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Flexible sensors for hand gesture recognition and human–machine interface (HMI) applications have witnessed tremendous advancements during the last decades. Current state‐of‐the‐art sensors placed on fingers or embedded into gloves are incapable of fully capturing all hand gestures and are often uncomfortable for the wearer. Herein, a flake‐sphere hybrid structure of reduced graphene oxide (rGO) doped with polystyrene (PS) spheres is fabricated to construct the highly sensitive, fast response, and flexible piezoresistive sensor array, which is ultralight in the weight of only 2.8 g and possesses the remarkable curved‐surface conformability. The flexible wrist‐worn device with a five‐sensing array is used to measure pressure distribution around the wrist for accurate and comfortable hand gesture recognition. The intelligent wristband is able to classify 12 hand gestures with 96.33% accuracy for five participants using a machine learning algorithm. To showcase our wristband, a real‐time system is developed to control a robotic hand via the classification results, which further demonstrates the potential of this work for HMI applications.

The goal of this work is to extend prior work on cardiac MR Fingerprinting (cMRF) using rosette k-space trajectories to enable simultaneous T1, T2, and proton density fat fraction (PDFF) mapping in the heart. A rosette trajectory designed for water-fat separation at 1.5T was used in a 2D ECG-triggered 15-heartbeat cMRF sequence. Water and fat specific T1 and T2 maps were generated from the cMRF data. A PDFF map was also retrieved using Hierarchical IDEAL by segmenting the rosette cMRF data into multiple echoes. The accuracy of rosette cMRF in T1, T2, and PDFF quantification was validated in the ISMRM/NIST phantom and an in-house built fat fraction phantom, respectively. The proposed method was also applied for myocardial tissue mapping of healthy subjects and cardiac patients at 1.5T. T1, T2, and PDFF values measured using rosette cMRF in the ISMRM/NIST phantom and the fat fraction phantom agreed well with the reference values. In 16 healthy subjects, rosette cMRF yielded T1 values which were 80~90 ms higher than spiral cMRF and MOLLI. T2 values obtained using rosette cMRF were ~3 ms higher than spiral cMRF and ~5 ms lower than conventional T2-prep bSSFP method. Rosette cMRF was also able to detect abnormal T1 and T2 values in cardiomyopathy patients and may provide more accurate maps due to effective fat suppression. In conclusion, this study shows that rosette cMRF has the potential for efficient cardiac tissue characterization through simultaneous quantification of myocardial T1, T2, and PDFF.

Abstract Wearable devices can be used for monitoring vital physical and physiological signs remotely, as well as for interacting with computers. Widespread adoption of wearables is somewhat hindered by the duration time they can be used without re‐recharging. To ensure uninterrupted operation, these devices need a constant and battery‐less energy supply. Scavenging energy from the wearable's surroundings is, therefore, an essential step towards achieving genuinely autonomous and self‐powered devices. While energy harvesting technologies may not completely eliminate the battery storage unit, they can ensure a maximum duration of use. Piezoelectric energy harvesting is a promising and efficient technique to generate electricity for powering wearable devices in response to body movements. Consequently, we systematically survey the range of technologies used for scavenging energy from the human body, with a particular focus on the upper‐limb area. According to our review and in comparison to other upper limb locations, highest power densities can be achieved from piezoelectric transducers located on the wrist. For short and fast battery charging needs, we therefore review the range of materials, architectures and devices used to scavenge energy from these upper‐limb areas. We provide comparisons as well as recommendations and possible future directions for harvesting energy using this promising technique.

