Birth In Rats Research Articles

Histopathological Changes of the Heart After Neonatal Dexamethasone Treatment: Studies in 4-, 8-, and 50-Week-Old Rats

Dexamethasone (Dex), for prevention of chronic lung disease in preterm infants, showed potential negative long-term effects. Studies regarding long-term cardiovascular effects are lacking. We investigated possible histopathological myocardial changes after neonatal Dex in the young and adult rat heart. Rats were treated with Dex on d 1, 2, and 3 (0.5, 0.3, and 0.1 mg/kg) of life. Control-pups received saline. At 4, 8, and 50 wk after birth rats were killed and anatomic data collected. Heart tissue was stained with hematoxylin and eosin, Cadherin-periodic acid schiff, and sirius red for cardiomyocyte morphometry and collagen determination. Presence of macrophages and mast cells was analyzed. Cardiomyocyte length of the Dex-treated rats was increased in all three age groups, whereas ventricular weight was reduced. Cardiomyocyte volumes were increased at 50 wk indicating cellular hypertrophy. Collagen content gradually increased with age and was 62% higher in Dex rats at 50 wk. Macrophage focus score and mast cell count were also higher. Neonatal Dex affects normal heart growth resulting in cellular hypertrophy and increased collagen deposition in the adult rat heart. Because previous studies in rats showed premature death, suggesting cardiac failure, cardiovascular follow-up of preterm infants treated with glucocorticoids should be considered.

Isoflurane Inhibits Growth but Does Not Cause Cell Death in Hippocampal Neural Precursor Cells Grown in Culture

Isoflurane causes long-term hippocampal-dependent learning deficits in rats despite limited isoflurane-induced hippocampal cell death, raising questions about the causality between isoflurane-induced cell death and isoflurane-induced cognitive function. Neurogenesis in the dentate gyrus is required for hippocampal-dependent learning and thus constitutes a potential alternative mechanism by which cognition can be altered after neonatal anesthesia. The authors tested the hypothesis that isoflurane alters proliferation and differentiation of hippocampal neural progenitor cells. Multipotent neural progenitor cells were isolated from pooled rat hippocampi (postnatal day 2) and grown in culture. These cells were exposed to isoflurane and evaluated for cell death using lactate dehydrogenase release, caspase activity, and immunocytochemistry for nuclear localization of cleaved caspase 3. Growth was assessed by cell counting and BrdU incorporation. Expression of markers of stemness (Sox2) and cell division (Ki67) were determined by quantitative polymerase chain reaction. Cell fate selection was assessed using immunocytochemistry to stain for neuronal and glial markers. Isoflurane did not change lactate dehydrogenase release, activity of caspase 3/7, or the amount of nuclear cleaved caspase 3. Isoflurane decreased caspase 9 activity, inhibited proliferation, and decreased the proportion of cells in s-phase. messenger ribonucleic acid expression of Sox2 (stem cells) and Ki67 (proliferation) were decreased. Differentiating neural progenitor cells more often select a neuronal fate after isoflurane exposure. The authors conclude that isoflurane does not cause cell death, but it does act directly on neural progenitor cells independently of effects on the surrounding brain to decrease proliferation and increase neuronal fate selection. These changes could adversely affect cognition after isoflurane anesthesia.

RNA interference for CFTR attenuates lung fluid absorption at birth in rats

BackgroundSmall interfering RNA (siRNA) against αENaC (α-subunit of the epithelial Na channel) and CFTR (cystic fibrosis transmembrane conductance regulator) was used to explore ENaC and CTFR function in newborn rat lungs.MethodsTwenty-four hours after trans-thoracic intrapulmonary (ttip) injection of siRNA-generating plasmid DNA (pSi-0, pSi-4, or pSi-C2), we measured CFTR and ENaC expression, extravascular lung water, and mortality.ResultsαENaC and CFTR mRNA and protein decreased by ~80% and ~85%, respectively, following αENaC and CFTR silencing. Extravascular lung water and mortality increased after αENaC and CFTR-silencing. In pSi-C2-transfected isolated DLE cells there were attenuated CFTR mRNA and protein. In pSi-4-transfected DLE cells αENaC mRNA and protein were both reduced. Interestingly, CFTR-silencing also reduced αENaC mRNA and protein. αENaC silencing, on the other hand, only slightly reduced CFTR mRNA and protein.ConclusionThus, ENaC and CFTR are both involved in the fluid secretion to absorption conversion around at birth.

