Miracle-dz/UniFAR-FTUs huggingface dataset:
and Vascular Technologists React to Chronic Stress

Burnout is an individual's reaction to chronic stress. Using the Maslach Burnout Inventory, this study surveyed a sample of sonographers and vascular technologists in the state of Tennessee.The objec - tives of the study were to (1) determine whether there is a relationship of individual demographic characteristics, job-related variables, and/or career- related variables to the 3 sequential stages of burn- out; (2) determine at what levels do sonographers and vascular technologists experience burnout com- pared to a national norm; and (3) determine whether sonographers and vascular technologists could iden- tify methods of diminishing chronic stress in the workplace environment.Statistical analysis indi- cated that sonographers and vascular technologists experience moderate levels of all 3 sequential stages of burnout.
Silk Fibroin-Based Biomaterials for Biomedical Applications: A Review

Since it was first discovered, thousands of years ago, silkworm silk has been known to be an abundant biopolymer with a vast range of attractive properties. The utilization of silk fibroin (SF), the main protein of silkworm silk, has not been limited to the textile industry but has been further extended to various high-tech application areas, including biomaterials for drug delivery systems and tissue engineering. The outstanding mechanical properties of SF, including its facile processability, superior biocompatibility, controllable biodegradation, and versatile functionalization have allowed its use for innovative applications. In this review, we describe the structure, composition, general properties, and structure-properties relationship of SF. In addition, the methods used for the fabrication and modification of various materials are briefly addressed. Lastly, recent applications of SF-based materials for small molecule drug delivery, biological drug delivery, gene therapy, wound healing, and bone regeneration are reviewed and our perspectives on future development of these favorable materials are also shared.
Experience of nurses who work with children with palliative care needs: A mixed-method systematic review

Abstract Objective The importance of palliative care education for nurses has been recognized worldwide. The study aims to explore the experiences of nurses working with children with palliative care needs and to identify any related educational needs. Methods The electronic databases of CINAHL, Cochrane, PubMed, OVID, Social Care Online, Web of Science, Scopus, and ProQuest were searched for the period 2000–2015. Results Finding revealed that working with children with palliative care needs is an emotionally struggling job for nurses, especially when they try to manage the transition of pediatric patients from curative to palliative care. Staffing level and time constraints comprise a major obstacle in pediatric palliative care. Focusing on invasive treatment and technology in spite of the feelings that it will not improve patients' health status intensifies the feeling of guilt and helplessness for nurses. Finally, nurses asserted the importance of receiving pediatric palliative care education, especially how to communicate with children with palliative care needs and their families. Significance of results Further research is recommended with regard to nurses' experience in communication with children with palliative care needs. Nursing education in pediatric palliative care is significantly important, especially how to communicate with children with palliative care needs and their families.
Optimizing the Diagnostic Criteria for Standard (250-μg) and low Dose (1-μg) Adrenocorticotropin Tests in the Assessment of Adrenal Function

ACTH stimulation is the standard test for assessment of adrenal function. It was suggested that the low dose (1 μg) would be more sensitive for detecting mild secondary adrenal insufficiency than the usual dose of 250 μg. The aim of this study was to find the optimal diagnostic criteria and to compare standard dose test (SDT) with the low dose test (LDT). A group of patients treated with corticosteroids for the 6 months was considered to have hypothalamo-pituitary-adrenal impairment. Studies were performed in 14 corticosteroid-treated and 28 control subjects in random order on 2 consecutive days. Tests were analyzed using the receiver operating characteristic curve method. The best test was cortisol increment at 15 min of the LDT. It was significantly better than the cortisol concentration at 15 min of the SDT, the best test during the SDT (receiver operating characteristic curve area and 95% confidence interval: LDT, 0.997 and 0.956–0.999; SDT, 0.827 and 0.662–0.929; P = 0.0113). For the cortisol increme.
The impact of renal function on efficacy and safety of new oral anticoagulant in atrial fibrillation patients

