• The Journal of the Institute of Internet, Broadcasting and Communication
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• v.22 no.3
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• pp.111-116
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• 2022

In the paper, A prototype Fetal Heart Monitor, mini - size, was designed and produced for pre-mothers to measure the rate and rhythm of their features's heart at home.Pre-mothers could listen fetal heart rhythm through an inner bluetooth speaker ant the monitor. LED colors show the frequency of fetal heart rate variability on the monitor. All measured health information, by ultrasonic resonator and bluetooth speaker, is linked to a mother's smart phone. A test verified this simple measuring device helps users discover the symptoms of fetal health. Patients using at home devices usefully prevent sudden cardiac death and myocardial infraction by discovering symptoms.

• Clinical and Experimental Pediatrics
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• v.45 no.7
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• pp.928-932
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• 2002

Perinatal atrial flutter is a potentially lethal arrhythmia. Management of this disorder is difficult and controversial. Fetal atrial flutter is a serious and life threatening rhythm disorder particulary when it causes hydrops; it may be associated with fetal death or neurological damage. Although the initial episode of flutter may be difficult to control, recurrence of atrial flutter after successful resolution of the arrhythmia seems highly unlikely and long-term prognosis is excellent. We experienced a case of a atrial flutter diagnosed in utero at $38^{+6}$ weeks' gestation by fetal cardiac echocardiography. He was treated with maternal digoxin, but he continued to have atrial flutter until delivery. Restoration of sinus rhythm occured with propafenone therapy in this patient after failure of initial digoxin therapy and direct current cardioversion.

• Journal of Microbiology and Biotechnology
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• v.18 no.9
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• pp.1590-1598
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• 2008

Cell proliferation and differentiation are critical processes in a developing fetal rat brain, during which programmed cell death (PCD) also plays an important role. One of the decisive factors for PCD is Bcl-2 family proteins, where Bax induces cell death, whereas Bcl-2 acts as an inhibitor of PCD. As maternal drinking is known to cause fetal alcohol syndrome (FAS) or malformation of the fetal brain during pregnancy, the objective of the present study was to investigate whether maternal ethanol exposure alters the PCD-related Bax and Bcl-2 protein expression during fetal brain development. Pregnant female rats were orally treated with 10% ethanol and the subsequent expressions of the Bax and Bcl-2 proteins examined in the fetal brain, including the forebrain, midbrain, and hindbrain, from gestational day (GD) 15.5 to GD 19.5, using Western blots, in situ hybridization, and immunohistochemistry. With regard to the ratio of Bcl-2 to Bax proteins (Bcl-2/Bax), the Bax protein was dominant in the forebrain and midbrain of the control GD 15.5 fetuses, except for the hindbrain, when compared with the respective ethanol-treated groups. Moreover, Bcl-2 became dominant in the midbrain of the control GD 17.5 fetuses when compared with the ethanol-treated group, representing an alternation of the natural PCD process by ethanol. Furthermore, a differential expression of the Bcl-2 and Bax proteins was found in the differentiating and migrating zones of the cortex, hippocampus, thalamus, and cerebellum. Thus, when taken together, the present results suggest that ethanol affects PCD in the cell differentiation and migration zones of the prenatal rat brain by modulating Bax and Bcl-2 expression in an age- and area-dependent manner. Therefore, this is the first evidence that ethanol may alter FAS-associated embryonic brain development through the alteration of Bax and Bc1-2 expression.

• Proceedings of the Korean Society of Toxicology Conference
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• 2006.11a
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• pp.55-64
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• 2006

