There were no differences in perceived sleep quality, difficulty falling asleep, or daytime alertness between groups.
 
  People who co-use cocaine and cannabis may report reduced sleep time relative to those who only use cocaine. Co-use of cannabis may exacerbate sleep difficulties in people who use cocaine by decreasing total sleep time, although it is important to note that the groups each reported similar sleep quality. Implications for treatment and directions for future research are discussed.
 People who co-use cocaine and cannabis may report reduced sleep time relative to those who only use cocaine. Co-use of cannabis may exacerbate sleep difficulties in people who use cocaine by decreasing total sleep time, although it is important to note that the groups each reported similar sleep quality. Implications for treatment and directions for future research are discussed.
  There is substantial experimental evidence to support the view that Ginkgo biloba L. (Ginkgoaceae), a traditional Chinese medicine known to treating stroke, has a protective effect on the central nervous system and significantly improves the cognitive dysfunction caused by disease, including alzheimer disease (AD), vascular dementia, and diabetic encephalopathy. Although a number of studies have reported that ginkgolide B (GB), a diterpenoid lactone compound extracted from Ginkgo biloba leaves, has neuroprotective effects, very little research has been performed to explore its potential pharmacological mechanism on astrocytes under abnormal glutamate (Glu) metabolism in the pathological environment of AD.
 
  We investigated the protective effect and mechanism of GB on Glu-induced astrocytes injury.
 
  Astrocytes were randomly divided into the control group, Glu group, GB group, and GB+IWP-4 group.The CCK-8 assay was used to determine relative cell viability in vitro. Furthermore, RNA sequencing (RNA-seq) was ive effect on astrocytes, and promoted Glu transporter gene and protein expression caused by Glu.
 
  Our findings demonstrate that GB may play a protective role in Glu-induced astrocyte injury by regulating the Hippo and Wnt pathways. GB was closely associated with the Wnt pathway by promoting expression of the Glu transporter and inhibiting Glu-induced injury in astrocytes.
 Our findings demonstrate that GB may play a protective role in Glu-induced astrocyte injury by regulating the Hippo and Wnt pathways. GB was closely associated with the Wnt pathway by promoting expression of the Glu transporter and inhibiting Glu-induced injury in astrocytes.
  Moringa oleifera Lam. leaf (MOL), a rich source of protein and phenolics, was traditionally used to treat various diseases including headaches, fevers, sore throat and dyslipidemia.  https://www.selleckchem.com/products/ABT-888.html  Recently, MOL was reported to possess antioxidant, anti-dyslipidemia and hepato-renal protective activities, indicating that MOL could become a potential agent to improve metabolic disorders associated with hyperuricemia. The antihyperuricemic effect of MOL hydrolysate (MOLH) with high contents of phenolics and peptides remains unknown.
 
  The aim of this study is to investigate xanthine oxidase (XO) inhibitory activity of MOLH, to clarify phenolic and peptide profiles of MOLH, and to evaluate possible mechanism underlying the antihyperuricemic effect of MOLH.
 
  MOLH was prepared by enzymatic hydrolysis using commercial trypsin. XO inhibitory activity was determined by XO reaction-UPLC-MS coupling method. The chemical profiles of the phenolic and peptide fractions of MOLH were determined by UPLC-QTOF-MS/MS. The antihyperuricemic e metabolic disorders associated with hyperuricemia by its multiple actions on liver MDA (p<0.001), serum CRE (p<0.05at 500mg/kg) and serum TG (p<0.001).
 
  The results provided scientific evidence that MOLH rich in phenolics and peptides ameliorated hyperuricemia and metabolic disorders. This study validated the potential use of MOLH for regulation of hyperuricemia.
 The results provided scientific evidence that MOLH rich in phenolics and peptides ameliorated hyperuricemia and metabolic disorders. This study validated the potential use of MOLH for regulation of hyperuricemia.
  Cross-cultural comparison of plants used during lactation and the postpartum period offers insight into a largely overlooked area of ethnopharmacological research. Potential roles of phytochemicals in emerging models of interaction among immunity, inflammation, microbiome and nervous system effects on perinatal development have relevance for the life-long health of individuals and of populations in both traditional and contemporary contexts.
 
  Delineate and interpret patterns of traditional and contemporary global use of medicinal plants ingested by mothers during the postpartum period relative to phytochemical activity on immune development and gastrointestinal microbiome of breastfed infants, and on maternal health.
 
  Published reviews and surveys on galactagogues and postpartum recovery practices plus ethnobotanical studies from around the world were used to identify and rank plants, and ascertain regional use patterns. Scientific literature for 20 most-cited plants based on frequency of publication was nd contributes phytochemicals absent in most contemporary diets and patterns of ingestion, with potential impacts on allergic, inflammatory and other conditions. Polyphenolics and other phytochemicals are widely immunologically active, present in breast milk and predominately non-toxic. Systematic analysis of phytochemicals in human milk, infant lumen and plasma, and immunomodulatory studies that differentiate maternal ingestion during lactation from pregnancy, are needed. Potential herb-drug interaction and other adverse effects should remain central to obstetric advising, but unless a plant is specifically shown as harmful, considering potential contributions to health of individuals and populations, blanket advisories against postpartum herbal use during lactation appear empirically unwarranted.Oxidopamine (6-hydroxydopamine, 6-OHDA) is a toxin commonly used for the creation of experimental animal models of Parkinson's disease, attention-deficit hyperactivity disorder, and Lesch-Nyhan syndrome. Its exact mechanism of action is not completely understood, although there are many indications that it is related to the generation of reactive oxygen species (ROS), primarily in dopaminergic neurons. In certain experimental conditions, oxidopamine may also cause programmed cell death via various signaling pathways. Oxidopamine may also have a significant impact on chromatin structure and nuclear structural organization in some cells. Today, many researchers use oxidopamine-associated oxidative damage to evaluate different antioxidant-based pharmacologically active compounds as drug candidates for various neurological and non-neurological diseases. Additional research is needed to clarify the exact biochemical pathways associated with oxidopamine toxicity, related ROS generation and apoptosis. In this short review, we focus on the recent research in experimental physiology and pharmacology, related to the cellular and animal experimental models of oxidopamine - mediated toxicity.