Miracle-dz/UniFAR-FTUs huggingface dataset:
Assessing adaptation and mitigation potential of roadside trees under the influence of vehicular emissions: A case study of Grevillea robusta and Mangifera indica planted in an urban city of India

The ever-increasing vehicle counts have resulted in a significant increase in air pollution impacting human and natural ecosystems including trees, and physical properties. Roadside plantations often act as a first defense line against the vehicular emissions to mitigate the impacts of pollutants. However, they are themselves vulnerable to these pollutants with varying levels of tolerance capacity. This demands a scientific investigation to assess the role of roadside plantation for better management and planning for urban sprawl where selected trees could be grown to mitigate the impacts of harmful pollutants. The present study assesses the impacts of vehicular emissions on the adaptation and mitigation potential of two important roadside tree species i.e. Grevillea robusta and Mangifera indica planted along roadsides in the capital city of Uttarakhand. Uttarakhand is one of the Indian Western Himalayan State and its capital city is situated on the foothills of Himalaya. The adaptation and mitigation potential were evaluated by studying the response of pollutants on the functional traits which drive the physiology of the trees. The CO2 assimilation rate, transpiration rate, stomatal conductance, water use efficiency (WUE), air pollution tolerance index (APTI), copper and proline accumulation, dust removal efficiency (DRE), leaf thickness and cooling created by plantation were studied to evaluate the response of trees exposed to roadside traffics. To compare the influence of pollutants, traits of trees grown in a control site with few or absence of vehicular movement were compared with the roadside trees. The control site represented part of a reserve forest where human interference is controlled and human-induced activities are prohibited. The vehicular frequency was found to modulate tree characteristics. The tree characteristics representing WUE, APTI, proline and copper accumulation, leaf thickness, cooling impact, and DRE were enhanced significantly, while the decreased CO2 assimilation rate was observed near roadside trees compared to the control site. We found both of the species to perform well to be used as one of the potential species for roadside and urban greening. However, there is a need to assess the potential of other species in reference to the present study.
Sweating Disorders.

PURPOSE OF REVIEW This article reviews disorders of sweating, including hyperhidrosis and anhidrosis due to central or peripheral autonomic nervous system causes. RECENT FINDINGS Disorders of thermoregulation and sweating may manifest with hyperhidrosis or hypohidrosis/anhidrosis. Primary disorders of hyperhidrosis may significantly impact quality of life yet tend to be benign. Many sweating disorders present with compensatory hyperhidrosis due to areas of anhidrosis. Anhidrosis may occur due to either central or peripheral damage to the autonomic nervous system. The thermoregulatory control of sweating involves central pathways from the hypothalamus to the brainstem and then spinal cord as well as projections to peripheral structures, including the sympathetic chain ganglia, peripheral nerves, and eccrine sweat glands. Disruption at any point of this pathway may lead to impaired sweating. Characterization of sweating dysfunction helps localize different autonomic disorders to guide diagnosis and may allow for evaluation of treatment effect. SUMMARY Sweating dysfunction manifests in myriad ways, including essential hyperhidrosis, complete anhidrosis with heat intolerance, and compensatory hyperhidrosis due to anhidrosis, and often indicates involvement of underlying central or peripheral autonomic dysfunction.
Ex vivo investigation on internal tunnel approach/internal resin infiltration and external nanosilver-modified resin infiltration of proximal caries exceeding into dentin

