Spitzer Space Telescope observatory planning and scheduling team

Launched as the space infrared telescope facility (SIRTF) in August, 2003 and renamed in early 2004, the Spitzer space telescope is performing an extended series of science observations at wavelengths ranging from 3 to 180 microns. The California Institute of Technology is the home of the Spitzer Science Center (SSC) and operates the science operations system (SOS), which supports science operations of the observatory. A key function supported by the SOS is the long-range planning and short-term scheduling of the observatory. This paper describes the role and function of the SSC observatory planning and scheduling team (OPST), its operational interfaces, processes, and tools

Loss of murine Paneth cell function alters the immature intestinal microbiome and mimics changes seen in neonatal necrotizing enterocolitis

Necrotizing enterocolitis (NEC) remains the leading cause of gastrointestinal morbidity and mortality in premature infants. Human and animal studies suggest a role for Paneth cells in NEC pathogenesis. Paneth cells play critical roles in host-microbial interactions and epithelial homeostasis. The ramifications of eliminating Paneth cell function on the immature host-microbial axis remains incomplete. Paneth cell function was depleted in the immature murine intestine using chemical and genetic models, which resulted in intestinal injury consistent with NEC. Paneth cell depletion was confirmed using histology, electron microscopy, flow cytometry, and real time RT-PCR. Cecal samples were analyzed at various time points to determine the effects of Paneth cell depletion with and without Klebsiella gavage on the microbiome. Deficient Paneth cell function induced significant compositional changes in the cecal microbiome with a significant increase in Enterobacteriacae species. Further, the bloom of Enterobacteriaceae species that occurs is phenotypically similar to what is seen in human NEC. This further strengthens our understanding of the importance of Paneth cells to intestinal homeostasis in the immature intestine

Acceleration of small intestine development and remodeling of the microbiome following hyaluronan 35 KDa treatment in neonatal mice

The beneficial effects of human milk suppressing the development of intestinal pathologies such as necrotizing enterocolitis in preterm infants are widely known. Human milk (HM) is rich in a multitude of bioactive factors that play major roles in promoting postnatal maturation, differentiation, and the development of the microbiome. Previous studies showed that HM is rich in hyaluronan (HA) especially in colostrum and early milk. This study aims to determine the role of HA 35 KDa, a HM HA mimic, on intestinal proliferation, differentiation, and the development of the intestinal microbiome. We show that oral HA 35 KDa supplementation for 7 days in mouse pups leads to increased villus length and crypt depth, and increased goblet and Paneth cells, compared to controls. We also show that HA 35 KDa leads to an increased predominance of Clostridiales Ruminococcaceae, Lactobacillales Lactobacillaceae, and Clostridiales Lachnospiraceae. In seeking the mechanisms involved in the changes, bulk RNA seq was performed on samples from the terminal ileum and identified upregulation in several genes essential for cellular growth, proliferation, and survival. Taken together, this study shows that HA 35 KDa supplemented to mouse pups promotes intestinal epithelial cell proliferation, as well as the development of Paneth cells and goblet cell subsets. HA 35 KDa also impacted the intestinal microbiota; the implications of these responses need to be determined

Tumor Necrosis Factor Induces Developmental Stage-Dependent Structural Changes in the Immature Small Intestine

Background. Premature infants are commonly subject to intestinal inflammation. Since the human small intestine does not reach maturity until term gestation, premature infants have a unique challenge, as either acute or chronic inflammation may alter the normal development of the intestinal tract. Tumor necrosis factor (TNF) has been shown to acutely alter goblet cell numbers and villus length in adult mice. In this study we tested the effects of TNF on villus architecture and epithelial cells at different stages of development of the immature small intestine. Methods. To examine the effects of TNF-induced inflammation, we injected acute, brief, or chronic exposures of TNF in neonatal and juvenile mice. Results. TNF induced significant villus blunting through a TNF receptor-1 (TNFR1) mediated mechanism, leading to loss of villus area. This response to TNFR1 signaling was altered during intestinal development, despite constant TNFR1 protein expression. Acute TNF-mediated signaling also significantly decreased Paneth cells. Conclusions. Taken together, the morphologic changes caused by TNF provide insight as to the effects of inflammation on the developing intestinal tract. Additionally, they suggest a mechanism which, coupled with an immature immune system, may help to explain the unique susceptibility of the immature intestine to inflammatory diseases such as NEC

Paneth cell ontogeny in term and preterm ovine models

IntroductionPaneth cells are critically important to intestinal health, including protecting intestinal stem cells, shaping the intestinal microbiome, and regulating host immunity. Understanding Paneth cell biology in the immature intestine is often modeled in rodents with little information in larger mammals such as sheep. Previous studies have only established the distribution pattern of Paneth cells in healthy adult sheep. Our study aimed to examine the ontogeny, quantification, and localization of Paneth cells in fetal and newborn lambs at different gestational ages and with perinatal transient asphyxia. We hypothesized that ovine Paneth cell distribution at birth resembles the pattern seen in humans (highest concentrations in the ileum) and that ovine Paneth cell density is gestation-dependent.MethodsIntestinal samples were obtained from 126–127 (preterm, with and without perinatal transient asphyxia) and 140–141 (term) days gestation sheep. Samples were quantified per crypt in at least 100 crypts per animal and confirmed as Paneth cells through in immunohistochemistry.ResultsPaneth cells had significantly higher density in the ileum compared to the jejunum and were absent in the colon.DiscussionExposure to perinatal transient asphyxia acutely decreased Paneth cell numbers. These novel data support the possibility of utilizing ovine models for understanding Paneth cell biology in the fetus and neonate