Epinephrine administration at birth prevents long-term changes in dopaminergic parameters caused by Cesarean section birth in the rat

Obstetric complications involving birth hypoxia are implicated in the etiology of disorders with dopaminergic dysfunction, such as schizophrenia. Cesarean section (C-section) birth in both humans and rats is associated with increased mild respiratory distress and with reduced levels of circulating catecholamines at birth, which normally serve to prime the lungs and activate other processes promoting extrauterine adaptation. Using a rat model, it has been found that C-section birth can produce long-term changes in central nervous system (CNS) dopamine function, compared to vaginal birth. The present experiments tested if administering exogenous epinephrine at birth could reverse long-term changes in dopaminergic parameters in C-sectioned rats. In the absence of stress at adulthood, no differences were observed between C-sectioned and vaginally born rats in levels of in vivo tyrosine hydroxylase (TH) activity and dopamine transporter (DAT) binding. However, after repeated mild stress at adulthood, C-sectioned rats showed increased TH activity in nucleus accumbens and increased DAT in dorsal striatum and accumbens, compared to vaginally born controls. A single injection of epinephrine to C-sectioned rats just after birth prevented the increased TH activity and DAT binding seen in C-sectioned rats after repeated mild stress at adulthood. There was also a trend for epinephrine at birth to partially reverse an increase in amphetamine-induced locomotion seen in C-sectioned rats at adulthood. These results suggest that variations in levels of circulating catecholamines in the neonate at the time of birth could contribute to subtle long-term changes in CNS function.

Ontogenetic noradrenergic lesion alters histaminergic activity in adult rats

To determine whether noradrenergic nerves might have a modulatory role on the sensitivity or reactivity of histaminergic receptor systems in brain, behavioral effects of the respective histamine H1, H2 and H3 antagonists S(+)chlorpheniramine, cimetidine and thioperimide in control adult rats were compared to the effects in adult rats that had been lesioned as neonates with the noradrenergic neurotoxin DSP-4. On the 1st and 3rd days after birth rat pups were treated with either saline or DSP-4 (50 mg/kg sc), then returned to their home cages with the dam. At 8 weeks when rats were tested, S(+)chlorpheniramine (10 mg/kg ip) was found to increase locomotor activity in intact and DSP-4 lesioned rats, while cimetidine (5 mg/kg, ip) and thioperimide (5 mg/kg, ip) increased activity several-fold solely in the DSP-4 group. Exploratory activity, nociceptive activity, and irritability were little altered by the histamine antagonists, although oral activity was increased by thioperimide in intact and lesioned rats, and by cimetidine or S(+)chlorpheniramine in DSP-4 rats. High performance liquid chromatography with electrochemical detection was used to determine that DSP-4 produced a 90% reduction in frontal cortex, hippocampus and hypothalamus, with a 90% elevation of NE in cerebellum--reflecting reactive sprouting of noradrenergic fibers consequent to lesion of noradrenergic tracts projecting to proximal brain regions. These findings indicate that perinatal noradrenergic fiber lesioning in rat brain is associated with an altered behavioral spectrum by histamine H1, H2 and H3 receptor antagonists, thereby implicating histaminergic systems as modulators of noradrenergic systems in brain.