The fetal central nervous system (CNS) is sensitive to diverse environmental factors, such as alcohol, heavy metals, irradiation, mycotoxins, neurotransmitters, and DNA damage, because a large number of processes occur during an extended period of development. Fetal neural damage is an important issue affecting the completion of normal CNS development. As many concepts about the brain development have been recently revealed, it is necessary to compare the mechanism of developmental abnormalities induced by extrinsic factors with the normal brain development. To clarify the mechanism of fetal CNS damage, we used one experimental model in which 5-azacytidine (5AZC), a DNA damaging and demethylating agent, was injected to the dams of rodents to damage the fetal brain. 5AzC induced cell death (apoptosis)and cell cycle arrest in the fetal brain, and it lead to microencephaly in the neonatal brain. We investigated the mechanism of apoptosis and cell cycle arrest in the neural progenitor cells in detail, and demonstrated that various cell cycle regulators were changed in response to DNA damage. p53, the guardian of genome, played a main role in these processes. Further, using DNA microarray analysis, tile signal cascades of cell cycle regulation were clearly shown. Our results indicate that neural progenitor cells have the potential to repair the DNA damages via cell cyclearrest and to exclude highly affected cells through the apoptotic process. If the stimulus and subsequent DNA damage are high, brain development proceeds abnormally and results in malformation in the neonatal brain. Although the mechanisms of fetal brain injury and features of brain malformation afterbirth have been well studied, the process between those stages is largely unknown. We hypothesized that the fetal CNS has the ability to repair itself post-injuring, and investigated the repair process after 5AZC-induced damage. Wefound that the damages were repaired by 60 h after the treatment and developmental processes continued. During the repair process, amoeboid microglial cells infiltrated in the brain tissue, some of which ingested apoptotic cells. The expressions of genes categorized to glial cells, inflammation, extracellular matrix, glycolysis, and neurogenesis were upregulated in the DNA microarray analysis. We show here that the developing brain has a capacity to repair the damage induced by the extrinsic stresses, including changing the expression of numerous genes and the induction of microglia to aid the repair process.

• Journal of Veterinary Clinics
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• v.18 no.2
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• pp.146-151
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• 2001

This study was carried out to find if the X-irradiation being used for clinical diagnosis during pregnancy would affect fetal development and cause fetal malformation in rats or not. To determine the dose and irradiation frequency of X-irradiation and gestation period by which fetal development would be affected when irradiated during pregnancy, seventy-two Sprague Dawley female rats (8 weeks old) were used for the experiment and grouped into three according to different gestation period of 5-8 days, and 6-12 days of gestation. Experimental rats were irradiated on the daily irradiation conditions of 40, 60, 80 kvp(kilo volt peak), 150 mA(milliampere), 0.25 sec and 4 times/day for both 5-8 days and 10-13 days of gestation, and 100 kvp, 100 mA, 2 min. and 4 times/day for 6-12 days of gestation. Rats were put in a small dark box when irradiated, which animals were sacrificed on the 20th day of gestation and mean litter size, fetal body weight, fetal crown-rump length(CRL) were investigated along with pathological findings. 1. Litter size were significantly decreased in the rats which were irradiated by both 60 and 80 kvp during 5 to 8 days of gestation and by 100 kvp during 6-12 days of gestation compared to those from the control rats(p<0.05) 2. Fetal body weight was significantly decreased in the fetus from the rats which were irradiated by both 60-80 kvp during 5-8 days of gestation and by 100 kvp during 6-12 days of gestation compared to those from the control rats(p<0.05). 3. There was no significant difference of fetal crown-rump length between all the experimental rats and the controls. 4. Fetal absorption, fetal death, and fetal malformation were not observed in the fetus form the rats irradiated by 40-80 kvp during 5-8 and 10-13 days of gestation, however, the pathological findings were found in those from the rats irradiated by 100 kvp during 6-12 days of gestation. 5. The harmful effect of x-irradiation on fetal development was estimated to occur when irradiated during 5-8 days of gestation. These results indicated that even X-irradiation for clinical diagnosis could affect fetal development in the early embryonic stage and when the fetus were exposed to frequent and prolonged x-irradiation with over dose.

• Toxicological Research
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• v.19 no.3
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• pp.181-187
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• 2003

Effects of repeated treatment with butylated hydroxyanisole (BHA) on the induction of glutathione S-transferases (GSTs) and teratogenicity of cyclophosphamide were investigated in rats. Pregnant rats were orally treated with BHA (50 mg/kg) for 7 days, from days 6 to 12 of gestation, and intraperitoneally challenged with cyclophosphamide (15 mg/kg) 2 hr after the final treatment. On day 20 of gestation, the maternal and fetal abnormalities were examined. Separately, a part of rats was sacrificed for the assay of hepatic and placental GSTs activities on day 12 of gestation following 7-day treatment with BHA. Cyclophosphamide, administered on day 12 of gestation, induced 43.2% of fetal death and resorption, and 100% of malformations in live fetuses, in contrast to low fetal resorption (8.7%) and malformations (8%) in control group. The malformations include cranial defect and exencephaly (100%), micrognathia and tongue extrusion (100%), limb defects (40%), renal pelvic dilatation (39%), and cleft palate (15%). Interestingly, BHA induced GSTs activities by 62% and 46% over the control in liver and placenta, respectively, and remarkably reduced the fetal resorption (13.9%) and malformations, resulting in 62% of cranial defect and exencephaly, 68% of micrognathia and tongue extrusion, 29% of limb defects, and 14% of renal pelvic dilatation. Taken together, it is suggested that a long-term pretreatment with BHA could substantially prevent fetuses from abortion and malformations following intrauterine exposure to teratogens including cyclophosphamide by inducing phase II antioxidant enzymes such as GSTs.

