Well-Aligned Au/TiO2 Nanorods by Magnetron Sputtering with Enhanced Photocatalytic Properties.

In this work, we demonstrate the feasibility of preparing Au/TiO2 nanorods via a dc magnetron sputtering at room temperature and heat-treatment at 500 °C in air for 2 h. The heat treatment leads to the migration of Au atoms into TiO2 nanofilm to form Au/TiO2 nanorods with Au nanoparticles embedded in the TiO2 nanorods of anatase phase. The Au nanoparticles in the TiO2 nanorods suppress the charge recombination. These Au/TiO2 nanorods showed high absorption and intensive response to the visible light and had improved photocatalytic properties in comparison with pure TiO2 nanoparticles formed by using similar method.

[The effect of edaravone on MAPKs signal pathway associated with Abeta(25-35) treatment in PC12 cells].

OBJECTIVE: To explore whether edaravone protects cells damage via mitogen-activated protein kinases (MAPKs) signal pathway, and which procedure of p38 be affected so as to add theories for AD pathogenesis and treatments. METHODS: According to different drugs treated, PC12 cells in vitro were divided into four groups. Negative control group: cells were treated with media alone. AD model group: cells were treated with 30 pmol/L Abeta(25-35). Inhibitor control group: cells were treated with 10 micromol/L SB203580 Cp38 mitogen-activated protein kinase (p38) inhibitor], 10 micromol/L SP600125 [c-Jun NH2 terminal kinase (JNK) inhibitor], or 10 micromol/L PD98059 extracelular signal regulated kinase (ERK) inhibitor]. Low-dose, middle-dose and high-dose edaravone group: cells plated for 24 hours treated with 30 micromol/L Abeta(25-35) and co-treated with 20, 40, 80 micromol/L edaravone 3 hours, respectively. The morphology of the treated cells were observed, the p-p38, p-JNK and p-ERK proteins in each group were tested by the Western blot. The p38 mRNA were tested in each group above (only add SB203580 10 micromol/L in third group) by the real time PCR. RESULTS: (1) The p-p38 protein was significantly increased in model control group compared with that in negative control group (P<0.05). The p-p38 protein in the inhibitor group and edaravone groups was decreased significantly (P<0.05) when compared with that in model control group. The p-p38 proteins were significantly increased in the three edaravone groups compared with that in inhibiter control group (P<0.05). The p-p38 protein in middle-dose edaravone group was decreased compared with that in low-dose edaravone group (P<0.05). There was no relationship in dose-dependent manner about edaravone. Compared with three edaravone groups, the p-p38 protein was lower than it in high-dose edaravone & inhibiter group (P<0.05). (2) The p-JNK protein was significantly increased in model control group compared with that in negative control group (P<0.05). The p-JNK protein in the inhibitor group was decreased compared with that in model control group (P<0.05). (3) No significantly difference of p-ERK protein concentration was observed in other groups when compared with that in negative control group (P>0.05 each). (4) Compared with negative control group, the p38 mRNA in model control group was significantly increased, and it was significantly decreased in inhibitor control group (P<0.05 each). In 40 micromol/L and 80 micromol/L edaravone groups, the p38 mRNA was significantly decreased compared with that in model control group, and it still was decreased compared with that in inhibitor control group (P<0.05). The p38 mRNA in 40 micromol/L edaravone group was the lowest among three edaravone groups, and it was obviously different from that in 20 micromol/L and 80 micromol/L edaravone groups (P<0.05). CONCLUSION: Abeta(25-35) could increase the p-p38 and p-JNK protein expression in cultured PC12 cells, but there was no obviously expression of p-ERK protein. These indicated that Abeta(25-35) might activate MAPKs signal pathway, especially p38 and JNK, and lead to PC12 cell damage. Edaravone could decrease p38 mRNA induced-Abeta(25-35), which indicated edaravone could protect PC12 cell damage via blocking p38 signal pathway in mRNA stage and protein stage simultaneously. Hence, it is promising that edaravone would be a new medicine for AD.

Induction of apoptosis by total flavonoids from Scutellaria barbata D. Don in human hepatocarcinoma MHCC97-H cells via the mitochondrial pathway.

