Miracle-dz/UniFAR-FTUs huggingface dataset:
The effect of aromatherapy with rose and lavender on anxiety, surgical site pain, and extubation time after open‐heart surgery: A double‐center randomized controlled trial

To determine the effect of aromatherapy with rose and lavender on the patient outcomes after open‐heart surgery (OHS). In the clinical trial, patients were randomized to four groups. One group received routine care, the placebo group received a cotton swab soaked in water and the other two groups received either a cotton swab containing three drops of rose or lavender essence (0.2 ml). A total of 160 patients were randomized into four groups. Intergroup anxiety was not significantly different; however, the reciprocal time‐group effect was significant among the four groups. The extubation time was significant among the four groups which related to rose essence group compared with the control group (p < .001) and placebo group (p = .029). The surgical site pain was significant in the rose essence and lavender groups compared to the control group. Aromatherapy can reduce extubation time, surgical site pain severity, and anxiety in patients undergoing OHS
The effect of extrinsic Wnt/β‐catenin signaling in Muller glia on retinal ganglion cell neurite growth

Muller glia are the predominant glial cell type in the retina, and they structurally and metabolically support retinal neurons. Wnt/β‐catenin signaling pathways play essential roles in the central nervous system, including glial and neuronal differentiation, axonal growth, and neuronal regeneration. We previously demonstrated that Wnt signaling activation in retinal ganglion cells (RGC) induces axonal regeneration after injury. However, whether Wnt signaling within the adjacent Muller glia plays an axongenic role is not known. In this study, we characterized the effect of Wnt signaling in Muller glia on RGC neurite growth. Primary Muller glia and RGC cells were grown in transwell co‐cultures and adenoviral constructs driving Wnt regulatory genes were used to activate and inhibit Wnt signaling specifically in primary Muller glia. Our results demonstrated that activation of Wnt signaling in Muller glia significantly increased RGC average neurite length and branch site number. In addition, the secretome of Muller glia after induction or inhibition of Wnt signaling was characterized using protein profiling of conditioned media by Q Exactive mass spectrometry. The Muller glia secretome after activation of Wnt signaling had distinct and more numerous proteins involved in regulation of axon extension, axon projection and cell adhesion. Furthermore, we showed highly redundant expression of Wnt signaling ligands in Muller glia and Frizzled receptors in RGCs and Muller glia. Therefore, this study provides new information about potential neurite growth promoting molecules in the Muller glia secretome, and identified Wnt‐dependent target proteins that may mediate the axonal growth.
Early Aphasia Rehabilitation Is Associated With Functional Reactivation of the Left Inferior Frontal Gyrus

Background and Purpose—Early poststroke aphasia rehabilitation effects and their functional MRI (fMRI) correlates were investigated in a pilot, controlled longitudinal study. Methods—Twelve patients with mild/moderate aphasia (8 Broca, 3 anomic, and 1 Wernicke) were randomly assigned to daily language rehabilitation for 2 weeks (starting 2.2 [mean] days poststroke) or no rehabilitation. The Aachen Aphasia Test and fMRI recorded during an auditory comprehension task were performed at 3 time intervals: mean 2.2 (T1), 16.2 (T2), and 190 (T3) days poststroke. Results—Groups did not differ in terms of age, education, aphasia severity, lesions volume, baseline fMRI activations, and in task performance during fMRI across examinations. Rehabilitated patients significantly improved in naming and written language tasks (P<0.05) compared with no rehabilitation group both at T2 and T3. Functional activity at T1 was reduced in language-related cortical areas (right and left inferior frontal gyrus and middle temporal g.
Metabolomics Benefits from Orbitrap GC–MS—Comparison of Low- and High-Resolution GC–MS