Study Question: What are the features of FAM71D (Family with sequence similarity 71, member D) expression and is there an association between FAM71D expression and sperm motility?Summary Answer: FAM71D, a novel protein exclusively expressed in the testis, is located in sperm flagella and is functionally involved in sperm motility.What Is Known Already: Some testis-specific proteins have been reported as potential diagnostic biomarkers to evaluate the spermatogenesis process and sperm quality. We have identified a novel testis-specific protein, FAM71D, through microarray data analysis, yet little is known about its expression and function.Study Design, Size, Duration: FAM71D mRNA and protein expression was quantified during mouse testis development. Its localization in germ cells was detected by dual-labeled immunostaining in testis sections and sperm smears. The clinical significance was assessed by comparing FAM71D expression in spermatozoa from normozoospermic controls and asthenozoospermic patients.Participants/materials, Setting, Methods: Testes were dissected from C57BL/6 J male mice at postnatal ages of 1, 2, 3, 4, 6, 8 weeks and 6 months, and sperm was collected from cauda epididymides of adult mice by the swim-up method. Human spermatozoa were isolated from 100 human semen samples by density gradient Percoll centrifugation. RT-qPCR and western blot were performed to semi-quantify the expression of FAM71D in mouse testis, and in the ejaculated spermatozoa of normozoospermic controls and asthenozoospermic patients. Immunofluorescence staining was used to detect the localization of FAM71D. Co-immunoprecipitation assay was performed to evaluate the interaction between FAM71D and calmodulin. An antibody blocking assay was employed to assess the role of FAM71D in sperm motility.Main Results and the Role Of Chance: Our results showed that FAM71D was exclusively expressed in the testis in an age-dependent manner. FAM71D expression exhibited dynamic change in the cytoplasm of spermatids during spermiogenesis and was finally retained in sperm flagella. FAM71D could interact with calmodulin. Use of anti-FAM71D antibody on sperm significantly decreased sperm motility. Expression level of FAM71D was markedly reduced in the ejaculated spermataozoa of asthenozoospermic patients (P < 0.05), and this was correlated with sperm progressive motility (r = 0.7435, P < 0.0001).Large Scale Data: N/A.Limitations, Reasons For Caution: The sample size was limited and it is necessary to verify the correlation of FAM71D expression with sperm motility in larger cohorts. Furthermore, our results were descriptive and follow-up studies would be needed to elucidate the detailed role of FAM71D in sperm motility.Wider Implications Of the Findings: This is the first systematic study to document the expression of endogenous FAM71D and a function for FAM71D in sperm motility. It provides new insights into our understanding of sperm motility regulation and causes of male infertility.Study Funding/competing Interests: This study was funded by the National Natural Science Foundation of China, Guangdong Natural Science Foundation and the Shenzhen Project of Science and Technology. The authors have no competing interests. [ABSTRACT FROM AUTHOR]

Sturge-Weber syndrome (SWS) is a rare neurocutaneous disorder whose etiology remains unclear. To investigate the genetic contribution underlying this disease, the genetic variants of a 4-generation family with a history of SWS was analyzed in the present study. SWS was diagnosed in 3 of the family members (II-1, III-11 and IV-6). Sanger sequencing was performed to identify mutations in G protein subunit aq (GNAQ) and RAS p21 protein activator 1 exons in the 3 patients with SWS and other unaffected family members. Notably, a non-synonymous single-nucleotide variant at codon 183 on exon 4 of the GNAQ gene was identified as the only pathogenic site. This variant generated a substitution of arginine (R) with glutamine and resulted in a change of function of the encoded protein. Evolutionary conservation analysis revealed that the mutated residue 183 (R) of GNAQ is highly conserved across several vertebrate species. Furthermore, an immunofluorescence staining assay demonstrated that the substitution of arginine with glutamine resulted in a change in the sub-cellular localization of the GNAQ recombinant protein in vitro. These findings may aid in the development of novel diagnostic markers and/or therapeutic targets for the treatment of patients with familial SWS. [ABSTRACT FROM AUTHOR]

