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Relationship between capillary angiogenesis, fiber type, and fiber size in chronic systemic hypoxia. Am J Physiol Heart Circ Physiol 281: H241-H252, 2001.--Whether chronic hypoxia causes angiogenesis in skeletal muscle is controversial. Male Wistar rats, 5-6 wk of age, were kept at constant 12% 02 for 3 wk, and frozen sections of their postural soleus (SOL), phasic extensor digitorum longus (EDL), and tibialis anterior (TA) muscles were compared with those of normoxic controls. Capillary supply increased in SOL muscles [capillary-to-fiber ratio (C/F) = 2.55 [+ or -] 0.09 hypoxia vs. 2.17 [+ or -] 0.06 normoxia; capillary density (CD) = 942 [+ or -] 14 hypoxia vs. 832 [+ or -] 20 [mm.sup.-2] normoxia, P [is less than] 0.01] but not in EDL muscles (C/F = 1.44 [+ or -] 0.04 hypoxia vs. 1.42 [+ or -] 0.04 normoxia; CD = 876 [+ or -] 52 hypoxia vs. 896 [+ or -] 24 [mm.sup.-2] normoxia). The predominantly glycolytic cortex of TA muscles showed higher C/F after hypoxia (1.79 [+ or -] 0.09 vs. 1.53 [+ or -] 0.05 normoxia, P [is less than] 0.05), whereas the mainly oxidative TA core with smaller fibers showed no change in capillarity. The region of the SOL muscle with large-sized (mean fiber area 2,843 [+ or -] 128 [micro][m.sup.2]) oxidative fibers (90% type I) had a higher C/F (by 30%) and CD (by 25%), whereas there was no angiogenesis in the region with sparse (76%) and smaller-sized (2,200 [+ or -] 85 [micro][m.sup.2]) type I fibers. Thus systemic hypoxia differentially induces angiogenesis between and within hindlimb skeletal muscles, with fiber size contributing either directly (via a metabolic stimulus) or indirectly (via a mechanical stimulus) to the process. capillary growth; histochemistry; hypoxemia; oxygen transport; rat

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Puberty and metamorphosis are two major developmental transitions linked to the reproductive maturation. In mammals and vertebrates, the central brain acts as a gatekeeper, timing the developmental transition through the activation of a neuroendocrine circuitry. In addition to reproduction, these neuroendocrine axes and the sustaining genetic network play additional roles in metabolism, sleep and behavior. Although neurohormonal axes regulating juvenile-adult transition have been classically considered the result of convergent evolution (i.e., analogous) between mammals and insects, recent findings challenge this idea, suggesting that at least some neuroendocrine circuits might be present in the common bilaterian ancestor Urbilateria. The initial signaling pathways that trigger the transition in different species appear to be of a single evolutionary origin and, consequently, many of the resulting functions are conserved with a few other molecular players being co-opted during evolution., Competing Interests: DD was employed by company Sartorius Netherlands BV. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Barredo, Gil-Marti, Deveci, Romero and Martin.)

Background/aim: Basal level of follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2), and antral follicle count are used as predictors of ovarian reserve before starting ovulation induction. We aimed to investigate the predictor potential of early follicular phase FSH/LH ratio on controlled ovarian hyperstimulation-intracytoplasmic sperm injection (COH-ICSI) cycle outcomes., Materials and Methods: This retrospective cohort study was conducted with 648 COH-ICSI cycles performed between 2012 and 2014. Cycles were classified according to their basal FSH/LH ratio, group 1(G1) = FSH/LH ratio < 2, N = 473 and group 2(G2) = FSH/LH ratio ≥ 2, N = 175. Demographic characteristics and stimulation parameters were evaluated. Retrieved total oocyte count (TOC), mature oocyte count (MOC), transferred embryo number, and pregnancy results were obtained and transferred to computer by SPSS 21.0 programme., Results: TOC and MOC of G1 were significantly higher than those of G2. The total gonadotrophin doses of G2 were significantly higher than G1. There was no significant difference between groups for transferred embryo number. Pregnancy and live birth rates were similar in both groups., Conclusion: In our population, increased FSH/LH ratio did not affect the rates of pregnancy and live birth negatively., Competing Interests: The authors declare that there is no conflict of interest to disclose., (This work is licensed under a Creative Commons Attribution 4.0 International License.)

