Clinical activity and safety of sintilimab, bevacizumab, and TMZ in patients with recurrent glioblastoma.

PURPOSE: There are limited and no standard therapies for recurrent glioblastoma. We herein report the antitumour activity and safety of sintilimab, bevacizumab and temozolomide (TMZ) in recurrent glioblastoma. METHODS: We retrospectively analysed eight patients with recurrent glioblastoma treated with sintilimab (200 mg) every three weeks + bevacizumab (10 mg/kg) every three weeks + TMZ (200 mg/m²orally) (5 days orally every 28 days for a total of four weeks). The primary objective was investigator-assessed median progression-free survival(mPFS). Secondary objectives were to assess the 6-month PFS, objective response rate (ORR) and duration of response (DOR) accroding to RANO criteria. RESULTS: The mPFS time for 8 patients was 3.340 months (95% CI: 2.217-4.463), The longest PFS was close to 9 months. Five patients were assessed to have achieved partial response (PR), with an overall remission rate of 62.5%, Four patients experienced a change in tumour volume at the best response time of greater than 60% shrinkage from baseline, and one patient remained progression free upon review, with a DOR of more than 6.57 months. The 6-month PFS was 25% (95% CI: 5.0-55.0%). Three patients had a treatment-related adverse events, though no grade 4 or 5 adverse events occurred. CONCLUSION: In this small retrospective study, the combination regimen of sintilimab, bevacizumab and TMZ showed promising antitumour activity in treatment of recurrent glioblastoma, with a good objective remission rate.

PITPNC1 Suppress CD8+ T cell immune function and promote radioresistance in rectal cancer by modulating FASN/CD155.

BACKGROUND: Radioresistance is a primary factor contributing to the failure of rectal cancer treatment. Immune suppression plays a significant role in the development of radioresistance. We have investigated the potential role of phosphatidylinositol transfer protein cytoplasmic 1 (PITPNC1) in regulating immune suppression associated with radioresistance. METHODS: To elucidate the mechanisms by which PITPNC1 influences radioresistance, we established HT29, SW480, and MC38 radioresistant cell lines. The relationship between radioresistance and changes in the proportion of immune cells was verified through subcutaneous tumor models and flow cytometry. Changes in the expression levels of PITPNC1, FASN, and CD155 were determined using immunohistochemistry and western blotting techniques. The interplay between these proteins was investigated using immunofluorescence co-localization and immunoprecipitation assays. Additionally, siRNA and lentivirus-mediated gene knockdown or overexpression, as well as co-culture of tumor cells with PBMCs or CD8+ T cells and establishment of stable transgenic cell lines in vivo, were employed to validate the impact of the PITPNC1/FASN/CD155 pathway on CD8+ T cell immune function. RESULTS: Under irradiation, the apoptosis rate and expression of apoptosis-related proteins in radioresistant colorectal cancer cell lines were significantly decreased, while the cell proliferation rate increased. In radioresistant tumor-bearing mice, the proportion of CD8+ T cells and IFN-γ production within immune cells decreased. Immunohistochemical analysis of human and animal tissue specimens resistant to radiotherapy showed a significant increase in the expression levels of PITPNC1, FASN, and CD155. Gene knockdown and rescue experiments demonstrated that PITPNC1 can regulate the expression of CD155 on the surface of tumor cells through FASN. In addition, co-culture experiments and in vivo tumor-bearing experiments have shown that silencing PITPNC1 can inhibit FASN/CD155, enhance CD8+ T cell immune function, promote colorectal cancer cell death, and ultimately reduce radioresistance in tumor-bearing models. CONCLUSIONS: PITPNC1 regulates the expression of CD155 through FASN, inhibits CD8+ T cell immune function, and promotes radioresistance in rectal cancer.

A retrospective review of non­intestinal­type adenocarcinoma of nasal cavity and paranasal sinus.