Abstract Background and objectives This meta-analysis was to investigate the efficacy and safety of new oral anticoagulant (NOAC) in atrial fibrillation (AF) patients with renal function insufficiency, and to explore whether renal decline occurs in AF patients with NOAC and its impact on outcomes. Methods and results In AF patients with mild renal insufficiency, the NOAC was associated with significantly lower rates of stroke (odds ratio [OR], 0.78; 95% confidence interval [CI], 0.67–0.91; P < .05). Lower rates of bleeding were significantly observed in NOAC group (OR, 0.85; 95% CI, 0.75–0.97; P < .05). In AF patients with moderate renal impairment, similar results were revealed (OR for stroke or systemic embolism, 0.80; 95% CI, 0.67–0.95, P < .05; OR for major bleeding, 0.78; 95% CI, 0.59–1.03; P = .07). During the follow-up, pooled data revealed that NOAC showed a less renal toxicity, but the difference did not reach statistical significance (creatinine clearance decline: −0.12 mL/min [−0.84, 0.61 mL/min]). We have revealed that the NOACs were associated with significantly lower rates of stroke or systemic embolism (hazard ratio [HR], 0.66; 95% CI, 0.42–0.89; P < .05) and lower rates of bleeding (HR, 0.93; 95% CI, 0.70–1.16; P = .153) in AF patients with worsening renal function. Conclusions NOAC may have the potentiality to be at least as effective as warfarin and may equal safety outcomes in AF patients with renal impairment. Renal decline during therapeutics may be less likely happened in NOAC than warfarin dose. NOAC may reveal good efficacy and safety outcomes in these scenarios. Further detailed research is needed to gain more clear profile on this new anticoagulant.
Response to Liu et al.

RELATIONSHIP BETWEEN RECURRENT ACUTE PANCREATITIS AND CHRONIC PANCREATITIS The clinicopathologic definitions of recurrent acute pancreatitis (RAP) and chronic pancreatitis (CP) are based on distinguishing clinical features of complex syndromes (e.g., .1 episode of AP for the diagnosis of RAP and morphologic features of fibrosis for the diagnosis of CP) with no reference to etiology. In the 1960s, attempts were made to distinguish RAP from CP ((1), see also Etemad and Whitcomb (2)), but the discovery that gain-of-function mutations p.R122H or p.N29I in the cationic trypsinogen gene (PRSS1) cause AP and RAP (primary phenotype), with a subset later developing CP, clarified the progressive relationship between these clinical syndromes (3). The etiology-based, progressive relationship between RAP and CP is specifically defined in the Mechanistic Definition of CP (4), a new definition that has been accepted by the major pancreatic societies (5). Multiple studies, including the meta-analysis (6) noted by Liu et al., confirm the relationship between RAP and CP, but they do not infer that all RAP becomes CP nor that CP requires RAP. Note also that the diagnosis of RAP does not preclude the diagnosis of CP or vice versa, and they can occur in the same person at the same time. The evidence that Liu et al. use to argue against including RAP with CP in our analysis is based on an article by Cavestro et al. (7). However, this article is now a decade out of date, grossly underpowered (RAP n 5 64; CP n 5 142), and only looked at 1 variant inMCP-1, 1 in SPINK1, and 33 cystic fibrosis-causing variants in CFTR. Their limited data suggested that genetic variants cause RAP but not CP.More recent studies that are larger and/or that have deeper genotyping demonstrate that RAP and CP have common etiologies and that time and persistent injury or inflammation, or additional risk factors that are present within a subset of RAP patients, cause progression to CP (8–12). Finally, the etiology of diabetes mellitus (DM) is linked to the pancreatic beta cell, not the acinar or duct cells that contribute to the etiology of RAP and CP. The fact that even one episode of AP clearly increases risk of DM (13) suggests that in some patients, susceptibility to DM is clearly linked to exocrine pancreatic injury and inflammation—which takes the forms of AP, RAP, and CP.
Combined Effect of Cadmium and Lead on Durum Wheat