Effects of acupuncture on the intrastriatal hemorrhage-induced caspase3 expression and newly cell birth in rats

Background: Intracerebral hemorrhage is one of the most devastating types of stroke. Caspases are essential players in apoptotic cell death both as initiators and executioners. The v-Fos FBJ murine osteosarcoma viral oncogene homolog (Fos, c-Fos) is an immediate early gene, and Fos expression is sometimes used as a marker for stimuli-induced changes in the metabolic activity of neurons. The expressions of caspase3 and Fos are enhanced with neuroregeneration and with neuronal cell death, respectively. Cells proliferation the dentate gyrus of adult rodents is enhanced by certain pathologic events as seizures and ischemic insult, and such up-regulation of cell proliferation occurring during pathologic situations is thought to be a compensatory response to lesion-induced cell death in the brain. In the present study, we investigated the effects of acupuncture on the intrastriatal hemorrhage-induced caspase3 expression in the striatum and on the Fos expression and cell proliferation in the dentate gyrus of rats.Methods: For this study, immunohistochemistry for caspase3, Fos and 5-bromo-2′-deoxyuridine (BrdU) was performed.Results: Caspase3 expression in the striatum was increased by intrastriatal hemorrhage. Fos expression and cell proliferation in the dentate gyrus of rats with intracerebral hemorrhage were also increased. Acupunctural treatment, especially at the ST36 acupoint, suppressed the intracerebral hemorrhage-induced caspase3 expression in the stratum, and it also inhibited expression of Fos and cell proliferation in the dentate gyrus.Conclusion: In the present study, we have shown that acupuncture treatment has a neuroprotective effect on intrastrstriatal hemorrhage-induced neuronal cell death, and this suggests that acupuncture can aid in the recovery of the central nervous system following stroke.

The critical period for thyroid hormone responsiveness through thyroid hormone receptor isoform α in the postnatal small intestine

During second and third weeks after birth in rats, serum thyroid hormone level is elevated. In this study, we investigated the jejunal expression of thyroid hormone receptor (TR) α in developing rats. The TRα-1 mRNA level and TRα-1/TRα-2 mRNA ratio increased two-fold from 5 to 13 days after birth. This high level of TRα-1 mRNA was maintained until 20 days and then decreased to the basal level by the end of weaning period at 27 days; however, the level of TRα-2 mRNA remained unchanged throughout the developmental period. The increase in the TRα-1/TRα-2 mRNA ratio from 5 to 13 days was accompanied by an initial rise in the levels of mRNA for hexose transporters in the jejunum. Administration of T 3 during the suckling period (8–13 days) caused a 50% increase in the TRα-1/TRα-2 mRNA ratio, while administration of T 3 on days 12–17 and days 16–21, but not on days 22–27, caused a two to four-fold increase in the levels of mRNA for hexose transporters. These results suggest that a transient variation in the TRα-1/TRα-2 expression ratio is closely related to the critical period of thyroid hormone responsiveness for hexose transporters expression in the developing rat jejunum.

Formation of the structural and ultrastructural organization of the striatum in early postnatal ontogenesis of rats in altered conditions of embryonic development

Light (Nissl and Golgi methods) and electron microscopy methods were used to study the formation of the structure of the striatum during the first two weeks after birth in rats subjected to acute hypoxia at different times of embryogenesis. The dynamics of the physiological development of the same population of rats were studied in parallel. Hypoxia at day 13.5 of embryogenesis was found to lead to delayed neurogenesis (delayed establishment of elements of the neuropil and differentiation of cells) and abnormalities in the structure of the striatum (degeneration, particularly chromatolysis, of neurons and the appearance of glial nodes). Morphometric analysis demonstrated a decrease in the total number of cells in the striatum; small changes in large neurons were seen. Hypoxia at day 18.5 of embryogenesis produced no significant changes. Structural abnormalities were accompanied by changes in the process of the animals' physiological development. The data obtained here show that changes in the conditions of embryogenesis (hypoxia) during the period of the most intense proliferation of neuroblasts in the forebrain lead to impairment of the process of formation of striatal nervous tissue and the body as a whole in the period of early postnatal ontogenesis.

