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Objective: To observe the clinical efficacy of the Zhuang medicine Yingbupu decoction on stage I and II acute kidney injury through sequential test. Methods: The open one-way qualitative response sequential design of experiments was adopted, and the patients with AKI in phase I and II who met the inclusion criteria were divided into the treatment group and the control group according to the order of hospitalization by random number table. On the basis of basic treatment, the treatment group was treated with Zhuang medicine Yingbupu decoction, and the control group was treated with Jinshuibao tablet. The clinical efficacy, TCM syndrome score, 24 h urine volume, serum creatinine (Scr), microalbumin in urine (mAlb), neutrophil Gelatinase related lipid delivery albumin (NGAL) of the two groups were compared, and the adverse reactions and complications of the two groups were observed. Results: After 14 d of treatment, when the treatment group reached the 10th case, the experimental line contacted the upper bound U-line and reached the experimental standard to terminate the experiment. The effective hypothesis was accepted, and it was believed that the Zhuang medicine Yingbupu decoction had a therapeutic effect on stage I and II AKI. The conclusion was drawn that the treatment group received the Zhuang medicine Yingbupu. The clinical effective rate and improvement days were similar between the two groups, and there was no significant difference (P>0.05). However, the integral value of traditional Chinese medicine syndrome in the treatment group was lower than that in the control group (P<0.05), After treatment, the Scr, mAlb, and NGAL levels of patients in both groups were lower than before treatment(P<0.05). After treatment, the Scr, mAlb, and NGAL values in the treatment group were significantly lower than those in the control group(P<0.05). After treatment, the 24-hour urine volume in both groups was higher than that before treatment, and the values in the treatment group were significantly higher than those in the control group (P<0.05). During the treatment period, there were no significant adverse reactions or complications in either group. Conclusion: The Zhuang medicine Yingbupu decoction is effective in treating stage I and II AKI, and the Zhuang medicine Yingbupu can significantly improve the symptoms and quality of life of patients with stage I and II AKI. Its improvement of renal function is better than that of Jinshuibao tablets, and its safety is good. [ABSTRACT FROM AUTHOR]

The tensile and compressive tests on woven carbon fiber epoxy resin composite specimens in different hygrothermal environments were carried out. The moisture absorption, tensile and compressive properties, fracture morphology and dynamic mechanical properties were analyzed. The influence of hygrothermal environments on tensile and compressive properties was investigated. The results show that the absorption process of carbon fiber epoxy composites satisfies Fick's law, and its saturated moisture absorption rate is about 0.86%. After moisture absorption, the surface of specimens becomes smooth, the phenomenon of few fibers pull-out and resin damage occurs, but no chemical reaction and no new substances is generated. After moisture absorption at 130℃, the retention rate of tensile properties is 96%, but the retention rate of compression properties is only 69%. The glass transition temperature of composite laminates after moisture absorption decreases by 33℃ compared with that in dry state.

Dipeptidyl peptidase 4 (DPP4) inhibitors(oral hypoglycemic agents)have beneficial effects during the early stages of diabetes. In this study, we evaluated the role of DPP4inhibitorsonthe biological functions of cultured human endothelial progenitor cells (EPCs). After treating EPCs with the DPP4 inhibitors sitagliptin and vildagliptin, we examined the mRNA expression of DPP4, vascular endothelial growth factor (VEGF),VEGF receptor 2 (VEGFR-2),endothelial nitric oxide synthase (eNOS), caspase-3,stromal cell-derived factor-1 (SDF-1), chemokine (C-X-C motif) receptor 4 (CXCR4) were measured by RT-PCR. The protein expression of SDF-1 and CXCR4 was determined by Western blot; cell proliferation was tested by the MTT method, and DPP4 activity was determined by a DPP4 assay. Our results revealed that DPP4 expression and activity were inhibited following the treatment with various doses of DPP4 inhibitors. Cell proliferation and the expression of VEGF, VEGFR-2andeNOS were up regulated, while cell apoptosis was inhibited by DPP4 inhibitors in a dose-dependent manner. DPP4 inhibitors activated the SDF-1/CXCR4 signaling pathway, shown by the elevated expression of SDF-1/CXCR4. This further proved that after the SDF-1/CXCR4 signaling pathway was blocked by its inhibitor ADM3100, the effects of DPP4 inhibitors on the proliferation and apoptosis, and the expression of VEGF, VEGFR-2and eNOS of EPCs were significantly reduced. These findings suggest that DPP4 inhibitors promote the biological functions of human EPCs by up regulating the SDF-1/CXCR4 signaling pathway.

