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The drug-injury relief system in Taiwan was implemented 20 years ago with the goal of providing timely relief for drug injuries incurred by the proper use of legal drugs. This system utilizes a nonlitigation expert review process to evaluate drug-injury relief applications, and 2,732 applications have been reviewed from 1999-2016. Of these, 1,572 applications received relief payments, an approval rate of 58%. Average review timeframes per application have decreased from 248 days (2003-2011) to 182 days (2012-2016). Most adverse drug reactions (ADRs) for approved cases involved skin and subcutaneous tissue disorders (67%), with allopurinol being the primary culprit drug. A recent decline observed for such ADRs may reflect the influences of promotional activities and policy initiatives carried out according to informed analysis from drug-injury relief applications, which suggests that the drug-injury relief system can also play an important public health role in enhancing drug safety.

We previously showed that microRNA-429 (miR-429) played an important role in epithelial–mesenchymal transition (EMT) of urothelial cell carcinoma of the bladder. We herein evaluated the expression of miR-429 in bladder cancer and its potential relevance to clinicopathological characteristics and patient survival. Relative expression levels of miR-429 in surgical bladder cancer tissue specimens obtained from 76 patients with bladder cancer were measured by chromogenic in situ hybridization. miR-429 expression was significantly higher in specimens from alive patients than expired patients in both of 5-year overall survival (OS) (0.59 ± 0.09 vs. 0.27 ± 0.12; p

Introduction 18F‐fluorodeoxyglucose (FDG)‐PET metabolic patterns of brain differ among autoimmune encephalitis with different neuronal surface antigens. In this case report, we compared the topographical relationship of cerebral glucose metabolism and antigen distribution in the patients with anti‐NMDAR and anti‐AMPAR encephalitis. Literature review summarized the common features of brain metabolism of autoimmune encephalitis. Methods The cerebral glucose metabolism was evaluated by FDG‐PET/CT during acute‐to‐subacute stage of autoimmune encephalitis and after treatment. The stereo and quantitative analysis of cerebral metabolism used standardized z‐score and visualized on three‐dimensional stereotactic surface projection. To map NMDAR and AMPAR in human brain, we adopted genetic atlases from the Allen Institute and protein atlases from Zilles's receptor densities. Results The three‐dimensional stereotactic surface projection displayed frontal‐dominant hypometabolism in a 66‐year‐old female patient with anti‐AMPAR encephalitis and occipital‐dominant hypometabolism in a 29‐year‐old female patient with anti‐NMDAR encephalitis. Receptor density maps revealed opposite frontal–occipital gradients of AMPAR and NMDAR, which reflect reduced metabolism in the correspondent encephalitis. FDG‐PET hypometabolic areas possibly represent receptor hypofunction with spatial correspondence to receptor distributions of the autoimmune encephalitis. The reversibility of hypometabolism was in line with patients' cognitive improvement. The literature review summarized six features of metabolic anomalies of autoimmune encephalitis: (a) temporal hypermetabolism, (b) frontal hypermetabolism and (c) occipital hypometabolism in anti‐NMDAR encephalitis, (d) hypometabolism in association cortices, (e) sparing of unimodal primary motor cortex, and (e) reversibility in recovery. Conclusions The distinct cerebral hypometabolic patterns of autoimmune encephalitis were representative for receptor hypofunction and topographical distribution of antigenic receptors. The reversibility of hypometabolism marked the clinical recovery of autoimmune encephalitis and made FDG‐PET of brain a valuable diagnostic tool., Glucose metabolism patterns were different in anti‐AMPAR and anti‐NMDAR encephalitis. Hypometabolism was frontal‐dominant in anti‐AMPAR encephalitis but occipital‐dominant in anti‐NMDAR encephalitis. The topographical differences might be related to receptor density.

