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Biomedical subjects

Ying Jin

Publications and source records attributed to Ying Jin.

At least 37 records · Page 2Linked to original sources

Molecular cloning, expression, purification, and characterization of shorter forms of human glutamic decarboxylase 67 in an E. coli expression system.

Previously, we reported the presence of truncated form of human brain l-glutamic decarboxylase 65 (tGAD65) in vivo as well as in vitro and found that tGAD65 was more active than the full-length GAD65 (Wei et al., J. Biomed. Sci., 10: 617-624, 2003). Here, we report the presence of two shorter forms of hGAD67, namely, hGAD67 (Delta1-70) and hGAD(67) (Delta1-90), referring to a deletion of 1-70 and 1-90 amino acids from the N-terminal, respectively. The molecular masses of hGAD67 (Delta1-70) and hGAD67 (Delta1-90) were found to be 59 kDa and 57 kDa, respectively. Both shorter forms were cloned, expressed, and characterized. In contrast to hGAD65, the shorter forms of hGAD67 were much less active than the full-length due to decrease in affinity of PLP towards the shorter enzymes. Both the full-length and one of the shorter forms of GAD67 were detected in porcine brain extract. Furthermore, the full-length GAD67 could be converted to both shorter forms by crude brain extract, suggesting that an endogenous protease may be present in the brain, which is responsible for the conversion. The cleavage of GAD67 seems to be Ca+(2)-dependent. The model for the conversion of GAD from full-length GAD to shorter forms of GAD and its physiological implications was proposed.

Animals↗

Ethanol inhibits monocyte chemotactic protein-1 expression in interleukin-1{beta}-activated human endothelial cells.

The aim of this study was to determine the effect of ethanol (EtOH) on endothelial monocyte chemotactic protein-1 (MCP-1) expression. IL-1beta increased the production of MCP-1 by human umbilical vein endothelial cells from undetectable levels to approximately 900 pg/ml at 24 h. EtOH dose-dependently inhibited IL-1beta-stimulated MCP-1 secretion as determined by ELISA: 25 +/- 1%, 35 +/- 7%, and 65 +/- 5% inhibition for 1, 10, and 100 mM EtOH, respectively, concomitant with inhibition of monocyte adhesion to activated endothelial cells. Similarly, EtOH dose-dependently inhibited IL-1beta-stimulated MCP-1 mRNA expression. Experiments with actinomycin D demonstrated that EtOH decreased the stability of MCP-1 mRNA. In addition, EtOH significantly reduced NF-kappaB and AP-1 binding activity induced by IL-1beta and inhibited MCP-1 gene transcription. Binding of (125)I-labeled MCP-1 to its receptor (CCR2) on THP-1 human monocytic cells was not affected by EtOH treatment. Modulation of the expression of MCP-1 represents a mechanism whereby EtOH could inhibit atherogenesis by blocking the crucial early step of monocyte adhesion and subsequent recruitment to the subendothelial space. These actions of EtOH may underlie, in part, its cardiovascular protective effects in vivo.

Cell Adhesion↗

Determination of optical properties of normal and adenomatous human colon tissues in vitro using integrating sphere techniques.

