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Schwannoma is a slowly-growing, benign tumor that originates from the Schwann cell and is rarely found in the auricle. In this article, we describe a 20-year-old male patient with an approximately 2 cm auricular mass located in the antitragus of the left ear. The mass was slowlygrowing following an auricular trauma. The mass was completely removed by local excision and the histopathologic review confirmed the diagnosis as an auricular schwannoma. Characteristic immunohistochemical findings may be helpful in differential diagnosis of other tumors. Herein, we present with a literature review a rare case of auricular schwannoma following a trauma.

Melanoma is a dangerous form of skin cancer that results in the demise of patients at the developed stage. Researchers have attempted to develop automated systems for the timely recognition of this deadly disease. However, reliable and precise identification of melanoma moles is a tedious and complex activity as there exist huge differences in the mass, structure, and color of the skin lesions. Additionally, the incidence of noise, blurring, and chrominance changes in the suspected images further enhance the complexity of the detection procedure. In the proposed work, we try to overcome the limitations of the existing work by presenting a deep learning (DL) model. Descriptively, after accomplishing the preprocessing task, we have utilized an object detection approach named CornerNet model to detect melanoma lesions. Then the localized moles are passed as input to the fuzzy K -means (FLM) clustering approach to perform the segmentation task. To assess the segmentation power of the proposed approach, two standard databases named ISIC-2017 and ISIC-2018 are employed. Extensive experimentation has been conducted to demonstrate the robustness of the proposed approach through both numeric and pictorial results. The proposed approach is capable of detecting and segmenting the moles of arbitrary shapes and orientations. Furthermore, the presented work can tackle the presence of noise, blurring, and brightness variations as well. We have attained the segmentation accuracy values of 99.32% and 99.63% over the ISIC-2017 and ISIC-2018 databases correspondingly which clearly depicts the effectiveness of our model for the melanoma mole segmentation.

This study examines conscious judgments of perceptual similarity between foreign and native structures, focusing on vowel epenthesis following coda stops in English nonwords borrowed into Korean. In a similarity judgment experiment, Korean listeners heard a triplet consisting of an English stop-final form and two Korean forms, one ending in a stop and one ending in stop-vowel; then they indicated which of the two Korean forms the English form sounded more similar to. This study investigated six different predictors: release, voicing and place of coda stop, vowel tenseness, final stress, and word length. Similarity judgment choices showed that Korean CVCV is judged as more similar to English CVC than Korean CVC when the English final stop is released or dorsal or when the English word is monosyllabic. Although this result confirms that stop release is indeed a major factor explaining vowel insertion in this context, no effects of stop voicing and vowel tenseness are not compatible with the perceptual similarity hypothesis, which is surprising since they have been previously argued to involve acoustic cues affecting L2 speech perception. These findings support the need for further research that concentrates more on direct perception rather than judgments of perceptual similarity.

Background: Active participation of clients in rehabilitation is a crucial factor for improved outcomes. A few studies have investigated how to measure patient engagement to given rehabilitation therapies compared to intervention developments. In this study, we aimed to examine the possibility of assessing patient engagement by analyzing features computed from autonomic nervous responses with machine learning algorithms, such as naïve bayes classifier (NB), random forest (RF), support vector machine (SVM), and neural network (NN). Methods: Autonomic nervous responses were collected from 56 older adults with moderate to mild cognitive impairment using a wearable device during rehabilitation therapy sessions under two different conditions designed to induce different levels of engagement. 32 features were obtained from the autonomic nervous system responses and used to determine the client engagement levels. In addition, feature selection methods were applied to reduce redundant information. Client engagement during rehabilitation therapy sessions was rated by therapists using Pittsburgh Rehabilitation Participation Scale (PRPS). In addition, subjective feelings were quantified by participants using Self-Assessment Manikin (SAM). The data collected under the different conditions were labelled as having a higher or lower degree of engagement, and classification performance was tested with the algorithms. Results: It was found that the mean scores of PRPS and the valence dimension of the participants were significantly different between the conditions confirming the successful induction of varying levels of engagement from the participants. The worst performance was observed when the classifiers were trained with all features (mean classification accuracy: 81.6%) whereas the highest mean accuracy was observed when classifiers were trained with the top 5 features (85.6%) selected by minimum-Redundancy-Maximum-Relevance (mRMR) than other combinations of feature sets. The best classification accuracy of different degrees of rehabilitation participation was achieved with SVM (87.7%) in combination with the top 5 ranked features, which indicates that the feature selection methods employed in this study did not only lead to a reduction in the number of features, but also a slight improvement in the classification performance. On the other hand, RF consistently performed better than NB and NN when combined with the mRMR feature selection method, suggesting RF is the most robust classifier among the tested classifiers for determining the degree of client engagement in rehabilitation. Conclusions: Engagement in rehabilitation can be realized by utilizing autonomic nervous responses and machine learning algorithms as a way of involving clients in the process of engagement assessment while requiring their minimal cognitive efforts.

