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OBJECTIVE Atherosclerosis (AS) is a chronic inflammatory disease characterized by the accumulation of lipids, vascular fibrosis, and inflammation. Paeonol (Pae) is a natural phenolic compounds isolated from a traditional Chinese medicine, Cortex Moutan, which exhibits anti-AS effects. Our previous work demonstrated that gut microbiota plays an important role during AS treatment as it affects the efficacy of Pae. However, the mechanism of Pae in protect?ing against vascular fibrosis as related to gut microbiota has yet to be elucidated. To investigate the anti-fibrosis effect of Pae on AS mice and demonstrate the underlying gut microbiota-dependent mechanism. METHODS ApoE-/- mice were fed with high-fat-diet (HFD) to replicate the AS model. HE and Masson staining were used to observe the plaque forma?tion and collagen deposition. Gut microbiota alteration and short-chain fatty acids (SCFAs) production were analyzed through 16S rRNA sequencing and LC-MS/MS. The frequency of immune cells in spleen were phenotyped by flow cytometry. The mRNA expression of aortic inflammatory cytokines were detected by qRT-PCR. The protein expression of LOX and fibrosis related indicators were examined by Western blotting. RESULTS Pae restricted the development of AS and collagen deposition. Notably, the anti-fibrosis effect of Pae was achieved by regulating the gut microbiota. 16S rRNA sequencing and LC-MS/MS data indicated that the relative abundance of SCFAs-producing bacteria and SCFAs production was increased. Additionally, Pae administration selectively up-regulated the frequency of regulatory T (Treg) cells as well as down-regulated the ratio of T helper type 17 (Th17) cells in the spleen of AS mice, improving the Treg/Th17 balance. In addition, as expected, Pae intervention significantly down-regulate the mRNA expression levels of pro-inflammatory cytokines IL-1β, IL-6, TNF-αand IL-17 in the aorta tissue, up-regulate the levels of anti-inflammatory factor IL-10, a marker of Treg cells. Finally, Pae's intervention in the gut microbiota resulted in the restoration of the balance of Treg/Th17, which indirectly down-regulated the protein expression level of LOX and fibrosis-related indicators (MMP-2/9 and collagenⅠ/Ⅲ). CONCLUSION Pae attenuates vascular fibrosis in a gut microbiota-dependent manner. The under?lying protective mechanism is associated with the improved Treg/Th17 balance in spleen mediated through the increased microbiota-derived SCFAs production.
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Objective:To explore the effect of Trichosanthis Fructus-Allii Macrostemonis Bulbus medicine on the proliferation and autophagy levels of aortic plaque vascular smooth muscle cells （VSMCs） in ApoE<sup>-/-</sup> mice with atherosclerosis （AS）. Method:A total of 40 ApoE<sup>-/-</sup> mice were fed with high-fat diet to replicate AS animal models. They were randomly divided into model group， Trichosanthis Fructus-Allii Macrostemonis Bulbus group， rapamycin group and atorvastatin group， and 10 mice with normal diet C57BL/6J mice were the blank group. The blank group and the model groups were given normal saline by gavage， while Trichosanthis Fructus-Allii Macrostemonis Bulbus group， rapamycin group and atorvastatin group were given corresponding drugs by gavage for 8 weeks. After the experiment， the mice were sacrificed. Total cholesterol （TC）， triglyceride （TG）， high-density lipoprotein cholesterol （HDL-C） and low-density lipoprotein cholesterol （LDL-C） levels were detected by the Microplate reader， the ratio of the aortic plaque area to the total area was observed and measured by staining with aortic gross oil red O. Western blot method was used to detect the proliferation-related protein proliferating cell nuclear antigen （PCNA） and <italic>α</italic>-smooth muscle actin （<italic>α</italic>-SMA） levels of VSMCs in the aortic media. Transmission electron microscopy was used to observe the autophagosomes of VSMCs and detect the expressions of VSMCs autophagy-related proteins Beclin-1， light chain proteinⅡ （LC3Ⅱ） and p62. Result:Compared with the model group， the Trichosanthis Fructus-Allii Macrostemonis Bulbus group showed significant reduction in the aortic lipid accumulation and plaque area of AS mice and the levels of TC， TG， LDL-C （<italic>P</italic><0.01） and increase of HDL-C （<italic>P</italic><0.05）. Trichosanthis Fructus-Allii Macrostemonis Bulbus significantly reduced the levels of proliferation-related antigens PCNA and <italic>α</italic>-SMA in aortic VSMCs （<italic>P</italic><0.01）， and inhibited the excessive proliferation of VSMCs. Trichosanthis Fructus-Allii Macrostemonis Bulbus significantly up-regulated Beclin-1 and LC3Ⅱ in aortic VSMCs protein expression， decreased p62 accumulation （<italic>P</italic><0.01）， increased the expressions of VSMCs autophagosomes， and increased the autophagy level of VSMCs. Conclusion:Trichosanthis Fructus-Allii Macrostemonis Bulbus regulates blood lipid levels in AS mice， and inhibits the excessive proliferation of aortic VSMCs and plaque formation in the aorta of AS mice. The mechanism may be related to the up-regulation of the autophagy activity of VSMCs.