Non-intestinal adenocarcinoma of nasal cavity and paranasal sinuses (n-ITAC) is a heterogeneous tumor, which has rarely been reported in previous studies. Most high-grade n-ITAC has poor prognosis and there is a lack of classic therapeutic strategy. The present study examined using the PACS system of Nanfang Hospital of Southern Medical University between January 2000 and June 2020. It searched the keyword 'n-ITAC' and selected pathology. A total of 15 consecutive patients were searched. Finally, the present study analyzed a total of 12 n-ITAC patients. The follow-up time was 47 months on average. For low-grade (G1) tumors, 1 and 3-year overall survival (OS) rate were 100 and 85.7% respectively, while for high-grade (G3) tumors, 1 and 3-year OS rates were 80.0 and 20.0% respectively. Pathological grade may be an adverse prognostic factor (P=0.077). The OS of the surgery group was significantly superior to that of the non-surgery group (3-year OS was 63.6 vs. 0%, P=0.0009). Surgery is an indispensable means of treatment. The OS of patients with positive incisal margin was lower compared with that of patients with negative margin (P=0.186), suggesting that complete resection may be one of the prognostic factors. Patients with high risk factors received radiotherapy. The radiation dose was 66-70 Gy/33F for patients with positive margin or non-operation and was 60 Gy/28F for those with negative margin. Most of the patients received prophylactic irradiation of cervical area. Therefore, the prognosis of pathological high-grade n-ITAC is poor. Surgery is the most effective and an indispensable treatment for n-ITAC. For patients with high risk factors, surgery combined with radiotherapy may be a reasonable treatment. With regard to the cover range of radiotherapy, the primary tumor combined with lymph node drainage area is often used in Nanfang Hospital of Southern Medical University and the total dose of radiotherapy can be reduced if the surgical margin is negative.

Pan-Genome Analysis of TIFY Gene Family and Functional Analysis of CsTIFY Genes in Cucumber.

Cucumbers are frequently affected by gray mold pathogen Botrytis cinerea, a pathogen that causes inhibited growth and reduced yield. Jasmonic acid (JA) plays a primary role in plant responses to biotic stresses, and the jasmonate-ZIM-Domain (JAZ) proteins are key regulators of the JA signaling pathway. In this study, we used the pan-genome of twelve cucumber varieties to identify cucumber TIFY genes. Our findings revealed that two CsTIFY genes were present in all twelve cucumber varieties and showed no differences in protein sequence, gene structure, and motif composition. This suggests their evolutionary conservation across different cucumber varieties and implies that they may play a crucial role in cucumber growth. On the other hand, the other fourteen CsTIFY genes exhibited variations in protein sequence and gene structure or conserved motifs, which could be the result of divergent evolution, as these genes adapt to different cultivation and environmental conditions. Analysis of the expression profiles of the CsTIFY genes showed differential regulation by B. cinerea. Transient transfection plants overexpressing CsJAZ2, CsJAZ6, or CsZML2 were found to be more susceptible to B. cinerea infection compared to control plants. Furthermore, these plants infected by the pathogen showed lower levels of the enzymatic activities of POD, SOD and CAT. Importantly, after B. cinerea infection, the content of JA was upregulated in the plants, and cucumber cotyledons pretreated with exogenous MeJA displayed increased resistance to B. cinerea infection compared to those pretreated with water. Therefore, this study explored key TIFY genes in the regulation of cucumber growth and adaptability to different cultivation environments based on bioinformatics analysis and demonstrated that CsJAZs negatively regulate cucumber disease resistance to gray mold via multiple signaling pathways.

Comparative Effectiveness of Abiraterone and Enzalutamide in Patients With Metastatic Castration-Resistant Prostate Cancer in Taiwan.

Background: Abiraterone and enzalutamide are widely used as first-line treatment for metastatic castration-resistant prostate cancer (mCRPC); however, their efficacy in mCRPC has been inconsistently demonstrated in other outcome studies from real-world databases. The aim of our study was to assess the comparative effectiveness of abiraterone and enzalutamide in patients with mCRPC using real-world data from Taiwan. Methods: This retrospective cohort population-based study included patients identified in the Taiwan National Health Insurance Research Database who had been diagnosed with mCRPC and who had taken abiraterone or enzalutamide between December 2014 and August 2017. The study's outcome evaluated the differences in overall survival (OS) and time to treatment failure (TTF) between abiraterone and enzalutamide over a 15-month follow-up period. The patients were followed from the index date to when the outcome occurred, to December 31, 2018, or to the patients' withdrawal from the National Health Insurance program. The estimated relative treatment effects of abiraterone and enzalutamide on OS and TTF were adjusted by the inverse probability of treatment weighting (IPTW) using the Kaplan-Meier method and a Cox proportional hazards model. Results: The abiraterone and enzalutamide groups consisted of 1,046 and 118 patients, respectively. After IPTW adjustment, 1,164 patients in the abiraterone group and 1,158 in the enzalutamide group underwent an outcome evaluation. Enzalutamide showed a similar OS rate to that of abiraterone (57.58% vs. 49.51%, p = 0.095 by log-rank test). Enzalutamide significantly reduced the risk of death for mCRPC when compared with abiraterone [adjusted hazard ratio (aHR), 0.828; 95% CI 0.731-0.938]. However, similar results were not observed in the TTF outcomes (63.84% vs. 67.79%, p = 0.2651 by log-rank test; aHR, 0.902; 95% CI 0.812-1.002). Conclusion: In conclusion, enzalutamide was associated with better OS for mCRPC than abiraterone in the Taiwan population. Our study showed that there was no statistically significant difference in TTF between enzalutamide and abiraterone. Studies with longer surveillance of enzalutamide and abiraterone using real-world databases are needed.