AIM: The purpose of the present study is to compare the optical properties of normal human colon mucosa/submucosa and muscle layer/chorion, and adenomatous human colon mucosa/submucosa and muscle layer/chorion in vitro at 476.5, 488, 496.5, 514.5 and 532 nm. We believe these differences in optical properties should help differential diagnosis of human colon tissues by using optical methods. METHODS: In vitro optical properties were investigated for four kinds of tissues: normal human colon mucosa/submucosa and muscle layer/chorion, and adenomatous human colon mucosa/submucosa and muscle layer/chorion. Tissue samples were taken from 13 human colons (13 adenomatous, 13 normal). From the normal human colons a total of 26 tissue samples, with a mean thickness of 0.40 mm, were used (13 from mucosa/submucosa and 13 from muscle layer/chorion), and from the adenomatous human bladders a total of 26 tissue samples, with a mean thickness of 0.40 mm, were used (13 from mucosa/submucosa and 13 from muscle layer/chorion). The measurements were performed using a double-integrating-sphere setup and the optical properties were assessed from these measurements using the adding-doubling method that was considered reliable. RESULTS: The results of measurement showed that there were significant differences in the absorption coefficients and scattering coefficients between normal and adenomatous human colon mucosa/submucosa at the same wavelength, and there were also significant differences in the two optical parameters between both colon muscle layer/chorion at the same wavelength. And there were large differences in the anisotropy factors between both colon mucosa/submucosa at the same wavelength, there were also large differences in the anisotropy factors between both colon muscle layer/chorion at the same wavelength. There were large differences in the value ranges of the absorption coefficients, scattering coefficients and anisotropy factors between both colon mucosa/submucosa, and there were also large differences in these value ranges between both colon muscle layer/chorion. There are the same orders of magnitude in the absorption coefficients for four kinds of colon tissues. The scattering coefficients of these tissues exceed the absorption coefficients by at least two orders of magnitude. CONCLUSION: There were large differences in the three optical parameters between normal and adenomatous human colon mucosa/submucosa at the same laser wavelength, and there were also large differences in these parameters between both colon muscle layer/chorion at the same laser wavelength. Large differences in optical parameters indicate that there were large differences in compositions and structures between both colon mucosa/submucosa, and between both colon muscle layer/chorion. Optical parameters for four kinds of colon tissues are wavelength dependent, and these differences would be useful and helpful in clinical applications of laser and tumors photodynamic therapy (PDT).

Adenomatous Polyposis Coli↗

Mode of action of taurine as a neuroprotector.

Previously, it has been shown that taurine exerts its protective function against glutamate-induced neuronal excitotoxicity through its action in reducing glutamate-induced elevation of intracellular free calcium, [Ca2+]i. Here, we report the mechanism underlying the effect of taurine in reducing [Ca2+]i. We found that taurine inhibited glutamate-induced calcium influx through L-, P/Q-, N-type voltage-gated calcium channels (VGCCs) and NMDA receptor calcium channel. Surprisingly, taurine had no effect on calcium influx through NMDA receptor calcium channel when cultured neurons were treated with NMDA in Mg2+-free medium. Since taurine was found to prevent glutamate-induced membrane depolarization, we propose that taurine protects neurons against glutamate excitotoxicity by preventing glutamate-induced membrane depolarization, probably through its effect in opening of chloride channels and, therefore, preventing the glutamate-induced increase in calcium influx and other downstream events.

Animals↗

Mutation analysis of PAX6 gene in a large Chinese family with aniridia.

BACKGROUND: Mutations in PAX6 gene have been shown to be the genetic cause of aniridia, which is a severe panocular eye disease characterised by iris hypoplasia. However, there is no study to do genetic analysis of aniridia, although there are several case reports in China. Here, we describe a mutation analysis of PAX6 in a large Chinese family with aniridia. METHODS: Genomic DNA from venous blood samples was prepared. Haplotype analysis was performed with two genetic markers (D11S904 and D11S935). Fourteen exons of the PAX6 gene were amplified from genomic DNA. Polymerase chain reaction (PCR) products of each exon were analysed by single strand conformational polymorphism (SSCP). The PCR products having an abnormal pattern were sequenced to confirm the mutation. RESULTS: Significant evidence for allele sharing in affected patients was detected suggesting that PAX6 mutation links to aniridia in this family. An extra band corresponding to exon 9 in PAX6 was found by single strand conformational polymorphism analysis in all the aniridia patients in this family, but not detected in the unaffected members. A mutation of C to T was detected by sequencing at the nucleotide 1080 that converts the Arg codon (CGA) to the termination codon (TGA). CONCLUSIONS: Aniridia is caused by a nonsense mutation of PAX6 gene in the large Chinese kindred. Genetic test is important to prevent the transmission of aniridia to their offsprings in the kindred by prenatal diagnosis.

Aniridia↗

Effect of apocalmodulin on recombinant human brain glutamic acid decarboxylase.