Scutellaria barbata D. Don, a traditional Chinese medicine, reportedly possesses antitumor activity against a variety of tumors. In the present study, we investigated the cytotoxic effect of total flavonoids from S. barbata (TF-SB) on human hepatocarcinoma cells and the underlying molecular mechanisms regarding the effect were explored. TF-SB treatment significantly reduced the cell viability of human HCC MHCC97-H cells in a dose-dependent manner. Further flow cytometric analysis showed that the apoptosis rate of MHCC97-H cells increased and the mitochondrial membrane potential (∆ψm) of MHCC97-H cells decreased after TF-SB treatment. DNA ladder showed that TF-SB induced a significant increase in DNA fragmentation in MHCC97-H cells. Reverse transcription PCR and Western blot analysis revealed that the expression levels of Smac, Apaf-1, Cytochrome c, Caspase-9, and Caspase-3 were upregulated in a dose-dependent manner and after treatment with different concentrations of TF-SB for 48 h. These results suggest that TF-SB induces apoptosis in MHCC97-H cells through the mitochondrial pathway.

Five-year remission without disease progression in a patient with relapsed/refractory multiple myeloma with extramedullary disease treated with LCAR-B38M chimeric antigen receptor T cells in the LEGEND-2 study: a case report.

BACKGROUND: Multiple myeloma remains incurable despite treatment advancements over the last 20 years. LCAR-B38M Cells in Treating Relapsed/Refractory Multiple Myeloma was a phase 1, first-in-human, investigator-initiated study in relapsed/refractory multiple myeloma conducted at four sites in China. The study used LCAR-B38M chimeric antigen receptor-T cells expressing two B-cell maturation antigen-targeting single-domain antibodies designed to confer avidity, and a CD3ζ signaling domain with a 4-1BB costimulatory domain to optimize T-cell activation and proliferation. This chimeric antigen receptor construct is identical to ciltacabtagene autoleucel. In the LEGEND-2 study (n = 57, Xi'an site), overall response rate was 88%; median (95% CI) progression-free survival and overall survival were 19.9 (9.6-31.0) and 36.1 (26.4-not evaluable) months, respectively; and median follow-up was 25 months. This case study reports on a patient with relapsed/refractory multiple myeloma (λ light chain type) who was treated with LCAR-B38M chimeric antigen receptor T cells in the LEGEND-2 study (Xi'an site); he had received five prior lines of treatment and had extensive extramedullary lesions. CASE PRESENTATION: The patient, a 56-year-old Asian male, received cyclophosphamide (500 mg daily × 3 days) as lymphodepletion therapy and a total dose of 0.5 × 106 chimeric antigen receptor + T cells/kg split into three infusions (days 1, 24, and 84 from June to August 2016). He experienced grade 2 cytokine release syndrome after the first infusion; all symptoms resolved with treatment. No cytokine release syndrome occurred following the second and third infusions. His λ light chain levels decreased and normalized 20 days after the first infusion, and extramedullary lesions were healed as of January 2018. He has sustained remission for 5 years and received no other multiple myeloma treatments after LCAR-B38M chimeric antigen receptor T cell infusion. As of 30 October 2020, the patient is still progression-free and has maintained minimal residual disease-negative (10-4) complete response status for 52 months. CONCLUSIONS: This case provides support that treatment with LCAR-B38M chimeric antigen receptor T cells can result in long-term disease remission of 5 or more years without disease progression in a heavily pretreated patient with extensive extramedullary disease and no other treatment options.

Four-year follow-up of LCAR-B38M in relapsed or refractory multiple myeloma: a phase 1, single-arm, open-label, multicenter study in China (LEGEND-2).