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Background@#Some long non-coding RNAs (lncRNAs) have been found to contribute to cisplatin resistance. Here, we identified a novel lncRNA that was downregulated in cisplatin-resistant to ovarian cancer (OC) cells and aimed to examine the contribution of LINC01508 to cisplatin resistance in OC cells. @*Methods@#Differences in the lncRNA expression profile between OV2008 and C13K cells were assessed by lncRNA expression microarray. The expression of LINC01508 in ovarian epithelial cells, four OC cells, and OC, benign ovary tumor and normal ovary, cisplatin-resistant and non-resistant OC specimens were evaluated by quantitative real-time polymerase chain reaction (qPCR). The role of LINC01508 in OC cisplatin-resistant was evaluated by cell counting kit-8 (CCK-8), flow cytometry, colony formation, wound healing, Transwell, and tumor growth inhibition study in vivo. The clinical associations of LINC01508 in OC were evaluated using correlation analysis. The effects of verteporfin (VP) on cisplatin were explored to reveal the function of the hippo-YAP pathway on the cisplatin tolerance of C13K. @*Results@#LINC01508 was downregulated in cisplatin-resistant OC cells and platinum-resistant OC tissue (p<0.01). LINC01508 downregulation was correlated with tumor size, residual tumor, and platinum resistance. The overexpression of LINC01508 improves in vitro and in vivo sensitivity to cisplatin while predicts the poor overall survival which need further follow-up research. The increased level of LINC01508 could suppress the cisplatin resistance of OC cells through the inhibition of the hippo-YAP pathway. @*Conclusions@#The study proposes that dysregulation of LINC01508 expression results in resistance of OC to cisplatin through the inhibition of the hippo-YAP pathway.
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The aim of this paper was to investigate the effect and mechanism of paeonol on peritoneal macrophage M1 polarization in mice, explore whether the intervention action is related to the down-regulation of miR-155 and the inhibition of downstream JAK1-STAT1 pathway, and provide a new idea for the molecular mechanism of paeonol against atherosclerosis(AS). Lipopolysaccharide(LPS) and interferon-γ(IFN-γ) were used to stimulate macrophages for 24 hours to establish the M1 polarization model, and paeonol was given 24 hours before co-stimulation to provide a pre-protective effect on cells. CCK-8 assay was used to detect the cells damage induced by LPS and IFN-γ co-stimulation; flow cytometry was used to detect the expression of M1 surface markers F4/80 and CD86. ELISA was used to detect the secretion of interleukin 6(IL-6) and tumor necrosis factor-α(TNF-α) in supernatant. RT-qPCR was used to detect the expression of miR-155, and Western blot was used to detect the protein expression at JAK1-STAT1-SOCS1 pathway. The results showed that LPS and IFN-γ had no obvious damage to the cells at the optimal concentration, but they induced macrophages polarized to M1, resulted in high expression of M1 type marker factors F4/80 and CD86 on the cell surface, and increased secretion of IL-6 and TNF-α on the cell surface(P<0.05 or P<0.01). Paeonol significantly reduced the LPS and IFN-γ-induced high expression of F4/80 and CD86, the secretion of inflammatory factors IL-6 and TNF-α(P<0.05 or P<0.01), decreased the expression level of miR-155, significantly down-regulated the protein phosphorylation level of JAK1-STAT1 and up-regulated the protein expression of SOCS1(P<0.01) in RAW264.7 cells. The results showed that paeonol could inhibit M1 polarization of macrophages by down-regulating cell surface marker factors and inflammatory factors secreted by cells, which may be related to the down-regulation of miR-155 expression and the inhibition JAK1-STAT1 pathway activation.
