Diagnostic value of combined serological markers in the detection of acute cerebral infarction.

ABSTRACT: To evaluate the value of the combination schemes of 10 serological markers in the clinical diagnosis of acute cerebral infarction.The level of total cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol, high-sensitivity C-reactive protein, homocysteine (HCY), lipoprotein-related phospholipase A2, ischemia-modified albumin, complement C1q, and lipoprotein a were analyzed in 154 patients with acute ischemic cerebral infarction. The optimized diagnostic combination for acute cerebral infarction was explored by calculating the maximum area under the receiver operating characteristic curves (AUC).The levels of total cholesterol, triglycerides, low-density lipoprotein cholesterol, high-sensitivity C-reactive protein, HCY, lipoprotein-related phospholipase A2, ischemia-modified albumin, complement C1q, and lipoprotein a were significantly higher in the patient vs the control group. Moreover, the positive rate of HCY reached 89.9%. The analysis of the receiver operating characteristic curve of each index and their combinations showed that the minimum AUC of HDL-C alone was 0.543, while the maximum AUC of HCY was 0.853. A multiple logistic regression analysis indicated that HDL-C was a slightly significant variate in the diagnosis of acute cerebral infarction.The value of individual serological markers in the diagnosis of acute cerebral infarction was slightly significant, while the combination of the markers significantly improved the efficiency of its diagnosis.

Recent Advances on the Model, Measurement Technique, and Application of Single Cell Mechanics.

Since the cell was discovered by humans, it has been an important research subject for researchers. The mechanical response of cells to external stimuli and the biomechanical response inside cells are of great significance for maintaining the life activities of cells. These biomechanical behaviors have wide applications in the fields of disease research and micromanipulation. In order to study the mechanical behavior of single cells, various cell mechanics models have been proposed. In addition, the measurement technologies of single cells have been greatly developed. These models, combined with experimental techniques, can effectively explain the biomechanical behavior and reaction mechanism of cells. In this review, we first introduce the basic concept and biomechanical background of cells, then summarize the research progress of internal force models and experimental techniques in the field of cell mechanics and discuss the latest mechanical models and experimental methods. We summarize the application directions of cell mechanics and put forward the future perspectives of a cell mechanics model.

A Connection Method between Ultrahard PtW8 Wire and a Au Thick Film Based on Parallel-Gap Resistance Microwelding.

To meet the application requirements of a thermal gas sensor, it is necessary to realize a bond connection between PtW8 wire with a Au thick film. However, the physical properties, such as the melting point and hardness, of the two materials differ greatly. In this study, the parallel-gap resistance microwelding was introduced into the bonding connection between PtW8 wire and a Au thick film in the thermal gas sensor. The feasibility of the method was analyzed theoretically and the experimental system was established and studied. A scanning electron microscope (SEM) was used to analyze the morphology of the cross-section of the welded joint. The results showed that there was no obvious transition layer at the interface region but there were relatively dense welds. At the same time, it was found that the melted Au wetted and climbed on the surface of the platinum-tungsten alloy, which may have been the key to forming the joint. Elements were observed to have a spatial distribution gradient within the cross-section of the welding line, revealing that mutual diffusion occurred in the parallel-gap resistance microwelding, where this diffusion behavior may be the basic condition for forming the joint. Finally, the influence of the welding voltage, time, and force on the joint strength was also studied, where the joint strength could be up to 5 cN.

Design and Verification of Humidity Sensors Based on Magnesium Oxide Micro-Arc Oxidation Film Layers.

Humidity detection range is an important indicator for measuring the performance of humidity sensors, but semiconductor humidity sensors often face the problems of narrow detection ranges and insufficient detection sensitivities. In this paper, a magnesium oxide (MgO) humidity sensor based on micro-arc oxidation (MAO) technology was designed to solve these problems by simultaneously using impedance and capacitance as the response signals, as well as by normalizing the output of the two signals. The experimental results showed that the average output of the micro-arc MgO ceramic film, with impedance as the response signal, could reach 150 in the low relative humidity(RH) range (11.3-67% RH), which was much higher than its sensitivity in the high humidity range (< 1), and the film showed fast response (13 s) and recovery (61 s). Under high humidity conditions (67-97.3% RH), with capacitance as the response signal, the output of the micro-arc MgO was as high as 120. Therefore, the micro-arc MgO humidity sensor with impedance, and the sensor with capacitance as the response signal, demonstrated good stability in low humidity and in high humidity environments, respectively, indicating that the method of selecting appropriate response signals for different humidity environments can be applied to extend the humidity detection range of sensing material, and to improve the humidity detection capability of a sensor.

