Miracle-dz/UniFAR-FTUs huggingface dataset:
Expand your body when you look at yourself: The role of the posture in a mirror exposure task

Mirror exposure (ME) is one of the main components of the treatment of patients with eating disorders symptomatology and it has shown its effectiveness in improving several outcomes (e.g., body dissatisfaction). However, the study as to what body posture should be adopted to maximize its effectiveness has been neglected. From embodied cognition and emotion theories, the adoption of an expansive (vs. contractive) body posture has been associated with positive changes in cognitive and emotional responses. The objective of this study was to analyze the effect of adopting an expansive (vs. contractive) posture before an ME task on body-related emotions and cognitions, as well as to analyze the possible moderator and mediator variables of these relationships. The sample was composed of 68 women (age: M = 21.74, SD = 3.12) with high scores on body dissatisfaction. Participants were randomly assigned to the expansive or contractive condition, where the openness of the arms/legs and the back position were manipulated. Posture was monitored by an electronic device and participants filled out several self-reported measures. ANCOVAs, moderation, mediation, and moderated mediated analyses were performed. Results showed that women in the expansive condition showed higher positive emotions after the ME. Moreover, exploratory analyses showed that adopting an expansive posture improved positive emotions, leading to improvements in negative emotions, body image satisfaction, and appraisal of the person’s own body. Psychological interventions should explore the value of holding an expansive posture before the ME in women with body dissatisfaction.
High corrosion resistance Ni-reduced graphene oxide nanocomposite coating

Abstract This paper presents a high corrosion resistance Ni-graphene composite coating fabricated by co-electrodeposition on Cu substrate. First, GO was synthesized by improved Hummers’ method, and then different concentrations of GO aqueous solution were introduced to Ni Watt’s bath. During electrodeposition, GO and Ni ions were reduced simultaneously to form composite coating. The phase structure and morphology were covered by X-ray diffraction and scanning electron microscopy analysis, respectively. Atomic force microscopy (AFM) was employed to identify the surface topography of the coatings. Raman spectroscopy, Fourier transform infrared spectroscopy (FTIR), and electrochemical impedance spectroscopy (EIS) were used to study the synthesis of GO and its reduction during the plating process. Corrosion resistance of nanocomposite and that of pure Ni coating were compared by applying potentiodynamic polarization spectroscopy (PDS). The results showed that by increasing the amount of graphene oxide in solution, there has been a significant reduction in corrosion current density. As the EIS result showed, the high amount of GO reduction was obtained in GO concentration of 0.6 mg ml−1 and current density of 8 A dm−2. It is in a good agreement with data obtained from PDS. Analyses showed that the corrosion current density of corresponding coating was improved up to 0.2 μA cm−2, which means an improvement of about 100 times compared to pure Ni coating.
Intramuscular triglyceride synthesis: importance in muscle lipid partitioning in humans.

Intramuscular triglyceride (IMTG) concentration is elevated in insulin-resistant individuals and was once thought to promote insulin resistance. However, endurance-trained athletes have equivalent concentration of IMTG compared with individuals with type 2 diabetes, and have very low risk of diabetes, termed the "athlete's paradox. " We now know that IMTG synthesis is positively related to insulin sensitivity, but the exact mechanisms for this are unclear. To understand the relationship between IMTG synthesis and insulin sensitivity, we measured IMTG synthesis in obese control subjects, endurance-trained athletes, and individuals with type 2 diabetes during rest, exercise, and recovery. IMTG synthesis rates were positively related to insulin sensitivity, cytosolic accumulation of DAG, and decreased accumulation of C18:0 ceramide and glucosylceramide. Greater rates of IMTG synthesis in athletes were not explained by alterations in FFA concentration, DGAT1 mRNA expression, or protein content. IMTG synthesis during exercise in Ob and T2D indicate utilization as a fuel despite unchanged content, whereas IMTG concentration decreased during exercise in athletes. mRNA expression for genes involved in lipid desaturation and IMTG synthesis were increased after exercise and recovery. Further, in a subset of individuals, exercise decreased cytosolic and membrane di-saturated DAG content, which may help explain insulin sensitization after acute exercise. These data suggest IMTG synthesis rates may influence insulin sensitivity by altering intracellular lipid localization, and decreasing specific ceramide species that promote insulin resistance.
High glucose induces podocyte epithelial-to-mesenchymal transition by demethylation-mediated enhancement of MMP9 expression

