Effect of Intensive and Repetitive Heat Exposure on the Sudomotor Activity.

The sweating response is modulated in two different ways depending on adaptation conditions. In this work, we examined sudomotor activities before and after intensive and repetitive heat exposure. Nine male volunteers were exposed to 30-min half-body immersion in hot water (42 ± 0.5°C) at the same time of day on alternate days for 3 weeks. All experiments were performed in an automated climate chamber. Tympanic (Tty) and skin (Ts) temperatures were measured. Mean body temperature (mTb) was calculated. Sudomotor activities, including sweat onset time, sweat rate and volume, activated sweat gland density (ASGD) and output (ASGO), were tested in four regions of the skin: chest, abdomen, upper back and thigh. Basal Tty and mTb were found to decrease by 0.15°C (P < 0.05) and 0.16°C (P < 0.05), respectively. As a typical data (upper back), sweat onset time increased by 33.6% (P < 0.05) after heat acclimation. After heat acclimation, sweat rate decreased by 14.7% (P < 0.05), sweat volume decreased by 15.5% (P < 0.05) and ASGO also decreased by 11.1% (P < 0.05). ASGD decreased by 4.1% after heat acclimation without statistical significance. The data suggest that intensive and repetitive heat exposure induces suppression of sudomotor activities within 3 weeks.

Seasonal acclimation in sudomotor function evaluated by QSART in healthy humans.

The quantitative sudomotor axon reflex testing (QSART) is a classic test of routine postganglionic sudomotor function. We investigated sudomotor function by QSART after summer (July 2012) and winter (January 2013) seasonal acclimation (SA) in the Republic of Korea. QSART with acetylcholine (ACh) iontophoresis were performed to determine directly activated (DIR) and axon reflex-mediated (AXR1, 2) sweating rate. Onset time of axon reflex, activated sweat gland density (ASGD), activated sweat gland output (ASGO), tympanic and skin temperatures (Tty, Tsk), basal metabolic rate (BMR), and evaporative loss volume changes were measured. Tympanic and mean body temperature (Tb; calculated from Tty, Tsk) were significantly lower after summer-SA than that of winter-SA. Sweat onset time was delayed during winter-SA compared to that after summer-SA. BMR, AXR(1), AXR(2), and DIR sweat rates, ASGD and ASGO, and evaporative loss volume were significantly diminished after winter-SA relative to after summer-SA. In conclusion, changes in sweating activity measured by QSART confirmed the involvement of the peripheral nervous system in variation of sudomotor activity in seasonal acclimation.

Beneficial effect of Oligonol supplementation on sweating response under heat stress in humans.

Oligonol is a low-molecular weight polyphenol that possesses antioxidant and anti-inflammatory properties. However, nothing is known regarding the impact of Oligonol on sudomotor activity. This study investigated the effects of Oligonol supplementation on sudomotor activity during heat load in humans. Initially, we conducted a placebo-controlled, cross-over trial where participants took a daily dose of Oligonol 200 mg or placebo for one week. After a 2 week washout period, the subjects were switched to the other study arm. As a heat load, half-body immersion into hot water (42 ± 0.5 °C for 30 min) was performed in an automated climate chamber. Tympanic and skin temperatures were measured. Sudomotor activity, including onset time, sweat rate (SR) and volume (SV), active sweat gland density (ASGD), and sweat gland output (SGO), was tested in four or eight areas of skin. When compared with placebo, Oligonol attenuated increases in tympanic and skin temperatures after the heat load. There was an increasing trend in local sweat onset time, but there was a decrease in local SR, SV, ASGD, and SGO for Oligonol compared to placebo. The mean ASGD was significantly higher in the Oligonol group than in the placebo group for 10, 20, and 30 min. This study demonstrates that Oligonol appears to be worthy of consideration as a natural supplement to support more economical use of body fluids against heat stress.

Oligonol supplementation affects leukocyte and immune cell counts after heat loading in humans.