Irinotecan plus cisplatin compared with etoposide plus cisplatin in patients with previously untreated extensive-stage small cell lung cancer: A meta-analysis.

OBJECTIVE: To systematically review the effect and safety of irinotecan plus cisplatin (IP) compared with etoposide plus cisplatin (EP) in patients with previously untreated extensive-stage small cell lung cancer (E-SCLC). MATERIALS AND METHODS: Databases including PubMed, The Cochrane Library, EMBASE, China National Knowledge Infrastructure, VIP, and WanFang Data were searched for the randomized controlled trials (RCTs) about IP compared with EP in patients with previously untreated E-SCLC from the establishment to June 2016. Two reviewers independently screened literature, extracted data and assessed the methodological quality of included studies. Then meta-analysis was performed using RevMan 5.3 software (Cochrane Collaboration, Oxford, UK). RESULTS: A total of 12 RCTs involving 2030 patients were finally included. Meta-analysis showed that compared with EP regimen, IP regimen significantly improved the 1- and 2-year survival rates of the patients with previously untreated E-SCLC (risk ratio [RR] = 1.16, 95% confidence interval [CI] [1.03-1.31], P = 0.02; RR = 1.79, 95% CI [1.22-2.61], P = 0.003, respectively). However, there was no significant difference between IP regimen and EP regimen in the objective response rate (ORR) (RR = 1.07, 95% CI [0.99-1.15], P = 0.10) and disease control rate (DCR) (RR = 1.03, 95% CI [0.96-1.10], P = 0.38). The incidence of Grade 3/4 leukopenia, neutropenia, anemia, and thrombocytopenia of IP regimen was sigificantly lower than EP regimen (all P < 0.05), the incidence of Grade 3/4 nausea/vomiting and diarrhea of IP regimen was sigificantly higher than EP regimen (all P < 0.05). CONCLUSION: IP regimen significantly improves the 1- and 2-year survival rates, but not significantly improves the ORR and DCR, compared with EP regimen in patients with previously untreated E-SCLC. IP regimen has less Grade 3 or 4 hematological adverse events. IP regimen is an alternative of EP regimen in patients with previously untreated E-SCLC.

Down regulation of G protein-coupled receptor 137 expression inhibits proliferation and promotes apoptosis in leukemia cells.

BACKGROUND: G protein-coupled receptors (GPR) are involved in a wide range of physiological processes, some of which, however, can be hijacked by tumor cells. Over-expression of G protein-coupled receptors 137 (GPR137) are associated with the growth of tumor cells, but under-expression of GPR137 has shown to inhibit cell proliferation in several different types of cancers. Currently, the role of GPR137 in leukemia is still unclear. In this study, the effect of under-expression of GPR137 on inhibiting the proliferation of leukemia cells is explored, to identify a novel target for leukemia treatment. MATERIALS AND METHODS: In this study, lentivirus-mediated RNA interference (RNAi) was employed to investigate the role of GPR137 in two leukemia cell lines K562 and HL60. The gene expression of GPR137 was analyzed by RT-PCR and its protein expression was determined by Western blot. Flow cytometry and Annexin V/7-AAD Apoptosis Detection Kit was used respectively in cell cycle and apoptosis analysis. The protein expression of CyclinD1, CDK4, BCL-2 and caspase-3 were also determined. RESULTS: There was high level of constitutive expression of GPR137 in leukemia cancer cell lines K562 and HL60. Lentivirus-mediated RNAi could significantly down-regulate gene and protein expression of GPR137 in both cell lines. Down regulation of GPR137 was associated with the reduction in proliferation rate and colony forming capacity. In addition, down regulation of GPR137 arrested cells in the G0/G1 phase of cell cycle and induced apoptosis in both leukemia cell lines K562 and HL60. CONCLUSIONS: The expression of GPR137 is associated with the proliferation of leukemia cell lines. Down regulation of GPR137 could inhibit proliferation and promote apoptosis in leukemia cells, which makes it a promising bio-marker and therapeutic target to treat patients with leukemia.

