The relationship between depression and periodontal diseases.

OBJECTIVE: A cross-sectional study was conducted to investigate whether depression is associated with periodontal diseases in a representative sample of South Korean adults Methods: We used data from the sixth Korea National Health and Nutrition Examination Survey (KNHANES VI), conducted in 2014. We included in this study 4328 participants aged over 20 years (1768 males and 2560 females). Depression was assessed with the Patient Health Questionnaire (PHQ-9) and history of physician-diagnosed depression. Periodontal diseases were assessed a gingival bleeding, calculus and periodontal pockets. The data were analyzed using the chi-square test and multiple logistic regression. RESULTS: People with any periodontal diseases tended to be old, male, married, low income, poor education, blue-collar occupation, diabetes mellitus, hypertension, overweight, smoking, not using dental floss or interdental brush in univariate analysis. Neither self-reported nor diagnosed depression was associated with the presence of any or severe periodontal disease in the total sample. In participants aged 20-29 years only, the presence of any periodontal disease was associated with self-reported depression (OR, 2.031; 95% CI, 1.011-4.078). In the same age group, the presence of severe periodontal disease was associated with both self-reported depression (OR, 6.532; 95% CI, 2.190-19.483) and diagnosed depression (OR, 7.729; 95% CI, 1.966-30.389). CONCLUSION: Self-reported depression was significantly associated with the presence of any or severe periodontal disease, and diagnosed depression was significantly associated with severe periodontal diseases only in participants aged 20-29 years.

Optical clearing agent reduces scattering of light by the stratum corneum and modulates the physical properties of coenocytes via hydration.

BACKGROUND: The interaction between light and the skin determine how the skin looks to the human eye. Light can be absorbed, scattered, and reflected by different components of the skin in a variety of different ways. Here, we focus on the scattering properties of the outmost layer, the stratum corneum (SC). However, we currently have limited methods with which to distinguish the scattering of light by SC from the changes due to other components of the skin. MATERIALS AND METHODS: Dark-field images of tape-striped corneocytes were used in vitro to study the differences in light scattered by the SC and other skin components. Several optical clearing agents (OCAs) were tested for their ability to reduce light scattering. Physical properties of the SC (water content, keratin configuration, and volume) after OCA treatment were investigated using FT-IR, confocal Raman microscopy, and 3D laser microscopy. RESULTS: Urea derivatives, several reducing sugars, and sugar alcohols, which were used as OCA in optics and also used as humectants in cosmetic area, could reduce scattering. However, unlike dehydration in optics, penetration of water into the keratin was increased at low OCA concentrations. In such conditions, the volume of corneocytes was increased but their stiffness was reduced. CONCLUSION: By analyzing the tape-striped SC, we were able to measure the changes in the optical and physical properties of corneocytes in response to OCAs. Hydration of the SC layer by OCAs reduces light scattering from the corneocytes and would be helpful in moisturizing the skin and helping the skin look healthy.

SET kinetics of electrochemical metallization cells: influence of counter-electrodes in SiO2/Ag based systems.

The counter-electrode material in resistively switching electrochemical metallization cells (ECMs) is a crucial factor influencing the nucleation of conductive filaments, the equilibrium electrode potentials, and kinetics in the devices, and hence the overall switching characteristics. Here, we demonstrate the influence of the counter-electrode (CE) material on the SET events and the importance of appropriate choice and combination of materials. The counter-electrode material influences the counter-electrode processes at the CE/insulator interface and consequently determines the metal ion concentration in the cells. We measured the switching kinetics for SiO2/Ag based ECM cells using different counter-electrode materials with different electrocatalytic activities towards water reduction, namely platinum, ruthenium, and iridium oxide, as well as titanium nitride and tantalum. The experimental results are fitted using a physical simulation model and are analysed for the limiting factors for fast SET kinetics.

Capsaicin attenuates spermatogenic cell death induced by scrotal hyperthermia through its antioxidative and anti-apoptotic activities.