Abnormal expression of matrix metalloproteinase 9 (MMP9) is correlated with podocyte epithelial-to-mesenchymal transition (EMT) in diabetic nephropathy (DN). However, the mechanisms underlying this process are not well defined. Site-specific demethylation may sustain high expression levels of target genes. In the present study, in order to investigate the association between DNA demethylation of MMP9 promoter and podocyte EMT in DN, human podocytes were cultured in high-glucose (HG) medium and a rat model of DN was established by intraperitoneal injection of streptozotocin (STZ) to determine whether site-specific demethylation of the MMP9 promoter was involved in regulating podocyte EMT in DN. The MTT assay was used to assess the effects of HG culture on the growth of podocytes, and the demethylation status of the MMP9 promoter was assessed by bisulfite sequencing polymerase chain reaction. mRNA and protein expression levels of MMP9, α-smooth muscle actin (α-SMA), podocalyxin and fibronectin-1 in podocytes were assessed by reverse transcription-quantitative PCR (RT-qPCR) and western blot analyses. The results demonstrated that HG treatment up regulated the expression of MMP9, α-SMA and fibronectin-1, but down regulated the expression of podocalyxin in podocytes. The MMP9 promoter region was revealed to contain a variety of demethylated CpG sites, and HG treatment reduced the rate of MMP9 promotermethylation, which, in turn, enhanced its promoter activity. In summary, these data suggested that demethylation of the MMP9 promoter may serve an important role in podocyte EMT in DN. The demethylation status of the MMP9 promoter maybe used as an important prognostic marker of DN in clinic.
Sensory Eye Dominance in Treated Anisometropic Amblyopia

Amblyopia results from inadequate visual experience during the critical period of visual development. Abnormal binocular interactions are believed to play a critical role in amblyopia. These binocular deficits can often be resolved, owing to the residual visual plasticity in amblyopes. In this study, we quantitatively measured the sensory eye dominance in treated anisometropic amblyopes to determine whether they had fully recovered. Fourteen treated anisometropic amblyopes with normal or corrected to normal visual acuity participated, and their sensory eye dominance was assessed by using a binocular phase combination paradigm. We found that the two eyes were unequal in binocular combination in most (11 out of 14) of our treated anisometropic amblyopes, but none of the controls. We concluded that the treated anisometropic amblyopes, even those with a normal range of visual acuity, exhibited abnormal binocular processing. Our results thus suggest that there is potential for improvement in treated anisometropic amblyopes that may further enhance their binocular visual functioning.
MicroRNA-138-5p regulates neural stem cell proliferation and differentiation in vitro by targeting TRIP6 expression

Research on neural stem cells (NSCs) has recently focused on microRNAs (miRNAs), a class of small non-coding RNAs that have crucial roles in regulating NSC proliferation and differentiation. In the present study, a quantitative-polymerase chain reaction assay revealed that the expression of miRNA (miR)-138-5p was significantly decreased during neural differentiation of NSCs in vitro. Overexpression of miR-138-5p reduced NSC proliferation and increased NSC differentiation. Furthermore, suppression of miR-138-5p via transfection with a miRNA inhibitor enhanced NSC proliferation and attenuated NSC differentiation. Additionally, expression of thyroid hormone receptor interacting protein 6 (TRIP6), a critical regulator of NSCs, was negatively correlated with the miR-138-5p level. A luciferase assay demonstrated that miR-138-5p regulate TRIP6 by directly binding the 3′-untranslated region of the mRNA. Additionally, upregulation of TRIP6 rescued the NSC proliferation deficiency induced by miR-138-5p and abolished miR-138-5p-promoted NSCs differentiation. By contrast, downregulation of TRIP6 produced the opposite effect on proliferation and differentiation of NSCs transfected with anti-miR-138-5p. Taken together, the data suggest that miR-138-5p regulates NSCs proliferation and differentiation, and may be useful in developing novel treatments for neurological disorders via manipulation of miR-138-5p in NSCs.
FAK Regulates Intestinal Epithelial Cell Survival and Proliferation during Mucosal Wound Healing