Knockdown of immature colon carcinoma transcript 1 induces suppression of proliferation, S-phase arrest and apoptosis in leukemia cells.

Immature colon carcinoma transcript 1 (ICT1), a human mitochondrial translation release factor, is a ribosome-dependent codon-independent peptidyl-tRNA hydrolase. ICT1-deficiency has been recognized as a cell growth inhibitor of hepatoblastoma and glioblastoma multiforme. To explore the role of ICT1 in human leukemia, 2 short hairpin RNAs (shRNAs) targeting ICT1 sequences were designed in leukemia U937 cells. The successful infection of ICT1 in the U937 cells was observed under a fluorescence microscope and further quantified by western blotting and quantitative real-time PCR (qRT-PCR) analysis. Tetrazolium dye (MTT) assay revealed a significant decrease in proliferation of ICT1-knockdown U937 cells on the fourth and fifth day as compared with the control. Depletion of ICT1 resulted in an increase in S phase and sub-G1 (representing cell apoptosis) fractions. Annexin V-APC/7-AAD staining assay confirmed that knockdown of ICT1 played a crucial role in boosting early and late apoptotic programs in U937 cells. Downregulation of ICT1 also altered cyclin A2 transcription expression, caspase-3 activity and p21 protein expression. Additionally, decreased levels of heat shock protein 27 (HSP27) phosphorylation at Ser78 was correlated with knockdown of ICT1 in U937 cells. Thus, we concluded that the regulatory role of ICT1 in leukemia may be used as a potential therapeutic target for the treatment of leukemia.

Knockdown of eukaryotic translation initiation factor 3 subunit D (eIF3D) inhibits proliferation of acute myeloid leukemia cells.

Various eukaryotic translation initiation factors (eIFs) have been implicated in carcinoma development. Eukaryotic translation initiation factor 3 subunit D (eIF3D) has recently been shown to regulate the growth of several types of human cancer cells. However, the function of eIF3D in acute myeloid leukemia (AML) remains unclear. In this study, we investigated the expression of eIF3D in three AML cell lines and a lymphoblast cell line, and found that eIF3D was expressed in all four leukemia cell lines. To explore the role of eIF3D in AML cell proliferation, lentivirus-mediated RNA interference was applied to knock down the expression of eIF3D in U937 cells. The expression of eIF3D was significantly downregulated in U937 cells after eIF3D knockdown, as confirmed by quantitative real-time PCR (qRT-PCR) and Western blot analysis. Knockdown of eIF3D significantly inhibited proliferation of U937 cells. Furthermore, flow cytometry analysis revealed that eIF3D silencing induced cell cycle arrest at the G2/M phase, ultimately leading to apoptosis. Our results indicate that eIF3D plays a key role in the proliferation of AML cells, and suggest that eIF3D silencing might be a potential therapeutic strategy for leukemia.

Marine drug Haishengsu increases chemosensitivity to conventional chemotherapy and improves quality of life in patients with acute leukemia.

BACKGROUND: Pharmacological management of acute leukemia remains a challenge. A seashell protein Haishengsu (HSS) has been found to exert anticancer activities in recent in vitro studies. The aim of this study was to determine whether the addition of HSS to the conventional chemotherapies would increase chemosensitivity and improves quality of life in patients with acute leukemia. METHODS: Two hundred and forty-eight patients with acute leukemia were enrolled in a double-blind, and placebo-controlled study. In addition to conventional chemotherapy, 142 patients received HSS and 106 received placebo. In an in vitro study, the expression of P-gp was evaluated by flow cytometry in a drug-resistant leukemia cell line (K562/ADM cells). Sorcin was examined by Western blot. RESULTS: The complete remission rates in the HSS treatment group were all higher than in the placebo group with non-relapsing leukemia and relapsed leukemia (p<0.05). Less patients in the HSS group experienced gastrointestinal side effects from chemotherapy, whereas more patients had increased food take and an increase in Karnofsky performance status (KPS) score (p<0.01). In vitro, the expression of P-gp and sorcin in the HSS treated cells were lower than in the control group cells (p<0.01). CONCLUSION: When added to conventional chemotherapy, HSS improves the complete remission rates and quality of life in patients with acute leukemia. The in vitro findings indicate that suppression of P-gp and sorcin genes in leukemia cells may be involved in the beneficial effects of HSS.

shRNA-mediated RPS15A silencing inhibits U937 acute myeloid leukemia cell proliferation and enhances apoptosis.

