Biomedical subjects

W Mu

Publications and source records attributed to W Mu.

43 records · Page 3Linked to original sources

PubMed1996

[Gas chromatographic analysis of molinate residue in rice].

We have developed a method for determining molinate residue in rice by gas chromatography. In our study, the rice sample was extracted with acetonewater (1 + 1). After filtering, the filtrate was acidified to pH 3.0-3.5 and re-extracted with petroleum. The extract was cleaned up on a florisil column and followed by analysis with GC/FPD. The linear range of the method was 0-5 micrograms/ml. the detection limit was 0.013 mg/kg for a rice sample of 20 g. The average recoveries of spiked samples ranged from 87.0%-96.7%. The relative deviation standard was less than 5.7%. The experimental verification of this method by extramural departments and its application to determination of rice samples demonstrate that this method is sensitive, reliable and suitable for analysis of molinate residue in rice.

Azepines↗

PubMed1995

Interleukin-1 receptor antagonist halts the progression of established crescentic glomerulonephritis in the rat.

The pathogenic role of interleukin-1 (IL-1) in the progression of established rat crescentic glomerulonephritis was investigated by administration of the interleukin-1 receptor antagonist (IL-1ra). Passive accelerated antiglomerular basement membrane (GBM) disease was induced in three groups of six rats. One group was killed on day 7 with no treatment. The other groups received a constant infusion of IL-1ra or saline from day 7 until being killed on day 21. All animals developed moderate glomerular injury, a significant loss of renal function and marked histological damage including crescent formation by day 7. Saline treated animals showed a significant deterioration in these parameters over days 7 to 21. In contrast, animals treated with the IL-1ra over this period showed stabilization of glomerular injury (protein-uria; P < 0.001) and a recovery of normal renal function (creatinine clearance; P < 0.05). Histologically, IL-1ra treatment suppressed glomerular cell proliferation (PCNA expression; P < 0.001) and significantly inhibited crescent formation (P < 0.005), glomerular sclerosis (P < 0.005), tubular atrophy (P < 0.05) and interstitial fibrosis (P < 0.05). A key finding was that IL-1ra treatment not only stopped renal leukocyte accumulation over days 7 to 21 (P < 0.01), but that treatment also suppressed immune activation of the infiltrate (P < 0.01). In conclusion, this study provides direct evidence that IL-1 plays a key role in the progressive/chronic phase of renal injury in experimental crescentic glomerulonephritis and indicates that IL-1ra treatment may be of therapeutic benefit in human rapidly progressive crescentic glomerulonephritis.

Analysis of Variance↗

PubMed1995

Local macrophage proliferation in the progression of glomerular and tubulointerstitial injury in rat anti-GBM glomerulonephritis.

The aim of this study was to examine the contribution of local proliferation in the development of macrophage accumulation and macrophage-mediated injury in rat anti-GBM glomerulonephritis. Using double immunohistochemistry staining of monocyte/macrophages plus the proliferating cell nuclear antigen (PCNA) or bromodeoxyuridine (BrdU) incorporation, we found that the initial accumulation of ED1+ macrophages in the kidney on day 1 of disease was due to an influx of circulating monocytes. However, large numbers of proliferating macrophages (ED1+PCNA+cells), including mitotic macrophages, were present within the glomerulus and interstitium during disease progression (days 7 to 21), accounting for up to 62% of the total macrophage population and giving an excellent correlation with total macrophage accumulation (glomerulus, r = 0.92; interstitium, r = 0.94; both P < 0.001). These proliferating cells had a monocyte phenotype (ED1+ED2-ED3-), but this marked proliferative activity was restricted to the diseased kidney since no PCNA expression or BrdU incorporation was evident within circulating blood monocytes. Proliferating macrophages were almost exclusively localized in areas of severe tissue damage and they correlated significantly with glomerular and tubulointerstitial lesions (P < 0.001), proteinuria (P < 0.001) and creatinine clearance (P < 0.01). In marked contrast, glomerular PCNA- macrophages failed to correlate with these parameters. In conclusion, this study has demonstrated that local macrophage proliferation is the major mechanism of macrophage accumulation during the progression of rat anti-GBM glomerulonephritis. Furthermore, it suggests that proliferating macrophages are potent local effector cells in the mediation of progressive renal injury in this disease.

Animals↗

PubMed1995

A novel, simple, reliable, and sensitive method for multiple immunoenzyme staining: use of microwave oven heating to block antibody crossreactivity and retrieve antigens.