Nobiletin, a bioactive polymethoxylated flavone (5,6,7,8,3(') ,4(') -hexamethoxyflavone), is abundant in citrus fruit peel. Although nobiletin exhibits antitumor activity against various cancer cells, the effect of nobiletin on glioma cells remains unclear. The aim of this study was to determine the effects of nobiletin on the human U87 and Hs683 glioma cell lines. Treating glioma cells with nobiletin (20-100 µm) reduced cell viability and arrested the cell cycle in the G0/G1 phase, as detected using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and propidium iodide (PI) staining, respectively; however, nobiletin did not induce cell apoptosis according to PI-annexin V double staining. Data from western blotting showed that nobiletin significantly attenuated the expression of cyclin D1, cyclin-dependent kinase 2, cyclin-dependent kinase 4, and E2 promoter-binding factor 1 (E2F1) and the phosphorylation of Akt/protein kinase B and mitogen-activated protein kinases, including p38, extracellular signal-regulated kinase, and c-Jun N-terminal kinase. Our data also showed that nobiletin inhibited glioma cell migration, as detected by both functional wound healing and transwell migration assays. Altogether, the present results suggest that nobiletin inhibits mitogen-activated protein kinase and Akt/protein kinase B pathways and downregulates positive regulators of the cell cycle, leading to subsequent suppression of glioma cell proliferation and migration. Our findings evidence that nobiletin may have potential for treating glioblastoma multiforme.

Growing evidence has indicated that opioids enhance replication of human immunodeficiency virus and hepatitis C virus in target cells. However, it is unknown whether opioids can enhance replication of other clinically important viral pathogens. In this study, the interaction of opioid agonists and human influenza A/WSN/33 (H1N1) virus was examined in human lung epithelial A549 cells. Cells were exposed to morphine, methadone or buprenorphine followed by human H1N1 viral infection. Exposure to methadone differentially enhanced viral propagation, consistent with an increase in virus adsorption, susceptibility to virus infection and viral protein synthesis. In contrast, morphine or buprenorphine did not alter H1N1 replication. Because A549 cells do not express opioid receptors, methadone-enhanced H1N1 replication in human lung cells may not be mediated through these receptors. The interaction of methadone and H1N1 virus was also examined in adult mice. Treatment with methadone significantly increased H1N1 viral replication in lungs. Our data suggest that use of methadone facilitates influenza A viral infection in lungs and might raise concerns regarding the possible consequence of an increased risk of serious influenza A virus infection in people who receive treatment in methadone maintenance programs.

The shape and size of monodisperse Fe3 O4 nanoparticles (NPs) are controlled using a chemical solution synthesis in the presence of the surfactant cetylpyridinium chloride (CPC). Cubic Fe3 O4 NPs surrounded by six {100} planes are obtained in the absence of CPC. Increasing the CPC content during synthesis causes the shape of the resulting Fe3 O4 NPs to change from cubic to truncated cubic, cuboctahedral, truncated octahedral, and finally octahedral. During this evolution, the predominantly exposed planes of the Fe3 O4 NPs vary from {100} to {111}. The shape control results from the synergistic effect of the pyridinium cations, chloride anions, and long-chain alkyl groups of CPC, which is confirmed by comparison with NPs synthesized in the presence of various related cationic surfactants. The size of the cubic Fe3 O4 NPs can be tuned from 50 to 200 nm, by changing the concentration of oleic acid in the reaction solution. The Fe3 O4 NPs exhibit shape-dependent saturation magnetization, remanent magnetization, and coercivity.

Immunotherapy using bacille Calmette-Guerin (BCG) instillation is the mainstay treatment modality for superficial urothelial cancer (UC) through toll-like receptor (TLR) activation of cognitive immune response. We investigated the roles of TLR7 in the activation of apoptosis in UC cells after BCG treatment. The in vitro cytotoxicity effect of BCG on UC cells was measured by a modified 3-(4,5-dimethylthiazo-2-yl)-2,5-diphenyl tetrazolium assay. Expressions of TLR7 mRNA and protein in native UC cells prior to and after BCG treatment were analyzed using real-time quantitative polymerase chain reaction and western blot methods. Phagocytotic processes after BCG treatment in UC cells were observed microscopically using a specific immunostain, subsequent cellular apoptosis-related signals induced by TLR7 were analyzed by western blot. Low-grade UC cells, TSGH8301, showed significant cellular death (4.23-fold higher than the high-grade UC cells T24 and J82) when treated with BCG and the BCG cytotoxicity was displayed in a dose–time-dependent manner. TSGH8301 cells had the highest content of TLR7 mRNA, 7.2- and 4.5-fold higher than that of T24 and J82 cells, respectively. TLR7 protein expression was also significantly increased in TSGH8301 cells. Phagocytosis-related markers, including beclin 1, ATG2, and LC3, were increased when TSGH8301 cells were treated by BCG. Interleukin-1 receptor-associated kinases 2 and 4 were also increased markedly in TSGH8301 cells. On the contrary, cellular apoptosis of TSGH8301 cells decreased by 34% when TLR7 activation was suppressed by the TLR antagonist IRS661 after BCG treatment. Our findings suggest that well differentiated TCC cells have higher expression of TLR7 and BCG can drive cellular death of TCC cells directly via TLR7 activation and related apoptotic pathway.