Background Following damage to the intestinal epithelium, restoration of epithelial barrier integrity is triggered by a robust proliferative response. In other tissues, focal adhesion kinase (FAK) regulates many of the cellular processes that are critical for epithelial homeostasis and restitution, including cell migration, proliferation and survival. However, few studies to date have determined how FAK contributes to mucosal wound healing in vivo. Methodology and Principal Findings To examine the role of FAK in intestinal epithelial homeostasis and during injury, we generated intestinal epithelium (IE)-specific conditional FAK knockout mice. Colitis was induced with dextran-sulfate-sodium (DSS) and intestinal tissues were analyzed by immunohistochemistry and immunoblotting. While intestinal development occurred normally in mice lacking FAK, FAK-deficient animals were profoundly susceptible to colitis. The loss of epithelial FAK resulted in elevated p53 expression and an increased sensitivity to apoptosis, coincident with a failure to upregulate epithelial cell proliferation. FAK has been reported to function as a mechanosensor, inducing cyclin D1 expression and promoting cell cycle progression under conditions in which tissue/matrix stiffness is increased. Collagen deposition, a hallmark of inflammatory injury resulting in increased tissue rigidity, was observed in control and FAK knockout mice during colitis. Despite this fibrotic response, the colonic epithelium in FAK-deficient mice exhibited significantly reduced cyclin D1 expression, suggesting that proliferation is uncoupled from fibrosis in the absence of FAK. In support of this hypothesis, proliferation of Caco-2 cells increased proportionally with matrix stiffness in vitro only under conditions of normal FAK expression; FAK depleted cells exhibited reduced proliferation concomitant with attenuated cyclin D1 expression. Conclusions In the colon, FAK functions as a regulator of epithelial cell survival and proliferation under conditions of mucosal injury and a mechanosensor of tissue compliance, inducing repair-driven proliferation in the colonic epithelium through upregulation of cyclin D1.
Icariin improves acute kidney injury and proteinuria in a rat model of pregnancy-induced hypertension

Icariin has previously been demonstrated to attenuate hyperglycemia-induced renal injury, however the renoprotective effects of icariin in a rat model of pregnancy-induced hypertension (PIH) remain to be elucidated. The present study aimed to investigate the effect of icariin on PIH-induced acute kidney injury (AKI) and proteinuria. Following 18 days of icariin treatment between day 1 and day 18 of gestation, which was combined with NG-nitro-L-arginine methyl ester (L-NAME) treatment between day 12 and day 18 of gestation to induce PIH, the 24 h urine protein level, blood urea nitrogen and serum creatinine were measured by using the Coomassie Brilliant Blue method, a commercial enzymatic kit and the picric acid method, respectively. Renal tissues were collected at day 18 of gestation for hematoxylin and eosin staining and immunohistochemistry. The mRNA expression of AGT and protein expression of angiotensin II (Ang II) in the kidneys of control and PIH rats was investigated by reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively, to determine the effect of icariin on components of the renin-angiotensin system. The results demonstrated that L-NAME treatment in pregnant rats resulted in significant increases in systolic blood pressure (SBP) and diastolic blood pressure, in addition to the induction of severe proteinuria. The significant increase in SBP and proteinuria in PIH rats was prevented by icariin. L-NAME-induced AKI resulted in profound renal histological alterations, including mesangial expansion and glomerular lesions. L-NAME administration exerted a marked decrease in the mRNA and protein expression levels of nephrin in the kidneys from PIH rats compared with control group. Furthermore, upregulation of circulating and renal Ang II levels in PIH rats was observed. However, icariin treatment significantly reversed the L-NAME-induced downregulation of nephrin and upregulation of circulating and renal Ang II levels in PIH rats. These results demonstrated that icariin administration improved urinary protein excretion levels and renal tissue damage in PIH rats, and the underlying mechanism was mediated in part, via upregulation of nephrin expression and downregulation of Ang II.
Spectroscopic Imaging of Aluminum Containing Plasma