Background/aim: To investigate the possible differences in endometrial leukocyte subtype distribution between women with unexplained infertility and normal fertile women and to determine whether there is a correlation between endometrial leukocyte counts and plasma cytokine levels in unexplained infertility. Materials and methods: This case-control study involved 79 infertile and 40 fertile women. Peripheral venous blood samples and endometrial samples were obtained on day 21 of the menstrual cycle. Plasma interleukin-4 (IL4), IL6, IL10, IL17, IL35, interferongamma (IFN-g), tumor necrosis factor-alpha (TNF-a), transforming growth factor-beta (TGF-b), and suppressor of cytokine signaling-3 (SOCS3) levels were determined by enzyme-linked immunosorbent assay. Endometrial CD8, CD56, and CD163 counts were detected by immunohistochemistry. Results: CD8 and CD56 counts were significantly higher, while CD163 count was significantly lower in infertile women than in fertile women. Plasma SOCS3, IL35, and IL4 levels of the infertile group were significantly lower than those of the fertile group (P < 0.01); the remaining cytokine levels were significantly higher in the infertile group than in the fertile group (P < 0.01). Conclusion: We observed aberrant cytotoxic immune activity in infertile women. The interaction between plasma SOCS3 levels and staining degree of endometrial leukocytes may be either the reason for or result of infertility leading to unavailability of the environment for implantation.

Aim: To investigate the effectiveness of intraperitoneal vitamin C (VC) and vitamin E (VE) in the prevention of postoperative adhesion formation in a rat uterine horn model., Methods: Twenty-eight Wistar albino rats were divided into four groups in which: control group, the abdomen was opened and closed without any intervention; adhesion group, a 2-cm linear incision was performed on the uterine horn and closed; VC group, VC was administrated i.p., and 15 min later a 2-cm incision was performed on the uterine horn and closed; and VE group, VE was administrated i.p., and 15 min later a 2-cm incision was performed on the uterine horn and closed. Re-laparotomy was performed 15 days later. Right uterine horn adhesions were evaluated according to macromorphological characteristics and tissue sections were further examined for fibrosis, angiogenesis and vascular endothelial growth factor (VEGF), type I collagen and malondialdehyde (MDA) scoring. Kruskal-Wallis anova and Mann-Whitney U-test were utilized for statistical analysis., Results: Adhesion area and also strength were significantly lower in the VC group and the VE group compared with the adhesion group. Fibrosis and angiogenesis scores were observed to be significantly higher in the adhesion group compared with the VC group and the VE group. MDA and VEGF immunoreactivity were also found to be significantly lower in the VC group and the VE group compared with the adhesion group. However, there was no significant difference between the VC group and the VE group with respect to all the above parameters., Conclusion: Administration of VC or VE i.p. was observed to be effective in the prevention of postoperative adhesion formation in an experimental model., (© 2014 The Authors. Journal of Obstetrics and Gynaecology Research © 2014 Japan Society of Obstetrics and Gynecology.)