All-optical modulation based on silicon quantum dot doped SiOx:Si-QD waveguide is demonstrated. By shrinking the Si-QD size from 4.3 nm to 1.7 nm in SiOx matrix (SiOx:Si-QD) waveguide, the free-carrier absorption (FCA) cross section of the Si-QD is decreased to 8 × 10−18 cm2 by enlarging the electron/hole effective masses, which shortens the PL and Auger lifetime to 83 ns and 16.5 ps, respectively. The FCA loss is conversely increased from 0.03 cm−1 to 1.5 cm−1 with the Si-QD size enlarged from 1.7 nm to 4.3 nm due to the enhanced FCA cross section and the increased free-carrier density in large Si-QDs. Both the FCA and free-carrier relaxation processes of Si-QDs are shortened as the radiative recombination rate is enlarged by electron–hole momentum overlapping under strong quantum confinement effect. The all-optical return-to-zero on-off keying (RZ-OOK) modulation is performed by using the SiOx:Si-QD waveguides, providing the transmission bit rate of the inversed RZ-OOK data stream conversion from 0.2 to 2 Mbit/s by shrinking the Si-QD size from 4.3 to 1.7 nm.

Exposure to benzidine has been known to induce human cancers, particularly bladder carcinomas. In this study, the zebrafish model was used to investigate the developmental toxicity of benzidine. Embryos at 6 h postfertilization (hpf) that were exposed to benzidine exhibited embryonic death in a dose- and time-dependent manner. Benzidine induced malformations in zebrafish, such as small brain development, shorter axes, and a slight pericardial edema. High concentrations (50, 100, and 200 µM) of benzidine triggered widespread apoptosis in the brain and dorsal neurons, as evidenced by acridine orange and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assays. Real-time polymerase chain reaction analysis also showed that benzidine treatment affected p53, bax, and noxa expression. Decreases in specific brain markers, such as emx1 in the telencephalon, ngn1 in differentiated neurons, and otx2 in the midbrain, were observed in benzidine-treated embryos at 24 hpf. Conversely, no overt changes to pax2.1 expression in the midbrain-hindbrain boundary were found. Moreover, the use of Tg(HuC:GFP) zebrafish showed that benzidine caused a malformation of the telencephalon region. Our findings show that benzidine exposure triggers widespread apoptosis in the zebrafish brain and dorsal neurons, resulting in the development of an abnormal telencephalon.

In mammals, a distinct RNA polymerase II form, RNAPII(G) contains a novel subunit Gdown1 (encoded by POLR2M), which represses gene activation, only to be reversed by the multisubunit Mediator co-activator. Here, we employed single-particle cryo-electron microscopy (cryo-EM) to disclose the architectures of RNAPII(G), RNAPII and RNAPII in complex with the transcription initiation factor TFIIF, all to ~19 A. Difference analysis mapped Gdown1 mostly to the RNAPII Rpb5 shelf-Rpb1 jaw, supported by antibody labelling experiments. These structural features correlate with the moderate increase in the efficiency of RNA chain elongation by RNAP II(G). In addition, our updated RNAPII-TFIIF map showed that TFIIF tethers multiple regions surrounding the DNA-binding cleft, in agreement with cross-linking and biochemical mapping. Gdown1's binding sites overlap extensively with those of TFIIF, with Gdown1 sterically excluding TFIIF from RNAPII, herein demonstrated by competition assays using size exclusion chromatography. In summary, our work establishes a structural basis for Gdown1 impeding initiation at promoters, by obstruction of TFIIF, accounting for an additional dependent role of Mediator in activated transcription.