The development of improved mass spectrometers and supporting computational tools is expected to enable the rapid annotation of whole metabolomes. Essential for the progress is the identification of strengths and weaknesses of novel instrumentation in direct comparison to previous instruments. Orbitrap liquid chromatography (LC)–mass spectrometry (MS) technology is now widely in use, while Orbitrap gas chromatography (GC)–MS introduced in 2015 has remained fairly unexplored in its potential for metabolomics research. This study aims to evaluate the additional knowledge gained in a metabolomics experiment when using the high-resolution Orbitrap GC–MS in comparison to a commonly used unit-mass resolution single-quadrupole GC–MS. Samples from an osmotic stress treatment of a non-model organism, the microalga Skeletonema costatum, were investigated using comparative metabolomics with low- and high-resolution methods. Resulting datasets were compared on a statistical level and on the level of individual compound annotation. Both MS approaches resulted in successful classification of stressed vs. non-stressed microalgae but did so using different sets of significantly dysregulated metabolites. High-resolution data only slightly improved conventional library matching but enabled the correct annotation of an unknown. While computational support that utilizes high-resolution GC–MS data is still underdeveloped, clear benefits in terms of sensitivity, metabolic coverage, and support in structure elucidation of the Orbitrap GC–MS technology for metabolomics studies are shown here.
Effects of Aroma Inhalation on Stress, Fatigue and Depression among Nurses Working in Intensive Care Unit

Copyright c Korea Institute of Dermatological Sciences. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Effects of Aroma Inhalation on Stress, Fatigue and Depression among Nurses Working in Intensive Care Unit
Social networks in mild-to-moderate Alzheimer disease: longitudinal relationships with dementia severity, cognitive function, and adverse events

Abstract Objectives Poor social networks are associated with a greater likelihood of cognitive decline, dementia, and other adverse health outcomes in later life. However, these relationships have been poorly explored in those with established Alzheimer Disease (AD), who may represent a particularly vulnerable group. Methods Analysis of data from the NILVAD study. We assessed social networks (Lubben Social Network Scale [LSNS]), cognition (Alzheimer’s disease Assessment Scale [ADAS-Cog]) and dementia severity (Clinical Dementia Rating, Sum of Boxes [CDR-Sb]) in older adults with mild-moderate AD at baseline and at 18 months. Results 464 participants with mild-to-moderate AD were included (73.1 ± 8.3 years; 61.9% female). At baseline, a poor social network was significantly associated with a greater dementia severity, but not greater cognitive impairment. Rather than a poor social network predicting greater cognitive decline over 18 months, a greater baseline dementia severity predicted a decline in social network over 18 months (β: −0.22, −0.42 – −0.02, p = 0.034). Finally, a poor social network was associated with a significantly increased likelihood of experiencing serious adverse events (IRR: 1.41, 1.06–1.89, p = 0.019). Discussion As dementia progresses, older adults with AD are more likely to experience a decline in social network. Further, having a poor social network was associated with a greater likelihood of experiencing serious adverse events. These findings add novel insight into the complex relationship between social networks, dementia progression and adverse events in AD, and underscore the importance of developing and maintaining social networks in AD.
Low mtDNA diversity in a highly differentiated population of spinner dolphins (Stenella longirostris) from the Fernando de Noronha Archipelago, Brazil

Spinner dolphins (Stenella longirostris, Gray 1828) are widely distributed in tropical waters around the world. Although they occur in large, pelagic groups in the Eastern Tropical Pacific, elsewhere in the Pacific they are found in small and genetically isolated populations associated with islands. This species is considered to be “Least Concern” (LC) by the World Conservation Union (IUCN). To assess genetic diversity and population structure of an island-associated population in the South Atlantic Ocean we surveyed 162 spinner dolphins throughout the Fernando de Noronha Archipelago of the northeast coast of Brazil using ten microsatellite loci and sequencing a 413-bp section of the mitochondrial DNA (mtDNA) control region. Eleven mtDNA haplotypes were identified and haplotype diversity (h) and nucleotide diversity (π) were 0.3747 and 0.0060, respectively. Median-Joining Network revealed the presence of two very divergent haplotypes and F-statistics indicated some heterogeneity between two sampling years. All microsatellite loci were polymorphic (Ho: 0.767; He: 0,764) but, revealed no detectable substructure. We also compared the mtDNA haplotypes from Noronha to 159 haplotypes representing 893 individuals from 14 locations worldwide. We found that the two common haplotypes from the Fernando de Noronha Archipelago were absent in all other populations. These comparisons showed that Noronha spinner dolphins are likely more differentiated than other island populations, suggesting that they form societies with strong site fidelity mediated by females.
The impact of residual mitral regurgitation after MitraClip therapy in functional mitral regurgitation