This study was performed to examine whether capsaicin, the main pungent ingredient of red peppers, exerts protective effects against testicular injuries induced by transient scrotal hyperthermia. Capsaicin (0.33 mg kg-1 ) was administered subcutaneously to mice one hour before heat stress (HS) in a 43°C water bath for 20 min. After 7 days, mice exposed to HS showed low testicular weight, severe vacuolisation of seminiferous tubules followed by loss of spermatogenic cells, and appearance of multinucleated giant cells and remarkable TUNEL-positive apoptotic cells, as well as weak immunoreactivity of phospholipid hydroperoxide glutathione peroxidase (PHGPx) in spermatogenic cells. Levels of lipid peroxidation and heat shock 70-kDa protein 1 (Hsp72) and BCL2-associated X protein (Bax) mRNA were greatly increased, but PHGPx, manganese superoxide dismutase (MnSOD), and B-cell lymphoma-extra large (Bcl-xL) mRNAs were significantly diminished in the testes by HS. However, capsaicin pre-treatment significantly suppressed the spermatogenic cell death, oxidative stress (levels of MDA, PHGPx immunoreactivity, and Hsp72, PHGPx, and MnSOD mRNA) and apoptosis (levels of TUNEL-positive cells, and Bcl-xL and Bax mRNA) in testes by HS. These suggest that capsaicin has a protective effect against spermatogenic cell death induced by scrotal hyperthermia through its antioxidative and anti-apoptotic activities.

AIMP1 downregulation restores chondrogenic characteristics of dedifferentiated/degenerated chondrocytes by enhancing TGF-ß signal.

Dedifferentiation and degeneration of chondrocytes critically influences the efficiency of cartilage repair. One of the causes is the defect of transforming growth factor (TGF)-ß signaling that promotes chondrogenic differentiation and degeneration. In the present study, we found that aminoacyl-tRNA synthetase-interacting multifunctional protein 1 (AIMP1) negatively regulates TGF-ß signaling via interactions with Smad2 and Smad3 in immunoprecipitation assay and luciferase assay. In addition, we observed that the AIMP1 expression level was significantly increased in osteoarthritis (OA) patient-derived degenerated chondrocytes compared with healthy control. So, we hypothesized that downregulation of AIMP1 using small-interfering RNA (siRNA) technology in dedifferentiated (collected at passage #6) and degenerated (obtained from OA-affected areas) chondrocytes could lead to recover TGF-ß signaling in both chondrocytes. Indeed, AIMP1 downregulation restored TGF-ß signaling by promoting phosphorylation of Smad2 and Smad3, which shows redifferentiated characteristics in both dedifferentiated and degenerated chondrocytes. Additionally, implantation analyses using in vivo mouse model clearly showed that AIMP1 downregulation resulted in the increased chondrogenic potential as well as the enhanced cartilage tissue formation in both dedifferentiated and degenerated chondrocytes. Histological analyses clarified that AIMP1 downregulation increased expression levels of collagen type II (Col II) and aggrecan, but not Col I expression. Taken together, these data indicate that AIMP1 downregulation using siRNA is a novel tool to restore TGF-ß signaling and thereby increases the chondrogenic potential of dedifferentiated/degenerated chondrocytes, which could be further developed as a therapeutic siRNA to treat OA.

Intracellular annexin A2 regulates NF-κB signaling by binding to the p50 subunit: implications for gemcitabine resistance in pancreatic cancer.

Annexin A2 (ANXA2) expression is highly upregulated in many types of cancer. Although cell surface localization of ANXA2 has been reported to have a critical role in the progression and metastasis of a variety of tumors, including pancreatic cancer, the biological role of intracellular ANXA2 is not fully understood. Herein the role of intracellular ANXA2 was investigated in a pancreatic cancer cell line. We first determined whether ANXA2 is involved in NF-κB signaling pathways. ANXA2 bound to the p50 subunit of NF-κB in a calcium-independent manner, and the ANXA2-p50 complex translocated into the nucleus. Furthermore, ANXA2 increased the transcriptional activity of NF-κB in both the resting and activated states and upregulated the transcription of several target genes downstream of NF-κB, including that encoding interleukin (IL)-6, which contributes to anti-apoptotic signaling. In Mia-Paca2 cells, we determined the effects of wild-type ANXA2 and an ANXA2 mutant, Y23A, which suppresses the cell surface localization, on upregulation of NF-κB transcriptional activity and secretion of IL-6. Both wild-type and Y23A ANXA2 induced anti-apoptotic effects in response to treatment with tumor necrosis factor-α or gemcitabine. Based on these results, we suggest that ANXA2 mediates resistance to gemcitabine by directly increasing the activity of NF-κB. Collectively, these data may provide additional information about the biological role of ANXA2 in pancreatic cancer and suggest that ANXA2 is a potential biomarker for the drug resistance phenotype and a candidate therapeutic target for the treatment of pancreatic cancer.