When an English word ending in a stop is adapted to Korean, a vowel is variably inserted after the final stop. Vowel insertion in this position is surprising because voiceless stops are permissible in coda position in Korean and it is not motivated by Korean native phonology. This study examines five factors that have been hypothesized to affect the likelihood of vowel insertion, i.e., tenseness of the pre-final vowel, voicing and place of the English final stop, word size and final stress. These possibilities were tested using a corpus of Korean loanwords whose source word ends in a stop. Patterns of vowel insertion were classified as no vowel insertion, vowel insertion, or optional vowel insertion, and analyzed using multinomial regression modeling. The results confirmed that all the relevant factors significantly increased the likelihood of vowel insertion and optional vowel insertion patterns relative to no vowel insertion patterns compared with the reference condition rates. These findings suggest that particular features indeed impact production patterns in loanword phonology. My Results support the need for further research into how other possible auditory factors such as stop release may shape speech perception in loanword adaptation.

Obstructive uropathy is a clinical condition that can lead to chronic kidney disease. However, treatments that can prevent the progression of renal injury and fibrosis are limited. Farrerol (FA) is a natural flavone with potent antioxidant and anti-inflammatory properties. Here, we investigated the effect of FA on renal injury and fibrosis in a mouse model of unilateral ureteral obstruction (UUO). Mice underwent a sham or UUO operation and received intraperitoneal injections of FA (20 mg/kg) daily for 8 consecutive days. Histochemistry, immunohistochemistry and immunofluorescence staining, TdT-mediated dUTP nick end labeling assay, Western blotting, gene expression analysis, and biochemical tests were performed. FA attenuated renal dysfunction (p < 0.05) and ameliorated renal tubular injury (p < 0.01) and interstitial fibrosis (p < 0.001) in UUO mice. FA alleviated 4-hydroxynonenal expression (p < 0.001) and malondialdehyde levels (p < 0.01) by regulating pro-oxidant and antioxidant enzymes. Apoptosis in the kidneys of UUO mice was inhibited by FA (p < 0.001), and this action was accompanied by decreased expression of cleaved caspase-3 (p < 0.01). Moreover, FA alleviated pro-inflammatory cytokine production (p < 0.001) and macrophage infiltration (p < 0.01) in the kidneys of UUO mice. These results suggest that FA ameliorates renal injury and fibrosis in the UUO model by inhibiting oxidative stress, apoptosis, and inflammation.

