A terminal guidance scheme for lifting body entry vehicles

Perturbation feedback guidance for terminal phase of lifting body entry vehicl

Exogenous overexpression of nerve growth factor in the urinary bladder produces bladder overactivity and altered micturition circuitry in the lumbosacral spinal cord

<p>Abstract</p> <p>Background</p> <p>Exogenous NGF or saline was delivered to the detrusor smooth muscle of female rats for a two-week period using osmotic mini-pumps. We then determined: (1) bladder function using conscious cystometry; (2) organization of micturition reflexes using Fos protein expression in lumbosacral (L5-S1) spinal cord neurons; (3) calcitonin gene-related peptide (CGRP)-immunoreactivity (IR) in lumbosacral spinal cord segments.</p> <p>Methods</p> <p>An osmotic pump infused 0.9% NaCl (n = 6) or NGF (n = 6)(2.5 μg/μl solution; 0.5 μl/hr) for two weeks into the bladder wall. NGF bladder content was determined by enzyme-linked immunoassays. Bladder function was assessed with conscious cystometry. Immunohistochemical and imaging techniques were used to determine the distribution of Fos-IR cells and CGRP expression in the L5-S1 spinal cord in saline and NGF-treated rats two hours after intravesical saline distention. Fos expression and CGRP-IR in NGF-treated rats with bladder distention was compared to that observed in cyclophosphamide (CYP; 75 mg/kg; i.p.) treated rats with bladder distention.</p> <p>Results</p> <p>Two-week infusion of NGF into the bladder wall increased bladder weight, reduced bladder capacity (60%), reduced the intercontraction interval (60%) and increased the amplitude of non-voiding contractions. NGF treatment and intravesical saline distention (2 hr) increased expression of Fos protein in L6-S1 spinal cord and altered the distribution pattern of Fos-IR cells. CGRP-IR in the lumbosacral spinal cord was also increased after NGF treatment.</p> <p>Conclusion</p> <p>These data suggest that NGF infusion into the bladder wall induces bladder overactivity, can reveal a "nociceptive" Fos expression pattern in the spinal cord in response to a non-noxious bladder stimulus and increases CGRP-IR in the lumbosacral spinal cord.</p

Total Energy Expenditure and Body Composition of Children with Developmental Disabilities

Background Obesity prevalence is increased in children with developmental disabilities, specifically in children with spina bifida and Down syndrome. Energy expenditure, a critical aspect of weight management, has been extensively studied in the typically developing population, but not adequately studied in children with developmental disabilities. Objective Determine energy expenditure, fat-free mass and body fat percentile and the impact of these findings on recommended caloric intake in children with spina bifida and Down syndrome. Methods/Measures This pilot study included 36 children, 18 with spina bifida, 9 with Down syndrome and 9 typically developing children. Half of the children with spina bifida were non-ambulatory. Doubly labeled water was used to measure energy expenditure and body composition. Descriptive statistics described the sample and MANOVA and ANOVA methods were used to evaluate differences between groups. Results Energy expenditure was significantly less for children with spina bifida who primarily used a wheelchair (p = .001) and children with Down syndrome (p = .041) when compared to children without a disability when adjusted for fat-free mass. However, no significant difference was detected in children with spina bifida who ambulated without assistance (p = .072). Conclusions Children with spina bifida and Down syndrome have a significantly decreased energy expenditure which directly impacts recommended caloric intake. No significant difference was detected for children with spina bifida who ambulated, although the small sample size of this pilot study may have limited these findings. Validating these results in a larger study is integral to supporting successful weight management of these children