Aggregation-Induced Emission-Based Vaccine Improves Potential Antitumor Immunotherapy.

Recently, immunomodulation based on biomaterials has held great promise for preventing and treating cancer. Tumor vaccination can be considered as one of promising immunotherapies, compared with the vaccines for infectious disease, it still stays in its infant. Herein, we designed a near-infrared-emitting AIEgens (named TPE-Ph-DCM) based vaccine as an adjuvant in enhancing immune response. AIE-based photodynamic vaccine exhibited efficiently enhancement of the DC?s antigen prestation and elicited antigen-specific cytotoxic T lymphocyte functionality, and significantly inhibited B16-OVA tumor growth prophylactically and therapeutically in mice model. This study is expected to provide a scientific basis for developing effective and safe tumor vaccines.

Glucocorticoid resistance induced by ANXA5 overexpression in B-cell acute lymphoblastic leukemia.

Development of chemo­resistance is ultimately responsible for treatment failure and relapse in B-cell acute lymphoblastic leukemia (B-ALL). However, the mechanism underlying glucocorticoid (GC) resistance remains unclear. This study was performed to identify GC resistance-related genes using the transcriptome chip from the GEO database, and preliminarily analyze drug resistance mechanism in B-ALL. Here, we found that ANXA5 expression was upregulated in B-ALL cells and high-level ANXA5 was associated with dexamethasone (DEX) resistance. Then, small interfering RNA (siRNA) was designed to silence ANXA5 expression in the B-ALL cell lines, and the apoptotic rate of cells treated with DEX was detected by flow cytometry. As a result, cell apoptosis was dramatically promoted in B-ALL cells following silencing of ANXA5 and DEX administration versus that in ANXA5-silenced alone or DEX-treated alone cells. It was further found that down-regulation of ANXA5 in B-ALL cells significantly increased the relative amount of cleaved Caspase 3 and Caspase 9 induced by DEX. Collectively, inhibition of ANXA5 gene expression may represent a novel method to restore the sensitivity of treatment-resistant B-ALL tumors to GC-induced cell death, which is of important clinical significance to overcome drug resistance associated with B-ALL.

Questions Frequently Asked of Healthcare Professionals: A 2-Year Data Survey Conducted at a Medical Center.

In this descriptive, retrospective study, we analyzed the types of questions posed by healthcare professionals to drug counselors at a medical center and the types of provision of pharmaceutical advice solicited to improve pharmaceutical care quality and establish clear directions for clinical pharmacist training. We collected 8,558 questions posed by healthcare professionals (physicians, 38%; pharmacists, 39%; nurses, 23%) from the electronic drug information record system from May 2013 to April 2015 in one medical center. Overall, 52% and 45% of calls came from outpatient and inpatient departments, respectively. Telephone was the main route of provision of pharmaceutical advice (total, 6,035 questions; 72%), and hospital/electronic formulary was the main reference type (43%). The top 10 topics were dosage, alternatives, drug name, usage, adverse drug reactions, medication suggestion, drug compatibility, national health insurance criteria, mechanism, and indications. Pharmacological classification inquiries most frequently addressed antimicrobial agents (20%), and vancomycin was the top single drug. Finally, 67% of calls were completed in 5 minutes. Our results suggest that the systematic organization of issues into a searchable database would reduce inquiry durations and improve work efficiency. Furthermore, the availability of various search tools and methods would quickly provide healthcare professionals with provision of drug information needed to improve patient medication safety.

Optimal donor for severe aplastic anemia patient requiring allogeneic hematopoietic stem cell transplantation: A large-sample study from China.

