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The thermohydraulic effect of microstructuring of the heat transfer surfaces of plate heat exchanger was studied experimentally. The aim of this enhancement strategy is to raise the heat transfer coefficient for the evaporation and condensation of the refrigerant in a vapor compression cycle up to the same level as typical single-phase heat transfer coefficients, when water is used as a secondary fluid. This would result in a better overall heat transfer performance. Titanium herringbone corrugated plates with no microstructure, micro-bump structures created by press rolling and femtosecond-laser-produced microstructures were studied. At first studies of the microstructured plates were performed in a visualization setup using 380 × 380 mm corrugated plate segments. Heat transfer and pressure drop were measured for liquid single-phase flow and evaporation with low vapor quality (x < 0.1). For the single-phase situation, the heat transfer coefficient of the microstructured plates dropped up to 5%, depending on the mass flux, while the pressure drop is not affected. For the evaporation situation, the heat transfer coefficient increased by about 25%, while the pressure drop stayed unchanged within the measurement uncertainty range. A second set of experiments was performed in an industrial-sized vapor compression cycle using R134a with a 100 kW plate evaporator and a 150 kW plate condenser. The microstructured plates gave a very moderate increase of less than 10% in heat transfer within the condenser, but a strong increase of about 40% in the evaporator as compared to the smooth plates. [ABSTRACT FROM AUTHOR]

Numerous studies have used human chorionic gonadotrophin (HCG) administration to study the response of the primate ovary to gonadotrophin stimulation. These studies are generally performed in the luteal phase with very few studies of the follicular phase. We have studied the effect of both HCG and gonadotrophin releasing hormone (GnRH) agonist administered at the early follicular phase in normally cycling baboons (Papio cynocephalus). Five baboons were treated with increasing doses of HCG for 5 consecutive days starting on day 1 of the cycle and three untreated baboons served as controls. Follicular and luteal phase lengths were determined and serum samples were assayed for progesterone, oestradiol and 17α-OH progesterone. In a separate study, six baboons were treated with GnRH agonist (WY-40972) on days 2-6 of the cycle and saline-treated baboons served as controls (n = 5). Mean peak progesterone concentrations (± SE) during the treatment interval were 3.88 ± 0.56 ng/ml in HCG-treated baboons compared to 0.19 ± 0.07 ng/ml in controls (P <0.001). A similar significant increase (P <0.001) in serum 17α-OH progesterone concentrations was also observed (6.13 ± 1.12 ng/ml versus 1.13 ± 0.49 ng/ml). In association with the increase in luteal steroids there was also a significant prolongation of menstrual cycle length from 32.7 ± 1.2 days in controls to 46.8 ± 4.9 days in HCG-treated baboons (P <0.05), which involved prolongation of the follicular phase (16.7 ± 1.2 days to 29.0 ± 4.6 days, P <0.05) with no difference in luteal phase length or progesterone concentrations. In GnRH agonist-treated baboons, mean (± SE) cycle length was prolonged to 46.3 ± 1.6 days and in saline-treated controls was 32.8 ± 0.8 days (P <0.001), again this was completely represented by the change in follicular phase length, from 13.4 ± 0.7 days in controls to 27.2 ± 2.1 days in agonist-treated baboons (P <0.001). In contrast, there was no significant difference in luteal phase length between these two groups (19.4 ± 0.7 versus 19.2 ± 1.0 days). The prolongation of the follicular phase was accompanied by significant increases in both progesterone (P <0.01) and oestradiol (P <0.01) during GnRH agonist treatment above control concentrations. Luteal phase concentrations of these hormones were not different from controls. These results demonstrate the previously unreported finding that gonadotropin stimulation will rescue the corpus luteum in the next follicular phase. [ABSTRACT FROM PUBLISHER]

