• The Korean Journal of Physiology
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• v.27 no.1
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• pp.13-25
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• 1993

To study the regulation of amniotic fluid volume and electrolyte concentration by the Membranes surrounding the amniotic fluid, the rate of $Li^+$ disappearance from amniotic sac of expired fetuses were examined while increasing the amniotic volume and osmolarity in rabbits. After intraamniotic injection of 1 ml isosmotic saline (about 20% of the amniotic fluid volume) containing 15 mM LiCl and 0.5 g/L Censored, the time courses of $Li^+$ and Censored disappearance were determined. From there the $Li^+$ clearance through the extrafetal routes was estimated and compared with that obtained from living fetuses. The volume, $Na^+$ concentration and osmolarity of amniotic fluid were measured and their relationships with $Li^+$ disappearance were evaluated. The fellowing results were obtained: 1. The rate of disappearance from amniotic fluid of living fetuses during the first 30 minutes was strikingly higher for $Li^+$ than for Censored, suggesting that extrafetal routes exist. At 60 and 90 minutes, however, the disappearance rate of $Li^+$ was less than that of Censored, suggesting the possibility of $Li^+$ reentry through fetal urination. 2. The disappearance of $Li^+$ from the amniotic fluid of the expired fetus was substantial, although lower than that of living fetuses, throughout the experimental period. 3. The $Na^+$ concentration and the osmolarity of the amniotic fluid of expired fetus measured 30 minutes after an intraamniotic injection of isoosmotic saline showed wide variation, but thereafter they changed gradually towards the normal extracellular fluid level. 4. When the amniotic fluid was iso- or hyposmolar, the rate of $Li^+$ disappearance from the amniotic fluid of the expired fetuses showed little variation. However, when the amniotic fluid was hyperosmolar, the rate at 30 minutes was markedly lower than those of isosmotic or hyposmotic amniotic fluid. At 90 minutes, the rate of $Li^+$ disappearance in hyperosmolar fluid reached a similar level to the rate in isosmolar fluid. 5. The intraamniotic injection of 400 mOsm/L saline solution decreased the disappearance rate of $Li^+$ from expired fetuses, while the injection of mannitol into the maternal vein induced no significant change. From these results it is concluded that: 1) a significant amount of $Li^+$ may leave the amniotic fluid via filtration through the membranes surrounding the amniotic fluid, 2) during hyperosmolar challenge to amniotic fluid, osmotic bulk flow might counteract the filterable loss, and 3) $Li^+$ disappearance might continue even after the volume and osmolarity of the amniotic fluid have recovered to control values.

• Asian-Australasian Journal of Animal Sciences
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• v.19 no.1
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• pp.19-25
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• 2006

The effect of vitamin E supplementation on plasma ${\alpha}$-tocopherol level, total antioxidant level and reproductive performance in Murrah buffaloes was studied during periparturient period. Twenty-four advance pregnant buffaloes were randomly divided into four equal groups as $T_1$, $T_2$, $T_3$ and $T_4$ and were supplemented with 0, 1,000, 1,500 and 2,000 IU of ${\alpha}$-tocopheryl acetate (Merck) from 60 days prepartum to 30 days postpartum and 0, 500, 750 and 1,000 IU from 30 to 60 days postpartum, respectively. Blood samples were collected at -60, -45, -30, -15, -7, 0, 7, 15, 30 and 60 days of parturition and were analyzed for plasma ${\alpha}$-tocopherol and total antioxidant activity (TAA). The intake of DM, CP and TDN did not vary among different groups. Plasma ${\alpha}$-tocopherol and TAA around parturition (-7 to 15 day) in $T_3$ and $T_4$ were significantly higher than the control group. There was 17% reduction in retention of fetal membranes (RFM) and metritis in $T_4$ than control. The post partum estrus interval averaged 58.00, 55.33, 51.83 and 43.00 days in $T_1$, $T_2$, $T_3$ and $T_4$ respectively. There was significant reduction in days open in both $T_3$ and $T_4$ in comparison to $T_1$ group (127,130 Vs.146). All the vitamin E supplemented groups showed reduction in days open than their previous lactation performance. Supplementation of vitamin E at $1,500IU\;d^{-1}$ from 60 day prepartum to 30 day post partum to buffaloes exhibited beneficial effect on plasma ${\alpha}$-tocopherol level and TAA around parturition and continuation of its supplementation at $1,000IU\;d^{-1}$ from 30 to 60 days of lactation improved post partum reproductive performance of buffaloes.

• Journal of Biomedical Engineering Research
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• v.41 no.3
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• pp.138-145
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• 2020

Adipocytes are the main constituent of adipose tissue. Understanding the molecular basis of adipogenesis is pivotal to finding the therapeutic targets for treatment of obesity. Melatonin is associated with obesity and its mechanism is currently under intensive investigation. The objective of this study was to investigate the effect of melatonin on adipogenesis in differentiating preadipocytes. 3T3-L1 preadipocytes were cultured in Dulbecco's modified Eagle's medium (DMEM) containing 5% calf serum at 37℃ with 5% CO₂ in a humidified incubator. Differentiation was induced using DMEM with 10% fetal bovine serum supplemented with MDI two days after cell confluence (day 0). Cells were treated with 0, 10 and 100 μM melatonin on either day 0 or day 5. 72 hours after each treatment, lipid accumulation was measured by oil red O staining. Proteins were resolved by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and transferred to membranes. As a result, lipid accumulation decreased with melatonin treatment. ERK pathway, activated when differentiation is induced, also decreased with an increase in melatonin concentration. Furthermore, the expression of key adipogenic factors, C/EBPα, C/EBPβ, and PPARγ, were reduced by melatonin treatment. These results imply that melatonin may inhibit the process of adipogenesis and may have a role as a new anti-obesity agent.