HLA-haploidentical hematopoietic stem cell transplantation (HSCT) may be an option for severe aplastic anemia (SAA) patients. However, to date, no large-sample studies have been performed to determine which types of SAA patients are suitable for HLA-haploidentical HSCT. We retrospectively studied 189 consecutive patients with SAA who underwent HLA-identical or HLA-haploidentical HSCT at seven transplant centers in China. Propensity score matching (PSM) was applied in this study to reduce the influence of potential confounders. The 5-year overall survival (OS) rate was 72.0% in the HLA-haploidentical group and 76.5% in the HLA-identical group. The median time to achieve engraftment and the incidence of acute GVHD/chronic GVHD were not significantly different between the two groups. In the subgroup analysis, the outcome of patients older than 40 years in the HLA-haploidentical group was significantly poorer than that of patients younger than 40 years in the same group and that of patients older than 40 years in the HLA-identical group. Based on the above results, we suggest that HLA-haploidentical relative HSCT should be considered as a valid alternative option for patients younger than 40 years with SAA for whom no matched sibling donor is available.

In Vitro Study on Influences of UGT1A8 Gene Polymorphisms on Mycophenolate Mofetil Metabolism.

OBJECTIVES: Mycophenolate mofetil is a first-line drug after organ transplant, but there are differences in metabolism of mycophenolate mofetil among individuals. The UDP glucuronosyltransferase enzyme is the key metabolic enzyme for mycophenolate mofetil, and UGT1A8 gene polymorphisms may affect the elimination of mycophenolate mofetil in patients. Here, we conducted an in vitro study to explore the relation between UGT1A8 gene polymorphisms and mycophenolate mofetil metabolism. MATERIALS AND METHODS: Five mutant loci overexpression vectors (UGT1A8 128C>T, 157C>A, 431C>T, 518C>G, and 830G>A) were constructed by genetic recombination and site-directed mutagenesis. We used Lipo2000 (Invitrogen, Carlsbad, CA, USA) to transfect the vectors into HEK293 cells. Mycophenolic acid, the active ingredient of mycophenolate mofetil, was added to different groups of cells. We then used the liquid chromatography tandem-mass spectrometry technique to detect production of the metabolite 7-O-mycophenolic acid glucuronide and to evaluate activity of the UDP glucuronosyltransferase enzyme in cells with different overexpression vectors. RESULTS: Mutations of UGT1A8 157C>A and 518C>G vectors can lead to increased activity of UDP glucuronosyltransferase enzymes and increased production of the 7-O-mycophenolic acid glucuronide metabolite, which showed 116% (P < .001) and 107% (P = .0191) production changes of 157C>A and 518C>G mutations, respectively, relative to wild-type UGT1A8. However, mutations of UGT1A8 431C>T and 830G>A loci resulted in decreased activity of UDP glucuronosyltransferase enzymes and decreased production of the metabolite, respectively showing 62.9% (P < .001) and 9.05% (P < .001) activity relative to wild-type UGT1A8. UGT1A8 128C>T had little effect on enzyme activity, with 96.8% activity relative to wild-type UGT1A8 (P = .0569). CONCLUSIONS: Our results showed that UGT1A8 gene polymorphisms can affect the activity of UDP glucuronosyltransferase enzyme, which may influence the elimination of mycophenolate mofetil in different patients.

Developing an App by Exploiting Web-Based Mobile Technology to Inspect Controlled Substances in Patient Care Units.

We selected iOS in this study as the App operation system, Objective-C as the programming language, and Oracle as the database to develop an App to inspect controlled substances in patient care units. Using a web-enabled smartphone, pharmacist inspection can be performed on site and the inspection result can be directly recorded into HIS through the Internet, so human error of data translation can be minimized and the work efficiency and data processing can be improved. This system not only is fast and convenient compared to the conventional paperwork, but also provides data security and accuracy. In addition, there are several features to increase inspecting quality: (1) accuracy of drug appearance, (2) foolproof mechanism to avoid input errors or miss, (3) automatic data conversion without human judgments, (4) online alarm of expiry date, and (5) instant inspection result to show not meted items. This study has successfully turned paper-based medication inspection into inspection using a web-based mobile device.

Long noncoding RNA HULC promotes cell proliferation by regulating PI3K/AKT signaling pathway in chronic myeloid leukemia.