Oligonol is a low-molecular-weight form of polyphenol and has antioxidant and anti-inflammatory activity, making it a potential promoter of immunity. This study investigates the effects of oligonol supplementation on leukocyte and immune cell counts after heat loading in 19 healthy male volunteers. The participants took a daily dose of 200 mg oligonol or a placebo for 1 week. After a 2-week washout period, the subjects were switched to the other study arm. After each supplement, half-body immersion into hot water was made, and blood was collected. Then, complete and differential blood counts were performed. Flow cytometry was used to enumerate and phenotype lymphocyte subsets. Serum concentrations of interleukin (IL)-1ß and IL-6 in blood samples were analyzed. Lymphocyte subpopulation variables included counts of total T cells, B cells, and natural killer (NK) cells. Oligonol intake attenuated elevations in IL-1ß (an 11.1-fold change vs. a 13.9-fold change immediately after heating; a 12.0-fold change vs. a 12.6-fold change 1h after heating) and IL-6 (an 8.6-fold change vs. a 9.9-fold change immediately after heating; a 9.1-fold change vs. a 10.5-fold change 1h after heating) immediately and 1 h after heating in comparison to those in the placebo group. Oligonol supplementation led to significantly higher numbers of leukocytes (a 30.0% change vs. a 21.5% change immediately after heating; a 13.5% change vs. a 3.5% change 1h after heating) and lymphocytes (a 47.3% change vs. a 39.3% change immediately after heating; a 19.08% change vs. a 2.1% change 1h after heating) relative to those in the placebo group. Oligonol intake led to larger increases in T cells, B cells, and NK cells at rest (p < 0.05, p < 0.05, and p < 0.001, respectively) and immediately after heating (p < 0.001) in comparison to those in the placebo group. In addition, levels of T cells (p < 0.001) and B cells (p < 0.001) were significantly higher 1 h after heating in comparison to those in the placebo group. These results demonstrate that supplementation with oligonol for 1 week may enhance the immune function under heat and suggest a potential useful adjunct to chemotherapy in malignant diseases.

Age- and sex-related differences in sudomotor function evaluated by the quantitative sudomotor axon reflex test (QSART) in healthy humans.

The aim of the present study was to quantitatively investigate the age and sex-related differences in sudomotor function in healthy humans. The quantitative sudomotor axon reflex test (QSART) with iontophoresis (2 mA for 5 min) and 10% acetylcholine (ACh) was performed to determine axon reflex-mediated (AXR), with and without iotophoresis (AXR(1) and AXR(2), respectively), and directly activated (DIR) sweating. All experiments were conducted under thermoneutral conditions (temperature 24.0 ± 0.5°C; relative humidity 40 ± 3%). In general, men had enhanced values of onset time of AXR, sweat rates, activated sweat gland density (SGD) and activated sweat gland output (SGO) than women, but not in all cases. The onset time of AXR (r(2)  = 0.567; P < 0.001) was positively correlated with advancing age, whereas sweat rates of AXR(1) and AXR(2) (r(2)  = 0.571 and r(2)  = 0.486, respectively; P < 0.0001), DIR (r(2)  = 0.594; P < 0.0001), SGD (r(2)  = 0.496; P < 0.0001) and SGO (r(2)  = 0.551; P < 0.0001) were negatively correlated in both men and women with advancing age. The results demonstrate that an attenuation of sudomotor function occurs with aging in both sexes. Moreover, the findings showed a progressive increase in onset time and a decrease in sweat rates, SGD and SGO with increasing age in both sexes. A variation in sweat function was found between sexes, but not in all age groups.

Comparison of peripheral sudomotor sensitivity to acetylcholine in endurance and non-endurance trained male subjects.

INTRODUCTION: We investigated the effect of endurance and non-endurance training on peripheral sudomotor sensitivity. METHODS: The quantitative sudomotor axon reflex test (QSART) was performed. RESULTS: Endurance-trained subjects (ET, long-distance runners) had a significantly shorter onset time of sweating, greater sweat volume, increased density of activated sweat glands and sweat gland output per single activated gland, greater volume of transepidermal water loss, and higher skin temperature compared with those in the other 2 groups [non-endurance-trained group (NET), sedentary control group (CT)]. NET subjects (baseball players) had a tendency to increase in these variables; thus, some values were greater than control subjects. CONCLUSIONS: These results suggest that endurance training much more effectively modifies sudomotor sensitivity than non-endurance training.