BACKGROUND: LCAR-B38M is a chimeric antigen receptor T cell product with two binding domains targeting B cell maturation antigen. Our previous reports showed a remarkable efficacy of LCAR-B38M in patients with relapsed/refractory multiple myeloma (RRMM) at a median follow-up of 2 years. Here, we report long-term safety and efficacy data from a median follow-up of 4 years. METHODS: LEGEND-2 was a phase 1, single-arm, open-label study conducted in four registered sites in China. Seventy-four participants with RRMM received LCAR-B38M treatment. Lymphodepletion was performed using cyclophosphamide or cyclophosphamide plus fludarabine. LCAR-B38M, at a median dose of 0.513 × 106 cells/kg, was intravenously administered either in three split infusions or in a single infusion. The primary objective was the safety of LCAR-B38M, and the secondary objective was efficacy. RESULTS: As of May 25, 2021, the median follow-up was 47.8 months. All patients experienced ≥ 1 adverse events (AEs). Grade ≥ 3 AEs were observed in 45/74 (60.8%) patients. Cytokine release syndrome (CRS) occurred in 68/74 (91.9%) cases; 7 (9.5%) had grade ≥ 3 CRS. One patient experienced grade 1 central nervous system toxicity. The overall response rate was 87.8%. Fifty-four out of 74 (73.0%) patients achieved complete response. The median progression-free survival was 18.0 months, and the median overall survival for all patients was not reached. The median duration of response was 23.3 months. Four patients experienced viral infection more than 6 months post-infusion, and four patients developed second primary non-hematological malignancies at a median time of 11.5 months post-CAR-T cell transfer. CONCLUSIONS: The 4-year follow-up data of LCAR-B38M therapy demonstrated a favorable long-term safety profile and a durable response in patients with RRMM. Trial registration Clinicaltrials.gov NCT03090659 (retrospectively registered on March 27, 2017); ChiCTR-ONH-17012285.

Involvement of oxidative stress in the relapse of acute myeloid leukemia.

The aims of the present study were to determine the level of oxidative stress and the salient factors leading to the relapse of acute myeloid leukemia (AML). Oxidative stress-related parameters and the expressions of specific genes were monitored in 102 cases of AML during a pretreatment period from a primary status to a relapse status. In addition, age-matched healthy subjects were classified as controls. The activities of adenosine deaminase and xanthine oxidase were higher in the relapse condition, whereas those of glutathione peroxidase, monoamine oxidase, and superoxide dismutase, and the total antioxidant capacity (T-AOC) were lower in the primary condition and in controls. Of particular note, levels of advanced oxidation protein products, malondialdehyde, and 8-hydroxydeoxyguanosine were also significantly higher in relapse patients. Furthermore, real-time PCR with SYBR Green revealed that the expression levels of human thioredoxin (TRX) and indoleamine 2,3-dioxygenase were increased in relapse patients. Pearson correlation analysis revealed that the T-AOC was positively correlated with GSH but negatively correlated with 8-OHdG, TRX, and indoleamine 2,3-dioxygenase. Linear regression showed that a low T-AOC and up-regulated TRX expression were the independent factors correlated with relapse. A strong association between oxidative stress and the incidence of disease relapse was observed, which has potential prognosis implications. These results indicate that oxidative stress is a crucial feature of AML and probably affects the development and relapse of AML.

[Effects of artemisinin on proliferation, apoptosis and Caspase-3 expression of rat mesangial cell].

OBJECTIVE: To study the effects of artemisinin on proliferation, apoptosis and Caspase-3 active of rat mesangial cell. METHODS: Rat mesangial cells were incubated with different concentrations of artemisinin, the proliferation, apoptosis and Caspase-3 active of rat mesangial cell were measured by MTT assay, fluorescent inverted microscope and enzyme-labeled analytical instruments respectively. RESULTS: Compared with control group, the proliferation and Caspase-3 expression of mesangial cell of three other groups were significantly different (P < 0.01). Compared with dexamethasone group, there were significant difference effects of proliferation and Caspase-3 expression of mesangial cell in other two groups of identical concentration drugs (P < 0. 01), especially in the artemisinin + glucocorticoid (ArtGC) group, and the effects of three different drugs on the mesangial cell Caspase-3 expression, proliferation and apoptosis had the tendency of depend on dosage, and mass mortality of mesangial cell in the mediate-dosage and high-dosage ArtGC group. CONCLUSION: Artemisinin could inhibit the proliferation of mesangial cell, enhance the expression of Caspase-3 and promote the apoptosis in a dose-dependent manner.

Identification and functional characterization of the novel acute monocytic leukemia associated antigen MLAA-34.

