Gestational sleep deprivation is associated with higher offspring body mass index and blood pressure

Study ObjectivesThe objective of this study was to evaluate the association between gestational sleep deprivation and childhood adiposity and cardiometabolic profile.MethodsData were used from two population-based birth cohorts (Rhea study and Amsterdam Born Children and their Development study). A total of 3,608 pregnant women and their children were followed up until the age of 11 years. Gestational sleep deprivation was defined as 6 or fewer hours of sleep per day, reported by questionnaire. The primary outcomes included repeated measures of body mass index (BMI), waist circumference, body fat, serum lipids, systolic and diastolic blood pressure (DBP) levels in childhood. We performed a pooled analysis with adjusted linear mixed effect and Cox proportional hazards models. We tested for mediation by birthweight, gestational age, and gestational diabetes.ResultsGestational sleep deprivation was associated with higher BMI (beta; 95% CI: 0.7; 0.4, 1.0 kg/m²) and waist circumference (beta; 95% CI: 0.9; 0.1, 1.6 cm) in childhood, and increased risk for overweight or obesity (HR; 95% CI: 1.4; 1.1, 2.0). Gestational sleep deprivation was also associated with higher offspring DBP (beta; 95% CI: 1.6; 0.5, 2.7 mmHg). The observed associations were modified by sex (all p-values for interaction < 0.05); and were more pronounced in girls. Gestational diabetes and shorter gestational age partly mediated the seen associations.ConclusionsThis is the first study showing that gestational sleep deprivation may increase offspring’s adiposity and blood pressure, while exploring possible mechanisms. Attention to glucose metabolism and preterm birth might be extra warranted in mothers with gestational sleep deprivation.     

Characterization of the oncogenic activity of the novel TRIM59 gene in mouse cancer models

A novel TRIM family member, TRIM59 gene was characterized to be upregulated in SV40 Tag oncogene-directed transgenic and knockout mouse prostate cancer models as a signaling pathway effector. We identified two phosphorylated forms of TRIM59 (p53 and p55) and characterized them using purified TRIM59 proteins from mouse prostate cancer models at different stages with wild-type mice and NIH3T3 cells as controls. p53/p55-TRIM59 proteins possibly represent Ser/Thr and Tyr phosphorylation modifications, respectively. Quantitative measurements by ELISA showed that the p-Ser/Thr TRIM59 correlated with tumorigenesis, whereas the p-Tyr-TRIM59 protein correlated with advanced cancer of the prostate (CaP). The function of TRIM59 was elucidated using short hairpin RNA (shRNA)-mediated knockdown of the gene in human CaP cells, which caused S-phase cell-cycle arrest and cell growth retardation. A hit-and-run effect of TRIM59 shRNA knockdown was observed 24 hours posttransfection. Differential cDNA microarrray analysis was conducted, which showed that the initial and rapid knockdown occurred early in the Ras signaling pathway. To confirm the proto-oncogenic function of TRIM59 in the Ras signaling pathway, we generated a transgenic mouse model using a prostate tissue-specific gene (PSP94) to direct the upregulation of the TRIM59 gene. Restricted TRIM59 gene upregulation in the prostate revealed the full potential for inducing tumorigenesis, similar to the expression of SV40 Tag, and coincided with the upregulation of genes specific to the Ras signaling pathway and bridging genes for SV40 Tag-mediated oncogenesis. The finding of a possible novel oncogene in animal models will implicate a novel strategy for diagnosis, prognosis, and therapy for cancer.     

Increased PLA2 activity in individuals at ultra-high risk for psychosis

European Archives of Psychiatry and Clinical Neuroscience - Phospholipase A2 is the main enzyme in the metabolism of membrane phospholipids. It comprises a family of enzymes divided into iPLA2,...     

