Seasonal Acclimatization in Summer versus Winter to Changes in the Sweating Response during Passive Heating in Korean Young Adult Men.

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<0.001). Changes in basal metabolic rate increased significantly after winter-SA (p< 0.001), and tympanic temperature and mean body temperature were significantly lower after summer-SA (p<0.05). In conclusion, central sudomotor acitivity becomes sensitive to summer-SA and blunt to winter-SA in Rebubic of Korea. These results suggest that the body adjusts its temperature by economically controlling the sweating rate but does not lower the thermal dissipation rate through a more effective evaporation scheme after summer-SA than that after winter-SA.

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.

Long distance runners present upregulated sweating responses than sedentary counterparts.

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<0.01, n = 16), DIR sweat rate (r2 = 0.584, P<0.001, n = 16), sweat output per gland (r2 = 0.539, P<0.01, n = 16). There was no correlation between VO2max and activated sweat glands. These findings suggest that habitual long-distance running results in upregulation of the peripheral sweating mechanisms in humans. Additional research is needed to determine the molecular mechanism underlying these changes. These findings complement the existing sweating data in long-distance runners.

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.

Acute exercise induces FGF21 expression in mice and in healthy humans.

Fibroblast growth factor 21 (FGF21) plays an important role in the regulation of energy homeostasis during starvation and has an excellent therapeutic potential for the treatment of type 2 diabetes in rodents and monkeys. Acute exercise affects glucose and lipid metabolism by increasing glucose uptake and lipolysis. However, it is not known whether acute exercise affects FGF21 expression. Here, we showed that serum FGF21 level is increased in mice after a single bout of acute exercise, and that this is accompanied by increased serum levels of free fatty acid, glycerol and ketone body. FGF21 gene expression was induced in the liver but not in skeletal muscle and white adipose tissue of mice after acute exercise, and further, the gene expression levels of hepatic peroxisome proliferator-activated receptor α (PPARα) and activating transcription factor 4 (ATF4) were also increased. In addition, we observed increased FGF21 level in serum of healthy male volunteers performing a treadmill run at 50 or 80% VO2max. These results suggest that FGF21 may also be associated with exercise-induced lipolysis in addition to increased catecholamines and reduced insulin.

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.

Fabrication and biocompatibility of novel bilayer scaffold for skin tissue engineering applications.

In this study, a novel bilayer scaffold composed of electrospun polycaprolactone and poly(lacto-co-glycolic acid) (PCL/PLGA) membrane and glutaraldehyde (3.5% v/v) cross-linked chitosan/gelatin hydrogel was fabricated using two methods: electrospinning of the membrane onto the lyophilized hydrogel (BS-1) and membrane underlaying and casting method (BS-2). The morphology of the fabricated scaffolds was examined by scanning electron microscope (SEM). Mechanical strength, porosity, swelling capacity, and biodegradation rates of the scaffolds were also characterized. The in vitro biocompatibility of the materials was investigated by assessing cytotoxicity and cell proliferation on the material was measured using MTT assay. In addition, cell adhesion on the material was investigated by SEM. The BS-2 was grafted in Sprague-Dawley rats to determine its in vivo behavior and biocompatibility. The experimental results showed that the addition of the membrane layer to the hydrogel decreased swelling and degradation rates and provided ease of handling during implantation. Grafted BS-2 showed normal wound healing and no major inflammatory reaction was observed.

Fabrication of multilayer ZrO2-biphasic calcium phosphate-poly-caprolactone unidirectional channeled scaffold for bone tissue formation.

We developed a continuously porous scaffold with laminated matrix and bone-like microstructure by a multi-pass extrusion process. In this scaffold, tetragonal ZrO2, biphasic calcium phosphate and poly-caprolactone layers were arranged in a co-axially laminated unit cell with a channel in the center. The entire matrix phase had a laminated microstructure of alternate lamina of tetragonal ZrO2, biphasic calcium phosphate and poly-caprolactone--biphasic calcium phosphate with optimized designed thickness and channeled porosity. Each of the continuous pores was coaxially encircled by the poly-caprolactone--biphasic calcium phosphate layer, biphasic calcium phosphate layer and finally tetragonal ZrO2 layer, one after the other. Before extrusion, 5 vol% graphite powder was mixed with tetragonal ZrO2 to ensure pores in the outer layer and connectivity among the lamellas. The design strategy is aimed to incorporate a lamellar microstructure like the natural bone in the macro-scaled ceramic body to investigate the strengthening phenomenon and pave the way for fabricating complex microstructure of natural bone could be applied for whole bone replacement. The final fabricated scaffold had a compressive strength of 12.7 MPa and porosity of 78 vol% with excellent cell viability, cell attachment and osteocalcin and collagen expression from cultured MG63 cells on scaffold.

In vitro and in vivo evaluation of electrospun PCL/PMMA fibrous scaffolds for bone regeneration.

