RÉSUMÉ
OBJECTIVE@#To explore the renal pathology and cytogenetic features in the multiple myeloma (MM) patients with renal impairment.@*METHODS@#The clinical data of newly diagnosed MM patients with renal impairment in our hospital from January 2009 to January 2019 were analyzed retrospectively, and the relationship between FISH results and results of renal pathological exanimation was analyzed statistically by using SPSS 20.0.@*RESULTS@#A total of 20 patients underwent renal biopsy, included 12 males and 8 females. FISH result showed that out of 20 patients, 7 cases presented interstitial nephritis, among which 3 cases were negative for FISH, and in the remaining cases the rate of IgH rearrangement, 1q21 amplification, RB1 deletion, D13S319 deletion, and P53 deletion detection was 42.86%, 28.57%, 28.57%, 28.57% and 14.29% respectively, the detection positive rate was statistically significantly lower as compared with total probe positive rate (P<0.01). There were 6 cases of cast nephropathy, among which IgH rearrangement, the rate of 1q21 amplification, RB1 deletion, D13S319 deletion, and P53 deletion detection was 66.67%, 50%, 66.67%, 50% and 0% respectively. Compared with the total probe positive rate, there was no statistical significance (P>0.05). There were 4 cases of acute tubular necrosis, among which the detection rates of IgH rearrangement, 1q21 amplification, RB1 deletion, D13S319 deletion, and P53 deletion was 100%, 50%, 50%, 25% and 25%, respectively. Compared with the total probe positive rate, there was no statistical significance (P>0.05). There were one case of amyloidosis, and one case of tubular nephropathy with amyloidosis, the detection with 5 probes were all positive. One case of light chain deposition disease was positive for RB1 gene deletion + D13S319 gene deletion.@*CONCLUSION@#FISH in the MM patients with different renal pathological changes is characterized by heterogeneity, which can be used to predict the risk of renal damage and speculate possible renal pathological types to guide prognosis.
Sujet(s)
Femelle , Humains , Mâle , Aberrations des chromosomes , Analyse cytogénétique , Cytogénétique , Hybridation fluorescente in situ , Myélome multiple , Études rétrospectivesRÉSUMÉ
<p><b>BACKGROUND</b>Acute lung injury (ALI) is a serious and common condition for which there are currently no specific strategies for treatment. Recent studies have suggested that bone marrow-derived multipotent mesenchymal stem cells (MSCs) may have therapeutic applications in multiple clinical disorders. We explored the biological effects of MSCs during endotoxin-induced ALI and the mechanisms involved.</p><p><b>METHODS</b>MSCs were isolated from male rat bone marrow and the ALI model was induced by intravenous endotoxin injection. Female rats were sacrificed at 6 hours, 24 hours, 4 days, 1 week and 3 weeks post-injection of MSCs or saline and the lung tissue, bronchoalveolar lavage fluid, and serum were harvested for analysis. We further evaluated the survival of the rats and examined the effects of endotoxin-induced injury on the interaction between alveolar macrophages (AMs) and MSCs in ex vivo.</p><p><b>RESULTS</b>There was a significant decrease in numbers of neutrophils in bronchoalveolar lavage fluid (P < 0.05), and myeloperoxidase activity in the lung (P < 0.01), and of TNF-α and IL-1β in serum (P < 0.05) in the MSC treated rats at 4 days. Furthermore, MSC treated rats exhibited improved survival, lower lung injury score, higher concentration of IL-10 in the serum and a reduced hydroxyproline content, but these differences were not statistically significant. Moreover, co-cultures of MSCs and AMs had significantly reduced levels of TNF-α, IL-1β and macrophage inflammatory protein (MIP)-1α and significantly increased levels of IL-10 (P < 0.05) in the culture supernatants.</p><p><b>CONCLUSIONS</b>Treatment with intravenous injection of bone marrow-derived MSCs have beneficial effects on endotoxin-induced ALI in rats. The beneficial effect might be achieved through the engraftment of differentiated MSCs in the lungs and appears derive more from their capacity to secrete soluble factors that modulate immune responses.</p>
Sujet(s)
Animaux , Femelle , Mâle , Rats , Lésion pulmonaire aigüe , Métabolisme , Thérapeutique , Cellules de la moelle osseuse , Biologie cellulaire , Cellules cultivées , Techniques de coculture , Endotoxines , Toxicité , Poumon , Métabolisme , Anatomopathologie , Macrophages alvéolaires , Biologie cellulaire , Transplantation de cellules souches mésenchymateuses , Cellules souches mésenchymateuses , Biologie cellulaire , Physiologie , Myeloperoxidase , Métabolisme , Répartition aléatoire , Rat WistarRÉSUMÉ