Abstract Aim Human Immunodeficiency Virus (HIV) patients commonly experience dyspnea for which an immediate cause may not be always apparent. In this prospective cohort study of HIV patients with exercise limitation, we use cardiopulmonary exercise testing (CPET) coupled with exercise cardiovascular magnetic resonance (CMR) to elucidate etiologies of dyspnea. Methods and results Thirty-four HIV patients on antiretroviral therapy with dyspnea and exercise limitation (49.7 years, 65% male, mean absolute CD4 count 700) underwent comprehensive evaluation with combined rest and maximal exercise treadmill CMR and CPET. The overall mean oxygen consumption (VO2) peak was reduced at 23.2 ± 6.9 ml/kg/min with 20 patients (58.8% of overall cohort) achieving a respiratory exchange ratio > 1. The ventilatory efficiency (VE)/VCO2 slope was elevated at 36 ± 7.92, while ventilatory reserve (VE: maximal voluntary ventilation (MVV)) was within normal limits. The mean absolute right ventricular (RV) and left ventricular (LV) contractile reserves were preserved at 9.0% ± 11.2 and 9.4% ± 9.4, respectively. The average resting and post-exercise mean average pulmonary artery velocities were 12.2 ± 3.9 cm/s and 18.9 ± 8.3 respectively, which suggested lack of exercise induced pulmonary artery hypertension (PAH). LV but not RV delayed enhancement were identified in five patients. Correlation analysis found no relationship between peak VO2 measures of contractile RV or LV reserve, but LV and RV stroke volume correlated with PET CO2 (p = 0.02, p = 0.03). Conclusion Well treated patients with HIV appear to have conserved RV and LV function, contractile reserve and no evidence of exercise induced PAH. However, we found evidence of impaired ventilation suggesting a non-cardiopulmonary etiology for dyspnea.

Constructing a three-dimensional (3D) multifunctional hosting architecture and subsequent thermal infusion of molten Li to produce advanced Li composite is an effective strategy for stable Li metal anode. However, the pure liquid Li is difficult to spread across the surface of various substrates due to its large surface tension and poor wettability, hindering the production and application of Li composite anode. Herein, heteroatomic Ca is doped into molten Li to generate Li-Ca alloy, which greatly regulates the surface tension of the molten alloy and improves the wettability against carbon cloth (CC). Moreover, a secondary network composed of CaLi2 intermetallic compound with interconnected ant-nest-like lithiophilic channels is in situ formed and across the primary scaffold of CC matrix by infiltrating molten Li-Ca alloy into CC and then cooling treatment (LCAC), which has a larger and lithiophilic surface to enable uniform Li deposition into interior space of the hybrid scaffold without Li dendrites. Therefore, LCAC exhibits a long-term lifespan for 1100 h under a current density of 5 mA cm-2 with fixed areal capacity of 5 mAh cm-2. Remarkably, full cells paired with practical-level LiFePO4 cathode of 2.45 mAh cm-2 deliver superior performance.

Renal cell carcinoma (RCC) is the most common type of malignant tumor of the adult kidney and has a poor prognosis. MicroRNAs (miRs) are important in a wide range of biological and pathological processes, including cell differentiation, migration, growth, proliferation, apoptosis and metabolism. The present study aimed to determine the role exerted by miR-30a-5p in the tumorigenesis of RCC. The expression levels of miR-30a-5p in RCC tissues and RCC-derived cells were demonstrated to be significantly downregulated by real-time quantitative polymerase chain reaction (RT-qPCR). Wound scratch assay, cell proliferation assay and flow cytometric analysis revealed that the abilities of migration and proliferation of the RCC-derived cells were suppressed, whereas cell apoptosis was promoted, when miR-30a-5p was overexpressed in these cells. N-acetylgalactos aminyltransferase 7 (GALNT7) was predicted to be one target gene of miR-30a-5p by bioinformatics analysis. Luciferase reporter assay, RT-qPCR and western blotting were performed to confirm that GALNT7 is the direct conserved target of miR-30a-5p. These results suggested that miR-30a-5p has a tumor-suppressive role in the tumorigenesis of RCC. [ABSTRACT FROM AUTHOR]

Renal cell carcinoma (RCC) is the most common type of kidney cancer in adults, which is associated with poor prognosis and high recurrence. Long non-coding RNAs (lncRNAs) have been reported to be dysregulated in cancer and to be important in the regulation of carcinogenesis, thus suggesting that this class of molecules may be used as biomarkers in cancer. The lncRNA urothelial carcinoma associated 1 (UCA1) has been observed to be upregulated and tofunction as an oncogene in certain types of cancer; however, the role of UCA1 in RCC remains to be elucidated. The present study aimed to determine the expression and function of UCA1 in RCC. Quantitative polymerase chain reaction (qPCR) was used to determine the expression levels of UCA1 in 46 paired RCC and adjacent normal tissue samples. Furthermore, qPCR was used to determine the expression levels of UCA1 in four RCC cell lines compared with the human embryonic kidney 293T cell line. The impact of UCA1 on cell migration, proliferation and apoptosis was investigated by wound scratch assay, MTT and flow cytometry, respectively. The results of the present study demonstrated that UCA1 expression levels were significantly increased in RCC tissues and cells, as compared with the controls. Ectopic expression and gene silencing of UCA1 in RCC cell lines exerted opposite effects on cellular proliferation, migration and apoptosis, and the results suggested that UCA1 may function as an oncogene in RCC. These results indicated that UCA1 may be considered as a promising biomarker for diagnosis, and a therapeutic target in RCC. Further research is required to elucidate the role and target genes of UCA1 in RCC. [ABSTRACT FROM AUTHOR]

