Miracle-dz/UniFAR-FTUs huggingface dataset:
Large-Scale Screening Assay to Measure Epidermal Growth Factor Internalization

Recently, we showed that the internalization of the epidermal growth factor (EGF) receptor is inhibited by hydrogen peroxide (H202) in human fibroblasts. In order to test the effect of various stress conditions on receptor internalization and to test a variety of antioxidants in their capacity to prevent or reduce the H202-induced inhibition of internalization, a screening assay was developed to measure the internalization in 96-well plates. In this assay, cells are exposed to biotin-conjugated EGF and the amount of internalized EGF is detected with horseradish peroxidase-conjugated streptavidin. We show that the results obtained by this new assay are comparable with those from internalization studies performed with radioactive labeled EGF. Therefore, the cellular internalization assay as presented here is a reliable method to measure EGF receptor internalization. Moreover, because elaborate processing of the cells is not required, the assay is a relatively fast and inexpensive method to study ligand-induced internalization in 96-well plates and thereby is suitable for large-scale screening of compounds or conditions interfering with this internalization.
Effects of Combined T‐ and B‐Cell Deficiency on Murine Ischemia Reperfusion Injury

B and T cells have been implicated in the pathogenesis of renal ischemia reperfusion injury (IRI); however, it is unknown if B and T cells interact in early injury responses, as seen in adaptive immune responses. Recent evidence has shown that B‐cell deficient and T‐cell deficient mice are partially protected from renal IRI. Renal IRI was induced in recombinase activating gene (RAG)‐1 deficient mice, which lack both B and T cells. RAG‐1 deficient mice from two different background strains were not protected from renal IRI. Adoptive transfer of either B or T cells into RAG‐1 deficient mice led to a significant protection of renal injury, which was independent of effects on neutrophil trafficking. Neutrophil depletion in RAG‐1 deficient mice did not protect from IRI. While deficiency of either B or T cells reduced IRI, combined lack of both is not protective. These results demonstrate that complex interactions between B and T cells are likely occurring in kidney IRI.
Research on Cooperative Game and Dynamic Mechanism of Industry-University-Research Synergistic Innovation

Innovation is the main engine of economic development. Building the industry-university-research synergistic innovation mechanism is an important measure to promote the implementation of innovation-driven development strategy. Based on the game theory, this thesis studies the cooperation strategies of industry, university and research in the process of synergistic innovation, constructs the payment functions of the four cooperation strategies, and analyzes the results of different strategies. From both the internal and external dimensions, this thesis further explores the dynamic factors and their mechanism of industry-university-research synergistic innovation and puts forward three targeted suggestions which are improving the distribution of benefits and risks, strengthening the guiding role of government and improving the intermediary service system. Keywords—enterprises, universities and institutes; synergistic Innovation; game theory; dynamic mechanism
Wing morphology and flight behavior of pelecaniform seabirds

The selective pressures associated with flight are significant factors in shaping the morphology of volant forms. Tropical seabirds are of particular interest because of their long foraging bouts, which can last hundreds of kilometers in search of unpredictable (spatially and temporally) resources. Here, we contrast wing loading (WL), aspect ratio (AR), and planform shape among five pelecaniform seabirds and correlate morphological diversity with known differences in flight strategies. Overall, WL and AR scaled with body mass. The Great Frigratebird had lower WL than that predicted, whereas the Red‐tailed Tropicbird had higher WL than that predicted. The tropicbird also exhibited a lower AR than that predicted. Visualization of planform shape was accomplished by using Thin‐plate spline relative warp analysis (TPS/RWA), and three major regions of variations were discovered: wing base, mid‐wing, and distal wing/wing tip. As expected, the three boobies were more similar than either the tropicbird or the frigatebird. The tropicbird had a broader distal wing and more rounded wing tip, associated with its greater use of flapping flight. The frigatebird showed the greatest deviation in the distal wing and wing tip associated with the high maneuverability required for aerial pursuit and kleptoparasitism. By using TPS/RWA, important differences were detected in planform shape that would have otherwise gone unnoticed when using only WL and AR. These differences correlated strongly with parameters such as maneuverability, flapping, and soaring flight. J. Morphol. , 2007. © 2007 Wiley‐Liss, Inc.
Calf Lung Surfactant Recovers Surface Functionality After Exposure to Aerosols Containing Polymeric Particles.

