Interactions Between Depression, Alcohol Intake, and Smoking on the Risk of Acute Coronary Syndrome.

OBJECTIVE: Our study hypothesizes that the interaction between depression, alcohol intake, and smoking status can significantly influence the risk of acute coronary syndrome (ACS). We aim to investigate the magnitude of the association between depression and ACS risk and explore how alcohol intake and smoking status affect this association. METHODS: We used data from the Korean Genome and Epidemiology Study. The primary exposure of interest was the presence of depression, as measured using the Beck Depression Inventory score at baseline. The primary outcome was the occurrence of ACS observed in the biennial follow-up surveys. We used Cox proportional regression analysis to estimate the effect of depression on ACS incidence. We conducted interaction and joint effect analyses to explore the interactions between depression and health-related habits including alcohol intake and smoking with regard to ACS incidence. RESULTS: During 16 years of follow-up among 3,254 individuals, we documented 88 cases of new-onset ACS (2.2 cases per 1,000 personyears). We found no association between depression and ACS risk; furthermore, the effect of depression on ACS risk by alcohol intake and smoking status did not differ significantly. In the analysis to observe the joint effect of smoking and depression, the multivariate hazard ratios of ACS were 1.26 (95% confidence interval [CI], 0.67-2.36) for non-smoking and depression, 1.52 (95% CI, 0.83-2.82) for smoking and non-depression, and 2.79 (95% CI, 1.21-6.41) for smoking and depression compared with non-smoking and non-depression. CONCLUSION: Our study reveals the combined effect of depression and smoking on ACS risk, highlighting the potential benefits of concurrent interventions for both depression and smoking for cardiovascular health.

Two-Dimensional calcium silicate nanosheets for trapping atmospheric water molecules in humidity-immune gas sensors.

In humid conditions, water vapor can easily neutralize the surface active sites of metal oxide sensors, leading to a lowering in the sensitivity of the gas sensor and a resultant inaccurate signal in practical applications. Herein, we present a new hybrid sensor by introducing a two-dimensional calcium silicate (CS) nanosheet as a water-trapping layer in SnO2 nanowires. Unlike the heavily wrinkled and aggregated morphology of conventional CS nanosheets, our nanosheet in the hybrid material is ultrathin and flat. Moreover, it was grown in the empty spaces between the spider-web-like networks of SnO2 nanowires without covering the nanowire surface. These two morphological features improve moisture trapping with minimal reduction in the active sensing area. Consequently, stable and sensitive gas detection under humid conditions was achieved in this hybrid sensor. The superior humidity-independent sensing is ascribed to the preferential adsorption of water molecules on hydroscopic CS nanosheets through the hydrogen bond. Based on density functional theory calculations, we determined that the improved gas response is driven by the additional formation of oxygen vacancy in SnO2 due to the diffusion of aliovalent Ca ions from the CS nanosheet.

Changes in liver stiffness measurement during antiviral therapy in patients with chronic hepatitis B.

BACKGROUND/AIMS: The usefulness of liver stiffness measurement (LSM) for monitoring changes in fibrosis and inflammation in chronic hepatitis B (CHB) patients receiving antiviral therapy is unknown. The aim of this study was to evaluate changes in liver stiffness and correlate them with changes in serological markers and histology in CHB patients receiving entecavir. METHODOLOGY: The study included 38 patients with CHB and 24 cirrhotic patients with CHB. All patients received entecavir for over 12 months. Liver stiffness was measured by transient elastography at baseline and after 48wks of therapy. Liver biopsy was performed on 15 patients at baseline and during therapy. RESULTS: Among 62 treated patients, 51 (82.2%) achieved HBV DNA <50 copies/mL and 43 (69%) achieved alanine aminotransferase (ALT) normalization at 48wks. The median liver stiffness value at baseline was 15.1 kPa (5.6-75.0) and decreased significantly to 8.8kPa (3.0-33.8) after 48wks. A decrease in liver stiffness value during therapy correlated significantly with decreases in albumin (r=-0.357, p=0.004), bilirubin (r=0.342, p=0.007), ALT (r=0.319, p=0.012), and aspartate aminotransferase (AST) (r=0.353, p=0.005) concentrations. Decreases in liver stiffness values correlated significantly with improvement in necroinflammatory scores. CONCLUSION: We suggest that LSM can reflect the changes of necroinflammation in patients with chronic hepatitis B receiving antiviral therapy.

