Objective To learn the domestic investigation into pulmonary cryptococcosis in the 22 years.Methods We retrieved the literature about pulmonary cryptococcosis included in CMCC,and summarized the clinical data of 67 patients suffering from pulmonary cryptococcosis.Results The clinical situation and radiological manifestation of pulmonary cryptococcosis were diverse and nonspecific.Cryptococcal meningitis was the commonest complication(31.34%).Almost all patients with pulmonary cryptococcosis were once misdiagnosed.Final diagnosis mainly depended on the smear,culture or pathological examination of various clinical specimens.Therapeutic tool involved resection with operation and the application of anti-fungi drugs.Conclusion To increase the cognition to the disease is the key to increase the final diagnosis rate.Therapeutical effect of anti-fungi drugs should be emphasized,especially the application in preoperation and postoperation can decrease the dissemination of cryptococcus after operation,which might result in cryptococcal meningitis.

BACKGROUNDPathology is the "gold standard" of the diagnosis of lung cancer, but at present there are few articles about evaluating the value of cytopathological check. The aim of this study is to evaluate the value of cytopathological check in the diagnosis of primary bronchogenic carcinoma of the lung.

METHODSA total of 552 samples' cytopathological results of 248 patients from January 2003 to May 2005 in this hospital were retrospectively analyzed. The samples included pleural fluids (110 for 68 patients), materials from lung puncture (33 for 31 patients), smears of transcatheter bronchial brushing (152 for 138 patients), bronchoalveolar lavage fluids (30 for 26 patients) and sputa (227 for 118 patients).

RESULTSThe positive results of different specimens were as follow: the pleural fluids was 69.12%, the materials from lung puncture 67.74%, the smears of transcatheter bronchial brushing 65.22%, the bronchoalveolar lavage fluids 23.08% and sputa 21.19% respectively. The positive rates of the pleural fluids, the materials from lung puncture and the smears of transcatheter bronchial brushing were higher than that of the bronchoalveolar lavage fluids and sputa (P < 0.01). There was no significant difference among the positive rates of the pleural fluids, the materials from lung puncture and the smears of transcatheter bronchial brushing, and between the positive rates of the bronchoalveolar lavage fluids and sputa (P > 0.05).

CONCLUSIONSThe cytopathological examination is helpful for the diagnosis of primary bronchogenic carcinoma of the lung, and is one of the important ways to the diagnosis of primary bronchogenic carcinoma of the lung.

Purpose: Four and a half LIM protein 1 (FHL1) is involved in breast cancer (BC) development, but the regulatory mechanism involved remain unclear. In the present study, we examined the role of FHL1 in BC development. Methods: The expression of FHL1, miR-183-5p, and miR-96-5p in BC tissues was analyzed using StarBase analysis. FHL1 expression in BC tissues, a normal human breast epithelial cell line, and BC cell lines was detected using quantitative reverse transcription polymerase chain reaction (qRT-PCR). The relationship between FHL1 and miR-183-5p/miR-96-5p was analyzed via Pearson's rank correlation, TargetScan, and a dual-luciferase reporter assay. BT549 and MDA-MB-231 cells were transfected with either FHL1 and miR-183-5p mimics, or siFHL1 and a miR-183-5p inhibitor, respectively. The viability, colony number, migration, invasion, and tube length of BT549 and MDA-MB-231 cells were examined using cell counting kit-8, colony formation, wound-healing, Transwell, and tube formation assays, respectively. The levels of FHL1, vascular endothelial growth factor (VEGF), p53, E-cadherin, N-cadherin, and vimentin were quantified using western blotting and qRT-PCR. Results: FHL1 expression was downregulated in BC tissues and cells, whereas miR-183-5p and miR-96-5p were upregulated in BC tissues (negative correlation with FHL1 expression).FHL1 overexpression inhibited the viability, colony number, migration, and invasion of BC cells and the expression of VEGF, N-cadherin, and vimentin, and increased the expression of FHL1, p53, and E-cadherin in BT549 cells. Furthermore, a miR-183-5p mimic reversed these effects of FHL1 overexpression, whereas FHL1 silencing caused opposite results to those observed in MDA-MB-231 cells; however, this was reversed by a miR-183-5p inhibitor. Conclusion Our study suggests that miR-183-5p promotes cell proliferation, metastasis, and angiogenesis by negatively regulating FHL1 in BC.