Lithium metal is a promising anode material for high energy density batteries, which is restricted from practical application by the issues including lithium dendrite, parasitic reaction and volumetric change. Herein, a strategy combing bulk and surface modification is proposed to address these problems. The bulk modification is to use Ni foam as three dimensional (3D) scaffold for direct infusion of molten Li resulting in the formation of Li-Ni composite anode, which reduces actual current density by increasing specific surface area and alleviates volumetric change in the process of Li stripping/plating. And the surface modification is to coat with ZnF2 film via sputtering, which is acted as artificial protective layer for controlling interfacial side reaction. The symmetric cell consisting of ZnF2 coated Li-Ni composite electrodes exhibits low overpotential (about 45 mV) and stable cycling over 900 h at 1 mA cm−2. Furthermore, the cell with LiCoO2 cathode delivers 110 mAh g−1 at 1 C rate after 500 cycles. Keywords: Lithium metal anode, Composite lithium, Nickel foam, Lithium dendrite, Surface modification, Lithium battery

Clear cell renal cell carcinoma (ccRCC) is the predominant and most aggressive type of kidney malignancy, however, the mechanism underlying its carcinogenesis remains to be elucidated. The present study aimed to determine the expression and function of microRNA (miR)-429 in ccRCC carcinogenesis. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-429 in ccRCC specimens. Following transfection of miR-429 synthetic mimics, the expression of miR-429 was examined and cell proliferation, cell migration, apoptosis and luciferase assays were conducted in ccRCC cell lines. The results demonstrated that expression of miR-429 was decreased in ccRCC cells. In addition, upregulation of miR-429 by transfection of mimics reduced cellular proliferation and migration, and induced apoptosis in ACHN and 786-0 cell lines. Furthermore, miR-429 decreased the 3'UTR luciferase activity of vascular endothelial growth factor (VEGF) and c-MYC, and RT-qPCR analysis demonstrated that the cancer cells transfected with miR-429 mimics exhibited decreased expression of VEGF, but not c-MYC. To the best of our knowledge, the present study was the first to reveal that downregulated miR-429 functioned as a tumor suppressor by restraining cellular proliferation and migration, and inducing apoptosis, as well as targeting VEGF in ccRCC cells. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRNAs/miRs) serve an important role in the regulation of carcinogenic pathways. RCC is the most prevalent kidney cancer that occurs in adults. miRNAs have gained increasing attention due to their association with RCC tumorigenesis, serving as biomarkers for early detection and progression monitoring, and as potential targets for molecular therapy. Upregulation of miRNA-142-3p has been previously identified in RCC tissues by microarray profile, however, its expression and function in RCC have not yet been validated. In the present study, quantitative polymerase chain reaction was performed to quantify the relative expression of miR-142-3p in 53 paired RCC and adjacent normal tissues. Furthermore, wound healing, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and flow cytometry assays were performed to analyze the impacts of miR-142-3p on cellular migration, proliferation and apoptosis. The results demonstrated that miR-142-3p was significantly upregulated in RCC tissues compared with adjacent normal tissues. Downregulation of miR-142-3p, induced by chemically synthesized miR-142-3p inhibitor, significantly suppressed cell migration and proliferation, and promoted cell apoptosis in 786-O and ACHN cells, supporting the theory that miR-142-3p may function as an oncogene in RCC. The potential clinical significance of miR-142-3p, as a biomarker and therapeutic target, provides rationale for further investigation into the miR-142-3p-mediated molecular pathway and how it is associated with RCC development. [ABSTRACT FROM AUTHOR]

