Prevalence of Metabolic Syndrome and Its Components among Japanese Workers by Clustered Business Category.

The present study was a cross-sectional study conducted to reveal the prevalence of metabolic syndrome and its components and describe the features of such prevalence among Japanese workers by clustered business category using big data. The data of approximately 120,000 workers were obtained from a national representative insurance organization, and the study analyzed the health checkup and questionnaire results according to the field of business of each subject. Abnormalities found during the checkups such as excessive waist circumference, hypertension or glucose intolerance, and metabolic syndrome, were recorded. All subjects were classified by business field into 18 categories based on The North American Industry Classification System. Based on the criteria of the Japanese Committee for the Diagnostic Criteria of Metabolic Syndrome, the standardized prevalence ratio (SPR) of metabolic syndrome and its components by business category was calculated, and the 95% confidence interval of the SPR was computed. Hierarchical cluster analysis was then performed based on the SPR of metabolic syndrome components, and the 18 business categories were classified into three clusters for both males and females. The following business categories were at significantly high risk of metabolic syndrome: among males, Construction, Transportation, Professional Services, and Cooperative Association; and among females, Health Care and Cooperative Association. The results of the cluster analysis indicated one cluster for each gender with a higher prevalence of metabolic syndrome components; among males, a cluster consisting of Manufacturing, Transportation, Finance, and Cooperative Association, and among females, a cluster consisting of Mining, Transportation, Finance, Accommodation, and Cooperative Association. These findings reveal that, when providing health guidance and support regarding metabolic syndrome, consideration must be given to its components and the variety of its prevalence rates by business category and gender.

Association of thioautotrophic bacteria with deep-sea sponges.

We investigated microorganisms associated with a deep-sea sponge, Characella sp. (Pachastrellidae) collected at a hydrothermal vent site (686 m depth) in the Sumisu Caldera, Ogasawara Island chain, Japan, and with two sponges, Pachastrella sp. (Pachastrellidae) and an unidentified Poecilosclerida sponge, collected at an oil seep (572 m depth) in the Gulf of Mexico, using polymerase chain reaction-denaturing gradient gel electrophoresis (PCR-DGGE) directed at bacterial 16S rRNA gene sequences. In the PCR-DGGE profiles, we detected a single clearly dominant band in each of the Characella sp. and the unidentified Poecilosclerida sponge. BLAST search of their sequences showed that they were most similar (>99% identity) to those of the gammaproteobacterial thioautotrophic symbionts of deep-sea bivalves from hydrothermal vents, Bathymodiolus spp. Phylogenetic analysis of the near-full length sequences of the 16S rRNA genes cloned from the unidentified Poecilosclerida sponge and Characella sp. confirmed that they were closely related to thioautotrophic symbionts. Although associations between sponges and methanotrophic bacteria have been reported previously, this is the first report of a possible stable association between sponges and thioautotrophic bacteria.

Aging enhances susceptibility to cigarette smoke-induced inflammation through bronchiolar chemokines.

Cigarette smoking and aging are major risk factors for chronic obstructive pulmonary disease. An unsolved question is whether elderly lungs are particularly vulnerable to cigarette smoke (CS) exposure. In this study, we used a mouse model to test the hypothesis that aging increases the susceptibility to CS-induced pulmonary inflammation. We subjected 9-week-old and 69-week-old C57BL/6J mice to CS (whole-body exposure, 90 min/d), and evaluated neutrophil infiltration in the lungs, the levels of keratinocyte-derived chemokine (KC) and macrophage inflammatory protein (MIP)-2 in bronchoalveolar lavage fluid, and mRNA expression in bronchiolar epithelium retrieved by laser capture microdissection. The 69-week-old mice showed a greater number of neutrophils and higher levels of bronchiolar KC and MIP-2 expression than 9-week-old mice after 9 days of CS exposure. Furthermore, single CS exposure induced the rapid up-regulation of KC and MIP-2 in bronchiolar epithelium in both 9-week-old and 69-week-old mice, and the much higher levels in 69-week-old mice were associated with greater nuclear translocation of NF-kappaB. In contrast, no age-related differences were observed in the bronchiolar expression of NF-E2-related factor 2-regulated antioxidant and detoxification genes, heme oxygenase-1, reduced nicotinamide adenine dinucleotide phosphate quinone reductase 1, and glutamate-cysteine ligase, modifier unit, or antioxidant activity in bronchoalveolar lavage fluid, regardless of CS exposure. In summary, aging increases susceptibility to CS-induced inflammation in a mouse model, and robust mRNA up-regulation and nuclear translocation of NF-kappaB in bronchiolar epithelium may be involved.