Dihydroartemisinin (DHA) has anticancer effects on multiple tumors, including those associated with breast cancer. This study aimed to investigate the mechanism causing DHA-reversing cisplatin (DDP) resistance in breast cancer. Relative mRNA and protein levels were tested using a qRT-PCR and western blot assay. Cell proliferation, viability, and apoptosis were evaluated using colony formation, MTT, and flow cytometry assays, respectively. Interaction of STAT3 and DDA1 was measured via a dual-luciferase reporter assay. The results showed that DDA1 and p-STAT3 levels were dramatically elevated in DDP-resistant cells. DHA treatment repressed proliferation and induced apoptosis of DDP-resistant cells by suppressing STAT3 phosphorylation; the inhibition ability was positively proportional to the DHA concentration. DDA1 knockdown inhibited cyclin expression, promoted G0/G1 phase arrest, restrained cell proliferation, and induced apoptosis of DDP-resistant cells. Furthermore, knockdown of STAT3 restrained proliferation and induced apoptosis and G0/G1 cell cycle arrest of DDP-resistant cells by targeting DDA1. DHA could restrain tumor proliferation of breast cancer via enhancing drug sensitivity of DDP-resistant cells through the STAT3/DDA1 signaling pathway. [ABSTRACT FROM AUTHOR]

The specific mechanism of gingerol in cerebral ischemia remains unknown. A neuroprotective function for miR‐210 in cerebral ischemia has been identified. The brain‐derived neurotrophic factor (BDNF)‐mediated signaling pathway protects against cerebral ischemic injury. This investigation aimed to determine whether gingerol plays a neuroprotective role in cerebral ischemia via the miR‐210/BDNF axis. N2a cells subjected to 10 h of hypoxia and 4 h of reoxygenation were treated with 5, 10, or 20 μmol/L gingerol. The levels of viability, apoptosis, and proteins in N2a cells were determined using MTT assays, flow cytometry, and western blotting, respectively. The binding relationship between BDNF and miR‐210 was studied using a dual luciferase reporter assay. The expression levels of miR‐210 and BDNF were determined using qPCR. Gingerol repressed the increase in apoptosis and decrease in viability observed in response to hypoxia/reoxygenation. Gingerol increased Bcl‐2, BDNF, and TrkB levels and reduced Bax and cleaved caspase 3 levels after hypoxia/reoxygenation. Gingerol evoked decreased expression of miR‐210. Inhibition of miR‐210 resulted in increased viability and reduced apoptosis along with increased levels of Bcl‐2, BDNF, and TrkB and reduced levels of Bax and cleaved caspase 3 after hypoxia/reoxygenation. Additionally, the miR‐210 mimic reversed changes induced by gingerol. The cotransfection of the miR‐210 mimic and wild type BDNF led to decreased luciferase activity. BDNF was negatively regulated by miR‐210. BDNF siRNA reversed these changes evoked by miR‐210 inhibition. Gingerol ameliorated hypoxia/reoxygenation‐stimulated neuronal damage by regulating the miR‐210/BDNF axis, indicating that gingerol is worthy of further application in cerebral ischemia therapy. [ABSTRACT FROM AUTHOR]

Background: Hypoxic-ischemic encephalopathy (HIE) occurs when an infant's brain has not received adequate oxygen and blood supply, resulting in ischemic and hypoxic damage. Currently, supportive care and hypothermia therapy have been the standard treatment for HIE. However, there are still over 20% of treated infants died and 19–30% survived with significant disability. HIE animal model was first established by Rice et al., involving the ligation of one common carotid artery followed by hypoxia. In this study, we investigated human umbilical cord blood (HUCB) and its two components mononuclear cell (MNC) and red cell fraction (RCF) in both short and long term study using a modified HIE rat model. Methods: In this modified HIE model, both common carotid arteries were occluded, breathing 8% oxygen in a hypoxic chamber for 60-min, followed by the release of the common carotid arteries ligature, mimicking reperfusion injury. For cell therapeutic study, cells were intravenously injected to HIE rat pups, and both behavioral and histological changes were assessed at selected time points. Result: Statistically significant behavioral improvements were demonstrated on Day 7 and 1 month between saline treated HIE rats and UCB/MNC treated rats. However, at 3 months, the therapeutic improvements were only showed between saline treated HIE animals and MNC treated HIE rats. For histological analysis 1 month after cell injection, the number of functional neurons were statistically increased between saline treated HIE and UCB/MNC/RCF treated HIE rats. At 3 months, the significant increase in functional neurons was only present in MNC treated HIE rats. Conclusion: We have used a bilateral temporary occlusion of 60 min, a moderately brain damaged model, for cell therapeutic studies. HUCB mononuclear cell (MNC) therapy showed benefits in neonatal HIE rats in both short and long term behavioral and histological assessments. [ABSTRACT FROM AUTHOR]

