Cerebral arteriolar pathology in a 32-year-old patient with CADASIL.
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Adult↗
Biomedical subjects
Q Miao
Publications and source records attributed to Q Miao.
Roles of an extracellular matrix (ECM) receptor and ECM processing enzymes in demyelinating canine distemper encephalitis.
Canine distemper virus (CDV) belongs to the genus Morbillivirus of the Paramyxoviridae family. Due to the central nervous system (CNS) tropism of the virus and associated neuropathological changes, demyelinating canine distemper encephalitis (CDE) represents a relevant model for human demyelinating diseases like multiple sclerosis. The present review decribes the role of CD44 antigen (CD44), the principle cell surface receptor for hyaluronate and extracellular matrix (ECM) processing enzymes (matrix metalloproteinases [MMPs]) and their inhibitors (TIMPs) in the pathogenesis of demyelination. In acute and subacute CDE, a plaque-associated CD44 up-regulation is found that parallels astrocyte activation. Likewise, MMPs and TIMPs are prominently up-regulated in these lesions and are expressed mostly by astrocytes and microglia. In chronic lesions, CD44 expression declines together with the number of glial fibrillary acidic protein (GFAP) positive astrocytes. In addition, in this plaque type, CD44 is expressed on the cell membrane of perivascular mononuclear cells. In this phase, a decrease of MMP and TIMP expressions apart from MMP-11, -12, and -13 is obvious. In summary, CD44 and MMPs might be associated with the onset of demyelination and may interact to initiate ECM disturbances. Ligation of CD44 in the early phase may induce chemokines and cytokines and hence initiate and perpetuate the inflammatory process. In the chronic phase, it is conceivable that a MMP-TIMP imbalance may be the motor for lesion progression with a simultaneous influx of CD44-positive activated immune cells.
Animals↗
Phosphatidic acid-phosphatidylethanolamine interaction and apocytochrome c translocation across model membranes.
The translocation of apocytochrome c (apocyt.c) across large unilamellar vesicles (LUVs) constructed from mixtures of anionic and zwitterionic phospholipids, phosphatidylethanolamine (PE) and phosphatidylcholine (PC), has been studied. It was shown that the import ratio of horse heart apocyt.c in LUVs composed of phosphatidic acid (PA) combined with PE and PC (62+/-10%) was much higher than that in LUVs made of PE and PC plus any other acidic phospholipid species (20+/-5%). This feature was shared by tuna heart and chicken heart apocyt.c. In addition, the greater efficiency of the PA/PE/PC system versus others in facilitating apocyt.c translocation was maintained using synthetic anionic phospholipids with the same acyl chains. Besides, apocyt.c induces more leakage of entrapped fluorescein sulphonate (FS) from the interior of PA/PC/PE vesicles compared with phosphatidylglycerol (PG)/PC/PE ones. By measuring the intrinsic fluorescence emission spectrum and the accessibility of the preprotein to the fluorescence quencher, acrylamide, differences could be detected in the conformational changes of apocyt.c as a consequence of its interaction with PA/PE/PC and PG/PE/PC vesicles, respectively. Particularly notable is that PE is indispensable for the PA/PE/PC system to most efficiently facilitate apocyt.c translocation across the model membranes. With the fraction of PE increasing from 0 to 30 mol%, the translocation efficiency of apocyt.c as well as its ability to induce FS efflux was significantly enhanced in PA-containing LUVs, whereas this was not observed in the case of replacement of PA by PG or phosphatidylserine. It is also interesting to note that in LUVs containing PA, dioleoyl-PE, but not dielaidoyl-PE, can exert such influences, indicative of the role of non-bilayer formation propensity. On the basis of these results it is postulated that PA might increase the bilayer-destabilizing effects of PE, and hence increase the translocation efficiency of apocyt.c and its leakage-induction ability.
Animals↗
Leakage and aggregation of phospholipid vesicles induced by the BH3-only Bcl-2 family member, BID.