Cell cycle-dependent Cdc25C phosphatase determines cell survival by regulating apoptosis signal-regulating kinase 1.

Cdc25C (cell division cycle 25C) phosphatase triggers entry into mitosis in the cell cycle by dephosphorylating cyclin B-Cdk1. Cdc25C exhibits basal phosphatase activity during interphase and then becomes activated at the G2/M transition after hyperphosphorylation on multiple sites and dissociation from 14-3-3. Although the role of Cdc25C in mitosis has been extensively studied, its function in interphase remains elusive. Here, we show that during interphase Cdc25C suppresses apoptosis signal-regulating kinase 1 (ASK1), a member of mitogen-activated protein (MAP) kinase kinase kinase family that mediates apoptosis. Cdc25C phosphatase dephosphorylates phospho-Thr-838 in the activation loop of ASK1 in vitro and in interphase cells. In addition, knockdown of Cdc25C increases the activity of ASK1 and ASK1 downstream targets in interphase cells, and overexpression of Cdc25C inhibits ASK1-mediated apoptosis, suggesting that Cdc25C binds to and negatively regulates ASK1. Furthermore, we showed that ASK1 kinase activity correlated with Cdc25C activation during mitotic arrest and enhanced ASK1 activity in the presence of activated Cdc25C resulted from the weak association between ASK1 and Cdc25C. In cells synchronized in mitosis following nocodazole treatment, phosphorylation of Thr-838 in the activation loop of ASK1 increased. Compared with hypophosphorylated Cdc25C, which exhibited basal phosphatase activity in interphase, hyperphosphorylated Cdc25C exhibited enhanced phosphatase activity during mitotic arrest, but had significantly reduced affinity to ASK1, suggesting that enhanced ASK1 activity in mitosis was due to reduced binding of hyperphosphorylated Cdc25C to ASK1. These findings suggest that Cdc25C negatively regulates proapoptotic ASK1 in a cell cycle-dependent manner and may play a role in G2/M checkpoint-mediated apoptosis.

Spin90 deficiency increases CXCL13-mediated B cell migration.

SPIN90 regulates actin dynamics, which is important for cell migration control. CXCL13-mediated B cell migration is essential for B cell immune responses. In this study, we investigated the role of SPIN90 in CXCL13-mediated B cell migration using Spin90 gene-deficient mice. Our chemokinesis analysis and transwell cell migration assay showed that SPIN90 is involved in CXCL13-mediated B cell migration. Moreover, the level of CXCR5, which is CXCL13 receptor, was increased in SPIN90-deficient B cells compared with wild-type B cells. Overall, our data suggest that SPIN90 plays an important role in B cell immune responses through the regulation of CXCL13-mediated B cell migration.

Reactive oxygen species-responsive miR-210 regulates proliferation and migration of adipose-derived stem cells via PTPN2.