BMI as a Predictor for Potential Difficult Tracheal Intubation in Males

Introduction: Difficult tracheal intubation is a common source of mortality and morbidity insurgical and critical care settings. The incidence reported of difficult tracheal intubation is 0.1 to 13%and reaches 14% in the obese population. The objective of our retrospective study was to investigateand compare the utility of BMI as indicator of difficult tracheal intubation in males and females.Material and methods: We performed a retrospective chart review of patients who underwentabdominal surgeries with ASA I to V under general anesthesia requiring endotracheal intubation. Thefollowing information was obtained from medical records for analysis: gender, age, height, weight,BMI, length of patient stay in the Post Anesthesia Care Unit (PACU), past medical history of sleepapnea, Mallampati score, and the ASA classification assigned by the anesthesia care providerperforming the endotracheal intubation.Results: Of 4303 adult patients, 1970 (45.8%) men and 2333 (54.2%) women, were enrolled in thestudy. Within this group, a total of 1673 (38.9%) patients were morbidly obese. The average age of thestudy group was 51.4 ± 15.8 and the average BMI was 29.7 ± 8.2 kg/m². The overall incidence of theencountered difficult intubations was 5.23%, or 225 subjects. Thus, our results indicate that BMI is areliable predictor of difficult tracheal intubation predominantly in the male population; another strongpredictor, with a positive linear correlation, being the Mallampati score.Conclusions: In conclusion, our data shows that BMI is a reliable indicator of potential difficult trachealintubation only in male surgical patients

Self-Compassion and Depressive Symptoms as Determinants of Sensitive Parenting: Associations with Sociodemographic Characteristics in a Sample of Mothers and Toddlers

Parenting that is sensitive and responsive to children’s needs has been shown to support children’s optimal growth and development in many cultural contexts. Numerous studies suggest that self-compassion is positively related to sensitive parenting. Despite growing research interest linking self-compassion to responsive parenting, there are considerable gaps in the literature. The current study examined the associations between self-compassion, depressive symptoms, socioeconomic status, and sensitive parenting. Data was obtained from a cohort study of 300 families in central Ohio enrolled when children were a mean (SD) calendar age of 18.2 (0.7) months. Children of all gestational ages at birth are included, and 37% were born preterm (<37 weeks’ gestation). Observational protocols were used to determine maternal sensitivity in a semi-structured play setting. Self-compassion was assessed with the Self-Compassion Scale when children were 24 months old. Self-compassion was not associated with sociodemographic characteristics including maternal education, household income, child sex and gestational age. In unadjusted regression models, depressive symptoms were related to sensitive parenting (B = −0.036, SE = 0.016, p = 0.03), but self-compassion was not a statistically significant predictor (p = 0.35) of sensitivity, and neither self-compassion nor depressive symptoms were statistically significant predictors of sensitive parenting after adjustment for covariates. Considerations for future studies are discussed

Extracellular deposition of matrilin-2 controls the timing of the myogenic program during muscle regeneration.

Here, we identify a role for the matrilin-2 (Matn2) extracellular matrix protein in controlling the early stages of myogenic differentiation. We observed Matn2 deposition around proliferating, differentiating and fusing myoblasts in culture and during muscle regeneration in vivo. Silencing of Matn2 delayed the expression of the Cdk inhibitor p21 and of the myogenic genes Nfix, MyoD and Myog, explaining the retarded cell cycle exit and myoblast differentiation. Rescue of Matn2 expression restored differentiation and the expression of p21 and of the myogenic genes. TGF-β1 inhibited myogenic differentiation at least in part by repressing Matn2 expression, which inhibited the onset of a positive-feedback loop whereby Matn2 and Nfix activate the expression of one another and activate myoblast differentiation. In vivo, myoblast cell cycle arrest and muscle regeneration was delayed in Matn2(-/-) relative to wild-type mice. The expression levels of Trf3 and myogenic genes were robustly reduced in Matn2(-/-) fetal limbs and in differentiating primary myoblast cultures, establishing Matn2 as a key modulator of the regulatory cascade that initiates terminal myogenic differentiation. Our data thus identify Matn2 as a crucial component of a genetic switch that modulates the onset of tissue repair

The critical role of intracellular zinc in adenosine A2 receptor activation induced cardioprotection against reperfusion injury