Objective: Diffusion spectrum imaging (DSI) was used to quantitatively study the changes in the trigeminal cistern segment in patients with trigeminal neuralgia (TN) and to further explore the value of acquiring DSI data from patients with TN. Methods: To achieve high-resolution fiber tracking, 60 patients with TN and 35 healthy controls (HCs) were scanned with conventional magnetic resonance imaging (MRI) and DSI. The patients and the members of the control group were compared within and between groups. The correlations between quantitative parameters of DSI and the visual analog scale (VAS), and symptom duration and responsible vessel types were analyzed. Results: Compared with unaffected side of patients in the TN group, the affected side showed significantly decreased quantitative anisotropy (QA) (p < 0.001), fractional anisotropy (FA) (p = 0.001), and general FA (GFA) (p < 0.001). The unaffected side exhibited significantly decreased QA (p + 0.001), FA (p = 0.001), and GFA (p < 0.001) and significantly increased axial diffusivity (AD) (p = 0.036) compared with the affected side of patients in the TN group and the average values of HCs. There were significantly decreased QA (p = 0.046) and FA (p = 0.008) between the unaffected side of patients and the average values of HCs. GFA can evidently distinguish arteries, veins, and features of unaffected side in TN patients. Conclusion: Using high-resolution fiber tracking technology, DSI can provide quantitative information that can be used to detect the integrity of trigeminal white matter in patients with TN and can improve the understanding of the disease mechanism. [ABSTRACT FROM AUTHOR]

Background: Recent investigations have suggested that long noncoding RNA (lncRNA) MIR22HG is commonly dysregulated in multiple types of malignancies. Nevertheless, the role of these MIR22HG in human colorectal carcinoma (CRC) are not well explored. Materials and Methods: Quantitative real-time polymerase chain reaction (qPCR) and in situ hybridization (ISH) assay were used to measure the expression of MIR22HG. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, and migration, as well as invasion assays, were utilized to determine the roles of MIR22HG on growth, apoptosis, migration, and invasiveness of CRC cell. The expression of E-cadherin and N-cadherin was measured using Western blotting and immunohistochemistry staining assay. CRC cell growth in vivo was analyzed using nude mice xenograft. Results: The qPCR and ISH assay revealed that MIR22HG was downregulated in CRC sample compared with in normal tissue. MIR22HG was also significantly downexpressed in CRC cells compared with that in normal colonic epithelial cell line. Overexpression of MIR22HG inhibited the growth, migration ability, and invasiveness of CRC cell in vitro. In addition, MIR22HG suppressed the epithelial-mesenchymal transition (EMT) and induced the apoptosis of human CRC cell. Moreover, the authors demonstrated that MIR22HG inhibited the tumor growth of CRC cell and regulated the expression of EMT markers (E-cadherin and N-cadherin) in vivo. Conclusion: Altogether, these results imply that lncRNA MIR22HG restrained the aggressive phenotypes of CRC cell. [ABSTRACT FROM AUTHOR]