Renal cell carcinoma (RCC) is the most common type of renal tumor, which has a poor prognosis. Improvements in understanding the underlying molecular biology of RCC has led to systemic treatments, which have markedly improved patient outcomes. Therefore, it is necessary and worthwhile to identify novel biomarkers for RCC. MicroRNAs (miRNAs) have been found to be important in a wide range of biological and pathological processes, including cell differentiation, migration, growth, proliferation, apoptosis and metabolism. Aberrant expression of miRNA-130b has previously been reported in tumors, however, its role in RCC remains to be elucidated. In the present study, the upregulation of miR-130b was observed in RCC tissues and cell lines using reverse transcription-quantitative polymerase chain reaction analysis, which was consistent with previous microRNA profiling in RCC. Furthermore, the effects of miR-130b on cell migration, proliferation and apoptosis were examined using a wound scratch assay, an MTT assay and flow cytometric analysis, respectively. The results demonstrated that the downregulation of miR-130b by a synthesized inhibitor inhibited cell migration, suppressed cell proliferation and induced RCC cell apoptosis. The present study was the first, to the best of our knowledge, to suggest that miR-130b may be a promising biomarker for diagnosis and a therapeutic target for the treatment of RCC. Further investigations are required to examine the roles and target genes of miR-130b in RCC. [ABSTRACT FROM AUTHOR]

Renal cell carcinoma (RCC) is the most common type of kidney cancer in adults and is associated with a poor prognosis due to a lack of early-warning signs, protean clinical manifestations, and resistance to radiotherapy and chemotherapy. Recently, increasing evidence has suggested that microRNAs (miRNAs) are involved in the proliferation, invasion and apoptosis of various types of human cancer cells. In a previous study, miRNA expression profiles from renal cell carcinoma (RCC) revealed that expression of miR-20b-5p was significantly downregulated in RCC tissues. The aim of this study was to investigate the expression and functional significance of miR-20b-5p in RCC. The expression of miR-20b-5p was quantified in 48 paired RCC tissues and cell lines, and compared with adjacent normal tissues and the 293T cell line by reverse transcription-quantitative polymerase chain reaction. The functional impact of miR-20b-5p on cell proliferation, cell migration and apoptosis in the 786-O and ACHN RCC cell lines, was determined by an 3-(4,5-dimethylthiazol-2-yl) -2,5-diphenyltetrazolium bromide assay, a scratch assay and flow cytometry. To the best of our knowledge, the present study was the first to reveal that miR-20b-5p was downregulated in RCC tissues and cell lines. It also demonstrated that upregulation of miR-20b-5p inhibited cellular migration and proliferation, and promoted cellular apoptosis, suggesting that miR-20b-5p functioned as a potential tumor suppressor. However, further studies are required to fully determine the effects of miR-20b-5p and the miR-20b-5p-mediated molecular pathway in RCC and other types of cancer. In conclusion, these results imply that miR-20b-5p may be a biomarker for early detection and prognosis prediction, as well as a therapeutic target for RCC. [ABSTRACT FROM AUTHOR]