We have previously applied the method of serologic analysis of recombinant cDNA expression library (SEREX) on acute monocytic leukemia to identify monocytic leukemia-associated antigens. Using this approach, we identified a novel gene, MLAA-34, which exclusively reacted with sera from allogeneic leukemia patients but not with normal donor sera. Here, we further characterized its gene structure and explored the function. We first determined both 5' and 3' end by RLM-RACE and cloned full-length cDNA of MLAA-34 in U937 cell line. Analysis of full cDNA sequence showed that MLAA-34 is highly homologous to known human gene CAB39L, but differs from two transcript splice variants of CAB39L. Thus, we propose that MLAA-34 is a novel CAB39L's splice variant associated with acute monocytic leukemia. Because the functions of MLAA-34 and CAB39L are both very unclear, then we investigated the role of MLAA-34 in U937 cell line using RNA interference technology. The results showed that the downregulation of MLAA-34 expression significantly suppressed the proliferation of U937 cells in vitro, and increased the spontaneous apoptosis of these leukemia cells. All these data indicated that MLAA-34 may be a novel anti-apoptotic factor related closely to carcinogenesis or progression of acute monocytic leukemia. The anti-apoptotic pathways of MLAA-34 remain further exploration. This study warrants further investigations to verify MLAA-34 as a promising antigen and a molecular target for therapeutic applications in acute monocytic leukemia.

[Cloning of New Antigen Gene MLAA-34 Promoter and Identification of Core Region in Acute Monocytic Leukemia].

OBJECTIVE: To clone the promoter sequence of acute monocytic leukemia new antigen gene.MLAA-34 and identify its promoter core region. METHODS: The full-length fragment of MLAA-34 gene promoter region was amplified by PCR, then was ligated into pGL3-Basic vector, and the recombinant plasmid was cloned. Constructed a series of MLAA-34 gene promoter 5' flanking region truncated plasmid. These recombinant plasmids were transfected into U937 and HEK293 cells, and the dual luciferase reporter gene was used to detect the promoter activity of each fragment to determine the minimum active region. Transcription factor binding sites were analyzed by bioinformatics methods. RESULTS: The recombinant plasmid containing MLAA-34 promoter sequence and its truncated plasmid were successfully constructed, and the promoter activity was significantly increased as compared with the empty vector (P＜0.001). The minimal active region of MLAA-34 located between 402 bp and 200 bp. It contained multiple transcription factor binding sites such as E2F1, MZF-1, SP1, USF2 and STAT3. CONCLUSION: The promoter of luciferase reporter gene has been successfully constructed with different deletion fragments of MLAA-34, and its core promoter region may contain multiple transcription factor sequence.

[Effects of Transcription Factor MZF-1 on Transcriptive Regulation of Acute Monocytic Leukemia-related Gene MLAA-34].

OBJECTIVE: To investigate the transcriptional regulation of transcription factor MZF-1 on acute monocytic leukemia-related gene MLAA-34. METHODS: The effect of MZF-1 on the transcriptional activity of MLAA-34 gene promoter was analyzed by luciferase reporter gene detection system and site-directed mutation technique. The EMSA and ChIP assay were used to verify whether MZF-1 directly and specifically binds to the core region of MLAA-34 promoter. The over-expression vector and interference vector of MZF-1 were constructed to transfect U937 cells, and RT-PCR and Western blot were used to detect the transcription and expression changes of MLAA-34 gene. RESULTS: The transcription factor MZF-1 had a regulatory effect on MLAA-34 gene expression, and the relative luciferase activity was decreased after MZF-1 binding point mutation (P<0.01). EMSA and ChIP experiments demonstrated that MZF-1 could directly bind to MLAA-34 promoter and play a regulatory role. In the over-expression test, the increase of MZF-1 could up-regulate the expression of MLAA-34 (P<0.05). In the interference test, the decrease of MZF-1 could down-regulate the expression of MLAA-34 (P<0.05). CONCLUSION: Transcription factor MZF-1 can bind to the transcriptional regulatory region on the promoter of MLAA-34 gene and promote the transcription of MLAA-34 gene in acute monocytic leukemia.