In this work, we report that the recombinant glutathione S-transferase (GST)-human L-glutamic acid decarboxylase (HGAD) isoforms, 65-kDa L-glutamic acid decarboxylase (GAD) (GST-HGAD65) fusion protein or free truncated HGAD65, were activated by apocalmodulin (ApoCaM) to an extent of 60%. Both truncated forms of GAD67 (tGAD67), HGAD67(Delta1-70) and HGAD67(Delta1-90), were markedly activated by ApoCaM to an extent of 141 and 85%, respectively, while GST-HGAD67 was not significantly affected. The activation appears to be due to an increase of GAD affinity for its cofactor, pyridoxal phosphate (PLP). This conclusion is based on the following observations. Firstly, the V(max) of GAD was increased when ApoCaM was present whereas the affinity for the substrate, glutamate, was not affected. Secondly, the affinity of GAD for PLP was increased in the presence of ApoCaM. Thirdly, results from calmodulin-agarose affinity column chromatography studies indicated a direct interaction or binding between ApoCaM and GAD. Fourthly, ApoCaM was found to be copurified with GAD65/GAD67 by anti-GAD65/67 immunoaffinity column using rat brain extract. Hence, it is proposed that a conformational change is induced when ApoCaM interacts with GAD65 or tGAD67, resulting in an increase of GAD affinity for PLP and the activation of GAD. The physiological significance of the interaction between GAD and ApoCaM is discussed.

Animals↗

Sodium ferulate prevents amyloid-beta-induced neurotoxicity through suppression of p38 MAPK and upregulation of ERK-1/2 and Akt/protein kinase B in rat hippocampus.

AIM: To observe whether an amyloid beta (Abeta)-induced increase in interleukin (IL)-1beta was accompanied by an increase in the p38 mitogen-activated protein kinase (MAPK) pathway and a decrease in the cell survival pathway, and whether sodium ferulate (SF) treatment was effective in preventing these Abeta-induced changes. METHODS: Rats were injected intracerebroventricularly with Abeta25-35. Seven days after injection, immunohistochemical techniques for glial fibrillary acidic protein (GFAP) were used to determine the astrocyte infiltration and activation in hippocampal CA1 areas. The expression of IL-1beta, extracellular signal-regulated kinase (ERK), p38 MAPK, Akt/protein kinase B (PKB), Fas ligand and caspase-3 were determined by Western blotting. The caspase-3 activity was measured by cleavage of the caspase-3 substrate (Ac-DEVD-pNA). Reverse transcription-polymerase chain reaction was used to analyze the changes in IL-1beta mRNA levels. RESULTS: Intracerebroventricular injection of Abeta25-35 elicited astrocyte activation and infiltration and caused a strong inflammatory reaction characterized by increased IL-1beta production and elevated levels of IL-1beta mRNA. Increased IL-1beta synthesis was accompanied by increased activation of p38 MAPK and downregulation of phospho-ERK and phospho-Akt/PKB in hippocampal CA regions prepared from Abeta-treated rats, leading to cell death as assessed by activation of caspase-3. SF significantly prevented Abeta-induced increases in IL-1beta and p38 MAPK activation and also Abeta-induced changes in phospho-ERK and phospho-Akt/PKB expression levels. CONCLUSION: SF prevents Abeta-induced neurotoxicity through suppression of p38 MAPK activation and upregulation of phospho-ERK and phospho-Akt/PKB expression.

Amyloid beta-Peptides↗

[The expression of TGF-beta1 and bFGF after LASEK and the effects of 20% ethanol exposure on corneal wound healing].