This dissertation aims to characterize laser-induced plasma from a physics point of view as warm, dense matter. Use of nominal nanosecond pulsed laser radiation initiates a plasma with electron temperatures of the order of 10 electron volts and electron densities of the order of air species densities at standard ambient temperature and pressure. For laser ablation and/or optical breakdown at or near a solid surface, the electron density can amount to be 1000 times greater. Spectroscopic investigations of the plasma emissions provide a method by which the electron density, temperature, and shockwave expansion may be determined. Of particular interest are the earliest of times following ablation of an aluminum target sample. At these times, observed spectral line profiles become distorted due to self-absorption affects. Here, experimental corrections to self-absorbed Al 394.4 and 396.15 nm, ground state transitions and the hydrogen Balmer series alpha, beta, and gamma lines are calculated by retroreflecting the plasma emission back through the plasma volume. The plasma are initiated by laser ablating an Al alloy 6061 target sample in a 90 percent hydrogen and 10 percent nitrogen gas atmosphere at 840 Torr with 1064 nm Nd:YAG 14 ns laser pulses. Electron densities are calculated by fitting the corrected profiles to Voigt profiles. The widths of the lines are used with empirically developed formulas to infer the electron density. The temperature of the plasma is found by using the Boltzmann plot method constructed from the Balmer series lines. Spatially resolved, diatomic molecular aluminum monoxide spectra are fit to theory spectra to infer the plasma temperature along the axis of the laser incidence at time delays greater than 2.5 microseconds following target ablation. Computer tomography methods, including Abel inversion, are used to find the radial profile of the inferred temperatures. Finally, a series of measurements of the plasma shockwave are presented to determine the geometry of the shock front expansion using the shadowgraph imaging technique.
Improving the healthcare response to domestic violence and abuse in sexual health clinics: feasibility study of a training, support and referral intervention

Objectives Sexual health and gynaecological problems are the most consistent and largest physical health differences between abused and non-abused female populations. Sexual health services are well placed to identify and support patients experiencing domestic violence and abuse (DVA). Most sexual health professionals have had minimal DVA training despite English National Institute for Health and Care Excellence recommendations. We sought to determine the feasibility of an evidence-based complex DVA training intervention in female sexual health walk-in services (IRIS ADViSE: Identification and Referral to Improve Safety whilst Assessing Domestic Violence in Sexual Health Environments). Methods An adaptive mixed method pilot study in the female walk-in service of two sexual health clinics. Following implementation and evaluation at site 1, the intervention was refined before implementation at site 2. The intervention comprised electronic prompts, multidisciplinary training sessions, clinic materials and simple referral pathways to IRIS ADViSE advocate-educators (AEs). The pilot lasted 7 weeks at site 1 and 12 weeks at site 2. Feasibility outcomes were to assign a supportive DVA clinical lead, an IRIS ADViSE AE employed by a local DVA service provider, adapt electronic records, develop local referral pathways, assess whether enquiry, identification and referral rates were measurable. Results Both sites achieved all feasibility outcomes: appointing a supportive DVA clinical lead and IRIS ADViSE AE, establishing links with a local DVA provider, adapting electronic records, developing local referral pathways and rates of enquiry, identification and referral were found to be measurable. Site 1: 10% enquiry rate (n=267), 4% identification rate (n=16) and eight AE referrals. Site 2: 61% enquiry rate (n=1090), a 7% identification rate (n=79) and eight AE referrals. Conclusions IRIS ADViSE can be successfully developed and implemented in sexual health clinics. It fulfils the unmet need for DVA training. Longer-term evaluation is recommended.
Endothelium-dependent vasodilation in the brachial artery is impaired in smokers: effect of vitamin C.