Glioblastoma multiforme (GBM) is the most frequent, lethal, and aggressive tumor of the central nervous system in adults. In this study, we found for the first time that moschamindole (MCD), a rare phenolic amide with 8/6/6/5/5 rings, is a major bioactive constituent derived from Phragmites communis Trin (Poaceae) that exhibits a potential cytotoxic effect on both TMZ‐resistant GBM cell lines and xenograft models. MCD‐induced intrinsic apoptosis signals and mitochondrial dysfunction were confirmed by cell cycle arrest, caspase‐3/7 activation, and membrane potential depolarization. Furthermore, investigations exploring the mechanism showed that MCD specifically inhibits Mia40‐mediated oxidative folding of mitochondrial intermembrane space (IMS) proteins via PCR assay and immunoblot analysis. MCD relies on its positive charge to associate with mitochondrial oxidative respiration, thus blocking energy metabolism and inducing apoptosis. Overexpression and upregulation of Mia40 were proven to reverse MCD‐induced apoptosis and were correlated with the chemoresistance of GBM in vitro and in vivo, respectively. Taken together, our study demonstrates that Mia40 is a potential target of the chemoresistance of glioblastoma and suggests that MCD might be a potential agent for the individualized treatment of chemoresistant GBM based on mitochondrial metabolic characteristics and Mia40 expression. [ABSTRACT FROM AUTHOR]

Glioblastoma multiforme (GBM) is a highly aggressive type of brain tumour. Patients with GBM respond poorly to chemotherapy and have poor survival outcomes. Neuron-glial antigen 2 (NG2), also known as chondroitin sulphate proteoglycan 4 (CSPG4), has been shown to contribute to critical processes, such as cell survival, proliferation, and chemotherapy resistance, during glioma progression. In this study, we found that furanodienone (FUR), a diene-type sesquiterpene isolated from the rhizomes of Rhizoma curcumae, exhibited a potential cytotoxic effect on temozolomide (TMZ)-resistant GBM cells in vitro by inhibiting CSPG4 and related signalling pathways. Studies investigating the mechanism demonstrated that FUR suppressed CSPG4-Akt-ERK signalling, inflammatory responses, and cytokine levels but activated caspase-dependent pathways and mitochondrial dysfunction. Furthermore, an immunofluorescence assay and a dual-luciferase reporter assay revealed that inhibition of EGR1-mediated transcription might have contributed to the FUR-dependent blockade of CSPG4 signalling and glioma cell survival. These results established a link between FUR-induced CSPG4 inhibition and the suppression of EGR1-dependent transcription. Attenuation of ERK1/2 and cytokine signalling might have generated the EGR1-dependent negative feedback loop of the CSPG4 pathway during FUR-induced apoptosis. These findings suggested that FUR could be a therapeutic candidate for the treatment of malignant glioma via targeting CSPG4 signalling. [ABSTRACT FROM AUTHOR]

A new bismuth(V)-based coordination complex Bi(phenyl)3(2,3-dfa)2 (1) based on two different donor organic ligands has been obtained by the reaction between triphenylbismuth, hydrogen peroxide, and 2,3-difluorobenzoic acid (molar ratio 1:1:2, respectively) in ether. The structure compound of 1 was established by singe crystal X-ray diffraction (SCXRD) and its phase purity was confirmed via the power X-day diffraction measurements (PXRD). The SXRD analysis reveals that the structure of 1 locates in the space group P-1 with the central Bi atom possessing a distorted trigonal-bipyramidal coordination with acylate groups in the axial positions. Furthermore, the morphology of complex 1 could be downsized into nanosized region via a green hand grinding technique. In addition, the anti-skin cancer activity of 1 in nano-region has been studied via cell counting Kit-8 (CCK-8) assay and flow cytometric analysis, which reveals its promising anticancer activity. [ABSTRACT FROM AUTHOR]

Objective: This study aims to improve the coagulation time, strength, and construction cost of magnesium phosphate cement. Methods: We analyzed the microstructure changes in the hardened magnesium phosphate cement paste through qualitative analysis, quantitative test, microscopic examination, and research regarding adding different concentrations of acetic acid on magnesium phosphate cement slurry time, effects of flow resistance, and mechanical properties. Results: When a moderate amount of AA was used, the setting time of MAPC mortar was significantly prolonged but was later reduced as the concentration increased. In the early phase, the degree of MAPC mortar hydration increased, whereas compressive strength significantly increased initially and increased slowly in the later phase. The crystal morphology and size of MAPC hydrates changed, and hardened MAPC became more compact in structure. The AA absorbed some ammonia in the MAPC condensation. Conclusion: Acetic acid can effectively regulate coagulation time, induce early hydration reaction rate, and improve the performance of magnesium phosphate cement, which can reduce the construction cost of magnesium phosphate cement. [ABSTRACT FROM AUTHOR]