New Insights into Biological Roles of Relaxin and Relaxin-related Peptides

In the 1920s, a relaxin peptide was first identified in serum from pregnant guinea pigs and has been shown to play important roles in the regulation of uterine contraction and parturition [1]. The importance of relaxin signaling in the parturition process was demonstrated through a series of classic experiments involving passive immunization [2– 11]. Immunization with a monoclonal antirelaxin antibody to neutralize endogenous relaxin during the antepartum period (days 12–22 of gestation) reduces cervical growth and extensibility, and disrupts labor and birth in rats. Approximately 20–25% of fetuses and placenta were retained in utero on day 24 whereas neither fetuses nor placenta were retained in control rats [6,8]. Importantly, this treatment has no effect on the weights of other reproductive tissues (uterus, placenta, and ovary), the number of fetuses, or fetus viability [7]. Cervices obtained from antirelaxin antibody-treated rats were much smaller and less extensible than cervices obtained from control rats. Using the same approach, it was shown that relaxin also effects the growth of the vagina during pregnancy. Antirelaxin antibody treatment leads to lower vaginal wet weight, dry weight, length, diameter, inner surface area, and DNA content [8]. Biochemically, it has been shown that relaxin stimulates matrix metalloproteinase I activity in cultured guinea pig cervical cells [12], leading to degradation of the extracellular matrix. Likewise, relaxin significantly increases the secretion of active matrix metalloproteinase-2 and -9 protein into uterine fluid of gilt, leading to increased extracellular proteolysis during the remodeling of reproductive tissues [13]. In human, treatment of lower uterine segment fibroblasts with relaxin results in a higher expression of procollagenase protein and mRNA levels, stimulates prostromelysin-1 protein and mRNA levels, but inhibits expression of the tissue inhibitor of metalloproteinase1 protein [14]. In addition, treatment of human cervical stromal cells with relaxin leads to the secretion of several stromal metalloproteinases [15]. Thus, one of the major roles of relaxin in the reproductive tract is the activation of different proteases important for extracellular matrix degradation and tissue remodeling. Comparative genomic analysis showed that in humans there are a total of seven peptides relaxin1, relaxin2, INSL3/RLF, INSL4/EPIL, INSL5/RLF2, INSL6/RLF1, and relaxin3/INSL7 sharing close phylogenetic relatedness in the relaxin subfamily [16–22]. Among these peptides, relaxin1 and relaxin2 share >90% identity and represent co-orthologs of the relaxin peptide in other mammals. Relaxin2 is mainly expressed in the reproductive tissues such as ovarian corpus luteum from which the hormone circulates during the luteal phase of the menstrual cycle and during pregnancy in women [23]. In contrast, relaxin1 is produced by deciduae and trophoblasts; with relaxin2, they could play a paracrine function at the placental site [24]. Similar to relaxins, INSL3, INSL5, and INSL6 are expressed in gonads of a variety of mammals [17,18,20,21]. In contrast, relaxin3/INSL7 and the primate-specific INSL4 are mainly found in brain and placenta, respectively [19,22]. The physiological importance of relaxins and INSL3 has become more clear with advances in the studies of various genetic models; however, the roles of other family peptides remain to be investigated. Although the ovary is the main source of relaxin during pregnancy, relaxin is expressed in a variety of tissues, including brain, uterus, prostate, heart, and kidney [25], and has been shown to exert effects in a variety of nonreproductive tissues. Recent identification of relaxin

Cesarean plus anoxia at birth induces hyperresponsiveness to locomotor activity by dopamine D2 agonist

