Miracle-dz/UniFAR-FTUs huggingface dataset:
The Patient Experience: Informing Practice through Identification of Meaningful Communication from the Patient’s Perspective

(1) Background: There is limited empirical knowledge concerning aspects of healthcare that contribute to a good patient experience from the patient’s perspective and how patient feedback informs service development. (2) Aim: To examine the issues that influence the effectiveness of communication on patient satisfaction, experience and engagement, in an acute National Health Service (NHS) setting, through identification of the patient’s requirements and expectations. (3) Method: Data was gathered from a large teaching hospital using a Friends and Family Test (FFT) and a communication specific survey. Both surveys captured patient narrative to identify predominant influences to explain the quantitative responses. (4) Results: The key priorities for patients are involvement in their care and receiving the right amount of information to support this. However, the delivery of compassionate care was identified as having the most influence on the likelihood of patients to recommend an acute NHS Trust. (5) Conclusion: The findings support a broader understanding of the constituents of an all-encompassing patient experience from the patient’s perspective. (6) Implications: healthcare organizations need to focus their resources on how to improve patient/provider communication to support patients to be true partners in their care.
Formation of microscale and nanoscale structures on surface irradiated with energetic beams

Single crystalline InP was ablated in air with p-polarized Ti:sapphire femtosecond laser at a fixed laser fluence of 82 mJ/cm. Ripples parallel to the laser polarization direction were found by scanning electron microscopy and atomic force microscopy to form for laser pulses ranging from 50 to 1000, whereas flower-like structures appeared for laser pulses of 10 and above. Analysis by x-ray photoelectron spectroscopy showed formation of indium and phosphorus oxides on the irradiated surface and the amounts of oxides increased with increasing number of laser pulses. The oxide formation is attributed to chemical reaction between the ultrafast laser ablation plume and oxygen in air, and formation of the flower-like structures is shown to be related to deposition of the oxides on the irradiated surface. Pacs Codes: 79.60. –i; 82.53. –k; 81.65. Mq; 79.20. Ds
In vivo 18F-AV-1451 tau PET signal in MAPT mutation carriers varies by expected tau isoforms

Objective To evaluate 18F-AV-1451 tau PET binding among microtubule-associated protein tau (MAPT) mutation carriers. Methods Using a case-control study, we quantitatively and qualitatively compared tau PET scans in 10 symptomatic and 3 asymptomatic MAPT mutation carriers (n = 13, age range 42–67 years) with clinically normal (CN) participants (n = 241, age range 42–67 years) and an Alzheimer disease (AD) dementia cohort (n = 30, age range 52–67 years). Eight participants had MAPT mutations that involved exon 10 (N279K n = 5, S305N n = 2, P301L n = 1) and tend to form 4R tau pathology, and 5 had mutations outside exon 10 (V337M n = 2, R406W n = 3) and tend to form mixed 3R/4R tau pathology. Results Tau PET signal was qualitatively and quantitatively different between participants with AD, CN participants, and MAPT mutation carriers, with the greatest signal intensity in those with AD and minimal regional signal in MAPT mutation carries with mutations in exon 10. However, MAPT mutation carriers with mutations outside exon 10 had uptake levels within the AD range, which was significantly higher than both MAPT mutation carriers with mutations in exon 10 and controls. Conclusions Tau PET shows higher magnitude of binding in MAPT mutation carriers who harbor mutations that are more likely to produce AD-like tau pathology (e.g., in our series, the non–exon 10 families tend to accumulate mixed 3R/4R aggregates). Exon 10 splicing determines the balance of 3R and 4R tau isoforms, with some mutations involving exon 10 predisposing to a greater proportion of 4R aggregates and consequently a lower level of AV-1451 binding, as seen in this case series, thus supporting the notion that this tau PET ligand has specific binding properties for AD-like tau pathology.
Varicella-Zoster Virus ORF63 Protects Human Neuronal and Keratinocyte Cell Lines from Apoptosis and Changes Its Localization upon Apoptosis Induction