Role of corticotrophin-releasing factor in the stress-induced dilation of esophageal intercellular spaces.

Corticotrophin-releasing factor (CRF) plays a major role in coordinating stress responses. We aimed to test whether blocking endogenous CRF activity can prevent the stress-induced dilation of intercellular spaces in esophageal mucosa. Eighteen adult male rats were divided into 3 groups: 1) a non-stressed group (the non-stressed group), 2) a saline-pretreated stressed group (the stressed group), 3) and an astressin-pretreated stressed group (the astressin group). Immediately after completing the experiments according to the protocol, distal esophageal segments were obtained. Intercellular space diameters of esophageal mucosa were measured by transmission electron microscopy. Blood was sampled for the measurement of plasma cortisol levels. Mucosal intercellular spaces were significantly greater in the stressed group than in the non-stressed group. Mucosal intercellular spaces of the astressin group were significantly smaller than those of the stressed group. Plasma cortisol levels in the stressed group were significantly higher than in the non-stressed group. Pretreatment with astressin tended to decrease plasma cortisol levels. Acute stress in rats enlarges esophageal intercellular spaces, and this stress-induced alteration appears to be mediated by CRF. Our results suggest that CRF may play a role in the pathophysiology of reflux-induced symptoms or mucosal damage.

Stress-induced alterations in mast cell numbers and proteinase-activated receptor-2 expression of the colon: role of corticotrophin-releasing factor.

This study was performed in order to assess whether acute stress can increase mast cell and enterochromaffin (EC) cell numbers, and proteinase-activated receptor-2 (PAR2) expression in the rat colon. In addition, we aimed to investigate the involvement of corticotrophin-releasing factor in these stress-related alterations. Eighteen adult rats were divided into 3 experimental groups: 1) a saline-pretreated non-stressed group, 2) a saline-pretreated stressed group, and 3) an astressin-pretreated stressed group. The numbers of mast cells, EC cells, and PAR2-positive cells were counted in 6 high power fields. In proximal colonic segments, mast cell numbers of stressed rats tended to be higher than those of non-stressed rats, and their PAR2-positive cell numbers were significantly higher than those of non-stressed rats. In distal colonic segments, mast cell numbers and PAR2-positive cell numbers of stressed rats were significantly higher than those of non-stressed rats. Mast cell and PAR2-positive cell numbers of astressin-pretreated stressed rats were significantly lower than those of saline-pretreated stressed rats. EC cell numbers did not differ among the three experimental groups. Acute stress in rats increases mast cell numbers and mucosal PAR2 expression in the colon. These stress-related alterations seem to be mediated by release of corticotrophin-releasing factor.

[Add on lamivudine to adefovir monotherapy for the treatment of lamivudine-resistant chronic hepatitis B patients].

BACKGROUND/AIMS: Add on adefovir (ADV) to ongoing lamivudine (LAM) has been recommended as a standard therapy for the treatment of LAM resistance. In the past, switch to ADV monotherapy was suggested as an option for the treatment of LAM resistance, leading to frequent development of ADV resistance. However, ADV monotherapy has been still used in LAM-resistant patients because of low cost in Korea. The aims of this study were to evaluate the virologic response and virologic breakthrough during adding on LAM in LAM-resistant patients receiving ADV monotherapy. METHODS: The study population comprised 99 patients with LAM-resistance. We divided them into 3 groups (Group 1: switch to ADV monotherapy, N=58, Group 2: add on ADV to ongoing LAM, N=25, Group 3: add on LAM to ADV monotherapy, N=16). HBV DNA levels were assessed at baseline and every 3 months during therapy. Serum HBV DNA levels were measured by bDNA assay or the COBAS TaqMan(TM) HBV test. RESULTS: The median treatment duration for group 1, group 2, and group 3 was 42.0, 20.6, and 31.8 (18.7 mon. of ADV13.1 mon. of LAM) months, respectively. Cumulative rate of virologic breakthrough in group 1 was 5.2%, 19.0%, and 25.9% at 12, 24, and 36 months of treatment, respectively. Virologic breakthrough was not detected in group 2 and group 3 (p=0.016, group 1 vs. group 2 or 3). In group 3, median serum HBV DNA levels were 4.22 log10 copies/mL prior to LAM administration. Median serum HBV DNA changes from baseline (log10 copies/mL) were -0.91, -1.93, -1.87 and -1.74 at week 12, 24, 36 and 48, respectively. CONCLUSIONS: Later add on LAM to ADV monotherapy prevented the development of ADV resistance in patients with LAM resistance effectively, comparable to ADV add on to continuing LAM therapy.

