Interpersonal Relationships among University Safety Professionals: The Impact of a Safety Departmentf

PresentationForming strong interpersonal relationships enables an organization or individual to achieve more favorable outcomes. The objectives of this study were to examine the frequency of interpersonal interactions among safety professionals (SPs) employed at Taiwanese universities and the factors that affected this frequency. To accomplish these objectives, we mailed questionnaires to a simple random sampling of 200 university SPs. Moreover, an interpersonal relationship scale was developed in this study; exploratory factor and internal consistency analyses revealed that the scale was valid and reliable. Results derived from the questionnaire revealed that in SP interpersonal relationships, general affairs department personnel, laboratory or internship unit supervisors, and teaching staff ranked highest in frequency of interactions. Multivariate analysis of variance results showed that establishing a safety department exerted a statistically significant effect on SP interpersonal relationships. SPs employed by universities with safety departments interacted more frequently with both internal and external relationships. Therefore, we suggest that universities without a safety department establish such a department to strengthen the labor safety and health structure, thereby benefitting SPs in fulfilling responsibilities to promote safety and health management

Removing Infragravity‐Wave‐Induced Noise from Ocean‐Bottom Seismographs (OBS) Data Deployed Offshore of Taiwan

Vertical ocean‐bottom seismograph (OBS) data at frequencies below 0.05 Hz are contaminated by noise induced by infragravity waves. We constructed the transfer function between pressure and velocity data from OBSs deployed in Taiwan waters to remove the wave pressure‐induced noise from seismic recordings. Data were analyzed from five portable broadband OBSs deployed each for 10 months at water depths from 1740 to 4600 m and from a cabled, shallow‐buried seismograph (EOS1) installed on the seafloor at 300 m depth. Removing long‐period noise from these OBS data improves the identification of teleseismic phases such as P, S, SS, Pdiff, and PKIKP that are otherwise ambiguous or unidentifiable. For EOS1, infragravity‐wave signals completely mask the P and S waveforms in the 10–50 s period band suitable for centroid moment tensor (CMT) solutions for most of the local events. Application of the transfer functions to predict and remove wave deformation yielded clean prominent P and S waveforms at these periods and aided in the CMT determination for small events jointly with land stations. The relative amplitudes of the wavenumber‐normalized transfer function for some of the OBSs are mostly determined by the thickness of the sediment at the OBS site

Sialylation of vasorin by ST3Gal1 facilitates TGF-β1-mediated tumor angiogenesis and progression.

ST3Gal1 is a key sialyltransferase which adds α2,3-linked sialic acid to substrates and generates core 1 O-glycan structure. Upregulation of ST3Gal1 has been associated with worse prognosis of breast cancer patients. However, the protein substrates of ST3Gal1 implicated in tumor progression remain elusive. In our study, we demonstrated that ST3GAL1-silencing significantly reduced tumor growth along with a notable decrease in vascularity of MCF7 xenograft tumors. We identified vasorin (VASN) which was shown to bind TGF-β1, as a potential candidate that links ST3Gal1 to angiogenesis. LC-MS/MS analysis of VASN secreted from MCF7, revealed that more than 80% of its O-glycans are sialyl-3T and disialyl-T. ST3GAL1-silencing or desialylation of VASN by neuraminidase enhanced its binding to TGF-β1 by 2- to 3-fold and thereby dampening TGF-β1 signaling and angiogenesis, as indicated by impaired tube formation of HUVECs, suppressed angiogenesis gene expression and reduced activation of Smad2 and Smad3 in HUVEC cells. Examination of 114 fresh primary breast cancer and their adjacent normal tissues showed that the expression levels of ST3Gal1 and TGFB1 were high in tumor part and the expression of two genes was positively correlated. Kaplan Meier survival analysis showed a significantly shorter relapse-free survival for those with lower expression VASN, notably, the combination of low VASN with high ST3GAL1 yielded even higher risk of recurrence (p = 0.025, HR = 2.967, 95% CI = 1.14-7.67). Since TGF-β1 is known to transcriptionally activate ST3Gal1, our findings illustrated a feedback regulatory loop in which TGF-β1 upregulates ST3Gal1 to circumvent the negative impact of VASN

High Prevalence of Mutations in Quinolone-resistance-determining Regions and mtrR Loci in Polyclonal Neisseria gonorrhoeae Isolates at a Tertiary Hospital in Southern Taiwan

Background/PurposeThe emergence of multidrug-resistant Neisseria gonorrhoeae is a great challenge in controlling gonorrhea. This study was conducted to survey the prevalence of molecular mechanisms of antimicrobial resistance among 45 clinical isolates of N. gonorrhoeae collected at a university hospital in Southern Taiwan during 1999-2004.MethodsMutations in mtrR loci and quinolone-resistance-determining regions (QRDRs) were examined by gene sequencing. Polymerase chain reactions with specific primers were performed to detect ermA, ermB, ermC, and ermF. Serogroups and serovars were determined by commercial kits.ResultsThe percentage of multidrug resistance, that is, resistance to penicillin, tetracycline, erythromycin, and ciprofloxacin, among the 45 isolates was 40%. Ceftriaxone and spectinomycin were active against all isolates in vitro. The frequency of mutations in the QRDR and mtrR promoter was 82.2% and 93.3%, respectively. Eighty-two percent of the isolates carried mutations both in the QRDR and mtrR loci. Of nine mutation profiles with QRDR mutations (n =37), gyrA-Ser91Phe/gyrA-Asp95Gly/parC-Ser87Arg was the most common type (56.8%). Acquired genes for rRNA methylase were detected in 11 isolates (10 ermB and 1 ermA). Twenty-seven serovars were identified and all belonged to serogroup B, which suggested that multiple clones of N. gonorrhoeae were circulating in the community in the Tainan area.ConclusionThe high prevalence of multidrug resistance caused by varied resistance mechanisms in N. gonorrhoeae limits the drug choice. Ongoing surveillance of antimicrobial resistance and discovery of new effective antibiotic therapy are warranted in endemic areas