OBJECTIVE: To assess the effects of 20% ethanol used in LASEK on corneal wound healing. METHODS: Forty-eight eyes from 24 rabbits were deepithelialized by two techniques. The epithelium were detached with either 20% ethanol (applied for 30 seconds) or mechanical scraping, then ablated was performed. The number of superficial stromal keratocytes was counted and the morphologic changes were observed. Expression of TGF-beta1 and bFGF mRNAs was detected and analyzed by reverse transcription-polymerase chain reaction and immunocytochemical methods at 1, 7, 30 and 90 days after the surgery. RESULTS: One day after the surgery, the expression of TGF-beta1 and bFGF in the keratocytes in both treated groups was lower than that of the normal controls. Seven days after the surgery, the expression of TGF-beta1 and bFGF in both treated groups was greater than that of the normal controls (P < 0.01). The expression in the alcohol-treated group was greater than that of the surgical-treated group (P < 0.01). The expression of TGF-beta1 and bFGF reached the peak 30 days after the surgery, no significant difference was detected between the alcohol-treated and surgical-treated groups. There was no significant difference in expression level between the alcohol-treated and surgical-treated groups 3 months after the surgery; as well as between treated groups and normal group. The amount of TGF-beta1 and bFGF mRNA was positively correlated with the number of keratocytes. The correlation coefficient between TGF-beta1 and bFGF mRNA and the number of the keratocytes was 0.744 (P < 0.01) and 0.738 (P < 0.01) in the alcohol-treated group; and was 0.664 (P < 0.01) and 0.785 (P < 0.01) in the surgical-treated group, respectively. CONCLUSIONS: The expression of TGF-beta1 and bFGF mRNA undergo a dynamic process of "decrease-increase-normal". Although ethanol has a slight toxic effect on rabbit epithelial cells, but the effects do not persist over time, therefore, it is relatively safe to use the alcohol treatment in the LASEK.

Animals↗

[Comprehensive staging surgery in treatment of malignant ovarian germ cell tumor].

OBJECTIVE: To evaluate the impact of comprehensive staging surgery on relapse and survival of malignant ovarian germ cell tumor (MOGCT). METHODS: The clinical data of 127 MOGCT cases treated in Peking Union Medical College Hospital from June 1980 to June 2003 were analyzed retrospectively. All the data about comprehensive staging surgery during primary surgery were collected, and other factors related to prognosis were also collected at the same time. COX model was applied in multivariate analysis related to relapse and survival. RESULTS: Among 127 patients, 45 (35.4%) received comprehensive staging surgery. Seventy-one cases (55.9%) received satisfied cytoreduction with residual tumor < 2 cm, 11 cases (8.7%) with residual tumor > or = 2 cm, and another 45 cases (35.4%) were undetermined. Seventy-five cases (59.1%) received cisplatin, etoposide, and bleomycin (BEP) or cisplatin, vinblastine, and bleomycin (PVB) chemotherapy, 18 cases (14.2%) received vincristine, actinomycin D, cyclophosphamide (VAC) chemotherapy, and 34 cases (26.8%) received other regimens or no chemotherapy. During the follow up period, 7 of 45 patients relapsed in patients who received compressive staging surgery, while the latter was not a significant factor (P = 0.061). Chemotherapy regimen and residual tumor were the significant factors related to the relapse (P < 0.05). All the patients were followed up for 2-254 months. Chemotherapy regimen and residual tumor were also the significant factors related to survival (P < 0.05). Compressive staging surgery showed no significant effect on survival (P > 0.05). CONCLUSIONS: The critical treatment for MOGCT is satisfactory cytoreduction surgery plus standard chemotherapy. Comprehensive staging surgery shows no significant impact on the prognosis of MOGCT patients.

Adolescent↗

[Lymphadenectomy in the treatment of malignant ovarian germ cell tumor].

