Social nicotine dependence in Australian dental undergraduate students

Objectives: This study aimed to investigate dental undergraduate students’ tobacco usage and social nicotine dependence in Australia. A special interest was to identify the role of factors such as age, gender, year of dental education and cohabitants’ smoking status for social nicotine dependence. Materials and methods: A sample of 252, first‐to‐fifth year undergraduate students in an Australian dental school was used. Each completed a self‐administered questionnaire. Results: The smoking rate was 4.8%. Current smokers displayed higher social nicotine dependence than those that had never smoked (t = 3.1, df = 244, P = 0.002). Dental undergraduate students that showed higher social nicotine dependence (P = 0.001, OR = 1.3, 95% CI: 1.1–1.6), or that had smoking cohabitants (P = 0.016, OR = 4.8, 95% CI: 1.3–17.0), were more likely to smoke. Students’ social nicotine dependence increased with year of dental study (P = 0.043, β = 0.4, t = 2.0). Social nicotine dependence enhanced tobacco usage among Year‐1‐to‐4 students (P = 0.005, OR = 1.4, 95% CI: 1.1–1.7) but not Year‐5 undergraduates (P = 0.432). Conclusions: Social nicotine dependence has become a developing issue in dental education. Tobacco control should be highlighted in the dental curriculum. Future investigations into the effects of dental education on social nocotine dependence and tobacco usage are indicated.     

Association of oral sodium phosphate purgative use with acute kidney injury

Oral sodium phosphate (OSP) is a commonly used purgative before colonoscopy. There have been numerous reports of acute phosphate nephropathy attributed to the use of OSP. This study evaluated the association between the use of OSP and acute kidney injury (AKI) in an observational, retrospective, cohort study. Of 9799 patients who underwent colonoscopy and had serum creatinine values recorded within 365 days before and after the procedure, AKI, defined as > or =50% increase in baseline serum creatinine, was identified in 114 (1.16%). After adjustment for significant covariates in a multiple logistic regression model, the use of OSP was associated with increased risk for AKI (odds ratio 2.35; 95% confidence interval 1.51 to 3.66; P < 0.001) with an adjusted number need to harm of 81. Age was also independently associated with AKI in this cohort; therefore, until larger, prospective studies define the population at risk for acute phosphate nephropathy, the use of polyethylene glycol-based purgatives should be considered for older patients and possibly for those with comorbid medical conditions.     

Changes in biochemical processes in cerebellar granule cells of mice exposed to methylmercury

At postnatal day 34, male and female C57BL/6J mice were exposed orally once a day to a total of five doses totaling 1.0 or 5.0 mg/kg of methylmercuric chloride or sterile deionized water in moistened rodent chow. Eleven days after the last dose cerebellar granule cells were acutely isolated to measure reactive oxygen species (ROS) levels and mitochondrial membrane potential using CM-H(2)DCFDA and TMRM dyes, respectively. For visualizing intracellular calcium ion distribution using transmission electron microscopy, mice were perfused 11 days after the last dose of methylmercury (MeHg) using the oxalate-pyroantimonate method. Cytosolic and mitochondrial protein fractions from acutely isolated granule cells were analyzed for cytochrome c content using Western blot analysis. Histochemistry (Fluoro-Jade dye) and immunohistochemistry (activated caspase 3) was performed on frozen serial cerebellar sections to label granule cell death and activation of caspase 3, respectively. Granule cells isolated from MeHg-treated mice showed elevated ROS levels and decreased mitochondrial membrane potential when compared to granule cells from control mice. Electron photomicrographs of MeHg-treated granule cells showed altered intracellular calcium ion homeostasis ([Ca(2+)](i)) when compared to control granule cells. However, in spite of these subcellular changes and moderate relocalization of cytochrome c into the cytosol, the concentrations of MeHg used in this study did not produce significant neuronal cell death/apoptosis at the time point examined, as evidenced by Fluoro-Jade and activated caspase 3 immunostaining, respectively. These results demonstrate that short-term in vivo exposure to total doses of 1.0 and 5.0 mg/kg MeHg through the most common exposure route (oral) can result in significant subcellular changes that are not accompanied by overt neuronal cell death.     

Perfluorooctanoic acid induced developmental toxicity in the mouse is dependent on expression of peroxisome proliferator activated receptor-alpha.

Perfluorooctanoic acid (PFOA) is a member of a family of perfluorinated chemicals that have a variety of applications. PFOA persists in the environment and is found in wildlife and humans. In mice, PFOA is developmentally toxic producing mortality, delayed eye opening, growth deficits, and altered pubertal maturation. PFOA activates peroxisome proliferators-activated receptor-alpha (PPARalpha), a pathway critical to the mode of induction of liver tumors in rodents. The present study uses 129S1/SvlmJ wild-type (WT) and PPARalpha knockout (KO) mice to determine if PPARalpha mediates PFOA-induced developmental toxicity. Pregnant mice were dosed orally from gestation days 1-17 with water or 0.1, 0.3, 0.6, 1, 3, 5, 10, or 20 mg PFOA/kg. PFOA did not affect maternal weight, embryonic implantation, number, or weight of pups at birth. At 5 mg/kg, the incidence of full litter resorptions increased in both WT and KO mice. In WT, but not KO, neonatal survival was reduced (0.6 mg/kg) and eye opening was delayed (1 mg/kg). There was a trend across dose for reduced pup weight (WT and KO) on several postnatal days (PND), but only WT exposed to 1 mg/kg were significantly different from control (PND7-10 and 22). Maternal factors (e.g., background genetics) did not contribute to differences in postnatal mortality, as PFOA induced postnatal mortality in heterozygous pups born to WT or KO dams. In conclusion, early pregnancy loss was independent of PPARalpha expression. Delayed eye opening and deficits in postnatal weight gain appeared to depend on PPARalpha expression, although other mechanisms may contribute. PPARalpha was required for PFOA-induced postnatal lethality and expression of one copy of the gene was sufficient to mediate this effect.     

