[Epidemiologic and clinical characteristics of 59 persons suspecting of being infected by the HIV virus despite having repeated negative laboratory findings].

OBJECTIVE: To describe the epidemiologic characteristics and clinical manifestations of 59 persons recruited via an internet chat group who complained of AIDS-like symptoms, so as to formulate effective intervention strategies and measures. METHODS: Case was defined as onset of any three of the following self-reported AIDS-like symptoms in a member of relevant "internet chat groups": persistent low grade fever, rash, swollen lymph node, fatigue, diarrhea, weight loss and low CD4(+)T count. We administered an internet-based questionnaire, and invited 59 of the 88 case-persons for voluntary physical examination and laboratory testing. RESULTS: The 59 case-persons came from 22 provinces; 54 (91.5%) were men; the median age was 34 (range: 22-53) years; 84.7% of them had high-risk sexual behaviors before the onset of self-reported symptoms. The median time interval from exposure to onset was 15 d (range: 1-365 d). Blood specimens for all the 59 case-persons were tested negative for HIV and syphilis antibodies. There was also no evidence of Xenotropic murine leukemia virus-related virus infection. One case-person was tested positive for hepatitis C virus antibody. The average CD4(+)T lymphocyte count was 707/µl. Of the 59 case-persons, 57 (96.6%) sought medical care from multiple providers; 40 were diagnosed to have no physical disorders. CONCLUSION: None of the 59 case-persons had any evidence of infection with HIV or any other infectious agents that could explain their self-reported symptoms.

[The mechanisms and effects of lutein on inducing the cell differentiation of human esophagus cancer EC9706].

OBJECTIVE: The purpose of the study was to explore the effects and molecular mechanisms of lutein on the differentiation of esophagus cancer EC9706 cell. METHODS: EC9706 cells were seeded in 1640 medium before the addition of test compounds. The respective test compound was added in fresh medium and the control cell received the vehicle (DMSO) or Fluorouracil. The proliferation and cell cycle of EC9706 were determined by MTT assay and flow cytometry, respectively. The change in cytomorphology was investigated by using HE staining. Proliferation and differentiation cells were checked and observed by methyl green-pyronine staining. The protein expression of cyclin D1 was detected by immunohistochemistry. RESULTS: Compared with the DMSO control group, the proliferation of the EC9706 cells treated with lutein (100 microg/mL and 150 microg/mL) could markedly be decreased and the cell cycle was blocked at G0/G1 phage which caused significant changes in the cytomorphology of EC9706 cell line, and the cell malignant degree tended to drop down, the protein expression of cyclin D1 was also down-regulated significantly. CONCLUSION: Lutein can inhibit the proliferation of EC9706 cell, and promote the cancer cell differentiation. cyclin D1 may be involved in cell proliferation and differentiation events in esophageal cancer EC9706 cell, which is regulated by lutein.

[Effects and mechanism of lutein on apoptosis of esophageal carcinoma EC9706 cells].

OBJECTIVE: To study the effects of lutein on apoptosis and its mechanism. METHOD: The cells of human esophageal carcinoma EC9706 were grown in RPMI medium containing 10% bovine serum and were treated with lutein at 100 microg x mL(-1) concentration. Flow cytometry was employed to investigate the effects of lutein on cell apoptosis of EC9706 cells. Histochemistry was performed to determine apoptosis-related protein expresion. RESULT: Flow cytometry analyses revealed that lutein increased EC9706 cell apoptosis ratio when treated with lutein 100 microg x mL(-1) at 96 h. Lutein decreased the expression of Bcl-2 protein and increased the expression of Bax protein in EC9706 cells. CONCLUSION: Lutein could inhibit mitosis and stimulate apoptosis of EC9706 cells. The apoptotic effect may result from the down-regulation of expression of Bcl-2 and up-regulation expression of Bax.