RCIP was interpreted and reported as relative risk (RR) with 95% confidence intervals (CI) adjusted for gender, age cancer diagnosis, education, comorbidity, and sick leave weeks.
 
  Across cancer diagnoses 69 (83.1%) and 215 (81.4%) returned to work in the intervention and control group, respectively. No statistical effect was seen (RR 1.08 (95% CI 0.98-1.19)). Repeating the analyses solely for participants with breast cancer (
   = 290) showed a significant effect of the intervention (RR 1.12 (95% CI 1.01-1.23)).
 
  More than 80% returned to work in both groups. However, no statistical difference in RTW effect was seen across cancer diagnoses within one year from being exposed to an early, individually tailored vocational rehabilitation intervention compared with usual municipal RTW management.
 
  ISRCTN50753764.
 ISRCTN50753764.Introduction Ischemic stroke and traumatic brain injury are leading causes of acute mortality, and in the longer run, major causes of significant mental and physical impairment. Most of the brain neuronal cell death in the minutes and hours following an ischemic stroke or brain trauma is mediated by the process of excitotoxicity, in which sustained elevations of extracellular glutamate, reflecting a failure of ATP-dependent mechanism which sequester glutamate in neurons and astrocytes, drive excessive activation of NMDA receptors. Areas covered A literature search was undertaken to clarify the molecular mechanisms whereby excessive NMDA activation leads to excitotoxic neuronal death, and to determine what safe nutraceutical agents might have practical potential for rescuing at-risk neurons by intervening in these mechanisms. Expert opinion Activation of both NADPH oxidase and neuronal nitric oxide synthase in the microenvironment of activated NMDA receptors drives production of superoxide and highly toxic peroxynitrite. This leads to excessive activation of PARP and p38 MAP kinase, mitochondrial dysfunction, and subsequent neuronal death. Heme oxygenase-1 (HO-1) induction offers protection via inhibition of NADPH oxidase and promotion of cGMP generation. Phase 2-inductive nutraceuticals can induce HO-1, and other nutraceuticals can mimic the effects of its products biliverdin and carbon monoxide.Shortened telomeres are associated with aging and age-related diseases. Oxidative stress is thought to be a major contributor to telomere shortening, and antioxidants may be able to mitigate these effects.  https://www.selleckchem.com/products/gsk963.html  Ergothioneine is a naturally occurring amino acid with potent antioxidant properties. In order to investigate ergothioneine's effects on telomere length, we cultured primary human fibroblasts under standard and oxidative (10 µM H2O2) conditions and treated cells with 0.04, 0.1, 0.3, or 1.0 mg/ml ergothioneine for 8 weeks. Telomere length measurements were performed using high-throughput quantitative fluorescent in situ hybridization (HT Q-FISH). Treatment with ergothioneine transiently increased relative telomerase activity after 24 h (p  less then  0.05 for all concentrations). Under oxidative conditions, ergothioneine treatment resulted in significantly longer median telomere length and 20th percentile telomere length, and significantly reduced the percentage of short telomeres ( less then 3 kilobase pairs) for all treatment concentrations after 8 weeks. Telomere shortening rate was also reduced. Overall, ergothioneine demonstrated beneficial effects by decreasing the rate of telomere shortening and preserving telomere length under oxidative stress conditions. Our data support a potential role for ergothioneine in oxidative stress-related conditions and healthy aging.
  Cerebral ischemia/reperfusion (I/R) causes memory and learning impairments and apoptosis in the hippocampus. The aim of present study aimed to investigate the anti-apoptotic effects of silymarin-loaded chitosan nanoparticles (SM-CS-NPs) on the expression of Bcl-2 and Caspase-3 genes in hippocampal neurons after I/R injury.
 
  SM and SM-CS-NPs were orally administered (15 mg/kg) for 14 days, and then cerebral I/R injury was induced by the bilateral common carotid artery occlusion (BCCAO). One day after I/R induction, memory and learning impairments and various biochemical estimations were assessed.
 
  Our results indicated that SM-CS-NPs improved I/R-induced memory and learning impairments and oxidative damage in the hippocampal region. The qRT-PCR analysis indicated that SM-CS-NPs pretreatment inhibited I/R-induced neuronal apoptosis by increasing the expression of Bcl-2 and decreasing the expression of Caspase-3 in the hippocampus.
 
  These findings suggest that SM-CS-NPs exert neuroprotective effects, and the neuroprotection is likely to be associated with the regulation of Bcl-2 and Caspase-3, leading to inhibition of apoptotic cell death in hippocampal neurons.
 These findings suggest that SM-CS-NPs exert neuroprotective effects, and the neuroprotection is likely to be associated with the regulation of Bcl-2 and Caspase-3, leading to inhibition of apoptotic cell death in hippocampal neurons.Introduction Heart failure (HF) affects over 6 million Americans and approximately 650,000 new cases are diagnosed annually, with patients evenly split between HFrEF and HFpEF. Recent advances in therapy for these patients have been limited to pharmaceutical agents, with CRT remaining the most reliable device therapy option since its advent almost twenty years ago. In 2019, after almost two decades without the introduction of a new device therapy for the treatment of moderate HF, the FDA approved CCM® therapy, delivered by the Optimizer Smart device, for patients with NYHA Class III HF who are on guideline-directed medical therapy (GDMT), in normal sinus rhythm (NSR), and with EF ranging from 25% to 45%, and who are ineligible for CRT.Areas covered Multiple clinical trials support the use of CCM to improve quality of life, functional class, and 6-min hall walk distance. This article will discuss the science behind CCM therapy, the presumed mechanisms of action, the pre-clinical studies that shaped subsequent endeavors, and the clinical trials that support its use.Expert opinion The introduction of CCM therapy bridges a therapeutic gap for patients with few or no other therapeutic options for NYHA III heart failure.