Objective: To investigate the plasma levels of interleukin-4 (IL-4), IL-6, IL-10, tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), transforming growth factor-beta (TGF-beta), IL-17, IL-35 and suppressor of cytokine signaling 3 (SOCS3) in the women with history of idiopathic recurrent pregnancy loss (RPL) and in the fertile controls., Methods: This study was conducted with 60 idiopathic RPL cases and 40 age-matched fertile controls. Mid-follicular plasma levels of IL-17, IFN-gamma, TNF-alpha, TGF-beta, IL-6, IL-4, IL-10, SOCS3 and IL-35 were assayed by an enzyme linked immunosorbent assay., Results: The mean age of RPL and control cases were 31.6 ± 0.6 and 32.1 ± 0.7 years, respectively. While plasma IL-35 and SOCS3 levels of RPL group were significantly lower than that of the control group; IFN-gamma, TNF-alpha, IL-4, IL-6, IL-10, IL-17 and TGF-beta levels of RPL group were significantly higher than that of the control group. The comparison of cytokine ratios between RPL and control groups indicated significantly high TNF-alpha/IL-10, TNF-alpha/IL-4, IFN-gamma/IL-10, IFN-gamma/IL-6 and IFN-gamma/IL-4 ratios in the RPL group. IL-35/IL-17 ratio was significantly low in the RPL group compared to that in the control group. Overstimulation of TNF-alpha presented moderate influence on recurrent miscarriage risk., Conclusion: Decreased SOCS3 and IL-35 plasma levels and increased Th1/Th2 cytokine ratios in RPL cases pointed out the supression of anti-inflammatory process and this supression might play an important role in the pathogenesis of idiopathic RPL.

Unlabelled: Abstract Objective: To research the hypothesis of preeclampsia (PE) is associated with increased systemic inflammatory responses of Th1-type as well as decreased Th2-type responses; we evaluated the maternal plasma levels of IFN-gamma, TNF-alpha, TGF-beta, IL-4, IL-6, IL-10, IL-17, IL-35 and SOCS3 in preeclamptic and healthy pregnants., Methods: This study was conducted with 40 preeclamptic (study group) and 40 normotensive pregnant (control) women in third trimester when they were admitted to the labor and delivery unit. The extracted maternal plasma samples were assayed by an enzyme-linked immunosorbent assay. Statistical analysis was performed by SPSS 16.0 version., Results: While IFN-gamma and TGF-beta levels of preeclamptic women were significantly higher (p < 0.01), IL-35 and IL-17 levels of preeclamptic women were significantly lower (p < 0.01) than those of controls. The ratios of IFN-gamma/IL-10, IFN-gamma/IL-6, IFN-gamma/IL-4 were significantly high and ratio of IL-35/IL-17 was significantly low in the PE group compared to those in the control group. Maternal plasma SOCS3 levels showed negative correlation with blood pressure and proteinuria severity, but none of the cytokines showed influence on blood pressure and proteinuria after adjusting for maternal and gestational age., Conclusions: Increased IFN-gamma/TGF-beta production and reduced IL-35/IL-17/SOCS3 production in preeclamptic women may lead to less cytokine inhibitory activity in PE, which may account for the increased proteinuria and blood pressure in PE.

Implantation necessitates complex interactions among the developing embryo, decidualizing endometrium, and developing maternal immune tolerance and/or alterations in cellular and humoral immune responses. Overstimulation of T helper 1 (Th1) or Th2 cytokines in systemic and local environments, alterations of the prevalence of IL17 and regulatory T cell (Treg) cytokines have also been suggested to contribute to the pathogenesis of implantation failure. We aimed to investigate the plasma levels of IL4, IL6, IL10, TNFα, IFNγ, TGFβ, IL17, IL35, and SOCS3 in infertile and fertile women. This case-control study was conducted with 80 women suffering from unexplained infertility and 40 fertile women. Peripheral venous blood samples were drawn on day 21 of the menstrual cycle. The extracted plasma samples were assayed by an enzyme linked immunosorbent assay. Statistical analysis was performed using SPSS version 16.0. Our main findings were as follows: despite the significantly high IL17 and IL35 plasma levels of infertile women, IL35/IL17 ratio was significantly lower in the infertile group compared with that in the fertile group; SOCS3 plasma levels showed an inverse relation with plasma levels of all cytokines except IL35; increased plasma IL17 levels (>3.42 pg/mL) have a negative impact on fertility; TNFα/IL10, IFNγ/IL10, IFNγ/IL6, and IFNγ/IL4 ratios were significantly higher in infertile group compared with those in the fertile group. It is not possible to show the major immunological factor(s) of unexplained infertility, but our findings point out that the decreased suppressor activity of the immune system may play a role in implantation failure., (Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)