The effects of running a 308 km ultra-marathon on cardiac markers.

The aim of this study was to investigate the expression of cardiac strain and damage in 18 male marathoners with average age of 52.8 ± 5.0 years running at a 308 km ultra-marathon. Blood samples were collected at pre-race, 100 km, 200 km and 308 km check points for the analysis of cardiac muscle injury markers, creatine kinase (CK), creatine kinase-myocardial band (CK-MB), cardiac troponin I (cTnI) and cardiac muscle strain marker, N-terminal pro-brain natriuretic peptide (NT-proBNP). The CK levels increased 1127.2 ± 507.9 IU/L, 5133.8 ± 2492.7 IU/L and 4958.4 ± 2087.9 IU/L at 100 km, 200 km and 308 km, respectively, compared to the pre-race levels. The CK-MB levels increased 20.2 ± 11.2 ng/mL, 73.3 ± 35.6 ng/mL and 68.6 ± 42.6 ng/mL at 100, 200 and 308 km, respectively, compared to the pre-race levels. The CK-MB/CK ratio showed that the CK-MB mass index was within the normal range (<2.5%) at 100 km, 200 km and 308 km. The cTnI levels showed no significant difference in all check points. The NT-proBNP levels increased 146.55 ± 92.7 pg/mL, 167.95 ± 111.9 pg/mL and 241.23 ± 121.2 pg/mL at 100, 200 and 308 km, respectively, compared to the pre-race levels. The normal CK-MB mass index (<5.0 ng/mL) and the absence of an increase in the cTnI levels during the 308 km ultra-marathon suggested that no myocardial injury despite an elevation in CK-MB. The increase in NT-proBNP levels probably resulted from continuous hemodynamic cardiac stress and represents a transient physiological myocardial protective response.

Left ventricular hypertrophy, diastolic dysfunction, pulse pressure, and plasma ET-1 in marathon runners with exaggerated blood pressure response.

This study was conducted to study left ventricular hypertrophy (LVH), diastolic dysfunction, pulse pressure (PP), and plasma endothelin (ET)-1 level in amateur marathon runners with an exaggerated blood pressure response (EBPR) to exercise. The study participants included normotensive marathon runners (NM, n = 15), EBPR marathon runners (EBPR, n = 17), normotensive sedentary individuals (CON, n = 13), and hypertensive patients (HTN, n = 14). An integrated M-mode/2-dimensional echocardiographic analysis was performed. Plasma ET-1 levels at resting were measured using a commercial ELISA kit. LV wall thickness and end-diastolic dimensions as well as LV mass index (LVMI) were higher in EBPR than in CON. There were no differences in systolic function among the groups. Analysis of diastolic function, such as lower Em and higher E/Em ratio on TDI, showed a worse relaxation pattern in EBPR. Despite LVH, NM subjects showed no abnormality of LV diastolic dysfunction. HTN subjects in the early stage of their disease showed a slightly modified LV structural and diastolic function, but there was no statistical difference compared with CON. The E/Em ratio was significantly correlated with PP and LVMI. LVMI was significantly correlated with PP. There was a significant difference in plasma ET-1 concentration between marathon runners and hypertensive subjects. We demonstrated that marathon runners with EBPR showed an increase in LVMI and diastolic dysfunction more than HTN subjects in the early stage. PP was significantly related to these two variables. Caution should be exercised when connecting LVH and diastolic dysfunction with plasma ET-1 concentration in all marathon runners.

Oligonol supplementation attenuates body temperature and the circulating levels of prostaglandin E2 and cyclooxygenase-2 after heat stress in humans.

