Miracle-dz/UniFAR-FTUs huggingface dataset:
Poor emotional responsiveness in clinical hypertension: Reduced accuracy in the labelling and matching of emotional faces amongst individuals with hypertension and prehypertension

Psychological factors are known to play an important part in the origin of many medical conditions including hypertension. Recent studies have reported elevated blood pressure (even in the normal range of variation) to be associated with a reduced responsiveness to emotions or ‘emotional dampening’. Our aim was to assess emotional dampening in individuals with more extreme blood pressure levels including prehypertensives (N = 58) and hypertensives (N = 60) by comparing their emotion recognition ability with normotensives (N = 57). Participants completed novel facial emotion matching and facial emotion labelling tasks following blood pressure measurement and their accuracy of emotion recognition and average response times were compared. The normotensives demonstrated a significantly higher accuracy of emotion recognition than the prehypertensives and the hypertensives in labelling of facial emotions. This difference generalised to the task where two facial halves (upper & lower) had to be matched on the basis of emotions. In neither the labelling nor matching emotion conditions did the groups differ in their speed of emotion processing. Findings of the present study extend reports of ‘emotional dampening’ to hypertensives as well as to those at-risk for developing hypertension (i.e. prehypertensives) and have important implications for understanding the psychological component of such medical conditions as hypertension.
Binary Coding for Partial Action Analysis with Limited Observation Ratios

Traditional action recognition methods aim to recognize actions with complete observations/executions. However, it is often difficult to capture fully executed actions due to occlusions, interruptions, etc. Meanwhile, action prediction/recognition in advance based on partial observations is essential for preventing the situation from deteriorating. Besides, fast spotting human activities using partially observed data is a critical ingredient for retrieval systems. Inspired by the recent success of data binarization in efficient retrieval/recognition, we propose a novel approach, named Partial Reconstructive Binary Coding (PRBC), for action analysis based on limited frame glimpses during any period of the complete execution. Specifically, we learn discriminative compact binary codes for partial actions via a joint learning framework, which collaboratively tackles feature reconstruction as well as binary coding. We obtain the solution to PRBC based on a discrete alternating iteration algorithm. Extensive experiments on four realistic action datasets in terms of three tasks (i.e., partial action retrieval, recognition and prediction) clearly show the superiority of PRBC over the state-of-the-art methods, along with significantly reduced memory load and computational costs during the online test.
Pyroptosis by caspase11/4‐gasdermin‐D pathway in alcoholic hepatitis in mice and patients

Alcoholic hepatitis (AH) continues to be a disease with high mortality and no efficacious medical treatment. Although severe AH is presented as acute on chronic liver failure, what underlies this transition from chronic alcoholic steatohepatitis (ASH) to AH is largely unknown. To address this question, unbiased RNA sequencing and proteomic analyses were performed on livers of the recently developed AH mouse model, which exhibits the shift to AH from chronic ASH upon weekly alcohol binge, and these results are compared to gene expression profiling data from AH patients. This cross‐analysis has identified Casp11 (CASP4 in humans) as a commonly up‐regulated gene known to be involved in the noncanonical inflammasome pathway. Immunoblotting confirms CASP11/4 activation in AH mice and patients, but not in chronic ASH mice and healthy human livers. Gasdermin‐D (GSDMD), which induces pyroptosis (lytic cell death caused by bacterial infection) downstream of CASP11/4 activation, is also activated in AH livers in mice and patients. CASP11 deficiency reduces GSDMD activation, bacterial load in the liver, and severity of AH in the mouse model. Conversely, the deficiency of interleukin‐18, the key antimicrobial cytokine, aggravates hepatic bacterial load, GSDMD activation, and AH. Furthermore, hepatocyte‐specific expression of constitutively active GSDMD worsens hepatocellular lytic death and polymorphonuclear leukocyte inflammation. Conclusion: These results implicate pyroptosis induced by the CASP11/4‐GSDMD pathway in the pathogenesis of AH. (Hepatology 2018;67:1737‐1753).
Assessing Hyperactivation and Deactivation Strategies of the Caregiving Behavioral System: Psychometric Studies of the Portuguese Version of the Caregiving System Scale