The thermal challenge associated with cold acclimation (CA) and hibernation requires effective cardio-respiratory function over a large range of temperatures. We examined the impact of acute cooling in a cold-naïve hibernator to quantify the presumed improvement in cardio-respiratory dysfunction triggered by CA, and estimate the role of the autonomic nervous system in optimising cardiac and respiratory function. Golden hamsters (Mesocricetus auratus) were held at a 12 h:12 h light:dark photoperiod and room temperature (21°C euthermic control) or exposed to simulated onset of winter in an environmental chamber, by progression to 1 h:23 h light:dark and 4°C over 4 weeks. In vivo acute cooling (core temperature Tb=25°C) in euthermic controls led to a hypotension and bradycardia, but preserved cardiac output. CA induced a hypertension at normothermia (Tb=37°C) but on cooling led to decreases in diastolic pressure below euthermic controls and a decrease in cardiac output, despite an increase in left ventricular conductance. Power spectral analysis of heart rate variability suggested a decline in vagal tone on cooling euthermic hamsters (Tb=25°C). Following CA, vagal tone was increased at Tb=37°C, but declined more quickly on cooling (Tb=25°C) to preserve vagal tone at levels similar to euthermic controls at Tb=37°C. For the isolated heart, CA led to concentric hypertrophy with decreased end-diastolic volume, but with no change in intrinsic heart rate at either 37 or 25°C. Mechanical impairment was noted at 37°C following CA, with peak developed pressure decreased by 50% and peak rate-pressure product decreased by 65%; this difference was preserved at 25°C. For euthermic hearts, coronary flow showed thermal sensitivity, decreasing by 65% on cooling (T=25°C). By contrast, CA hearts had low coronary flow compared with euthermic controls, but with a loss of thermal sensitivity. Together, these observations suggest that CA induced a functional impairment in the myocardium that limits performance of the cardiovascular system at euthermia, despite increased autonomic input to preserve cardiac function. On acute cooling this autonomic control was lost and cardiac performance declined further than for cold-naïve hamsters, suggesting that CA may compromise elements of cardiovascular function to facilitate preservation of those more critical for subsequent rewarming.

The consequences of acute hypothermia include impaired cardiovascular performance, ultimately leading to circulatory collapse. We examined the extent to which this results from intrinsic limitations to cardiac performance or physiological dysregulation/autonomic imbalance, and whether chronic cold exposure could ameliorate the impaired function. Wistar rats were held at a 12 h:12 h light:dark (L:D) photoperiod and room temperature (21°C; euthermic controls), or exposed to a simulated onset of winter in an environmental chamber by progressive acclimation to 1 h:23 h L:D and 4°C over 4 weeks. In vivo, acute cold exposure (core temperature, T(b)=25°C) resulted in hypotension (approximately -20%) due to low cardiac output (approximately -30%) accompanying a bradycardia (approximately -50%). Cold acclimation (CA) induced only partial compensation for this challenge, including increased coronary flow at T(b)=37°C (but not at T(b)=25°C), maintenance of ventricular capillarity and altered sympathovagal balance (increased low:high frequency in power spectral analysis, PSA), suggesting physiological responses alone were insufficient to maintain cardiovascular performance. However, PSA showed maintenance of cardiorespiratory coupling on acute cold exposure in both groups. Ex vivo cardiac performance revealed no change in intrinsic heart rate, but a mechanical impairment of cardiac function at low temperatures following CA. While CA involved an increased capacity for β-oxidation, there was a paradoxical reduction in developed pressure as a result of adrenergic down-regulation. These data suggest that integrated plasticity is the key to cardiovascular accommodation of chronic exposure to a cold environment, but with the potential for improvement by intervention, for example with agents such as non-catecholamine inotropes.