Transient global anoxia after Cesarean birth in rats may produce alterations in the subcortical DA function and related behaviors. The reports only tested the behavioral changes induced by a general DA agonist, such as amphetamine or apomorphine, in adult rats. Here we investigated the role of perinatal anoxia on the locomotion induced by a specific dopamine (DA) agonist and its relation to the DA D1-like and D2-like receptors, measured by autoradiography at two different ages, prepubertal (35 days old, P35) and postpubertal (60 days old, P60). Cesarean birth with or without (C-only) an additional period of 10 min of the anoxia was done in Sprague-Dawley rats, and the effects of the DA D1-like and D2-like agonist and their receptors were studied at P35 and P60. In addition, a third group of animals born vaginally served as the control. The quantitative autoradiography study of the DA D1-like and D2-like receptors revealed an enhancement of the DA D1-like receptor levels in the nucleus accumbens (NAcc) and dorsolateral part of the caudate-putamen in the prepubertal C-only animals. The postpubertal C-only rats showed a decrease in the levels of DA D2-like receptors in the NAcc. However, quinpirole, a DA D2 agonist (0.125 and 0.25 mg/kg, s.c.), induced a dose-dependent increase of the locomotor activity in the animals born by Cesarean with anoxia at birth at both ages. Our results suggest that Cesarean with or without anoxia at birth may mediate differently the neurodevelopmental aspects of the dopaminergic system before and after puberty.

Postnatal growth of the carotid body

The size of the carotid body (CB) is increased significantly during the postnatal period. Type I cells in the CB are the chemoreceptive element and possess many neuron-like characteristics. In contrast to previous opinions that the number of type I cells is determined before birth, we have found that type I cells continue to proliferate over a period of at least 1 month after birth in rats. The proliferation of type I cells is influenced by oxygen concentration in ambient air. Specifically, hyperoxia inhibits the type I cell proliferation, resulting in small CBs throughout life and the permanent impairment of CB chemoreception. On the other hand, hypoxia enhances the type I cell proliferation. Whether hypoxia causes long-lasting effects on CB morphology and function remains to be determined. Besides type I cell proliferation, other cellular components in the CB undergo proliferation and growth as well. In the nearby petrosal ganglion and superior cervical ganglion, both involved in CB chemoreception, cellular proliferation is limited to glial cells and no proliferation of neurons is observed. Also, expression of neurotrophic factors, particularly, BDNF and GDNF, is observed in type I cells of neonatal rats. Taken together, the CB undergoes significant morphological and functional changes during the postnatal period over at least 1 month. This process can be altered by oxygen concentration in ambient air.

Birth of rats following nuclear exchange at the 2-cell stage.

We report full-term development of nuclear transfer embryos following nuclear exchange at the 2-cell stage. Nuclei from 2-cell rat embryos were transferred into enucleated 2-cell embryos and developed to term after transfer to recipients (NT2). Pronuclear exchange in zygotes was used for comparison (NT1). Zygotes and 2-cell embryos were harvested from 4-week-old female Sprague-Dawley rats. Nuclear transfer was performed by transferring the pronuclei or karyoplasts into the perivitelline space of recipient embryos followed by electrofusion to reconstruct embryos. Fused couplets were cultured for 4 or 24 h before being transferred into day 1 pseudopregnant recipients (Hooded Wistar) at the 1- or 2-cell stage. In vitro culture was also carried out to check the developmental competence of the embryos. In vitro development to the blastocyst stage was not significantly different between the two groups (NT1, 34.3%; NT2, 45.0%). Two of three recipients from NT1 and two of five recipients from NT2 became pregnant. Six pups (3 from NT1, 3 from NT2) were delivered from the four foster mothers. Three female pups survived; 2 from NT1 and 1 from NT2. At 2 months of age these pups appeared healthy, and were mated with Sprague-Dawley males. One rat derived from NT1 delivered 15 pups (5 males, 10 females) as did the rat from NT2 (7 males, 8 females). Our results show that by using karyoplasts from 2-cell stage embryos as nuclear donors and reconstructing them with enucleated 2-cell embryos, healthy rats can be produced.