Cigarette smoking has been shown to cause endothelial dysfunction. To examine the effects of vitamin C and cigarette smoking on endothelium-dependent vasodilation, we measured the lumen diameter and flow velocity of the brachial arteries at rest, during reactive hyperemia following transient arterial occlusion, and after sublingual nitroglycerin (0.3 mg) in smokers ( n = 20) and nonsmokers ( n = 20) with high-resolution ultrasound after infusion of saline or saline plus vitamin C (10 mg/min for 20 min). We also performed the same study in smokers ( n = 15) before and 10 min after cigarette smoking. In addition, we measured the serum levels of vitamin C and the plasma levels of thiobarbituric acid-reactive substances (TBARS) as an index of lipid peroxidation. The smokers had lower vitamin C levels, higher TBARS levels, and showed impairment of flow-dependent vasodilation (5.3 ± 1.9 vs. 9.2 ± 1.5%, P < 0.0001) compared with nonsmokers. Vitamin C administration improved the impairment of flow-dependent vasodilation (5.3 ± 1.9 to 9.0 ± 3.2%, P < 0.001) and decreased TBARS in smokers but not in nonsmokers. Furthermore, cigarette smoking acutely worsened the impairment of flow-dependent vasodilation (5.4 ± 1.8 to 1.5 ± 1.3%, P < 0.01) and increased TBARS. We conclude that 1) endothelium-dependent vasodilation in the brachial arteries is impaired in smokers and this impairment is improved by vitamin C administration in association with a decrease in TBARS and 2) cigarette smoking produces acute impairment of endothelium-dependent vasodilation in smokers in association with an increase in TBARS.
A 30/35GHz phased array transmitter front-end with >+14dBm Psat and 10° phase/5-bit amplitude resolution for advanced beamforming

A 30/35 GHz dual-band phased array transmitter (TX) front-end is demonstrated in a 0.25um SiGe:C BiCMOS process. The front-end provides variable phase shifts from 0°~360° with a ~10° resolution. A 5-bit amplitude resolution is achieved for advanced beamforming algorithms. Accurate transmitted beam patterns can be generated by applying a genetic algorithm with the achieved phase and amplitude resolution. The front-end transmits a >+14dBm saturation output power with >+15dB gain and >+22dBm OIP3 at 30/35GHz.
The design of a theory-based intervention to improve medication adherence in chronic pain patients

Abstract Objective: Non-adherence to pain medication is common in chronic pain patients and may result in unfavorable treatment outcomes. Interventions to improve adherence behavior often fail to significantly change medication use. In this report, we describe the application of a theoretical psychological model of behavior change in order to design an intervention to improve medication adherence in chronic pain patients. Methods: This study applies the Behavior Change Wheel framework and the Behavior Change Techniques Taxonomy to design a theory-based intervention to improve pain medication use. Available literature was used to extract determinants of adherence in chronic pain patients. Results: Selected target behaviors to improve medication adherence are: share agreement on follow up policy, monitor medication adherence, provide patient education routinely, discuss attitudes and concerns towards pain medication, develop medication taking habits and use medication reminders. The intervention consists of three components in which relevant behavior change techniques are applied: (1) changes in the electronic patient data management systems to enable medical staff to apply target behaviors; (2) bi-annual education of medical staff to commit the team to the proposed intervention and provide feedback; (3) routine and mandatory education of chronic pain patients following prescription of pain medication. Conclusions: To improve medication adherence in chronic pain patients, most interventions should be focused on providers of pain therapy. Prescribing chronic pain medication should be seen as part of a larger treatment regimen including adequate follow-up, adherence monitoring and patient education during the course of treatment.