It is believed that HPV infection can result in the death of placental trophoblasts and cause miscarriages or preterm birth. In clinical cases of placental villi positive for HPV DNA reported by other authors, contamination is suspected in the act of crossing the cervical canal.  https://www.selleckchem.com/products/ly2157299.html  We analyzed placental samples of women who resorted to elective abortion obtained by hysterosuction of ovular material, bypassing any contact with the cervical canal and vagina.
 
  We studied the chorionic villi of the placenta of 64 women who resorted to voluntary termination of pregnancy, in the first trimester. To avoid contamination of the villi by the cervical canal, we analyzed placental samples obtained by hysterosuction of ovular material, bypassing any contact with the cervical canal and vagina. All samples of chorionic villi were manually selected from the aborted material and subjected to research for HPV DNA.
 
  HPV DNA was detected in 10 out of 60 women (16.6%). The HPV DNA identified in the placenta belonged to genotypes 6, 16, 35, 53, and 90.
 
  The study shows that papillomavirus DNA can infect the placenta and that placenta HPV infection can occur as early as the first trimester of pregnancy.
 The study shows that papillomavirus DNA can infect the placenta and that placenta HPV infection can occur as early as the first trimester of pregnancy.
  Many studies have proposed that the pathogenesis of obesity has a genetic basis, with an important risk factor being the presence of polymorphisms in the region of the TMEM18 gene, which plays a significant role in feeding behaviour; however, subsequent studies among different ethnic populations and age groups have shown inconsistent results. Therefore, this present meta-analysis examines the relationship between TMEM18 polymorphisms with the risk of obesity with regard to age group and ethnic population.
 
  A literature database search was conducted for available relevant studies investigating the association between obesity risk and the presence of rs6548238, rs4854344, rs11127485, rs2867125 and rs7561317 polymorphisms in TMEM18. Pooled odds ratio (OR) and 95% confidence intervals (95% CI) were calculated by either a fixed-effects model or random effect model based on a heterogeneity test. The meta-analysis of rs6548238 and its surrogates examined the relationships between 53 395 obesity cases and 123 972 e that differences exist between ethnic populations and age groups, supporting those of a previous study showing the various effects of genetic factors on age and ethnic groups.
  Endoplasmic reticulum (ER) stress is a common feature of Parkinson's disease (PD), and several PD-related genes are responsible for ER dysfunction. Recent studies suggested LRRK2-G2019S, a pathogenic mutation in the PD-associated gene LRRK2, cause ER dysfunction, and could thereby contribute to the development of PD. It remains unclear, however, how mutant LRRK2 influence ER stress to control cellular outcome. In this study, we identified the mechanism by which LRRK2-G2019S accelerates ER stress and cell death in astrocytes.
 
  To investigate changes in ER stress response genes, we treated LRRK2-wild type and LRRK2-G2019S astrocytes with tunicamycin, an ER stress-inducing agent, and performed gene expression profiling with microarrays. The XBP1 SUMOylation and PIAS1 ubiquitination were performed using immunoprecipitation assay. The effect of astrocyte to neuronal survival were assessed by astrocytes-neuron coculture and slice culture systems. To provide in vivo proof-of-concept of our approach, we measured Ee correlation between mutant LRRK2 and pathophysiological ER stress in PD, and suggest a plausible model that explains this connection.
 Our findings reveal a novel regulatory mechanism involving XBP1 in LRRK2-G2019S mutant astrocytes, and highlight the importance of the SHP/PIAS1/XBP1 axis in PD models. These findings provide important insight into the basis of the correlation between mutant LRRK2 and pathophysiological ER stress in PD, and suggest a plausible model that explains this connection.
  The most common cause of respiratory failure in premature infants is respiratory distress syndrome. Historically, respiratory distress syndrome has been treated by intratracheal surfactant injection followed by mechanical ventilation. In view of the risk of pulmonary injury associated with mechanical ventilation and subsequent chronic pulmonary lung disease, less invasive treatment modalities have been suggested to reduce pulmonary complications.
 
  148 neonates (with gestational age of 28 to 34 weeks) with respiratory distress syndrome admitted to Imam Khomeini Hospital in Ahwaz in 2018 were enrolled in this clinical trial study. 74 neonates were assigned to duo positive airway pressure (NDUOPAP) group and 74 neonates to nasal continuous positive airway pressure (NCPAP) group. The primary outcome in this study was failure of N-DUOPAP and NCPAP treatments within the first 72h after birth and secondary outcomes included treatment complications.
 
  there was not significant difference between DUOPAP (4.1 %) and in the CPAP group.
 
  IRCT20180821040847N1 , Approved on 2018-09-10.
 IRCT20180821040847N1 , Approved on 2018-09-10.
  An urgent transition to more sustainable diets is necessary for the improvement of human and planetary health. One way to achieve this is for sustainable practices to become mainstream. We estimated the potential health impact of wider adoption of dietary practices deemed by consumers, researchers and stakeholders in Sweden to be niche, sustainable and with the potential to be scaled up.
 
  A life table method was used to estimate the impact - changes in years of life lost (YLL) - over periods of 20 and 30 years in the Swedish population had the practices been adopted in 2010-11, when the last national adult dietary survey was conducted. The practices modelled were reducing red and processed meat (by 25, 50 and 100%), and assuming, for each stage, replacement by an equal weight of poultry/fish and vegetables +/- legumes; reducing milk intake (by 25, 50 and 100%); and reducing sugar-sweetened beverage intake (by 25, 50 and 100%). Using population data together with data on cause-specific mortality and relative risks for diet-disease outcomes, impacts were estimated for each scenario separately and in combination, for the outcomes ischaemic heart disease (IHD), ischaemic stroke, diabetes type 2 and colorectal cancer.