An observational and theoretical view of the radial distribution of HI gas in galaxies

We analyze the radial distribution of HI gas for 23 disk galaxies with unusually high HI content from the Bluedisk sample, along with a similar-sized sample of "normal" galaxies. We propose an empirical model to fit the radial profile of the HI surface density, an exponential function with a depression near the center. The radial HI surface density profiles are very homogeneous in the outer regions of the galaxy; the exponentially declining part of the profile has a scale-length of $\sim 0.18$ R1, where R1 is the radius where the column density of the HI is 1 M$_{\odot}$ pc$^{-2}$. This holds for all galaxies, independent of their stellar or HI mass. The homogenous outer profiles, combined with the limited range in HI surface density in the non-exponential inner disk, results in the well-known tight relation between HI size and HI mass. By comparing the radial profiles of the HI-rich galaxies with those of the control systems, we deduce that in about half the galaxies, most of the excess gas lies outside the stellar disk, in the exponentially declining outer regions of the HI disk. In the other half, the excess is more centrally peaked. We compare our results with existing smoothed-particle hydrodynamical simulations and semi-analytic models of disk galaxy formation in a $\Lambda$ Cold Dark Matter universe. Both the hydro simulations and the semi-analytic models reproduce the HI surface density profiles and the HI size-mass relation without further tuning of the simulation and model inputs. In the semi-analytic models, the universal shape of the outer HI radial profiles is a consequence of the {\em assumption} that infalling gas is always distributed exponentially. The conversion of atomic gas to molecular form explains the limited range of HI surface densities in the inner disk. These two factors produce the tight HI mass-size relation.Comment: 15 pages, 14 figures, submitted to MNRA

In high glucose protein kinase C-ζ activation is required for mesangial cell generation of reactive oxygen species

In high glucose protein kinase C-ζ activation is required for mesangial cell generation of reactive oxygen species.BackgroundWe postulated that in mesangial cells exposed to high glucose, protein kinase C-ζ (PKC-ζ) is necessary for the generation of reactive oxygen species (ROS) by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and that the requirement of PKC-ζ for filamentous (F)-actin disassembly may involve ROS. To identify signaling mechanisms relevant to PKC-ζ activation and ROS generation, including phosphoinositide 3 kinase (PI3 kinase), we examined mesangial cell stimulation with platelet-derived growth factor (PDGF).MethodsIn primary rat mesangial cells cultured in 5.6mmol/L or 30mmol/L D-glucose, PKC-ζ expression was identified with immunoblotting and activity was analyzed in cell membrane immunoprecipitates and by confocal immunofluorescence imaging. ROS generation was measured by dichlorofluorescein fluorescence using confocal microscopy and was inhibited by transfection of antisense against NADPH subunits p22phox or p47phox or with Tempol. F-actin disassembly was observed by dual-channel confocal fluorescence imaging. PI3 kinase activity was detected by immunoblotting of phosphorylated Akt.ResultsIn high glucose, generation of NADPH oxidase-dependent ROS was dependent on PKC-ζ. Conversely, sustained PKC-ζ activity was dependent on ROS generation, suggesting a positive feedback. PKC-ζ-dependent F-actin disassembly in high glucose required ROS generation. PDGF stimulated NADPH oxidase generation of ROS through a PKC-ζ mechanism that was independent of Akt phosphorylation and remained unchanged in high glucose.ConclusionIn high glucose, mesangial cell PKC-ζ is required for ROS generation from NADPH oxidase similar to PDGF stimulation of PKC-ζ-dependent ROS generation through a pathway independent of PI3 kinase. F-actin disassembly in high glucose also requires ROS. A positive feedback loop occurs between ROS and the activation of PKC-ζ in high glucose

Rosiglitazone Prevents High Glucose-Induced Vascular Endothelial Growth Factor and Collagen IV Expression in Cultured Mesangial Cells

Peroxisome proliferator-activated receptor (PPARγ), a ligand-dependent transcription factor, negatively modulates high glucose effects. We postulated that rosiglitazone (RSG), an activator of PPARγ prevents the upregulation of vascular endothelial growth factor (VEGF) and collagen IV by mesangial cells exposed to high glucose. Primary cultured rat mesangial cells were growth-arrested in 5.6 mM (NG) or 25 mM D-glucose (HG) for up to 48 hours. In HG, PPARγ mRNA and protein were reduced within 3 h, and enhanced ROS generation, expression of p22phox, VEGF and collagen IV, and PKC-ζ membrane association were prevented by RSG. In NG, inhibition of PPARγ caused ROS generation and VEGF expression that were unchanged by RSG. Reduced AMP-activated protein kinase (AMPK) phosphorylation in HG was unchanged with RSG, and VEGF expression was unaffected by AMPK inhibition. Hence, PPARγ is a negative modulator of HG-induced signaling that acts through PKC-ζ but not AMPK and regulates VEGF and collagen IV expression by mesangial cells

Seizure After Local Anesthesia for Nasopharyngeal Angiofibroma

We report a young male patient who experienced seizure after local injection of 3 mL 2% lidocaine with epinephrine 1:200,000 around a recurrent nasal angiofibroma. After receiving 100% oxygen via mask and thiamylal sodium, the patient had no residual neurologic sequelae. Seizure immediately following the injection of local anesthetics in the nasal cavity is probably due to injection into venous or arterial circulation with retrograde flow to the brain circulation. Further imaging study or angiography should be done before head and neck surgeries, especially in such highly vascular neoplasm