MitraClip therapy for the treatment of functional mitral regurgitation (FMR) is an increasingly used intervention for high‐risk surgical patients. The aim of this observational study was to assess the impact of residual mitral regurgitation (rMR) at discharge on long‐term outcome after MitraClip therapy in patients with FMR.
Effect of the Sodium-Glucose Cotransporter 2 Inhibitor, Dapagliflozin, on Genitourinary Infection in an Animal Model of Type 2 Diabetes

Purpose To investigate the effect of dapagliflozin, a sodium-glucose cotransporter 2 inhibitor, on inflammatory cytokines of urogenital tissue in a rat model of type 2 diabetes (T2DM) to infer pharmaceutical influence of dapagliflozin on genitourinary infection or inflammation. Methods Study animals were divided into the following 4 groups of 10 animals each: (1) the Otsuka Long-Evans Tokushima Fatty (OLETF)-DA group treated with dapagliflozin at 1.0 mg/kg/day, (2) the OLETF-VO group treated with voglibose at 0.6 mg/kg/day, (3) the control group (OLETF-CO) given water, and (4) the Long-Evans Tokushima Otsuka (LETO) rats were included as nondiabetic control group. Changes in blood glucose, 24-hour urine volume, and urine glucose were measured. The interleukin-1β (IL-1β) and interleukin-18 (IL-18) levels in the bladder and the urethra were quantified, respectively. Results The urine glucose level and the 24-hour urine volume at 12 weeks of treatment were significantly higher in the OLETF-DA group than that in any other group (P<0.05). The cytokine analysis of the bladder and urethra showed higher IL-18 and IL-1β in the OLETF-DA and the OLETF-CO groups than that in the OLETF-VO and LETO groups (P<0.05). The cytokine levels did not differ between the OLETF-DA and the OLETF-CO groups, and the level of IL-18 in the OLETF-DA group was higher in the urethra than in the bladder. Conclusions This study revealed that dapagliflozin increased the urine glucose concentration, resulting in an inflammatory response remain in the urogenital tract as the untreated diabetic rats. Therefore, when treating patients with T2DM with dapagliflozin, careful attention should be paid to genitourinary infection or inflammation.
Convolutional Neural Network Technology in Endoscopic Imaging: Artificial Intelligence for Endoscopy

Recently, significant improvements have been made in artificial intelligence. The artificial neural network was introduced in the 1950s. However, because of the low computing power and insufficient datasets available at that time, artificial neural networks suffered from overfitting and vanishing gradient problems for training deep networks. This concept has become more promising owing to the enhanced big data processing capability, improvement in computing power with parallel processing units, and new algorithms for deep neural networks, which are becoming increasingly successful and attracting interest in many domains, including computer vision, speech recognition, and natural language processing. Recent studies in this technology augur well for medical and healthcare applications, especially in endoscopic imaging. This paper provides perspectives on the history, development, applications, and challenges of deep-learning technology.
Bioinformatics analysis of gene expression profiles of Inclusion body myositis

Inclusion body myositis (IBM) is a disease with a poor prognosis and limited treatment options. This study aimed at exploring gene expression profile alterations, investigating the underlying mechanisms and identifying novel targets for IBM. We analysed two microarray datasets (GSE39454 and GSE128470) derived from the Gene Expression Omnibus (GEO) database. The GEO2R tool was used to screen out differentially expressed genes (DEGs) between IBM and normal samples. Gene Ontology（GO）function and Kyoto Encyclopedia of Genes and Genomes（KEGG）pathway enrichment analysis were performed using the Database for Annotation, Visualization and Integrated Discovery to identify the pathways and functional annotation of DEGs. Finally, protein‐protein interaction (PPI) networks were constructed using STRING and Cytoscape, in order to identify hub genes. A total of 144 upregulated DEGs and one downregulated DEG were identified. The GO enrichment analysis revealed that the immune response was the most significantly enriched term within the DEGs. The KEGG pathway analysis identified 22 significant pathways, the majority of which could be divided into the immune and infectious diseases. Following the construction of PPI networks, ten hub genes with high degrees of connectivity were picked out, namely PTPRC, IRF8, CCR5, VCAM1, HLA‐DRA, TYROBP, C1QB, HLA‐DRB1, CD74 and CXCL9. Our research hypothesizes that autoimmunity plays an irreplaceable role in the pathogenesis of IBM. The novel DEGs and pathways identified in this study may provide new insight into the underlying mechanisms of IBM at the molecular level.
Germ-Free Swiss Webster Mice on a High-Fat Diet Develop Obesity, Hyperglycemia, and Dyslipidemia

