measure for the clinical management of patients with iNPH-P.This study was conducted to investigate the effects of hot-melt extrusion (HME)-processed copper (Cu) sulfate supplementation on the growth performance, gut microbiota, metabolic function of Cu, and bioavailability of Cu in weanling pigs fed a corn-soybean meal basal diets. A total of 180 piglets (Yorkshire × Landrace × Duroc) of mixed-sex randomly were allotted to six treatments on the basis of initial average body weight (6.36 ± 0.39 kg) to six dietary treatments. There were six replicates in each treatment with 5 pigs per replicates. The dietary treatments included levels of CuSO4 (IN6, 6 mg Cu/kg diets; IN125, 125 mg Cu/kg diets), nano-CuSO4 (HME6, 6 mg Cu/kg diets; HME65, 65 mg Cu/kg diets; and HME125, 125 mg Cu/kg diets), and Cu-methionine (ORG125, 125 mg Cu/kg diets). The weanling pigs fed diets supplemented with the HME65 and HME125 showed a greater body weight and feed intake compared with IN6 and IN125 (P  less then  0.05). The weaning pigs fed diets supplemented with the HME125 showed the highest datment (P  less then  0.05). Taken together, these results suggest that the HME65 can be an alternative to IN125 in weanling pigs due to the greater overall average daily gain, improved villus height, and higher bioavailability.Cadmium pollution is serious heavy metal pollution in environmental pollution and impacts on livestock productivity. However, the effect and mechanisms of cadmium toxicity on the broiler remain unclear. This study aimed to explore the liver oxidative damage and reveal the related long non-coding RNA (lncRNA) expression patterns in the broiler liver with cadmium exposure. The broilers were fed with diets containing CdCl2 and detected the oxidative stress indexes in the liver tissues. Transcriptome sequencing of broiler liver was performed to identify cadmium exposure-related differentially expressed lncRNAs (DElncRNAs). The functions and pathways of DElncRNAs were analyzed by GO and KEGG. The sequencing results were verified by the quantitative real-time polymerase chain reaction. Cadmium exposure induced tissue structure disorder, focal hemorrhage, and irregular hepatocytes in the broiler liver, and significantly decreased GSH level and enzyme activities, and increased MDA expression in the liver. A total of 74 DElncRNAs were obtained in cadmium group compared with the control group, which were enriched in the GO terms, including intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator, branched-chain amino acid biosynthetic process. The enriched KEGG pathways, including lysine biosynthesis, valine, leucine and isoleucine biosynthesis, and pantothenate and CoA biosynthesis, were related to oxidative stress. PCR analysis indicated that the changes in ENSGALG00000053559, ENSGALG00000053926, and ENSGALG00000054404 expression were consistent with sequencing. Our results provide novel lncRNAs involved in oxidative stress in the broiler liver with cadmium exposure.Grape seed proanthocyanidins (GSP) are known as condensed tannins and have been used as an anti-oxidant in various neurodegenerative diseases. In our study, GSP was used as a daily dietary supplement and the neuroprotective effects were evaluated on the retinal ganglion cells (RGCs) in the retinal tissues in glaucomatous DBA/2D (D2) mice. D2 mice and age-matched non-glaucomatous DBA/2J-Gpnmb+ (D2-Gpnmb+) mice were fed with GSP or a control diet for up to 6 months. The intraocular pressure (IOP), RGC survival, glial fibrillary acidic protein (GFAP), the levels of apoptotic proteins, and the expression of oxidative stress markers in retinal tissues were determined. In our study, the neuroprotective effects of GSP on retinal tissues were confirmed, as evidenced by (a) GSP inhibited the IOP elevation in D2 mice; (b) GSP enhanced RGC survival and mediated the apoptotic protein expression; (c) GSP suppressed GFAP expression; and (d) the oxidative stress and the levels of mitochondrial reactive oxygen species were regulated by GSP. Our findings indicate that GSP has promising potential to preserve retinal tissue functions via regulating oxidative stress and mitochondrial functions.Aberrant production of adipokines, a group of adipocytes-derived hormones, is considered one of the most important pathological characteristics of obesity. In individuals with obesity, beneficial adipokines, such as adiponectin are downregulated, whereas leptin and other pro-inflammatory adipokines are highly upregulated. Hence, the imbalance in levels of these adipokines is thought to promote the development of obesity-linked complications. However, the mechanisms by which adipokines contribute to the pathogenesis of various diseases have not been clearly understood. Inflammasomes represent key signaling platform that triggers the inflammatory and immune responses through the processing of the interleukin family of pro-inflammatory cytokines in a caspase-1-dependent manner. Beyond their traditional function as a component of the innate immune system, inflammasomes have been recently integrated into the pathological process of multiple metabolism- and obesity-related disorders such as cardiovascular diseases, diabetes, fatty liver disease, and cancer.