ABSTRACT There are many facets of varicella-zoster virus (VZV) pathogenesis that are not fully understood, such as the mechanisms involved in the establishment of lifelong latency, reactivation, and development of serious conditions like postherpetic neuralgia (PHN). Virus-encoded modulation of apoptosis has been suggested to play an important role in these processes. VZV open reading frame 63 (ORF63) has been shown to modulate apoptosis in a cell-type-specific manner, but the impact of ORF63 on cell death pathways has not been examined in isolation in the context of human cells. We sought to elucidate the effect of VZV ORF63 on apoptosis induction in human neuron and keratinocyte cell lines. VZV ORF63 was shown to protect differentiated SH-SY5Y neuronal cells against staurosporine-induced apoptosis. In addition, VZV infection did not induce high levels of apoptosis in the HaCaT human keratinocyte line, highlighting a delay in apoptosis induction. VZV ORF63 was shown to protect HaCaT cells against both staurosporine- and Fas ligand-induced apoptosis. Confocal microscopy was utilized to examine VZV ORF63 localization during apoptosis induction. In VZV infection and ORF63 expression alone, VZV ORF63 became more cytoplasmic, with aggregate formation during apoptosis induction. Taken together, this suggests that VZV ORF63 protects both differentiated SH-SY5Y cells and HaCaT cells from apoptosis induction and may mediate this effect through its localization change during apoptosis. VZV ORF63 is a prominent VZV gene product in both productive and latent infection and thus may play a critical role in VZV pathogenesis by aiding neuron and keratinocyte survival. IMPORTANCE VZV, a human-specific alphaherpesvirus, causes chicken pox during primary infection and establishes lifelong latency in the dorsal root ganglia (DRG). Reactivation of VZV causes shingles, which is often followed by a prolonged pain syndrome called postherpetic neuralgia. It has been suggested that the ability of the virus to modulate cell death pathways is linked to its ability to establish latency and reactivate. The significance of our research lies in investigating the ability of ORF63, a VZV gene product, to inhibit apoptosis in novel cell types crucial for VZV pathogenesis. This will allow an increased understanding of critical enigmatic components of VZV pathogenesis.
Dietary carbohydrate and postexercise synthesis of proglycogen and macroglycogen in human skeletal muscle.

This study examined the role of carbohydrate (CHO) ingestion on the resynthesis of two pools of glycogen, proglycogen (PG) and macroglycogen (MG), in human skeletal muscle. Nine males completed an exhaustive glycogen depletion exercise bout at 70% maximal O2 consumption on two occasions. Subsequent 48-h dietary interventions consisted of either high (HC, 75% of energy intake) or low (LC, 32% of energy intake) CHO diets. Muscle biopsies were taken at exhaustion (EXH) and 4, 24, and 48 h later. The total muscle glycogen (Gt) at EXH for the HC and LC conditions was not significantly different, and the MG represented ∼12% of the Gt. From EXH to 4 h, there was an increase in the PG only for HC and no change in MG in either diet ( P < 0.05). From 4 to 24 h, the concentration of PG increased in both conditions ( P < 0.05). Between 24 and 48 h, in HC the majority of the increase in Gt was due to the MG pool ( P < 0.05). The MG and PG concentrations for HC were significantly greater than for LC at 24 and 48 h ( P < 0.05). At 48 h the MG represented 40% of the Gt for the HC diet and only 21% for the LC diet. There was no change in the net rates of synthesis of PG or MG over 48 h for LC ( P < 0.05). The net rate of PG synthesis from 0 to 4 h for HC was 16 ± 1.68 mmol glucosyl units ⋅ kg dry wt-1 ⋅ h-1, which was threefold greater than for LC ( P < 0.05). The net rate of PG synthesis decreased significantly from 4 to 24 h for HC, whereas the net rate of MG synthesis was not different over 48 h but was significantly greater than in LC ( P< 0.05). The two pools are synthesized at very different rates; both are sensitive to CHO, and the supercompensation associated with HC is due to a greater synthesis in the MG pool.
Acute and chronic hypokalemia sensitize the isolated heart to hypoxic injury.