Ribosomal protein S15a (RPS15A), which is a component of the 40S ribosomal subunit, is able to promote mRNA/ribosome interaction during the early stage of translation. Previous studies have demonstrated that RPS15A regulates cell growth and is involved in several types of human cancer. The aim of the present study was to investigate the role of RPS15A in acute myeloid leukemia (AML). Lentivirus­delivered short hairpin RNA (shRNA) was used to silence RPS15A expression in the U937 AML cell line. Subsequently, the effects of RPS15A silencing on cell viability, cell cycle progression and apoptosis were investigated. The results indicated that RPS15A knockdown significantly inhibited cell growth. Furthermore, flow cytometric analysis demonstrated that the majority of U937 cells were arrested in G0/G1 phase and sub­G1 phase after RPS15A knockdown, as determined using propidium iodide staining. In addition, U937 cells underwent apoptosis in response to RPS15A silencing, as determined using Annexin V/7­aminoactinomycin D staining. In conclusion, the present study provides novel evidence indicating that RPS15A modulates AML cell growth in vitro, and may be considered a novel therapeutic target for the treatment of AML.

Prognostic value of PD-1 and TIM-3 on CD3+ T cells from diffuse large B-cell lymphoma.

OBJECTIVE: To investigate the expression of PD-1 and TIM-3 in CD3+ T cells in patients with diffuse large B-cell lymphoma (DLBCL). METHODS: A retrospective analysis was conducted on data from 46 patients with newly diagnosed DLBCL and 30 healthy people. Flow cytometry was used to detect the expression of PD-1 and TIM-3 before and after chemotherapy. RESULTS: Compared to healthy control, the expression of PD-1 and TIM-3 in patients with DLBCL was increased in CD3+ T cells. There is no significant change of PD-1 and TIM-3 in patients with stage I/II DLBCL, however, they were markedly increased in patients with stage III/IV DLBCL. The expression of PD-1 and TIM-3 elevated in DLBCL patients with B symptoms, IPI score >2 points and high level of LDH and Ki-67. After four courses of standard chemotherapy, PD-1 and TIM-3 expression level decreased. The treatment efficiency is higher in patients with low expression of PD-1 and TIM-3 than in patients with high PD-1 and TIM-3 expression. CONCLUSION: DLBCL patients have high expression level of PD-1 and TIM-3, which are related to DLBCL staging. PD-1 and TIM-3 expression levels are also related to the efficiency of chemotherapy. PD-1 and TIM-3 expression levels may be used as an indicator of chemotherapeutic efficacy in patients with DLBCL.

ß-catenin induces A549 alveolar epithelial cell mesenchymal transition during pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease characterized by expansion of the fibroblast and myofibroblast population and extracellular matrix deposition. Although the pathogenic mechanisms of IPF remain to be fully elucidated, there is emerging evidence that fibroblasts and myofibroblasts may be derived partially from alveolar epithelial cells by epithelial­mesenchymal transition (EMT). In the present study, A549 cells were treated with different concentrations of Wnt1 and the results indicated that the mRNA and protein expression levels of vimentin, α­smooth muscle actin (α­SMA) and collagen Ⅰ gradully increased and those of E­cadherin gradully decreased in a concentration­dependent manner. Furthermore, the A549 cells were transfected with ß­catenin plasmid cells, revealing phenotypic changes in the cells from a pebble to a fusiform shape. The mRNA and protein expression levels of of vimentin, α­SMA and collagen Ⅰ increased significantly, whereas those of E­cadherin decreased significantly. The present study examined the roles of alveolar epithelial cell injury and profibrogenic cytokine release in EMT and their association with the Wnt/ß­catenin signaling pathway in a mouse model of bleomycin­induced pulmonary fibrosis. Bronchoalveolar fluid was obtained 7 days after treatment with bleomycin and the A549 cells were incubated for 48 h. An increase in the expression levels of the mesenchymal markers, α­SMA, vimentin and collagen Ⅰ, and a concomitant decrease in the expression of the epithelial marker, E­cadherin were observed. This corresponded with an increased expression of ß­catenin. When the A549 cells were infected with a lentivirus expressing ß­catenin shRNA, no significant increase was observed in the expression of the mesenchymal cell markers and the expression of E­cadherin did not decrease. These findings demonstrated that activation of the Wnt signaling pathway was capable of inducing an EMT program in the lung epithelial cells through ß­catenin and that injured alveolar epithelium activated the Wnt/ß­catenin signaling pathway, thereby inducing the expansion of the fibroblast/myofibroblast population through EMT. These results suggested that ß­catenin was involved in the formation of lung fibrosis and may provide a theoretical basis for the treatment of IPF.