According to attachment theory, the main goal of the caregiving behavioral system is to relieve others’ distress and promote their health and welfare. This is accomplished through a set of caregiving behaviors that are the primary strategy of this system. However, some individuals develop nonoptimal or secondary strategies (hyperactivation or deactivation). The Caregiving System Scale (CSS) is a self-report measure that assesses these nonoptimal caregiving strategies. This study examined the factor structure of the Portuguese version of the CSS using a bifactor model and a 2-factor correlated model; it also examined validity evidence for CSS scores in relation to other relevant variables. The sample comprised 417 women from the general population who completed the CSS, with a subsample of 124 women completing additional measures of attachment, mental representations of caregiving, compassion, and difficulties in emotional regulation. The bifactor model showed the best fit to the data, supporting an orthogonal and reliable 2-factor structure (Hyperactivation and Deactivation). This model also suggested that the Hyperactivation scale is multidimensional. With regard to the validity evidence for the CSS, the results showed that individuals engaged in volunteering activities presented lower levels of deactivation than those who were not engaged in these activities. The CSS scores also correlated as expected with the other measures. In conclusion, this study supports the utilization of Deactivation and Hyperactivation subscales as 2 statistically distinct constructs and demonstrates that the Portuguese version is an adequate measure of nonoptimal caregiving strategies.
Interaction of copper wood preservatives and adhesives

Compared to other substrates, wood is generally easy to bond. However, adhesion is diminished when the wood surface is covered by chemicals, whether natural oils and resins or added chemicals. Among the chemicals added to wood are fire retardants and wood preservatives. Chromated copper arsenate (CCA) has been widely used to protect wood against rot and termites, but concern about the toxicity of arsenic is leading companies to turn to other treatment chemicals (1). The two most prominent chemicals for replacing CCA in treating wood are ammonical copper quat (ACQ) and copper azole (CAz). Most treatment chemicals tend to reduce the strength of wood bonds (2). In fact, the bonds of CCA-treated wood have been found to be less durable than those of untreated wood (3). The lack of adhesion is usually revealed by an environmental resistance test, which is critical since preservative-treated wood is often exposed to water. Exposure to water and drying is a severe test for wood adhesion since the bond has to withstand the expansion and shrinking that occurs when the wood picks up and loses moisture content, as well as the thermal expansion and contraction of the wood (4). The reduced adhesion of treated wood can be the result of a number of factors. For example, nodules of CCA on the wood surface can limit adhesion (5). However, treatment with CCA does not accelerate the cure of the adhesive (6). There is little in the literature on bonds of ACQand CAz-treated woods.
Rib kinematics during lung ventilation in the American alligator (Alligator mississippiensis): an XROMM analysis

ABSTRACT The current hypothesis regarding the mechanics of breathing in crocodylians is that the double-headed ribs, with both a capitulum and tuberculum, rotate about a constrained axis passing through the two articulations; moreover, this axis shifts in the caudal thoracic ribs, as the vertebral parapophysis moves from the centrum to the transverse process. Additionally, the ventral ribcage in crocodylians is thought to possess additional degrees of freedom through mobile intermediate ribs. In this study, X-ray reconstruction of moving morphology (XROMM) was used to quantify rib rotation during breathing in American alligators. Whilst costovertebral joint anatomy predicted overall patterns of motion across the ribcage (decreased bucket handle motion and increased calliper motion), there were significant deviations: anatomical axes overestimated pump handle motion and, generally, ribs in vivo rotate about all three body axes more equally than predicted. The intermediate ribs are mobile, with a high degree of rotation measured about the dorsal intracostal joints, especially in the more caudal ribs. Motion of the sternal ribs became increasingly complex caudally, owing to a combination of the movements of the vertebral and intermediate segments. As the crocodylian ribcage is sometimes used as a model for the ancestral archosaur, these results have important implications for how rib motion is reconstructed in fossil taxa, and illustrate the difficulties in reconstructing rib movement based on osteology alone. Summary: Using XROMM to test how well joint anatomy predicts rib motion during breathing in crocodylians, our best living model for the earliest archosaurs.
Shape Memory Polymers in Fiber Composite Structures for Shape Adjustment