This ex vivo proof-of-concept study aimed to investigate the effect of nanosilver particles (AgNP) added to a conventional infiltrant resin (Icon) on external penetration into natural proximal enamel caries exceeding into dentin after internal tunnel preparation and internal infiltration. Carious lesions (ICDAS codes 2/3) of extracted human (pre-)molars revealing proximal caries radiographically exceeding into dentin (E2/D1 lesions) were preselected. Then, 48 of those specimens showing demineralized areas transcending the enamel-dentin border as assessed by means of near-infrared light transillumination (DIAGNOcam) were deproteinized (NaOCl, 5%). Using an internal tunnel approach, occlusal cavities central to the marginal ridge were prepared. Excavation of carious dentin, total etch procedure (H3PO4, 40%), and internal resin infiltration (FITC-labeled) followed, along with final restorations (flowable composite resin). Outer lesion surfaces were etched (HCl, 15%) prior to external infiltration (RITC-labeled). Group 1 (control; n = 24) used non-modified infiltrant, while an infiltrant/AgNP mixture (20 nm; 5.5 wt%) was used with experimental Group 2 (n = 24). Non-infiltrated pores of cut lesions were stained (Berberine), and specimens were analyzed using confocal laser scanning microscopy. Compared to the non-filled infiltrant, incorporation of AgNP had no effect on the resin’s external penetration. Between the groups, no significant differences regarding internal or external infiltration could be detected, and non-infiltrated lesion areas did not differ significantly (p>0.109; t-test). The internal tunnel preparation in combination with both an internal resin infiltration and an additional external infiltration approach using a nanosilver-modified infiltrant resin leads to increased infiltrated lesion areas, thus occluding and adhesively stabilizing the porous volume of the demineralized enamel. While exerting antimicrobial effects by the nanosilver particles, this approach should have the potential as a viable treatment alternative for proximal lesions extending into dentin, thus avoiding the sacrifice of sound enamel, postponing the frequently inevitable restoration/re-restoration cycle of conventional proximal caries treatment, and improving dental health.
The Cohesin Complex Subunit ZmSMC3 Participates in Meiotic Centromere Pairing in Maize[CC-BY]

In addition to its role in sister chromatid cohesion, the cohesin complex subunit ZmSMC3 participates in meiotic centromere pairing in maize to ensure accurate chromosome segregation. Meiosis consists of two highly conserved nuclear divisions, which allow eukaryotes to maintain their chromosome number through sexual reproduction. The successful completion of meiosis depends on homologous chromosome pairing. Centromere interactions during early meiotic prophase I facilitate homologous chromosome pairing, but the underlying mechanism is unclear. Here, we performed chromatin immunoprecipitation-mass spectrometry analysis of maize (Zea mays) anthers during early meiotic prophase I using anti-centromeric histone H3 (CENH3) antibodies and determined that the cohesin subunit Structural Maintenance of Chromosome3 (SMC3) interacts with CENH3 during this period. SMC3 is enriched at centromeres and along chromosome arms in threads from leptotene to pachytene and might promote interactions between homologous centromeres. We observed dysfunctional SMC3 assembly in meiotic-specific maize mutants with defective centromere pairing. In SMC3 RNAi meiocytes, centromere pairing defects were observed during early meiotic prophase I, SMC3 was weakly associated with centromeres, and SMC3 did not localize to the chromosome arms. In wild-type mitosis, SMC3 is associated with chromatin and is enriched at centromeres from prophase to anaphase. CRISPR-Cas9-induced Zmsmc3 mutants showed premature loss of sister chromatid cohesion and mis-segregation of chromosomes in mitotic spreads. Our findings suggest that in addition to sister chromatid cohesion, ZmSMC3 participates in meiotic centromere pairing.
Macrophage migration inhibitory factor may contribute to hypertrophy of lumbar ligamentum flavum in type 2 diabetes mellitus

Previous studies have implicated the proinflammatory To the Editor: Lumbar spinal canal stenosis (LSCS) is a common disease among older individuals. Hypertrophic factors including interleukin (IL)-1a, IL-6, tumor necrosis lumbar ligamentum flavum (LLF) plays a vital role in the pathogenesis of LSCS. The physiological LLF is a kind of dense connective tissue with thickness of 2 to 4 mm, which is mainly composed of fibroblasts and extracellular matrix (ECM). ECM contains elastic, collagen fibers and ground substances. The distribution characteristics of fibers show that a large number of elastic fibers are mixed with a small amount of the collagen fibers; mainly type I and type III collagen fibers. These fibers are arranged tightly and regularly along the direction of column’s axis. The LLF is located in the dorsal part of the dura mater of the spinal canal, and it attaches to the upper border and lower parts of anterior surfaces of the laminas. The hypotrophy of LLF is the consequence of several factors such as aging, inflammatory process, stress loading and genetic predisposition. Once the hypertrophy of LLF occurs, it can cause the stenosis for the central spinal canal, nerve root canal and intervertebral foramen. This pathology can lead to low back pain, sciatica, and even urinary and bowel disorders.
Solubility Enhancement of Myricetin by Inclusion Complexation with Heptakis-O-(2-Hydroxypropyl)-β-Cyclodextrin: A Joint Experimental and Theoretical Study

