A laboratory scale combination process of anaerobic baffled reactor(ABR) with sequencing batch reactor(SBR) for treatment of real dyeing wastewater was studied.The effects of operational conditions were investigated.The results demonstrated that removal rates of COD,colour and aniline were 32%~95%,89%~99% and 50%~98%,respectively,the effluents of COD were 30.0 ~97.1mg/L,colour were 8 ~40 times dilution ratio,concentration of aniline were 0.20 ~0.95 mg/L,which could meet the National Discharge Criteria(GradeⅠ) under the operational conditions of HRTs of 24~36 h,organic loading rates of 0.43 ~2.46 kg COD/(m~(3)?d),the influent pH values of 6.5~8.0,ambient temperatures of 20℃~35℃ at the ABR stage and DOs of 2 mg/L,reaction times of 3~10h,settle times of 2 h at the SBR stage.

This study was aimed to investigate the effects of oxaliplatin on human multiple myeloma cell line RPMI-8226 and its mechanism. The proliferation inhibitory rate of RPMI8226 cells was assayed by MTT, the morphological changes of RPMI-8226 cells were observed by inverted fluorescent microscopy and transmission electron microscopy, the apoptosis rate and the cell cycle distribution of RPMI-8226 cells were detected by flow cytometry, The effects of oxaliplatin on the expression of Bcl-2, caspase-8, caspase-3 mRNA were tested by RT-PCR, Bcl-2 protein expression of RPMI-8226 cells was analyzed by Western blot. The results showed that oxaliplatin could inhibit the proliferation of RPMI-8226 cells in time and dose-dependent manners. Cell number in oxaliplatin group was significantly less than that in control group under light microscope, and the growth arrangement was irregular, apoptotic cells could be seen. Under electron microscope, typical apoptotic morphological and ultrastructural changes could be observed. Flow cytometry results showed that oxaliplatin could induce apoptosis of RPMI-8226 cells, the difference have statistical significance (P < 0.05). Oxaliplatin mainly arrested RPMI-8226 cells in the S phase (P < 0.05). The expression of Bcl-2 mRNA did not have apparent change, while the expression of caspase-8, caspase-3 mRNA increased (P < 0.05). Western blot results suggested that the expression of Bcl-2 protein had no obvious change. It is concluded that the oxaliplatin can induce apoptosis of RPMI-8226 cells, activating the death receptor pathway and arresting cell cycle may be two of the related mechanisms, Bcl-2 gene has unobservable effects in the process of oxaliplatin-induced cell apoptosis.
Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Caspase 8 ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Multiple Myeloma ; metabolism ; pathology ; Organoplatinum Compounds ; pharmacology ; Proto-Oncogene Proteins c-bcl-2 ; metabolism

This study was aimed to investigate the effects of docetaxel on proliferation and apoptosis of multiple myeloma cell line RPMI8226 and its mechanism. The inhibitory rate of multiple myeloma cells was detected by MTT, the morphological and ultrastructural changes of RPMI8226 cells were observed by using inverted fluorescent microscope and transmission electron microscope, the apoptosis-inducing effect of docetaxel on RPMI-8226 cells was determined by flow cytometry with Annexin-V FITC/PI staining, the cell distribution in cell cycle of RPMI-8226 cells was assayed using flow cytometry with PI staining; the effect of docetaxel on expression of BCL-2, caspase-8, caspase-3 mRNA was detected by semiquantitative RT-PCR, the expression changes of BCL-2 protein in RPMI-8226 cells before and after treatment with docetaxel were measured by using Western blot. The results indicated that 0.25 - 8.0 µg/ml docetaxel obviously inhibited the proliferation of RPMI-8226 cells in both time- and dose-dependent manners. Cell number of docetaxel-treated group was significantly less than control group under inverted fluorescent microscope, and the cell arrangement was irregular, necrotic cells could be seen occasionally. By transmission electron microscope, the morphological and ultrastructural changes of cell typical apoptosis could be observed, a few necrotic cells could be captured, too. Compared with control group, docetaxel induced the apoptosis of RPMI-8226 cell line (P < 0.01). Docetaxel mainly arrested RPMI-8226 cells in the G(2)/M phase (P < 0.01). The expression of BCL-2 mRNA decreased (P < 0.05), while the mRNA expression of caspase-8 and caspase-3 increased (P < 0.05). Western blot indicated that BCL-2 protein expression also decreased (P < 0.05). It is concluded that docetaxel can inhibit the proliferation of RPMI-8226 cells by inducing cell apoptosis. Activation of the mitochondrial and death receptor pathways of apoptosis may be involved in the docetaxel-induced apoptosis, cell cycle arrest may also play an important role in the apoptosis mechanism.
Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Caspase 8 ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Multiple Myeloma ; metabolism ; pathology ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Taxoids ; pharmacology