We examined the effects of acute and/or chronic hypokalemia on responses to 30 min of hypoxia and recovery in the isolated, perfused heart model. We found that both acute hypokalemia and chronic hypokalemia impaired contractility [expressed as maximum slope of pressure increase over time (dP/d t): 501 ± 49 and 529 ± 48 vs. 1,302 ± 118 mmHg/s, P < 0.01] and recovery of ATP concentrations (determined with31P NMR spectroscopy: 30 ± 6 and 40 ± 10 vs. 67 ± 5% initial, P < 0.05) at 30 min of recovery. Moreover, the combination of acute hypokalemia and chronic hypokalemia had additive effects (dP/d t 166 ± 15 mmHg/s and ATP 21 ± 7% initial, both P < 0.01). We also measured cytosolic calcium with surface fluorescence spectroscopy after indo 1 loading. Acute hypokalemia and acute hypokalemia + chronic hypokalemia increased cytosolic calcium (averaged throughout the cardiac cycle) during and after hypoxia (390- to 460-nm ratio at 30 min of recovery: 0.46 ± 0.07 and 0.65 ± 0.07 vs. 0.18 ± 0.03, P < 0.01), whereas control and chronic hypokalemia hearts had only small changes with hypoxia and recovery. Finally, when we examined mitochondria isolated from hearts perfused under experimental conditions, we found that chronic hypokalemia-alone mitochondria and chronic hypokalemia + acute hypokalemia mitochondria had marked impairment of state 3 respiration compared with control hearts (52 ± 13 and 50 ± 9 vs. 128 ± 10 natm ⋅ min-1 ⋅ mg protein-1 with succinate as substrate, P < 0.01), whereas acute hypokalemia mitochondria demonstrated only subtle changes. These data suggest that both acute hypokalemia and chronic hypokalemia impair cardiac responses to hypoxia. The mechanism may involve impairment of calcium metabolism, but cytosolic calcium alterations do not explain all of the metabolic and functional effects of acute hypokalemia and chronic hypokalemia in the setting of hypoxia.
The immune system prevents recurrence of transplanted but not autochthonous antigenic tumors after oncogene inactivation therapy

Targeted oncogene inactivation by small molecule inhibitors can be very effective but tumor recurrence is a frequent problem in the clinic. Therapy by inactivation of the cancer‐driving oncogene in transplanted tumors was shown to be augmented in the presence of T cells. However, these experiments did not take into account the long‐term, usually tolerogenic, interaction of de novo malignancies with the immune system. Here, we employed mice, in which SV40 large T (Tag) and firefly luciferase (Luc) as fusion protein (TagLuc) could be regulated with the Tet‐on system and upon activation resulted in tumors after a long latency. TagLuc inactivation induced profound tumor regression, demonstrating sustained oncogene addiction. While tumor relapse after TagLuc inactivation was prevented in immunocompetent mice bearing transplanted tumors, autochthonous tumors relapsed or recurred after therapy discontinuation indicating that the immune system that coevolved with the malignancy over an extended period of time lost the potency to mount an efficient anti‐tumor immune response. By contrast, adoptively transferred CD8+ T cells targeting the cancer‐driving oncogene eradicated recurrent autochthonous tumors, highlighting a suitable therapy option in a clinically relevant model.
Graph Measures of Node Strength for Characterizing Preictal Synchrony in Partial Epilepsy

The reference electrophysiological pattern at seizure onset is the "rapid discharge," as visible on intracerebral electroencephalography (EEG). This discharge typically corresponds to a decrease of synchrony across brain areas. In contrast, the preictal period can exhibit patterns of increased synchrony, which can be quantified by network measures. Our objective was to compare preictal synchrony with a quantification of the rapid discharge as provided by the epileptogenicity index (EI). We investigated 24 seizures from 12 patients recorded by stereotaxic EEG (SEEG). Seizures were classified visually as containing preictal synchrony or not. We computed pairwise nonlinear correlation (h(2)) across channels in the 8 sec preceding the rapid discharge. The sum of ingoing and outgoing links (IN and OUT node strength), as well as the sum of all links (total strength, TOT) were computed for each region. We tested several filtering schemes, and quantified the capacity of each strength measure to serve as a detector of regions with high EI values using a receiver operating characteristic (ROC) analysis. We found that the best correspondence between node strength and EI was obtained for the OUT and TOT measures, for signals filtered in the 15-40 Hz band-that is, for the band corresponding to the spiky part of epileptic discharges. In agreement with these results, we also found that the ROC results were improved when considering only seizures with visible synchronous patterns in the preictal period. Our results suggest that measuring strength of preictal connectivity graphs can bring useful clinical information on the epileptogenic zone.
MAPK superfamily activation in human airway smooth muscle: mitogenesis requires prolonged p42/p44 activation.