J. Neurochem. (2012) 122, 147–161. Abstract The mechanisms that regulate synapse formation and maintenance are incompletely understood. In particular, relatively few inhibitors of synapse formation have been identified. Receptor protein tyrosine phosphatase σ (RPTPσ), a transmembrane tyrosine phosphatase, is widely expressed by neurons in developing and mature mammalian brain, and functions as a receptor for chondroitin sulfate proteoglycans that inhibits axon regeneration following injury. In this study, we address RPTPσ function in the mature brain. We demonstrate increased axon collateral branching in the hippocampus of RPTPσ null mice during normal aging or following chemically induced seizure, indicating that RPTPσ maintains neural circuitry by inhibiting axonal branching. Previous studies demonstrated a role for pre-synaptic RPTPσ promoting synaptic differentiation during development; however, subcellular fractionation revealed enrichment of RPTPσ in post-synaptic densities. We report that neurons lacking RPTPσ have an increased density of pre-synaptic varicosities in vitro and increased dendritic spine density and length in vivo. RPTPσ knockouts exhibit an increased frequency of miniature excitatory post-synaptic currents, and greater paired-pulse facilitation, consistent with increased synapse density but reduced synaptic efficiency. Furthermore, RPTPσ nulls exhibit reduced long-term potentiation and enhanced novel object recognition memory. We conclude that RPTPσ limits synapse number and regulates synapse structure and function in the mature CNS.

BACKGROUND:Monascus-fermented products have featured in Chinese cuisine for thousands of years and are widely used as food colourants and dietary materials in many Asian countries. Rice and dioscorea fermented with Monascus purpureus NTU 568 have health-promoting attributes in vitro and in vivo. The aim of this study was to investigate the immunomodulatory and antioxidant effects of polysaccharides from red mould rice (RMRP) and red mould dioscorea (RMDP) in Raw 264.7 cells. RESULTS: The results showed the antioxidant capabilities (including scavenging, chelating, inhibition of lipid peroxidation, and reducing power) of RMRP and RMDP at a concentration of 10 mg mL−1. RMRP and RMDP also stimulated cell proliferation, nitric oxide production, phagocytosis and cytokine production (including IL1-β, IL-6 and TNF-α) in Raw 264.7 cells. CONCLUSION: These findings demonstrate that RMRP and RMDP have antioxidant and immunomodulation potential to be developed as novel dietary supplements. Copyright © 2011 Society of Chemical Industry

Overexpression of hypoxia-inducible factor-1 alpha is noted during the invasive and metastatic process of transitional cell carcinoma. It will upregulate vascular endothelial growth factor (VEGF) and drive proliferation, invasiveness, metastasis, and antiapoptotic ability of cancer cells. We proposed that tyrosine kinase receptor inhibitor, sunitinib malate—(Sutent; Pfizer Inc., Taiwan), combined with chemotherapeutic drug may present synergistic cytotoxic enhancement to transitional cell carcinoma cells with subsequent inhibition of their cellular behaviors, including proliferation, invasiveness, and metastatic activity. The contents of VEGF-A in mouse bladder tumor cells (MBT-2) and culture medium were detected by quantification-polymerase chain reaction and Western blot individually. The inhibitory concentrations of various chemotherapeutic drugs, sunitinib, and their combination treatment in MBT-2 were determined by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay. Microchamber transmembrane migration assay was applied in evaluation of the inhibitory effects of different dosages of sunitinib and combination treatment on tumor cells. The cell cycle and apoptosis were analyzed after combination therapy by flow cytometry. Variation in apoptotic pathway was elucidated by Western blot using specific antibodies with cleaved PARP and caspase-3. Metastatic animal model mimicked by tail vein injection of MBT-2 cells was used to evaluate the treatment efficiency in tumor weight and survival rate. The mRNA and protein level of VEGF-A in MBT-2 cells increased by 70% at 48 hours interval under hypoxia stress condition. In MTT assay, MBT-2 cells had shown the highest sensitivity to epirubicin. Sunitinib combined with epirubicin had shown a synergistic cytotoxic effect to MBT-2 cells. Sunitinib and its combination with epirubicin showed significant inhibition on MBT-2 cells migration in microchambers. G2/M phase arrest and increased subG1 in cell cycle was seen in the epirubicin and sunitinib combination treatment group. The activation of apoptosis pathway was confirmed by increased cleaved caspase-3 and cleaved PARP in MBT-2 cells. In tail vein tumor inoculation C3H mice model, epirubicin alone and sunitinib combination therapy decreased tumor growth in lungs with marginal effect. Sunitinib and epirubicin combination had shown a synergistic cytotoxic effect and inhibited cell migration ability in MBT-2 cells. The combination can induce cell cycle arrest at G2/M phase and increase subG1 cells. Metastatic animal study also showed that sunitinib combined with epirubicin has a marginal effect on inhibition of tumor growth of lungs. The tyrosine kinase receptor inhibitor-targeted combined chemotherapy regimen may provide as a new treatment modality for advanced bladder cancer in the future.

