• Proceedings of the Korean Society of Medical Physics Conference
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• 2006.08a
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• pp.71-71
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• 2006

• Journal of Radiation Protection and Research
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• v.31 no.4
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• pp.203-210
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• 2006

Purpose : To estimate the dose to the embryo/fetus of a pregnant patient with brain tumors, and to design an shielding device to keep the embryo/fetus dose under acceptable levels Materials and Methods : A shielding wall with the dimension of 1.55 m height, 0.9 m width, and 30 m thickness is fabricated with 4 trolleys under the wall. It is placed between a Patient and the treatment head of a linear accelerator to attenuate the leakage radiation effectively from the treatment head, and is placed 1 cm below the lower margin of the treatment field in order to minimize the dose to a patient from the treatment head. An anti-patient scattering neck supporters with 2 cm thick Cerrobend metal is designed to minimize the scattered radiation from the treatment fields, and it is divided into 2 section. They are installed around the patient neck by attach from right and left sides. A shielding bridge for anti-room scattered radiation is utilized to place 2 sheets of 3 mm lead plates above the abdomen to setup three detectors under the lead sheets. Humanoid phantom is irradiated with the same treatment parameters, and with and without shielding devices using TLD, and ionization chambers with and without a build-up cap. Results : The dose to the embryo/fetus without shielding was 3.20, 3.21, 1.44, 0.90 cGy at off-field distances of 30, 40, 50, and 60 cm. With shielding, the dose to embryo/fetus was reduced to 0.88, 0.60, 0.35, 0.25 cGy, and the ratio of the shielding effect varied from 70% to 80%. TLD results were 1.8, 1.2, 0.8, 1.2, and 0.8 cGy. The dose measured by the survey meter was 10.9 mR/h at the patient's surface of abdomen. The dose to the embryo/fetus was estimated to be about 1 cGy during the entire treatment. Conclusion : According to the AAPM Report No 50 regarding the dose limit of the embryo/fetus during the pregnancy, the dose to the embryo/fetus with little risk is less than 5 cGy. Our measurements satisfy the recommended values. Our shielding technique was proven to be acceptable.

• Proceedings of the Korean Society of Embryo Transfer Conference
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• 2002.11a
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• pp.34-36
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• 2002

Epidermal growth factor (EGF) and insulin-like growth factor-I (IGF-I) have been shown to stimulate proliferation and differentiation of various somatic cells, including placental trophoblasts and also to enhance fetal growth and development when maternally administered. Since an increase of the expression of placental EGF and IGF-I receptors in rat, mouse, and human with the gestation advanced, both EGF and IGF-I were considered to play pivotal roles on fetal growth by regulating some function of placental cells. Amino acids are crucial importance for both maternal and fetal requirements of energy source and essential constituent of fetal mass during pregnancy. Impaired fetal and placental uptake of amino acids has been observed in several models of growth retardation in the rat. Amino acid is concentrated in the fetal side through active transport by amino acid transporters and is one of the important metabolic fuels for the fatal growth. Therefore, at first plasma amino acid concentrations in mothers and fetuses were measured as an index of uphill transport across the placenta associated with EGF and IGF-1. The EGF administration at the concentration of 0, 0.1, or 0.2 $\mu\textrm{g}$/g to pregnant rats from day 18 to 21 of gestation apparently increased fetal/maternal ratio of serum proline concentration and also fatal growth in EGF dose-dependent manner. When IGF-I in doses of 0, 1, 2, and 4 $\mu\textrm{g}$/g were administrated, the ratio of leucine, isoleucine, tryptophan, phenylalanine, tyrosine and also fetal growth significantly increased with a dose-dependent manner. These results suggested that EGF and IGF-I enhanced fatal growth by, as one of its possible mechanisms, promoting placental activity to transfer some amino acid supplies from the mother to the fetus in late pregnancy.

• Journal of Oral Medicine and Pain
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• v.25 no.2
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• pp.241-245
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• 2000

In this case report, I discussed the diagnosis and treatment of two pregnant women with temporomandibular disorders(TMD) who visited the Department of Oral Medicine, PNUH. Also, I reviewed some investigations of diagnosis and treatment of TMD in pregnant women. The obtained results were as follows; 1. No single X-ray diagnostic procedure for TMD results in radiation dose that threatens the well-being of the developing embryo and fetus. 2. Most non-steroidal anti-inflammatory drugs(NSAIDs) have commonly used because these drugs are considered to be nonteratogenic, but these agents are not recommended for routine use after 3rd trimester. 3. Electro-acupuncture stimulation therapy(EAST) is contraindicated for 1st trimester, and ultrasonic deep heat therapy, microwave deep heat therapy, low level laser therapy, myo-monitor are not contraindicated for pregnant women but clinician must consider some risk of adverse fetal effects. 4. The occlusal stabilization splint may be used for pregnant women, if it is fabricated indirectly. 5. Surgical treatment is contraindicated for pregnant women.

• Biomedical Science Letters
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• v.17 no.3
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• pp.231-238
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• 2011

During pregnancy, stress induces maternal glucocorticoid secretion, which in turn is known to affect structural malformation, retardation of growth, reduced birth weight of the fetus. As Hox genes are master transcription factors which fulfill critical roles in embryonic development, we aimed to explore the possibility that alterations of the Hox gene expression might be involved in stress-induced malformation. The pregnant mice were injected with dexamethasone at a dose of 1 mg/kg or 10 mg/kg on day 7.5, 8.5 and 9.5 p.c. (post coitum), as well as saline as control. Embryos of E11.5 and E18.5 were obtained by sacrificing pregnant animals. Weight and crown-rump length (CRL) were measured. RT-PCR was performed to examine the Hox gene expression levels. Embryos given dexamethasone at day 7.5~9.5 p.c. had small CRL and weighed less both in E11.5 and E18.5. The percentage of embryos showing abnormalities was high in groups received high dose of dexamethasone. To define the molecular basis for abnormal embryonic development, we analyzed the Hox gene expression pattern and found that many Hox genes display altered expression. Effects of prenatal dexamethasone treatment on embryonic development might be associated with the aberrant Hox gene expression.