Oligonol, a phenolic production from lychee, has been reported to exhibit anti-oxidative and anti-inflammatory effects. This study investigated the effect of Oligonol supplementation on circulating levels of prostaglandin E2 (PGE2) and cyclooxygenase (COX)-2, as well as body temperature, after heat stress in 17 healthy human male volunteers (age, 21.6±2.1 years). All experiments were performed in an automated climate chamber (26.0°C±0.5°C, relative humidity 60%±3.0%, air velocity less than 1 m/sec) between 2 and 5 p.m. Subjects ingested an Oligonol (100 mg)-containing beverage or placebo beverage before half-body immersion into hot water (42°C±0.5°C for 30 min). Tympanic and skin temperatures were measured and mean body temperatures were calculated. Serum concentrations of PGE2 and COX-2 were analyzed before, immediately after, and 60 min after immersion. Oligonol intake significantly prevented elevation of tympanic (temperature difference: 0.17°C at Post, P<.05; 0.17°C at Re-60, P<.05) and mean body temperatures (temperature difference: 0.18°C at Post, P<.05; 0.15°C at Re-60, P<.05), and lowered concentrations of serum PGE2 (increased by 13.3% vs. 29.6% at Post, P<.05) and COX-2 (increased by 15.6% vs. 21.8% at Post, P<.05), compared to placebo beverage. Our result suggests that Oligonol has the potential to suppress increases in body temperature under heat stress, and this is associated with decreases in serum levels of PGE2 and COX-2.

Heat acclimation affects circulating levels of prostaglandin E2, COX-2 and orexin in humans.

We examined serum levels of prostaglandin E2 (PGE2), cyclooxygenase (COX)-2 and orexin before and after heat acclimation (HA) to test the hypothesis that decreased basal body temperature due to HA correlate with circulating levels of these key thermoregulatory molecules. Nine healthy human male volunteers were recruited (age, 21.9±2.7 years). The subjects were exposed to half-body immersion in hot water (42±0.5°C) at the same time of day (2-5p.m.) on alternate days for 3 weeks. The HA protocol included 10 bouts of 30min immersion. All experiments were performed in an automated climate chamber (temperature, 26.0±0.5°C; relative humidity, 60±3.0%; air velocity, <1m/s). Tympanic and skin temperatures were measured, and mean body temperature was calculated. The difference in body weight was used to estimate total sweat loss. Serum levels of PGE2, COX-2 and orexin were analyzed before and after HA. Body temperature decreased significantly (P<0.05) after HA, whereas sweat volume increased significantly (P<0.01). Serum PGE2, COX-2 and orexin concentrations decreased significantly compared to those at pre-acclimation (P<0.001, P<0.01, P<0.01, respectively). Our data suggest that decreased basal body temperature after HA is associated with decreases in thermoregulatory molecules, such as PGE2, COX-2 and orexin.

Leukocyte chemotactic cytokine and leukocyte subset responses during ultra-marathon running.

PURPOSE: The aim of this study was to assess leukocyte chemotactic cytokine and leukocyte subset responses during ultra-marathon running. Leukocyte chemokines such as interleukin (IL)-8, interferon gamma-induced protein-10 (IP-10), regulated upon activation, normal T-cell expressed and secreted (RANTES), and eotaxin are involved in leukocyte recruitment. METHODS: Among 60 male amateur endurance runner volunteers, 18 finished the course (a 308 km continuous race from Kanghwado to Kangneung, South Korea). Their average age, height, and body mass were 52.8 ± 5.0 years, 167.6 ± 5.2 cm, and 64.5 ± 1.2 kg, respectively. Blood samples were collected at 0, 100, 200, and 308 km during the race for analysis of white blood cells and serum concentrations of IL-8, IP-10, RANTES, eotaxin, IL-6, creatine kinase (CK), and C-reactive protein (CRP). RESULTS: Muscle and liver damage indicators (IL-6, CK, and CRP) were maximally elevated as a result of marathon running. Total leukocytes, neutrophils, and monocytes increased significantly during the event (leukocytosis, neutrophilia, and monocytosis, respectively). However, lymphocytes and eosinophils decreased significantly during the event (lymphopenia and eosinopenia, respectively). Serum levels of the neutrophil chemokine IL-8 increased maximally at 100 km and were maintained. Monocyte-lymphocyte chemokine IP-10 concentration decreased during the latter part of the race. The eosinophil chemokine eotaxin decreased gradually during the race, and no difference was observed in eosinophil chemokine RANTES levels. CONCLUSION: These observations indicate that prolonged endurance ultra-marathon running was associated with significant systemic inflammation and perturbation in leukocyte subsets. Leukocyte chemotactic cytokines such as IL-8, IP-10, eotaxin showed similar patterns of responses in related leukocyte subsets, but RANTES did not.