With the increasingly more serious environmental pollution in China in recent years, effective intervention with PM25-induced health risks has become a major scientific issue to be addressed urgently in medical research field in China. NOD-like receptors (NLRs) are a family of cytoplasmic pattern-recognition receptors that have critical roles in innate immunity. On the basis of study progresses in international cardiovascular disease research "Fine particulate matter exposure is a modifiable risk factor for the morbidity and mortality of cardiovascular diseases", and with reference to the current understanding of pulmonary inflammation and oxidative stress in PM2.5-induced acute coronary syndrome, this study intended to investigate whether intracellular pattern recognition NL-RP3 plays a important role in the inital event of PM2.5 induced vessel inflammation as a foreign matter in the process of plaque destabilization and to thoroughly explore the underlying mechanisms responsible for PM2.5-induced acute cardiovascular events. On the other hand, it also studies the feasibility of using traditional Chinese medicine to treat plaque destabilization cause by PM2.5 exposure and discuss it's pathogenesis and intervention strategy based on TCM theory. This paper in order to provide scientific basis for social focal issues in public health proactively and offers the references for relevant research.
Air Pollutants ; toxicity ; Animals ; Environmental Exposure ; adverse effects ; Humans ; Medicine, Chinese Traditional ; methods ; Particulate Matter ; toxicity ; Plaque, Atherosclerotic ; chemically induced ; drug therapy ; mortality

Objective To investigate the anti-oxidative effects of alprostadil on contrast-induced nephropathy(CIN)after percuteous coronary intervention (PCI)in patients with chronic kidney disease(CKD).Methods A total of 200 patients with CKD were enrolled in our hospital.According to the random number table was divided into alprostadil 100 cases,100 cases of conventional treatment group.The levels of serum creatinine (Scr),creatinine clearance (eGFR),serum cystatin C (ScysC)and 8-hydroxy-deoxyguanine (8-OHdG)were observed before and after operation at 72 h and 7 d after operation.Results The incidence of CIN in the alprostadil group was significantly lower than that in the conventional treatment group (6% vs 12%,P<0.05).There was no significant difference in the level of Scr,eGFR,ScysC and 8-OHdG between the alprostadil group and the conventional treatment group (P>0.05).The level of Scr in the alprostadil group was significantly lower than that in the conventional treatment group at 72 h and 7 d after operation.The level of eGFR was significantly higher than that of the conventional treatment group (P<0.05).The levels of ScysC and 8-OHdG in the two groups were significantly higher than those before operation at 72 h and 7 d(P>0.05).The levels of ScysC and 8-OHdG in the alprostadil group were significantly lower than those in the conventional treatment group at 72 h and 7 d after PCI(P<0.05).Conclusion Alprostadil may improve the oxidative stress in patients with CKD and provide a preventive effect on CIN.

Objective To develop a field medical equipment maintenance trailer for patrol inspection and maintenance of medical equipment in wartime and peace time.Methods A field medical equipment maintenance trailer was constructed with the components of a shelter,a chassis,an electrical system and etc.The shelter had a power supply area on the front side,two working areas on left and right sides,a control area on the rear side and a support mechanism covered with a rainproof tarpaulin;The chassis was composed mainly of a frame,a traction mechanism,a steering mechanism,a suspension,a braking system and etc;the electrical system was made up of a power supply unit and a control unit.Results The maintenance trailer carrying a variety of maintenance tools and spare parts was trailed with the transport vehicle during maneuvering and driven electrically during equipment maintenance,which was ready for use immediately after deployment so as to meet the needs for rapid maintenance of medical equipment.Conclusion The maintenance trailer gains advantages in internal layout,mobility and security,and can be used to inspect and maintain medical equipment and to transport spare parts and maintenance tools.[Chinese Medical Equipment Journal,2023,44(11):114-116]