Decreased airway expression of vascular endothelial growth factor in cigarette smoke-induced emphysema in mice and COPD patients.

Vascular endothelial growth factor (VEGF) signaling is crucial for lung structure maintenance. Although VEGF deficiency plays a role in the pathogenesis of emphysema in animals, little is known about VEGF expression levels and functions, as well as VEGF receptors, in airway epithelial cells, which are in direct contact with the environment. In this study, C57BL/6J mice were exposed to cigarette smoke (CS) for short (approximately 10 days) and long (4-24 wk) time periods, and bronchiolar expressions of VEGF and its receptors VEGFR-1 and VEGFR-2 were examined. The relationships between the expressions of VEGF, VEGFR-1, and VEGFR-2 and smoking histories and/or chronic obstructive pulmonary disease (COPD) were examined in humans. The mRNA levels were quantified in bronchiolar epithelium harvested by laser capture microdissection in both mouse and human lung tissues or in human bronchial epithelium harvested by bronchoscopic brushing. The VEGF protein level was assessed by immunohistochemistry or enzyme-linked immunosorbent assay. Repeated CS exposure downregulated bronchiolar expressions of VEGF and both VEGF receptors at various time points prior to the development of emphysema. In humans, bronchiolar VEGF was significantly decreased in smokers with COPD compared to lifelong nonsmokers, as well as to smokers without COPD; however, there was no difference in bronchiolar VEGF levels between lifelong nonsmokers and smokers without COPD. On the other hand, bronchiolar VEGFR-2 was downregulated in smokers with and without COPD compared to lifelong nonsmokers. These findings suggest the association of downregulation of bronchiolar VEGF and its receptors with cigarette smoking and COPD.

Bronchiolar chemokine expression is different after single versus repeated cigarette smoke exposure.

BACKGROUND: Bronchioles are critical zones in cigarette smoke (CS)-induced lung inflammation. However, there have been few studies on the in vivo dynamics of cytokine gene expression in bronchiolar epithelial cells in response to CS. METHODS: We subjected C57BL/6J mice to CS (whole body exposure, 90 min/day) for various periods, and used laser capture microdissection to isolate bronchiolar epithelial cells for analysis of mRNA by quantitative reverse transcription-polymerase chain reaction. RESULTS: We detected enhanced expression of keratinocyte-derived chemokine (KC), macrophage inflammatory protein-2 (MIP-2), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta (IL-1beta) by bronchial epithelial cells after 10 consecutive days of CS exposure. This was mirrored by increases in neutrophils and KC, MIP-2, TNF-alpha, and IL-1beta proteins in the bronchoalveolar lavage (BAL) fluid. The initial inhalation of CS resulted in rapid and robust upregulation of KC and MIP-2 with concomitant DNA oxidation within 1 hr, followed by a return to control values within 3 hrs. In contrast, after CS exposure for 10 days, this initial surge was not observed. As the CS exposure was extended to 4, 12, 18 and 24 weeks, the bronchiolar KC and MIP-2 expression and their levels in BAL fluid were relatively dampened compared to those at 10 days. However, neutrophils in BAL fluid continuously increased up to 24 weeks, suggesting that neutrophil accumulation as a result of long-term CS exposure became independent of KC and MIP-2. CONCLUSION: These findings indicate variable patterns of bronchiolar epithelial cytokine expression depending on the duration of CS exposure, and that complex mechanisms govern bronchiolar molecular dynamics in vivo.

In vitro evaluation of low-intensity pulsed ultrasound in herniated disc resorption.