Married Black men's opinions as to why Black women are disproportionately single: A qualitative study

Abstract This study's purpose was to explore the reasons Black women are disproportionately single according to the unique viewpoint of married Black men. The sample comprises 52 married Black men who resided in northeast Georgia (mean age = 43). Qualitative interviews were conducted in 2010 as part of the Pathways to Marriage study. The authors analyzed the data in a collaborative fashion and utilized content analyses to explore the relationships in the data, which were derived from qualitative interviews with the men. Findings on the reasons for the disproportionality of singlehood among Black women reflected these four themes: gender relations, marriage education and socialization, individual development, and a preference for gay/lesbian relationships. Recommendations for future research are discussed. Recent estimates highlight an important trend-Black women are less likely to enter into marriage or remarry than are Blac

Transactivation of EGFR by LPS induces COX-2 expression in enterocytes

Necrotizing enterocolitis (NEC) is the leading cause of gastrointestinal morbidity and mortality in preterm infants. NEC is characterized by an exaggerated inflammatory response to bacterial flora leading to bowel necrosis. Bacterial lipopolysaccharide (LPS) mediates inflammation through TLR4 activation and is a key molecule in the pathogenesis of NEC. However, LPS also induces cyclooxygenase-2 (COX-2), which promotes intestinal barrier restitution through stimulation of intestinal cell survival, proliferation, and migration. Epidermal growth factor receptor (EGFR) activation prevents experimental NEC and may play a critical role in LPS-stimulated COX-2 production. We hypothesized that EGFR is required for LPS induction of COX-2 expression. Our data show that inhibiting EGFR kinase activity blocks LPS-induced COX-2 expression in small intestinal epithelial cells. LPS induction of COX-2 requires Src-family kinase signaling while LPS transactivation of EGFR requires matrix metalloprotease (MMP) activity. EGFR tyrosine kinase inhibitors block LPS stimulation of mitogen-activated protein kinase ERK, suggesting an important role of the MAPK/ERK pathway in EGFR-mediated COX-2 expression. LPS stimulates proliferation of IEC-6 cells, but this stimulation is inhibited with either the EGFR kinase inhibitor AG1478, or the selective COX-2 inhibitor Celecoxib. Taken together, these data show that EGFR plays an important role in LPS-induction of COX-2 expression in enterocytes, which may be one mechanism for EGF in inhibition of NEC

Multi-Platform Next-Generation Sequencing of the Domestic Turkey (Meleagris gallopavo): Genome Assembly and Analysis

The combined application of next-generation sequencing platforms has provided an economical approach to unlocking the potential of the turkey genome

Role of Physical Activity and Fitness in the Characterization and Prognosis of the Metabolically Healthy Obesity Phenotype: a Systematic Review and Meta-Analysis

The aims of the present article are to systematically review and meta-analyze the existing evidence on: 1) differences in physical activity (PA), sedentary behavior (SB), cardiorespiratory fitness (CRF) and muscular strength (MST) between metabolically healthy obesity (MHO) and metabolically unhealthy obesity (MUO); and 2) the prognosis of all-cause mortality and cardiovascular disease (CVD) mortality/morbidity in MHO individuals, compared with the best scenario possible, i.e., metabolically healthy normal-weight (MHNW), after adjusting for PA, SB, CRF or MST. Our systematic review identified 67 cross-sectional studies to address aim 1, and 11 longitudinal studies to address aim 2. The major findings and conclusions from the current meta-analysis are: 1) MHO individuals are more active, spend less time in SB, and have a higher level of CRF (yet no differences in MST) than MUO individuals, suggesting that their healthier metabolic profile could be at least partially due to these healthier lifestyle factors and attributes. 2) The meta-analysis of cohort studies which accounted for PA (N = 10 unique cohorts, 100% scored as high-quality) support the notion that MHO individuals have a 24-33% higher risk of all-cause mortality and CVD mortality/morbidity compared to MHNW individuals. This risk was borderline significant/non-significant, independent of the length of the follow-up and lower than that reported in previous meta-analyses in this topic including all type of studies, which could be indicating a modest reduction in the risk estimates as a consequence of accounting for PA. 3) Only one study has examined the role of CRF in the prognosis of MHO individuals. This study suggests that the differences in the risk of all-cause mortality and CVD mortality/morbidity between MHO and MHNW are largely explained by differences in CRF between these two phenotypes

Reductions in ozone at high concentrations of stratospheric halogens

An increase in the concentration of inorganic chlorine to levels comparable to that of oxidized reactive nitrogen could cause a significant change in the chemistry of the lower stratosphere leading to a reduction potentially larger than 15% in the column density of ozone. This could occur, for example by the middle of the next century, if emissions of man-made chlorocarbons were to grow at a rate of 3% per year. Ozone could be further depressed by release of industrial bromocarbon