Exogenous zinc can protect cardiac cells from reperfusion injury, but the exact roles of endogenous zinc in the pathogenesis of reperfusion injury and in adenosine A2 receptor activation-induced cardioprotection against reperfusion injury remain unknown. Adenosine A1/A2 receptor agonist 5′-(N-ethylcarboxamido) adenosine (NECA) given at reperfusion reduced infarct size in isolated rat hearts subjected to 30 min ischemia followed by 2 h of reperfusion. This effect of NECA was partially but significantly blocked by the zinc chelator N,N,N′,N′-tetrakis-(2-pyridylmethyl) ethylenediamine (TPEN), and ZnCl2 given at reperfusion mimicked the effect of NECA by reducing infarct size. Total tissue zinc concentrations measured with inductively coupled plasma optical emission spectroscopy (ICPOES) were decreased upon reperfusion in rat hearts and this was reversed by NECA. NECA increased intracellular free zinc during reperfusion in the heart. Confocal imaging study showed a rapid increase in intracellular free zinc in isolated rat cardiomyocytes treated with NECA. Further experiments revealed that NECA increased total zinc levels upon reperfusion in mitochondria isolated from isolated hearts. NECA attenuated mitochondrial swelling upon reperfusion in isolated hearts and this was inhibited by TPEN. Similarly, NECA prevented the loss of mitochondrial membrane potential (ΔΨm) caused by oxidant stress in cardiomyocytes. Finally, both NECA and ZnCl2 inhibited the mitochondrial metabolic activity. NECA-induced cardioprotection against reperfusion injury is mediated by intracellular zinc. NECA prevents reperfusion-induced zinc loss and relocates zinc to mitochondria. The inhibitory effects of zinc on both the mPTP opening and the mitochondrial metabolic activity may account for the cardioprotective effect of NECA

Neurophysiological modeling of bladder afferent activity in the rat overactive bladder model

The overactive bladder (OAB) is a syndrome-based urinary dysfunction characterized by “urgency, with or without urge incontinence, usually with frequency and nocturia”. Earlier we developed a mathematical model of bladder nerve activity during voiding in anesthetized rats and found that the nerve activity in the relaxation phase of voiding contractions was all afferent. In the present study, we applied this mathematical model to an acetic acid (AA) rat model of bladder overactivity to study the sensitivity of afferent fibers in intact nerves to bladder pressure and volume changes. The afferent activity in the filling phase and the slope, i.e., the sensitivity of the afferent fibers to pressure changes in the post-void relaxation phase, were found to be significantly higher in AA than in saline measurements, while the offset (nerve activity at pressure ~0) and maximum pressure were comparable. We have thus shown, for the first time, that the sensitivity of afferent fibers in the OAB can be studied without cutting nerves or preparation of single fibers. We conclude that bladder overactivity induced by AA in rats is neurogenic in origin and is caused by increased sensitivity of afferent sensors in the bladder wall

TCF4 sequence variants and mRNA levels are associated with neurodevelopmental characteristics in psychotic disorders

TCF4 is involved in neurodevelopment, and intergenic and intronic variants in or close to the TCF4 gene have been associated with susceptibility to schizophrenia. However, the functional role of TCF4 at the level of gene expression and relationship to severity of core psychotic phenotypes are not known. TCF4 mRNA expression level in peripheral blood was determined in a large sample of patients with psychosis spectrum disorders (n=596) and healthy controls (n=385). The previously identified TCF4 risk variants (rs12966547 (G), rs9960767 (C), rs4309482 (A), rs2958182 (T) and rs17512836 (C)) were tested for association with characteristic psychosis phenotypes, including neurocognitive traits, psychotic symptoms and structural magnetic resonance imaging brain morphometric measures, using a linear regression model. Further, we explored the association of additional 59 single nucleotide polymorphisms (SNPs) covering the TCF4 gene to these phenotypes. The rs12966547 and rs4309482 risk variants were associated with poorer verbal fluency in the total sample. There were significant associations of other TCF4 SNPs with negative symptoms, verbal learning, executive functioning and age at onset in psychotic patients and brain abnormalities in total sample. The TCF4 mRNA expression level was significantly increased in psychosis patients compared with controls and positively correlated with positive- and negative-symptom levels. The increase in TCF4 mRNA expression level in psychosis patients and the association of TCF4 SNPs with core psychotic phenotypes across clinical, cognitive and brain morphological domains support that common TCF4 variants are involved in psychosis pathology, probably related to abnormal neurodevelopment