This study was purposed to explore the mechanisms of cladribine (2-CdA)-inducing apoptosis of multiple mycloma RPMI 8226 cells. The MTT method was used to determine cell proliferation after being treated with 2-CdA. Apoptosis and cell cycle progression were examined by flow cytometry. Transmission electron microscopy was used to observe ultrastructural changes of RPMI 8226 cells. RT-PCR and Western blot were used to analyze the mRNA and protein expression levels of BCL-2, MCL-2 and caspase-3 respectively. The results showed that the 2-CdA inhibited proliferation of RPMI 8226 cells in time and dose-dependent manner. Typical apoptotic morphological and ultrastructure changes could be observed by electron microscopy. Flow cytometry showed that 2-CdA induced myeloma cell apoptosis and arrested myeloma cells in the G2/M phase. The mRNA expression of BCL-2 and MCL-1 decreased but that of caspase-3 not apparently changed. Western blot results suggested that the change trend of BCL-2 MCL-1 and caspase-3 was the same as result of RT-PCR. It is concluded that 2-CdA exhibits inhibitory effects on RPMI 8226 cells in vitro. Activating the mitochondrial and death receptor pathways of apoptosia may be the potential mechanism, meanwhile, the cell cycle arrest may also play a critical role in apoptosis.
Apoptosis ; drug effects ; Caspase 3 ; Cell Division ; Cell Line, Tumor ; Cell Proliferation ; Cladribine ; pharmacology ; Humans ; Multiple Myeloma ; pathology ; Proto-Oncogene Proteins c-bcl-2

This study was aimed to investigate the effects of mitoxantrone on proliferation and apoptosis of human multiple myeloma cell line RPMI-8226 and its mechanism. The inhibitory rate of RPMI8226 cells proliferation was assayed by MTT, the morphological changes of RPMI-8226 cells were observed by inverted flurescent microscopy and transmission electron microscopy, the apoptosis rate and the cell cycle distribution of RPMI-8226 cells were detected by flow cytometry. The effects of mitoxantrone on the expression of BCL-2, BAX, caspase-3 mRNA were detected by RT-PCR, the BCL-2, BAX, caspase-3 protein expression of RPMI-8226 cells was analyzed by Western blot. The results showed that mitoxantrone could inhibit the proliferation of RPMI-8226 cells in time- and dose-dependent manners. Light microscopy showed that the cell number in mitoxantrone group was significantly less than that in control group and the cell growth arrangement was irregular, apoptotic cells could be seen. Under electron microscope, typical apoptotic morphological and ultrastructural changes could be observed, these results confirmed that the mitoxantrone could induce apoptosis of RPMI-8226 cells, the difference have statistical significance (P < 0.05). The 1.0 µg/ml low concentration of mitoxantrone mainly arrested RPMI-8226 cells in the G2/M phase(P < 0.05), and the 2.0 µg/ml high concentration of mitoxantrone mainly arrested RPMI-8226 cells in the S phase (P < 0.05). The expression of BCL-2 mRNA decreased (P < 0.05),while the expression of BAX, caspase-3 mRNA increased (P < 0.05). Western blot indicated that BCL-2 protein expression also decreased (P < 0.05) and BAX, caspase-3 protein expression increased. It is concluded that the mitoxantrone can inhibit the proliferation of RPMI-8226 cells by inducing cell apoptosis. Activation of the mitochondrial and death receptor pathways of apoptosis may be involved in the mitoxantrone-induced apoptosis, the cell cycle arrest may also play an important role in the apoptosis mechanism.
Apoptosis ; drug effects ; Caspase 3 ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Mitoxantrone ; pharmacology ; Multiple Myeloma ; pathology ; Proto-Oncogene Proteins c-bcl-2