Scaffolds were fabricated by electrospinning using polycaprolactone (PCL) blended with poly(methyl methacrylate) (PMMA) in ratios of 10/0, 7/3, 5/5 and 3/7. The PCL/PMMA ratio affected the fiber diameter, contact angle, tensile strength and biological in vitro and in vivo properties of the scaffolds, and the 7/3 ratio resulted in a higher mechanical strength than 5/5 and 3/7. In vitro cytotoxicity and proliferation of MG-63 osteoblast cells on these blended scaffolds were examined by MTT assay, and it was found that PCL/PMMA blends are suitable for osteoblast cell proliferation. Confocal images and expression of proliferating cell nuclear antigen confirmed the good proliferation and expression of cells on the 7/3 PCL/PMMA fibrous scaffolds. In vivo bone formation was examined using rat models, and bone formation was observed on the 7/3 PCL/PMMA scaffold within 2 months. In vitro and in vivo results suggest that 7/3 PCL/PMMA scaffolds can be used for bone tissue regeneration.

Effect of coenzyme Q10 and Ardisia japonica Blume on plasma and liver lipids, platelet aggregation, and erythrocyte Na efflux channels in simvastatin-treated guinea pigs.

Forty guinea pigs were divided into four groups and fed 0.04% cholesterol based control diet, plus 0.05% simvastatin, and statin plus 0.1% CoQ10 or 10% Ardisia Japonica Blume (AJB) leave powder for 4 weeks. Plasma total cholesterol levels decreased significantly in all groups fed the statin-containing diet compared with that in guinea pigs fed the control diet (P < 0.01). Plasma and liver triglycerides decreased significantly in the statin plus CoQ10 group compared with those in the control (both P < 0.05). Maximum platelet aggregation was significantly higher in the statin plus CoQ10 group than that in the other groups (P < 0.05). Na-K ATPase activity increased in the statin group and decreased in the statin plus CoQ10 group (P < 0.01). Na-K co-transport and Na passive transport decreased significantly in the control group compared with those in the other groups (both P < 0.05). Intracellular Na was highest in the statin group and lowest in the statin plus CoQ10 group and was correlated with Na-K ATPase activity. Thiobarbituric acid reactive substance production in platelet-rich plasma and liver tended to decrease in the statin plus CoQ10 group compared with those in the other groups. Plasma glutamic-pyruvic transaminase and glutamic-oxaloacetic transaminase increased significantly in the statin group compared with those in the control (P < 0.05). These result suggest that antioxidant rich AJB did not have positive effects on cardiovascular disease parameters. The statin plus CoQ10 seemed to decrease cholesterol more efficiently than that of statin alone.

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.

Tropical Malaysians and temperate Koreans exhibit significant differences in sweating sensitivity in response to iontophoretically administered acetylcholine.

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 (P < 0.0001). 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 (P < 0.0001). The Temperate-N group also had a 17.8% (P < 0.0001) 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 (P < 0.01). 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.

Parameter estimation for mathematical models of NKCC2 cotransporter isoforms.

An optimization problem, formulated using a nonlinear least-squares approach, was used to estimate parameters for kinetic models of the three isoforms of the kidney-specific Na-K-2Cl (NKCC2) cotransporter. Specifically, the optimization problem estimates the magnitude of model parameters (i.e., off-binding and translocation rate constants) by minimizing the distance between model unidirectional fluxes and published unidirectional (86)Rb(+) uptake curves for the A, B, and F isoforms of the NKCC2 cotransporter obtained in transfected Xenopus oocytes. By using different symmetry assumptions, NKCC2 models with five, six, seven, or eight parameters were evaluated. The optimization method identified parameter sets that yielded computed unidirectional fluxes consistent with the uptake data. However, the parameter values were not unique, in that systematic exploration of the parameter space revealed alternative parameter sets that fit the data with similar accuracy. Finally, we demonstrate that the optimization method can identify parameter sets for the three transporter isoforms that differ only in ion binding affinities, a result that is consistent with a published mutagenesis analysis of the molecular and structural bases for the differences in (86)Rb(+) uptake among the A, B, and F isoforms. These NKCC2 cotransporter models will facilitate the development of larger scale models of ion transport by thick ascending limb cells.

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.

The Influence of Alpha-fetoprotein on Natural Suppressor Cell Activity and Ehrlich Carcinoma Growth.

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 (1.100>rho>1.090 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.

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.

Prolonged residence of temperate natives in the tropics produces a suppression of sweating.

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<0.0001), and AXR(1) (P<0.0004), AXR(2) (P<0.0001), and DIR (P<0.0001) sweating responses were larger in JRJ than in TRJ. AXR and DIR sweating volumes (P<0.0001) were negatively correlated, and sweat onset times (P<0.0001) were positively correlated with the duration of residence in the tropics (2 to 13 years). The observed attenuation of sweating in TRJ suggests that temperate natives may acquire heat tolerance with improved sweating economy similar to tropical natives after prolonged residence in the tropics.