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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 (P0.01, 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.

This study investigated the anti-inflammatory effects of Pellinus linteus (PL) extract supplementation in healthy young men. The subjects were 18 healthy young males 20 years of age that were given 1.5 L of 0.12% PL extract orally (n=8) or a placebo (control group, n=10) daily for 4 weeks. The body composition, the white blood cell (WBC) count and differential as well as the serum cortisol, interleukin (IL)-1β, and IL-6 concentrations were measured before and after the supplementation. Serum concentrations of cortisol and IL-1β at rest after oral supplementation were significantly decreased compared to before treatment (p

Natives of the tropics are able to tolerate high ambient temperatures. This results from their long-term residence in hot and often humid tropical climates. This study was designed to compare the peripheral mechanisms of thermal sweating in tropical natives with that of their temperate counterparts. Fifty-five healthy male subjects including 20 native Koreans who live in the temperate Korean climate (Temperate-N) and 35 native tropical Malaysian men that have lived all of their lives in Malaysia (Tropical-N) were enrolled in this study after providing written informed consent to participate. Quantitative sudomotor axon reflex testing after iontophoresis (2 mA for 5 min) with 10% acetylcholine (ACh) was used 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, and oral and skin temperature changes were measured. The sweat onset time of AXR (nicotinic-receptor-mediated) was 56 s shorter in the Temperate-N than in the Tropical-N subjects (P0.0001). The nicotinic-receptor-mediated sweating activity AXR (1), and the muscarinic-receptor-mediated sweating activity DIR, in terms of sweat volume, were 103% and 59% higher in the Temperate-N compared to the Tropical-N subjects (P0.0001). The Temperate-N group also had a 17.8% (P0.0001) higher active sweat gland density, 35.4% higher sweat output per gland, 0.24 degrees C higher resting oral temperature, and 0.62 degrees C higher resting forearm skin temperature compared to the Tropical-N subjects (P0.01). ACh iontophoresis did not influence oral temperature, but increased skin temperature near where the ACh was administered, in both groups. These results suggest that suppressed thermal sweating in the Tropical-N subjects was, at least in part, due to suppressed sweat gland sensitivity to ACh through both recruitment of active sweat glands and the sweat gland output per each gland. This physiological trait guarantees a more economical use of body fluids, thus ensuring more efficient protection against heat stress.

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.

Tropical natives possess heat tolerance due to the ability to off-load endogenous and exogenous heat efficiently using a minimum amount of sweat. On the other hand, exposure of temperate natives to heat results in exaggerated production of sweat, of which part is lost by dripping and, thus, not available for evaporation. How sweating is modified in natives of temperate climate zones by prolonged residence in the tropics is not well-understood. The aim of this study was to investigate possible changes in the peripheral sweating mechanisms. Sweating responses to iontophoretically applied acetylcholine (ACh) were compared between Japanese subjects having either permanently resided in Japan (Japan resident Japanese, JRJ) or having stayed in the tropics for 2 years or longer (Tropics resident Japanese, TRJ). Quantitative sudomotor axon reflex tests by iontophoresis of ACh (10%, 2 mA for 5 min) were applied to determine directly activated (DIR) and axon reflex-mediated sweating during [AXR(1)] and after [AXR(2)] ACh iontophoresis. The sweat onset time of AXR(1) was 0.6 min shorter in JRJ than in TRJ (P

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.

Tropical subjects regulate core temperature with less amount of sweat against heat compared to temperate subjects through long-term heat-acclimatization. The purpose of the study is to determine whether acclimatization in tropical subjects decay during a stay in temperate area. The aim of this study, therefore, was to investigate the possible changes in the peripheral sweating mechanisms. Local sweating response activated by acetylcholine (ACh) applied iontophoretically among Malaysians with varying duration of stay in Japan and Japanese resident subjects. Directly activated (DIR) and axon reflex (AXR)-mediated sweating during ACh iontophoresis were measured by capacitance hygrometer (quantitative sudomotor axon reflex test, QSART) QSART was performed in a thermoneutral condition (24±0.5 °C, 40±3% rh). The sweat onset-time after the current loading was 1.05 min shorter in Malaysian with long-term stay in Japan (MLJ) than in Malaysian, and the AXR(1), AXR(2) and DIR sweating in MLJ were larger than Malaysian. From these results, suppressed neuroglandular response to ACh was confirmed in Malaysians. It is suggested that long-term heat-acclimatization acquired in tropical subjects may decay after immigration to temperate area.