Objective: To present a retrospective analysis of the prenatal diagnosis and the outcome of fetuses diagnosed with central nervous system (CNS) anomalies., Materials and Methods: We reviewed the medical records and ultrasound data of 69 cases diagnosed with CNS anomalies from 2007 to 2008. We described the prenatal diagnosis, associated findings, and outcome of these patients., Results: Sixty-nine patients were diagnosed with CNS anomalies. Of these, 31 had ventriculomegaly + hydrocephaly, 14 had spina bifida + meningomyelosel, 5 had choroid plexus cyst, 5 had Dandy Walker malformation, 3 had sacrocoxigeal teratoma, 2 had encephalosel, 1 had microcephaly, and 1 had Arnold Chiari malformation. Eight amniocentesis, three cord blood sampling, and two fetal reduction procedure were performed. Nine pregnancy termination and 36 delivery were performed. Neurosurgical correction was performed for neonates with spina bifida, hydrocephaly and sacrocoxigeal teratoma. Twenty-one neonates were discharged with cure, 4 neonates with follow-up, 7 neonates with paraplegia, and 13 neonates died., Conclusion: The outcome of fetuses with CNS anomalies was shown to depend mainly on the degree of neural tube defect and the associated anomalies were the most important factors in surviving.

The cardiovascular and ventilatory responses of the Wistar rat (a non-hibernator) and the Syrian hamster (a hibernator) to acute and chronic cold exposure were investigated. The acute lowering of core temperature (T(c) = 22 degrees C, hypothermia) compared with normothermia (T(c) = 37 degrees C) and hyperthermia (T(c) = 40 degrees C) was used to examine the underlying differences in the extent of cold adaptation. In euthermic rats, acutely induced hypothermia resulted in a pronounced reduction in heart rate (f(H) reduced by 55%; P < 0.01), a modest but significant elevation of mean arterial blood pressure (mABP increased by 16%; P < 0.05), and a marked reduction in respiratory frequency (f(R) reduced by 64%; P < 0.01). All parameters returned to baseline values on returning T(c) to 37 degrees C, with a modest overshoot on acute hyperthermia. These data are consistent with the depressive effect of low temperature on biological rate functions and increased vagal tone in the cold, while matching f(R) to a lowered metabolic rate (MO(2)). Cold acclimation had little effect on this pattern of response, suggesting that any adaptive increase in thermogenesis is limited. Euthermic hamsters also showed a significant reduction in f(H) on acute cooling (74%; P < 0.01). In contrast to rats, hamsters developed a significant decrease in mABP (52%; P < 0.01) and maintained a relatively high f(R) (4%; n.s.). These data suggest a resetting of the baroreflex and relative hyperventilation, consistent with an elevated MO(2) associated with enhanced nonshivering thermogenesis. Cold acclimation had little effect on thermal sensitivity, though the response curves were displaced to produce a relative hypertension and tachycardia at a given T(c). These data suggest a reduced cardiorespiratory coupling in the hibernator compared with the non-hibernator.

Objectives: Normal muscle growth is accompanied by capillary proliferation, which usually lags behind the increase in muscle size, causing a decline in mean capillary density (CD). It is not known, however, how the capillary distribution is affected and what impact it has on the oxygenation of the muscle., Methods: The capillarization of soleus muscles of rats (64-425 g) was determined with the method of capillary domains. As well as quantifying CD, capillary to fiber ratio (C:F), and fiber size, this method provides a measure of the heterogeneity of capillary spacing. Capillary locations were used to mathematically model oxygenation levels within the muscle., Results: The increase in muscle mass was largely attributable to 5-fold increase in fiber size, accompanied by a more than 3-fold rise in C:F. The mismatch between rates of angiogenesis and muscle growth resulted in a decrease in CD. However, the heterogeneity of capillary spacing was unaffected (heterogeneity index logRSD: 0.091 +/- 0.013; mean +/- SD) as was muscle PO2, with modal values between 4 and 60 mmHg (0.5 and 8 kPa)., Conclusions: Angiogenesis during normal muscle growth does not maintain CD, but with similar heterogeneity of capillary spacing it preserves the potential for adequate intramuscular oxygenation.