Cadmium (Cd) and lead (Pb) are two toxic heavy metals (HMs) whose presence in soil is generally low. However, industrial and agricultural activities in recent years have significantly raised their levels, causing progressive accumulations in plant edible tissues, and stimulating research in this field. Studies on toxic metals are commonly focused on a single metal, but toxic metals occur simultaneously. The understanding of the mechanisms of interaction between HMs during uptake is important to design agronomic or genetic strategies to limit contamination of crops. To study the single and combined effect of Cd and Pb on durum wheat, a hydroponic experiment was established to examine the accumulation of the two HMs. Moreover, the molecular mechanisms activated in the roots were investigated paying attention to transcription factors (bHLH family), heavy metal transporters and genes involved in the biosynthesis of metal chelators (nicotianamine and mugineic acid). Cd and Pb are accumulated following different molecular strategies by durum wheat plants, even if the two metals interact with each other influencing their respective uptake and translocation. Finally, we demonstrated that some genes (bHLH 29, YSL2, ZIF1, ZIFL1, ZIFL2, NAS2 and NAAT) were induced in the durum wheat roots only in response to Cd.
Enhanced Neuroprotective Effects of Panax ginseng G115® and Ginkgo biloba GK501® Combinations In Vitro Models of Excitotoxicity

Neurological-related disorders are seen as an increasingly important aspect of welfare. While conventional medicine is still the mainstay for the treatment of these diseases, it is becoming apparent that patients are also seeking more natural and preventative interventions. Panax ginseng G115® and Ginkgo biloba GK501® extracts alone or in combination were used in two in vitro experimental models of primary cultures exposed to excitotoxicity: rat organotypic hippocampal slices exposed to either 5 µM kainic acid or 10 µM N-Methyl-d-aspartate for 24 hours, and mixed cortical cells exposed to 300 µM NMDA for 10 min. Cell death in the Cornu Ammonis areas CA3 or CA1 subregions of slices was quantified by measuring propidium iodide fluorescence, whereas in cortical cells, it was assessed by measuring the amount of lactate dehydrogenase. In slices, treatment with extracts alone or in combination significantly attenuated CA3 and CA1 damage induced by exposure to kainic acid or NMDA, respectively. A similar neuroprotective effect was observed in cortical cells exposed to NMDA. Analysis of cell signaling pathways found that the two extracts induced an increase of the phosphorylation and they reversed the decrease of phosphorylation of ERK1/2 and Akt induced by kainic acid and NMDA in organotypic hippocampal slices. These results suggest that P. ginseng G115® and G. biloba GK501® extracts may mediate their effects by activating phosphorylation of ERK1/2 and Akt signaling pathways, protecting against excitotoxicity-induced damage in in vitro models.
Neuroprotective effects of mitoquinone and oleandrin on Parkinson’s disease model in zebrafish

Abstract Aim: The aim of this study is to investigate the possible protective effects of mitoquinone and oleandrin on rotenone induced Parkinson’s disease in zebrafish. Materials and methods: Adult zebrafish were exposed to rotenone and mitoquinone for 30 days. Biochemical parameters were determined by spectrophotometric method and Parkinson’s disease-related gene expressions were determined by reverse transcription polymerase chain reaction method. Measurement of neurotransmitters was performed by liquid chromatography tandem-mass spectrometry instrument. The accumulation of synuclein was demonstrated by immunohistochemical staining. In vitro thiazolyl blue tetrazolium bromide method was applied to determine the mitochondrial function of synaptosomal brain fractions using rotenone as a neurotoxic agent and mitoquinone and oleandrin as neuroprotective agents. Results: Mitoquinone improved the oxidant-antioxidant balance and neurotransmitter levels that were disrupted by rotenone. Mitoquinone also ameliorated the expressions of Parkinson’s disease-related gene expressions that were disrupted by rotenone. According to thiazolyl blue tetrazolium bromide assay results, mitoquinone and oleandrin increased mitochondrial function which was decreased due to rotenone exposure. Conclusion: Based on the results of our study, positive effects of mitoquinone were observed in Parkinson’s disease model induced by rotenone in zebrafish.
Neurology and Neuroscience: Two Cultures, Common Destiny?