Tropical subjects regulate core temperature with less amount of sweat against heat compared to temperate subjects through long-term heat-acclimatization. The purpose of the study is to determine whether acclimatization in tropical subjects decay during a stay in temperate area. Local sweating response activated by acetylcholine (ACh) applied iontophoretically among Malaysians (n=26) with varying duration of stay in Japan and Japanese residents subjects (J-R n=30). Based on their length of stay, Malaysian subjects were divided into three groups, group M-S (n=9) with a duration of stay oflto 12 months, M-M (n=7) with 13 to 36 months and M-L (n=10) with 37 to 72 months. ACh, the primary transmitter for sudomotor innervation, was iontophoretically administered on the forearm. Sweating response elicited directly (DIR) and indirectly via axon reflex (AXR) were evaluated by quantitative sudomotor axon reflex test. The onset-time of AXR was shortened with the longer duration of stay among Malaysian subjects (P

We investigated the sweating response during passive heating (partial submersion up to the umbilical line in 42±0.5℃ water, 30 min) after summer and winter seasonal acclimatization (SA). Testing was performed in July during the summer, 2011 [summer-SA; temp, 25.6±1.8℃; relative humidity (RH), 82.1±8.2%] and in January during the winter, 2012 (winter-SA; temp, -2.7±2.9℃; RH, 65.0±13.1%) in Cheonan (126°52'N, 33.38'E), Republic of Korea. All experiments were carried out in an automated climatic chamber (temp, 25.0±0.5℃: RH, 60.0±3.0%). Fifteen healthy men (age, 23.4±2.5 years; height, 175.0±5.9 cm; weight, 65.3±6.1 kg) participated in the study. Local sweat onset time was delayed during winter-SA compared to that after summer-SA (p< 0.001). Local sweat volume, whole body sweat volume, and evaporative loss volume decreased significantly after winter-SA compared to those after summer-SA (p

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.

This paper presents the low power architecture of CalmRISC, a low power 8-bit microcontroller consuming only 0.1 mW per MIPS at 3.0 V, and its efficient coprocessor interface. The architectural consideration of CalmRISC for low power consumption is presented. Some low power circuit design schemes as well as an efficient coprocessor interface scheme in CalmRISC are proposed and discussed. Finally, the implementation results of CalmRISC and MAC816, one of its DSP coprocessors, as well as C-compiler issues are presented.

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

The paper presents the low power architecture of CalmRISC, a low power 8-bit microcontroller consuming only 0.1 mW per MIPS at 3.0 V, and its efficient coprocessor interface. The architectural consideration of CalmRISC for low power consumption is presented. Some low power circuit design schemes, as well as an efficient coprocessor interface scheme in CalmRISC are proposed and discussed.

In this paper, a single chip 16-bit microcontroller which is integrated with DMA controller, interrupt controller and timer is designed. The CPU core adopts 5-stage pipeline technique and the microcode ROM is configured as 38-bit/spl times/512-word. PMU (power management unit) has 3 operating modes, one of which can be applied to a specific application system to minimize the power dissipation. It is laid out in a 0.6 mm CMOS triple metal single poly process. About 200,000 transistors are integrated on a 7.8 mm/spl times/7.6 mm die.