Objective: To determine if free beta-human chorionic gonadotropin (hCG) serum levels at the 10th-14th week of gestation were different in groups of women who had experienced pregnancy complications., Study Design: The obstetric records of women who had uncomplicated pregnancies when they consented to donate blood for biochemical research purposes early in pregnancy were reviewed. Two hundred thirteen of these women had donated blood at the 10th-14th week of gestation. Of these, 135 had uneventful pregnancies and delivered at term, 19 delivered before 37 weeks'gestation, 10 had fetuses small for gestational age, 4 developed pregnancy-induced hypertension, 7 developed gestational diabetes, 10 aborted spontaneously, 4 had an intrauterine fetal death after 20 weeks' gestation, and 24 were lost to follow-up. After the clinical groups had been identified, the 213 maternal serum stored samples were thawed and free beta-hCG measured by enzyme-linked immunosorbent assay. After normalization of the data, ANOVA was used to compare mean gestational age and mean free beta-hCG levels within groups., Results: The overall mean gestational age at maternal blood sampling was 12.5 weeks. All groups had similar gestational ages at blood sampling (P = .18). The overall mean free beta-hCG serum level was 18.05 mIU/mL. Only the group of women who went on to experience spontaneous abortions had significantly lower free beta-hCG lev- els (mean, 10.45 mIU/mL; P < .03), Conclusion: Our data suggest that of the groups with obstetric complications evaluated, only the group of women who experienced spontaneous abortions had significantly different serum levels of free beta-hCG at the 10th-14th week of gestation.

Objective: A number of investigations have examined the effect of exercise on leptin concentrations, because leptin is associated with obesity, satiety, and reproductive function. High-intensity exercise is known to increase testosterone, an inhibitor of leptin. The objective of the study was to determine whether the leptin responses to a progressive, intermittent exercise protocol were related to serum testosterone concentrations. Most previous studies have examined leptin responses to low or moderately high exercise intensities. A second objective was to determine whether leptin responses were different than previous experiments using intermittent moderate and high-intensity exercise., Methods: Well-trained runners completed strenuous intermittent exercise consisting of treadmill running at 60, 75, 90, and 100% VO(2 max) and a subsequent resting control trial was also conducted., Results: There were significant increases in mean serum levels of leptin and testosterone with both quickly returning to baseline during recovery, but no relationship between the two hormones was found. After examining individual data for both hormones, it was discovered that subjects could be classified as leptin responders or nonresponders, whereas testosterone increased in all subjects. Responders had elevated serum leptin levels at baseline and exhibited increases after high-intensity exercise, whereas nonresponders did not show changes in leptin during exercise., Conclusions: Data suggest testosterone levels do not acutely affect leptin responses to exercise or 1-h of recovery. Moreover, varied leptin responses to intense exercise in comparable well-trained runners was observed and was associated with baseline leptin concentrations.

We determined developmental changes in circulating levels of the soluble leptin receptor (sOB-R), leptin, and gonadal hormones in human subjects. In both sexes the rise in leptin with age was associated with a decline in sOB-R, and age-related changes in both parameters preceded the pubertal rise in gonadal hormones. Leptin levels above 10 ng/ml were a strong predictor of sOB-R concentrations, but this predictive value decreased as leptin declined. In young subjects there were no gender differences in serum leptin, but boys had higher sOB-R levels. In adults neither leptin nor sOB-R changed with age, but serum leptin was higher and sOB-R was lower in women than men. There was a significant negative correlation between sOB-R and leptin in women, but not men. The data suggest that bioavailable leptin in the circulation may be increasing more rapidly during development than indicated by total leptin levels, and that these changes may serve as one of the signals to the central nervous system that metabolic conditions are adequate to support pubertal development. Furthermore, the study provides suggestive evidence that leptin regulates the secretion of its own binding protein, but it also appears that an additional gender-specific, leptin-independent, regulatory mechanism is functional before puberty.

