Assessment of Effects of Air Pollution on Daily Outpatient Visits using the Air Quality Index

Background

The air quality index (AQI) is widely used to characterize the quality of ambient air. Chinese cities officially report the AQI on a daily basis. To assess the possible effects of air pollution on daily outpatient visits, we examined the association between AQI and the daily outpatient count.

Methods

Daily data on outpatient visits to each clinical department were collected from the Z county hospital of Datong City, China. The collection period was between 5 April and 30 June, 2012. Daily AQI data and meteorological information were simultaneously recorded. We compared outpatient counts between the index days and comparison days, and calculated Pearson’s product moment correlation coefficient between outpatient counts and AQI levels.

Results

The average AQI level for index days was significantly higher than that for comparison days. No significant difference was observed in temperature or relative humidity between index days and comparison days. The outpatient counts for pediatrics were significantly higher on index days than on comparison days, and no significant difference was noted in other clinical departments. The outpatient counts for pediatrics positively correlated with the AQI level, and no correlation was noted in other clinical departments.

Conclusion

The present study assessed the association between daily outpatient visits and air pollution using AQI. The results obtained suggest that air pollution could increase the outpatient count for pediatrics.     

Immunohistochemistry of γ‐H2AX as a method of early detection of urinary bladder carcinogenicity in mice

Phosphorylated histone H2AX (γ‐H2AX) has been demonstrated as a DNA damage marker both in vitro and in vivo. We previously reported the effects of genotoxic carcinogens in the urinary bladder of rats by immunohistochemical analysis of γ‐H2AX using samples from 28‐day repeated‐dose tests. To evaluate the application of γ‐H2AX as a biomarker of carcinogenicity in the bladder, we examined species differences in γ‐H2AX formation in the urinary bladder of mice. Six‐week‐old male B6C3F₁ mice were treated orally with 12 chemicals for 4 weeks. Immunohistochemical analysis demonstrated that N‐butyl‐N‐(4‐hydroxybutyl)nitrosamine, p‐cresidine and 2‐acetylaminofluorene (2‐AAF), classified as genotoxic bladder carcinogens, induced significant increases in γ‐H2AX levels in the bladder urothelium. In contrast, genotoxic (2‐nitroanisole, glycidol, N‐nitrosodiethylamine and acrylamide) and non‐genotoxic (dimethylarsinic acid and melamine) non‐bladder carcinogens did not upregulate γ‐H2AX. Importantly, 2‐nitroanisole, a potent genotoxic bladder carcinogen in rats, significantly increased the proportion of γ‐H2AX‐positive cells in rats only, reflecting differences in carcinogenicity in the urinary bladder between rats and mice. Significant upregulation of γ‐H2AX was also induced by uracil, a non‐genotoxic bladder carcinogen that may be associated with cell proliferation, as demonstrated by increased Ki67 expression. 2‐AAF caused γ‐H2AX formation mainly in the superficial layer, together with reduced and disorganized expression of uroplakin III, unlike in rats, suggesting the mouse‐specific cytotoxicity of 2‐AAF in umbrella cells. These results suggest γ‐H2AX is a useful biomarker reflecting species differences in carcinogenicity in the urinary bladder.     

Non-linear association between ankle-brachial pressure index and prevalence of silent cerebral infarction in Japanese patients with type 2 diabetes

ObjectivePatients with peripheral artery disease (PAD), defined as having low ankle-brachial pressure index (ABI), have increased risk for incident stroke compared with those without PAD. We aimed to reveal whether ABI abnormality, especially high ABI is associated with prevalent silent cerebral infarction (SCI) in type 2 diabetic patients.MethodsWe studied 538 Japanese type 2 diabetic patients, 227 women and 311 men, with a mean [±SD] age of 64 ± 11 years. All patients underwent cranial magnetic resonance imaging (MRI). Values of ABI were classified as low (<0.9), normal (0.9≤ and <1.3), and high (1.3≤). Logistic regression model was used to calculate odds ratio and 95% confidence interval (95% CI) for prevalent SCI.ResultsThe mean ABI among the overall 538 patients was 1.09 ± 0.16. Low and high ABI values were found in 52 (9.7%) and 33 (6.1%) patients, respectively. SCI was detected in 297 (55.2%) patients. The prevalence in patients with low, normal, and high ABI values were 88.5%, 49.7%, and 78.8 (p < 0.001), respectively. In the multivariate logistic regression analysis, both patients with high and low ABI were significantly increased risk of prevalent SCI (odds ratio 4.53, 95% CI 1.67–12.34, p = 0.003 and odds ratio 3.50, 95% CI 1.50–10.29, p = 0.005), independently of other traditional cardiovascular risk factors, than those with normal ABI.ConclusionsBoth high and low ABI may be strongly associated with prevalent SCI in Japanese patients with type 2 diabetes.     