Body composition and bone measurements in intra-uterine growth retarded and early postnatally undernourished male and female rats at the age of 6 months: comparison with puberty

Undernutrition in early life may permanently change body structure, physiology and metabolism and leads to chronic diseases in later life. To test whether malnutrition during different critical time periods around birth in the rat has long-lasting effects on body composition and skeletal growth, we examined body weight and body composition in pubertal rats and adult rats of 6 months after pre- and postnatal malnutrition. Prenatal malnutrition or intra-uterine growth retardation (IUGR) was induced by ligation of the uterine arteries on day 17 of gestation and postnatal food restriction (FR) by litter enlargement to 20 pups per mother from day 2 after birth until weaning (day 24). Pubertal markers were balanopreputial separation (BPS) in the male and vaginal opening (VO) in the female. IUGR as well as FR resulted in a persistent growth retardation. From birth in IUGR rats and from day 4 after birth in FR rats until 6 months of age body weight in male and female rats was significantly lower compared with controls ( P < 0.01 and P < 0.05). Although total body bone mineral content (TBBMC) did not differ between male IUGR rats and controls at BPS, at the age of 6 months TBBMC was significantly lower ( P < 0.01) compared with controls. At BPS as well as at 6 months of age, TBBMC was significantly lower in male FR rats compared with controls ( P < 0.05 and P < 0.01). In the female IUGR rats TBBMC was significantly lower compared with controls at VO ( P < 0.01) and 6 months ( P < 0.05). TBBMC in the female FR rats was significantly lower at VO ( P < 0.01), but did not differ from controls at the age of 6 months. For both IUGR and FR male and female rats these differences disappeared after adjusting for body weight. Body composition in terms of total fat mass, percentage fat and percentage lean did not differ from controls in male and female IUGR rats at 6 months and the same results were observed in the female FR rats. However, in the male FR rats, total fat mass and percentage fat were significantly lower compared with controls ( P < 0.01 and P < 0.05), while the percentage lean mass was significantly higher ( P < 0.05). We conclude that different critical time periods of malnutrition around birth have different effects later in life on growth, which do not disappear at least after 6 months of life. With respect to body composition, only in the FR male rats, differences are found in total fat mass and the balance of percentage fat mass and lean mass. At time of puberty and at the age of 6 months bone mass adjusted for body weight does not seem to be affected by perinatal undernutrition.

Anoxia at birth induced hyperresponsiveness to amphetamine and stress in postpubertal rats

Several evidences suggest that transient global anoxia after Caeraean section birth in rats produces behavioral changes related to dopaminergic transmission. However, all of the reports tested the behavioral changes in adult rats. Here we investigated the role of perinatal anoxia on behavioral paradigms related to dopamine (DA) such as novel environment, saline injection, d-amphetamine, apomorphine and stress-induced changes in locomotor activity at prepubertal and postpubertal ages. All these dimensions of behavior can be affected in schizophrenia. Caesarean section birth with or without an additional period of anoxia was performed in Sprague–Dawley rats and their behaviors were studied at P35 and P56, respectively. In addition, a third group of animals born vaginally served as control. No significant differences in saline injection and d-amphetamine-induced locomotion were observed when the three groups of rats at P35 were compared. However, stress-induced locomotor activity was significantly increased in the Caesarean birth plus anoxia at P35, while after puberty (at P56), saline injection, d-amphetamine and stress-induced locomotion were significantly enhanced in the Caesarean birth plus anoxia compared to its control groups. The data suggests that anoxia at birth mediates differently the functional development and maturation of DA behaviors in adult rats.

Sex-differences in adrenocortical responsiveness during development in rats

It is known that the stress hyporesponsive period (SHRP), which seems to be related to an immature hypothalamo-pituitary-adrenal (HPA) regulatory system, occurs during the first 2 weeks after birth in rats. In the present study, we investigated the effects of sex-steroid hormones on adrenocortical responsiveness to adrenocorticotropic hormone (ACTH) in neonatal rats. The levels of cyclic adenosine 3′,5′-monophosphate (cAMP), corticosterone, and adenylate cyclase activity increased with the dose of ACTH in adrenal cells of males and females in vitro. The ACTH responsiveness in adrenal cells increased with age (7–35 days of age), that is, the loss in responsiveness to ACTH just after birth began to recover in 14–35-day-old rats, but the responsiveness in 14-day-old rats was attenuated in males compared with females. Although castration markedly augmented the responsiveness in male rats, testosterone-replacement in the castrated male rats inhibited the enhancement. Furthermore, the responsiveness in 14-day-intact female rats was suppressed by treatment with testosterone. Expression levels of ACTH receptor mRNA in adrenals increased with age in the female rat, but not in the male. Castration enhanced the level of ACTH receptor mRNA to three-fold of that in intact male rats at 14 days of age, but replacement treatment with testosterone in castrated male rats lowered the elevated levels. Testicular androgens are thought to evoke a gender-specific response in neonates, and the temporal decrease of adrenal ACTH-responsiveness might be due to the topically immature adrenal system as well as the central nervous system in mammals.