Clinical and genetic analysis of Korean patients with Marfan syndrome: possible ethnic differences in clinical manifestation

Yoo E‐H, Woo H, Ki C‐S, Lee HJ, Kim D‐K, Kang I‐S, Park P, Sung K, Lee CS, Chung T‐Y, Moon JR, Han H, Lee S‐T, Kim J‐W. Clinical and genetic analysis of Korean patients with Marfan syndrome: possible ethnic differences in clinical manifestation. Marfan syndrome (MFS) is an autosomal dominant disorder of the fibrous connective tissue caused by mutations in the fibrillin‐1 (FBN1) gene. Although clinical and genetic analyses have been performed in various populations, there have been few studies in Korea. The aim of this study was to investigate the clinical characteristics and genetic background of Korean patients with MFS. In 39 Korean patients with MFS who met the Ghent criteria, the most common clinical finding was aortic dilatation and/or dissection (94.9%), whereas only 35.9% of patients had ectopia lentis. The majority of MFS patients had fewer than four of the skeletal findings required to fulfill the major skeletal Ghent criterion for MFS. Only 21% of Korean patients had major skeletal abnormalities and most cases showed only minor skeletal involvement. FBN1 gene mutations were detected in 35 out of 39 patients (89.7%), which is similar to rates presented in the previous reports. These results suggest that some clinical features in Korean patients with MFS differed from those reported in Western MFS patients.     

Extending the effects of spike-timing-dependent plasticity to behavioral timescales

Activity-dependent modification of synaptic strengths due to spike-timing-dependent plasticity (STDP) is sensitive to correlations between pre- and postsynaptic firing over timescales of tens of milliseconds. Temporal associations typically encountered in behavioral tasks involve times on the order of seconds. To relate the learning of such temporal associations to STDP, we must account for this large discrepancy in timescales. We show that the gap between synaptic and behavioral timescales can be bridged if the stimuli being associated generate sustained responses that vary appropriately in time. Synapses between neurons that fire this way can be modified by STDP in a manner that depends on the temporal ordering of events separated by several seconds even though the underlying plasticity has a much smaller temporal window.     

spa typing of methicillin-resistant Staphylococcus aureus isolated from domestic animals and veterinary staff in the UK and Ireland

OBJECTIVES: Region X of the protein A gene (spa) was sequenced from methicillin-resistant Staphylococcus aureus (MRSA) isolates originating from animals, humans and the environment at veterinary hospitals in the UK and Ireland. MRSA transmission between animals and veterinary staff was assessed on the basis of spa typing, PFGE and epidemiological data. METHODS: MRSA isolates from dogs (n = 27), horses (n = 9), cats (n = 6), staff (n = 22) and environmental surfaces (n = 3) were analysed by PFGE and spa typing. Known contacts between human and animal MRSA carriers were ascertained from the veterinary hospitals. RESULTS: All feline, most canine (96%) and human (82%) isolates showed PFGE profiles that were either indistinguishable (subtype A1) or closely related (subtypes A2-A10) to that of the epidemic clone EMRSA-15 (CC22), whereas most equine isolates (88%) were related to CC8 (types C, D, E and G). spa polymorphism enabled discrimination among MRSA strains assigned to the same PFGE type. Fifteen spa types clustering into two distinct groups were detected, with t032 being the most prevalent (48%). The spa and PFGE types of MRSA isolated from seven staff members were the same as those of strains isolated from infected animals attended by the staff. CONCLUSIONS: Irrespective of geographical origin, MRSA isolated from equine and small animal hospitals generally clustered into two distinct clonal complexes, CC8 and CC22, respectively. The combined use of spa and PFGE typing allowed better discrimination than each method used individually, and provided useful information on MRSA transmission between animal and human individuals.     

MxA gene expression in juvenile dermatomyositis peripheral blood mononuclear cells: association with muscle involvement

Juvenile dermatomyositis (JDM), a systemic vasculopathy, is characterized by inflammation of skin and muscle. Muscle biopsies from untreated JDM patients show upregulation of type I interferon (IFN)-inducible genes, including myxovirus resistance protein A (MxA). The present study examines whether MxA mRNA expression in peripheral blood mononuclear cells (PBMC) from JDM patients: (1) is elevated compared to healthy controls, (2) reflects disease activity, and (3) changes with the onset of clinically effective treatment. MxA mRNA expression in JDM PBMC obtained at the initial clinic visit was elevated compared to controls and was positively correlated with Disease Activity Score (DAS) for muscle, but not with DAS for skin, suggesting that damage to skin and muscle in JDM may each have a discrete pathophysiology. During the course of clinically effective treatment, decrease in muscle symptoms was associated with a decrease in PBMC MxA mRNA expression.