• The Korean Journal of Physiology
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• v.29 no.1
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• pp.81-89
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• 1995

The effects of prolactin and vasopressin on the regulation of amniotic fluid (AF) volume and its $Na^{+}$ concentration $([Na^{+}])$ through the membrane surrounding the AF during increase in AF volume due to fetal urination were studied. About 70% of AF volume was replaced with normal isotonic saline solution. Isotonic saline solution (0.5 ml) containing Censored and LiCl was introduced into each amniotic sac. Vasopressin (25 ng/ml) or prolactin (1 mg/ml) of AF was then injected into experimental amniotic sac. The concentrations of Congored, $Li^{+}$, and $Na^{+}$ were measured at 30 and 60 min intervals after injection. Af samples with decreased Censored concentration ([CR]) during the period of 30 - 60 min were analyzed. The percentage change of $[Na^{+}]$ and the rate of $Li^{+}$ movement during this period were calculated, and the effects of vasopressin and prolactin on them were evaluated. Fellowing results were obtained: 1. The rate of reduction of [CR] in the AF was retarded by vasopressin or prolactin injection. 2. The rate of reduction of $[Li^{+}]$ in the AF was also retarded by vasopressin or prolactin injection. 3. The rate of reduction of $[Li^{+}]$ in the AF was less retarded by vasopressin than that of [CR]. 4. $[Na^{+}]$ changed to approach to the normal level, but this was markedly retarded by prolactin injection. 5. Direction of $Li^{+}$ movement was correlated with the change in $[Na^{+}]$ but it always moved out of the amniotic sac even when the $[Na^{+}]$ increased in vasopressin injected AF. From the above results, it is suggested that vasopressin in the AF triggers the fetus to urinate, and then the membranes surrounding the AF regulate osmolarity by efflux of $Na^{+}$. We suggest that prolactin facilitates water outflow across the amniotic membrane during increase in AF volume, in contrast to a constant volume, whereas regulation of $[Na^{+}]$ is partly restricted by prolactin.

• Biomedical Science Letters
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• v.2 no.2
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• pp.175-185
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• 1996

The mitogen-activated protein(MAP) kinase signal transduction pathway represents an important mechanism by which mitogen, such as serum and PMA, regulate cell proliferation and differentiation. Target substrates of the MAP kinase are located within several compartments containing plasma membranes and nucleus. We now report that serum addition induces proliferation of the P388 murine leukemia cell, but PMA does not, while both serum and PMA treatment cause translocation of the MAP kinase, mainly p42$^{mapk}$ isoform, from cytosol into the nucleus, which was monitored by immunoblot analysis using polyclonal anti-ERK1 antibodies. We investigated whether the MAP kinase was capable of phosphorylating c-Jun protein and GST-fusion proteins, the P562$^{kk}$N-terminal peptides (1-77 or 1-123 domain) of the T cell tyrosine kinase, using the partially purified MAP kinase by SP-sephadex C-50, phenyl superose and Mono Q column chromatography. We found that the partially purified MAP kinase was able to phosphorylate c-Jun protein and the GST-fusion protein expressed using E.coli DH5$\alpha$ which is transformed with pGEX-3Xb plasmid vector carrying of p562$^{kk}$N-terminal peptide-encoding DNA. These results imply that tyrosine kinase receptor/Ras/Raf/MAP kinase pathway is a major mechanism for mitogen-induced cell proliferation in P388 murine leukemia cell and that the various MAP kinase isoforms may have their own target substrates located in distinct subcellular compartments.

• Neonatal Medicine
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• v.18 no.1
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• pp.158-162
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• 2011

Preterm infants with oligohydramnios after preterm premature rupture of membranes can present with severe respiratory distress immediately after birth, and the most common cause is pulmonary hypoplasia. Unlike infants with pulmonary hypoplasia, some cases have shown dramatic improvement with aggressive ventilatory support during the initial 1-2 days of distress: those patients have been defined as having dry lung syndrome. It is assumed that oligohydramnios leads to functional pulmonary hypoplasia by compression of the fetal lungs: some of the improvement in dry lung syndrome may thus have resulted from inflation of compressed lung tissue and increase of lung compliance. We report two incidences of dry lung syndrome that were treated successfully with high inflation pressure and inhaled nitric oxide (NO): these are the first dry lung syndrome cases to be reported in Korean infants.

• Journal of Genetic Medicine
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• v.8 no.1
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• pp.71-75
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• 2011

A male infant was diagnosed with obstetric brachial plexus injury, congenital muscular torticollis and cleft palate 17 days after birth. His mother presented with gestational diabetes and premature rupture of membranes. Although it is possible that these three disorders arose independently, it is very likely that all three have the same etiologic cause, and we propose that a possible mechanism for this concurrence is related to maternal gestational diabetes. Maternal hyperglycemia mostly affects fetal structures deriving from the neural crest, including the palatine bone, and may have caused the cleft palate observed in this case. Gestational diabetes is also associated with increased frequency of large for gestational age infants and, by extension, with increased risk of birth injuries such as obstetric brachial plexus injury or congenital muscular torticollis associated with large for gestational age infants. Since the children of mothers with gestational diabetes are at increased risk for congenital defects such as cleft palate as well as being large for gestational age, precautions indicated for each respective disorder must be taken during prenatal testing and during birth. However, further studies of more cases are required to evaluate whether the concurrence of obstetric brachial plexus injury, congenital muscular torticollis and cleft palate in this case are complications specifically associated with gestational diabetes or just a simple coincidence.