Cisplatin is a chemotherapeutic agent widely used in the treatment of various cancers, but its application is often limited due to complications such as acute kidney injury (AKI). Orexins are hypothalamic neuropeptides that modulate the sleep-wake cycle, neuroendocrine function, and the autonomic nervous system. Emerging evidence suggests that orexin A (OXA) has anti-inflammatory and neuroprotective effects in animal models of neuroinflammatory diseases of the central nervous system. However, the effect of OXA on kidney diseases has not been examined. Here, we investigated whether OXA has a protective effect in a murine model of cisplatin-induced AKI. Intraperitoneal administration of OXA ameliorated renal dysfunction, and histological abnormalities in mice injected with cisplatin. OXA inhibited cisplatin-induced oxidative stress through the modulation of prooxidant and antioxidant enzymes. This peptide reduced apoptotic cell death by inhibiting the p53-mediated pathway in mice injected with cisplatin. OXA also alleviated cisplatin-induced cytokine production and macrophage infiltration into injured kidneys. Taken together, these results showed that OXA ameliorates cisplatin-induced AKI via antioxidant, anti-apoptotic, and anti-inflammatory actions. This peptide could be a potential therapeutic agent for cisplatin-induced AKI.

The purpose of this study is to investigate gait in patients with neurological disorders using accelerometers. Accelerometers were placed on both ankles of participants undergoing gait analysis. Data were collected during the 10-min walk test from healthy participants (n = 20) and patients with neurological deficits (n = 22) scheduled for surgery. Additional data were obtained after surgery for comparison. Both the time and frequency domain features were compared between healthy participants and patients. The interval between successive heel-strikes differed significantly, as did that between successive toe-offs. These features were correlated in healthy participants but not in patients, for whom the correlation coefficients tended to increase after surgery, indicating that the correlations can be used to monitor gait recovery and ankle-worn accelerometers were effective in collecting data for gait monitoring.

Sepsis-related acute kidney injury (AKI) is a worldwide health problem, and its pathogenesis involves multiple pathways. Lipopolysaccharide (LPS) is an endotoxin that induces systemic inflammatory responses. Melittin, a main constituent of bee venom, exerts several biological activities such as antioxidant, anti-inflammatory, and antiapoptotic actions. However, whether melittin protects against endotoxin-induced AKI remains undetermined. Here, we aimed to examine the potential action of melittin on LPS-induced renal injury and explore the mechanisms. We showed that acute renal failure and structural damage after injection of LPS were markedly attenuated by administration of melittin. The peptide also suppressed expression of markers of direct tubular damage in kidneys of the LPS-treated mice. Mechanistically, melittin reduced systemic and renal levels of cytokines and inhibited renal accumulation of immune cells with concomitant suppression of nuclear factor kappa-B pathway. Increased amounts of lipid peroxidation products after LPS treatment were largely decreased by melittin. Additionally, the peptide decreased expression of nicotinamide adenine dinucleotide phosphate oxidase 4 and enhanced nuclear factor erythroid-2-related factor 2-mediated antioxidant defenses. Moreover, melittin inhibited apoptotic and necroptotic cell death after LPS treatment. Lastly, we showed that melittin improved the survival rate of LPS-injected mice. These results suggest that melittin ameliorates endotoxin-induced AKI and mortality through inhibiting inflammation, oxidative injury, and apoptotic and necroptotic death of tubular epithelial cells.

A novel mathematical model is envisaged to scrutinize the Darcy Forchheimer 3D Powell Eyring nanofluid flow in a porous medium. Flow is taken under the influence of zero mass flux and convective boundary conditions at the surface and a chemical reaction in the mass equation. The heat transfer flow is scrutinized with non-linear thermal radiation. Entropy generation analysis of the envisioned model is also conducted. The Homotopy Analysis method to yield the series solutions for the envisioned model. The graphs are plotted to witness the characteristics of several parameters versus velocity, heat, and mass distributions and are well cogitated accordingly. The findings show that the velocity is decreasing the function of Darcy-Forchheimer number. Further, the Biot number large values boost the fluid temperature. The outcomes obtained in the analysis are substantiated when compared with a published result in the literature. An outstanding matching is achieved in this regard.