Survival advantages of multicellular spheroids vs. monolayers of HepG2 cells in vitro.

Mammalian cells grow in three-dimensions (3-D) in vivo. Commonly used two-dimensional (2-D) cell cultures are inadequate to recreate the biological microenvironment of tumor cells. The potentially different outcomes from 2-D and 3-D culture systems may have a significant impact on the relevance of experimental findings. The purpose of this study was to characterize the human hepatoma cell line HepG2 in 2-D and 3-D cultures. HepG2 cells in 2-D and 3-D cultures were treated with cisplatin, 5-fluorouracil, and adriamycin and were analyzed by scanning electron microscopy and transmission electron microscopy. Cell cycle progression and apoptosis were detected by flow cytometry. Inhibition of cell proliferation was quantified by MTT assay. The expression of E-cadherin, CD44v6, VEGF, KDR, endostatin, Bax, and cytochrome-c were analyzed by immunohistochemical (IHC) staining. As compared to the 2-D monolayer culture, the 3-D multicellular spheroids (MCS) of HepG2 cells featured a greater fraction of cells in G1 phase and were organized with more abundant cell-cell adhesion. In addition, cells in MCS were significantly less apoptotic in maintenance culture media and were more resistant to drug-induced apoptosis. E-cadherin, CD44v6, VEGF, KDR, endostatin, and cytochrome-c levels were increased in MCS as compared to 2-D cell cultures. In conclusion, MCS conferred differentiated phenotypes including increased cell-cell adhesion and G1 phase cell cycle arrest, enhanced cellular resistance to apoptosis, and upregulated angiogenic potential. Based on our data, a multicellular morphological hierarchy may sustain the growth/survival advantages of cancer cells in vivo. Therefore, a 3-D culture system should be the preferred technique for cancer biology investigation.

Clinical study of Trilogy Detoxicating Therapy combined with routine Western medicine on patients with chronic renal failure.

OBJECTIVE: To investigate the mechanism of Trilogy Detoxicating Therapy in treating patients with chronic renal failure (CRF). METHODS: A total of 142 patients were assigned to the Trilogy Detoxicating Therapy group (the treatment group, 82 patients) and the Western medicine treatment group (the control group, 60 patients). All of the patients were treated with NovoNorm 1 mg and metformin hydrochloride tablets 0.15 g thrice per day for lowering the blood glucose, as well as Perindopril 4 mg twice daily for lowering blood pressure, recombinant human erythropoietin 2 000 U and a hypodermic injection thrice a week for rectifying anemia, 30 days as one course of treatment, and all patients were treated for two courses. Patients in the treatment group were treated with the Trilogy Detoxicating Therapy [dispersing the five-zang organs, expelling toxins through colonic dialysis and skin dialysis fumigation] in addition to the aforementioned drugs. Parameters observed and recorded in the study included renal function [serum creatinine (SCr), blood urea nitrogen (BUN)], blood lipids [triglyceride (TG), total cholesterol (TC), low-density lipoprotein C (LDL-C), high-density lipoprotein C (HDL-C)], plasma total protein (TP), hemoglobin (Hb), serum interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) before and after the treatment. RESULTS: After two courses of treatment, the levels of SCr, BUN, TG, TC, LDL-C, serum IL-6 and TNF-alpha decreased significantly, meanwhile HDL-C increased in the treatment group (P<0.05 or P<0.01). In contrast, no obvious changes of the above mentioned items occurred in the control group. In both groups, the levels of TP and Hb were significantly elevated (P<0.05 or P<0.01), but the changes were more obvious in the treatment group (P<0.01). CONCLUSION: Trilogy Detoxicating Therapy played a therapeutic role on patients with CRF possibly through lowering the levels of blood lipids, serum IL-6 and TNF-alpha.

[Detection of Novel Antigen MLAA-34 Gene Mutation in Acute Monocytic Leukemia and Its Correlation with Efficacy].

