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+/-0.5degrees C water, 30 min) after summer and winter seasonal acclimatization (SA). Testing was performed in July during the summer, 2011 [summer-SA; temp, 25.6+/-1.8degrees C; relative humidity (RH), 82.1+/-8.2%] and in January during the winter, 2012 (winter-SA; temp, -2.7+/-2.9degrees C; RH, 65.0+/-13.1%) in Cheonan (126degrees52'N, 33.38'E), Republic of Korea. All experiments were carried out in an automated climatic chamber (temp, 25.0+/-0.5degrees C: 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.

Effects of Ascorbic Acid on Osteoblast Differentiation in MC3T3-E1 Cells

OBJECTIVE: Vitamin C is an essential agent for cell differentiation for cell. However, for osteogenic differentiation a combined medium of vitamin C, phosphoglyceride and dexamethasone is used. Individual effect of vitamin C can be observed in terms of cell growth and proliferation and eventual differentiation to assess the effect of this chemical agent for using as bone growth. This work investigates the dose dependent effect of vitamin C on MC3T3-E1 type pre-osteoblast cell on cell proliferation and differentiation. METHODS: To investigate the dose dependent effect of vitamin C on MC3T3-E1 type pre-osteoblast cell predetermined amount of vitamin C was added to the medium and the medium was used for cell culture and cell differentiation. Relative cell viability and cell proliferation were checked to see the effect of vitamin C. Effect of dose dependent gene expression was carried out by reverse transcription-polymerase chain reaction with osteogenic differentiation specific genes. RESULTS: Cell viability and cell proliferation was increased in all culture time. The pre-osteoblast cells show significantly higher expression of osteoblast formation specific gene alkaline phosphatase, osteocalcin, and osteopontin at a higher dose of vitamin C. CONCLUSION: Higher doses of vitamin C with 50 microg/uL could significantly enhance the cell proliferation.

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.

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 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 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.

Long-Term Tropical Residency Diminishes Central Sudomotor Sensitivities in Male Subjects

Tropical natives (TROP) are capable of tolerating tropical heat because of their long-term adaptation to tropical environments. When exposed to heat stress, these natives tend to respond with lower sweat output, which is generally thought to be the result of heat acclimatization. The main objective of this study was to clarify central mechanisms inherent to suppressed thermal sweating in tropical natives (Malaysians) by comparing their sweating responses to those of temperate native (TEMP) (Koreans). This experiment was conducted in a thermoneutral climatic chamber (24+/-0.5 degrees C, 40+/-3% relative humidity). Heat loads were applied to each subject by the immersion of their lower legs in a hot water bath (43 degrees C for 30 min). Sweat onset-time and sweat volume were compared between TROP and TEMP. The sweat onset-times on four selected points on the body ranged from 10.25 to 13.47 min in TEMP subjects, and from 16.24 to 17.83 min in TROP subjects (p<0.001). The local sweat volumes at the same sites ranged from 4.30 to 9.74 mg/cm2 in TEMP subjects, and from between 1.80 to 4.40 mg/cm2 in TROP subjects (p<0.001). These results demonstrated a significant difference between TROP and TEMP subjects with regard to the manner in which they regulate their body temperatures when exposed to heat loads, and verified that long-term thermal adaptation blunts sweating sensitivities.

Comparison of Interleukin-8 Levels in Long-Distance Runners and Healthy Sedentary Non-Athletic Control Subjects

We have previously demonstrated that the level of leukocytes and neutrophils significantly increased immediately and 30 min after exercise. Interleukin-8 (IL-8) is an inflammatory cytokine that acts as a chemokine on neutrophils. In the present study, we evaluated the correlation between the number of neutrophils and leukocytes, and between the number of neutrophils and plasma IL-8 level. Long-distance trained runners (TRs, n = 10) and untrained sedentary control subjects (SEDs, n = 10) ran for one hour at 70% of heart rate reserve. In the TR, the number of neutrophils correlated significantly with the number of leukocytes in the blood. However, there was no correlation between the number of neutrophils and the plasma IL-8 concentration in both groups. Expressions of IL-8 protein and mRNA were markedly higher in the TRs as compared to the SEDs at three time intervals (pre-exercise, immediately after exercise, and post exercise). In conclusion, our results show that 1) the neutrophil level was dependent on the level of leukocytes 2) there was no correlation between the neutrophils count and plasma IL-8 concentration and 3) a higher plasma IL-8 level in athletes may be a unique characteristic of intensive training.

Sweating by Exercise Controls Body Temperature through Increase of Interleukin-1beta

This study was designed to investigate the expression and production of interleukin-1beta (IL-1beta) in human peripheral blood of trained runners and untrained controls after temporary moderate intensity exercise. Male long-distance trained runners (TR) and untrained sedentary control subjects (SED) ran for 1 h at 70% of heart rate reserve (HRR). IL-1beta gene and protein expressions were significantly higher in TR than those with SED at all 3 intervals examined independently. Significant increases in total sweat volume and oral temperature were observed after exercise in both groups, however, there were some differences between the groups. We conclude, therefore, that sweating due to exercise is associated with increase of IL-1beta and it is correlated with decrease of oral temperature.

