Biomedical subjects
Publications and source records attributed to K Techatraisak.
We present a case of familial 17alpha-hydroxylase/17,20 lyase (CYP17) deficiency in which the index case, a 14-year-old XX girl, led to the diagnosis of the condition in a 9-year-old XY sister. No mutations in the CYP 17 gene were found in any of the girls.
The molecular method for prenatal diagnosis in the first trimester was carried out on the second and third pregnancies of a family at risk of congenital adrenal hyperplasia (CAH). The first child, an 8-year-old daughter, was affected. The molecular and cytogenetic prenatal diagnosis on the second pregnancy revealed that the fetus which was a female had been affected. The pregnancy was then terminated. The couple presented with the third pregnancy at 8 weeks' gestation. The same approach revealed that the fetus, a male, was affected. The couple opted for continuation of pregnancy which was on-going at the time of the manuscript preparation. To our knowledge, this is the first family in Thailand who had molecular approach for prenatal diagnosis of CAH. This approach allows early information about the fetal status of the disease and, together with the result of fetal gender, will help early decision making in pregnancy management.
Cyclooxygenase (COX) is the first enzyme in the pathway in which arachidonic acid is converted to PGs, also called COX-metabolites. COX exists as COX-1 and COX-2 isoforms. Each COX-metabolite has different characters and functions. The amounts of each COX-metabolite produced in cells are also different depending on cell type and mitogen stimulated cells. These were thought to be autoregulation among COX-metabolites. Here, we have investigated the effects of COX-metabolites, such as PGI2, PGE2, PGF2alpha and U44069, on the induction of COX-2 in human umbilical vein endothelial cells (HUVEC) treated with LPS (1 microg/ml). COX activity was measured by the production of 6-keto-PGF1alpha, PGE2, PGF2alpha and TXB2 in the presence of exogenous arachidonic acids (10 microM for 10 min) using enzyme immunoassay (EIA). COX-1 and COX-2 protein was measured by immunoblotting using specific antibody. PGI2, PGE2, PGF2alpha or U44069, did not affect on basal COX activity in untreated HUVEC (24 h incubation). Untreated HUVEC contained COX-1 protein but not COX-2 protein. When HUVEC were treated with LPS (1 microg/ml for 24 h), COX activity and COX-2 protein was increased in a dose dependent manner. The increased COX activity in LPS (1 microg/ml) treated HUVEC was inhibited with PGE2 (0.03, 0.3 or 3 microM), but not PGI2, PGF2alpha or U44069, in a dose dependent manner. Similarly, COX-2 protein expression in LPS treated HUVEC was also inhibited with PGE2, but not PG2, PGF2alpha or U44069, in a dose dependent manner. These results suggested that PGE2, but not PGI2, PGF2alpha or TXA2 is a key in feedback regulation of COX-metabolites produced in HUVEC.
OBJECTIVE AND DESIGN: We investigated whether estrogen affected COX isoform expressed in human umbilical vein endothelial cells (HUVEC). MATERIALS AND METHODS: HUVEC were grown to confluence and replaced with fresh medium containing 17beta-estradiol (0.001, 0.01, 0.1 and 1 nM) or 17beta-estradiol (1 nM) plus staurosporine (0.1, 1 and 10 ng/ml) for 24 h, after which the supernatant medium was collected to measure 6-keto-PGF1alpha using enzyme immunoassay. To measure COX activity via exogenous substrates, the remaining cells were replaced with fresh medium containing arachidonic acid (10 microM for 10 min), and then the medium was removed to measure 6-keto-PGF1alpha. The COX isoform expressed in cells was detected by immunoblotting using specific antibody. RESULTS: 17beta-estradiol (0.001 to 1 nM) increased the production of 6-keto-PGF1alpha via either endogenous or exogenous substrate in a dose dependent manner. These increases were significantly inhibited when cells were coincubated with staurosporine. Interestingly, only COX-2 protein, but not COX-1 protein, was induced in 17beta-estradiol treated HUVEC and was also inhibited by staurosporine. CONCLUSION: Our data showed that 17beta-estradiol increased the release of PGI2 from HUVEC via the induction of COX-2 which was mediated through protein kinase C. The results suggested that COX-2 might have a role in the cardiovascular protective effect of estrogen.
We have shown the HUVEC from normal pregnancy contained COX-1 protein but not COX-2 protein and released 6-keto-PGF1 alpha 277 +/- 5 ng/ml (for 24 h). In contrast, HUVEC from preeclampsia contained both COX-1 and COX-2 protein and released significantly lesser amounts of 6-keto-PGF1 alpha (159 +/- 8 ng/ml for 24 h; p < 0.05). Thus, COX-2 is expressed in HUVEC from preeclampsia but not in normal pregnancy and affects the release of prostacyclin suggesting the involvement of COX-2 in the pathogenesis of preeclampsia. The development of selective inhibitors of COX-2 may have a potential role in prevention and treatment of preeclampsia.