A chemometric study using pattern recognition technology was carried out to characterize the geographic origins of the brown planthopper, Nilaparvata lugens. The concentrations of 23 trace elements (Mn, Mo, Cd, Ce, V, Th, Cs, Be, Tl, Fe, Nd, Pr, Se, Tm, Lu, Eu, Ho, Br, Dy, Gd, U, Sm and Er) in 53 samples from seven regions in southern China were determined using inductively coupled plasma mass spectrometry. The data obtained were successively evaluated using a multivariate statistical approach, namely, linear discriminant analysis, which allowed classification and discrimination of the N. lugens samples from Fuqing, Shaoguan, Hepu, Yongfu, Hengnan, Wan-an and Yongkang with high accuracy and a clear separation among the seven regions. The results show that pattern identification on the basis of trace elements in the bodies of N. lugens is feasible for determining the geographic origins of individuals.

Oral Diseases (2010) 16, 351–359 Objectives: To investigate the changes in the muscarinic receptor signaling pathway with submandibular gland (SMG) transplantation and whether carbachol improves secretion in transplanted SMGs. Materials and methods: SMG autotransplantation was performed in a rabbit model. Carbachol (1 μM) was infused into the transplanted glands from postoperative day 1–7. The expression of the M1 and M3 muscarinic receptors, aquaporin-5 (AQP5), and phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) was measured by RT-PCR, immunoblotting or immunofluorescence. The content of inositol 1, 4, 5-trisphosphate (IP3) was measured by radioimmunoassay. Results: Salivary flow of the transplanted SMGs was decreased after transplantation. As well, the expressions of M1 and M3 receptors and their downstream signaling molecules, IP3, p-ERK1/2 and AQP5, were all reduced. Atrophy of acinar cells was shown in transplanted glands. However, all these alterations were reversed after carbachol treatment for 7 days. Furthermore, carbachol directly increased the mRNA expression of AQP5 and phosphorylation of ERK1/2 in cultured neonatal rabbit SMG cells. Conclusion: A lack of acetylcholine and downregulation of the muscarinic receptor signaling pathway is involved in the early hypofunction of transplanted SMGs. Carbachol treatment could be a new therapeutic strategy to improve secretion and prevent the obstruction of Wharton’s duct in the early phase after SMG transplantation.

The urea hydrolysis method was used to prepare NiO-deposited YSZ composite powders. First, micrometer-sized YSZ particles were fabricated, and then the nanosized NiO particles were deposited on the surface of the YSZ particles. The microstructure of composite powders and the sintered bulk were further characterized with the aid of XRD, SEM, and TEM. The results indicated that the mesoporous and microsheet-like Ni(OH)2·xH2O (x=0–1) crystals were deposited on the surface of YSZ particles. As the concentration of Ni2+ ion in the stock solution increased, the deposited NiO content and thickness of NiO layer on the YSZ particle surface also increased. In addition, the YSZ particle size showed significant influence on the microstructure and conductivity of Ni/YSZ cermet anode produced by NiO-deposited YSZ composite powders. Such NiO-deposited YSZ composite powders can be easily sintered to form a continuous NiO network.

Triangular prism-like extended microtunnels (EMTs) can be easily formed in specially designed epitaxial lateral overgrowth GaN thick films by selective wet chemical etching in molten potassium hydroxide (KOH). In this study, extended microtunnels along the 〈100〉 and the 〈100〉 directions were fabricated and compared. If tunnels along the 〈100〉 direction, the {11} planes would be the etch stop plane. While the tunnels along 〈100〉 direction, the etch stop plane would become to {10} planes. The activation energies of wet chemical etch for the {11} planes and the {10} planes were determined to be 23.6 kcal/mol (1.02 eV) and 22.8 kcal/mol (0.99 eV) using Arrhenius plot. On the other hand, the etching depths of the tunnels along the 〈100〉 direction were more than twice the depths of the tunnels along the 〈100〉 direction during the same etching time. The highest etch rate of the tunnels along the axial direction can reach 1000 μm/hr in 〈100〉 direction, which is believed to be the highest etch rate of GaN ever reported. Additional crystal facet of m-plane in GaN was also observed in the sample with extended microtunnels along the 〈100〉 direction. (© 2008 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim)