As a jobbing neuroscientist with day-to-day responsibilities for teaching and research, I am about as far away from ‘practical neurology’ as any writer of an editorial in this journal is ever likely to be. I don’t see patients, I do not have to think about diagnosis, to treat, nor to pass on bad news. My subjects live in the animal rooms of the laboratory, turn up for their appointments on time, and have invasive licensed procedures in which the experimental conditions are precisely matched except for the one variable in which I am interested. It would seem that clinical neurology and neuroscience are two quite different cultures. However, we are not like the two cultures of Arts and Science that F.R. Levis and C.P. Snow argued about two generations ago (Snow 1993; see also: http://www.datasync.com/~/pwilz/snow1.htm). We have in common a shared interest in the organ of the human body from
Diurnal variations of amplitude of accommodation in different age groups

Clinical assessment of amplitude of accommodation (AA) involves measuring the ability of the eye to change its optical power and focus on near tasks/objects. AA gradually decreases with increasing age. However, details of age-related diurnal changes in AA are not well known. This study compared diurnal changes in AA in the adolescents, the twenties, and the forties age groups. Measurement of AA using the push-up method was performed in six sessions at two-hourly intervals for 154 subjects (48, 56, 50 subjects for the adolescents, twenties, and forties age groups, respectively); the first measurements were taken from 9:00–10:00 a.m. and the final measurements from 7:00–8:00 p.m. The mean AA was 14.67 D (highest: 16.15 D in the 3:00–4:00 p.m. session, lowest: 13.35 D in the 9:00–10:00 a.m. session) for the adolescent group; 11.13 D (highest: 11.69 D in the 3:00–4:00 p.m. session; lowest: 10.61 D in the 9:00–10:00 a.m. session) in the twenties group; and 5.53 D (highest: 5.80 D in the 1:00–2:00 p.m. session, lowest: 5.11 D in the 7:00–8:00 p.m. session) in the forties age group. The measured AA showed significant difference between sessions; however, diurnal variations were greater in the younger groups. The measured AA was low at the beginning of the day in the adolescents and twenties groups and low at the end of the day in the forties age group. All age groups showed a high AA during the afternoon hours of the day (1:00–4:00 p.m.). Since the difference between each session was larger in younger subjects, AA should be evaluated while taking the age-related diurnal variations into account.
PERSISTENT TAPETAL CELL2 Is Required for Normal Tapetal Programmed Cell Death and Pollen Wall Patterning1[OPEN]

PTC2, an AT-hook DNA binding protein, is required for tapetal programmed cell death and pollen wall patterning in rice. The timely programmed cell death (PCD) of the tapetum, the innermost somatic anther cell layer in flowering plants, is critical for pollen development, including the deposition and patterning of the pollen wall. Although several genes involved in tapetal PCD and pollen wall development have been characterized, the underlying regulatory mechanism remains elusive. Here we report that PERSISTENT TAPETAL CELL2 (PTC2), which encodes an AT-hook nuclear localized protein in rice (Oryza sativa), is required for normal tapetal PCD and pollen wall development. The mutant ptc2 showed persistent tapetal cells and abnormal pollen wall patterning including absent nexine, collapsed bacula, and disordered tectum. The defective tapetal PCD phenotype of ptc2 was similar to that of a PCD delayed mutant, ptc1, in rice, while the abnormal pollen wall patterning resembled that of a pollen wall defective mutant, Transposable Element Silencing Via AT-Hook, in Arabidopsis (Arabidopsis thaliana). Levels of anther cutin monomers in ptc2 anthers were significantly reduced, as was expression of a series of lipid biosynthetic genes. PTC2 transcript and protein were shown to be present in the anther after meiosis, consistent with the observed phenotype. Based on these data, we propose a model explaining how PTC2 affects anther and pollen development. The characterization of PTC2 in tapetal PCD and pollen wall patterning expands our understanding of the regulatory network of male reproductive development in rice and will aid future breeding approaches.
‘Should it fit? Yes. Does it fit? No’: Exploring the organisational processes of introducing a recovery-oriented approach to mental health in Australian private health care