BID is a BH3 domain-only member of the Bcl-2 family that acts as an apoptotic agonist in programmed cell death. After cleavage by caspase-8, the N-terminal of BID (N-BID) stays in the cytosol while the C-terminal of BID (C-BID) translocates to mitochondria, leading to cytochrome c release in vivo and in vitro. We have previously reported that BID or truncated BID (tBID) can induce the release of entrapped trypsin and cytochrome c from large unilamellar vesicles (LUVs). Further studies have been performed and are presented here; the results demonstrate that C-BID, like BID and tBID, induces vesicle leakage, whereas N-BID or the BID mutants BID (D59A) and BID (G94E) fail to have any significant effects. The affinity of the above-mentioned proteins for soybean phospholipid LUVs (SLUVs) decreased in an order similar to their leakage-inducing capability: tBID > BID > BID (D59A), while N-BID and BID (G94E) were unable to bind to the vesicles at all. BID-induced leakage was dependent on the lipid composition of vesicles. Acidic phospholipid (e.g. phosphatidic acid or phosphatidylglycerol) was necessary for BID-induced leakage while the presence of phosphatidylethanolamine or cholesterol reduced the leakage. It was also found C-BID is better able to penetrate the soybean phospholipid monolayer than BID or tBID. A further finding was that tBID, but not full-length BID, could stimulate the aggregation of SLUVs. Finally, Bcl-x(L), an apoptotic antagonist in programmed cell death, can prevent the aggregation of LUVs induced by tBID, but not the release of entrapped trypsin. It is postulated that two separate domains of tBID are responsible for inducing leakage and aggregation of phospholipid vesicles.
BH3 Interacting Domain Death Agonist Protein↗
A distinct mutational spectrum of p53 and K-ras genes in lung cancer of workers with silicosis.
Crystalline silica was recently classified as a human carcinogen by the International Agency for Research on Cancer (IARC). However, the direct genotoxic effect of silica in humans remains unclear. We examined the p53 and K-ras gene mutations in lung cancer in workers with silicosis (LCWS). DNA was extracted from paraffin-embedded tissues and examined by PCR-RFLP, PCR-SSCP, and DNA sequencing. The mutation frequencies of p53 gene were high, but the mutation distributions in exons and among the histological types of LCWS differed from those of common (i.e., not silicosis-related) lung cancer. Furthermore, no mutations in codon 12 of K-ras gene (predominant in common lung cancer) were found in LCWS. These findings in the mutational spectrum support a carcinogenic effect of silica dust at the DNA molecular level.
DNA Mutational Analysis↗
Adenosquamous lung carcinoma: clinical characteristics, surgical treament and prognosis.
OBJECTIVE: The effectiveness of surgical resection of adenosquamous carcinoma of the lung remains poorly defined because of the histology's relatively low frequency, the failure in most published series to separate adenosquamous carcinoma from the other variants of non-small cell lung carcinoma. To define the effectiveness of treatment of adenosquamous carcinoma, we have retrospectively reviewed our hospital experience over a 12-year period. METHODS: Retrospectively reviewed 22 cases of adenosquamous carcinoma who were surgically treated, except one patient, in the PUMCH from Jan. 1985 to Aug. 1997. This series constitutes the 1.9% of a total of 1 245 patients with all types of surgical treatment for the primary lung cancer during the same time. RESULTS: The adenosquanous carcinoma was mostly presented in the old patients with a mean age of 60 years and mostly located in the peripheral of lung (n = 20). The overall 5-year survival was 23%. Those with stage I tumors survival was only 18% (n = 13), stage II 5%. The survival in stage III tumos was not longer than 25 months and in stage IV survival was not longer than 12 months. CONCLUSION: Our results suggest that adenosquamous carcinoma of lung was a virulent tumor, which exhibited highly aggressive biological behavior with early lymph nodes metastasis (46%) and its prognosis was worse than that of both squamous cell carcinoma and adenocarcinoma.
Adult↗
[Evidence on the carcinogenicity of silica at DNA level in human].