Architecting today's embedded processor core faces several important design challenges: low power, high performance, and system-on-a-chip considerations. Moreover, support for high-level language constructs and operating systems becomes increasingly critical for acceptance to various applications. CalmRISC/sup TM/-32 effectively meets these challenges by incorporating a carefully designed instruction set, an energy-efficient pipeline design, debugging support with trace mode/CalmBreaker/sup TM/ (an in-circuit debugger), and a generic, yet efficient coprocessor interface. Using a 0.25 /spl mu/m static CMOS standard cell library and compiled datapath cells, the first implementation of CalmRISC/sup TM/-32 operates at 130 MHz (under worst conditions) and consumes 150 /spl mu/A/MHz at 2.5 V. This paper presents a brief description of the instruction set, the overall microarchitecture, and the coprocessor interface of CalmRISC/sup TM/-32.

Relatively few studies have investigated peripheral sweating mechanisms of long-distance runners. The aim of this study was to compare peripheral sweating mechanisms in male long-distance runners, and sedentary counterparts. Thirty six subjects, including 20 sedentary controls and 16 long-distance runners (with 7-12 years of athletic training, average 9.2±2.1 years) were observed. Quantitative sudomotor axon reflex testing (QSART) with iontophoresis (2 mA for 5 min) and 10% acetylcholine (ACh) were performed to determine axon reflex-mediated and directly activated (DIR, muscarinic receptor) sweating. Sweat onset time, sweat rate, number of activated sweat glands, sweat output per gland and skin temperature were measured at rest while maximum oxygen uptake (VO2max) were measured during maximal cycling. Sweat rate, activated sweat glands, sweat output per gland, skin temperature and VO2max were significantly higher in the trained runners than in the sedentary controls. Sweat onset time was significantly shorter for the runners. In the group of long-distance runners, significant correlations were found between VO2max and sweat onset time (r2 = 0.543, P

The aim of the present study was to determine the changes in cardiac makers and endothelin-1 (ET-1) in marathoners with exercise induced hypertension compared to normotensive controls before and after running a marathon. Among a total of 70 volunteers, 10 marathoners with systolic blood pressure (SBP) greater than 210 mmHg during a treadmill exercise stress test were selected as an exercise-induced hypertension group (EIH) and 10 marathoners with normal SBP were selected as a control group (CON). Blood was collected from all volunteers 2 h before and immediately after a marathon: creatinine kinase (CK), CK-MB, cardiac tropoin-I (cTnI), N-terminal pro-brain natriuretic peptide (NT-proBNP), and endothelin-1(ET-1). Cardiac markers, CK, CK-MB, and CK-MB/CK ratio significantly increased in both EIH and CON; significance was not observed between the groups. Significant increases were not observed in high sensitive-C reactive protein (hs-CRP) after the race nor between the groups. Significant increases in cTnI and NT-proBNP were observed after the race in both groups. In addition, EIH showed greater increase than CON after the race. In conclusion, increased vascular tone in EIH during a marathon increased blood pressure and myocardial burden which in turn increased myocardial cell membrane permeability to further increase myocardial tension to the point of cTnI release.

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

The influence of alpha-fetoprotein (AFP) on the bone marrow (BM) natural suppressor (NS) cells of intact Ehrlich carcinoma -bearing CBA mice was studied. Bone marrow NS cells were fractionated into three fractions by isopycnic centrifugation on percoll gradients: NS1 (rho=1.080 g/ml), NS2 (rho=1.090 g/ml) and NS3 (1.100rho1.090 g/ml). These fractions were highly different in their sensitivity to known NS cell inductors (interleukin (IL)-2, IL-3 or histamine). None of the NS fractions isolated from the intact mice spontaneously produced antiproliferative activity, however, they showed a high level of NS (antiproliferative and natural killer cell inhibitory) activity under the influence of AFP. A single injection of AFP to intact mice led to an increase of spontaneous NS activity and the inhibition of natural killer cell activity. NS activity, especially NS2, was increased in when tumor cells were subcutaneously inoculated three days after AFP injection. In the AFP-treated mice, the tumor mass at 14 days was 60% larger than that in the untreated mice. Our data confirmed that AFP is a tumor marker that can inhibit cancer immunity and plays a role in cancer pathogenesis.