Effect of the Wnt1/ß-catenin signalling pathway on human embryonic pulmonary fibroblasts.

Idiopathic pulmonary fibrosis (IPF) is a fibrotic lung disease associated with a high rate of mortality, characterised by an accumulation of fibroblasts/myofibroblasts in the fibroblastic foci (FF) and by an excessive deposition of extracellular matrix (ECM) in the lung parenchyma. The pathogenesis of this fatal disorder remains unclear. Previous evidence suggests that myofibroblasts are key effectors of the deposition of ECM. In the present study, human embryonic pulmonary fibroblast (HEPF) cells were incubated with different concentrations of Wnt1. The present study revealed that cell proliferation improved following stimulation using different concentrations of Wnt1 in a concentration-dependent manner. When the concentration exceeded 20 µg/l, cell proliferation was significant (P<0.05) and the cell expression of α-SMA, vimentin and collagen I mRNA, as well as protein expression, significantly increased (P<0.05). Bronchoalveolar lavage fluid (BALF) was then obtained from bleomycin (BLM)-induced models of pulmonary fibrosis. HEPF cells were cultured with Dulbecco's modified Eagle's medium plus BALF. The mRNA and protein expression of α-SMA, vimentin and collagen I significantly increased and these increases were associated with ß-catenin. Furthermore, following being infected with the lentivirus expressing ß-catenin shRNA, HEPF cells were cultured with BALF. However, the mRNA and protein expression of α-SMA, vimentin and collagen I did not increase significantly. The present study suggested that the Wnt1/ß-catenin signalling pathway can promote HEPF cell proliferation and induced HEPF cells can change into myofibroblasts and promote ECM deposition. These findings may provide a theoretical basis for the treatment of IPF.

Inhibition of epithelial-mesenchymal transition in A549 cell by transfected Napsin A.

BACKGROUND: Epithelial-mesenchymal transition is a cellular process characterized by the loss of cell adhesion, inhibition of E-cadherin expression, and increased cell mobility. Cells without Napsin A are susceptible to transition. Further studies are required to investigate whether this transition can be reversed by restoration of Napsin A. METHODS: A Napsin A expression vector PLJM1-Napsin A plasmid was constructed and then transfected into the epithelial cell line A549 by lentivirus transfection to obtain A549-PLJM1-Napsin A cell line. Cell proliferation was assayed by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide and cell cycle was measured by flow cytometry. The E-cadherin, type I collagen, and focal adhesion kinase mRNA level was detected by reverse transcription-polymerase chain reaction. The Napsin A, E-cadherin, type I collagen, and focal adhesion kinase protein level in A549 cells was detected by Western blotting. RESULTS: Transforming growth factor-b1 induced epithelial-mesenchymal transition in A549 cells, as demonstrated by significant reduction of E-cadherin mRNA and protein levels (P < 0.01) as well as up-regulation of type I collagen (P < 0.01). Transfection of Napsin A in A549 cells can partially block the transforming growth factor-b1-regulated expression of E-cadherin and type I collagen (P < 0.01). In addition, transforming growth factor-b1-induced cell proliferation was inhibited by Napsin A (P < 0.01). Further study demonstrated that Napsin A caused G(0)/G(1) arrest and inhibited the expression of focal adhesion kinase (P < 0.01), a key protein in the integrin signaling pathway, in the in vitro epithelial-mesenchymal transition model. CONCLUSIONS: Sustained Napsin A expression in A549 cells can inhibit the transforming growth factor-b1-induced epithelial-mesenchymal transition. This may be due to the Napsin A-mediated inhibition of focal adhesion kinase expression and integrin signaling pathway.