OBJECTIVE: To evaluate the impact of lymphadenectomy on the relapse and survival of malignant ovarian germ cell tumor (OGCT). METHODS: The clinical data of 102 OGCT cases treated in Peking Union Medical College Hospital from June 1980 to June 2003 were analyzed retrospectively. All the data about lymphadenectomy during primary and secondary surgery were collected, and other factors related to prognosis were also collected at the same time. Chi-squared test was applied in the univariate analysis related to relapse of disease. Cox model was applied in multivariate analysis related to relapse and survival of disease. RESULTS: Pelvic and paraaortic lymph node metastasis was not significantly related to prognosis in primary and secondary treated patients. Lymphadenectomy showed no significant impact on disease relapse and survival. In the primary treatment, International Federation of Gynecology and Obstetrics (FIGO) staging, chemotherapy regimen, residual tumor and lymphadenectomy were the significant factors related to the relapse. After being stratified for the chemotherapy regimen, lymphadenectomy was not significantly related to the relapse in bleomycin +etoposide +cisplatin or cisplatin +vincristine +bleomycin regimen group, and lymphadenectomy could prevent relapse in no chemotherapy or other chemotherapy regimen group. In relapsed patients, only residual tumor was significantly related to survival time after relapse. CONCLUSIONS: Pelvic lymph node metastasis is not the significant risk factor related to prognosis. Lymphadenectomy may have a beneficial effect on survival, although such effect is not significant. Although lymphadenectomy provides important information for prognosis, they provide little benefit to those patients already requiring chemotherapy based on the original operative findings. Lymphadenectomy should be performed to primary or relapsed patients by an expert surgical team.

Adolescent↗

[Multifactor analysis of relationship between the biological exposure to iodine and hypothyroidism].

OBJECTIVE: To assess the relationship between the biological exposure to iodine and hypothyroidism. METHODS: Logistic regression model was used to analyze the risk factors of hypothyroidism, according to the epidemiologic data of 3761 adults in 3 kinds of rural communities: mild iodine deficiency area (4 natural villages in Panshan County, Liaoning Province), more than adequate iodine (7 natural villages of Zhangwu County, Liaoning Province), and excessive iodine area (2 natural villages of Huanghua City, Hebei Province). RESULTS: More than adequate iodine and excessive iodine were independent risk factors of subclinical hypothyroidism (OR = 3.172 and 6.391, P < 0.05) and overt hypothyroidism (OR = 3.696 and 9.213, P < 0.05). When interactions of iodine exposure and thyroid peroxidase antibody (TPOAb) or thyroglobulin antibody (TgAb) were included, more than adequate iodine was still a risk factor of subclinical hypothyroidism (OR = 2.788, P < 0.01), but had no such effect on overt hypothyroidism. Interaction of more than adequate iodine and positive TgAb significantly affected subclinical hypothyroidism and overt hypothyroidism (OR = 2.656 and 3.347, P < 0.05). CONCLUSION: More than adequate and excessive iodine exposure are independent risk factors of hypothyroidism. The risk of hypothyroidism grows up and thyroid dysfunction becomes more serious with the increasing of the biological exposure to iodine.

Adult↗

Wwp2, an E3 ubiquitin ligase that targets transcription factor Oct-4 for ubiquitination.

The POU transcription factor Oct-4 is a master regulator affecting the fate of pluripotent embryonic stem cells. However, the precise mechanisms by which the activation and expression of Oct-4 are regulated still remain to be elucidated. We describe here a novel murine ubiquitin ligase, Wwp2, that specifically interacts with Oct-4 and promotes its ubiquitination both in vivo and in vitro. Remarkably, the expression of a catalytically inactive point mutant of Wwp2 abolishes Oct-4 ubiquitination. Moreover, Wwp2 promotes Oct-4 degradation in the presence of overexpressed ubiquitin. The degradation is blocked by treatment with proteasome inhibitor. Fusion of a single ubiquitin to Oct-4 inactivates its transcriptional activity in a heterologous Oct-4-driven reporter system. Furthermore, overexpression of Wwp2 in embryonic stem cells significantly reduces the Oct-4-transcriptional activities. Collectively, we demonstrate for the first time that Oct-4 can be post-translationally modified by ubiquitination and that this modification dramatically suppresses its transcriptional activity. These results reveal that the functional status of Oct-4, in addition to its expression level, dictates its transcriptional activity, and the results open up a new avenue to understand how Oct-4 defines the fate of embryonic stem cells.

Animals↗

Overexpression of XIAP inhibits apoptotic cell death in an oligodendroglial cell line.

