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1.
Chinese Journal of Cardiology ; (12): 277-280, 2006.
Article in Chinese | WPRIM | ID: wpr-295333

ABSTRACT

<p><b>OBJECTIVE</b>To evaluate the present status of pulmonary embolism (PE) misdiagnosis in China.</p><p><b>METHODS</b>Documents on PE misdiagnosis published in Chinese-language journals between 2001 and 2004 were identified by searching the China Hospital Knowledge Database in China National Knowledge Infrastructure Web (CNKI-CHKD). Retrospective review items include: patient symptoms, medical examination tools, treatments and prognosis, causes of death, hospitals involved. The recent situation on PE misdiagnosis was also compared to that in year between 1980 to 2000. The number of published literatures on PE and PE misdiagnosis from 1994 to 2004 was also searched.</p><p><b>RESULTS</b>(1) A total of 110 documents with 1540 misdiagnosed PE patients were found. The misdiagnosis time varies from 0.5 hour to 16 years and was 1.86 years on average. (2) Once the misdiagnosis be corrected, the prognosis could be improved by antithrombotic and thrombolytic therapies compared with those without antithrombotic and thrombolytic therapies (OR 11.67, 95% CI 5.861-23.249). The major causes of death were sudden death, resistant shock in patients without antithrombotic and thrombolytic therapies while the causes were sudden death, cerebral hemorrhage and resistant shock in PE patients received antithrombotic and thrombolytic therapies. (3) Literatures on PE misdiagnosis were most from provincial hospitals [37 papers with 547 cases (33.6%, 35.5%)] and municipal hospitals [43 papers with 671 cases (39.1%, 43.6%)]. (4) The number of papers published on PE and PE misdiagnosis from 1994 to 2004 increased steadily by an average of 26.6% and 9.1%, respectively. (5) PE was misdiagnosed to more than 70 kinds of diseases and the top 4 were coronary heart disease in 449 cases (26.8%), pneumonia in 217 cases (12.9%), congestive heart failure in 142 cases (8.5%) and pleurisy in 114 cases (6.8%).</p><p><b>CONCLUSIONS</b>(1) PE misdiagnosis is still a critical issue now in China and early diagnosis and effective treatment is essential for a better prognosis. (2) The differential diagnosis among PE and coronary heart disease and pneumonia need to be emphasized to avoid the PE misdiagnosis. (3) Efforts should be made through continuing education on clinical professionals to improve their knowledge on PE in China.</p>


Subject(s)
Adolescent , Adult , Aged , Aged, 80 and over , Child , Child, Preschool , Female , Humans , Male , Middle Aged , Young Adult , China , Diagnosis, Differential , Diagnostic Errors , Pulmonary Embolism , Diagnosis
2.
Journal of Applied Clinical Pediatrics ; (24)2006.
Article in Chinese | WPRIM | ID: wpr-639406

ABSTRACT

Objective To explore the causes of subclinical hypothyrodism in children and the effects of the interventional therapy with thyroixine on the course of it.Methods Two hundreds children with subclinical hypothyroidism were measured for thyroglobulin antibody(TGAb),thyroid microsomal antibody(TMAb) in the blood serum,examined by colord Dopplor ultrasonic,examined by fine needle aspiraton cytology of the throid and measured the rate of 131I absorbed by thyroid in order to find out the causes of the disease.Two hundreds cases were randomly divided into two groups on the base of the cause of diseases,treatment group 100 cases and control group 100 cases.The treatment group were treated by throxine 25-75 ?g/d and the therapeutic dosage were chosen with the normal value of free triiodothyronine(FT3),free thyroxine(FT4)and high sensitive thyrotropin(sTSH) in the blood serum .After one year thyroxine therapy were stopped.Thyroid function was examined 6 months later after stopping the thyroxine.Results Among all of the causes of subclinical hypothyroidism in children,Hasgumoto′s thyroiditis accounts for 56%,simple goiter accounts for 26%,antithyroid drug accounts for 6%,the lack of thyroxine substitution therapy on the hypothyroidism accounts for 5% and undefined causes accounts for 7% .The thyroid function could keep normal for 1 year with an alternative therapy with thyroxine on subclinical hypothyroidism in children.Half a year later after stopping thyroxine,the thyroid function turned normal in most of the children.There were obvious differences in the ratio of cure and the ratio of effectiveness between treatment group and control group (t=20.2,3.2 Pa