Asthma is frequently associated with abnormal airway smooth muscle (ASM) growth that may contribute to airway narrowing and hyperresponsiveness to contractile agents. Although numerous hormones and cytokines have been shown to induce human ASM (HASM) proliferation, the cellular and molecular mechanisms underlying HASM hyperplasia are largely unknown. Here we characterize the roles of the mitogen-activated protein kinase (MAPK) superfamily [p42/p44 MAPK, c-Jun amino-terminal kinase/stress-activated protein kinase (JNK/SAPK), and p38] in mediating hormone- and cytokine-induced HASM proliferation. Significant enhancement of [3H]thymidine incorporation in HASM cultures was observed only by treatment with agents (epidermal growth factor, platelet-derived growth factor, thrombin, and phorbol 12-myristate 13-acetate) that promoted a strong and sustained activation of p42/p44 MAPK. Significant activation of the JNK/SAPK and p38 pathways was only observed on stimulation with interleukin (IL)-1β and tumor necrosis factor-α, agents that did not appreciably stimulate HASM proliferation. Two different inhibitors of MAPK/extracellular signal-regulated kinase kinase (MEK), PD-98059 and U-0126, inhibited mitogen-induced [3H]thymidine incorporation in a manner consistent with their ability to inhibit p42/p44 activation. Elk-1 and activator protein-1 reporter activation by mitogens was similarly inhibited by inhibition of MEK, suggesting a linkage between p42/p44 activation, transcription factor activation, and HASM proliferation. These findings establish a fundamental role for p42/p44 activation in regulating HASM proliferation and provide insight into species-specific differences observed among studies in ASM mitogenesis.
A multilevel analysis of the relationship between parental migration and left-behind children’s macronutrient intakes in rural China

Abstract Objective China’s internal migration has left 61 million children living apart from their parent(s) in rural areas. The present study aimed to examine whether the relative contributions of macronutrients (protein, fat and carbohydrate) to total energy intake differ between children left behind by the father or mother, compared with children from intact families. Design Drawing on a longitudinal study, the China Health and Nutrition Survey (1997–2009), multilevel modelling analyses (level 1: occasions; level 2: children; level 3: villages) were performed. Setting Data from rural communities in nine provinces in China. Subjects Rural children (n 975; 555 boys and 420 girls) from 140 villages. Results Among boys of school age, being left behind by the father tended to reduce the relative protein intake by 0·70 % (P<0·01) compared with boys from intact families. Being left behind by at least the mother was more detrimental for young boys under the age of 6 years than paternal migration, reducing relative protein intake by 1·14 % (P<0·05). Parental migration was associated with a significant increase in young boys’ relative fat intake by 2·60 % (P<0·05). No significant associations were found for girls. Results suggest left-behind boys, especially in early life, are subject to a higher-fat and lower-protein diet compared with non-left-behind boys. This may put them at increased risk of being overweight or obese, or of suffering from stunted growth, when they grow up. Conclusions Public health policies should recognise the influences of parental migration on boys, especially maternal migration, and encourage a more balanced diet for children in rural China.
Psychosocial Modifiers of Immunocompetence in Medical Students

&NA; This study addressed the effects of a naturally occurring stressor on components of the immune response. Blood was drawn twice from 75 first‐year medical students, with a baseline sample taken one month before their final examinations and a stress sample drawn on the first day of final examinations. Median splits on scores from the Holmes—Rahe Social Readjustment Rating Scale and the UCLA Loneliness Scale produced a 2 X 2 X 2 repeated measures ANOVA when combined with the trials variable. Natural killer (NK) cell activity declined significantly from the first to the second sample. High scorers on stressful life events and loneliness had significantly lower levels of NK activity. Total plasma IgA increased significantly from the first to second sample, while plasma IgG and IgM, C‐reactive protein, and salivary IgA did not change significantly.
Asynchronous Gradient Push

We consider a multiagent framework for distributed optimization where each agent has access to a local smooth strongly convex function, and the collective goal is to achieve consensus on the parameters that minimize the sum of the agents’ local functions. We propose an algorithm wherein each agent operates asynchronously and independently of the other agents. When the local functions are strongly convex with Lipschitz-continuous gradients, we show that the iterates at each agent converge to a neighborhood of the global minimum, where the neighborhood size depends on the degree of asynchrony in the multiagent network. When the agents work at the same rate, convergence to the global minimizer is achieved. Numerical experiments demonstrate that asynchronous gradient push can minimize the global objective faster than the state-of-the-art synchronous first-order methods, is more robust to failing or stalling agents, and scales better with the network size.
Role of L-type Ca2+ channel in PACAP-induced adrenal catecholamine release in vivo.

