Star formation triggered by non-head-on cloud-cloud collisions, and clouds with pre-collision sub-structure

In an earlier paper, we used smoothed particle hydrodynamics (SPH) simulations to explore star formation triggered by head-on collisions between uniform-density 500 M clouds, and showed that there is a critical collision velocity, vCRIT. At collision velocities below vCRIT, a hub-and-spoke mode operates and delivers a monolithic cluster with a broad mass function, including massive stars (M 10 M) formed by competitive accretion. At collision velocities above vCRIT, a spider’s-web mode operates and delivers a loose distribution of small sub-clusters with a relatively narrow mass function and no massive stars. Here we show that,if the head-on assumption is relaxed, vCRIT is reduced. However, if the uniform-density assumption is also relaxed, the collision velocity becomes somewhat less critical: a low collision velocity is still needed to produce a global hub-and-spoke system and a monolithic cluster, but, even at high velocities, large cores – capable of supporting competitive accretion and thereby producing massive stars – can be produced. We conclude that cloud–cloud collisions may be a viable mechanism for forming massive stars – and we show that this might even be the major channel for forming massive stars in the Galaxy

Numerical simulations of triggered star formation

Feedback from massive stars is thought to be very important in regulating star formation on a range of scales. However, it is not clear if this feedback acts in a positive way by triggering star formation, or negatively by terminating it. In this thesis we investigate what role feedback plays in determining both the structure of molecular clouds and the rate of star formation, using Smoothed Particle Hydrodynamics. We begin by looking at how the evolution of an HII region is dependent on the amount of ionising radiation the exciting star produces. We then go on to explore the stellar populations created by cloud-cloud collisions and assess their ability to form high mass stars capable of producing large amounts of feedback. We then model the HII regions of these stars and determine what impact these have on star and structure formation. We find that there is a minimum stellar mass required to produce enough feedback to maintain an HII region. Below this value an HII region will either not form, or form and then implode. Above this value the HII region will act as a traditional HII region, and expand. When two clouds collide we �nd that they produce a shock compressed layer which forms �lamentary structures. The arrangement of these �laments is highly dependent on the collision velocity. Low velocity collisions produce a hub and spoke system in which competitive accretion dominates and produces a few very massive stars and a plethora of low mass stars. High velocity collisions produce lamentary networks that resemble a spider's web. In these spider's webs the stars form at nodes where multiple �laments meet. These nodes act as small local sites for star formation and form either a single, or small collection of stars. As a result stars formed in these systems tend to have a characteristic mass and there is less low mass or high mass star formation. However, we do find that eventually stars capable of producing signi�cant feedback form in all simulations. We model the HII regions of these stars and �find that they very quickly terminate star formation. They also produce very interesting bi-polar HII regions that are diffi�cult to interpret when viewed from some directions

Numerical simulations of triggered star formation

Feedback from massive stars is thought to be very important in regulating star formation on a range of scales. However, it is not clear if this feedback acts in a positive way by triggering star formation, or negatively by terminating it. In this thesis we investigate what role feedback plays in determining both the structure of molecular clouds and the rate of star formation, using Smoothed Particle Hydrodynamics. We begin by looking at how the evolution of an HII region is dependent on the amount of ionising radiation the exciting star produces. We then go on to explore the stellar populations created by cloud-cloud collisions and assess their ability to form high mass stars capable of producing large amounts of feedback. We then model the HII regions of these stars and determine what impact these have on star and structure formation. We find that there is a minimum stellar mass required to produce enough feedback to maintain an HII region. Below this value an HII region will either not form, or form and then implode. Above this value the HII region will act as a traditional HII region, and expand. When two clouds collide we �nd that they produce a shock compressed layer which forms �lamentary structures. The arrangement of these �laments is highly dependent on the collision velocity. Low velocity collisions produce a hub and spoke system in which competitive accretion dominates and produces a few very massive stars and a plethora of low mass stars. High velocity collisions produce lamentary networks that resemble a spider's web. In these spider's webs the stars form at nodes where multiple �laments meet. These nodes act as small local sites for star formation and form either a single, or small collection of stars. As a result stars formed in these systems tend to have a characteristic mass and there is less low mass or high mass star formation. However, we do find that eventually stars capable of producing signi�cant feedback form in all simulations. We model the HII regions of these stars and �find that they very quickly terminate star formation. They also produce very interesting bi-polar HII regions that are diffi�cult to interpret when viewed from some directions

Impact of geography on the control of type 2 diabetes mellitus: a review of geocoded clinical data from general practice

Objective: To review the clinical data for people with diabetes mellitus with reference to their location and clinical care in a general practice in Australia. Materials and methods: Patient data were extracted from a general practice in Western Australia. Iterative data-cleansing steps were taken. Data were grouped into Statistical Area level 1 (SA1), designated as the smallest geographical area associated with the Census of Population and Housing. The data were analysed to identify if SA1s with people aged 70 years and older, and with relatively high glycosylated haemoglobin (HbA1c) were significantly clustered, and whether this was associated with their medical consultation rate and treatment. The analysis included Cluster and Outlier Analysis using Moran’s I test. Results: The overall median age of the population was 70 years with more males than females, 53% and 47%, respectively. Older people (\u3e70 years) with relatively high HbA1c comprised 9.3% of all people with diabetes in the sample, and were clustered around two ‘hotspot’ locations. These 111 patients do not attend the practice more or less often than people with diabetes living elsewhere in the practice ( p=0.098). There was some evidence that they were more likely to be recorded as having consulted with regard to other chronic diseases. The average number of prescribed medicines over a 13-month time period, per person in the hotspots, was 4.6 compared with 5.1 in other locations ( p=0.26). Their prescribed therapy was deemed to be consistent with the management of people with diabetes in other locations with reference to the relevant diabetes guidelines. Conclusions: Older patients with relatively high HbA1c are clustered in two locations within the practice area. Their hyperglycaemia and ongoing cardiovascular risk indicates causes other than therapeutic inertia. The causes may be related to the social determinants of health, which are influenced by geography