The functionality of high precision composite parts might be affected by distortions caused by residual curing stresses. In order to compensate these distortions actuator patches consisting of shape memory polymers can be used for a post manufacturing shape adjustment. For the determination of necessary actuation properties an experimental method is developed. Methods for the shape sensing are introduced. Finite element models are used to investigate the structure-actuator interface for these soft actuator materials. An optimization process to determine optimal actuator configurations for the shape error minimization is developed. Obtained simulation results are verified with experiments in which significant shape error reductions are achieved.
Residential inter-zonal ventilation rates for exposure modeling

ABSTRACT Residential inter-zonal (e.g., between rooms) ventilation is comprised of fresh air infiltration in and exfiltration out of the whole house plus the “fresh” air that is entering (and exiting) the room of interest from other rooms or areas within the house. Clearly, the inter-zone ventilation rate in any room of interest will be greater than the infiltration/exfiltration ventilation rate of outdoor air for the whole house. The purpose of this study is to determine how much greater the inter-zonal ventilation rate is in typical U.S. residences compared to the whole house ventilation rate from outdoor air. The data for this statistical analysis came from HouseDB, a 1995 EPA database of residential ventilation rates. Analytical results indicate that a lognormal distribution provides the best fit to the data. Lognormal probability distribution functions (PDFs) are provided for various inter-zonal ventilation rates for comparison to the PDF for the whole house ventilation rates. All ventilation rates are expressed as air change rates per hour (ACH). These PDFs can be used as inputs to exposure models. This analysis suggests that if one were performing a deterministic analysis for unknown housing stocks in the U.S., a default mean and median ACH values of 0.4/hr and 0.3/hr, respectively, for whole house ventilation would be appropriate; and 0.7/hr and 0.6/hr, respectively, for inter-zonal ventilation.
BGP-15 prevents the death of neurons in a mouse model of familial dysautonomia

Significance Familial dysautonomia (FD) is a fatal genetic disorder that disrupts development of the peripheral nervous system (PNS) and causes progressive degeneration of the PNS and retina, ultimately leading to blindness. The underlying cellular mechanisms responsible for neuronal death in FD have been elusive. Using a mouse model that recapitulates impaired PNS development, we report here that developing peripheral neurons die in FD as the result of disruptions in mitochondrial and actin function. Cell death can be prevented in vivo by the small molecule BGP-15. Given that disrupted mitochondrial function appears to be a hallmark of neurodegenerative diseases, future studies on the efficacy of BGP-15 for mitigating neuronal loss in other disorders is warranted. Hereditary sensory and autonomic neuropathy type III, or familial dysautonomia [FD; Online Mendelian Inheritance in Man (OMIM) 223900], affects the development and long-term viability of neurons in the peripheral nervous system (PNS) and retina. FD is caused by a point mutation in the gene IKBKAP/ELP1 that results in a tissue-specific reduction of the IKAP/ELP1 protein, a subunit of the Elongator complex. Hallmarks of the disease include vasomotor and cardiovascular instability and diminished pain and temperature sensation caused by reductions in sensory and autonomic neurons. It has been suggested but not demonstrated that mitochondrial function may be abnormal in FD. We previously generated an Ikbkap/Elp1 conditional-knockout mouse model that recapitulates the selective death of sensory (dorsal root ganglia) and autonomic neurons observed in FD. We now show that in these mice neuronal mitochondria have abnormal membrane potentials, produce elevated levels of reactive oxygen species, are fragmented, and do not aggregate normally at axonal branch points. The small hydroxylamine compound BGP-15 improved mitochondrial function, protecting neurons from dying in vitro and in vivo, and promoted cardiac innervation in vivo. Given that impairment of mitochondrial function is a common pathological component of neurodegenerative diseases such as amyotrophic lateral sclerosis and Alzheimer’s, Parkinson’s, and Huntington’s diseases, our findings identify a therapeutic approach that may have efficacy in multiple degenerative conditions.
Effects of turf and cleat footwear on plantar load distributions in adolescent American football players during resisted pushing