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Animales , Ratones , Acetofenonas , Activación de Macrófagos , Macrófagos , MicroARNs , Factor de Transcripción STAT1RESUMEN
Objective To understand the prevalence and epidemiological characteristics of respiratory viruses in influenza-like illness in children during March 2017 to March 2018 in Qingdao. Methods A random selection of influenza surveillance cases (influenza-like illness, ILI) among children in Qingdao area was selected as the research object, and 359 cases were detected. Nasopharyngeal swabs were collected for multiple-fluorescence real-time reverse transcription-polymerase chain reaction nucleic acid detection to screen 9 kinds of respiratory viruses. Results Among the 359 Cases, 200 cases were positive for at least 1 kinds of viruses, and the positive rate was 55.71%(200/359). Among these 200 cases, the most positive numbers were influenza B Yamagata (IVB Yamagata) 29.50%(59/200), followed by enterovirus 15.00%(30/200), respiratory adenovirus (AdV) 13.50%(27/200), respiratory syncytial virus A (RSVA) 12.5%(25/200), influenza A H1N1(IVA H1N1) 10.00%(20/200), etc. 2 cases were 3 kinds of mixed viruses infected and 1 case was 4 kinds of mixed viruses infected. Conclusions Nine kinds of respiratory viruses are prevalent in Qingdao during March 2017 -March 2018. The main prevalence viruses contain influenza B Yamagata, enterovirus, respiratory adenovirus, respiratory syncytial virus A, influenza A H1N1. There is obvious seasonal distribution of influenza, respiratory syncytial virus, enterovirus, metapneumovirus. A mixed infection exists between 9 kinds of respiratory viruses, and mixed infection occurs in the month of the virus epidemic.
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This study is to investigate the role of endogenous CSE/H2S in regulating apoptosis of HepG2 cells. MTT and Trypan blue assay were performed to determine the effect of CSE inhibitor PAG and CSE siRNA on proliferation of HepG2. Production of H2S from HepG2 cells was assessed spectrophotometrically using N, N-dimethyl-p-phenylenediamine-dihydrochloride. Cells apoptosis was detected by means of double staining of Hoechst 33342 and PI with Array Scan V(TI)HCS600 High-Contents. Dihydroethidine (DHE) and 2', 7'-dichlorodihydrofluorescein diacetate (DCFH-DA) assay was used to determine intracellular superoxide anion and ROS level. Reduced glutathione (GSH) was determined by OxiSelect Total Glutathione Assay Kit. Recombinant plasmid pcDNA 3.1/myc-His(-)-CSE was constructed and transfected into 293T cells to rescue the ROS and GSH level to further investigate the effect of CSE/H2S on ROS and GSH. Western blotting was performed to test the effect of CSE siRNA on expression of activated caspase 3 and p-AKT and Nrf2 protein. The results showed that PAG and CSE siRNA could significantly decrease the production of H2S in HepG2 cells and inhibit the proliferation of HepG2 cells at a dose-dependent and time-dependent manner, respectively. PAG and CSE siRNA could promote the cell apoptosis of HepG2 cells. Moreover, PAG and CSE siRNA induced increased ROS generation and depletion of the critical antioxidant GSH and recombinant plasmid pcDNA 3.1/myc-His(-)-CSE rescued the level of ROS and GSH. Meanwhile, CSE siRNA increased the expression of activated caspase 3, but CSE siRNA did not affect the expression of p-AKT and Nrf2. These results suggested that the CSE/H2S pathway was involved in suppression of HepG2 cell growth and promoted apoptosis of HepG2 cells in an oxidative stress-dependent manner.