A survey of obstetricians willingness to practice collaboratively with midwives in Taiwan.

This study was designed to investigate obstetricians willingness to practice collaboratively with midwives in Taiwan. Systematic random sampling was used to access the 500 participants from the 2,256 registered members of the Association of Obstetrics and Gynecology of the Republic of China. A questionnaire and four open-ended questions were designed to examine obstetricians willingness to work collaboratively with midwives and other related factors. A total of 78 physicians returned the questionnaires, providing a response rate of 15.6%. Thirty-six (46.2%) of subjects worked as private obstetricians, with a mean age of 47.1 years. About 79.5% (n = 62) had over 10 years of experiences in their role. Fifty percent (n = 39) worked in areas with birth rats less than 50 infants per month. The findings of the current study demonstrate, regarding the seven midwifery practice items on the questionnaire, that all 78 obstetricians were unwilling to work collaboratively with midwives. However, results showed that if midwifery education were to be advanced to college level, the degree of willingness to work collaboratively with midwives improved significantly (t > 1.96, p <.05). Furthermore, 56.4% (n = 44) obstetricians would then agree to work collaboratively with midwives. However, 43.6% (n = 34) were unwilling to accept midwives as independent practitioners. Reasons included: unwillingness to share risks, worry about the incapability of midwives, worry that it would impair the professional image of physicians, and unwillingness to share interests. The authors conclude that advancing and enhancing midwifery education in Taiwan should be the first step to negotiate in order to raise the profile of midwives specifically and the midwifery profession generally. Ultimately, such a strategy would improve the quality of care provided to women and their infants and consequently improve the health and social well-being of present and future generations.

Interleukin-10 Administration and Bacterial Endotoxin-Induced Preterm Birth in a Rat Model

In Brief OBJECTIVE To determine whether intrauterine infusion of interleukin-10 prevents preterm delivery in rats treated with endotoxin. METHODS Pregnant rats underwent implantation of uterine catheters and were randomly assigned to receive intrauterine infusion of either normal saline, 50 μg lipopolysaccharide endotoxin, or 50 μg lipopolysaccharide with 500 ng interleukin-10 administered either concurrently or 24 hours later. The interval from infusion to delivery for each group was recorded, along with the number of live born pups and their birth weight. We calculated that to obtain a power of 80%, assuming a 24-hour difference in the treatment to delivery times between the test and control subjects, at least six animals would be needed in each group. RESULTS In females receiving lipopolysaccharide (50 μg) alone, the interval to delivery (P < .05), live birth rate (P < .05), and pup weight (P < .001) were reduced compared with the saline-infused controls. In contrast, females receiving interleukin-10 at the time of the endotoxin challenge or 24 hours after delivered at term with no difference in litter size or live birth weight compared with the controls. CONCLUSION Animals treated with both lipopolysaccharide and interleukin-10, administered concurrently or 24 hours after the endotoxin challenge, delivered normal weight pups at term with a similar litter size as the saline-infused controls. Interleukin-10 appears to be effective in preventing endotoxin-induced preterm birth and fetal wastage in pregnant rats. Interleukin-10 prevents endotoxin-induced preterm birth in a rat model.

Maternal reproductive experience enhances early postnatal outcome following gestation and birth of rats in hypergravity.