3.
Journal of Experimental Hematology ; (6): 999-1003, 2005.
Article in Chinese | WPRIM | ID: wpr-343840

ABSTRACT

The aim of this study was to investigate the mechanism to reverse the drug resistance of leukemia cells in tetrandrine (Tet) alone or in combination with droloxifen (Drol) by using protein chips and to lay the theoretical basis for the clinical applications. Three monoclonal antibodies against P-glycoprotein (P-gp), the multidrug resistance-associated protein (MRP1) and the breast cancer resistance protein (BCRP) were immobilized onto the agarose gel film-coated glass slides. Protein chips were prepared respectively from K562/A02 cells cultured for 12, 24 and 48 hours with Tet alone or in combination with Drol. The results showed that Tet alone or in combination with Drol could decrease only the expression of P-gp in a time-dependent manner, the effect for 48 hours as follows: Tet + Drol 82.620 +/- 3.227; Tet alone 86.440 +/- 2.906; Drol alone 87.230 +/- 2.049; control 93.670 +/- 2.748 (P < 0.05). However, down-regulation of P-gp by K562/A02 cells cultured with Tet alone or in combination with Drol began at 24 hours (Tet + Drol 85.270 +/- 3.095; control 93.670 +/- 2.748, P < 0.05). The results were coincident with that of FCM. It is concluded that Tet and Drol can downregulate the expression of P-gp in the time-dependent way. There is a significant difference between Tet alone and Tet combined with Drol at 24 hours (P < 0.05). The expression of MRP1 and BCRP are not closely correlated with the reversal mechanism of Tet and Drol, and which may be involved in the mechanism of this combination to reverse multidrug resistance in leukemia.


Subject(s)
Humans , ATP Binding Cassette Transporter, Subfamily G, Member 2 , ATP-Binding Cassette Transporters , ATP Binding Cassette Transporter, Subfamily B, Member 1 , Antineoplastic Agents , Pharmacology , Benzylisoquinolines , Pharmacology , Drug Resistance, Multiple , Drug Resistance, Neoplasm , Drug Synergism , K562 Cells , Leukemia , Metabolism , Pathology , Multidrug Resistance-Associated Proteins , Neoplasm Proteins , Protein Array Analysis , Tamoxifen , Pharmacology
4.
Chinese Journal of Oncology ; (12): 528-530, 2005.
Article in Chinese | WPRIM | ID: wpr-358580

ABSTRACT

<p><b>OBJECTIVE</b>To evaluate the use of protein array chips in detection of multidrug-resistance proteins.</p><p><b>METHODS</b>Human erythroleukemic cell line K562 and its doxorubicin-resistant counterpart K562/A02 were used in the study. Monoclonal antibodies against P-glycoprotein (P-gP), multidrug resistance-associated protein (MRP1) and breast cancer resistance protein (BCRP) were immobilized onto agarose film-coated glass. The antibody-cell binding was assessed by capturing K562 and K562/A02 cells. The protein array was observed under a microscope and the image was captured with a CCD camera. The expression levels of the three proteins were also measured by flow cytometry (FCM).</p><p><b>RESULTS</b>The expression of P-gP and BCRP in K562 was very low. However, MRP1 expression was high. P-gP and MRP1 were highly expressed in K562/A02, while the expression of BCRP was low. FCM results showed that the expression rate of P-gP, MRP1 and BCRP in K562 cells was 5.98% +/- 2.19%, 95.80% +/- 3.98%, 1.03% +/- 0.45%, respectively, while that in K562/A02 cells was 92.67% +/- 1.80%, 97.18% +/- 1.02%, 3.98% +/- 0.37%, respectively. The results of protein array method are consistent with those of FCM (P > 0.05).</p><p><b>CONCLUSION</b>It is feasible to develop a new protein array technique and to provide a novel method for multi-drug resistant cell detection, with a high throughput, high specificity, simple procedure and low cost.</p>


Subject(s)
Humans , ATP Binding Cassette Transporter, Subfamily G, Member 2 , ATP-Binding Cassette Transporters , ATP Binding Cassette Transporter, Subfamily B, Member 1 , Drug Resistance, Multiple , Genetics , Drug Resistance, Neoplasm , Genetics , K562 Cells , Multidrug Resistance-Associated Proteins , Neoplasm Proteins , Protein Array Analysis
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