Effect of Ultra-marathon (308 km) Race on Bone Metabolism and Cartilage Damage Biomarkers.

OBJECTIVE: To evaluate the potential effects of a 308-km ultra-marathon on bone and cartilage biomarkers. METHOD: Venous blood samples were collected at pre-race, 100 km, 200 km, and 308 km checkpoints. The following markers of cartilage damage and bone metabolism were studied: osteocalcin (OC), osteoprotegerin (OPG), and calcium, phosphorous, and cartilage oligomeric matrix protein (COMP). RESULTS: Blood samples were taken from 20 male runners at four different checkpoints. Serum COMP was increased by 194.1% (130.7% at 100 km and 160.4% at 200 km). Serum OPG was significantly increased by 158.57% at 100 km and 114.1% at 200 km compared to the pre-race measures. OC was transiently suppressed at 200 km. Serum calcium and phosphorous concentrations decreased compared to the pre-race measures. CONCLUSION: This study showed that the 308-km ultra-marathon induced several changes, including transient uncoupling of bone metabolism, increased bone resorption, suppressed bone formation, and bone turnover and had a major impact on cartilage structure.

Caffeine increases sweating sensitivity via changes in sudomotor activity during physical loading.

We assessed the effect of caffeine on sudomotor activity and sweating sensitivity during physical loading. Both physiological responses could occur due to energy expenditure. Subjects were 13 athletically trained males (22.1 ± 3.7 years old, 174.2 ± 5.4 cm tall, and weighing 70.9 ± 4.6 kg, with maximal oxygen consumption [VO(2)max] of 53.6 ± 4.4 mL/kg/minute). The study involved a within-subject, random, crossover design. Tests were performed following the ingestion of 3 mg/kg caffeine. The physical loading involved running for 30 minutes at 60% VO(2)max (24.0 ± 0.5°C, 40 ± 3.0% relative humidity). Tympanic temperature (TYMP) was significantly higher in the caffeine-consuming group (Caffe-I) at pre-exercise (40 minutes after caffeine intake and immediately before running) (P<.05). Mean body temperature (mT(b)) was significantly higher in the Caffe-I group at pre- and post-exercise (30 min after start of running) (P<.05). Onset time of localized sweating was significantly shorter in the Caffe-I group (P<.01), but localized sweat volume and active sweat gland output (per single gland) was significantly higher in the Caffe-I group (P<.001). Activated sweat gland density was significantly increased in the Caffe-I group on the abdomen and thigh (P<.01). In conclusion, caffeine ingestion caused not only increases in TYMP and mT(b) through thermogenesis, but also an increased sweating sensitivity via changes in sudomotor activity.

Effect of the Heat-exposure on Peripheral Sudomotor Activity Including the Density of Active Sweat Glands and Single Sweat Gland Output.

Tropical inhabitants are able to tolerate heat through permanent residence in hot and often humid tropical climates. The goal of this study was to clarify the peripheral mechanisms involved in thermal sweating pre and post exposure (heat-acclimatization over 10 days) by studying the sweating responses to acetylcholine (ACh), a primary neurotransmitter of sudomotor activity, in healthy subjects (n=12). Ten percent ACh was administered on the inner forearm skin for iontophoresis. Quantitative sudomotor axon reflex testing, after iontophoresis (2 mA for 5 min) with ACH, was performed to determine directly activated (DIR) and axon reflex-mediated (AXR) sweating during ACh iontophoresis. The sweat rate, activated sweat gland density, sweat gland output per single gland activated, as well as oral and skin temperature changes were measured. The post exposure activity had a short onset time (p<0.01), higher active sweat rate [(AXR (p<0.001) and DIR (p<0.001)], higher sweat output per gland (p<0.001) and higher transepidermal water loss (p<0.001) compared to the pre-exposure measurements. The activated sweat rate in the sudomotor activity increased the output for post-exposure compared to the pre-exposure measurements. The results suggested that post-exposure activity showed a higher active sweat gland output due to the combination of a higher AXR (DIR) sweat rate and a shorter onset time. Therefore, higher sudomotor responses to ACh receptors indicate accelerated sympathetic nerve responsiveness to ACh sensitivity by exposure to environmental conditions.