Aberrant expression of long noncoding RNA (lncRNA) HULC is associated with various human cancers. However, the role of HULC in chronic myeloid leukemia (CML) is unknown. In this study, we found that HULC was remarkably overexpressed in both leukemia cell lines and primary hematopoietic cells derived from CML patients. The increase in HULC expression was positively correlated with clinical stages in CML. Moreover, the knockdown of HULC significantly inhibited CML cell proliferation and induced apoptosis by repressing c-Myc and Bcl-2. Furthermore, inhibition of HULC enhanced imatinib-induced apoptosis of CML cells. Further experiments demonstrated that HULC silencing markedly suppressed the phosphorylation of PI3K and AKT, indicating that enhancement of imatinib-induced apoptosis by HULC inhibition is related with the reduction of c-Myc expression and inhibition of PI3K/Akt pathway activity. Furthermore, HULC could modulate c-Myc and Bcl-2 by miR-200a as an endogenous sponge. Taken together, these results reveal that HULC promotes oncogenesis in CML and suggest a potential strategy for the CML treatment.

Identification of Heme Oxygenase-1 as a Novel Predictor of Hematopoietic Stem Cell Transplantation Outcomes in Acute Leukemia.

OBJECTIVE: The main aim of this study was to determine the correlation between clinical outcome and heme oxygenase-1 (HO-1) expression before and after hematopoietic stem cell transplantation (HSCT) in acute leukemia. METHODS: HO-1 mRNA levels in 83 patients were measured using qRT-PCR. In a comparative analysis of HO-1 levels in relation to different post-transplant outcomes, the HO-1 threshold, determined via the receiver operating characteristic (ROC) curve, was effectively used to predict clinical relapse and acute graft-versus-host disease (aGVHD). The correlations among clinical relapse, aGVHD and HO-1 expression were analyzed based on this threshold. RESULTS: Leukemia risk stratification and relative expression of HO-1 before pretreatment had significant effects on clinical relapse. Leukemia risk stratification, relative expression of HO-1 after HSCT and the interval from diagnosis to transplantation had a significant influence on aGVHD. Both relapse and aGVHD appeared to be associated with relative HO-1 expression. The relative expression rate of HO-1 was 1.131-1.186 before pretreatment, and strongly associated with post-transplantation relapse. The relative expression rate of HO-1 was 1.102-1.144 after transplantation, and closely related to aGVHD. ROC curve analysis revealed high specificity and sensitivity of HO-1 expression in predicting relapse and aGVHD after allo-HSCT. CONCLUSIONS: HO-1 expression can be effectively used as a predictor of relapse as well as a diagnostic factor of aGVHD after transplantation for allo-HSCT patients with acute leukemia.

1-Alpha, 25-dihydroxyvitamin D3 alters the pharmacokinetics of mycophenolic acid in renal transplant recipients by regulating two extrahepatic UDP-glucuronosyltransferases 1A8 and 1A10.

Mycophenolic acid (MPA) is an important immunosuppressant broadly used in renal transplantation. However, the large inter-patient variability in mycophenolic acid (MPA) pharmacokinetics (PK) limits its use. We hypothesize that extrahepatic metabolism of MPA may have significant impact on MPA PK variability. Two intestinal UDP-glucuronosyltransferases 1A8 and 1A10 plays critical role in MPA metabolism. Both in silico and previous genome-wide analyses suggested that vitamin D (VD) may regulate intestinal UGT1A expression. We validated the VD response elements (VDREs) across the UGT1A locus with chromatin immunoprecipitation (ChIP) and luciferase reporter assays. The impact of 1-alpha,25-dihydroxyvitamin D3 (D3) on UGT1A8 and UGT1A10 transcription and on MPA glucuronidation was tested in human intestinal cell lines LS180, Caco-2 and HCT-116. The correlation between transcription levels of VD receptor (VDR) and the two UGT genes were examined in human normal colorectal tissue samples (n = 73). PK alterations of MPA following the parent drug, mycophenolate mofetil (MMF), and D3 treatment was assessed among renal transplant recipients (n = 10). Our ChIP assay validate three VDREs which were further demonstrated as transcriptional enhancers with the luciferase assays. D3 treatment significantly increased transcription of both UGT genes as well as MPA glucuronidation in cells. The VDR mRNA level was highly correlated with that of both UGT1A8 and UGT1A10 in human colorectal tissue. D3 treatment in patients led to about 40% reduction in both AUC0-12 and Cmax while over 70% elevation of total clearance of MPA. Our study suggested a significant regulatory role of VD on MPA metabolism and PK via modulating extrahepatic UGT activity.

miR-320a regulates cell proliferation and apoptosis in multiple myeloma by targeting pre-B-cell leukemia transcription factor 3.