Acetaminophen (APAP) can cause acute liver failure, but treatment options are still limited. Kahweol is the main diterpene compound of coffee and possesses antioxidant and anti-inflammatory properties. Emerging evidence suggests that this natural diterpene exerts favorable effects on several inflammatory diseases. However, the action of kahweol on APAP toxicity has not been addressed. The purpose of this study was to explore whether kahweol has a protective activity against APAP-induced hepatotoxicity and to investigate the mechanism. Administration of kahweol reduced serum levels of liver injury indicators and ameliorated histological abnormalities in APAP-treated mice. Kahweol inhibited lipid peroxidation and nucleic acid oxidation with restoration of glutathione content and stimulation of nuclear factor erythroid-2-related factor 2-dependent cellular defense system. Hepatocyte death was also decreased by kahweol, which was associated with inhibition of endoplasmic reticulum (ER) stress. Moreover, kahweol reduced hepatic levels of inflammatory mediators, inhibited nuclear factor-κB activation, and attenuated infiltration of neutrophils and macrophages. These findings suggest that kahweol has a protective activity against APAP-induced liver injury and this effect is related to the suppression of oxidative stress, hepatocyte death, ER stress, and inflammation.

As the coronavirus disease 2019 (COVID-19) pandemic continues, reinfection is likely to become increasingly common. However, confirming COVID-19 reinfection is difficult because it requires whole-genome sequencing of both infections to identify the degrees of genetic differences. Since the first reported case of reinfection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in the Republic of Korea in April 2020, four additional cases were classified as suspected reinfection cases. We performed whole-genome sequencing of viral RNA extracted from swabs obtained at the initial infection and reinfection stages of these four suspected cases. The interval between initial infection and reinfection of all four suspected cases was more than 3 months. All four patients were young (10-29 years), and they displayed mild symptoms or were asymptomatic during the initial infection and reinfection episodes. The analysis of genome sequences combined with the epidemiological results revealed that only two of the four cases were confirmed as reinfection, and both were reinfected with the Epsilon variant. Due to the prolonged COVID-19 pandemic, the possibility of reinfections with SARS-CoV-2 variants is increasing, as reported in our study. Therefore, continuous monitoring of cases is necessary.

Hepatocyte apoptosis and inflammation play important roles in cholestatic liver diseases. Bee venom-derived secretory phospholipase A2 (bvPLA2) has been shown to ameliorate various inflammatory diseases. However, whether bvPLA2 has a therapeutic effect against cholestatic liver disease has not been evaluated. Therefore, we investigated the effects of bvPLA2 on cholestatic liver injury and fibrosis in a murine model of 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet feeding. The administration of bvPLA2 ameliorated liver damage, cholestasis, and fibrosis in DDC diet-fed mice, as assessed by serum biochemical tests and histological examinations. In addition, bvPLA2 reduced myofibroblast accumulation, concomitant with suppression of transforming growth factor-β signaling cascade. The administration of bvPLA2 inhibited hepatocyte apoptosis in DDC diet-fed mice as represented by a reduction in the number of cells stained with terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling and suppression of caspase-3 activation. Moreover, bvPLA2 reduced cytokine production along with the inhibition of the nuclear factor kappa-B pathway. The number of regulatory T-cells was increased by bvPLA2, while the number of other immune cells, including neutrophils, macrophages, and CD8+ T-cells, was decreased. Our data indicate that the administration of bvPLA2 ameliorates cholestatic liver injury and fibrosis by inhibiting hepatocyte apoptosis and inflammation.

Hepatocyte apoptosis and inflammation play important roles in cholestatic liver diseases. Bee venom-derived secretory phospholipase A2 (bvPLA2) has been shown to ameliorate various inflammatory diseases. However, whether bvPLA2 has a therapeutic effect against cholestatic liver disease has not been evaluated. Therefore, we investigated the effects of bvPLA2 on cholestatic liver injury and fibrosis in a murine model of 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet feeding. The administration of bvPLA2 ameliorated liver damage, cholestasis, and fibrosis in DDC diet-fed mice, as assessed by serum biochemical tests and histological examinations. In addition, bvPLA2 reduced myofibroblast accumulation, concomitant with suppression of transforming growth factor-β signaling cascade. The administration of bvPLA2 inhibited hepatocyte apoptosis in DDC diet-fed mice as represented by a reduction in the number of cells stained with terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling and suppression of caspase-3 activation. Moreover, bvPLA2 reduced cytokine production along with the inhibition of the nuclear factor kappa-B pathway. The number of regulatory T-cells was increased by bvPLA2, while the number of other immune cells, including neutrophils, macrophages, and CD8+ T-cells, was decreased. Our data indicate that the administration of bvPLA2 ameliorates cholestatic liver injury and fibrosis by inhibiting hepatocyte apoptosis and inflammation.