• Neonatal Medicine
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• v.28 no.1
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• pp.59-63
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• 2021

An important, albeit rare, cause of fetal bradycardia is long QT syndrome (LQTS). Congenital LQTS is an ion channelopathy caused by mutations in genes encoding cardiac ion channel proteins. Fetal onset of LQTS imposes high risk of life-threatening tachyarrhythmias and sudden cardiac death. Here, we report the case of a female newborn with fetal onset of bradycardia and a 2:1 atrioventricular (AV) block. After birth, a 12-lead electrocardiogram (ECG) revealed bradycardia with QT prolongation of a corrected QT (QTc) interval of 680 ms and pseudo 2:1 AV block. Genetic testing identified a heterozygous Gly402Ser (c.1204G>A) mutation in CACNA1C, confirming the diagnosis of LQTS type 8 (LQT8). The patient received propranolol at a daily dose of 2 mg/kg. Mexiletine was subsequently administered owing to the sustained prolongation of the QT interval and pseudo 2:1 AV block. One week after mexiletine inception, the ECG still showed QT interval prolongation (QTc, 632 ms), but no AV block was observed. There were no life-threatening tachyarrhythmias in a follow-up period of 13 months.

• Journal of Veterinary Clinics
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• v.36 no.2
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• pp.116-118
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• 2019

A 2-year-old female Persian cat weighing 2.95 kg was admitted for dystocia. The levels of white blood cells and thrombocytes were decreased in blood analysis. In radiography and ultrasonography, there were four fetuses with no remarkable signs of blood flow and heartbeat. In particular, one of them showed symptom of Spalding's sign, which is a rare symptom that indicated overriding of the fetal cranial bones and shrinkage of the head with a decreased volume. It was reported that Spalding's sign is one of the strong indication of fetal death in human uterus and it occurs rarely with normal fetus without apparent reason prior to labor in human. This is the first report to provide the Spalding's sign in domestic cats and this will be applied in a strong presumptive evidence that fetal death has occurred with brain disruption sequence while pregnancy in domestic animals.

• Journal of the Korean Society of Radiology
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• v.14 no.5
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• pp.661-668
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• 2020

One of the causes of death for pregnant female is embolism, when a chest PA examination is performed. In addition, due to small doses, the examinations are performed for the purpose of preparing for pre-delivery emergency surgery or basic examination for pregnant female. Evaluating fetal doses through actual measurements is subject to ethical problems, Monte Carlo simulations assesses the organ and fetal doses of pregnant females according to week of pregnancy. The results of the simulations showed that the fetal dose decreased according to weeks of pregnancy and it showed a dose of about 0.1 mGy. The higher the density and thickness of the shielding material, the better the shielding effect. In addition, the dose reduction effect for each shielding material is between 40 and 98%. Afterwards, it is deemed necessary to study the reduction of fetal doses through various shielding characteristics and methods.

• Journal of radiological science and technology
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• v.18 no.1
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• pp.91-95
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• 1995

The ICR pregnant mice were irradiated at 1.5Gy in every 6 hours in the period of organogenesis in order to classify the stage specificity of the embryonic effects of radiation and the stage of development differentiation of the primordium of each major organ. Intrauterine death, fetal body weight and external malformation in live fetuses were observed on day 18 of gestation. There was no statistically significant difference in the intrauterine mortality at any stage organogenesis. The fetal body weight of the mice irradiated in the intermediate stage of organogenesis showed significantly lower. There were specific highly sensitive stages in the incidences of each external malformation, that is exencephalia, open eyelid, cleft palate, anomalies of extremities and anomalies of the tail. At these stage, the primordia of the major organs are established in ICR mice.