The effect of Oligonol intake on cortisol and related cytokines in healthy young men.

This study investigated the effects of Oligonol intake on cortisol, interleukin (IL)-1beta, and IL-6 concentrations in the serum at rest and after physical exercise loading. Nineteen healthy sedentary male volunteers participated in this study. The physical characteristics of the subjects were: a mean height of 174.2 +/- 2.7 cm, a mean weight of 74.8 +/- 3.6 kg and a mean age of 22.8 +/- 1.3 years. Each subject received 0.5 L water with Oligonol (100 mg/day) (n = 10) or a placebo (n = 9) daily for four weeks. The body composition, the white blood cell (WBC) and differential counts as well as the serum cortisol, IL-1beta, and IL-6 concentrations were measured before and after Oligonol intake. The cortisol concentration and serum levels of IL-1beta and IL-6 after Oligonol intake were significantly decreased compared to before treatment (P < 0.01, respectively). In addition, the rate of increase of these factors after exercise was decreased compared to the placebo group. There was no change in the WBC and differential cell counts. These results suggest that oral Oligonol intake for four weeks had a significant effect on inhibition of inflammatory markers in healthy young men.

Effect of supplementation with Ecklonia cava polyphenol on endurance performance of college students.

Ecklonia cava polyphenol (ECP) is a potent antioxidant and procirculatory agent that may contribute to improvement of endurance performance during highly intense exercise. This study evaluated the acute effect of an ECP-supplemented drink against a placebo on maximum endurance capacity and related physiological parameters. Twenty men 18-23 yr old volunteered as participants. Each performed 2 randomized trials with a 1-week interval between them. One trial was with ECP and the other with a placebo drink. Participants in this randomized, placebo-controlled, crossover design ingested either a placebo or ECP drink 30 min before each exercise trial. Time to exhaustion, VO(2max), and postexercise blood glucose and lactate levels were evaluated. ECP supplementation increased time to exhaustion (2.39 min) compared with placebo. This result was accompanied by a 6.5% higher mean VO(2max) in the ECP group, although the difference was not statistically significant. The blood glucose level in the ECP group at 3 min after exhaustive exercise was significantly higher than that of the placebo group (+ 9.9%). The postexercise blood lactate levels in the ECP group showed a decreasing trend compared with placebo, but it was nonsignificant. This study was not able to determine any physiological mechanisms behind the improved endurance performance, but, based on these results, it is speculated that the ECP supplementation may have contributed to enhanced oxidation of glucose and less production of lactate during intense exercise, possibly by its free-radical-scavenging and procirculatory activities. However, careful verification is required to elucidate the correct mechanism.

Beneficial effects of cardiac rehabilitation and exercise after percutaneous coronary intervention on hsCRP and inflammatory cytokines in CAD patients.

Recent studies showed that tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), as well as high-sensitive C-reactive protein (hsCRP) levels are predictive factors of cardiovascular risk. However, the effect of cardiac rehabilitation (CR) intervention in coronary artery disease (CAD) patients on these factors is not known. The aim of this study was to evaluate the effects of CR and exercise on hsCRP and inflammatory cytokine levels in patients with CAD after percutaneous coronary intervention (PCI). CAD patients who underwent PCI were divided into a CR and exercise group (CRE, n = 29) or a control group (CON, n = 10). CR and exercise consisted of 6 weeks supervised exercise training and 8 weeks home-based, self-managed exercise. Compared to pre-experimental levels, TNF-alpha (by 20.4%; p = 0.006) and IL-6 (by 49.0%; p < 0.0001), as well as hsCRP (by 59.4%; p < 0.0001), were markedly decreased after CR and exercise in CAD patients but not in control group, except for IL-6 (by 41.6%; p = 0.001). However, there was no significant alteration of adiposity-related variables such as BMI, percent body fat, and waist circumferences, in both groups. We suggest that CR and exercise in CAD patients after PCI induce significant reduction in hsCRP and inflammatory cytokines (TNF-alpha and IL-6), and marked increase in exercise tolerance and capacity.