Hydrotherapy versus conventional land-based exercise for the management of patients with osteoarthritis of the knee: a randomized clinical trial

BACKGROUND AND PURPOSE: This study was designed to evaluate the effectiveness of hydrotherapy in subjects with osteoarthritis (OA) of the knee compared with subjects with OA of the knee who performed land-based exercises. SUBJECTS AND METHODS: Sixty-four subjects with OA of the knee were randomly assigned to 1 of 2 groups that performed exercises for 18 weeks: a water-based exercise group and a land-based exercise group. The outcome measures included a visual analog scale (VAS) for pain in the previous week, the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC), pain during gait assessed by a VAS at rest and immediately following a 50-foot (15.24-m) walk test (50FWT), walking time measured at fast and comfortable paces during the 50FWT, and the Lequesne Index. Measurements were recorded by a blinded investigator at baseline and at 9 and 18 weeks after initiating the intervention. RESULTS: The 2 groups were homogenous regarding all parameters at baseline. Reductions in pain and improvements in WOMAC and Lequesne index scores were similar between groups. Pain before and after the 50FWT decreased significantly over time in both groups. However, the water-based exercise group experienced a significantly greater decrease in pain than the land-based exercise group before and after the 50FWT at the week-18 follow-up. DISCUSSION AND CONCLUSION: Both water-based and land-based exercises reduced knee pain and increased knee function in participants with OA of the knee. Hydrotherapy was superior to land-based exercise in relieving pain before and after walking during the last follow-up. Water-based exercises are a suitable and effective alternative for the management of OA of the knee.     

Emphysema induced by elastase enhances acute inflammatory pulmonary response to intraperitoneal LPS in rats

Abnormalities in lungs caused by emphysema might alter their response to sepsis and the occurrence of acute lung injury (ALI). This study compared the extension of ALI in response to intraperitoneal lipopolysaccharide (LPS) injection in Wistar rats with and without emphysema induced by elastase. Adult male Wistar rats were randomized into four groups: control, emphysema without sepsis, normal lung with sepsis and emphysema with sepsis. Sepsis was induced, and 24 h later the rats were euthanised. The following analysis was performed: blood gas measurements, bronchoalveolar lavage (BAL), lung permeability and histology. Animals that received LPS showed significant increase in a lung injury scoring system, inflammatory cells in bronchoalveolar lavage (BAL) and IL‐6, TNF‐α and CXCL2 mRNA expression in lung tissue. Animals with emphysema and sepsis showed increased alveolocapillary membrane permeability, demonstrated by higher BAL/serum albumin ratio. In conclusion, the presence of emphysema induced by elastase increases the inflammatory response in the lungs to a systemic stimulus, represented in this model by the intraperitoneal injection of LPS.     

Bacterial concentrations determine the ability to implant in the root canal system and translocate to lymph nodes in germ-free mice

The purpose of this study was to evaluate the influence of the infecting dose on bacterial colonization in root canal systems (RCS) and translocation to the submandibular lymph node (SML) of gnotobiotic (germ-free) mice. RCS were inoculated with 10(2) and 10(1) colony-forming units (CFU) of Enterococcus faecalis (ATCC 4083) or 10(5), 10(4), 10(3), and 10(2) CFU of Prevotella nigrescens (ATCC 33563). E. faecalis implanted in 83.3% of the cases, for both inocula. Translocation was detected in 58.3% of lymph nodes for the 10(2) CFU inoculum and in 33.3% of lymph nodes for the 10(1) CFU inoculum. P. nigrescens implanted in 25%, 16.7%, 8.3%, and 0%, for the 10(5), 10(4), 10(3), and 10(2) CFU inocula, respectively, and did not translocate at any of the concentrations used. These results indicate that E. faecalis was able to implant in the RCS and translocate to the SML, whereas P. nigrescens implanted in lower percentages in the RCS and did not translocate to the SML.     

Mutational analysis of nicotinic acetylcholine receptor beta2 subunit gene (CHRNB2) in a representative cohort of Italian probands affected by autosomal dominant nocturnal frontal lobe epilepsy

Twenty-four autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) probands were analyzed for the presence of V287L and V287M mutations in the CHRNB2 gene, which have been recently associated with the disease. In all patients, the involvement of the two additional loci reported as being associated with ADNFLE (CHRNA4 gene and chromosome 15q24 region) had been previously excluded. Mutational screening was performed by sequencing a polymerase chain reaction-amplified CHRNB2 DNA fragment, spanning the whole exon 5, which contains the V287L and V287M mutations and codes for approximately 65% of the mature protein. In none of the patients were mutations in the analyzed region of CHRNB2 found. These data, obtained in the largest ADNFLE cohort so far analyzed, demonstrate the rarity of the identified CHRNB2 mutations in ADNFLE patients.