Hypoxia enhances the proliferation and migration of adipose-derived stem cells (ASCs) via the generation of reactive oxygen species (ROS). Therefore, this study primarily investigated whether or not ROS generation could regulate microRNA-210 (miR-210) expression, and increase proliferation/migration of ASCs. In addition, we tried to identify the signaling pathways involved in miR-210 upregulation and the direct target genes of miR-210 that mediate these functions. Various sources of ROS generation such as hypoxia, antimycin, rotenone, and platelet-derived growth factor (PDGF)-BB upregulated miR-210 expression, and increased the proliferation/migration of ASCs. There is a positive feed-forward loop between ROS generation and miR-210, and miR-210 itself increases ROS generation by downregulation of iron-sulfur cluster scaffold homolog 2 (ISCU2). Although hypoxia-inducible factor-1α was not involved in miR-210 expression, pharmacological or small interfering RNA (siRNA)-driven inhibition of Akt and ERK1/2 molecules reduced miR-210 expression. Transfection of siRNAs of NF-κB and Elk1 also reduced miR-210 expression, indicating that these signaling pathways mediate miR-210 upregulation. Protein tyrosine phosphatase, non-receptor type 2 (PTPN2) was selected for miR-210 target gene, and it was downregulated by ROS generators or miR-210 mimic treatment. PTPN2 was first proven to be a direct miR-210 target in luciferase activity assay, and pharmacological inhibition or overexpression of PTPN2 regulated the proliferation and migration of ASC. In conclusion, ROS generation from diverse sources induces miR-210 expression in ASCs via PDGFR-ß, Akt and ERK pathways. Transcription of miR-210 expression is regulated by NF-κB and Elk1, and miR-210 increases the proliferation and migration of ASCs via ISCU2 and PTPN2 downregulation.

Secondhand smoke exposure and osteoporosis in never-smoking postmenopausal women: the Fourth Korea National Health and Nutrition Examination Survey.

SUMMARY: The association between secondhand smoke (SHS) exposure and lumbar and femoral neck osteoporosis was assessed in postmenopausal never-smoking Korean women. The presence of family members who actively smoked was associated with femoral neck osteoporosis. The number of cigarettes consumed by cohabitant smokers was positively associated with lumbar and femoral neck osteoporosis. INTRODUCTION: This study aimed to assess the association between SHS and postmenopausal osteoporosis. METHODS: Of 2,067 postmenopausal women (age, ≥55 years) participating in the Fourth Korea National Health and Nutrition Examination Survey, 925 never-smokers identified through interviews and urinary cotinine level verification were enrolled. Cross-sectional relationships between self-reported SHS exposure and osteoporosis of the lumbar vertebrae and femoral neck (defined using the World Health Organization T-score criteria) were investigated by bone densitometry. RESULTS: Participants having actively smoking family members showed increased adjusted odds ratio (aOR) for femoral neck osteoporosis compared with participants not exposed to SHS (aOR, 3.68; 95 % confidence interval [CI], 1.23-10.92). Participants whose cohabitant smokers consumed any number of cigarettes per day showed increased occurrences for lumbar and femoral neck osteoporosis compared with the nonexposed group. Participants whose cohabitant smokers consumed ≥20 cigarettes/day showed increased aORs for lumbar (aOR, 5.40; 95 % CI, 1.04-28.04) and femoral neck (aOR, 4.35; 95 % CI, 1.07-17.68) osteoporosis compared with participants not exposed to SHS. CONCLUSIONS: In postmenopausal never-smoking Korean women, exposure to SHS was positively associated with osteoporosis. This finding further emphasizes a need to identify vulnerable groups exposed to SHS to increase bone health.

Relationship between chewing ability and depressive symptoms.

OBJECTIVE: Depression, as one of the most common mental health problems, has many related factors. Recent studies have suggested chewing difficulties as a risk factor for depression in the elderly. This study seeks to investigate whether chewing ability is associated with depressive symptoms in a Korean population. METHODS: This study used data from the Fifth Korean National Health and Nutrition Examination Survey (KNHANES V) conducted in 2010. Self-reported questionnaires assessed depressive symptoms and chewing ability for the purposes of this study. A total of 6,255 subjects aged over 19 years were included for this study (2,704 males and 3,551 females). RESULTS: Comparing depressive symptoms with chewing ability (i.e., very poor, poor, moderate, good, and very good), the adjusted odds ratios (ORs) and confidence intervals (CI) were 1.05 (95% CI: 0.84-1.32) for good vs. very good (as a reference), 1.31 (95% CI: 1.00-1.73) for moderate vs. very good, 1.41 (95% CI: 1.12-1.78) for poor vs. very good, and 1.76 (95% CI: 1.16-2.76) for very poor vs. very good. CONCLUSION: This study suggests that subjects with reduced chewing ability were more susceptible to having depressive symptoms.