A case of testicular regression syndrome was reported. The patient was an 18 year old girl presenting with primary amenorrhoea. Physical examination revealed normal female external genitalia and underdeveloped secondary sexual characteristics. Hormonal profile indicated gonadal failure. Chromosome analysis revealed 46,XY karyotype. Diagnostic laparoscopy demonstrated undeveloped internal genital organs. Remnants of epididymis, vas deferens and seminiferous tubule were uncovered during exploratory laparotomy. Ontogeny of sexual differentiation and pathogenesis of testicular regression syndrome were reviewed and discussed.
To compare the efficiency of sperm preparation between the two-layer Percoll gradient and mini-Percoll methods, 50 normal and 33 abnormal semen samples from male partners of infertile couples were studied. The number of recovered spermatozoa, percentage of motility, percentage of normal morphology, and their survival at 24 and 48 hours were assessed. Both Percoll gradient techniques resulted in a significantly higher percentage of motility and percentage of normal morphology compared with the original semen samples (p < 0.0001). The two-layer Percoll gradient showed a higher sperm recovery than the mini-Percoll method (p < 0.001), but the latter resulted in a higher percentage of motility (p > 0.001) and a higher sperm survival rate at 24 hours (p < 0.05) than the former, regarding normal semen samples. These differences did not appear with abnormal semen samples when analyzed as a group. Considering each of the abnormal parameters separately, sperm recovery was significantly higher after the two-layer Percoll gradient in the case of astheno- and teratozoospermia (p < 0.05), but sperm survival at 48 hours was higher after the mini-Percoll gradient in the case of teratozoospermia (p < 0.05). It is concluded that both the two-layer Percoll gradient and mini-Percoll method can be used effectively for sperm preparation. The former yields a higher sperm recovery, but the latter should be considered regarding teratozoospermic samples and semen samples of very low volume.
OBJECTIVE: Dysregulation of 17 alpha-hydroxylase (CYP17) has been proposed as a cause of hyperandrogenism. We have determined the prevalence of a polymorphic allele in the CYP17 gene in sporadic patients with polycystic ovaries (PCOS) compared to a reference population, and to a group of hyperandrogenic individuals, to assess its significance to androgen production. PATIENTS AND DESIGN: DNA was isolated from EDTA blood samples from 69 patients with PCOS, 63 patients with congenital adrenal hyperplasia secondary to 21-hydroxylase deficiency and 124 consecutive patients attending for a full blood examination. The thymine (T) to cytosine (C) polymorphism at -34 base pairs (bp), denoted alleles A1 and A2 respectively, was detected by amplification of DNA followed by restriction enzyme digestion. MEASUREMENTS: Testosterone and LH. The frequency of alleles A1 and A2 in each of the subject groups was determined. RESULTS: The prevalences of the A1 and A2 alleles were 75 and 25% respectively in the PCOS group which was not significantly different from that in either the hyperandrogenic or the reference group. Neither allele segregated with hyperandrogenism. CONCLUSION: The polymorphism plays no apparent role in the dysregulation of CYP17.
To determine the incidence of etiologic factors responsible for primary amenorrhoea in Siriraj Hospital on the basis of clinical examination and laboratory investigations. A retrospective study was performed from the records of patients who attended the Reproductive endocrine Clinic at Siriraj Hospital from 1 September 1992 to 31 August 1995. During the 3 years of the study period, there were 110 cases of primary amenorrhoea. One hundred and one cases were analyzed: nine cases were excluded because the patients lost follow-up before the final diagnosis could be concluded. The two most common etiologic factors were mullerian agenesis (39.65%) and gonadal dysgenesis (32.69%). Mean age of the patients when they first consulted the physicians was 22.45 +/- 6.06 years. Karyotyping was done on 28 of 32 cases of gonadal dysgenesis; 46,XX karyotype was found in 50 per cent and 45,XO in 14.29 per cent of analyzed cases. Clinical examination gave wrong diagnosis of absent uterus in 4 cases who were in the hypoestrogenic stage with hypoplastic uterus; ultrasonography and laparoscopy gave the wrong diagnosis in 1 case each in our report. These patients successfully menstruated after hormonal replacement therapy. The incidence of etiologic causes and cytogenetic study of primary amenorrhoea in our study is different from earlier reports. Racial and environmental differences may play a role in these differences. The facilities of diagnostic tools may also play a part. However, both clinical examination and many laboratory investigations have to be completed before final diagnosis of etiologic causes of primary amenorrhoea are elucidated. Diagnosis based on inadequate data can be misleading.
A 50 g 1-h glucose test was studied in pregnant Thai women in order to find out the cut-off level for diagnosis of gestational diabetes. The gold standard for diagnosis of gestational diabetes. The gold standard for diagnosis of gestational diabetes was the standard OGTT. Among 23 patients diagnosed as having gestational diabetes following employing a standard test the cut-off value of 144 mg/dl accounted for the appropriate level for screening of gestational diabetes.