OBJECTIVE: To investigate the correlation of all exone mutation in MLAA-34 gene with chemotherapeutic efficacy for leukemia. METHODS: The expression level of MLAA-34 gene in 40 patients with AML-M5 and 5 healthy volunteers as control was detected by RT-PCR and its effect on chemotherapeutic efficacy were analyzed by RT-PCR; the effect of MLAA-34 gene mutation on overall survival (OS) and progression-free survival (PFS) of AML-M5 patients was analyzed by sequencing of all 12 exoues in MLAA-34 gene, the correlation between the mutation of prognostic genes important to leukemia and the mutation of MLAA-34 gene was explored. RESULTS: The expression level of MLAA-34 gene was significantly up-regulated as compared with that of healthy volunteers, moreover this up-regulation was related with a C59T SNP site located in second exon of MLAA-34 gene, meanswhile this SNP site is affinitive to the well-known mdecular markers of AML, inclinding Fms-like tyrosine kinase (FLT-3) and DNA methyltransferase-3A(DNAMT3A). The AML-M5 patients with high expression of MLAA-34 gene poorly responded to chemotherapy, the AML-M5 patients with MLAA-34 C59T mulation had even more high expression of MLAA-34 gene and significantly short OS and PFS in comparison with those of patients without C59T mutation. CONCLUSION: The C59T mutation in MLAA-34 gene is a high risk factor for recurrence of AML, and may be a cadidate target for treatment of AML.

A phase 1, open-label study of LCAR-B38M, a chimeric antigen receptor T cell therapy directed against B cell maturation antigen, in patients with relapsed or refractory multiple myeloma.

BACKGROUND: Chimeric antigen receptor (CAR) T cell therapy has demonstrated proven efficacy in some hematologic cancers. We evaluated the safety and efficacy of LCAR-B38M, a dual epitope-binding CAR T cell therapy directed against 2 distinct B cell maturation antigen epitopes, in patients with relapsed/refractory (R/R) multiple myeloma (MM). METHODS: This ongoing phase 1, single-arm, open-label, multicenter study enrolled patients (18 to 80 years) with R/R MM. Lymphodepletion was performed using cyclophosphamide 300 mg/m2. LCAR-B38M CAR T cells (median CAR+ T cells, 0.5 × 106 cells/kg [range, 0.07 to 2.1 × 106]) were infused in 3 separate infusions. The primary objective is to evaluate the safety of LCAR-B38M CAR T cells; the secondary objective is to evaluate the antimyeloma response of the treatment based on the general guidelines of the International Myeloma Working Group. RESULTS: At data cutoff, 57 patients had received LCAR-B38M CAR T cells. All patients experienced ≥ 1 adverse events (AEs). Grade ≥ 3 AEs were reported in 37/57 patients (65%); most common were leukopenia (17/57; 30%), thrombocytopenia (13/57; 23%), and aspartate aminotransferase increased (12/57; 21%). Cytokine release syndrome occurred in 51/57 patients (90%); 4/57 (7%) had grade ≥ 3 cases. One patient reported neurotoxicity of grade 1 aphasia, agitation, and seizure-like activity. The overall response rate was 88% (95% confidence interval [CI], 76 to 95); 39/57 patients (68%) achieved a complete response, 3/57 (5%) achieved a very good partial response, and 8/57 (14%) achieved a partial response. Minimal residual disease was negative for 36/57 (63%) patients. The median time to response was 1 month (range, 0.4 to 3.5). At a median follow-up of 8 months, median progression-free survival was 15 months (95% CI, 11 to not estimable). Median overall survival for all patients was not reached. CONCLUSIONS: LCAR-B38M CAR T cell therapy displayed a manageable safety profile and demonstrated deep and durable responses in patients with R/R MM. TRIAL REGISTRATION: ClinicalTrials.gov , NCT03090659 ; Registered on March 27, 2017, retrospectively registered.

Study on effect of yishen capsule in preventing recurrence of chronic glomerulonephritis.