Reactive oxygen species (ROS) are increased in inflammatory bowel disease (IBD) and have been implicated as mediators of intestinal inflammation. We investigated the hypothesis that N-acetylcysteine (NAC) as a glutathione (GSH) precursor attenuates disease progression in a murine dextran sodium sulfate (DSS)-induced colitis model. A colitis model was induced by adding 5% DSS into the drinking water for 7 days. BALB/c mice were injiciatur enema with saline, 5-ASA, N-acetylcysteine, respectively, and free drinking water as control group. DSS-treated mice developed severe colitis as shown by bloody diarrhea, weight loss, and pathologic involvement. Colon lengths were significantly decreased in DSS-treated mice with decreased GSH activity too (P < 0.01). ROS in the colon, the level of interleukin 1 beta (IL-1 beta) in colonic mucosa, serum tumor necrosis factor a (TNF-alpha), MPO, and MDA were significantly increased in DSS-treated animals (P < 0.01), with decreased PON1 activity (P < 0.01). However, NAC significantly decreased colonic MPO activity, ROS, TNF-alpha and IL-1 beta levels and increased PON1 activity and GSH concentration. Moreover, NAC attenuated the macroscopic colonic damage and the histopathologic changes-induced by DSS while similar to 5-ASA group. These results suggest that NAC may be effective in the treatment of colitis through its up-regulating PON1 and scavenging oxygen-derived free radicals. [ABSTRACT FROM AUTHOR]

Abstract: Ion mobility spectrometry (IMS) is a very fast, highly sensitive, and inexpensive technique, it permits efficient monitoring of volatile organic compounds like alcohols. In this article, positive ion mobility spectra for six alcohol organic compounds have been systematically studied for the first time using a high-resolution IMS apparatus equipped with a discharge ionization source. Utilizing protonated water cluster ions (H2O)nH+ as the reactant ions and clean air as the drift gas, alcohol organic compounds, ethanol, 1-propanol, 2-propanol, 1-butanol, 1-pentanol and 2-octanol, all exhibit product ion characteristic peaks in their respective ion mobility spectrometry, that is a result of proton transfer reactions between the alcohols and reaction ions (H2O)nH+. The mixture of these alcohols, including two isomers, has been detected, and the results showed that they could be distinguished effectively in the ion mobility spectrum. The reduced mobility values have been determined, which are in very well agreement with the traditional 63Ni-IMS experimental values. The exponential dilution method was used to calibrate the alcohol concentrations, and a detection limit available for the alcohols is in order of magnitude of a few ng/L. [Copyright &y& Elsevier]

Glioblastoma (GBM) is a highly aggressive brain tumor. During screening work, we found a new compound named phragmunis A (PGA), which is derived from the fruitbody of Trogia venenata , exhibits a potential cytotoxic effect on patient-derived recurrent GBM cells and temozolomide (TMZ)-resistant cell lines. The present study was designed to investigate the potential molecular mechanism of the anti-glioma effects of PGA in vitro and in vivo. Studies investigating the mechanism revealed that PGA diminished the binding efficiency of ETS family of transcription factor (ELK1) and Serum response factor (SRF), and suppressed ELK1-SRF complex-dependent transcription, which decreased the transcriptional levels of downstream genes Early growth response protein 1 (EGR1)-Polycomb ring finger (BMI1), thus inducing the imbalanced regulation between Myeloid cell leukaemia-1 (MCL1) and F-Box and WD repeat domain containing 7 (FBXW7). Finally, orthotopic xenograft models were established to confirm the anti-glioma effect of PGA on tumour growth. We showed, for the first time, that the cytotoxic effects of PGA occurred by inducing MCL1 inhibition and FBXW7 activation by blocking ELK1-SRF complex-dependent transcription. The blockage of ELK1-mediated transcription resulted in the suppression of EGR1-BMI1, which led to the upregulation of FBXW7 expression and downregulation of MCL1. These findings suggested that PGA could be a therapeutic drug candidate for the treatment of recurrent GBM by targeting the ELK1-SRF complex. [Display omitted] • Phragmunis A (PGA) is a new compound isolated from the fruitbody of Trogia venenata. • PGA could overcome temozolomide resistance and be a drug candidate for the treatment of GBM. • PGA could suppress the binding efficiency of ELK1-SRF and the complex-dependent transcription. • PGA could break the feedback between MCL1 and FBXW7 via inhibition of EGR1-BMI1. [ABSTRACT FROM AUTHOR]