A critical step for JNK activation: isomerization by the prolyl isomerase Pin1.

c-Jun N-terminal kinase (JNK) is activated by dual phosphorylation of both threonine and tyrosine residues in the phosphorylation loop of the protein in response to several stress factors. However, the precise molecular mechanisms for activation after phosphorylation remain elusive. Here we show that Pin1, a peptidyl-prolyl isomerase, has a key role in the JNK1 activation process by modulating a phospho-Thr-Pro motif in the phosphorylation loop. Pin1 overexpression in human breast cancer cell lines correlates with increased JNK activity. In addition, small interfering RNA (siRNA) analyses showed that knockdown of Pin1 in a human breast cancer cell line decreased JNK1 activity. Pin1 associates with JNK1, and then catalyzes prolyl isomerization of the phospho-Thr-Pro motif in JNK1 from trans- to cis-conformation. Furthermore, Pin1 enhances the association of JNK1 with its substrates. As a result, Pin1(-/-) cells are defective in JNK activation and resistant to oxidative stress. These results provide novel insights that, following stress-induced phosphorylation of Thr in the Thr-Pro motif of JNK1, JNK1 associates with Pin1 and undergoes conformational changes to promote the binding of JNK1 to its substrates, resulting in cellular responses from extracellular signals.

A prospective study of work stressors and the common cold.

BACKGROUND: Psychological stress is a risk factor for infectious diseases. Although psychological stress at work is considered an important problem for many workers, there is little evidence for the effect of work-related stress on infectious diseases. AIMS: To investigate whether work-related stress affected the occurrence of the common cold in South Korean workers in small- to medium-sized manufacturing companies. METHODS: We conducted a prospective study, involving 1241 workers. At the outset, we collected information regarding sociodemographic and work characteristics. At follow-up after 6 months, we asked subjects whether they had experienced common cold symptoms during the preceding 4 months. RESULTS: Male subjects experiencing stress at the outset were more likely to report having experienced the common cold at follow-up (odds ratios: high job demand group 1.74; 95% CI: 1.28-2.36; insufficient job control 1.42; 95% CI: 1.05-1.93; inadequate social support 1.40; 95% CI: 1.03-1.91). For females, no significant association between work stress and occurrence of the common cold was detected. CONCLUSIONS: Males experiencing work stress in job demand, job control and social support reported an increased occurrence of the common cold at follow-up but this association was not seen in females.

Total arsenic, mercury, lead, and cadmium contents in edible dried seaweed in Korea.

Total arsenic, mercury, lead, and cadmium contents were determined in 426 samples of seaweed sold in Korea in 2007-08. The average concentrations, expressed in mg kg(-1), dry weight, were: total arsenic 17.4 (less than the limit of detection [LOD] to 88.8), Hg 0.01 (from 0.001 to 0.050), lead 0.7 (less than the LOD to 2.7), and cadmium 0.50 (less than the LOD to 2.9). There were differences in mercury, cadmium, and arsenic content in seaweed between different kinds of products and between coastal areas. The intakes of total mercury, lead, and cadmium for Korean people from seaweed were estimated to be 0.11, 0.65, and 0.45 µg kg(-1) body weight week(-1), respectively. With respect to food safety, consumption of 8.5 g day(-1) of the samples analysed could represent up to 0.2-6.7% of the respective provisional tolerable weekly intakes established by the World Health Organization (WHO). Therefore, even if Korean people have a high consumption of seaweed, this study confirms the low probability of health risks from these metals via seaweed consumption.

Far upstream element-binding protein-1, a novel caspase substrate, acts as a cross-talker between apoptosis and the c-myc oncogene.

Far upstream element-binding protein-1 (FBP-1) binds to an upstream element of the c-myc promoter and regulates the c-myc mRNA level. Earlier, FBP-1 was identified as a candidate substrate of caspase-7. Here, we report that FBP-1 is cleaved by executor caspases, both in vitro and during apoptosis. Cleavage occurs at the caspase consensus site (DQPD(74)) located within the classical bipartite nuclear localization signal sequence. In cells subjected to apoptotic stimuli, the caspase-mediated cleavage of FBP-1 leads to its decreased presence in the nucleus, concomitant with the marked downregulation of c-Myc and its various target proteins. By contrast, cells transfected with a non-cleavable mutant of FBP-1 (D74A) maintain higher levels of c-Myc and are protected from apoptosis. On the basis of these results, we suggest that the oncogenic potential of c-Myc is 'switched off' after apoptosis induction as a consequence of the caspase-mediated cleavage of FBP-1.