OBJECTIVE: To observe the effect of yishen capsule (YSC) on preventing the recurrence of chronic glomerulonephritis (CGN) and to explore its mechanism preliminarily. METHODS: CGN patients were assigned to the treated group (61 cases) and the control group (48 cases) and all of them were orally administered with 4 mg of Perindopril twice a day, but 3 capsules of YSC, thrice a day, were given additionally to patients in the treated group. The therapeutic course for both groups was 18 months. The recurrence rate of CGN at the 6th, 12th, and 18th month in the two groups was observed and compared, and the changes of 24-h urinary protein quantity and T-lymphocyte subsets before and after treatment were observed as well. RESULTS: (1) Comparison of recurrence rate between the two groups showed insignificant difference at the 6th month, but it did show significant difference at the 12th and the 18th month, which was significantly decreased in the treated group than in the control group (P<0.05, P<0.01); (2) The 24-h urinary protein quantity at the 18th month decreased significantly in both groups (P<0.05, P<0.01), but in the treated group was more significant (P<0.01); (3) T-lymphocyte subsets showed no obvious change in the control group after treatment (P>0.05), while in the treated group, it showed significant increase in CD3, CD4 and CD4/CD8 (P<0.05 or P<0.01) and significant decrease in CD8 (P<0.05), and also the difference after treatment in T-lymphocyte subsets between the two groups was significant (P<0.05 or P<0.01). CONCLUSION: YSC has marked effects in reducing the recurrence of CGN and in decreasing urinary protein, and its mechanism might be related with its function in regulating the ratio of T-lymphocyte subsets to enhance the immunity of patients.

[Effect of Yishen capsule on serum vascular endothelial growth factor and cell immunity in patients with chronic glomerulonephritis].

OBJECTIVE: To explore the effect of Yishen capsule on the serum vascular endothelial growth factor (VEGF), the cell immunity and the theraphic. METHOD: Serum VEGF and T cell subsets were studied in 30 normal subjects and 83 patients before and after treatment. RESULT: Compare with normal subjects, CD3, CD4, CD4/CD8 were decreased, CD8 and serum VEGF were increased obviously (P <0. 05 or P <0. 01). After three months treatment with YiShen capsule, CD4/CD8 was increased, CD8 and serum VEGF were decreased significantly (P <0.05 or P <0.01). CONCLUSION: Yishen capsule can reduce the proteinuria, increase the function of immunity and improve the clinical symptom of patients with chronic glomerulonephritis, achieved the effects of allevating chronic glomerular sclerosis ultimately.

Iodine-125 Brachytherapy Prophylaxis after Radiofrequency Ablation Cannot Benefit Patients in High Risk of Locoregional Hepatocellular Carcinoma Recurrence.

This study evaluated if iodine-125 brachytherapy prophylaxis after radiofrequency ablation (RFA) prolongs time to recurrence (TTR) and overall survival (OS) of patients in high risk of locoregional hepatocellular carcinoma (HCC) recurrence. 116 patients with total tumor necrosis after RFA were divided into iodine-125 brachytherapy prophylaxis treatment group and control group. The primary endpoint was TTR, and secondary endpoints were OS and treatment-related adverse events. There were no significant differences among the baseline characteristics of two subgroups patients. The mean iodine-125 particles were 29.8 (26.59 ± 12.51 mCi) per patient. The mean follow-up was 25 months, and mean TTR of treatment and control groups were 21.7 and 15.9 months (P = 0.733); mean OS of two subgroups were 41.7 and 40.9 months (P = 0.316). There were no significant differences of 1-, 2-, 3-, 4-and 5-years TTR and OS and patients' immunity pre- and 1 month post-treatment. Extrahepatic metastasis was found to have a statistically significant influence on TTR, and AFP, extrahepatic metastasis were found to have a statistically significant influence on OS by multivariate analysis. There was no major complications and procedure related death. Iodine-125 brachytherapy prophylaxis after RFA can't improve TTR and OS of HCC patients who were in high risk of locoregional tumor recurrence.

[Application of serum surface-enhanced laser desorption/ionization proteomic patterns in distinguishing non-small cell lung cancer patients from healthy people].