Herniated disc (HD) is often resolved spontaneously without surgical intervention. HD resorption (HDR) is associated with abundant vascularization and infiltration of macrophages (Mphi) into the intervertebral disc (ID), as well as with high levels of matrix metalloproteinases (MMPs). Low-intensity pulsed ultrasound (LIPUS) accelerates bone fracture healing in clinical studies, and angiogenic factors are involved in the mechanism of action. In the present study, we examined the effects of LIPUS on HDR in a rat in vitro HD model. HDR was enhanced by LIPUS as measured by the change in the wet weight of the cultured ID. The secretion of tumor necrosis factor-alpha (TNF-alpha) and macrophage chemoattractant protein-1 (MCP-1) from Mphi into the culture medium was stimulated by LIPUS. LIPUS also enhanced matrix metalloproteinase-3 (MMP-3) maturation. Moreover, many apoptotic cell death were observed in the HDR groups with LIPUS exposure. These results suggest that LIPUS enhanced the HDR via MMP-3 activation through TNF-alpha and MCP-1 pathways. Although animal studies and clinical trial are needed to understand the LIPUS effects on HDR, LIPUS treatment might be an effective treatment for accelerating HDR.

Anaerobic degradation of cis-1,2-dichloroethylene and vinyl chloride by Clostridium sp. strain DC1 isolated from landfill leachate sediment.

The bacterial community structure of anaerobic enrichment cultures that are capable of degrading both cis-1,2-dichloroethylene (cis-DCE) and vinyl chloride (VC) and isolation of the organism responsible for the degradation were investigated. Denaturing gradient gel electrophoresis (DGGE) of a PCR-amplified 16S rRNA gene from the cultures showed the possible predominance of Clostridium species. One isolate, designated strain DC1, was closely related to members of Clostridiaceae, based on 16S rRNA gene analysis, and the highest sequence similarity (98.9%) was obtained for Clostridium saccarobutylicum. In culture experiments, strain DC1 was shown to degrade cis-DCE and VC during the stationary phase of growth without accumulation of VC and/or ethene. The bacterial growth was not linked to the degradation of cis-DCE and VC. Stoichiometric analysis revealed that two moles of chloride ions as released from one mole of cis-DCE during the incubation period, indicating that cis-DCE was fully dechlorinated. The results appear consistent with the presence of a mechanism of oxidative dechlorination rather than respiratory reductive dechlorination; the latter is accompanied by transient formation of dechlorinated ethenes from cis-DCE and VC.

Biodegradation of cis-1,2-dichloroethylene and vinyl chloride in anaerobic cultures enriched from landfill leachate sediment under Fe(III)-reducing conditions.

An anaerobic, Fe(III)-reducing enrichment culture, which originated from a sediment sample collected at a landfill in Nanji-do, Seoul, Korea, was capable of degrading cis-1,2-dichloroethylene (cis-DCE) and vinyl chloride (VC). Although it exhibited the ability under Fe(III)-reducing conditions, the chlorinated ethenes degradation was not linked to the Fe(III) reduction. During cis-DCE degradation, no VC, ethene, or ethane was detected through the experimental period. Also, this culture did not accumulate ethene and ethane during the VC degradation. It was unlikely that cis-DCE was reductively dechlorinated to VC and then the VC formed was dechlorinated fast enough. Because the kinetic data showed that the rate of cis-DCE degradation was 3.5 times higher than that of VC. Whereas glucose supported the culture growth and the degradation, formate, acetate, butyrate, propionate, lactate, pyruvate, and yeast extract did not. The results appeared consistent with the involvement of oxidative degradation mechanism rather than reductive dechlorination mechanism. The traits of the culture described here are unusual in the anaerobic degradation of chlorinated ethenes and may be useful for searching an effective organism and mechanism regarding anaerobic cis-DCE and VC degradation.

Pharmacological profiles of high-concentration (20 microg/g) tacalcitol ointment: effects on cutaneous inflammation, epidermal proliferation, and differentiation in mice.