Four cyclodextrins (CD) including β-cyclodextrin (β-CD), γ-cyclodextrin (γ-CD), heptakis-O-(2-hydroxypropyl)-β-cyclodextrin (HP-β-CD), and heptakis-O-(2, 6-di-O-methyl)-β-cyclodextrin (DM-β-CD) were used as solubilizer to study the solubility enhancement of myricetin. The results of the phase solubility study showed that the presence of CDs could enhance the solubility of myricetin by forming 1:1 complexes. Among all CDs, HP-β-CD had the highest solubilization effect to myricetin. The concentration of myricetin could be 1.60 × 10−4 moL/L when the presence of HP-β-CD reached 1.00 × 10−2 moL/L, which was 31.45 times higher than myricetin’s aqueous solubility. Subsequently, the HP-β-CD:myricetin complex was characterized by Fourier transform infrared spectroscopy (FT-IR), X-ray diffraction (XRD), and thermogravimetric analysis (TGA). In order to get an insight of the plausible structure of the complex, molecular docking was used to study the complexation process of HP-β-CD and myricetin. In the complex, the A ring and C ring of myricetin were complexed into the hydrophobic cavity of HP-β-CD, while the ring B was located at the wide rim of HP-β-CD. Four hydrogen bonding interactions were found between HP-β-CD and -OH groups of the guest in the HP-β-CD: myricetin complex. The complexation energy (△E) for the host-guest interactions was calculated with a negative sign, indicating the formation of the complex was an exergonic process. A 30-ns molecular dynamics simulation was conducted to the HP-β-CD: myricetin complex. Calculation results showed that no large structural deformation or position change were observed during the whole simulation time span. The average root-mean-square deviation (RMSD) changes of the host and guest were 2.444 and 1.145 Å, respectively, indicating the complex had excellent stability.
Hippocampal vascular reserve associated with cognitive performance and hippocampal volume

See Wiesmann and de Leeuw (doi:10.1093/brain/awz408) for a scientific commentary on this article. Hippocampal vascularization patterns vary between individuals. Using 7 Tesla time-of-flight angiography, Perosa et al. examine the impact of these differences in elderly adults with and without cerebral small vessel disease. A mixed hippocampal supply, as opposed to a single one, provides a hippocampal vascular reserve that protects against cognitive impairment.
Deciphering the role of the capsule of Klebsiella pneumoniae during pathogenesis: A cautionary tale

Extracellular capsule polysaccharides increase the cellular fitness under abiotic stresses and during competition with other bacteria. They are best‐known for their role in virulence, particularly in human hosts. Specifically, capsules facilitate tissue invasion by enhancing bacterial evasion from phagocytosis and protect cells from biocidal molecules. Klebsiella pneumoniae is a worrisome nosocomial pathogen with few known virulence factors, but the most important one is its capsule. In this issue, Tan et al. assess the fitness advantage of the capsule by competing a wild‐type strain against four different mutants where capsule production is interrupted at different stages of the biosynthetic pathway. Strikingly, not all mutants provide a fitness advantage. They suggest that some mutants have secondary defects altering virulence‐associated phenotypes and blurring the role of the capsule in pathogenesis. This study indicates that the K1 capsule in K. pneumoniae is not required for gut colonization but that it is critical for bloodstream dissemination to other organs. These results contribute to clarify the contradictory literature on the role of the Klebsiella capsule during infection. Finally, the varying fitness effects of different capsule mutations observed for K. pneumoniae K1 might apply also to other capsulated diderm bacteria that are facultative or emerging pathogens.
Thermal Stability of Octadecyltrichlorosilane and Perfluorooctyltriethoxysilane Monolayers on SiO2

Using in situ ultraviolet photoelectron spectroscopy (UPS) and X-ray photoelectron spectroscopy (XPS) measurements, the thermal behavior of octadecyltrichlorosilane (OTS) and 1H, 1H, 2H, and 2H-perfluorooctyltriethoxysilane (PTES) monolayers on SiO2 substrates has been investigated. OTS is thermally stable up to 573 K with vacuum annealing, whereas PTES starts decomposing at a moderate temperature between 373 K and 423 K. Vacuum annealing results in the decomposition of CF3 and CF2 species rather than desorption of the entire PTES molecule. In addition, our UPS results reveal that the work function (WF)of OTS remains the same after annealing; however WF of PTES decreases from ~5.62 eV to ~5.16 eV after annealing at 573 K.
Incidence and risk factors associated with pressure injury in patients with traumatic brain injury