Abstract Metatarsal and midfoot injuries are common in American football. Footwear design may influence injury rates by altering plantar foot loading patterns in these regions. The purpose of this study was to determine the effect of cleat design on in-shoe plantar foot loading during a football-specific, resisted pushing task. Twenty competitive football players (age 14.7 ± 1.8 years, height 1.72 ± 0.10 m, and mass 71.8 ± 26.9 kg) completed three trials of pushing a weighted sled at maximal effort in a standard shoe (CLEAT) and artificial turf-specific shoe (TURF), with flexible in-shoe force measuring insoles. Repeated measures ANOVAs identified mean differences in maximum force and relative load under all regions of the foot. Results showed higher forces in the CLEAT under the medial (p < 0.001) and lateral (p = 0.004) midfoot, central (p = 0.007) and lateral (p < 0.001) forefoot, and lesser toes (p = 0.01), but lower forces in the hallux (p = 0.02) compared to the TURF shoe. Additionally, relative loading was higher in the CLEAT under the medial (p < 0.001) and lateral (p = 0.002) midfoot and lateral (p < 0.001) forefoot, but lower in the medial forefoot (p = 0.006) and hallux (p < 0.001) compared to the TURF shoe. The two shoes elicited distinct plantar loading profiles and may influence shoe selection decisions during injury prevention or rehabilitation practices.
Immunotherapy of spontaneous mammary carcinoma with fusions of dendritic cells and mucin 1‐positive carcinoma cells

The tumour‐associated antigen mucin 1 (MUC1) is a multifunctional protein involved in protection of mucous membranes, signal transduction, and modulation of the immune system. More than 70% of cancers overexpress MUC1, making MUC1 a potential target for immunotherapy. In the present study, MUC1 transgenic mice were crossed with syngeneic strains that express the polyomavirus middle‐T oncogene (PyMT) driven by the mouse mammary tumour virus promoter long‐terminal repeat (MMTV‐LTR). The resultant breed (MMT mice) developed spontaneous MUC1‐expressing mammary carcinomas with 100% penetrance at 8–15 weeks of age. As found in human breast cancer, the mammary carcinoma in MMT mice arose in multiple stages. Immunization with fusions of dendritic cells and MUC1‐positive tumour cells (FC/MUC1) induced MUC1‐specific immune responses that blocked or delayed the development of spontaneous breast carcinomas. In contrast, there was no delay of tumour development in MMT mice immunized with irradiated MC38/MUC1 tumour cells. The efficacy of fusion cells was closely correlated with the timing of initial immunization. Immunization with FC/MUC1 initiated in MMT mice at < 1, 1–2 and 2–3 months of age rendered 33, 5 and 0% of mice free of tumour, respectively, up to 6 months. Whereas mice immunized in the later stage of tumour development succumbed to their disease, immunization resulted in control of tumour progression and prolongation of life. These results indicate that immunization with FC/MUC1 can generate an anti‐MUC1 response that is sufficient to delay the development of spontaneous mammary carcinomas and control tumour progression in MMT mice.
Noncalcemic adverse effects and withdrawals in randomized controlled trials of long-term vitamin D2 or D3 supplementation: a systematic review and meta-analysis