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Humanos , Alquinos , Farmacología , Apoptosis , Caspasa 3 , Metabolismo , Proliferación Celular , Cistationina gamma-Liasa , Genética , Metabolismo , Glutatión , Metabolismo , Glicina , Farmacología , Células HEK293 , Células Hep G2 , Sulfuro de Hidrógeno , Metabolismo , Factor 2 Relacionado con NF-E2 , Metabolismo , Plásmidos , Proteínas Proto-Oncogénicas c-akt , Metabolismo , ARN Interferente Pequeño , Genética , Especies Reactivas de Oxígeno , Metabolismo , Proteínas Recombinantes , Genética , Metabolismo , Transducción de Señal , TransfecciónRESUMEN
This study is to investigate the inhibitory effect and mechanism of prosapogenin A (PSA) on MCF7. MTT assay was performed to determine the inhibitory effect of PSA on MCF7 cells. PI/Hoechst 33342 double staining was used to detect cell apoptosis. RT-PCR was used to test the mRNA levels of STAT3, GLUT1, HK and PFKL. Western blotting was performed to determine the expression of STAT3 and pSTAT3 protein in MCF7 cells. The results showed that PSA could dose-dependently inhibit cell growth of MCF7 followed by IC50 of 9.65 micrmol x L(-1) and promote cell apoptosis of MCF7. Reduced mRNA levels of STAT3, HK and PFKL were observed in MCF7 cells treated with 5 micromol x L(-1) of PSA. PSA also decreased the level of pSTAT3 protein. STAT3 siRNA caused decrease of mRNA of GLUT1, HK and PFKL which indicated STAT3 could regulate the expressions of GLUT1, HK and PFKL. The results suggested that PSA could inhibit cell growth and promote cell apoptosis of MCF7 via inhibition of STAT3 and glycometabolism-related gene.
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Humanos , Antineoplásicos Fitogénicos , Farmacología , Apoptosis , Proliferación Celular , Transportador de Glucosa de Tipo 1 , Genética , Metabolismo , Hexoquinasa , Genética , Metabolismo , Células MCF-7 , Fosfofructoquinasas , Genética , Metabolismo , Plantas Medicinales , Química , ARN Mensajero , Metabolismo , Factor de Transcripción STAT3 , Genética , Metabolismo , Saponinas , Farmacología , Veratrum , QuímicaRESUMEN
Histone lysine methyltransferase EZH2 has been reported to be frequently overexpressed in hepatocellular carcinoma (HCC) tissues and associated with hepatocarcinogenesis. However, the exact mechanism of EZH2 up-regulation in HCC has not been determined. In this study, we used murine hepatocyte AML12 cells to investigate the role of hepatitis B virus X protein (HBx) in regulating the expression of mEZH2. Western blot analysis demonstrated that the expression level of mEZH2 protein in AML12 cells was up-regulated by HBx in a dose-dependent manner. To further investigate the mechanism of mEZH2 overexpression, the 2500 bp regulatory sequence upstream from the first exon of the mEZH2 gene was amplified from AML12 genomic DNA and constructed into a luciferase reporter plasmid. The luciferase activity of the mEZH2 promoter significantly increased in AML12 cells co-transfected with HBx plasmid, and deleting the -486/-214 promoter region decreased HBx-induced mEZH2 promoter activation by nearly 50%. The -486/-214 region was then analyzed in the TRANSFAC 6.0 database and a typical E2F1-binding site was found. Mutation of this E2F1-binding site or knockdown of E2F1 expression by RNAi led to a dramatic decrease in HBx-induced activation of the mEZH2 promoter and mEZH2 overexpression in AML12 cells. These results provide evidence that HBx up-regulates mEZH2 expression by transactivating the mEZH2 promoter through E2F1 transcription factor, thereby providing new epigenetic evidence for the carcinogenic effect of HBx.