Tankyrase inhibition ameliorates lipid disorder via suppression of PGC-1 alpha PARylation in db/db mice

Objective Human TNKS, encoding tankyrase 1 (TNKS1), localizes to a susceptibility locus for obesity and type 2 diabetes mellitus (T2DM). Here, we addressed the therapeutic potential of G007-LK, a TNKS-specific inhibitor, for obesity and T2DM. Methods We administered G007-LK to diabetic db/db mice and measured the impact on body weight, abdominal adiposity, and serum metabolites. Muscle, liver, and white adipose tissues were analyzed by quantitative RT-PCR and western blotting to determine TNKS inhibition, lipolysis, beiging, adiponectin level, mitochondrial oxidative metabolism and mass, and gluconeogenesis. Protein interaction and PARylation analyses were carried out by immunoprecipitation, pull-down and in situ proximity ligation assays. Results TNKS inhibition reduced body weight gain, abdominal fat content, serum cholesterol levels, steatosis, and proteins associated with lipolysis in diabetic db/db mice. We discovered that TNKS associates with PGC-1 alpha and that TNKS inhibition attenuates PARylation of PGC-1 alpha, contributing to increased PGC-1 alpha level in WAT and muscle in db/db mice. PGC-1 alpha upregulation apparently modulated transcriptional reprogramming to increase mitochondrial mass and fatty acid oxidative metabolism in muscle, beiging of WAT, and raised circulating adiponectin level in db/db mice. This was in sharp contrast to the liver, where TNKS inhibition in db/db mice had no effect on PGC-1 alpha expression, lipid metabolism, or gluconeogenesis. Conclusion Our study unravels a novel molecular mechanism whereby pharmacological inhibition of TNKS in obesity and diabetes enhances oxidative metabolism and ameliorates lipid disorder. This happens via tissue-specific PGC-1 alpha-driven transcriptional reprogramming in muscle and WAT, without affecting liver. This highlights inhibition of TNKS as a potential pharmacotherapy for obesity and T2DM.Peer reviewe

Muscle injury and impaired function, and insulin resistance in Chromogranin A knockout mice

Chromogranin A (CgA) is widely expressed in endocrine and neuroendocrine tissues as well as in the central nervous system. We observed CgA expression (mRNA and protein) in the gastrocnemius (GAS) muscle and found that performance of CgA-deficient Chga-KO mice in treadmill exercise was impaired. Supplementation with CgA in Chga-KO mice restored exercise ability suggesting a novel role for endogenous CgA in skeletal muscle function. Chga-KO mice display (i) lack of exercise-induced stimulation of pAKT, pTBC1D1 and phospho-p38 kinase signaling, (ii) loss of GAS muscle mass, (iii) extensive formation of tubular aggregates (TA), (iv) disorganized cristae architecture in mitochondria, (v) increased expression of the inflammatory cytokines Tnfα, Il6 and Ifnɣ, and fibrosis. The impaired maximum running speed and endurance in the treadmill exercise in Chga-KO mice correlated with decreased glucose uptake and glycolysis, defects in glucose oxidation and decreased mitochondrial cytochrome C oxidase activity. The lack of adaptation to endurance training correlated with the lack of stimulation of p38MAPK that is known to mediate the response to tissue damage. Since CgA sorts proteins to the regulated secretory pathway, we speculate that lack of CgA could cause misfolding of membrane proteins inducing aggregation of sarcoplasmic reticulum (SR) membranes and formation of tubular aggregates that is observed in Chga-KO mice. In conclusion, CgA deficiency renders the muscle energy deficient, impairs performance in treadmill exercise and prevents regeneration after exercise-induced tissue damage

Vascular function in the aging human brain during muscle exertion

: To determine how brain oxygenation is stably maintained during advancing age, cerebral oxygenation and hemoglobin were measured real-time at 10 Hz using near-infrared spectroscopy (NIRS) at rest (30 seconds) and during a 10-repeated handgrip strength test (30 seconds) for 834 adults (M/F = 45/55%) aged 20-88 y. The amplitude of cerebral hemodynamic fluctuation was reflected by converting 300 values of % oxygen saturation and hemoglobin of each 30-second phase to standard deviation as indicatives of brain oxygenation variability (BOV) and brain hemodynamic variability (BHV) for each participant. Both BOV (+21-72%) and BHV (+94-158%) increased during the maximal voluntary muscle exertions for all age levels (α < 0.05), suggesting an increased vascular recruitment to maintain oxygen homeostasis in the brain. Intriguingly, BHV was >100 folds for both resting and challenged conditions (α < 0.001) in >80% of adults aged above 50 y despite similar BOV compared with young age counterparts, indicating a huge cost of amplifying hemodynamic oscillation to maintain a stable oxygenation in the aging brain. Since vascular endothelial cells are short-lived, our results implicate a hemodynamic compensation to emergence of daily deficits in replacing senescent endothelial cells after age 50 y