Economical Sweating Function in Africans: Quantitative Sudomotor Axon Reflex Test

People in tropics have the ability to tolerate heat by residential permanence in the tropics. Previously, we have shown that African and Thai subjects who lived for whole their lives in only their respective countries sweat less under hot conditions than South Koreans who also lived whole their lives in Korea. The difference in sweating responses was attributed to the dissimilar central and peripheral sweating mechanisms operating in people from both groups. In the present study, acetylcholine (ACh), the primary transmitter for the sudomotor functions, was iontophoretically administered to South Koreans and Africans to determine the characteristic sudorific responses of their acclimatized biologic make-up to their respective environments. Using quantitative sudomotor axon reflex test (QSART), direct (DIR) and axon reflex (AXR) responses were evaluated. The findings revealed that the sweat onset-time among South Koreans was 0.91 min earlier than among Africans (P< 0.01). The axon reflex sweat volume of nicotine receptor activity AXR (1) and sweat volume of muscarinic receptor activity DIR (2) among South Koreans were 79% and 53% greater (P< 0.01), respectively. These results indicate that the reduced thermal sweating among Africans is at least in part attributed to the diminished sensitivity of sweat glands to ACh.

Mechanisms of Increase in Renal Blood Flow During Partial Ureteral Obstruction in Dogs / 대한신장학회잡지

Although tubuloglomerular feedback (TGF) is involved in ureteral obstruction-induced increase in renal blood flow (RBF), its contribution to RBF is not well established due to the concommitant increases in prostaglandin (PG) and renal interstitial fluid pressure (Pisf), both of which affect RBF one way or the other. Since Pisf and TGF are closely affected by renal hemodynamics, RBF will respond differently to increases in ureteral pressure depending on renal hemodynamic conditions. Therefore, the purpose of the present study was to investigate how the changes in renal hemodynamics affect the response of RBF to increases in ureteral pressure. The effect of PG on RBF was assessed by comparing the effects obtained before and after indomethacin, a cyclooxygenase inhibitor. Six anesthetized dogs were prepared with flow probes and inflatable silastic occluder around the renal artery, the ureteral catheter with its free end attached to a water reservoir, and the arterial and venous catheters. RBFs were obtained at ureteral pressures of 0, 15, and 40cmH2O during the maintenance of the renal artery pressure (RAP) at the level of systemic arterial pressure, 10mmHg above and below the lower autoregulatory limit of RBF (65+/-4 mmHg) both before and after indomethacin administration (10mg/kg). In response to the ureteral pressure of 40cmH2O, RBF increased from 172+/-6 to 185+/-10ml/min when RAP's were equal to systemic arterial pressure and decreased from 162+/-10 to 120+/-9 ml/min when RAP's were 55+/-4mmHg. Indomethacin pretreatment, depending on the level of RAP either prevented an increase or augmented a decrease in RBF in response to ureteral pressure elevation. This suggests that RAP-dependent changes in susceptibility of the renal venous system to compression by increased Pisf is the main mechanism by which the changes in renal perfusion pressure modulate the response of RBF to ureteral pressure elevation.

Prostaglandin in regulations of renal blood flow during partial ureteral obstruction in dogs

Ureteral obstruction causes increase in renal blood flow (RBF) and partial impairment of the autoregulation of RBF. Although increased renal prostaglandin production is responsible for the former, it is not clear whether or not it is also responsible for the latter. Therefore, we investigated the role which prostaglandins play in the autoregulation of RBF during an ureteral pressure elevation (40 cmH2O). Since the major mechanism of RBF autoregulation is the tubuloglomerular feedback studying the interaction between ureteral pressure and RBF autoregulation may reveal the role of prostaglandin in tubuloglomerular feedback. To pursue the purpose, six anesthetized dogs were prepared for the measurements of RBF, mean systemic and renal arterial pressure (RAP) and the manipulation of ureteral pressure. The autoregulation curves were determined during both control and elevation of the ureteral pressure, before and after the pretreatment with indomethacin, a cyclooxygenase inhibitor. The desired ureteral pressure was achieved by vertically elevating the water-filled reservoir connected to the ureteral catheter to 40 cm above the kidney level. In response to the elevation of the ureteral pressure, RBF increased from 170 +/- 8 ml cntdot min -1 to 189+/-8, and the systemic arterial pressure didn't change significantly. During spontaneous urine flow, RBF autoregulation was abolished when RAP was reduced to 59+/-3 mmHg. On the other hand, during the ureteral pressure elevation, the autoregulation curves shifted upward and rightward from control, and the pressure when RBF autoregulation was abolished was 74 +/- 3 mmHg. The pretreatment of the dogs with indomethacin failed to affect the lower limit of RBF autoregulation during both control (63 +/- 5 mmHg) and the elevated ureteral pressure (77 +/- 5 mmHg). Since RBF failed to increase in response to the elevated ureteral pressure, RBF autoregulation curves obtained during the elevated ureteral pressure shifted only rightward from indomethacin control. The results indicate that the increased intrarenal level of prostaglandin or prostaglandin-induced vasodilation does not appear to bear any relation to the reduction in the autoregulatory capacity during partial ureteral obstruction. It seems that the partial impairment of the autoregulation during acute ureteral obstruction is due to the consumption of tubuloglomerular feedback mechanism at spontaneous RAP and that prostaglandin is neither mediator nor effector of tubuloglomerular feedback mechanism.