A major goal of space life sciences research is to broaden scientific knowledge of the influence of gravity on living systems. Recent spaceflight and centrifugation studies demonstrate that reproduction and ontogenesis in mammals are amenable to study under gravitational conditions that deviate considerably from those typically experienced on Earth (1 x g). In the present study, we tested the hypothesis that maternal reproductive experience determines neonatal outcome following gestation and birth under increased (hyper) gravity. Primigravid and bigravid female rats and their offspring were exposed to 1.5 x g centrifugation from Gestational Day 11 either through birth or through the first postnatal week. On the day of birth, litter sizes were identical across gravity and parity conditions, although significantly fewer live neonates were observed among hypergravity-reared litters born to primigravid dams than among those born to bigravid dams (82% and 94%, respectively; 1.0 x g controls, 99%). Within the hypergravity groups, neonatal mortality was comparable across parity conditions from Postnatal Day 1 through Day 7, at which time litter sizes stabilized. Maternal reproductive experience ameliorated neonatal losses during the first 24 h after birth but not on subsequent days, and neonatal mortality was associated with changes in maternal care patterns. These results indicate that repeated maternal reproductive experience affords protection against neonatal losses during exposure to increased gravity. Differential mortality of neonates born to primigravid versus bigravid dams denotes gravitational load as one environmental mechanism enabling the expression of parity-related variations in birth outcome.

Interleukin-10 administration and bacterial endotoxin-induced preterm birth in a rat model

Objective: To determine whether intra-uterine infusion of interleukin-10 prevents preterm delivery in rats treated with endotoxin. Methods: Pregnant rats underwent implantation of uterine catheters and were randomly assigned to receive intrauterine infusion of either normal saline, 50 μg lipopolysaccharide endotoxin, or 50 μg lipopolysaccharide with 500 ng interleukin-10 administered either concurrently or 24 hours later. The interval from infusion to delivery for each group was recorded, along with the number of live born pups and their birth weight. We calculated that to obtain a power of 80%, assuming a 24-hour difference in the treatment to delivery times between the test and control subjects, at least six animals would be needed in each group. Results: In females receiving lipopolysaccharide (50 μg) alone, the interval to delivery ( P < .05), live birth rate ( P < .05), and pup weight ( P < .001) were reduced compared with the saline-infused controls. In contrast, females receiving interleukin-10 at the time of the endotoxin challenge or 24 hours after delivered at term with no difference in litter size or live birth weight compared with the controls. Conclusion: Animals treated with both lipopolysaccharide and interleukin-10, administered concurrently or 24 hours after the endotoxin challenge, delivered normal weight pups at term with a similar litter size as the saline-infused controls. Interleukin-10 appears to be effective in preventing endotoxin-induced preterm birth and fetal wastage in pregnant rats.

Electrophysiological properties of rat retinal Müller (glial) cells in postnatally developing and in pathologically altered retinae.

Retinal glial Müller cells are characterized by dominant K(+) conductances. The cells may undergo changes of their membrane currents during ontogeny and gliosis as described in rabbit and man. Although the rat retina is often used in physiological experiments, the electrophysiology of rat Müller cells is less well studied. The aim of the present study was to characterize their membrane currents in postnatal development and in two models of retinal degeneration. Freshly isolated cells were subjected to whole-cell patch clamp recordings. During the first 4 weeks after birth of rats, their Müller cells displayed an increase in all membrane currents, particularly in the inward currents elicited at hyperpolarizing potentials. The decrease of the membrane resistance from more than 760 MOmega to less than 50 MOmega was accompanied by a shift of the zero current potential from about -20 mV to -80 mV, similar as earlier observed in developing rabbit Müller cells. These developmental changes were found in pigmented Brown Norway rats as well as in rats with inherited retinal dystrophy (RCS rats). Moreover, an infection of Lewis rats with the Borna disease virus caused substantial neuroretinal degeneration but did not result in a strong reduction of inward currents and of the zero current potential of the Müller cells. Thus, rat Müller cells fail to change their basic membrane properties in two different models of retinal pathology. This is in contrast to human and rabbit Müller cells, which have been shown to undergo dramatic changes of their membrane physiology in response to retinal diseases and injuries.