Kidney cancer is the 14th most common cancer in the world and its prognosis remains poor due to difficult early detection and treatment. Therefore, the identification of biomarkers for early-stage renal cell carcinoma (RCC) is important. MicroRNA-106b (miR-106b) has been described as an oncogene in several types of human cancer. Previous microarray studies have suggested that miR-106b was significantly upregulated in RCC tissues compared with paired normal kidney tissues and may be a promising biomarker for the prediction of early metastasis following nephrectomy. The present study aimed to determine the expression and function of miR-106b in RCC. The expression of miR-106b in RCC tissues and cells, and in paired normal tissues and cells was determined by reverse transcription quantitative polymerase chain reaction, based on the previous sequencing results of miRNAs. Furthermore, a wound scratch assay, MTT assay and flow cytometry were performed to examine the functions of miR-106b on cell migration, proliferation and apoptosis. The results demonstrated that miR-106b was upregulated in RCC tissues and cell lines compared with control normal tissues and cell lines. Downregulation of miR-106b with a synthesized inhibitor suppressed cell migration and proliferation and induced renal cancer cell apoptosis, suggesting that miR-106b can be characterized as an oncogene in RCC. To the best of our knowledge, the present study was the first to reveal that miR-106b is upregulated and affects cellular migration, proliferation and apoptosis in RCC. Further studies are required to examine the role and target genes of miR-106b in RCC. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRNAs) have been demonstrated to exhibit abnormal expression patterns in various types of human cancer. The aim of the present study was to identify a novel tumor suppressor microRNA (miR) and investigate its physiological function and mechanism in renal cell carcinoma (RCC). The expression levels of miRNA (miR)-362-3p expres were measured in 47 pairs of RCC and adjacent normal tissue samples, using reverse transcription-quantitative polymerase chain reaction analysis. In addition, miR-362-3p was transfected into renal cancer cells to investigate its role in the regulation of cell proliferation, migration, invasion, apoptosis and cell cycle. Identification of the target gene of miR-362-3p was performed using luciferase reporter assays and western blot analyses. The results demonstrated that the expression levels of miR-362-3p were downregulated in the RCC tissue samples, compared with the adjacent normal tissue samples. The upregulation of miR-362-3p using a synthesized mimic suppressed the proliferation, migration and invasion of the renal cancer cells, and induced cell apoptosis and G1 phase arrest. Further experiments demonstrated that the overexpression of miR-362-3p resulted in decrease expression levels of nemo-like kinase. These results suggested that miR-362-3p functions as a tumor suppressor in RCC, and may serve as a potential molecular target in the treatment of RCC. [ABSTRACT FROM AUTHOR]

Androgens and the androgen receptor (AR) are of great importance to spermatogenesis and male fertility. AR knockout (ARKO) mice display a complete insensitivity to androgens and male infertility; however, the exact molecular mechanism for this effect remains unclear. In this study, we found that the expression levels of Prmt6 mRNA and protein were significantly up-regulated in the testes of ARKO mice compared to wild type (WT) mice. PRMT6 was principally localized to the nucleus of spermatogonia and spermatocytes by immunofluorescence staining. Furthermore, luciferase assay data showed that AR together with testosterone treatment suppressed Prmt6 transcription via binding to the androgen-responsive element (ARE) of the Prmt6 promoter. Moreover, knockdown of Prmt6 suppressed germ cells migration and promoted apoptosis. In addition, both of these cellular activities could not be enhanced by testosterone treatment. Taken together, these data indicate that PRMT6, which was down-regulated by AR and influenced cell migration and apoptosis of germ cells, could play a potentially important role in spermatogenesis. [ABSTRACT FROM AUTHOR]

MicroRNA (miR)-510-5p has been demonstrated to be involved in a number of types of malignancy; however, the function of miR-510-5p in renal cancer remains unclear. The present study aimed to determine the expression of miR-510-5p in renal cell carcinoma (RCC) specimens and analyzed the impact of miR-510-5p on renal cancer by 3-(4,5-dimethylthiazol-2-yl) -2,5-diphenyltetrazolium bromide, wound scratch and apoptosis assays. The results showed that miR-510-5p was significantly downregulated in RCC specimens compared with normal renal specimens. Overexpression of miR-510-5p by synthetic mature mimics reduced cell proliferation and migration and induced an increase in cell apoptosis, indicating that miR-510-5p may act as a tumor suppressor in RCC. The present study firstly revealed that downregulated miR-510-5p functioned as a tumor suppressor by reducing cellular proliferation and migration, and inducing apoptosis in RCC. Further research is required to define target genes of miR-510-5p to determine the cellular mechanism of miR-510-5p in the carcinogenesis of RCC. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRs) are small, endogenous noncoding RNAs that serve a significant function in various biologic processes, including those involved in cancer. The present study aimed to determine the expression and function of miR-16 in renal cell carcinoma (RCC). Quantitative polymerase chain reaction was used to quantify the expression of miR-16 in 48 paired RCC tissues and adjacent normal tissues. The impact of miR-16 on cell proliferation, migration and apoptosis was analyzed by transfecting miR-16 mature molecules into the renal cancer cell lines 786-O and ACHN. The results indicated that miR-16 was significantly upregulated in RCC tissues (P<0.05). Downregulation of miR-16 resulted in reduced cell proliferation and migration and increased levels of apoptosis, while overexpression of miR-16 resulted in accelerated cellular proliferation and migration, suggesting that miR-16 may function as an oncogene in RCC. The present study demonstrated for the first time, to the best of our knowledge, that miR-16 is upregulated in RCC and acts as an oncogene by inducing cellular proliferation, migration and reducing apoptosis. Further study of miR-16 in RCC may clarify the molecular mechanisms of RCC carcinogenesis and aid in the development of novel biomarkers and therapeutic options. [ABSTRACT FROM AUTHOR]