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Animales , Ratones , Sitios de Unión , Línea Celular , Factor de Transcripción E2F1 , Genética , Proteína Potenciadora del Homólogo Zeste 2 , Hepatocitos , Biología Celular , Metabolismo , Virología , N-Metiltransferasa de Histona-Lisina , Genética , Metabolismo , Plásmidos , Complejo Represivo Polycomb 2 , Regiones Promotoras Genéticas , Genética , ARN Interferente Pequeño , Genética , Transactivadores , Genética , Metabolismo , Transfección , Regulación hacia ArribaRESUMEN
The development of human endometrial carcinoma (HEC) is a complex pathologic process involves several oncogenes and tumor suppressor genes. The full-length paired-box gene 2 (pax2), a recently discovered oncogene, promotes cell proliferation and growth and inhibits apoptosis of HEC cells. Here, we examined the effect of pax2 small interfering RNA (siRNA) on the growth of transplanted HEC cells in nude mice. The expression of Pax2 in 21 cases of normal endometrium and 38 cases of HEC was examined by immohistochemistry (IHC). HEC models were developed by subcutaneously transferring HEC cells into nude mice, followed by treatment with empty lentivirus vector, lentivirus vector-based pax2 siRNA, and phosphate buffered saline, respectively. Four weeks later, tumor size was measured, tumor inhibition rate was calculated, and histological analyses were conducted after staining with hematoxylin and eosin. The expression of Pax2 and Bcl-2 was detected by Western blot; proliferating cell nuclear antigen (PCNA) was detected by IHC. Significant differences were observed in the positive rate of Pax2 between normal endometrium and HEC (14.2% vs. 60.5%, P < 0.01). The expression index of Pax2 in well differentiated tumors was 1.88 ± 1.68, much lower than that in tumors of moderate (3.07 ± 1.96, P < 0.05) or poor differentiation (5.45 ± 2.76, P <0.01). Tumor necrosis increased, nuclear basophilia stain decreased, tumor growth was inhibited, and PCNA, Pax2, and Bcl-2 expression was reduced in HEC models treated with pax2 siRNA. These results indicate that Pax2 expression is related to HEC tumor biology with the increased expression of Pax2 correlated to malignancy. pax2 siRNA down-regulates Pax2 expression and inhibits tumorigenesis of HEC in nude mice, possibly due to cell apoptosis and the inhibition of tumor proliferation induced by down-regulation of Bcl-2.
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Adulto , Anciano , Animales , Femenino , Humanos , Ratones , Persona de Mediana Edad , Apoptosis , Línea Celular Tumoral , Proliferación Celular , Regulación hacia Abajo , Neoplasias Endometriales , Metabolismo , Patología , Vectores Genéticos , Lentivirus , Genética , Ratones Endogámicos BALB C , Ratones Desnudos , Trasplante de Neoplasias , Factor de Transcripción PAX2 , Genética , Metabolismo , Antígeno Nuclear de Célula en Proliferación , Metabolismo , Proteínas Proto-Oncogénicas c-bcl-2 , Metabolismo , Interferencia de ARN , ARN Interferente Pequeño , Genética , Transfección , Carga TumoralRESUMEN
<p><b>OBJECTIVE</b>To study the effects of Saccharomyces albicans (S. albicans) on the cell cycle distribution and proliferation of human umbilical vein endothelial cell ECV304 cells in vitro.</p><p><b>METHODS</b>The line of ECV304 cultured in vitro were divided into four groups which were treated by S. albicans supernatant, S. albicans inactivated bacilli, supernatant and inactivated bacilli mixture, normal culture medium. The proliferous effect of ECV304 induced by supernatant, inactivated bacilli, supernatant and inactivated bacilli mixture using the methods of MTT, cell count, microscope and flow cytometry were conducted.</p><p><b>RESULTS</b>In the condition of different times and different culture concentrations, ECV304 cells incubated with 4-fold diluted S. albicans supernatant for 48 h increased the proliferation rate. The S and G2/M population of ECV304 cells increased after incubated with S. albicans supernatant for 40 h, which showed significant increasing cell proliferation index (PI) (P < 0.05). The PI of the cells treated by inactivated bacilli showed no significant change (P > 0.05).</p><p><b>CONCLUSION</b>S. albicans could induce ECV304 cell proliferation which depends on the release of metabolic products of S. albicans.</p>