Attitudes of students from south-east and east Asian countries to slaughter and transport of livestock

Attitudes to animals have been extensively studied for people in developed countries, but not for those in developing countries. The attitudes of prospective stakeholders in the livestock sectors in south-east and east Asia toward transport and slaughter were examined by surveying university students studying veterinary medicine and animal science in Malaysia, Thailand, China and Vietnam, with a total of 739 students taking part. Students had greater acceptability of transport than slaughter issues for livestock, and female students found most transport and slaughter issues of greater concern than male students. Veterinary students were more accepting of several issues than animal science students, in particular killing animals that were injured or ill. Religion had a major effect on attitudes. Muslim students found using animals that died naturally for products least acceptable. Compared to them, Hindu students were less accepting of killing injured or ill animals and Buddhist students less accepting of euthanasing healthy pets. Students with more experience of pets were less accepting of both transport and slaughter issues. It is concluded that concern was exhibited by future stakeholders in the SE and E Asian livestock industries for slaughter and, to a lesser extent, transport issues, although attitudes were influenced by their religion, gender and experience of pet-keeping

GT-repeat polymorphism in the heme oxygenase-1 gene promoter and the risk of carotid atherosclerosis related to arsenic exposure

<p>Abstract</p> <p>Background</p> <p>Arsenic is a strong stimulus of heme oxygenase (HO)-1 expression in experimental studies in response to oxidative stress caused by a stimulus. A functional GT-repeat polymorphism in the HO-1 gene promoter was inversely correlated to the development of coronary artery disease in diabetics and development of restenosis following angioplasty in patients. The role of this potential vascular protective factor in carotid atherosclerosis remains unclear. We previously reported a graded association of arsenic exposure in drinking water with an increased risk of carotid atherosclerosis. In this study, we investigated the relationship between HO-1 genetic polymorphism and the risk of atherosclerosis related to arsenic.</p> <p>Methods</p> <p>Three-hundred and sixty-seven participants with an indication of carotid atherosclerosis and an additional 420 participants without the indication, which served as the controls, from two arsenic exposure areas in Taiwan, a low arsenic-exposed Lanyang cohort and a high arsenic-exposed LMN cohort, were studied. Carotid atherosclerosis was evaluated using a duplex ultrasonographic assessment of the extracranial carotid arteries. Allelic variants of (GT)n repeats in the 5'-flanking region of the HO-1 gene were identified and grouped into a short (S) allele (< 27 repeats) and long (L) allele (≥ 27 repeats). The association of atherosclerosis and the HO-1 genetic variants was assessed by a logistic regression analysis, adjusted for cardiovascular risk factors.</p> <p>Results</p> <p>Analysis results showed that arsenic's effect on carotid atherosclerosis differed between carriers of the class S allele (OR 1.39; 95% CI 0.86-2.25; <it>p </it>= 0.181) and non-carriers (OR 2.65; 95% CI 1.03-6.82; <it>p </it>= 0.044) in the high-exposure LMN cohort. At arsenic exposure levels exceeding 750 μg/L, difference in OR estimates between class S allele carriers and non-carriers was borderline significant (<it>p </it>= 0.051). In contrast, no such results were found in the low-exposure Lanyang cohort.</p> <p>Conclusions</p> <p>This exploratory study suggests that at a relatively high level of arsenic exposure, carriers of the short (GT)n allele (< 27 repeats) in the HO-1 gene promoter had a lower probability of developing carotid atherosclerosis than non-carriers of the allele after long-term arsenic exposure via ground water. The short (GT)n repeat in the HO-1 gene promoter may provide protective effects against carotid atherosclerosis in individuals with a high level of arsenic exposure.</p

Effects of implementation of an online comprehensive antimicrobial-stewardship program in ICUs: A longitudinal study

AbstractBackground/purposeThe long-term effects of antimicrobial-stewardship programs in the intensive care units (ICUs) have not been adequately examined. We evaluated the impact of an online comprehensive antimicrobial stewardship program (OCASP) on the outcomes of patients in 200-bed medical/surgical ICUs over the course of 11 years.MethodsWe analyzed the records of adult patients admitted to ICUs during the 5 years before (n = 27,499) and the 6 years after (n = 33,834) implementation of an OCASP. Antimicrobial consumption, expenditures, duration of treatment, incidence of healthcare-associated infections (HAIs), prevalence of HAIs caused by antimicrobial-resistant strains, and crude or sepsis-related mortality of patients were analyzed. Segmented regression analyses of interrupted time series were used to assess the significance of changes in antimicrobial use.ResultsCompared to the patients in the pre-OCASP period, the patients in the post-OCASP period were older, had greater disease severity, longer ICU stays, and were more likely to receive antimicrobials, but had lower antimicrobial expenditures and crude and sepsis-related mortality. The trend of overall antimicrobial use [slope of defined daily dose/1000 patient-days vs. time) increased significantly before OCASP implementation (p < 0.001), but decreased significantly after implementation (p < 0.01). The administration duration of all classes of antibiotics were significantly shorter (p < 0.001) and the incidences of HAIs were significantly lower (p < 0.001) after implementation. However, there was an increase in the proportion of HAIs caused by carbapenem-resistant Acinetobacter baumannii relative to all A. baumannii infections.ConclusionImplementation of an OCASP in the ICUs reduced antimicrobial consumption and expenditures, but did not compromise healthcare quality