Abstract Aim To identify the prevalence of pressure injury in patients diagnosed with traumatic brain injury and analyse the risk factors involved during hospitalization. Methods This was a prospective study evaluating patients who were diagnosed with traumatic brain injury between November 2013 and September 2014. Patient characteristics, clinical and metabolic factors and therapeutic interventions, were evaluated within 30 days of hospital admission. Results Most of the 240 patients included in the study were male, young, and non‐Caucasian. The incidence of pressure injury was 18.8%. In terms of severity classification, the incidence of pressure injury was 2.7%, 23.2%, and 42.6% in mild, moderate, and severe traumatic brain injury, respectively. Pressure injury development was more likely in the first 10 days of hospitalization. A moderate or severe traumatic brain injury classification, the use of noradrenaline, and older age were pressure injury risk factors. The presence of pressure injury was associated with mortality within 30 days of hospitalization (P < .001). Conclusion The incidence of pressure injury was high in patients diagnosed with traumatic brain injury, especially in those whose injury was classified as severe. Older age, noradrenaline use, and a classification of moderate or severe traumatic brain injury were identified as pressure injury risk factors.
Restless legs syndrome is associated with mast cell activation syndrome.

STUDY OBJECTIVES Mast cell activation syndrome (MCAS) is an inflammatory and allergic disorder. We determined the prevalence of Restless Legs Syndrome (RLS) in MCAS since each common syndrome may be inflammatory in nature and associated with dysautonomia. METHODS MCAS subjects were evaluated for RLS by two standard questionnaires. Prevalence comparisons included spouse controls and two prevalence publications. MCAS diagnosis required mast cell (MC) symptoms in ≥2 organs plus ≥1 elevated MC mediators, improvement with MC-therapy, and/or increased intestinal MC density. Clinical variables were studied. RESULTS There were 174 MCAS subjects (146 F, 28 M, mean 44.8 years) and 85 spouse controls (12 F, 73 M, mean 50.9 years). MCAS subjects as a whole had a higher prevalence of RLS (40.8%) than spouse controls (12.9%) (P <0.0001) Male MCAS subjects had a higher prevalence of RLS (32.1%) than male controls (12.3%, OR 3.4, CI 1.2-9.7, p=0.025) American men (8.4%, OR 5.2, CI 2.2-12.0, p<0.001), and French men (5.8%, OR 7.7, CI 3.4-17.1, p<0.001). Female MCAS subjects also had a higher prevalence of RLS (42.5%) than female controls (16.7%) but this did not reach statistical significance perhaps due to the sample size of the female controls. On the other hand, female MCAS subjects had a statistically higher prevalence of RLS than American women (10.0%, OR 6.7, CI 4.5-9.7, p<0.0001) and French women (10.8%, OR 6.1, CI 4.4-8.6, p<0.0001). Conclusions RLS appears to be associated with MCAS. Effects of MC mediators, inflammation, immune mechanisms, dysautonomia, or hypoxia may theoretically activate RLS in MCAS.
HGF/c-Met Promote Renal Carcinoma Cancer Stem Cells Enrichment Through Upregulation of Cir-CCDC66

Increasing studies have suggested that circular RNAs play an important function in the process of numerous cancers. We aimed to investigate the possible role of cir-CCDC66 in renal carcinoma cancer. As cancer stem cells are responsible for the renal carcinoma cancer tumor growth and resistance to conventional therapy, we focus on the cir-CCDC66 influence on renal carcinoma cancer stem cells. In this study, we performed experiments in human renal tubular epithelial cell HK2 cells and several renal carcinoma cancer cancer cell lines. The results showed that cir-CCDC66 was upregulated not only in renal carcinoma cancer cancer cell lines but also in cancer stem cell spheres. What’s more, the results showed that cir-CCDC66 enhanced the cancer stem cell enrichment. Further mechanistic studies showed that hepatocyte growth factor/c-Met pathway was activated in cancer stem cell enrichment and responsible for the cir-CCDC66 upregulation. Inhibition of hepatocyte growth factor/c-Met could block cir-CCDC66-induced cancer stem cell enrichment. In conclusion, our research revealed a novel mechanism between hepatocyte growth factor/c-Met/cir-CCDC66 and cancer stem cell enrichment. We verified that cir-CCDC66 could be a promising biomarker and therapy target for renal carcinoma cancer treatment.
Adjuvant antibiotic‐loaded bone cement: Concerns with current use and research to make it work