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Humanos , Ciclo Celular , División Celular , Proliferación Celular , Células Endoteliales de la Vena Umbilical Humana , Saccharomyces , Venas UmbilicalesRESUMEN
<p><b>OBJECTIVE</b>To investigate the impact of the expression of S100P on the prognosis and tumor chemosensitivity in patients with resectable gastric cancer and its mechanisms.</p><p><b>METHODS</b>The expression of S100P was analyzed in 121 resected primary gastric cancer tissues by using tissue array of immunohistochemistry excised from January 2003 to December 2007. The patients received adjuvant chemotherapy with oxaliplatin. The pEGFP-S100P plasmid was constructed and was transfected into BGC823 cell line to establish gastric cancer cell line with over-expression of human S100P, BGC823-S100P. The expression level of S100P was determined by real-time PCR and Western blot assay. The chemosensitivity of BGC823-S100P cell line to oxaliplatin was detected by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT) assay.</p><p><b>RESULTS</b>The S100P was positively expressed in 64 tumors (52.9%, 64/121). Although there was no significant relation between the expression of S100P and tumor T staging (P = 0.683), N staging (P = 0.472), M staging (P = 0.770) and differentiation (P = 0.553), Wilcoxon test showed that the 5-year cumulative survival rate of patients with positive S100P expression was significantly higher than that of patients with negative expression (20.3% vs. 3.5%, P = 0.034). Furthermore, overexpressed of S100P was found in the BGC823 cell line, BGC823-S100P. The mRNA and protein level of S100P in pEGFP transfected BGC823-S100P cell lines were significantly higher than those in control group (8.42 ± 1.38 vs. 0.83 ± 0.11 and 3.52 ± 0.48 vs. 0.97 ± 0.19, all P < 0.05). It indicated with MTT assay that the half-inhibitory concentration (IC(50)) to oxaliplatin decreased in BGC823-S100P cells, and was significantly lower than that in vector-only transfected cells [(142 ± 16) mg/L vs. (266 ± 11) mg/L, P = 0.032].</p><p><b>CONCLUSIONS</b>S100P may also be a potentially novel independent prognostic factor in gastric cancer patients following curative resection. And it could improve the cumulative survival of the patients through enhancing the chemosensitivity of tumor cell line to oxaliplatin.</p>
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Adulto , Anciano , Anciano de 80 o más Años , Femenino , Humanos , Masculino , Persona de Mediana Edad , Proteínas de Unión al Calcio , Metabolismo , Quimioterapia Adyuvante , Proteínas de Neoplasias , Metabolismo , Compuestos Organoplatinos , Pronóstico , Estudios Retrospectivos , Neoplasias Gástricas , Quimioterapia , Metabolismo , Patología , Cirugía General , Resultado del TratamientoRESUMEN
<p><b>OBJECTIVE</b>To detect the expression of VEGF-C in nasopharyngeal carcinoma (NPC) and explore its relationship with proliferation and metastasis of NPC.</p><p><b>METHODS</b>Biopsy specimens of 62 NPC patients were divided into 2 equal portions, one for immunohistochemical staining with VEGF-C polyclonal antibody by streptavidin peroxidase method, another for flow cytometry with Ki67 antibody to analyze the proliferation of tumors. The patients were followed up periodically, and then their 3-year survival and the cause of death were statistically analyzed.