The alteration of p53 and K-ras gene in 36 lung cancers of workers occupationally exposed to silica (LCWS) was studied. DNA was extracted from paraffin\|embedded tissues and amplified by PCR. PCR-SS-CP analysis on exons 5, 7 and 8 of p53 gene revealed that 43.8% of mutations were clustered in exon 8 of p53 gene. In ordinary lung cancer, the mutation rate of exon 8 was fluctuated around 20%. The prevalence of mutations was the highest (70%) in small cell lung cancer (SCLC) and the lowest in adenocarcinoma(33%). In our study the mutation rate was high in adenocarcinoma(53.9%) and low in SCLC (30.8%). The K-ras gene of LCWS also revealed a different mutation pattern. Unexpectedly, no mutation was found at codon 12 in 36 LCWS by PCR-RFLP, which is the predominant mutation in K-ras gene in ordinary lung cancer. The point mutation study by DNA sequencing confirmed the absence of codon 12 mutation in K-ras gene in LCWS. The mutations observed in this study were frequently distributed in codons 13 and 15, principally a G-C transversion, instead of G-T transversion in ordinary lung cancer.
Adenocarcinoma↗
[Management of thoracic esophageal perforation].
OBJECTIVE: To compare surgical management of esophageal perforation on thoracic portion with nonoperative management. METHODS: Seventeen patients were treated for thoracic esophageal perforation at our department between 1962 and 1996. Among them, seven patients underwent nonoperative management. The remaining 10 had operative procedures (primary repair in 5, esophagostomy in 3, and drainage alone in 2 cases). RESULTS: Postoperative leakage occurred in 2 patients; among the two leakages, 1 required cervical esophagostomy, and 1 became a controlled fistula needed pleural drainage and feeding jejunostomy. One patient had anastomotic narrowing after esophagostomy. Of patients with nonoperative management, five survived (with 28% in-hospital mortality rate), Whereas only one patient, who was treated by surgical procedure, died (with 10% inhospital mortality rate). The mean hospital stay in nonoperative and operative group were (28.3 +/- 12.9) days and (57.6 +/- 52.7) days respectively. CONCLUSIONS: The clinical observation suggested that rapid diagnosis of thoracic esophageal perforations is essential and once the diagnosis of esophageal perforation is established, a appropriate management must be selected promptly.
Adult↗
[Subxiphoid pericardial window drainage in the management of large pericardial effusions].
OBJECTIVE: To choose a safe, effective, minimum invasive procedure for treatment of patients with a large pericardial effusion and cardiac tamponade. METHODS: Retrospective analysis of 30 cases with large pericardial effusion or cardiac tamponade diagnosed by echocardiography during four years (1993-1997). The subxiphoid pericardial window drainage and pericardial tissue biopsy was performed. RESULTS: The symptoms were improved immediately following the drainage. The drainage volume during operation was 200-2,000 ml, and postoperation was 0-2,000 ml. The drainage tube was kept in position for average of 5.6 days. With the echocardiography follow up, the pericardial effusion disappeared or remained only minimum fluid in 96.7% of the patients. The complications happened in 6 cases. The 30-days mortality was 6.7%. CONCLUSIONS: The subxiphoid pericardial window drainage procedure is the first choice for a safe, effective, minimal invasive and easy to do procedure for the patients with a large pericardial effusions or cardiac tamponade.
Adolescent↗
p53 gene mutations in asbestos associated cancers.
The accumulation of mutant p53 protein in cancer cells was observed by immunohistochemistry analysis. DNA was extracted from paraffin-embedded tissue. Exons 5, 7 and 8 were amplified and studied by PCR-SSCP and sequencing analysis. Ten cases of asbestos associated cancer tissue were studied, of which five cases had adenocarcinoma, and the other five had mesothelioma, squamous carcinoma, small cell lung cancer, adenosquamous carcinoma and malignant lymphoma respectively. Employing monoclonal antibody PAb1801, five cases were found to be mutant p53 protein positive. Seven cases were found to have mutations by PCR-SSCP. A total of 7 cases (8 mutations) were found to be positive and 4 cases were found to be positive by both of these analyses. Of the 8 mutations found by SSCP analysis, 4(50%, 4/8) were clustered in exon 8. A high mutation frequency was noticed in adenocarcinoma (80%, 4/5). Sequencing analysis on two specimens revealed two hotspot mutations. In codon 234, TAC for tyrosin was mutated to AAC for asparagine by a T to A transversion of the first letter. In codon 273, CGT for arginine was mutated to AGT for serine by a C to A transversion of the first letter. In conclusion, the mutation of p53 gene is common in asbestos associated cancers. However, the mutational spectrum of asbestos associated cancers might be different from that of non-asbestos associated cancers.