[Clinical efficacy of entecavir therapy and factors associated with treatment response in naive chronic hepatitis B patients].

BACKGROUND/AIMS: Entecavir is a potent and selective guanosine analogue that has demonstrated a significant antiviral efficacy against hepatitis B virus (HBV). The aim of this study was to characterize the response to entecavir and to examine the factors affecting that response. METHODS: We administered 0.5 mg of entecavir once daily for more than 12 months to 114 naive chronic hepatitis B (CHB) patients. We measured the levels of liver enzymes, serological markers, and serum HBV DNA at 3-month interval. RESULTS: Normalization of serum alanine aminotransferase levels was observed in 68.5% (76/114), 74.6% (85/114), and 81.6% (62/76) of patients after 6, 12, and 24 months of therapy, respectively. HBV DNA levels of <50 copies/mL (as evaluated by polymerase chain reaction) were observed in 43.9% (50/114), 71.1% (81/114), and 85.5% (65/76) of patients after 6, 12, and 24 months, respectively. Viral breakthrough was not observed. The rates of HBeAg loss and seroconversion were 43.5% (27/62) and 14.5% (9/62), respectively, after 12 months of therapy, and 56.4% (22/39) and 15.4% (6/39) after 24 months. The independent factor associated with PCR negativity was early virologic response (EVR; HBV DNA <2,000 copies/mL after 3 months of therapy, P<0.001). The independent factors predicting HBeAg loss were found to be serum albumin levels (P=0.041) and EVR (P=0.005). CONCLUSIONS: Entecavir induced excellent biochemical and virologic responses in naive CHB patients. EVR was an independent factor for predicting HBV PCR negativity and HBeAg loss.

[Ten cases of Fitz-Hugh-Curtis syndrome].

Fitz-Hugh-Curtis syndrome, a kind of perihepatitis, occurs approximately in 3 to 10 percent of patients with pelvic inflammatory disease. It is not easy to detect in clinical settings due to requirement of invasive methods for diagnosis, for example, like a laparoscopic examination. Now, it has become possible to recognize it easily with the aid of non-invasive methods including an abdominal dynamic CT scan and laboratory tests. Moreover, it can be improved after the oral administration of antibiotics. Therefore, noninvasive diagnosis is desirable. Herein, clinical characteristics of ten cases of Fitz-Hugh-Curtis syndrome are reported, with a review of the literature.

Assessment of estimated daily intakes of benzoates for average and high consumers in Korea.

A study was performed to evaluate the estimated daily intakes (EDI) of benzoates for the average and high (90th percentile) consumers by age and sex categories in Korea. The estimation of daily intakes of benzoates was based on individual dietary intake data from the National Health and Nutrition Survey in 1998 and on the determination of benzoates in eight food categories. The EDI of benzoates for average consumers of different age groups ranged from 0.009 to 0.025 mg kg(-1) bw day(-1). For high consumers, the range of EDI of benzoates was 0.195-1.878 mg kg(-1) bw day(-1). The intakes represented 0.18-0.50% of the acceptable daily intake (ADI) of benzoates for average consumers and 3.9-37.6% of the ADI for high consumers. Foods that contributed most to the daily intakes of benzoates were mixed beverages and soy sauce in Korea.