</p><p><b>RESULTS</b>Of the 62 patients, the percentage of VEGF-C positive cells in the tumors ranged from 0 - 82%, 17 (27.4%) were negative, 13 (21.0%) weak positive, 18 (29.0%) moderate positive and 14 (22.6%) strong positive. Ki67 positive tumor cells ranged from 0 - 52%, 40 cases (64.5%) showed low expression which include 15 cases of negative, 22 (35.5%) showed high expression. There was a direct relationship between the expression of VEGF-C and Ki67 (r = 0.323, P < 0.05). The 3-year survival rate of 62 patients was 66.1%. The expression of VEGF-C in the patients with positive lymph node was much higher than that with negative lymph node (P < 0.01). Among the 8 patients with distant metastasis, their VEGF-C expression was strong positive while among the 21 disease free survival patients, their VEGF-C expression was (-) or (+) account for 80.9%. An inverse correlation was found between the VEGF-C expression and prognosis of NPC patients, but the difference has no statistical significance (r = -0.219, P > 0.05).</p><p><b>CONCLUSION</b>High expression of VEGF-C is related with proliferation and metastasis of NPC cells. It is not an independent prognostic factor, but a predictive marker of disease-free survival of NPC patients.</p>
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Adulto , Anciano , Femenino , Humanos , Masculino , Persona de Mediana Edad , Proliferación Celular , Supervivencia sin Enfermedad , Estudios de Seguimiento , Regulación Neoplásica de la Expresión Génica , Antígeno Ki-67 , Metabolismo , Ganglios Linfáticos , Patología , Metástasis Linfática , Neoplasias Nasofaríngeas , Metabolismo , Patología , Radioterapia , Estadificación de Neoplasias , Tasa de Supervivencia , Factor C de Crecimiento Endotelial Vascular , MetabolismoRESUMEN
<p><b>BACKGROUND</b>Improvement of clinical symptoms following hyperbaric oxygen (HBO) treatment of neuropsychiatric disorders arising from traumatic brain injury was proved by our previous study. This study was aim to obtain the evidence of other changes.</p><p><b>METHODS</b>Three hundred and ten patients with neuropsychiatric disorders arising from traumatic brain injury were treated twice with hyperbaric oxygen. Cerebral single photon emissions computed tomography (SPECT) images and computed tomography scans (CT) before and after hyperbaric oxygen treatment, were compared.</p><p><b>RESULTS</b>Before treatment, the proportion of abnormal cerebral changes detected by SPECT was 81.3% but only 15.2% by CT. After HBO treatment, 70.3% of SPECT scans showed no abnormalities and these patients were clinically improved. Treatment improved regional cerebral blood flow.</p><p><b>CONCLUSION</b>SPECT was much more sensitive than CT in the diagnosis of neuropsychiatric disorders following hyperbaric oxygen treatment of neuropsychiatric disorders arising from traumatic brain injury.</p>
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Adolescente , Adulto , Anciano , Niño , Femenino , Humanos , Masculino , Persona de Mediana Edad , Lesiones Encefálicas , Oxigenoterapia Hiperbárica , Trastornos Mentales , Diagnóstico , Terapéutica , Enfermedades del Sistema Nervioso , Diagnóstico , TerapéuticaRESUMEN
<p><b>OBJECTIVE</b>To determine the correlation between results of ATP bioluminescence tumor chemosensitivity assay (ATP-TCA) of human ovarian cancer specimens in vitro and clinical chemo-therapeutic responses of patients.</p><p><b>METHODS</b>Thirty-four freshly taken ovarian cancer specimens (28 cases) and ascites (6 cases) and 9 chemotherapeutic drugs were tested in vitro for cancer chemosensitivity by ATP-TCA.</p><p><b>RESULTS</b>Among the 34 ovarian cancer cases, the efficacy of ATP-TCA is 94.0%, the sensitivity, the specificity, the positive and negative predicting values, and an overall predicting value in vitro and vivo were 90.0%, 91.7%, 94.7%, 84.6% and 90.6%, respectively.</p><p><b>CONCLUSION</b>The results of ATP-TCA assay are correlated well with clinical treatment responses. The assay may be an important and useful method for individual-based chemotherapy of cancers.</p>
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Adulto , Anciano , Femenino , Humanos , Persona de Mediana Edad , Adenosina Trifosfato , Metabolismo , Antineoplásicos , Farmacología , Usos Terapéuticos , Protocolos de Quimioterapia Combinada Antineoplásica , Usos Terapéuticos , Carcinoma , Quimioterapia , Patología , Cisplatino , Farmacología , Ciclofosfamida , Farmacología , Resistencia a Antineoplásicos , Ensayos de Selección de Medicamentos Antitumorales , Métodos , Mediciones Luminiscentes , Neoplasias Ováricas , Quimioterapia , Patología , Paclitaxel , Farmacología , Valor Predictivo de las Pruebas , Sensibilidad y EspecificidadRESUMEN