BACKGROUND Recent studies have shown that colloidal particles can disrupt the interfacial properties of lung surfactant and thus key functional abilities of lung surfactant. However, the mechanisms underlying the interactions between aerosols and surfactant films remain poorly understood, as our ability to expose films to particles via the aerosol route has been limited. The aim of this study was to develop a method to reproducibly apply aerosols with a quantifiable particle dose on lung surfactant films and investigate particle-induced changes to the interfacial properties of the surfactant under conditions that more closely mimic those in vivo. METHODS Films of DPPC and Infasurf® were exposed to aerosols containing polystyrene particles generated using a Dry Powder Insufflator™. The dose of particles deposited on surfactant films was determined via light absorbance. The interfacial properties of the surfactant were studied using a Langmuir-Wilhelmy balance during surfactant compression to film collapse and cycles of surface compression and expansion at a fast cycling rate within a small surface area range. RESULTS Exposure of surfactant films to aerosols led to reproducible dosing of particles on the films. In film collapse experiments, particle deposition led to slight changes in collapse surface pressure and surface area of both surfactants. However, longer interaction times between particles and Infasurf® films resulted in time-dependent inhibition of surfactant function. When limited to lung relevant surface pressures, particles reduced the maximum surface pressure that could be achieved. This inhibitory effect persisted for all compression-expansion cycles in DPPC, but normal surfactant behavior was restored in Infasurf® films after five cycles. CONCLUSIONS The observation that Infasurf® was able to quickly restore its function after exposure to aerosols under conditions that better mimicked those in vivo suggests that particle-induced surfactant inhibition is unlikely to occur in vivo due to an aerosol exposure.
Design of a continuous passive and active motion device for hand rehabilitation

This paper presents the design of a novel, portable device for hand rehabilitation. The device provides for CPM (continuous passive motion) and CAM (continuous active motion) hand rehabilitation for patients recovering from damage such as flexor tendon repair and strokes. The device is capable of flexing/extending the MCP (metacarpophalangeal) and PIP (proximal interphalangeal) joints through a range of motion of 0° to 90° for both the joints independently. In this way, typical hand rehabilitation motions such as intrinsic plus, intrinsic minus, and a fist can be achieved without the need of any splints or attachments. The CPM mode is broken into two subgroups. The first mode is the use of preset waypoints for the device to cycle through. The second mode involves motion from a starting position to a final position, but senses the torque from the user during the cycle. Therefore the user can control the ROM by resisting when they are at the end of the desired motion. During the CPM modes the device utilizes a minimum jerk trajectory model under PD control, moving smoothly and accurately between preselected positions. CAM is the final mode where the device will actively resist the movement of the user. The user moves from a start to end position while the device produces a torque to resist the motion. This active resistance motion is a unique ability designed to mimic the benefits of a human therapist. Another unique feature of the device is its ability to independently act on both the MCP and PIP joints. The feedback sensing built into the device makes it capable of offering a wide and flexible range of rehabilitation programs for the hand.
Reduced complexity on mobile sensor deployment and coverage hole healing by using adaptive threshold distance in hybrid Wireless Sensor Networks

The hybrid deployment of wireless sensors with static and mobile nodes in the monitoring area is an important issue to cover a maximum sensing area with a limited number of nodes. Furthermore, mobile sensor nodes can relocate themselves to improve coverage area in the network. In this paper, we propose a method that reduces the complexity on the relocation of initial deployment and coverage hole healing of mobile sensor nodes in the hybrid Wireless Sensor Networks (WSNs). Our method finds the best-ordered ways of mobile nodes' movement to give the shortest distance movements for mobile nodes in WSN. Adaptive threshold distance is used to eliminate the consideration of some mobile nodes, which are already occupied or situated within the threshold distance from optimal new positions. The simulation results show that the proposed methods can give much smaller calculation time to find the shortest paths for the movements of mobile nodes in WSN.
Hepatoma‐derived growth factor promotes growth and metastasis of hepatocellular carcinoma cells