Cholestatic liver diseases can progress to end-stage liver disease and reduce patients’ quality of life. Although their underlying mechanisms are still incompletely elucidated, oxidative stress is considered to be a key contributor to these diseases. Heme oxygenase-1 (HO-1) is a cytoprotective enzyme that displays antioxidant action. It has been found that this enzyme plays a protective role against various inflammatory diseases. However, the role of HO-1 in cholestatic liver diseases has not yet been investigated. Here, we examined whether pharmacological induction of HO-1 by cobalt protoporphyrin (CoPP) ameliorates cholestatic liver injury. To this end, a murine model of 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet feeding was used. Administration of CoPP ameliorated liver damage and cholestasis with HO-1 upregulation in DDC diet-fed mice. Induction of HO-1 by CoPP suppressed the DDC diet-induced oxidative stress and hepatocyte apoptosis. In addition, CoPP attenuated cytokine production and inflammatory cell infiltration. Furthermore, deposition of the extracellular matrix and expression of fibrosis-related genes after DDC feeding were also decreased by CoPP. HO-1 induction decreased the number of myofibroblasts and inhibited the transforming growth factor-β pathway. Altogether, these data suggest that the pharmacological induction of HO-1 ameliorates cholestatic liver disease by suppressing oxidative stress, hepatocyte apoptosis, and inflammation.

Indian Emergency Departments (EDs) encounter a significant number of toxicologic cases each year, approximately half of which are attempts at deliberate self-harm. The objective of this study was t...

Leaf senescence is an integrated response of the cells to develop age information and various environmental signals. Thus, some of the genes involved in the response to environmental changes are expected to regulate leaf senescence. Light acts not only as the primary source of energy for photosynthesis but also as an essential environmental cue that directly control plant growth and development including leaf senescence. The molecular mechanisms linking light signaling to leaf senescence have recently emerged, exploring the role of Phytochrome-Interacting Factors (PIFs) as a central player leading to diverse senescence responses, senescence-promoting gene regulatory networks (GRNs) involving PIFs, and structural features of transcription modules in GRNs. The circadian clock is an endogenous time-keeping system for the adaptation of organisms to changing environmental signals and coordinates developmental events throughout the life of the plant. Circadian rhythms can be reset by environmental signals, such as light-dark or temperature cycles, to match the environmental cycle. Research advances have led to the discovery of the role of core clock components as senescence regulators and their underlying signaling pathways, as well as the age-dependent shortening of the circadian clock period. These discoveries highlight the close relationship between the circadian system and leaf senescence. Key issues remain to be elucidated, including the effect of light on leaf senescence in relation to the circadian clock, and the identification of key molecules linking aging, light, and the circadian clock, and integration mechanisms of various senescence-affecting signals at the multi-regulation levels in dynamics point of view.