The effect on the recovery profile of a change from enflurane to desflurane during the latter part of anaesthesia.

This study compared emergence and recovery characteristics after either enflurane anaesthesia or crossover from enflurane to desflurane anaesthesia. At an estimated 1 h prior to the end of operation, enflurane was either reduced (group E, n = 23) or replaced with desflurane (group X, n = 23). At the end of the operation, emergence and recovery characteristics of the two groups were compared. The crossover technique accelerated recovery compared with enflurane anaesthesia. The time taken for the eyes to open in response to painful pinching or a verbal command, and to regain awareness of age and name, were significantly shorter after crossover anaesthesia than after enflurane anaesthesia. The digit symbol substitution test and serial seven test scores were significantly better in patients subjected to crossover anaesthesia than in those subjected to enflurane anaesthesia. We conclude that, during surgery, the substitution of enflurane with desflurane in the latter part of anaesthesia can improve recovery.

Effects of hypoxia-inducible factor-1alpha expression and C4d deposition in implantation biopsies on renal allograft.

Upregulation of hypoxia-inducible factor-1alpha (HIF-1alpha) in response to ischemic states has been suggested to have a role in the development of chronic allograft nephropathy. Deposition of C4d in the peritubular capillaries of renal allografts has been reported to be a sensitive marker of acute humoral rejection. The purpose of this study was to determine the effects of HIF-1alpha expression and C4d deposition in implantation biopsies of renal allografts. Implantation biopsies and 22 rejection proved biopsies were performed in 54 renal transplant recipients between December 1996 and July 1999. The mean follow-up was 82.8 months. Immunohistochemical studies were performed using a mouse monoclonal antibody for HIF-1alpha expression and a rabbit polyclonal antibody for C4d detection. HIF-1alpha was demonstrated in 19 of 54 implantation biopsies (35%), and C4d deposition in one (1.9%). The HIF-1alpha-positive group included a higher percentage of deceased donor organs (66.4% vs 17.1%; P = .002) and longer mean cold ischemia times (261.3 +/- 231 vs 103 +/- 40 min; P = .008) compared with the HIF-1alpha-negative group. The relative risks (95% confidence intervals) of expression of HIF-1alpha for allograft rejection, chronic allograft nephropathy, and graft loss were 1.53 (0.82-2.87), 0.61 (0.06-5.50), and 2.45 (0.62-9.85). The C4d-positive patient developed acute accelerated rejection on postoperative day 4. In the present study, the expression of HIF-1alpha showed a significant correlation with the use of a deceased donor kidney and with cold ischemia time. However, there were no significant effects on the prognosis for a graft after implantation of a kidney with HIF-1alpha expression.

G1 to S phase transition protein 1 induces apoptosis signal-regulating kinase 1 activation by dissociating 14-3-3 from ASK1.

Apoptosis signal-regulating kinase 1 (ASK1), a member of the mitogen-activated protein kinase kinase kinase family, plays a critical role in mediating apoptosis signals initiated by a variety of death stimuli such as hydrogen peroxide and tumor necrosis factor-alpha. Owing to its critical role in inducing apoptosis, the activity of ASK1 is tightly regulated by various mechanisms such as post-translational modifications and protein-protein interactions. Here we describe the identification of G(1) to S phase transition protein 1 (GSPT1), which is associated with protein translation, as a regulator of ASK1. GSPT1 interacts with ASK1 and enhances ASK1-induced apoptotic activity through the activation of caspase-3. In vitro kinase assay data show that GSPT1 enhances ASK1 autophosphorylation and its kinase activity. Cell cycle-dependent GSPT1 induction and small interfering RNA analyses show that ASK1 autophosphorylation is dependent on the expression level of endogenous GSPT1 in cells. GSPT1 inhibits the binding of ASK1 to the 14-3-3 protein, an ASK1 inhibitor, while GSPT1 has no effect on the interaction between ASK1 and TRAF2, a C-terminal-binding activator of ASK1. Thus, our results reveal a novel role of GSPT1 in the regulation of ASK1-mediated apoptosis.