Objectives: We sought to determine what differences, if any, existed between white and Mexican American women with polycystic ovary syndrome (PCOS) and whether the same values for fasting insulin, fasting glucose/insulin ratio, and homeostasis model assessment (HOMA) might be applied when screening both ethnic groups for insulin resistance., Study Design: Eighty-three consecutive women suspected to have PCOS but who demonstrated absence of other endocrine disorders comprised the study population. Nineteen healthy ovulatory women volunteered as controls. Fasting serum samples were obtained for determination of thyroid-stimulating hormone (TSH), prolactin, glucose, insulin, free and total testosterone, 17-hydroxyprogesterone, and dehydroepiandrosterone sulfate in the early proliferative phase. An oral glucose load was administered, and blood samples for glucose and insulin were drawn at 1, 2, and 3 hours. Those with impaired glucose tolerance or diabetes mellitus were excluded from our final study population. Four different groups were defined: (1) women with PCOS and insulin resistance, (2) women with PCOS without insulin resistance, (3) women with irregular cycles but without PCOS or another identifiable endocrinopathy, and (4) regular, cycling control subjects. Each group was subdivided by ethnicity (white or Mexican American). A total of 65 white and 37 Mexican American women were studied, including control subjects., Results: Among all study participants, Mexican American women with PCOS had significantly higher mean values for body mass index, fasting insulin, and HOMA but lower mean fasting glucose/insulin levels than white women. When group 1 patients (PCOS with insulin resistance) were compared between ethnic groups, mean fasting insulin and HOMA levels were significantly lower and glucose/insulin ratios higher in white than in Mexican American women. A single cutoff value for insulin resistance in PCOS was insensitive when applied to both ethnic groups. A fasting insulin value >20 microU/mL, HOMA value > 3.8, and glucose/insulin value <7.2 were reasonable screening values in our population of white women, whereas a fasting insulin value >23 microU/mL, HOMA value >4.5, and glucose/insulin ratio <4.0 were feasible screening values in Mexican American women., Conclusions: We conclude that (1) Mexican American women with PCOS are more insulin resistant than white women, (2) the incidence of insulin resistance is higher in Mexican American women with PCOS than in white women, (3) a single "screening" value for PCOS-related insulin resistance screening cannot be applied to both white and Mexican American women, and (4) normative values for insulin resistance screening in the PCOS population should be individualized for different racial or ethnic populations.

Leptin, a product of both adipose tissue and the placental syncytiotrophoblast and a potential regulator of primate conceptus development, increases in the maternal circulation with advancing gestation. This increase may be potentiated by estrogens, which also increase as pregnancy progresses. In the present study adipose tissue was collected from nonpregnant (n = 5) baboons (Papio sp) and in baboons during early (days 58-62; n = 5), mid (days 98--102; n = 5), and late (days 158-162; n = 5) pregnancy (term, approximately 184 days). Additionally, placental estrogen production was inhibited in pregnant baboons by the removal of fetal androgen precursors via fetectomy at midgestation, with tissues collected from fetectomized (n = 5) baboons approximately 60 days later. Leptin, estrogens, and androgens were quantitated in maternal serum by RIA. Leptin (LEP) and leptin receptor (LEP-R(L) and LEP-R(S) isoforms) messenger ribonucleic acids (mRNAs) were quantitated by competitive RT-PCR, and leptin concentrations were determined by RIA in maternal adipose and placental villous tissues. Although LEP transcript abundance in adipose tissues was unchanged as a result of pregnancy or with advancing gestation, the leptin protein level was higher (P < 0.02) in pregnant baboons in early gestation than in nonpregnant baboons and increased with gestational age (P < 0.04). Maternal serum estrogens (estradiol and estrone) and androgens (androstenedione and testosterone) were lower (P < 0.0001) in fetectomized baboons than in intact controls. Serum leptin concentrations were unchanged by fetectomy, but the abundance of LEP mRNA transcripts was lower (P < 0.003) in sc adipose tissue and 3-fold higher (P < 0.05) in placenta. Similarly, the leptin protein level declined (P < 0.05) in sc adipose tissue and increased (P < 0.05) in placenta in fetectomized baboons. Although LEP-R(L) mRNA levels were unchanged after fetectomy, placental LEP-R(S) transcript abundance was lower (P < 0.04) than in pregnancy-intact baboons matched for gestational age. Results suggest that both adipose tissue and the placenta may contribute to maternal hyperleptinemia during normal primate pregnancy. Furthermore, the withdrawal of placental steroids results in the enhanced placental leptin production that is commensurate with a decline in production by sc adipose tissue.