A calorie-dense diet is a well-established risk factor for obesity and metabolic syndrome (MetS), whereas the role of the intestinal microbiota (IMB) in the development of diet-induced obesity (DIO) is not completely understood. To test the hypothesis that Swiss Webster (Tac:SW) mice can develop characteristics of DIO and MetS in the absence of the IMB, we fed conventional (CV) and germ-free (GF) male Tac:SW mice either a low-fat diet (LFD; 10% fat derived calories) or a high-fat diet (HFD; 60% fat derived calories) for 10 weeks. The HFD increased feed conversion and body weight in GF mice independent of the increase associated with the microbiota in CV mice. In contrast to CV mice, GF mice did not decrease feed intake on the HFD and possessed heavier fat pads. The HFD caused hyperglycemia, hyperinsulinemia, and impaired glucose absorption in GF mice independent of the increase associated with the microbiota in CV mice. A HFD also elevated plasma LDL-cholesterol and increased hepatic triacylglycerol, free fatty acids, and ceramides in all mice, whereas hypertriglyceridemia and increased hepatic medium and long-chain acylcarnitines were only observed in CV mice. Therefore, GF male Tac:SW mice developed several detrimental effects of obesity and MetS from a high-fat, calorie dense diet.
IRE1α Disruption in Triple-Negative Breast Cancer Cooperates with Antiangiogenic Therapy by Reversing ER Stress Adaptation and Remodeling the Tumor Microenvironment

Pharmacologic IRE1α kinase inhibition reverses ultrastructural distension of the ER, normalizes the tumor vasculature, and remodels the cellular TME attenuating TNBC growth in mice. Cancer cells exploit the unfolded protein response (UPR) to mitigate endoplasmic reticulum (ER) stress caused by cellular oncogene activation and a hostile tumor microenvironment (TME). The key UPR sensor IRE1α resides in the ER and deploys a cytoplasmic kinase–endoribonuclease module to activate the transcription factor XBP1s, which facilitates ER-mediated protein folding. Studies of triple-negative breast cancer (TNBC)—a highly aggressive malignancy with a dismal posttreatment prognosis—implicate XBP1s in promoting tumor vascularization and progression. However, it remains unknown whether IRE1α adapts the ER in TNBC cells and modulates their TME, and whether IRE1α inhibition can enhance antiangiogenic therapy—previously found to be ineffective in patients with TNBC. To gauge IRE1α function, we defined an XBP1s-dependent gene signature, which revealed significant IRE1α pathway activation in multiple solid cancers, including TNBC. IRE1α knockout in TNBC cells markedly reversed substantial ultrastructural expansion of their ER upon growth in vivo. IRE1α disruption also led to significant remodeling of the cellular TME, increasing pericyte numbers while decreasing cancer-associated fibroblasts and myeloid-derived suppressor cells. Pharmacologic IRE1α kinase inhibition strongly attenuated growth of cell line–based and patient-derived TNBC xenografts in mice and synergized with anti-VEGFA treatment to cause tumor stasis or regression. Thus, TNBC cells critically rely on IRE1α to adapt their ER to in vivo stress and to adjust the TME to facilitate malignant growth. TNBC reliance on IRE1α is an important vulnerability that can be uniquely exploited in combination with antiangiogenic therapy as a promising new biologic approach to combat this lethal disease. Significance: Pharmacologic IRE1α kinase inhibition reverses ultrastructural distension of the ER, normalizes the tumor vasculature, and remodels the cellular TME, attenuating TNBC growth in mice.
What have we learned about renal protection from the cardiovascular outcome trials and observational analyses with SGLT2 inhibitors?