Context Recent randomized controlled trials (RCTs) provide evidence for a possible beneficial impact of vitamin D supplementation on health outcomes beyond bone health, but there are few reviews of noncalcemic adverse effects from long-term supplementation. Objective The aims of this systematic review of vitamin D supplementation in RCTs were as follows: to determine whether all adverse effects, when combined, are reported equally between treatment arms; to identify the most common noncalcemic adverse effects reported; and to ascertain whether withdrawal rates, as a marker of clinical adverse effects, differ between treatment arms. Data Sources The MEDLINE Ovid, Embase, and Cochrane Library databases were searched systematically up to May 2016. Study Selection Randomized controlled trials that met the following criteria were selected: administered vitamin D2 or D3 supplements for a minimum supplementation or follow-up period of 24 weeks, had a placebo/control group, and were conducted among adults (≥ 18 y). Data Extraction Two researchers independently screened studies for eligibility, extracted data, and carried out quality assessment of selected studies. A total of 128 studies with 52 297 participants were identified. A random-effects model was used to calculate risk ratios in a meta-analysis. Results Long-term vitamin D2 or D3 supplementation, compared with placebo, did not increase all adverse effects, when combined, as reported in 62 studies with 19 389 participants (relative risk [RR] = 0.97; 95%CI, 0.92-1.02). Vitamin D also did not increase the risk of the most common noncalcemic adverse effects: gastrointestinal symptoms were reported in 27 studies with 9189 participants (RR = 1.01; 95%CI, 0.87-1.17), and dermatological symptoms were reported in 8 studies with 1695 participants (RR = 1.33; 95%CI, 0.82-2.15). Vitamin D did not increase withdrawals from 123 studies with 41 861 participants (RR = 1.03; 95%CI, 0.96-1.09). However, participants given vitamin D were more likely to report withdrawals than those given placebo in studies in which calcium was given in both arms (RR = 1.16; 95%CI, 1.02-1.33) when compared with participants in studies in which calcium was not given in either arm (RR = 1.00; 95%CI, 0.95-1.06; P for interaction = 0.009). Conclusions Overall, these findings suggest that vitamin D, by itself, does not increase the risk of noncalcemic adverse effects.
P2X1‐regulated IL‐22 secretion by innate lymphoid cells is required for efficient liver regeneration

Paracrine signalling mediated by cytokine secretion is essential for liver regeneration after hepatic resection, yet the mechanisms of cellular crosstalk between immune and parenchymal cells are still elusive. Interleukin‐22 (IL‐22) is released by immune cells and mediates strong hepatoprotective functions. However, it remains unclear whether IL‐22 is critical for the crosstalk between liver lymphocytes and parenchymal cells during liver regeneration after partial hepatectomy (PH). Here, we found that plasma levels of IL‐22 and its upstream cytokine, IL‐23, are highly elevated in patients after major liver resection. In a mouse model of PH, deletion of IL‐22 was associated with significantly delayed hepatocellular proliferation and an increase of hepatocellular injury and endoplasmic reticulum stress. Using Rag1−/− and Rag2−/−γc−/− mice, we show that the main producers of IL‐22 post‐PH are conventional natural killer cells and innate lymphoid cells type 1. Extracellular adenosine triphosphate (ATP), a potent danger molecule, is elevated in patients immediately after major liver resection. Antagonism of the P2‐type nucleotide receptors, P2X1 and P2Y6, significantly decreased IL‐22 secretion ex vivo. In vivo, specific inhibition of P2X1 was associated with decreased IL‐22 secretion, elevated liver injury, and impaired liver regeneration. Conclusion: This study shows that innate immune cell‐derived IL‐22 is required for efficient liver regeneration and that secretion of IL‐22 in the regenerating liver is modulated by the ATP receptor, P2X1. (Hepatology 2016;63:2004‐2017)
Maternal CD8+ T‐cell depletion alleviates intrauterine inflammation‐induced perinatal brain injury

We investigated the mechanisms by which CD8+ T‐cell trafficking in placenta contributes to perinatal brain injury by studying effects of maternal CD8+ T‐cell depletion (DEP) in a mouse model of intrauterine inflammation (IUI). Maternal CD8+ T cells were depleted with anti‐CD8+ antibodies. IUI was induced with lipopolysaccharide (LPS). DEP was confirmed using flow cytometry. Preterm birth rate was evaluated. Offspring neurologic sequelae were assessed by Nissl staining, immune arrays, confirmatory individual TaqMan® gene assays, and neurobehavioral tests. DEP did not significantly prevent LPS‐induced preterm birth but improved neurobehavioral performance (P < .001) and increased cortical neuronal density (P < .05) in LPS‐exposed pups compared to controls. These changes were associated with decreased CCL3 and CXCL10 and increased CCL5 in DEP LPS‐exposed mice. We demonstrate that DEP reduces perinatal brain injury following IUI. This supports a role for maternal CD8+ T‐cell trafficking in placenta in mediating perinatal brain injury separate from preterm birth mechanisms.