1. This study describes the use of an oligodendroglial cell line (158N) to study the protective effects of X-chromosome-linked inhibitor of apoptosis (XIAP) overexpression. 2. 158N cells were transiently transfected with either pCMV-Myc-XIAP or control pCMV-Myc vector. At 48 h post-transfection, immunoblotting and immunocytochemical staining showed robust myc-XIAP overexpression in pCMV-Myc-XIAP transfected cells relative to pCMV-Myc-transfected cells and normal 158N cells. 158N cells were treated with either 100 nm staurosporine (STS) or 300 microM dopamine (DA) and cell survival/function determined using two cell viability assays. 3. Both STS and DA treatments resulted in increased apoptotic death of pCMV-Myc transfected cells. In contrast, there was significant decrease in apoptotic cell death in cells transfected with pCMV-Myc-XIAP. Finally, XIAP overexpression was found to significantly reduce caspase-3 enzyme activity levels in response to apoptotic stimuli. 4. These results provide evidence that XIAP overexpression promotes cell survival in a non-neuronal cell type derived from the central nervous system. In addition, these data suggest that the 158N oligodendroglial cell line is a suitable tool for transient transfection studies, which is a problem frequently encountered when attempting to introduce genes of interest in cultures of primary oligodendroglia.

Apoptosis↗

Isolation and analysis of water stress induced genes in maize seedlings by subtractive PCR and cDNA macroarray.

In order to identify genes induced during the water stress response in maize (Zea mays) seedlings, suppression subtractive hybridization (SSH) was performed using mixed cDNAs prepared from maize seedlings treated with 20% PEG as testers and cDNAs from unstressed maize seedlings as drivers. A forward subtractive cDNA library was constructed, from which 960 recombinant colonies were picked and amplified. Through differential screening of the subtractive cDNA library, 533 clones were identified as water stress induced. After sequencing, 190 unique expressed sequence tags (ESTs) were obtained by clustering and blast analysis, which included transcripts that had previously been reported as responsive to stress as well as some functionally unknown transcripts. The ESTs with significant protein homology were sorted into 13 functional categories. A cDNA marcoarray containing the 190 unique ESTs was used to analyze their expression profiles in maize seedling during both PEG treatment and natural drought. The results indicated that 67 ESTs in leaves and 113 ESTs in roots were significantly up-regulated by PEG-stress. 123 ESTs were found to be up-regulated for at least one time-course point in either maize leaves or roots. Correspondingly, 163 ESTs were significantly up-regulated by drought stress. Results from the hierarchical cluster analysis suggest that the leaves and roots of maize seedlings had different expression profiles after PEG treatment and that there was a lot of overlap between PEG- and drought-stress induced up-regulated transcripts. A set of transcripts has been identified, which have significantly increased expression and probably involved in water stress signaling pathway based on data analysis.

Cluster Analysis↗

The mitochondrial uncoupling agent 2,4-dinitrophenol improves mitochondrial function, attenuates oxidative damage, and increases white matter sparing in the contused spinal cord.

The purpose of this study was to investigate the potential neuroprotective efficacy of the mitochondrial uncoupler 2,4-dinitrophenol (DNP) in rats following a mild to moderate spinal cord contusion injury. Animals received intraperitoneal injections of vehicle (DMSO) or 5 mg/mL of DNP prior to injury. Twenty-four hours following surgery, mitochondrial function was assessed in mitochondria isolated from spinal cord synaptosomes. In addition, synaptosomes were used to measure indicators of reactive oxygen species formation, lipid peroxidation, and protein oxidation. Relative to vehicle-treated animals, pretreatment with DNP maintained mitochondrial bioenergetics and significantly decreased reactive oxygen species levels, lipid peroxidation, and protein carbonyl content following spinal cord injury. Furthermore, pretreatment with DNP significantly increased the amount of remaining white matter at the injury epicenter 6 weeks after injury. These results indicate that treatment with mitochondrial uncoupling agents may provide a novel approach for the treatment of secondary injury following spinal cord contusion.

2,4-Dinitrophenol↗

Study on switched reluctance generator.

The linear and non-linear math models of the switched reluctance generator (SRG) in generator mode were established in this work. The phase current and energy conversion process during generator operation were simulated by the linear math model. The non-linear math model was used to analyze the characteristics of the SRG operation in self-excitation mode and in separately-excitation mode. Some important findings on how the SRG is operated and controlled were obtained in this study, which provides theoretical basis for further design and experimental study.