We aimed to elucidate the effects of hepatoma‐derived growth factor (HDGF) on growth and metastasis of hepatocellular carcinoma (HCC) cells. Tissue microarrays with 236 HCC specimens and 18 extrahepatic metastases were utilized to detect the HDGF expression by immunohistochemistry. Meanwhile, HDGF expressions in HCC cell lines with different metastatic potentials were examined using immunofluorescence staining, real‐time PCR and western blotting. After HDGF silencing, the growth and metastatic potentials of HCC cells were evaluated by soft agar assay, invasion assay, together with tumorigenicity assay in nude mice. The gelatin zymography was performed by detecting MMP‐2 and MMP‐9 levels. Additionally, western blotting was conducted to determine the levels of total and phosphorylated ERK1/2, JNK, p38 and Akt. The results showed that HDGF was overexpressed in HCC metastasis tumour, and the expression increased with the differentiation degree of tumours (Grade I 44.0%, Grade II 48.4% and Grade III 65.6%). Consistently, HDGF levels were positively associated with the metastatic capability of HCC cells (MHCC97L < MHCC97H < HCCLM3). The growth and metastasis were suppressed by HDGF‐siRNA. Gelatinolytic activities were enhanced in the three metastatic HCC cell lines, but had no significant difference among them. The tumourigenicity and metastatic capability of HCCLM3 cells in nude mice were inhibited after silencing HDGF. Meanwhile, HDGF‐siRNA specifically suppressed the total and phosphorylated protein levels of ERK1/2, while not JNK, p38 and Akt. In conclusion, HDGF was overexpressed in HCC patients and cells, and HDGF might be closely correlated with HCC metastasis via regulating ERK signalling pathway. Copyright © 2016 John Wiley & Sons, Ltd.
Molecular Genetic Analysis of Appendiceal Mucinous Adenomas in Identical Twins, Including One With Pseudomyxoma Peritonei

Pseudomyxoma peritonei (PMP) is a clinical syndrome characterized by mucinous ascites and peritoneal lesions composed of histologically bland to low-grade adenomatous mucinous epithelium within pools of extracellular mucin, often with an associated mucinous adenoma of the appendix. There is evidence that the peritoneal lesions in PMP are clonally derived from the associated appendiceal adenoma. Little is known about the molecular genetic alterations or hereditary factors involved in the development of appendiceal mucinous tumors and PMP. We report the only known example of appendiceal mucinous adenomas in identical twin brothers, one of whom developed PMP. We analyzed the status of the K-RAS and APC genes in these tumors using digital polymerase chain reaction and digital single nucleotide polymorphism (SNP) assay. Identical K-RAS mutations were detected in the appendiceal adenoma and peritoneal tumor from the twin with PMP, whereas the adenoma from the other twin harbored a different mutation. Digital SNP analysis demonstrated loss of heterozygosity of APC only in the adenoma from the twin without PMP but not from the appendiceal or peritoneal tumors of the twin with PMP. The adjacent normal tissue in each case retained both APC alleles. The K-RAS mutational analysis supports the view that PMP is clonally derived from the associated appendiceal mucinous adenoma. The lack of loss of heterozygosity of APC in the adenoma and peritoneal tumor from the twin with PMP suggests that loss of heterozygosity of APC is not necessarily involved in the development of all appendiceal adenomas or PMP. The different types of mutations in K-RAS and the different allelic status of the APC locus in the tumors from both twins suggest that mutation in K-RAS and loss of heterozygosity of APC occurs somatically in adenomas and is independent of the identical genetic background of the twins.
Emergence of fluoroquinolone resistance in the native Campylobacter coli population of pigs exposed to enrofloxacin.

