While Medicaid expansion is associated with decreased uninsured rates and earlier cancer diagnoses, no study has demonstrated an association between Medicaid expansion and cancer mortality. Our primary objective was to quantify the relationship between early Medicaid expansion and changes in cancer mortality rates.
 
  We obtained county-level data from the National Center for Health Statistics for adults ages 20-64 who died from cancer from 2007-2009 (pre-expansion) and 2012-2016 (post-expansion). We compared changes in cancer mortality rates in early Medicaid expansion states (CA, CT, DC, MN, NJ, and WA) vs. non-expansion states through a difference-in-differences (DID) analysis using hierarchical Bayesian regression. An exploratory analysis of cancer mortality changes associated with the larger-scale 2014 Medicaid expansions was also performed.
 
  In adjusted DID analyses, we observed a statistically significant decrease of 3.07 (95% credible interval = 2.19 to 3.95) cancer deaths per 100,000 in early expansion vs. non-expansion states, which translates to an estimated decrease of 5,276 cancer deaths in the early expansion states during the study period. Expansion-associated decreases in cancer mortality were observed for pancreatic cancer. Exploratory analyses of the 2014 Medicaid expansions showed a decrease in pancreatic cancer mortality (-0.18 deaths per 100,000, 95% confidence interval = -0.32 to -0.05) in states that expanded Medicaid by 2014 compared to non-expansion states.
 
  Early Medicaid expansion was associated with reduced cancer mortality rates, especially for pancreatic cancer, a cancer with short median survival where changes in prognosis would be most visible with limited follow-up.
 Early Medicaid expansion was associated with reduced cancer mortality rates, especially for pancreatic cancer, a cancer with short median survival where changes in prognosis would be most visible with limited follow-up.
  Adverse medication events are associated with a significant number of hospital admissions, and the appropriate recording of these events plays a vital role in medication safety. We set out to analyse the time and extrapolated cost in reporting adverse drug reactions (ADRs).
 
  A time and motion study of the tasks involved in reviewing, assessing, reporting and communicating ADRs was done over a period of 2 months.
 
  We found a median of 69 min was needed in background work per ADR report.
 
  The commitment involved in the support of this program is considerable and will encourage further refinement to streamline the process.
 The commitment involved in the support of this program is considerable and will encourage further refinement to streamline the process.Recent studies demonstrate that histones are subjected to a series of short-chain fatty acid modifications that is known as histone acylations. However, the enzymes responsible for histone acylations in vivo are not well characterized. Here, we report that HBO1 is a versatile histone acyltransferase that catalyzes not only histone acetylation but also propionylation, butyrylation and crotonylation both in vivo and in vitro and does so in a JADE or BRPF family scaffold protein-dependent manner. We show that the minimal HBO1/BRPF2 complex can accommodate acetyl-CoA, propionyl-CoA, butyryl-CoA and crotonyl-CoA. Comparison of CBP and HBO1 reveals that they catalyze histone acylations at overlapping as well as distinct sites, with HBO1 being the key enzyme for H3K14 acylations. Genome-wide chromatin immunoprecipitation assay demonstrates that HBO1 is highly enriched at and contributes to bulk histone acylations on the transcriptional start sites of active transcribed genes.  https://www.selleckchem.com/products/Furosemide(Lasix).html  HBO1 promoter intensity highly correlates with the level of promoter histone acylation, but has no significant correlation with level of transcription. We also show that HBO1 is associated with a subset of DNA replication origins. Collectively our study establishes HBO1 as a versatile histone acyltransferase that links histone acylations to promoter acylations and selection of DNA replication origins.
  Comparisons between healthy controls (HCs) and individuals with mood disorders have shown more cognitive dysfunction among the latter group, in particular in bipolar disorder (BD). This study aimed to characterize the pattern of cognitive function of BD and major depressive disorder (MDD) and compare them to HC using the (CogState Research Battery) CSRB™.
 
  Participants were tested, comprising the following domains processing speed, attention, working memory, visual memory, executive functions, and verbal memory. Quality of life and functionality were also assessed. Multiple linear regression models were performed to examine the effect of demographic characteristics and functionality on cognitive outcomes separately for BD and MDD.
 
  Ninety individuals participated in the study, of which 32 had BD, 30 had MDD, and 28 were HC. Differences were found between both BD and MDD and HC for the composite cognitive score, with significant differences between BD and HC (Diff=-5.5, 95% CI=[-9.5, -1.5], p=0.005), and MDD and HC (Diff=-4.6, 95% CI=[-8.6, -0.5], p=0.025). There were overall significant differences in five cognitive domains processing speed (p=0.001 and p=0.004), attention (p=0.002), working memory (p=0.02), visual memory (p=0.021), and verbal memory (p=0.007). BD also presented worse performance than both MDD and HC, and MDD presented better performance than BD but worse than HC in quality of life and functionality. Multiple linear regression models were significative for education (p<0.001) and age (p=0.004) for BD and education (p<0.001) for MDD.
 
  In general, cognition is more affected in BD than MDD, which could be associated with functional and quality of life impairment.
 In general, cognition is more affected in BD than MDD, which could be associated with functional and quality of life impairment.Endometritis is an inflammatory disease of the endometrium, which is responsible for endometrial dysfunction, decidualization failure, and increased incidence of early pregnancy loss. SCM-198, a synthetic form of leonurine, is well known to possess anti-inflammatory effects. SCM-198 has been reported to display beneficial effects on endometritis. However, the specific mechanisms of SCM-198 in preventing endometritis remain unknown. In this study, we focused on the molecular mechanism of SCM-198 in inhibiting endometritis. The anti-inflammatory effects and the related signaling pathways of SCM-198 were studied in vitro using human endometrial stromal cells (hESCs). Reverse transcriptase-polymerase chain reaction and western blot analysis results demonstrated that SCM-198 markedly inhibited lipopolysaccharide (LPS)-induced endometrial inflammatory response by suppressing the LPS-JNK-cJUN/cFOS-TLR4-NF-κB pathway. The preventive and therapeutic effects of SCM-198 on endometrial inflammation were explored by using a mouse model of LPS-induced endometritis.