Background: Glioblastoma multiforme (GBM) is the most frequent, lethal and aggressive tumour of the central nervous system in adults. The discovery of novel anti-GBM agents based on the isocitrate dehydrogenase (IDH) mutant phenotypes and classifications have attracted comprehensive attention.Purpose: Diterpenoids are a class of naturally occurring 20-carbon isoprenoid compounds, and have previously been shown to possess high cytotoxicity for a variety of human tumours in many scientific reports. In the present study, 31 cassane diterpenoids of four types, namely, butanolide lactone cassane diterpenoids (I) (1-10), tricyclic cassane diterpenoids (II) (11-15), polyoxybutanolide lactone cassane diterpenoids (III) (16-23), and fused furan ring cassane diterpenoids (IV) (24-31), were tested for their anti-glioblastoma activity and mechanism underlying based on IDH1 mutant phenotypes of primary GBM cell cultures and human oligodendroglioma (HOG) cell lines.Results: We confirmed that tricyclic-type (II) and compound 13 (Caesalpin A, CSA) showed the best anti-neoplastic potencies in IDH1 mutant glioma cells compared with the other types and compounds. Furthermore, the structure-relationship analysis indicated that the carbonyl group at C-12 and an α, β-unsaturated ketone unit fundamentally contributed to enhancing the anti-glioma activity. Studies investigating the mechanism demonstrated that CSA induced oxidative stress via causing glutathione reduction and NOS activation by negatively regulating glutaminase (GLS), which proved to be highly dependent on IDH mutant type glioblastoma. Finally, GLS overexpression reversed the CSA-induced anti-glioma effects in vitro and in vivo, which indicated that the reduction of GLS contributed to the CSA-induced proliferation inhibition and apoptosis in HOG-IDH1-mu cells.Conclusion: Therefore, the present results demonstrated that compared with other diterpenoids, tricyclic-type diterpenoids could be a targeted drug candidate for the treatment of secondary IDH1 mutant type glioblastoma through negatively regulating GLS. [ABSTRACT FROM AUTHOR]

The thermally induced cross-linked esterification occurs for the formation of eccentric inorganic-polymeric nanoparticles. By taking advantage of eccentricity, Ag-PSMA eccentric structure is converted to raspberry-like Au-based Janus nanoparticles. [ABSTRACT FROM AUTHOR]

Kallmann syndrome (KS) is an inherited developmental disorder defined as the association of hypogonadotropic hypogonadism and anosmia or hyposmia. KS has been shown to be a genetically heterogeneous disease with different modes of inheritance. However, variants in any of the causative genes identified so far are only found in approximately one third of KS patients, thus indicating that other genes or pathways remain to be discovered. Here, we report a large Han Chinese family with inherited KS which harbors two novel variants, KAL1 c.146G>T (p.Cys49Phe) and mitochondrial tRNAcys (m.5800A>G). Although two variants can't exert obvious effects on the migration of GnRH neurons, they show the synergistic effect, which can account for the occurrence of the disorder in this family. Furthermore, the disturbance of the mitochondrial cysteinyl-tRNA pathway can significantly affect the migration of GnRH cells in vitro and in vivo by influencing the chemomigration function of anosmin-1. Our work highlights a new mode of inheritance underlay the genetic etiology of KS and provide valuable clues to understand the disease development. [ABSTRACT FROM AUTHOR]

Abstract: The selection of carrier transporting layer in polymer solar cells is an important issue because the nature and direction of carrier transport can be manipulated by inserting different functional layers in the device structure. In this work, we report a very efficient inverted polymer solar cell (PSC) system based on regioregular poly(3-hexylthiophene) and a n-type acceptor, bis-indene[C60]. With a pair of metal oxides and the insertion of TiO2 nanorods electron collecting layer between the ZnO thin film and the active layer, the device efficiency can be greatly improved. The contact area between the active layer and the electron collecting layer, as well as the thickness of active layer, can be increased with the incorporation of TiO2 nanorods. As a result, photocurrent can be enhanced due to more absorption of light and more charge separation interface. In addition, the larger contact area and the crystalline TiO2 nanorods provide a more efficient transporting route for the carriers to the cathode. The most efficient device demonstrated shows a high power conversion efficiency of 5.6% with the inverted structure. [Copyright &y& Elsevier]