This case-controlled study consisted of 2 parts. The objective of part 1 was to determine the relationship between DHEA, body mass index (BMI), and age in young males, young females, and postmenopausal (PM) females. Part 2 examined the effects of estrogen on DHEA by analyzing the relationship between DHEA and age in young females on and off oral contraceptives (OCs) and PM females on and off estrogen or hormone replacement therapy (ERT/HRT). The study was performed at the Obstetrics and Gynecology Clinic, Texas Tech Health Sciences Center-Amarillo, Exercise Physiology Laboratory at Southeastern Louisiana University, and Woman's Health Research Institute, Woman's Hospital, Baton Rouge, LA. Part 1 groups consisted of: (1) young males between the ages of 18 to 40 years; (2) normally cycling females off OCs, ages 18 to 40 years; and (3) PM females older than 40 years not receiving ERT/HRT. Part 2 groups consisted of: (1) normally cycling females on OCs, ages 18 to 40 years;, (2) normally cycling females off OCs, ages 18 to 40 years; (3) PM females 50 years or older not receiving ERT/HRT; and (4) PM females 50 years or older receiving ERT/HRT. The main outcome measure was serum DHEA concentrations. For part 1, there were significant (P <.05) inverse relationships between DHEA and age for young males; young females, off OCs; PM females, no ERT/HRT r = -.44, -.26, and -.25, respectively. There were no significant relationships between DHEA and BMI for any of the groups. DHEA concentrations were significantly higher in young males than young females even after accounting for age. For part 2, DHEA concentrations were significantly higher in young females off OCs compared with young females on OCs, and significantly higher in PM women off ERT/HRT than those on ERT\HRT. There were significant inverse relationships between DHEA and age for young females and PM females on and off ERT/HRT. From these findings, we conclude that there is an inverse relationship between DHEA and age for young males, young females off OCs, and PM females, no ERT/HRT. No relationship between BMI and DHEA was observed in these same 3 groups. These results agree with previous findings in young men, but differ from previous findings in obese young females. The data also suggest that estrogen treatment (OCs and ERT/HRT) suppresses DHEA concentrations in premenopausal and PM females, and that DHEA declines with age in PM females regardless of estrogen treatment., (Copyright 2001 by W.B. Saunders Company)

Leptin is a polypeptide hormone originally thought to be produced exclusively by adipocytes. Recently, however, both leptin messenger ribonucleic acid (mRNA) and leptin protein were identified in human placental trophoblast cells, suggesting a potential role in primate pregnancy. In the present study, venous blood samples were collected at 5-day intervals during gestation from baboons (Papio sp), an established model for the study of human pregnancy, as well as from nonpregnant baboons, and leptin concentrations were determined by RIA. Additionally, placental villous tissue was collected upon cesarean delivery at early (days 60-62; n = 5), mid (days 98-102; n = 5), and late (days 159-167; n = 5) gestation (term = approximately 184 days), and leptin mRNA was quantitated by competitive RT-PCR. Finally, in situ hybridization was employed to localize transcripts to specific placental cell types. Results determined that maternal leptin levels (mean +/- SEM), which were dramatically greater (P<0.01) than those in nonpregnant cycling baboons (1.4+/-0.1 ng/mL), increased (P<0.005) with gestational age from 63.6+/-10.4 ng/mL on day 60 of gestation to 157.8+/-16.1 near term. Levels declined to those found in cycling baboons by 15 days postdelivery. In contrast to maternal leptin concentrations, placental leptin mRNA decreased (P<0.02) with advancing pregnancy, as transcript abundance declined approximately 8-fold from early to late gestation. Maternal peripheral leptin concentrations were positively correlated (r = 0.66; P<0.001) whereas placental leptin mRNA levels were negatively correlated (r = -0.64; P<0.01) with gestational age. Expression of leptin mRNA transcripts, as evidenced by RT-PCR in villous tissue, was localized principally within syncytiotrophoblast by in situ hybridization. In summary, changes in maternal peripheral leptin concentrations and placental leptin mRNA abundance that occur commensurate with advancing gestational age may imply evolving roles for the polypeptide with advancing primate pregnancy. In this capacity, localization of leptin transcripts within the baboon syncytiotrophoblast suggests the potential for autocrine or paracrine interactions within this endocrinologically active tissue. Finally, both the similarities in leptin ontogeny in baboon and human pregnancy and the singular enhancement of maternal leptin levels inherent throughout baboon gestation emphasize the potential of this nonhuman primate model for the study of leptin action in the maternal-fetoplacental unit.