Phosphatidylinositol 4-phosphate 5-kinase alpha (PIPKα) regulates neuronal microtubule depolymerase kinesin, KIF2A and suppresses elongation of axon branches

Neuronal morphology is regulated by cytoskeletons. Kinesin superfamily protein 2A (KIF2A) depolymerizes microtubules (MTs) at growth cones and regulates axon pathfinding. The factors controlling KIF2A in neurite development remain totally elusive. Here, using immunoprecipitation with an antibody specific to KIF2A, we identified phosphatidylinositol 4-phosphate 5-kinase alpha (PIPKα) as a candidate membrane protein that regulates the activity of KIF2A. Yeast two-hybrid and biochemical assays demonstrated direct binding between KIF2A and PIPKα. Partial colocalization of the clusters of punctate signals for these two molecules was detected by confocal microscopy and photoactivated localization microscopy. Additionally, the MT-depolymerizing activity of KIF2A was enhanced in the presence of PIPKα in vitro and in vivo. PIPKα suppressed the elongation of axon branches in a KIF2A-dependent manner, suggesting a unique PIPK-mediated mechanism controlling MT dynamics in neuronal development.     

Constructing an index of physical fitness age for Japanese elderly based on 7-year longitudinal data: sex differences in estimated physical fitness age

A standardized method for assessing the physical fitness of elderly adults has not yet been established. In this study, we developed an index of physical fitness age (fitness age score, FAS) for older Japanese adults and investigated sex differences based on the estimated FAS. Healthy elderly adults (52 men, 70 women) who underwent physical fitness tests once yearly for 7 years between 2002 and 2008 were included in this study. The age of the participants at the beginning of this study ranged from 60.0 to 83.0 years. The physical fitness tests consisted of 13 items to measure balance, agility, flexibility, muscle strength, and endurance. Three criteria were used to evaluate fitness markers of aging: (1) significant cross-sectional correlation with age; (2) significant longitudinal change with age consistent with the cross-sectional correlation; and (3) significant stability of individual differences. We developed an equation to assess individual FAS values using the first principal component derived from principal component analysis. Five candidate fitness markers of aging (10-m walking time, functional reach, one leg stand with eyes open, vertical jump and grip strength) were selected from the 13 physical fitness tests. Individual FAS was predicted from these five fitness markers using a principal component model. Individual FAS showed high longitudinal stability for age-related changes. This investigation of the longitudinal changes of individual FAS revealed that women had relatively lower physical fitness compared with men, but their rate of physical fitness aging was slower than that of men.     

Effect of GDF-5 and BMP-2 on the expression of tendo/ligamentogenesis-related markers in human PDL-derived cells

Oral Diseases (2012) 18 , 206–212 Objectives: The effect of growth differentiation factor 5 and bone morphogenetic protein 2 on human periodontal ligament‐derived cells was investigated with special reference to tendo/ligamentogenesis‐related markers. Materials and Methods: Effects of each factor were analyzed by quantitative PCR for scleraxis and tenomodulin and by western blotting for scleraxis. After exposure to those factors, STRO‐1‐positive and STRO‐1‐negative fractions of human periodontal ligament tissues were isolated with an immunomagnetic cell sorting system, and the expression of scleraxis in each fraction was analyzed by western blotting. Non‐separated crude cells were used as a control. Results: Growth differentiation factor 5 and bone morphogenetic protein 2 did not increase alkaline phosphatase activity in crude periodontal ligament‐derived cells. Growth differentiation factor 5, but not bone morphogenetic protein 2, increased the expression of scleraxis in crude, STRO‐1‐positive and STRO‐1‐negative periodontal ligament‐derived cells. The expression of scleraxis in STRO‐1‐positive periodontal ligament‐derived cells was significantly less compared to that in crude P2 and STRO‐1‐negative periodontal ligament‐derived cells. Conclusion: Growth differentiation factor 5 induced the expression of scleraxis and may enhance tendo/ligamentogenesis in human periodontal ligament‐derived cells. The expression of scleraxis was higher in STRO‐1‐negative fraction, suggesting more differentiated state of the cells.     

Coexpression of SGLT1 and EGFR is associated with tumor differentiation in oral squamous cell carcinoma

Overexpression of epidermal growth factor receptor (EGFR) is associated with resistance to chemotherapy and radiotherapy, advanced tumor stage, invasion, metastasis and poor prognosis in malignant tumors. EGFR, therefore, has been an attractive molecular target for chemotherapy. However, the results of clinical studies using inhibitors of its kinase activity have not been promising because the response rates were at most 20%. Sodium-glucose co-transporter 1 (SGLT1) is a membrane protein that mediates the transport of glucose across cellular membranes. EGFR physically associates with and stabilizes SGLT1 to promote glucose uptake into cancer cells through a kinase-independent process. The purpose of this study was to investigate the coexpression of SGLT1 and EGFR and its relationships with clinicopathological features in oral squamous cell carcinoma (OSCC). SGLT1 and EGFR were detected in all OSCC cell lines, and the expression levels of SGLT1 were significantly correlated with those of EGFR. Pearson product?Cmoment correlation coefficient of SGLT1 and EGFR was 0.89 (P?=?0.016). The immunohistochemical study using the surgical specimens in 52 patients with tongue SCC also showed a significant correlation between SGLT1 and EGFR. Moreover, SGLT1/EGFR expression was inversely related to tumor differentiation among the 5 clinicopathological factors (P?=?0.004). SGLT1/EGFR coexpression might be required in the de-differentiation of OSCC, but further study is needed to clarify the implication of these proteins in the manifestation of malignancy and clinical significance.