miR-125a-5p has been previously described as a tumor suppressor in numerous malignancies, however the expression and function of miR-125a-5p in renal cell carcinoma (RCC) remains to be elucidated. In the present study, to explore the potential role of miR-125a-5p in RCC, quantitative polymerase chain reaction was used to determine the expression levels of miR-125a-5p in renal cancer tissues. The influence of miR-125a-5p on cell proliferation, migration and apoptosis was also determined, using an MTT assay, a wound scratch assay and flow cytometry, respectively. The expression of miR-125a-5p was shown to be decreased in RCC and the restoration of miR-125a-5p by synthetic mimics was shown to suppress cell proliferation and migration, and induce apoptosis. The present results indicate that miR-125a-5p may function as a tumor suppressor in RCC. The present study is, to the best of our knowledge, the first to demonstrate the downregulation of miR-125a-5p in RCC, and to show the role it has in affecting cellular proliferation, migration and apoptosis. Further research is needed to define the target genes of miR-125a-5p and explore the potential of miR-125a-5p as a diagnostic or a prognostic biomarker for RCC. [ABSTRACT FROM AUTHOR]

In this paper, we present an asymmetric rectangular ring resonator based on graphene nanoribbon. The finite-difference time-domain method for three-dimensional model is used to investigate the multiple Fano resonances which can be observed in the transmission spectrum. We also study the influence of graphene structure parameters and chemical potential on Fano resonance. Furthermore, we explore the application of this structure in refractive index sensing. The sensitivity to background refractive index can reach 16494 nm/RIU. This high sensitivity makes the structure a promising biosensor.

Reactive oxygen species (ROS) can cause cell injury and death via mitochondrial-dependent pathways, and supplementation with anti-oxidants has been shown to ameliorate these processes. The c-Jun NH2-terminal kinase (JNK) pathway has been shown to play a critical role in ROS-induced cell death. To determine if targeting catalase (CAT) to the mitochondria provides better protection than cytosolic expression against H2O2-induced injury, the following two approaches were taken: 1) adenoviral-mediated transduction was performed using cytosolic (CCAT) or mitochondrial (MCAT) CAT cDNAs and 2) stable cell lines were generated overexpressing CAT in mitochondria (n = 3). Cells were exposed to 250 μM H2O2, and cell survival, mitochondrial function, cytochrome c release, and JNK activity were analyzed. Although all viral transduced cells had a transient twofold increase in CAT activity, MCAT cells had significantly higher survival rates, the best mitochondrial function, and lowest JNK activity compared with CCAT and LacZ controls. The improved protection with MCAT was observed in primary type II lung epithelial cells and in transformed lung epithelial cells. In the three stable cell lines, cell survival directly correlated with extent of mitochondrial localization (r = 0.60572, P < 0.05) and not overall CAT activity (r = -0.4550 1, P < 0.05). Data indicate that targeting of antioxidants directly to the mitochondria is more effective in protecting lung epithelial cells against ROS-induced injury. This has important implications in antioxidant supplementation trials to prevent ROS-induced lung injury in critically ill patients. [ABSTRACT FROM AUTHOR]