This study was aimed to investigate the effects of sorafenib on proliferation and apoptosis of MM cell line RPMI-8226, and to explore the its potential anti-tumor mechanism. The inhibitory rate of multiple myeloma cell proliferation was tested by MTT. Transmission electron microscopy was used to observe morphological and ultrastructural changes of RPMI-8226 cells treated with sorafenib. The effects of sorafenib on the apoptosis and cell cycle of RPMI-8226 cells was detected by flow cytometry. The effects of sorafenib on the expression of caspase-3, BCL-2 and MCL-1 mRNA and protein were assayed by RT-PCR and Western blot respectively. The results showed that sorafenib (0-10.0 µmol/L) could obviously inhibit the proliferation of RPMI-8226 cells in time and dose-dependent manner. Flow cytometry results showed that sorafenib could induce apoptosis of RPMI-8226 cells, the difference was statistical significance (P < 0.05). Sorafenib mainly arrested RPMI-8226 cells in the G1 phase (P < 0.05). Typical apoptotic morphological and ultrastructural changes of MM cells could be observed under transmission electron microscope, Examination of cellular signaling pathways showed that sorafenib induced upregulation of cleaved-caspase-3 expression, and simultaneous downregulation of BCL-2 and MCL-1 expression. It is concluded that sorafenib displays anti-myeloma activity. Activating the death receptor pathway and arresting cell cycle may be two of the relatated mechanisms.
Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Caspase 3 ; Cell Cycle ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Multiple Myeloma ; drug therapy ; pathology ; Niacinamide ; analogs & derivatives ; pharmacology ; Phenylurea Compounds ; pharmacology ; Proto-Oncogene Proteins c-bcl-2 ; Signal Transduction

OBJECTIVETo investigate the feasibility and efficacy of rituximab combined with high-dose chemotherapy supported by autologous peripheral blood stem cell transplantation (ASCT) in patients with aggressive B-cell non-Hodgkin lymphoma (NHL).

METHODSTwenty-eight patients with aggressive B-cell NHL (22 newly diagnosed, 6 relapsed) were enrolled in this study. The high-dose chemotherapy included CHOP regimen (CTX + ADM + VCR + PDN) for the newly diagnosed patients and DICE (DEX + IFO + DDP + VP-16) or EPOCH (VP-16 + PDN + VCR + CTX + ADM) for the relapsed patients. Each patient received infusion of rituximab at a dose of 375 mg/m(2) for four times, on D1 before and on D7 of peripheral blood stem cell mobilization, and on D1 before and D8 after stem cell reinfusion.

RESULTSComplete remission was achieved in all patients after high dose chemotherapy and ASCT. At a median follow-up of 37 months, the estimated overall 4-year survival and progression-free survival rate for all patients were 75.0% and 70.3%, respectively, while both were 72.7% for the previously untreated patients. The therapy was generally well tolerated with few side-effects attributable to rituximab.

CONCLUSIONThese results suggest that adding rituximab to high-dose chemotherapy with peripheral blood stem cell transplantation is feasible and may be beneficial for patients with aggressive B-cell non-Hodgkin lymphoma.

Adolescent ; Adult ; Antibodies, Monoclonal, Murine-Derived ; adverse effects ; therapeutic use ; Antineoplastic Agents ; adverse effects ; therapeutic use ; Antineoplastic Combined Chemotherapy Protocols ; adverse effects ; therapeutic use ; Cisplatin ; adverse effects ; therapeutic use ; Combined Modality Therapy ; Cyclophosphamide ; adverse effects ; therapeutic use ; Dexamethasone ; adverse effects ; therapeutic use ; Disease-Free Survival ; Doxorubicin ; adverse effects ; therapeutic use ; Etoposide ; adverse effects ; therapeutic use ; Female ; Fever ; chemically induced ; etiology ; Humans ; Ifosfamide ; adverse effects ; therapeutic use ; Lymphoma, Large B-Cell, Diffuse ; therapy ; Male ; Middle Aged ; Peripheral Blood Stem Cell Transplantation ; Prednisolone ; adverse effects ; therapeutic use ; Prednisone ; adverse effects ; therapeutic use ; Prospective Studies ; Remission Induction ; Rituximab ; Survival Rate ; Vincristine ; adverse effects ; therapeutic use ; Vomiting ; chemically induced ; Young Adult