Adenocarcinoma↗
[Purification of PCR products from paraffin-embedded lung cancer tissue of pneumoconiosis cases].
A method of purification of PCR products from paraffin-embedded human lung tissue by low melting temperature agarose gel electrophoresis was developed. This method increased the specificity of PCR products of DNA from lung tissues with pneumoconiosis. The retrieved DNA fragments can be used for SSCP, sequencing and other molecular biology research.
Genes, p53↗
[PCR-SSCP and sequencing analysis on mutations of anti-oncogene p53 in asbestos-related lung cancer].
To explore the carcinogenic effect of asbestos at molecular level, we directly analyzed the mutations of exon 5, 7 and 8 of anti-oncogene p53 in paraffin-embedded human lung tissue affected by asbestos for the first time. Mutations of p53 gene located in exon 5, 7 and 8 were detected in 7 of 10 cases by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis. The mutation rate found in this study is 70%. Two cases were analyzed by PCR product direct sequencing and C-->A and T-->A transformations were detected. Mutation of p53 gene may be one of the characteristics of asbestos-related lung cancer.
Asbestos↗
[The research on p53 gene mutation in lung cancer tissue of silicotic patients by PCR-SSCR].
Using polymerase chain reaction single strand conformation polymorphism analysis (PCR-SSCP), the authors mutations in exon 5, 7 and 8 of the p53 gene in lung cancer tissue from 15 of 36 silicotic patients. Mutations existed in exon 5, exon 7 and exon 8, but occured more frequently in exon 8. The authors also found that p53 gene mutation rate in lung adenocarcinomas of silicotic patients was higher than that of those without silicosis. A single base substitution was found by DNA sequencing analysis in sample C8. As a result, No. 144 codon was mutated from CAG to AAG, so Gln was substituted by Lys. The authors' data suggest that p53 mutation may play an important role in the pathogenesis of lung cancer of silicotic patients.
Adenocarcinoma↗
Pulmonary leiomyosarcoma.
Three cases of pulmonary leiomyosarcoma were presented. The characteristic clinical features were described with review of literature. In comparison with bronchogenic carcinoma, the leiomyosarcoma has some characteristics: 1) On chest X-ray, it usually appears as a sharply demarcated, even density round mass, growing rapidly within the lung, it unusually accompanies with hilar or mediastinal lymph node metastasis; 2) The preoperative cytological or pathological diagnosis is difficult either by sputum smear or by bronchoscopic biopsy or by fine needle percutaneous aspiration biopsy; 3) Pathological differential diagnosis of leiomyosarcoma of lung from anaplastic lung cancer is difficult. In conclusion, the primary pulmonary leiomyosarcoma is a rare malignant tumor, detecting the present illness seriously, paying attention to the chest X-ray films characterize, early surgical resection is the only way to get diagnosis and effective treatment method.
Adult↗
[A preliminary study on p53 gene in lung cancer tissues of workers exposed to silica and welding fumes].