OBJECTIVE The effect of a single 5 day enrofloxacin treatment on the native Campylobacter coli population in conventionally weaned 5-week-old pigs was investigated. MATERIALS Twelve pigs were split into two groups of six: one group was treated with a therapeutic dose (15 mg/pig/day) of enrofloxacin and the other remained untreated to act as the control. Campylobacter coli were isolated from faecal samples and tested for ciprofloxacin resistance by measuring MIC values. Mutations in the quinolone resistance-determining region (QRDR) of the gyrA gene of resistant isolates were identified by sequencing and denaturing HPLC. Levels of enrofloxacin and its primary metabolite ciprofloxacin in the pig faeces were also measured by HPLC. RESULTS No quinolone-resistant C. coli (n = 867) were detected in any of the pigs prior to treatment, indicating <0.1% resistance in the group. Resistant C. coli were isolated from pigs for up to 35 days after treatment with a therapeutic dose. These resistant C. coli had MIC values of 128 mg/L and 8-16 mg/L for nalidixic acid and ciprofloxacin, respectively, and the same single point mutation causing a Thr-86 to Ile substitution in the QRDR was identified in each. The concentration of enrofloxacin in the pig faeces was 2-4 micro g/g faeces for the duration of the 5 day therapeutic treatment and was detected up to 10 days post-treatment. Ciprofloxacin was also measured and peaked at 0.6 micro g/g faeces in the treated group. CONCLUSION This study provides evidence that a single course of enrofloxacin treatment contributes directly to the emergence and persistence of fluoroquinolone resistance in C. coli.
The age distribution of primary open angle glaucoma.

Prevalence data for primary open angle glaucoma (POAG), taken from eight population surveys, was smoothed by curve-fitting to derive composite estimates with respect to quinqennial age groups from 40-44 to 85-89 years. These were applied to national population figures to provide a distribution of cases with respect to age. Estimated prevalence for age 40-89 years in mainly white Caucasian people was 1.2%, rising from 0.2% for those in their 40s to 4.3% for those in their 80s. Of the total cases, 7% were less than 55 years old, 44% were aged 55-74 years, and 49% were older. 'Implied incidence' was estimated from the prevalence results, being 0.11% per year in people aged 55 to 74 years. The analysis applied to relatively narrow definitions of POAG. If 'probable' cases and also 'ocular hypertensives requiring treatment' (of relevance for glaucoma screening) were included, the prevalence would be almost twice as high. Also, a larger proportion of potential cases for a screen would be less than 55 years old, partly because the average age of incident (i.e., newly developed) cases is less than that of prevalent (i.e., all existing) cases.
The Role of Chondroitinase as an Adjuvant to Peripheral Nerve Repair

Chondroitin sulfate proteoglycans (CSPGs) are potent inhibitors of neural regeneration in the peripheral nervous system. Following nerve injury, inhibitory CSPGs accumulate within the endoneurium and Schwann cell basal lamina of the distal nerve stump. The utilization of chondroitinase ABC (chABC) has led to a marked increase in the ability of injured axons to regenerate across gaps through the CSPG-laden extracellular matrix. Experimental models have repeatedly shown chABC to be capable of degrading the CSPGs that hinder neurite outgrowth. In this article, the characterization of CSPGs, their upregulation following peripheral nerve injury, and potential mechanisms behind their growth and inhibition are described. To date, the literature supports that the adjunct use of chABC may be beneficial to peripheral nerve repair in digesting inhibitory CSPGs. chABC has also shown some indication of synergism with other therapies, such as stem cell transplantation. Evidence supporting the use of chondroitinase as a treatment modality in nerve repair, either alone or in combination with other agents, is reviewed within. Finally, several shortcomings of chABC are addressed, notably its thermal stability and physiologic longevity - both hindering its widespread clinical adoption. Future studies are warranted in order to optimize the therapeutic benefits of the chondroitinase enzyme.
SRAM Design for 22-nm ETSOI Technology: Selective Cell Current Boosting and Asymmetric Back-Gate Write-Assist Circuit