Journal Article↗

[Clinical analysis of endometrial carcinoma patients aged 45 years and younger].

OBJECTIVE: To retrospectively analyze the clinical characteristics and outcomes of endometrial carcinoma patients aged 45 years and younger. METHODS: Fifty-two cases of endometrial carcinoma aged 45 years and younger were treated in Peking Union Medical College Hospital. They were further divided into group A (35 years of age and younger) and group B (older than 35 years). Clinical data of these patients were reviewed and the two groups were compared. RESULTS: Patients aged 45 years and younger accounted for 12.7% of all the endometrial carcinoma cases. About 50% of the patients were nulliparous, infertile or had irregular menstruation and endometrial hyperplasia, 29% were obese, 23% had polycystic ovaries. Eighty-three percent of the patients were stage [International Federation of Gynecology and Obstetrics (FIGO), 1988]. Group A had more polycystic ovaries and atypical endometrial hyperplasia than group B (53% vs 9%, 59% vs 26% respectively, P < 0.05). All group A patients were stage I endometrial carcinoma. In group B, 26% had high risk factors, and compared with group A, FIGO stage was higher (P < 0.05). Operation was the main treatment. Two patients were treated successfully with conservative high dose progestin. Two patients relapsed. CONCLUSIONS: There were high incidences of infertility, irregular menstruation, endometrial hyperplasia, obese and polycystic ovaries in patients aged 45 years and younger, indicating the relationship between endometrial carcinoma and estrogen. Most patients, especially those younger than 35 years, were stage I with few risk factors and good prognosis. Conservation of fertility and ovarian function should be considered in these patients.

Adenocarcinoma↗

Effect of different iodine intake on schoolchildren's thyroid diseases and intelligence in rural areas.

BACKGROUND: Reports are increasingly appearing on the side effects caused by excessive iodine intake. Our objective was to find out whether iodine excess would impair the thyroid function and intelligence of schoolchildren in rural areas of China. METHODS: A comparative epidemiological study was made on thyroid function and intelligence of the schoolchildren in the areas of low, moderate or excessive intake of iodine. In the area of low intake of iodine (Panshan, Liaoning province, median urinary iodine (MUI) was 99 microg/L), of moderate intake of iodine (Zhangwu, Liaoning Province, MUI was 338 microg/L) and of excessive intake of iodine (Huanghua, Hebei Province, MUI was 631 microg/L). The numbers of schoolchildren from each area selected to take part in a Chinese version of Raven's Test were 190, 236 and 313, respectively, and then 116, 110 and 112 of them were tested for thyroid function, thyroid autoantibody (TAA) and urinary iodine (UI). RESULTS: There were no significant differences in the incidences of overt hyperthyroidism, subclinical hyperthyroidism and overt hypothyroidism in Panshan, Zhangwu and Huanghua. But significant differences were found in the incidences of subclinical hypothyroidism (P = 0.001) in these three areas. The incidences of subclinical hypothyroidism in Huanghua and Zhangwu were 4.76 and 3.37 times higher than that in Panshan. TAA were negative in all the schoolchildren with subclinical hypothyroidism except for one. No significant difference was found among the rates of thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TGAb) in these three areas. Mean serum thyroglobulin (TG) value of Huanghua was markedly higher than those of the other two (P = 0.02). Mean serum TG value of Zhangwu was higher than that of Panshan but the difference was not significant. Mean IQ value of the schoolchildren in Huanghua was markedly higher than that for Zhangwu (P = 0.001). Mean IQ value of the schoolchildren in Panshan was lower than that of Huanghua and higher than that of Zhangwu but, again, the differences were not significant. CONCLUSIONS: The increase of iodine intake may increase the risk for schoolchildren of subclinical hypothyroidism. In the area of iodine excess, most of the subclinical hypothyroidism cases are not of autoimmune origin. No obvious effect of excess iodine was found on mental development of schoolchildren.

Child↗