<p><b>OBJECTIVE</b>To study the altering rule of coagulation function at molecular level in patients with secondary brain injury (SBI).</p><p><b>METHODS</b>Tissue factor (TF) and tissue factor pathway inhibitor (TFPI) were studied in 32 patients 1, 2, 3 and 7 days after craniocerebral injury. Repeated cranial CT scans and platelet counts were made simultaneously. Same measurements were done in 30 normal adults except CT scan.</p><p><b>RESULTS</b>No obvious difference was found in age, sex and platelet count between the injured and the normal groups. TFPI/TF decreased markedly in the first week after injury in patients with SBI, but only decreased on the 7th day in the patients without obvious SBI. For the patients who developed delayed intracranial hematoma (DIH) or hematoma enlargement, TF rose only 1 and 2 days after injury, but TFPI had a tendency to rise again after a fall on the 3rd day. For those patients who developed no DIH, TF rose all the time within the 1st week.</p><p><b>CONCLUSIONS</b>Decrease of TFPI/TF for a long time, especially within 3 days after injury, may be one of the most important reasons for SBI. High expression of TF for a relative short time and increase of TFPI after a fall within 3 days may be one of the important reasons for DIH or hematoma enlargement.</p>
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Adolescente , Adulto , Femenino , Humanos , Masculino , Persona de Mediana Edad , Anticoagulantes , Sangre , Traumatismos Craneocerebrales , Sangre , Coagulación Intravascular Diseminada , Sangre , Lipoproteínas , Sangre , Recuento de Plaquetas , Tromboplastina , Tomografía Computarizada por Rayos XRESUMEN
<p><b>OBJECTIVE</b>To investigate the heterogeneity of human breast cancer cells, their influence on biological behavior of tumor cells and clinical implications.</p><p><b>METHODS</b>The subpopulations of MCF-7 breast cancer cells were isolated by Percoll gradient centrifugation. DNA content and cell cycle distribution were detected with flow cytometry. Tumor chemosensitivity analysis was performed with MTT assay.</p><p><b>RESULTS</b>Heterogeneity was observed in DNA content and cell cycle distribution among four subpopulations of breast cancer cells, which were related to their proliferation ability and chemosensitivity results.</p><p><b>CONCLUSION</b>Hereditary instability and intrinsic characteristics of most tumor cells, not only lead to tumor progression and heterogeneity but also cause the loss of monoclonality and the generation of subclones. Further study on some profiles of tumor heterogeneity such as DNA content, cell cycle distribution and their influence on tumor proliferation and chemosensitivity may very well improve the clinical treatment.</p>
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Femenino , Humanos , Neoplasias de la Mama , Quimioterapia , Patología , Ciclo Celular , División Celular , Línea Celular Tumoral , Centrifugación por Gradiente de Densidad , ADN de NeoplasiasRESUMEN
<p><b>OBJECTIVE</b>To evaluate the effects of hyperbaric oxygen (HBO) therapy on patients with postbrain injury neural status.</p><p><b>METHODS</b>Two to 4 courses of HBO therapy and/or medications were used to treat 320 patients who were randomly divided into two groups. Assessment was made with (99m)Tc-ethyl cysteinate dimer ( (99m)Tc-ECD) single photon emission computed tomography (SPECT) before and after treatment.</p><p><b>RESULTS</b>There was a significant difference between the HBO therapy group and the non-HBO therapy group. HBO therapy was superior to medication treatment alone in the recovery of clinical symptoms, control of epilepsy, and resolution of hydrocephalus (P<0.01).</p><p><b>CONCLUSIONS</b>HBO therapy has specific curative effects on patients with postbrain injury neural status, and (99m)Tc-ECD SPECT could play an important role in diagnosing postbrain injury neural status and monitoring the therapeutic effects of HBO.</p>