Aberrant expression of microRNAs (miRNAs) is implicated in cancer development and progression. While miR-320a is reported to be deregulated in many malignancy types, its biological role in multiple myeloma (MM) remains unclear. Here, we observed reduced expression of miR-320a in MM samples and cell lines. Ectopic expression of miR-320a dramatically suppressed cell viability and clonogenicity and induced apoptosis in vitro. Mechanistic investigation led to the identification of Pre-B-cellleukemia transcription factor 3 (PBX3) as a novel and direct downstream target of miR-320a. Interestingly, reintroduction of PBX3 abrogated miR-320a-induced MM cell growth inhibition and apoptosis. In a mouse xenograft model, miR-320a overexpression inhibited tumorigenicity and promoted apoptosis. Our findings collectively indicate that miR-320a inhibits cell proliferation and induces apoptosis in MM cells by directly targeting PBX3, supporting its utility as a novel and potential therapeutic agent for miRNA-based MM therapy.

Over-expression of heme oxygenase-1 in peripheral blood predicts the progression and relapse risk of chronic myeloid leukemia.

BACKGROUND: There are limited eligible clinical markers at present to monitor the progress of chronic myeloid leukemia (CML). Heme oxygenase-1 (HO-1), as one of the most important oxidation-regulating enzymes in vivo, suggests the onset and progression of cancer when highly expressed. Furthermore, HO-1 level is related with the occurrence and development of hematological diseases. But the relationship between HO-1 expression and progression/relapse of CML has seldom been studied hitherto. This study aimed to investigate the relationship between them to find out a new molecular marker for prediction. METHODS: A total of 60 peripheral blood and bone marrow (BM) samples from 25 CML patients in different phases were collected respectively to detect the expressions of HO-1 and bcr/abl using real-time PCR. Routine blood test was performed to detect the changes of leukocyte and platelet counts. The proportion of primitive cells in BM was detected by flow cytometry. The relationship between high HO-1 expression and CML progression and relapse was explored by the analysis of variance by Wilcoxon test and linear regression analysis. The diagnostic accuracy and cutoff values were determined by receiver operating characteristic curve. RESULTS: Relative expression of HO-1 mRNA in CML patients peripheral blood was significantly higher than that of donors (P < 0.0001), which were 0.57±3.78 and (1.417±1.125)×10(-6), respectively. HO-1 expression level in CML patients was 0.061 5±0.062 4, which decreased to 0.009 4±0.006 7 upon CMoR, and remained remarkably higher 0.016 3±0.017 5 than that of normal donors (1.417±1.125)×10(-6), P < 0.001. When relapse occurred, HO-1 expression significantly increased from 0.020 6±0.021 0 to 3.852±10.285 in CMoR stage and undergoing relapse. According to progression of CML, HO-1 expression level in CML patients increased from CP (0.009 5±0.017 6) to AP (0.028 0±0.055 7) and then to BP (0.276 7 ± 0.447 0). And there was a linear correlation between HO-1 expression and proportion of primitive CML cells. The diagnostic accuracies and cutoff values of HO-1 expression for CML-CP, CML-AP, and CML-BP were 1.0, 0.748, and 0.965, respectively, as well as 0.000 070, 0.001 917, and 0.020 696, respectively. CONCLUSION: HO-1 may be a potential molecular indicator for the progression and relapse of CML.

WebBio, a web-based management and analysis system for patient data of biological products in hospital.

We selected HTML, PHP and JavaScript as the programming languages to build "WebBio", a web-based system for patient data of biological products and used MySQL as database. WebBio is based on the PHP-MySQL suite and is run by Apache server on Linux machine. WebBio provides the functions of data management, searching function and data analysis for 20 kinds of biological products (plasma expanders, human immunoglobulin and hematological products). There are two particular features in WebBio: (1) pharmacists can rapidly find out whose patients used contaminated products for medication safety, and (2) the statistics charts for a specific product can be automatically generated to reduce pharmacist's work loading. WebBio has successfully turned traditional paper work into web-based data management.