OBJECTIVE: To explore the application of serum surface-enhanced laser desorption/ionization (SELDI) marker patterns in distinguishing non-small cell lung cancer patients from healthy people by protein chip technology. METHODS: One hundred and sixty-three serum samples (123 patients with lung cancer and 40 healthy persons), were randomly divided into a training set [94 cases, 53 non-small cell lung cancer (NSCLC), 21 small cell lung cancer and 20 healthy persons] and a blinded test set (69 cases), were included for analysis by surface-enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF-MS). Five protein peaks at 11,493, 6,429, 8,245, 5,336 and 2,536 were automatically chosen for the system training and the development of a decision classification tree model (marker pattern). The accuracy of the model was tested with the blinded test set (an independent set of masked serum samples from 49 patients with NSCLC and 20 healthy persons). RESULTS: The model differentiated the patients with NSCLC from the healthy people with a sensitivity of 95.9% (71/74) and a specificity of 90.0% (18/20) in the training set and a sensitivity of 83.7%, and a specificity of 80.0% in the blinded set respectively. CONCLUSION: SELDI-TOF-MS technique can correctly distinguish NSCLC patients from healthy people, and it has the potential for the development of a screening test for the detection of NSCLC.

[Screening of Serum Markers in Primary Immune Thrombocytopenia].

OBJECTIVE: To analyze the serum protein fingerprints of immune thrombocytopenia (ITP) patients and healthy controls by using weak cation exchange nanometer magnetic beads and MALDI-TOF-MAS technology, to identify the proteins with different expression, to establish the diagnostic model for ITP and to explore the pathogenesis of ITP. METHODS: A total of 40 patients with ITP and 40 healthy controls were selected, the serum protein components were captured by using weak cation exchange nanaometer magnetic beads, the protein spectra of all specimens were detected by Autoflex II matrix assisted laser desorption/ionization time of flight mass spectrometry (MALDI- TOF-MS) and then the data were analyzed by CliprotoolsTM2.2 software, by which the distinct protein molecules were screened to set up ITP diagnostic model. To identify the established model, the sera of 20 ITP patients and 20 healthy controls were selected to make category and cross validations. RESULTS: The detection of Clinprot system and the analysis of CliprotoolsTM2.2 software showed that about 55 protein peaks were detected with the range of 700 Da to 10 000 Da of molecular weight in the protein spectrum of serum speciments from 40 ITP patients and 40 healthy controls. Compared with healthy controls, 19 protein expression peaks with statistically significant difference were found in ITP patients (P < 0.05), among them 5 expressions were up-regulated and 14 expressions were down-regulated. The diagnostic model on basis of Supervised Neural Network Algorithm (SNN) was established through 10 MS peaks with strongest capability in ITP group and control group automatically distinguished by software, and it is expected that the sensitivity of model group reached to 100%, and the specificity to 100%. The category validation showed that this diagnostic model correctly identificed all 20 ITP patients and 20 healthy controls, and in cross validation, the model sensitivity was 100% and the specificity was 100%. CONCLUSION: The ITP SNN model ertablished by using ChinProt System with high flax and good repetition is composed of 10 protein peaks with significant difference, this model can effectively distinguish ITP patients and healthy controls.

Fludarabine and busulfan as a reduced-toxicity myeloablative conditioning regimen in allogeneic hematopoietic stem cell transplantation for acute leukemia patients.

The optimal conditioning regimen for allogeneic hematopoietic stem cell transplantation (allo-HSCT) in acute leukemia remains undefined. We evaluated the outcomes in 30 patients with acute leukemia who underwent allo-HSCT from human leukocyte antigen-matched donors after conditioning with busulfan and fludarabine (BuFlu). The regimen comprised injection of busulfan 3.2 mg/kg daily on 4 consecutive days and fludarabine 30 mg/m2 daily for 4 doses. All 30 patients achieved hematopoiesis reconstitution with full donor chimerism confirmed by short tandem repeat DNA analysis. The most common regimen-related toxicity was mucositis (86.7%), followed by cytomegalovirus infection (80%). Serious regimen-related toxicities were rare. Acute graft vs. host disease (aGVHD) was detected in 46.7% of the patients; 33.4% had grade I-II aGVHD and 13.3% had grade III-IV aGVHD. Chronic GVHD (cGVHD) was noted in 20% of the patients. The overall survival and disease-free survival rates were 66.7 and 53%, respectively, with a median follow-up of 25 months for surviving patients. Therefore, BuFlu was an effective conditioning regimen with a low rate of transplant-related adverse effects and increased antileukemic effects in patients with acute leukemia undergoing allo-HSCT.