Antibiotic‐loaded bone cement (ALBC) is broadly used to treat orthopaedic infections based on the rationale that high‐dose local delivery is essential to eradicate biofilm‐associated bacteria. However, ALBC formulations are empirically based on drug susceptibility from routine laboratory testing, which is known to have limited clinical relevance for biofilms. There are also dosing concerns with nonstandardized, surgeon‐directed, hand‐mixed formulations, which have unknown release kinetics. On the basis of our knowledge of in vivo biofilms, pathogen virulence, safety issues with nonstandardized ALBC formulations, and questions about the cost‐effectiveness of ALBC, there is a need to evaluate the evidence for this clinical practice. To this end, thought leaders in the field of musculoskeletal infection (MSKI) met on 1 August 2019 to review and debate published and anecdotal information, which highlighted four major concerns about current ALBC use: (a) substantial lack of level 1 evidence to demonstrate efficacy; (b) ALBC formulations become subtherapeutic following early release, which risks induction of antibiotic resistance, and exacerbated infection from microbial colonization of the carrier; (c) the absence of standardized formulation protocols, and Food and Drug Administration‐approved high‐dose ALBC products to use following resection in MSKI treatment; and (d) absence of a validated assay to determine the minimum biofilm eradication concentration to predict ALBC efficacy against patient specific micro‐organisms. Here, we describe these concerns in detail, and propose areas in need of research.
The contribution of Parkin, PINK1 and DJ‐1 genes to selective neuronal degeneration in Parkinson's disease

Abstract Parkinson's disease (PD) is characterised by selective and severe degeneration of the substantia nigra pars compacta and the locus coeruleus (LC), which underlies the most prominent symptoms. Although α‐synuclein accumulation has long been established to play a causal role in the disease, it alone cannot explain the selective degenerative pattern. Recent evidence shows that the selective vulnerability could arise due to the large presence of cytosolic catecholamines and Ca2+ ions in the substantia nigra pars compacta and LC specifically that can be aberrantly affected by α‐synuclein accumulation. Moreover, each has its own toxic potential, and disturbance of one can exacerbate the toxic effects of the others. This presents a mechanism unique to these areas that can lead to a vicious degenerative cycle. Interestingly, in familial variants of PD, the exact same brain areas are affected, implying the underlying process is likely the same. However, the exact disease mechanisms of many of these genetic variants remain unclear. Here, we review the effects of the PD‐related genes Parkin, PINK1 and DJ‐1. We establish that these mutant varieties can set in motion the same degenerative process involving α‐synuclein, cytosolic catecholamines and Ca2+. Additionally, we show indications that model organisms might not accurately represent all components of this central mechanism, explaining why Parkin, PINK1 and DJ‐1 model organisms often lack a convincing PD‐like phenotype.
Cytotoxic CD4+ T lymphocytes may induce endothelial cell apoptosis in systemic sclerosis.

Systemic sclerosis (SSc) is an autoimmune fibrotic disease whose pathogenesis is poorly understood and lacks effective therapies. We undertook quantitative analyses of T cell infiltrates in the skin of thirty-five untreated patients with early diffuse SSc and here show that CD4+ cytotoxic T cells and CD8+ T cells contribute prominently to these infiltrates. We also observed an accumulation of apoptotic cells in SSc tissues, suggesting that recurring cell death may contribute to tissue damage and remodeling in this fibrotic disease. HLA-DR expressing endothelial cells were frequent targets of apoptosis in SSc, consistent with the prominent vasculopathy seen in patients with this disease. A circulating effector population of cytotoxic CD4+ T cells, which exhibited signatures of enhanced metabolic activity, was clonally expanded in systemic sclerosis patients. These data suggest that cytotoxic T cells may induce the apoptotic death of endothelial and other cells in systemic sclerosis. Cell loss driven by immune cells may be followed by overly exuberant tissue repair processes that lead to fibrosis and tissue dysfunction.