Mutations of suppressor gene p53 was studied in 36 cases of silica related lung cancer and 6 cases of welding fume related lung cancer with immunohistochemical and PCR-SSCP methods. Cancer tissues were embedded in paraffin and stored for 13.4 years in average. Results revealed that there was abnormal mobility shift of electrophoresis in 18 cases with 20 point mutations of 42 specimens tested, accounted for 42.9%, and 50% (10/20) of the mutations were clustered in exon 8. This finding differed from mutational spectrum of gene in non-occupational lung cancer, in which mutation frequency of exon 8 ranged from 17.5% to 23.5%. Gene mutation frequency in varied pathological categories of pneumoconiosis related lung cancer also differed from that in common lung cancer. In the latter, the highest one was in small cell lung cancer (70%) and the lowest in adenocarcinoma (33%), but in the former, the highest in adenocarcinoma (53.9%) and the lowest in small cell lung cancer (30.8%). Immunohistochemical observations also showed a very high prevalence of p53 gene mutation expression (46.9%). Sequencing, which was determined in two cases of this study, revealed that two point mutations all occurred in non-hotspot codon 144 of p53 gene. Difference in gene mutation spectrum suggests that there exist specific carcinogens and carcinogenesis in silica and welding fume related lung cancer.
Adenocarcinoma↗
Pulmonary leiomyosarcoma--report of three cases.
Three cases of pulmonary leiomyosarcoma were presented. The characteristic clinical features were described with review of literature. In comparison with bronchogenic carcinoma, the leiomyosarcoma has some characteristics: 1) On chest X-ray, it usually appears as a sharply demarcated, even density round mass, growing rapidly within the lung, it rarely accompanies with hilar or mediastinal lymph node metastasis. 2) The preoperative cytological or pathological diagnosis is difficult either by sputum smear or by bronchoscopic biopsy or by fine needle percutaneous aspiration biopsy. 3) Pathological differential diagnosis of leiomyosarcoma of lung from anaplastic lung cancer is difficult. In conclusion, the primary pulmonary leiomyosarcoma is a rare malignant tumor, detecting the present illness seriously, paying attention to the chest X-ray films characterize, early surgical resection is the only way to get diagnosis and effective treatment method.
Adult↗
[Inhibition of mRNA expression of silicotic collagen gene by tetrandrine].
Effects of tetrandrine (TT) on types I and III collagen gene mRNA in lung tissues of silicotic rats were studied with RNA dot blot and in situ hybridization by cDNA coding human and mouse Pro alpha 1 (I) and Pro alpha 1 (III) collagen. Results revealed types I and III collagen gene mRNA content in lung tissues of rats exposed to silica dust for two to four months was obviously greater than that in normal lung tissues (P < 0.05), and decreased significantly after treatment with TT (P < 0.05) by dot blot technique. In situ hybridization revealed silver granules of types I and III collagen gene mRNA were scattered in fibroblasts of alveolar septa in normal lung tissues, and in cellular nodes and thickened interstitia of silicotic tissues. It suggested aggregation of collagen in silicotic tissues was caused by enhancement of collagen gene expression, and TT could inhibit directly or indirectly transcription of collagen gene, and thus reduce synthesis of collagen protein in silicotic tissues.
Alkaloids↗
Ceruloplasmin or fibronectin synergism with quartz dust on stimulating collagen gene transcription in human 2BS fibroblast.
Human alpha 1(I), alpha 2(I) and alpha 1(III) cDNA probes and RNA dot hybridization were employed to quantitate collagen mRNA changes after adding silica dust into the media of human 2BS fibroblasts. At all dosages used (100, 200, 500 and 1000 micrograms), the alpha 1(I), alpha 2(I) and alpha 1(III) mRNA levels increased one day after dusting. At the same dosage of silica (100 micrograms), alpha 1(III) mRNA increased earlier than type I collagen mRNA did. The type I and type III collagen mRNA contents in the experimental groups were higher than those in control on days 3, 5, 7 and 9. The effect of ceruloplasmin (Cp) and fibronectin (Fn) on collagen mRNA synthesis was also studied, after adding silica dust, Cp or Fn into the media of human 2BS fibroblast. The results showed that Cp and Fn have stimulating effect on collagen mRNA production. When both Cp and silica dust were added into cell culture media, the collagen mRNA level was increased more than those of adding either Cp or silica dust alone. Similar situations were found for Fn. Cp (or Fn) synergism with silica dust on stimulating transcription of human collagen gene was suggested.
Cells, Cultured↗