The aim of the present study was to investigate whether the dihydropyridine-sensitive L-type Ca2+ channel is operative in adrenal catecholamine (CA) secretion induced by a novel neuropeptide, pituitary adenylate cyclase-activating polypeptide (PACAP), in anesthetized dogs. Plasma CA concentrations in adrenal venous and aortic blood were determined by a high-performance liquid chromatography method. All drugs tested were locally infused into the left adrenal gland via the left adrenolumbar artery. PACAP, with the isoform consisting of 27 (PACAP-27) and 38 (PACAP-38) amino acid residues, significantly increased CA output in a dose-dependent manner, with doses ranging from 5 to 500 ng and 7 to 700 ng, respectively. However, the amplitude of epinephrine response to PACAP-27 was three times greater than that obtained with PACAP-38 at the highest dose tested. In a separate group, a single dose of PACAP-27 (50 ng) induced highly reproducible CA responses when the same dose was repeated with an interval of 35 min. In dogs treated with nifedipine (50 μg), 5 min before the second administration of PACAP-27, the net CA response was significantly inhibited by ∼50% compared with that obtained in the presence of vehicle. A similar CA response to BAY K 8644 (5 μg) was completely abolished by the same dose of nifedipine. The present results indicate that both PACAP-27 and PACAP-38 have the direct local secretagogue effect on the adrenal medulla in vivo and that CA responses to PACAP-27 were greater than those observed with PACAP-38 at equivalent mole doses. The study suggests that the dihydropyridine-sensitive L-type Ca2+ channel is functionally involved in PACAP-induced adrenal CA secretion in the canine adrenal medulla in vivo.
Measurement of surface temperature of weld pools by infrared two colour pyrometry

In this research, two colour pyrometry was conducted to obtain the surface temperature of weld pools, in which the weld pool was photographed by a high speed camera during arc welding. Two wavelengths (950 and 980 nm) of light in the infrared range were selected from the thermal radiation light emitted from the weld pool at the instant when the arc was extinguished, using an imaging spectroscope. Consequently, in gas tungsten arc welding, it was shown that the surface temperature distribution of a weld pool is affected by the sulphur content in the base metal. It is thought that this temperature distribution is determined by the balance between the driving forces of viscous drag from the cathode jet of plasma and Marangoni surface tension. In gas metal arc welding, it was seen that the surface temperature distribution becomes uniform and the temperature is 1715–1845 K, which is obviously lower than that of the metal droplet.
Effects of estrogen and growth hormone on skeleton in the ovariectomized rat with hypophysectomy.

To investigate whether growth hormone (GH) and 17β-estradiol (E2) replacement can prevent osteopenia induced by pituitary and ovarian hormone deficiency [by hypophysectomy and ovariectomy (HX+OV)], we administered relatively low doses of GH (2.3 IU ⋅ kg-1 ⋅ day-1) and E2 (100 μg ⋅ kg-1 ⋅ wk-1) in experiment 1 and relatively high doses of GH (13.5 IU ⋅ kg-1 ⋅ day-1) and E2 (3,500 μg ⋅ kg-1 ⋅ wk-1) in experiment 2 to 2-mo-old HX+OV Sprague-Dawley rats for 6 wk. Our data show that the HX+OV of rats results in diminished periosteal bone formation, longitudinal bone growth, and decreased cancellous bone volume. Administration of either the low or high dose of GH to these rats increased their systemic growth, serum levels of osteocalcin, and cortical bone formation. Either low or high doses of GH or E2 alone only partially prevent cancellous bone loss. However, the combined treatment of GH plus E2 resulted in an additive increase in the cancellous bone mass. We conclude that the additive effect of GH plus E2 on cancellous bone is attributed to the suppressive effect of E2 on bone resorption and the anabolic effect of GH on bone formation.