<p><b>BACKGROUND</b>Toll-like receptor-4 (TLR-4) is integrally involved in lipopolysaccharide (LPS) signaling and has a requisite role in the activation of nuclear factor-κB (NF-κB). The exact mechanisms that lend perfluorocarbon (PFC) liquids a cytoprotective effect have yet to be elucidated. Therefore we examined in an in vitro model the cytoprotective effect of PFC on LPS-stimulated alveolar epithelial cellls (AECs).</p><p><b>METHODS</b>AECs (A549 cells, human lung adenocarcinoma cell line) were divided into four groups: control, PFC, LPS and LPS + PFC (coculture group) groups. Intercellular adhesion molecule-1 (ICAM-1) was detected by ELISA, tumor necrosis factor-α (TNF-α) and interleukin-8 (IL-8) were detected by radioimmunological methods. The expression of TLR-4 mRNA and protein was detected by real time PCR and Western blotting, respectively. The activation of NF-κB was detected by Western blotting (proteins of I-κBa and NF-κB p65).</p><p><b>RESULTS</b>ICAM-1, TNF-α and IL-8 were significantly increased in LPS-stimulated AECs groups. The expression of TLR-4 mRNA and protein in LPS-stimulated groups was markedly increased. Meanwhile, NF-κB was activated as indicated by the significant degradation of IκB-α and the significant release of NF-κB P65 and its subsequent translocation into the nucleus. There were no significant effects of PFC alone on any of the factors studied while the coculture group showed significant downregulation of the secretion of ICAM-1, TNF-α and IL-8, the expression of TLR-4 mRNA and the activity of NF-κB.</p><p><b>CONCLUSIONS</b>Taken together, our results demonstrate that LPS can induce AEC-related inflammatory injury via the activation of TLR-4 and subsequent activation of NF-κB. PFC is able to protect AECs from LPS-induced inflammatory injury by blocking the initiation of the LPS signaling pathway, which is indicated by the significant decrease of TLR-4 expression and NF-κB activation.</p>
Sujet(s)
Humains , Technique de Western , Lignée cellulaire tumorale , Cellules épithéliales , Allergie et immunologie , Fluorocarbones , Pharmacologie , Inflammation , Allergie et immunologie , Molécule-1 d'adhérence intercellulaire , Génétique , Métabolisme , Interleukine-8 , Génétique , Métabolisme , Lipopolysaccharides , Pharmacologie , Facteur de transcription NF-kappa B , Génétique , Métabolisme , Alvéoles pulmonaires , Biologie cellulaire , Réaction de polymérisation en chaine en temps réel , Récepteur de type Toll-4 , Génétique , Métabolisme , Facteur de nécrose tumorale alpha , Génétique , MétabolismeRÉSUMÉ
<p><b>BACKGROUND</b>Gefitinib, an inhibitor of epidermal growth factor receptor (EGFR) tyrosine kinase, is an effective treatment for epithelial tumors, including non-small cell lung cancer (NSCLC), and is generally well tolerated. However, some clinical trials revealed that gefitinib exposure caused lung fibrosis, a severe adverse reaction. This study investigated the effect of gefitinib on lung fibrosis in mice.</p><p><b>METHODS</b>We generated a mouse model of lung fibrosis induced by bleomycin to investigate the fibrotic effect of gefitinib. C57BL/6 mice were injected intratracheally with bleomycin or saline, with intragastric administration of gefitinib or saline. Lung tissues were harvested on day 14 or 21 for histology and genetic analysis.</p><p><b>RESULTS</b>The histological results showed that bleomycin successfully induced lung fibrosis in mice, and gefitinib prevented lung fibrosis and suppressed the proliferation of S100A4-positive fibroblast cells. In addition, Western blotting analysis revealed that gefitinib decreased the expression of phosphorylated EGFR (p-EGFR). Furthermore, quantitative real-time PCR (qRT-PCR) demonstrated that gefitinib inhibited the accumulation of collagens I and III.</p><p><b>CONCLUSIONS</b>These results reveal that gefitinib reduces pulmonary fibrosis induced by bleomycin in mice and suggest that administration of small molecule EGFR tyrosine kinase inhibitors has the potential to prevent pulmonary fibrosis by inhibiting the proliferation of mesenchymal cells, and that targeting tyrosine kinase receptors might be useful for the treatment of pulmonary fibrosis in humans.</p>
Sujet(s)
Animaux , Mâle , Souris , Bléomycine , Toxicité , Technique de Western , Collagène de type I , Génétique , Collagène de type III , Génétique , Souris de lignée C57BL , Inhibiteurs de protéines kinases , Utilisations thérapeutiques , Fibrose pulmonaire , Traitement médicamenteux , Quinazolines , Utilisations thérapeutiques , Récepteurs ErbB , Métabolisme , RT-PCRRÉSUMÉ