Impaired mucosal defense to acute colonic injury in mice lacking cyclooxygenase-1 or cyclooxygenase-2

To investigate roles in intestinal inflammation for the 2 cyclooxygenase (COX) isoforms, we determined susceptibility to spontaneous and induced acute colitis in mice lacking either the COX-1 or COX-2 isoform. We treated wild-type, COX-1–/–, COX-2–/–, and heterozygous mice with dextran sodium sulfate (DSS) to provoke acute colonic inflammation, and we quantified tissue damage, prostaglandin (PG) E2, and interleukin-1β. No spontaneous gastrointestinal inflammation was detected in mice homozygous for either mutation, despite almost undetectable basal intestinal PGE2 production in COX-1–/– mice. Both COX-1–/– and COX-2–/– mice showed increased susceptibility to a low-dose of DSS that caused mild colonic epithelial injury in wild-type mice. COX-2–/– mice were more susceptible than COX-1–/– mice, and selective pharmacologic blockade of COX-2 potentiated injury in COX-1–/– mice. At a high dose, DSS treatment was fatal to 50% of the animals in each mutant group, but all wild-type mice survived. DSS treatment increased PGE2 intestinal secretion in all groups except COX-2–/– mice. These results demonstrate that COX-1 and COX-2 share a crucial role in the defense of the intestinal mucosa (with inducible COX-2 being perhaps more active during inflammation) and that neither isoform is essential in maintaining mucosal homeostasis in the absence of injurious stimuli

The Effects of Etodolac, Nimesulid and Naproxen Sodium on the Frequency of Sister Chromatid Exchange after Enclused Third Molars Surgery

are frequently used in oral surgical procedures in dentistry. The evaluation of the frequency of sister chromatid exchange (SCE) is accepted as a reliable cytogenetic method to assess the genotoxic effects of environmental factors. Materials and Methods: In this study, the genotoxic effects of various NSAIDs were assessed in 30 patients to who they were administered following encluosed third molar surgery using SCE analysis before and after the operation. The frequency of SCE was evaluated before the operation and after 3 days of etodolac, nimesulid and naproxen use. Results: There was no statistically significant difference in the frequency of SCE between the preoperative and postoperative states in patients given etodolac, nimesulid or naproxen sodium. Conclusion: Short term use of selective and non-selective NSAIDs was not associated with a significant genotoxic effect that could be detected using the SCE method in peripheric lymphocytes. Key Words: Genotoxicity, sister chromatid exchange, oral surgery, non-steroidal anti-inflammatory drug

IL-10 Regulates Il12b Expression via Histone Deacetylation: Implications for Intestinal Macrophage Homeostasis

To prevent excessive inflammatory responses to commensal microbes, intestinal macrophages unlike their systemic counterparts do not produce inflammatory cytokines in response to enteric bacteria. Consequently, loss of macrophage tolerance to the enteric microbiota plays a central role in the pathogenesis of the inflammatory bowel diseases. Therefore, we examined whether the hyporesponsive phenotype of intestinal macrophages is programmed by prior exposure to the microbiota. IL-10, but not in vivo exposure to the microbiota, programs intestinal macrophage tolerance, as wild-type (WT) colonic macrophages from germ free and specific-pathogen free (SPF) derived mice produce IL-10 but not IL-12 p40 when activated with enteric bacteria. Basal and activated IL-10 expression is mediated through a MyD88 dependent pathway. Conversely, colonic macrophages from germ free and SPF derived colitis-prone Il10−/− mice demonstrated robust production of IL-12 p40. Next, mechanisms through which IL-10 inhibits Il12b expression were investigated. While Il12b mRNA was transiently induced in LPS-activated WT bone marrow derived macrophages (BMDMs), expression persisted in Il10−/− BMDMs. There were no differences in nucleosome remodeling, mRNA stability, NF-κB activation or MAPK signaling to explain prolonged transcription of Il12b in Il10−/− BMDMs. However, acetylated histone H4 (AcH4) transiently associated with the Il12b promoter in WT BMDMs, whereas association of these factors was prolonged in Il10−/− BMDMs. Experiments utilizing histone deacetylase (HDAC) inhibitors and HDAC3 shRNA indicate that HDAC3 is involved in histone deacetylation of the Il12b promoter by IL-10. These results suggest that histone deacetylation on the Il12b promoter by HDAC3 mediates homeostatic effects of IL-10 in macrophages

Altered Macrophage Function Contributes to Colitis in Mice Defective in the Phosphoinositide-3 Kinase Subunit p110δ

Innate immune responses are crucial for host defense against pathogens, but need to be tightly regulated to prevent chronic inflammation. Initial characterization of mice with a targeted inactivating mutation in the p110d subunit of phosphoinositide 3-kinase (PI3K p110δD910A/D910A) reveal defects in B- and T-cell signaling and chronic colitis. Here, we further characterize features of inflammatory bowel diseases (IBD) in these mice and investigate underlying innate immune defects

Major Depression Is a Risk Factor for Shorter Time to First Cigarette Irrespective of the Number of Cigarettes Smoked Per Day: Evidence From a National Population Health Survey

Article deposited according to Oxford Open Self-Archiving policy: http://www.oxfordjournals.org/oxfordopen/policies.html, January 12, 2012.YesFunding provided by the Open Access Authors Fund