Tegillarca granosa extract Haishengsu inhibits the expression of P-glycoprotein and induces apoptosis in drug-resistant K562/ADM cells.

This study was designed to investigate the effect and molecular mechanisms of Haishengsu (HSS), a protein extract from a shellfish Tegillarca granosaL., on a drug resistant leukemia cell line. Cultured K562/Adriamycin (ADM) cells were treated with HSS at 10, 20 and 40 microg/mL, respectively. The apoptosis and expression of p-glycoprotein was evaluated by flow cytometry. Expressions of caspase-3 and Bcl-2 were also evaluated. There was a significant dose-dependent increase in the apoptosis in the HSS treated K562/ADM cells (P < 0.05 and 0.01, respectively). The p-glycoprotein expression in the 40 microg/mL HSS group (14.8%) was lower than in the control (16.9%, P < 0.05) and the 10 microg/mL HSS group (7.3%, P < 0.05), but it was similar to the HSS 20 microg/mL group (10.7%, P > 0.05). The expressions of apoptosis-stimulating protein caspase-3 protein were increased, whereas the expressions of apoptosis-suppressing Bcl-2 were decreased in the HSS groups, as compared with the levels in the control group (P < 0.05). We conclude that HSS induces apoptosis of the Adriamycin-resistant K562/ADM cells. The enhanced expressions in caspase-3 and the reduced expressions in Bcl-2 protein may have contributed to the apoptosis-stimulating effect of HSS. The inhibition of p-glycoprotein suggests that HSS may diminish the resistance to Adriamycin and potentially enhance the therapeutic effects.

[Effect of Napsin A transfection into type II alveolar epithelial cells on pulmonary fibrosis].

OBJECTIVE: To study the in vitro effect and mechanism of Napsin A gene transfection into type II alveolar epithelial cells on pulmonary fibrosis. METHODS: A recombinant lentiviral plasmid PLJM1-Napsin A was constructed and transfected into human type II alveolar epithelial cell line A549. The model of pulmonary fibrosis was established by the in vitro stimulation of A549 cells by transforming growth factor beta-1 (TGF-ß1). The morphological changes were observed continuously under inverted microscopy. The proliferation of transgenic and non-transgenic cells was detected by MTT. To observe the degree of epithelial-mesenchymal transition (EMT) by TGF-ß1 intervening A549 cells, the expressions of E-cadherin and fibronectin were determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. Lastly the protein expression of focal adhesion kinase (FAK) was detected by Western blot to investigate the mechanism. RESULTS: The result of sequencing the recombinant lentiviral plasmid PLJM1-Napsin A was the same as the design sequence. Napsin A mRNA and protein were expressed in transgenic A549 cells (P<0.01). The model of pulmonary fibrosis was established successfully based on the morphology of transformed interstitial cell. As compared with the control group, the proliferation rate of transgenic cells decreased significantly (P<0.05). The mRNA and protein expression of E-cadherin significantly decreased in the model of pulmonary fibrosis (P<0.01), while the expression of fibronectin markedly increased (P<0.01). But the change rate of transgenic cells decreased (P<0.01, P<0.05). The expression of FAK was significantly elevated after the stimulation of TGF-ß1 (P<0.01). But the upward trend of the transgenic cells was smaller as compared with the control group (P<0.01). CONCLUSION: Pulmonary fibrosis may be suppressed by the transfection of Napsin A gene into type II alveolar epithelial cells. And the mechanism may be through the inhibition of integrin signal transduction.

Effect of haishengsu as an adjunct therapy for patients with advanced renal cell cancer: a randomized and placebo-controlled clinical trial.

OBJECTIVE: The purpose of this study was to investigate the effect of Haishengsu, an extract from Tegillarca L. granosa, on the effects and side-effects of immunotherapy in patients with advanced renal cell cancer. METHODS: Fifty-five (55) patients with renal cell cancer were randomly divided into a Haishengsu group (n = 27, 2.4 mg, intravenously for 15 days) and a control group (n = 28). All patients were also treated with interleukin-2, interferon-alpha, and fluorouracil. RESULTS: In the Haishengsu group, the prevalence of gastrointestinal reactions to the immunotherapy was lower than in the control group (18.5% versus 64.3%, p < 0.01). In comparison with the control group, more patients from the Haishengsu group had increased food intake (74.1% versus 14.3%, p < 0.01), weight gain (77.8% versus 10.7%, p < 0.01) or an increase in Karnofsky Performance Status score (55.6% versus 17.9%, p < 0.01). The remission rate of cancer in the Haishengsu group was higher than in the control group (51.9% and 21.4%, p < 0.01). CONCLUSIONS: Addition of Haishengsu to the conventional immunotherapy is associated with an increased remission rate in patients with advanced renal cell cancer. Haishengsu was also associated with a reduced rate of gastrointestinal side-effects from the immunotherapeutic agents, and an improvement in the physical functionality of the patients.