This article explores the implementation of an innovative approach to mental health care in a private health setting. Open Dialogue is a recovery-oriented approach to mental health that emerged in Finland, which emphasises family involvement, interdisciplinary collaboration and a flexible, needs-adapted approach. Early research is promising; however, little research has explored Open Dialogue outside Finland. This study aimed to explore the introduction of this approach at a private, inpatient young-adult mental health unit in Australia. Drawing on data from a long-term ethnographic field study that included 190 hours of observation and qualitative interviews, the findings show that despite staff members being inspired by and supportive of Open Dialogue, the existing ideology and organisational structures of the unit conflicted with the integration of Open Dialogue principles. Dialogical ways of working were challenged by medical dominance and emphasis on economic efficiencies. This study emphasises the importance of a ‘good’ fit between organisational cultures and innovations. It also highlights the challenges of moving towards recovery-oriented and family-focused models of care in the Australian neoliberal health care context. There is a need for organisational and ideological change in health services that is receptive to, and meaningfully supports, efforts to implement recovery-oriented care.
Cross-Talk between Lipoproteins and Inflammation: The Role of Microvesicles

Atherothrombosis is the principal underlying cause of cardiovascular disease (CVD). Microvesicles (MV) are small blebs originated by an outward budding at the cell plasma membranes, which are released in normal conditions. However, MV release is increased in pathophysiologic conditions such as CVD. Low density lipoprotein (LDL) and MV contribute to atherothrombosis onset and progression by promoting inflammation and leukocyte recruitment to injured endothelium, as well as by increasing thrombosis and plaque vulnerability. Moreover, (oxidized)LDL induces MV release and vice-versa, perpetuating endothelium injury leading to CVD progression. Therefore, MV and lipoproteins exhibit common features, which should be considered in the interpretation of their respective roles in the pathophysiology of CVD. Understanding the pathways implicated in this process will aid in developing novel therapeutic approaches against atherothrombosis.
Remote Ischemic Preconditioning and Diazoxide Protect from Hepatic Ischemic Reperfusion Injury by Inhibiting HMGB1-Induced TLR4/MyD88/NF-κB Signaling

Remote ischemic preconditioning (RIPC) is known to have a protective effect against hepatic ischemia-reperfusion (IR) injury in animal models. However, the underlying mechanism of action is not clearly understood. This study examined the effectiveness of RIPC in a mouse model of hepatic IR and aimed to clarify the mechanism and relationship of the ATP-sensitive potassium channel (KATP) and HMGB1-induced TLR4/MyD88/NF-κB signaling. C57BL/6 male mice were separated into six groups: (i) sham-operated control, (ii) IR, (iii) RIPC+IR, (iv) RIPC+IR+glyburide (KATP blocker), (v) RIPC+IR+diazoxide (KATP opener), and (vi) RIPC+IR+diazoxide+glyburide groups. Histological changes, including hepatic ischemia injury, were assessed. The levels of circulating liver enzymes and inflammatory cytokines were measured. Levels of apoptotic proteins, proinflammatory factors (TLR4, HMGB1, MyD88, and NF-κB), and IκBα were measured by Western blot and mRNA levels of proinflammatory cytokine factors were determined by RT-PCR. RIPC significantly decreased hepatic ischemic injury, inflammatory cytokine levels, and liver enzymes compared to the corresponding values observed in the IR mouse model. The KATP opener diazoxide + RIPC significantly reduced hepatic IR injury demonstrating an additive effect on protection against hepatic IR injury. The protective effect appeared to be related to the opening of KATP, which inhibited HMGB1-induced TRL4/MyD88/NF-kB signaling.
Treatment of severe acetaminophen-induced hepatocellular injury with prostaglandin E: Two case reports

Drugs have long been recognized as culprits in hepatocellular injury. Acetaminophen is one example of a commonly used over-the-counter medication that can cause severe centrolobular hepatic necrosis when ingested in large quantities in suicide attempts or unintentional overdoses. Acetaminophen hepatotoxicity is mediated by a toxic reactive metabolite formed from the parent compound by the cytochrome P450 mixed-function oxidase system of the hepatocyte. Conventional treatment of acetaminophen-induced liver injury consists of supportive measures and prevention of further drug absorption. In addition, in patients with high serum acetaminophen concentrations, the severity of hepatic necrosis appears to diminish with the timely use of sulfhydryl compounds such as N-acetyl cysteine. Two patients in whom acetaminophen hepatotoxicity was successfully treated using prostaglandin E1 are described.