Ultrafast Kerr effect switching in near-infrared two-photon absorption (TPA)-free and free-carrier-absorption (FCA)-free nonstoichiometric silicon carbide (SixC1−x) microring waveguides is performed and investigated. With pulsed return-to-zero on–off-keying (PRZ-OOK) stream for the Si-rich SixC1−x-based all-optical switches, the inversely modulated probe reveals an asymmetric bit shape data extinction ratio (ER) of only 8.7 dB owing to the TPA + FCA effect. By eliminating the FCA effects in nearly stoichiometric SixC1−x microring waveguide, the high-speed wavelength conversion of a data stream with an ER of 14 dB can be observed when coinciding the probe wavelength with the transmission dip. Slightly deviating the probe wavelength from the transmission dip, most probe power still remains in bus waveguide to cause a strong FCA effect to degrade the ER down to 7.4 dB. A symmetrically converted and inverted data stream with high on/off extinction can be observed in the C-rich SixC1−x-based microring waveguide with completely suppressed trailing-edge response. To further approach the upper limitation on bandwidth, the wavelength-converted and sign-reversible PRZ-OOK data switching at a bit rate up to 12 Gbit s−1 can be obtained with similar ER of better than 20 dB, as contributed mainly by the enhanced Kerr nonlinearity in the C-rich SixC1−x.

Objective The paradigm of global medical health has been re-characterised by a shift in its major focus from infectious disease to chronic illness. Opinions vary as to the declining emphasis on infectious disease. This paper provides clinicians with an understanding of a secular trend in medical education regarding the topic of infectious diseases over a period of 26 years. Methods A survey was carried out to evaluate coverage of infectious disease topics within recent general medicine textbooks and journals. Results The percentage of content dedicated to infectious disease has remained static in 2 major medical textbooks, whereas a trend towards decreasing coverage was shown in 4 major medical journals. Of 901 original articles published in 2000, 16·4% covered certain aspects of infectious disease, as compared with 20·9% of 790 articles published in 1985. Increasing rates of infectious disease mortality in developing countries were not consistently matched with the trend in coverage of infectious disease topics in either medical textbooks or journals. Conclusions Our data demonstrate that coverage of infectious disease topics in publications issued in developed countries was more indicative of global trends in disease mortality rather than those of developing countries. Medical education and knowledge, which are usually delivered by the rich nations where influential medical textbooks and journals are published, place less emphasis on infectious disease relative to the burden infectious disease places on the developing world.

Installation of a partially penetrating well (PPW) in which only a portion of the well casing is screened is becoming more common because it is very often the case that only a portion of the vertical thickness of the aquifer is contaminated. In this study, we present a mathematical model describing the contaminant transport towards a PPW. To construct the model, the radial and vertical components of the pore water velocity are first computed using an analytical solution for the steady-state drawdown distribution near a PPW. Next, the obtained radial and vertical components of the pore water velocity are incorporated into a three-dimensional axially symmetrical advection–dispersion equation in cylindrical coordinates from which the solute transport equation is derived. The Laplace transformed finite difference technique is then adopted to solve the governing equation. The case that contaminant plume is distributed only over the lowermost 20% vertical thickness of the aquifer is considered for simulation. Breakthrough curves at the extraction well and the total mass removal of the contaminant by pumping are both obtained to illustrate how the aquifer remediation using a PPW is affected by various site-specific hydrogeological parameters. Results demonstrate that the use of the PPW can effectively remove the contaminant only for the aquifer that has a large hydraulic conductivity anisotropy ratio and a small longitudinal dispersivity. The fully penetrating well performs equally or better than the PPW for an aquifer with large longitudinal dispersivity. Moreover, the temporal evolution of the contaminant plume is depicted to gain further insight into the contaminant transport towards a PPW affected by various hydrogeological parameters. The mathematical model presented herein provides a useful tool for designing an effective and efficient pump-and-treat system using a PPW. Copyright © 2010 John Wiley & Sons, Ltd.