Effect of a seashell protein Haishengsu on the immunological function of mice with Ehrlich ascites tumor.

This study was designed to investigate the effect of a seashell protein Haishengsu (HSS) on the immuno logical function in mice with Ehrlich ascites tumor. Ehrlich ascites tumor-bearing mice were divided into three HSS groups (25, 50 and 100 mg/kg, i.v., respectively), cyclophosphamide (10 mg i.p.) and control group. The immunological function was assessed by measuring the phagocytizing capacity of the peritoneal macrophages and neutrophils, as well as the number of spleen hemolytic plaque-forming cells. The percentage of blood T-lymphocytes was also evaluated. The number and the percentage of phagocytizing macrophages and neutrophils in the 50 and 100 mg/kg HSS groups were higher than in the control and the cyclophosphamide groups (P < 0.01). The hemolytic plaque-forming cells in the three HSS groups (10.8 +/- 1.2, 16.9 +/- 3.9 and 25.3 +/- 2.9, respectively), was greater than in the control (7.3 +/- 1.4), or the cyclophosphamide group (0.33 +/- 0.4) (all P < 0.01). In all HSS groups, the percentage of blood T3, T4 and T8 was higher than in the cyclophosphamide and the control group (all P < 0.01). We conclude that HSS has significant immune-modulating effect in mice with Ehrlich ascites tumor.

Antitumor effect of the seashell protein Haishengsu on Ehrlich ascites tumor: an experimental study.

The aim of the study was to investigate the in vivo effect of the seashell protein Haishengsu (HSS) on Ehrlich ascites tumor. Mice were inoculated with Ehrlich ascites tumor cells and randomly divided into three HSS groups and a control group. The survival times in the three HSS-treated groups was longer than in the control (P < 0.01) and the increased life span in the high-dose HSS group was greater than in the lower-dose groups (P < 0.05). In comparison with control group, the mice receiving pretreatment of HSS had longer survival times and greater life spans following inoculation of the ascites tumor (P < 0.05). HSS therefore prolongs survival times and increases the life spans of mice bearing Ehrlich ascites tumor. Pretreatment with HSS also diminishes the detrimental effect of Ehrlich ascites tumor on the prognosis of these animals.

Effect of Haishengsu on transplanted K562 and drug-resistant K562/ADM tumors: an experimental study.

PURPOSE: To evaluate the effect of Haishengsu (HSS) on transplanted K562 and drug-resistant K562/ADM tumors. METHODS: Mice were inoculated subcutaneously with K562 and K562/ADM cells, respectively. Tumour-bearing animals were divided into HSS, adriamycin, combination therapy (adriamycin plus HSS) and placebo groups. The anti-tumour effect was assessed by tumour growth curve and tumour inhibitory rate (IR). RESULTS: In animals inoculated with K562 cells, the inhibitory rates of high (1800mg/kg) and medium (900mg/kg ) dose HSS groups were 100% and 96.4%, respectively, which was higher than that in the adriamycin (88.9%) or the combination therapy groups (85.8%, P < 0.05). The inhibitory rate in the low-dose HSS group (53.4%) was lower than in all other groups (P < 0.01). In mice inoculated with K562/ADM cells, the inhibitory rates in the high, medium and low dose HSS groups were 100%, 95.9%, and 44.1%, respectively. In the adriamycin group, the inhibitory rate was 23.07%, which was lower than in the HSS group (P < 0.01). Pathological examination of tumour tissues from HSS-treated animals showed extensive necrosis and bleeding. CONCLUSIONS: Haishengsu inhibits the growth of transplanted K562 tumours in mice. It is also effective in suppressing the growth of drug-resistant K562/ADM tumors in this animal model.