As the semiconductor technology scales down, the read stability and write ability of a static random-access memory (SRAM) cell are degraded because of the increased mismatch among its transistors. Extremely thin silicon-on-insulator is one of the attractive candidates to reduce this mismatch, and it offers an independent back-gate control using a thin buried oxide. The implementation of back-gate control has recently attracted much interest to improve the read stability and write ability. In this paper, we propose a selective cell current (ICELL) boosting scheme (SIB) and an asymmetric back-gate control write-assist (ABC-WA) circuit. SIB enhances the read performance by selectively boosting ICELL of the SRAM cells. ABC-WA enhances the write ability by forward biasing the NMOSs at one side, which improves the write ability with reduction in the dynamic power overhead and without requiring a voltage generator. The proposed SRAM design improves the read performance and energy by 38.6% and 24.9%, respectively.
Effects of resistance training on bone mineral content and density in adolescent females.

Postmenarcheal adolescent girls performed resistance training (RT) for 26 weeks, which consisted of 4 sets of 13 exercises of varying and progressive intensity performed 3 times weekly on hydraulic resistance machines. Bone mineral was assessed by dual photon absorptiometry. Resistance training resulted in significant increases (pre-post) in biceps curl (21.4%), triceps press (21.5%), knee extension (25.1%), knee flexion (52.8%), and squat press (21.5%) strength. There were no significant differences between RT and control (C) groups initially, and no significant effects of training (pre-post) for total body (TB) or lumbar spine (LS) bone mineral content (BMC) or bone mineral density (BMD). The largest increases in LS bone mineral occurred during the first 13 weeks, and although not significant, the increases in LS BMC (g) (3.9 vs. 5.9%), LS BMC (g.cm-1) (2.6 vs. 5.9%), LS areal BMD (g.cm-2) (1.48 vs. 4.75%), and LS bone mineral apparent density (BMAD, g.cm-3) (0.47 vs. 4.13%) were greater in the RT compared with the C group during this period. In conclusion, resistance training resulted in a trend towards a transient increase in LS bone mineral during the first 13 weeks, but despite significant strength gains, there were no significant changes in TB or LS bone mineral after 26 weeks of training.
Eps1, a novel PDI‐related protein involved in ER quality control in yeast

PMA1 is an essential gene encoding the yeast plasma membrane [H+]ATPase. A pma1‐D378N mutant has a dominant‐negative effect on cell growth because both newly synthesized mutant and wild‐type Pma1 molecules are retained and degraded in the endoplasmic reticulum (ER). Like other substrates for ER‐associated degradation, Pma1‐D378N is stabilized in mutants defective in components of the ubiquitination machinery. A genetic selection was performed for eps (ER‐retained pma1 suppressing) mutants in which the growth defect caused by the D378N allele is suppressed. In an eps1 mutant, both mutant and wild‐type Pma1 molecules are allowed to travel to the plasma membrane; however, normal retention of resident ER proteins Shr3 and Kar2 is not perturbed. Eps1 is a novel membrane protein belonging to the protein disulfide isomerase (PDI) family, and Eps1 co‐localizes with Pma1‐D378N in the ER. In the absence of Pma1‐D378N, ER export of wild‐type Pma1 is not affected by eps1 deletion, but export of the plasma membrane protein Gas1 is delayed. Because Eps1 is required for retention and degradation of Pma1‐D378N, we propose a model in which Eps1 acts as a novel membrane‐bound chaperone in ER quality control.
Polymerase chain reaction multiplexing of microsatellites and single nucleotide polymorphism markers for quantitative trait loci mapping of wild house mice

We tested 96 microsatellites and 10 single nucleotide polymorphisms for their allelic distribution in two subspecies of the house mouse, Mus musculus musculus and M. m. domesticus. Sixty‐two microsatellites discriminated strain‐specific differences among nine wild‐derived ‘musculus’ and ‘domesticus’ and three ‘classical’ laboratory strains. For efficient genotyping, we optimized multiplex conditions using five microsatellites per polymerase chain reaction. All 10 single nucleotide polymorphisms were also optimized for simultaneous analysis in one reaction using SNaPshot multiplex. The uniform distribution of markers on autosomes and on the X chromosome makes these panels potentially useful tools for quantitative trait loci mapping of wild house mice.