Effect of cardiac rehabilitation and statin treatment on anti-HSP antibody titers in patients with coronary artery disease after percutaneous coronary intervention.

Accumulating evidence suggests that higher antibody titers to heat shock proteins (HSPs) are associated with the development and severity of atherosclerosis. The aim of this study was to evaluate the impact of cardiac rehabilitation therapy (CRT) or stain treatment (STT) or a combination of both (COM) on anti-HSP antibodies in patients with coronary artery disease (CAD) after percutaneous coronary intervention (PCI). Clinical evaluation of subjects was performed both at the commencement and completion of the 14 weeks of treatment. CRT consisted of a supervised 6 weeks of exercise following hospital discharge and 8 weeks of home stay exercise. Patients assigned to statin therapy were treated with 80 mg per day of fluvastatin. Blood samples from 39 patients were analyzed for antibodies to HSP60 and HSP70 by ELISA. Biochemical parameters, including lipids, high-sensitivity C reactive protein (hsCRP), and interleukin-6 (IL-6), were also analyzed. We found that CRT and COM reduced antibody titers to HSP60 and HSP70 in CAD patients (by 3.79 and 10.00% of anti-HSP60, and by 5.74 and 3.45% of anti-HSP70, respectively) but statin treatment reduced only antibody titers to HSP70 (by 3.83%). There was a significant correlation between antibody titers to HSP60 versus HSP70. Considering the fact that antibody titers to HSPs are associated with the autoimmune process in CAD, CRT and COM have greater effects on reduction in autoimmune reaction after PCI than statin treatment. This reduction was accompanied by greater improvements in blood biochemical variables, such as lipids, hsCRP, and IL-6 after CRT and COM.

Detection of enteroviruses and mammalian reoviruses in Korean environmental waters.

Using the standard total culturable virus assay-most probable number (TCVA-MPN) method, we evaluated a total of 348 samples, including surface water, finished water, and tap water samples, collected from randomly selected water treatment plants in Korea from August 2001 through July 2005 according to the Information Collection Rule. All the TCVA-positive samples were also subjected to integrated cell culture-PCR (ICC-PCR) methods for the detection of enteroviruses, hepatitis A virus, adenoviruses, and reoviruses. The most probable number of infectious units per 100 liters for the environmental water samples ranged from 0.5 to 47.3. Nine of the 13 TCVA-positive samples (69.2%) were found by ICC-PCR to be positive for human enteroviruses, which were confirmed to be coxsackievirus type B3, coxsackievirus type B4, coxsackievirus type B6, echovirus type 30, and vaccine strain poliovirus type 3 by direct sequencing. Eleven of the 13 TCVA-positive samples (84.6%) were found by ICC-PCR assay to be positive for reoviruses. The serotype of all the reoviruses was the same as reovirus type 1 by direct sequencing. Both enteroviruses and reoviruses were concurrently detected in seven TCVA-positive samples (53.8%).

Anti-obesity effect of Pinellia ternata extract in Zucker rats.

Pinellia ternata is known as the herb effective in removing dampness-phlegm, one of the causes of obesity in traditional Korean medicine. Pinellia ternata water extract (PE) was fed to rats after mixing with diet once a day (400 mg x kg(-1)) for 6 weeks. We investigated its effect on the thermogenesis and fatty acids oxidation with obese Zucker rats. We also determined the gene expression of uncoupling protein 1 (UCP1), peroxisome proliferators-activated receptor alpha (PPARalpha), and PPARgamma coactivator 1alpha (PGC1alpha). The PE treatment lowered the levels of triglyceride and free fatty acids (p<0.05) in blood of the obese rats and the body weight was also reduced slightly. It was also observed that PE significantly increased the expression of both UCP1 mRNA in brown adipose tissue (BAT) (p<0.001) and PPARalpha and PGC1alpha mRNA in white visceral adipose tissue (WAT) (p<0.05 and p<0.001, respectively), which may cause a reduction of obesity. These results suggested that PE would be able to affect anti-obesity through thermogenesis and fatty acid oxidation.