This study focused on the effects of tacalcitol (1,24 (R) (OH)2D3, TV-02) ointment (20 micro g/g) on cutaneous inflammation, epidermal proliferation, and differentiation and compared them with tacalcitol ointment (2 micro g/g) and other anti-psoriatic ointments using hairless mice. Tacalcitol ointment (0, 2 and 20 micro g/g) significantly inhibited 12-O-tetradecanoylphorbol 13-acetate (TPA)-induced cutaneous inflammation, histopathologically. The effect of tacalcitol ointment (20 micro g/g) on cutaneous inflammation was much stronger than that of tacalcitol ointment (0, 2 micro g/g), and as effective as calcipotriol ointment (50 micro g/g) or betamethasone valerate ointment (1.2 mg/g). Tacalcitol ointment (20 micro g/g) also significantly inhibited TPA-induced myeloperoxidase (MPO) activity, as effectively as calcipotriol ointment (50 micro g/g) or betamethasone valerate ointment (1.2 mg/g). The effect of tacalcitol ointment on epidermal proliferation [ornithine decarboxylase (ODC) activity] and differentiation [transglutaminase (TGase) activity] was dose-dependent from 0 micro g/g to 20 micro g/g. The effect of tacalcitol ointments on epidermal proliferation was significant at the doses of 2 micro g/g and 20 micro g/g, and that on epidermal differentiation was significant at the doses of 0.2 micro g/g or more. The effect of tacalcitol ointment (20 micro g/g) on epidermal differentiation was significantly stronger than tacalcitol ointment (2 micro g/g). In this study, tacalcitol ointment (20 micro g/g) was found to have a marked effect on cutaneous inflammation and improved effect on epidermal differentiation, although tacalcitol ointment (2 micro g/g) also had significant effects on epidermal proliferation and differentiation. These findings support the clinical effectiveness of tacalcitol ointment (20 micro g/g) against psoriasis.

Change in location of cytokine-induced neutrophil chemoattractants (CINCs) in pulmonary silicosis.

Rat cytokine-induced neutrophil chemoattractants (CINCs), which belong to the interleukin-8 family, are known to be induced by treatment with lipopolysaccharide (LPS). Recently, CINCs were grouped into four subtypes-CINC-1, CINC-2alpha, CINC-2beta, and CINC-3-and CINC-1 was considered to be a major isoform among the four CINCs in LPS-induced acute lung inflammation in rats. The purpose of this study was to investigate the change in location of CINCs with chronic inflammation induced by experimental pulmonary silicosis. Administration of silica particles induced lung granulomas. Immunohistochemical staining for CINCs showed that the number of cells positive for CINC-2alpha, CINC-2beta, and CINC-3 was increased, peaking at 1 day after treatment with silica particles, whereas CINC-1 was almost undetectable. We suggest that CINC-2alpha, CINC-2beta, and CINC-3 are the most important chemoattractants in the formation of granulomas in chronic inflammation.

Expression of hepatocyte growth factor mRNA in rat liver cirrhosis induced by N-nitrosodimethylamine as evidenced by in situ RT-PCR.

Hepatocyte growth factor (HGF) is a potent inducer of hepatocyte proliferation and is expressed during liver failure. In this study we used the in situ reverse transcriptase-polymerase chain reaction (RT-PCR) method to detect HGF mRNA expression in normal rat livers and cirrhotic rat livers induced by treatment with N-nitrosodimethylamine (DMN). In normal control livers, in situ RT-PCR detected HGF mRNA expression in Ito cells and Kupffer cells, both of which showed rounded morphologies. However, in the cirrhotic livers induced by DMN, HGF mRNA-positive cells were spindle-shaped and surrounded the hepatocytes located around the sinusoids. These cells appeared to be sinusoidal endothelial cells as well as Ito and Kupffer cells. Because it has been suggested that HGF expression is related to transforming growth factor-beta (TGF-beta) levels that may play an essential role in disease progression in cirrhotic livers, TGF-beta mRNA expression in normal and cirrhotic livers was also compared using in situ RT-PCR. Our results confirmed that expression of TGF-beta mRNA co-localized with HGF mRNA expression in the cirrhotic liver.