Over the past 5 years, sodium‐glucose cotransport 2 (SGLT2) inhibitors have been increasingly regarded as glycaemic agents with cardiovascular (CV) and renal protective effects. The CV benefits of SGLT2 inhibitors have been well established in patients with type 2 diabetes (T2D) and a range of CV comorbidities at baseline. Subsequently, the renal benefits of SGLT2 inhibitors were established in the CREDENCE trial, a dedicated renal outcome trial where canagliflozin reduced the primary composite renal outcome by 30%. In light of these trials, clinical practice guidelines have rapidly evolved, recommending the use of SGLT2 inhibitors as renal and cardioprotective agents in appropriate patient populations. Accordingly, it is important to have an in‐depth understanding of the evidence underlying the use of SGLT2 inhibitors in patients with T2D based on published clinical trials and real‐world evidence (RWE) studies, as well as information related to potential safety concerns. To accomplish this, we reviewed the evidence for renal protection and safety with SGLT2 inhibitors in the EMPA‐REG OUTCOME, CANVAS Program and DECLARE‐TIMI 58 CV safety trials, and in the growing body of evidence emerging from real‐world studies. This body of work has shown that SGLT2 inhibitors reduce the risk of surrogate renal endpoints such as albuminuria and mitigate the risk of hard renal endpoints including doubling of serum creatinine and end‐stage kidney disease in patients with T2D.
New insight into the role of substance P/neurokinin‐1 receptor system in breast cancer progression and its crosstalk with microRNAs

The neuropeptide substance P (SP) triggers a variety of tumor‐promoting signaling pathways through the activation of neurokinin‐1receptor (NK1R), a class of neurokinin G protein‐coupled receptors superfamily. Recent researches in our and other laboratories have shown the overexpression of both SP and NK1R in breast cancer (BC) patients. SP/NK1R signaling is strongly implicated in the pathogenesis of BC through affecting cell proliferation, migration, metastasis, angiogenesis, and resistance. Therefore, SP/NK1R signaling responses must be rigorously regulated; otherwise, they would contribute to a more aggressive BC phenotype. Recently, microRNAs (miRNAs) as a specific class of epigenetic regulators have been shown to regulate NK1R and thus, controlling SP/NK1R signaling responses in BC. This review summarizes the current knowledge of the role of SP/NK1R signaling and its therapeutic potentials in BC. We also provide an overview regarding the effects of miRNA‐mediated NK1R regulatory mechanisms in controlling BC tumorigenesis to gain a clearer view and thus better management of cancer.
Paneth Cell Alterations During Ischemia-reperfusion, Follow-up, and Graft Rejection After Intestinal Transplantation

Supplemental Digital Content is available in the text. Background. Ischemia-reperfusion injury is inevitable during intestinal transplantation (ITx) and executes a key role in the evolution towards rejection. Paneth cells (PCs) are crucial for epithelial immune defense and highly vulnerable to ischemia-reperfusion injury. We investigated the effect of ITx on PC after reperfusion (T0), during follow-up, and rejection. Moreover, we investigated whether PC loss was associated with impaired graft homeostasis. Methods. Endoscopic biopsies, collected according to center protocol and at rejection episodes, were retrospectively included (n = 28 ITx, n = 119 biopsies) Biopsies were immunohistochemically co-stained for PC (lysozyme) and apoptosis, and PC/crypt and lysozyme intensity were scored. Results. We observed a decrease in PC/crypt and lysozyme intensity in the first week after ITx (W1) compared with T0. There was a tendency towards a larger decline in PC/crypt (P = 0.08) and lysozyme intensity (P = 0.08) in W1 in patients who later developed rejection compared with patients without rejection. Follow-up biopsies showed that the PC number recovered, whereas lysozyme intensity remained reduced. This persisting innate immune defect may contribute to the well-known vulnerability of the intestine to infection. There was no clear evidence that PCs were affected throughout rejection. Conclusions. This study revealed a transient fall in PC numbers in the early post-ITx period but a permanent reduction in lysozyme intensity following ITx. Further research is needed to determine the potential clinical impact of PC impairment after ITx.