We report a simple and reliable method for detection of two or more antigens within tissue sections by indirect immunoenzyme staining using mouse monoclonal antibodies (MAbs). This technique involves treating sections with two 5-min microwave (MW) oven heatings between sequential rounds of three-layer immunoenzyme staining (mouse MAb, goat anti-mouse IgG, and mouse PAP or mouse APAAP) and color development. Discrete staining of cell surface, cytoplasmic, and nuclear antigens was evident within individual cells. This technique has a number of advantages over those currently available. First, MW treatment denatures bound antibody molecules, thereby completely blocking crossreactivity between sequential rounds of staining. This allows the use of primary (and other) antibodies raised in the same species and the use of a sensitive three-layer staining method. Second, antigen retrieval after MW treatment markedly increases the sensitivity of cytoplasmic and nuclear antigen detection. Third, inactivation of peroxidase and alkaline phosphatase enzymes present in PAP and APAAP complexes prevents inappropriate color development. Finally, this method can be used in both paraformaldehyde-fixed cryostat sections and formalin-fixed paraffin tissue sections. In conclusion, this is a simple, reliable, and sensitive technique that will be useful in many areas of diagnosis and research.

Animals↗

PubMed1995

Local macrophage proliferation in multinucleated giant cell and granuloma formation in experimental Goodpasture's syndrome.

Granuloma is a specialized form of inflammatory reaction featuring focal macrophage and T-cell accumulation and multinucleated giant cell formation. It is widely held that macrophage accumulation within granulomatous lesions results from recruitment of blood monocytes, whereas proliferation of monocyte/macrophages makes little contribution to this process. The present study of macrophage proliferation within immunologically induced granulomas in rat experimental Goodpasture's syndrome challenges the conventional view. In this disease, granulomatous lesions in the kidney and lung contained 60 to 70% macrophages of an ED1+ED2-ED3-blood monocyte phenotype. However, double immunohistochemistry showed that up to 75% of ED1+ macrophages within granulomatous lesions were proliferating on the basis of proliferating cell nuclear antigen expression and bromodeoxyuridine incorporation. In contrast, no proliferating cell nuclear antigen expression or bromodeoxyuridine incorporations was detected in blood monocytes, indicating that proliferation of ED1+ED2-ED3- cells was a localized event within granulomatous lesions. A second finding of note was that almost all ( > 95%) nuclei within multinucleated giant cells were positive for proliferating cell nuclear antigen, but these nuclei lacked bromodeoxyuridine incorporation. This suggests a novel mechanism of multinucleated giant cell formation involving fusion of macrophages in G1 phase, which then halts progression into S phase of the cell cycle. In conclusion, this study has found that local macrophage proliferation plays an important role in the pathogenesis of granuloma formation.

Animals↗

PubMed1993

[Gas chromatographic analysis of nicotine in indoor air].

An analytical method for the determination of nicotine in indoor air was developed. Air sample was collected in absorption solution of 1% NaHSO4. After alkalization and heptance extraction, the content of nicotine in the sample was determined by gas chromatography with FID. The average sampling efficiency was 93.6%. The recovery rate was 89.3%-105.5% (mean = 98.4%). The coefficient of variation was 1.7-4.1%. Under the sampling condition the detection limit was 0.01 microgram/m3. After discussing the stability and extraction efficiency of the sample, we found the air sample collected in the absorption solution was stable for at least 7 days in refrigerator. The field experimental results show that the method is simple, reliable and suitable for collecting and determining trace nicotine in indoor air.

Air Pollution, Indoor↗

PubMedDate not supplied

A functional role for osteopontin in experimental crescentic glomerulonephritis in the rat.

This study examined whether osteopontin (OPN), a molecule with monocyte chemotactic and adhesive activity, participates in macrophage-mediated renal disease, Accelerated anti-glomerular basement membrane glomerulonephritis was induced in groups of six rats. Animals were treated with a neutralizing anti-OPN or an irrelevant control antibody over days 0-7 (induction phase) or days 7-14 (established disease). Administration of the control antibody had no effect on the severity of the disease. In contrast, anti-OPN treatment significantly reduced glomerular injury (urinary protein excretion) and prevented a loss of renal function (creatinine clearance) during the induction of disease. This was accompanied by a significant reduction in renal macrophage and T-cell accumulation, T-cell activation, and histological injury (glomerular hypercellularity, segmental lesions, crescents, and tubulointerstitial lesions). An important finding was that anti-OPN treatment of established crescentic glomerulonephritis led to a significant reduction in glomerular injury and recovery of renal function in association with inhibition of macrophage and T-cell accumulation, T-cell activation, and histological damage. Anti-OPN treatment significantly inhibited the upregulation of OPN and its ligand CD44 but demonstrated no effect on upregulation of intercellular adhesion molecule-1 (ICAM-1) expression in the kidney. Interestingly, anti-OPN treatment significantly reduced skin swelling and leukocyte infiltration in the delayed type hypersensitivity response. However, anti-OPN treatment had no effect on the humoral immune response. In summary, this study has demonstrated that OPN plays a functional role in macrophage and T-cell accumulation and renal damage in both the induction and progression of a rat model of crescentic glomerulonephritis. Thus, OPN may be of pathological importance in human glomerulonephritis and in cell-mediated immune diseases generally.

Animals↗