The physiological, metabolic and anatomical adaptations of skeletal muscle to chronic cold exposure were investigated in Wistar rats (Rattus norvegicus), a species that defends core temperature, and Syrian hamsters (Mesocricetus auratus), which may adopt a lower set point under unfavourable conditions. Animals were exposed to a simulated onset of winter in an environmental chamber, progressively shortening photoperiod and reducing temperature from 12 h:12 h L:D and 22 degrees C to 1 h:23 h L:D and 5 degrees C over 4 weeks. The animals were left at 4 degrees C for a further 4 weeks to complete the process of cold-acclimation. M. tibialis anterior from control (euthermic) and cold-acclimated animals of similar mass showed a significant hyperactivity-induced hypertrophy in the rat, but a small disuse atrophy in the hamster. Little evidence was found for interconversion among fibre types in skeletal muscle on cold-acclimation, and only modest differences were seen in activity of oxidative or glycolytic enzymes in either species. However, adjustments in Type II fibre size paralleled the muscle hypertrophy in rat and atrophy in hamster. Cold-induced angiogenesis was present in the rat, averaging a 28 % increase in capillary-to-fibre ratio (C:F) but, as this was balanced by fibre hypertrophy across the whole muscle, there was no change in capillary density (CD). In contrast, the C:F was similar in both groups of hamsters, whereas CD rose by 33 % in line with fibre atrophy. Within distinct regions of the m. tibialis anterior, there was a correlation between angiogenesis and fibre size in rats, in which oxygen diffusion distance increased, but not in hamsters, in which there was a reduced oxygen diffusion distance. Consequently, the change in C:F was greatest (39 %) in the glycolytic cortex region of the m. tibialis anterior in rats. We conclude that non-hibernator and hibernator rodents improve peripheral oxygen transport following cold-acclimation by different mechanisms. In rats, an increase in fibre girth was accompanied by a true angiogenesis, while the improved apparent capillary supply in hamsters was due to smaller fibre diameters. These responses are consistent with the strategies of resisting and accommodating, respectively, an annual fall in environmental temperature.

We tested the hypothesis that alterations in arterioles in locomotor skeletal muscles in rats with myocardial infarction (MI), but before development of congestive heart failure (CHF), precede structural and functional changes commonly observed in limb muscle in association with CHF. Resting diameters of third- (A3) and fourth-order arterioles (A4) in extensor digitorum longus (EDL) muscle were significantly smaller in rats with nonfailing small and medium-sized MI compared with control animals. Dilation of A4 in response to 10(-4) M adenosine was significantly attenuated in both groups (P < 0.05), whereas dilation of A3 was unaltered. Microvessels from both groups of infarcted rats constricted to all doses of acetylcholine (10(-9), 10(-8), and 10(-7) M) and showed a significantly exaggerated vasoconstrictor response to norepinephrine (10(-9), 10(-8), and 10(-7) M) compared with microvessels in control rats (P < 0.05). Peak isometric tension of combined tibialis anterior and EDL muscles and muscle fatigue (final/peak tension x 100), measured during 5-min isometric supramaximal twitch contractions at 4 Hz, were similar in control and MI rats (218 +/- 7 vs. 213 +/- 15 g/g muscle and 52 +/- 1 vs. 51 +/- 9%, respectively; n = 5 for both). There was also no difference with respect to the proportion of oxidative fibers or capillary-to-fiber ratios. Our results indicate that, in rats with left ventricular dysfunction but without failure, decreased diameter and perturbations in reactivity of small arterioles precede alterations in skeletal muscle performance often seen at a later date in association with CHF. These findings are consistent with the notion of aberrant endothelial and smooth muscle function and may contribute to the maintenance of blood pressure after MI but before CHF.