<p><b>OBJECTIVE</b>To investigate the effect of baicalin on insulinoma cell line and the molecular mechanism involved.</p><p><b>METHODS</b>Light microscope, MTT assay, flow cytometry, gene analysis and Western Blot were applied to investigate the effects of baicalin on the cell proliferation, the cell cycle and the involved molecular mechanism.</p><p><b>RESULTS</b>After treatment with baicalin, the number of cells in mitotic stage and the survival rate of cells obviously decreased, and cell proliferation was inhibited in a drug concentration- and acting time-dependent manner, with the appearance of apoptotic insulinoma cells. During the apoptotic process, the activity of caspase-3 was elevated by baicalin in a time-dependent manner; with the increase of the concentration of baicalin, the number of cells in S-phase obviously decreased from 38.2% to 9.4%, while the percentage of cells in G0/G1 phase increased from 56.4% to 85.9%, indicating cells were arrested in G1-phase. Meanwhile, the activity of cyclin gene promoter obviously declined, and the expression of cyclin reduced remarkably.</p><p><b>CONCLUSION</b>Baicalin could induce apoptosis of insulinoma cells, which might be correlated with the activity of caspase-3, and inhibiting proliferation of insulinoma cells in a concentration- and time-dependent manner, in which the action of baicalin in down-regulating the gene transcription and expression of cyclin may play an important role.</p>
Sujet(s)
Animaux , Rats , Antinéoplasiques d'origine végétale , Pharmacologie , Apoptose , Technique de Western , Caspase-3 , Métabolisme , Lignée cellulaire tumorale , Prolifération cellulaire , Survie cellulaire , Relation dose-effet des médicaments , Flavonoïdes , Pharmacologie , Cytométrie en flux , Insulinome , Métabolisme , AnatomopathologieRÉSUMÉ
<p><b>OBJECTIVE</b>To review the species and distribution of the medicinal plants peculiar to Guizhou and provide evidence for application, protection and collection.</p><p><b>METHOD</b>Open-air investigation, data collection and specimen identification.</p><p><b>RESULT</b>More than eighty kinds of the medical plants peculiar to Guizhou have been identified.</p><p><b>CONCLUSION</b>Guizhou has a diversity of medicinal plants. The area of distribution of most species is restricted and the population is small. Some of the species have higher medicinal and scientific research values.</p>
Sujet(s)
Berberis , Classification , Chine , Conservation des ressources naturelles , Epimedium , Classification , Gynostemma , Classification , Pharmacognosie , Plantes médicinales , ClassificationRÉSUMÉ
OBJECTIVE@#To investigate the effect of baicalin on the proliferation of insulinoma cell line and the molecular mechanism involved.@*METHODS@#Such methods as light microscope, MTT assay, flow cytometry and Western blotting were applied to investigate the effects of baicalin (0, 100, 200, and 400 microg/ml baicalin treated for 24 h or 200 microg/ml baicalin treated at different time points) on the cell proliferation, cell survival rate, the cell cycle and related molecular mechanisms.@*RESULTS@#The number of proliferating cells obviously decreased with the increase of baicalin under the light microscope, and the survival rate of cells decreased as determined by MTT assay. After being treated with baicalin, the number of insulinoma cells in S-phase obviously decreased from 38.2% (0 microg/ml) to 9.4% (400 microg/ml), and the number of cells in phase G1 increased from 56.4% (0 microg/ml) to 85.9% (400 microg/ml). In the meantime, the expression of cyclin D1 was obviously declined by Western blotting.@*CONCLUSION@#Baica-lin can inhibit the proliferation of insulinoma cells, and the down-regulation of the expression of cyclin D1 might also be involved in these events.
Sujet(s)
Humains , Antinéoplasiques d'origine végétale , Pharmacologie , Lignée cellulaire tumorale , Prolifération cellulaire , Cycline D1 , Flavonoïdes , Pharmacologie , Insulinome , Anatomopathologie , Tumeurs du pancréas , AnatomopathologieRÉSUMÉ
OBJECTIVE@#To transform eukaryotic expression vector pEGFP-PDX-1 into marrow stromal cells by liposome and to optimize the conditions of transformation.@*METHODS@#The recombinant vector was identified by enzyme digestion analysis and sequencing. The recombinant plasmid was transformed into bone marrow stromal cells and it changed the quantity of DNA or liposome. The expression of PDX-1 gene in the transformed cells was detected by immunocytochemical staining.@*RESULTS@#Enzyme digestion analysis and sequencing showed that the interesting gene was integreted into the recombinant vector. We obtained satisfactory efficiency of transfection when the ratio of DNA and liposome was 1 : 1 or 1 : 2. The PDX-1 in the transformed cells was expressed by immunocytochemical staining.@*CONCLUSION@#The eukaryotic expression vector pEGFP-PDX-1 was constructed for the first time in China. We have enhanced the efficiency of transfection by optimizing the transformation conditions. It is possible to use the bone marrow stromal cells as seed cells in tissue-engineering.