Prolonged exposure to supraphysiological oxygen concentrations results in the generation of reactive oxygen species, which can cause significant lung injury in critically ill patients. Supplementation with human recombinant antioxidant enzymes (AOE) may mitigate hyperoxic lung injury, but it is unclear which combination and concentration will optimally protect pulmonary epithelial cells. First, stable cell lines were generated in alveolar epithelial cells (MLE12) overexpressing one or more of the following AOE: Mn superoxide dismutase (MnSOD), CuZnSOD, or glutathione peroxidase 1. Next, A549 cells were transduced with 50-300 particles/cell of recombinant adenovirus containing either LacZ or each of the three AOE (alone or in combination). Cells were then exposed to 95% O2 for up to 3 days, with cell number and viability determined daily. Overexpression of either MnSOD (primarily mitochondrial) or CuZnSOD (primarily cytosolic) reversed the growth inhibitory effects of hyperoxia within the first 48 h of exposure, resulting in a significant increase in viable cells (P < 0.05), with 1.5- to 3-fold increases in activity providing optimal protection. Protection from mitochondrial oxidation was confirmed by assessing aconitase activity, which was significantly improved in cells overexpressing MnSOD (P < 0.05). Data indicate that optimal protection from hyperoxic injury occurs in cells coexpressing MnSOD and glutathione peroxidase 1, with prevention of mitochondrial oxidation being a critical factor. This has important implications for clinical trials in preterm infants receiving SOD supplementation to prevent acute and chronic lung injury. [ABSTRACT FROM AUTHOR]

Though lithium (Li) metal is an ideal anode material for next-generation rechargeable batteries, its application has been seriously limited by security and cyclability issues as the result of uncontrollable Li dendrite growth. To solve this problem, this paper proposes a method to suppress Li dendrite growth using melamine-derived 3D porous carbon foam decorated with graphite intercalation compounds of Li (GICs-Li) as a Li host. GICs-Li, with excellent lithiophilicity, ensures uniform Li deposition, while the 3D porous carbon foam, with ultrahigh porosity and enlarged surface area, provides pathway for Li+ transport, accommodates Li deposition as well as reduces practical current density. Thus, dendrite-free morphology of composite Li anode is realized without additional heterogeneous lithiophilic particles. In symmetric cell configuration, the composite Li anode performs stably for 500 cycles at 10 mAcm−2. In full cell configuration with Li4Ti5O12 (LTO), it exhibits a large capacity retention rate (~91%) after 700 cycles at 1.0C. Keywords: Partly lithiated graphitic carbon foam, Lithium metal anode, 3D porous current collector, Lithium dendrite, Graphite intercalation compounds of Li

Aquaporin-4 (AQP4) plays an important role in regulating water exchange across the blood-brain barrier (BBB) and brain-cerebrospinal fluid interface. Studies on AQP-4 knockout mice (AQP4-KO) have reported considerable protection from brain edema induced by acute water intoxication and ischemic stroke, identifying AQP4 as a potential target for therapeutic interventions. However, the long-term effects of chronic AQP4 suppression are yet to be elucidated. In the current study, we evaluated the physiological and structural changes in adult AQP4-KO mice using magnetic resonance imaging (MRI) and immunohistochemical analysis. Water exchange across BBB was assessed by tracking an intravenous bolus injection of oxygen-17 (17O) water (H217O) using 17O-MRI. Cerebral blood flow (CBF) was quantified using arterial spin-labeling (ASL) MRI. Capillary density was determined by immunohistochemical staining for glucose transporter-1 (GLUT1). Compared to wildtype control mice, AQP4-KO mice showed a significant reduction in peak and steady-state H217O uptake despite unaltered CBF. Interestingly, a 22% increase in cortical capillary density was observed in AQP4-KO mice. These results suggest that increased cerebral vascularization may be an adaptive response to chronic reduction in water exchange across BBB in AQP4-KO mice.

The preparations of crystal titanium dioxide (TiO2) are often time-consuming multistep processes involving high temperature. Rapid and efficient methods to obtain TiO2 with anatase or rutile phase are desirable. In this paper, we describe an ultrafast single-step method to obtain urchin-like rutile TiO2 particles via microwave irradiation. In the procedure, TiCl4 aqueous solution was used as a reactant and toluene was used as a solvent. It takes only a few minutes without any further heat treatment. The samples were characterized by scanning electron microscopy (SEM), transmission electron microscopy (TEM), X-ray diffraction (XRD), and thermal gravimetric analysis (TGA). The effect of temperature, irradiation time and the ratio of precursor to solvent on the morphology and crystal structure were studied. The results show urchin-like rutile TiO2 with high stability is formed after only 5 min microwave irradiation at 135 °C.