Background: Toll-like receptor 4 (TLR4) is involved in the pathogenesis of arthritic diseases. The TLR4 inhibitor TAK-242 has shown potential as a possible treatment for rheumatoid arthritis in an adjuvant-induced arthritis rat model. However, further investigation of the anti-arthritis effect of TAK-242 in other animal models of arthritis disease is required. Objective: This study was conducted to examine the anti-arthritic effects and mechanisms of TAK-242 on curdlan-induced spondyloarthritis in SKG mice. Methods: Curdlan-injected SKG ZAP-70W163C mice were intraperitoneally administered with TAK-242 (3 mg/kg) every other day or anti-IL-23 antibody (100 μg) weekly for 9 weeks. The therapeutic effect of TAK-242 was evaluated in the SKG mice by measuring the inflammation level of foot, ileum, lung and tail by histology, the levels of proinflammatory cytokines in serum, bone mineral density (BMD) in femur and spine, and CD4+T cell subtypes Th1 and Th17 in spleen.Results: TAK-242 treatment significantly reduced clinical score, paw width, and colon length in SKG mice. Consistent with the therapeutic effect, TAK-242 also reduced peripheral arthritis and IL-17 expression in the foot and ileum tissues. It also inhibited inflammation of the lungs, ileum, paws, and tail and reduced serum levels of pro-inflammatory cytokines such as IL-6 and TNF-α. TAK-242 recovered the reduced bone density in the femur but not in the spine. Treatment with TAK-242 also suppressed the populations of Th1 and Th17 cells in the spleen of SKG mice.Conclusions: TAK-242 may show beneficial anti-arthritis effects by inhibiting the proliferation of pro-inflammatory Th1 and Th17 cells. Further research is needed for TAK-242 to be repositioned as a treatment for arthritis disease.

Olfactory receptors are ectopically expressed in extra-nasal tissues. The gut is constantly exposed to high levels of odorants where ectopic olfactory receptors may play critical roles. Activation of ectopic olfactory receptor 544 (Olfr544) by azelaic acid (AzA), an Olfr544 ligand, reduces adiposity in mice fed a high-fat diet (HFD) by regulating fuel preference to fats. Herein, we investigated the novel function of Olfr544 in the gut. In GLUTag cells, AzA induces the cAMP-PKA-CREB signaling axis and increases the secretion of GLP-1, an enteroendocrine hormone with anti-obesity effects. In mice fed a HFD and orally administered AzA, GLP-1 plasma levels were elevated in mice. The induction of GLP-1 secretion was negated in cells with Olfr544 gene knockdown and in Olfr544-deficient mice. Gut microbiome analysis revealed that AzA increased the levels of Bacteroides acidifaciens and microbiota associated with antioxidant pathways. In fecal metabolomics analysis, the levels of succinate and trehalose, metabolites correlated with a lean phenotype, were elevated by AzA. The function of Olfr544 in gut inflammation, a key feature in obesity, was further investigated. In RNA sequencing analysis, AzA suppressed LPS-induced activation of inflammatory pathways and reduced TNF-α and IL-6 expression, thereby improving intestinal permeability. The effects of AzA on the gut metabolome, microbiome, and colon inflammation were abrogated in Olfr544-KO mice. These results collectively demonstrated that activation of Olfr544 by AzA in the gut exerts multiple effects by regulating GLP-1 secretion, gut microbiome and metabolites, and colonic inflammation in anti-obesogenic phenotypes and, thus, may be applied for obesity therapeutics.

Cisplatin is an effective chemotherapeutic agent, but its clinical use is frequently limited by its nephrotoxicity. The pathogenesis of cisplatin-induced acute kidney injury (AKI) remains incompletely understood, but oxidative stress, tubular cell death, and inflammation are considered important contributors to cisplatin-induced renal injury. Kahweol is a natural diterpene extracted from coffee beans and has been shown to possess anti-oxidative and anti-inflammatory properties. However, its role in cisplatin-induced nephrotoxicity remains undetermined. Therefore, we investigated whether kahweol exerts a protective effect against cisplatin-induced renal injury. Additionally, its mechanisms were also examined. Administration of kahweol attenuated renal dysfunction and histopathological damage together with inhibition of oxidative stress in cisplatin-injected mice. Increased expression of nicotinamide adenine dinucleotide phosphate oxidase 4 and decreased expression of manganese superoxide dismutase and catalase after cisplatin treatment were significantly reversed by kahweol. Moreover, kahweol inhibited cisplatin-induced apoptosis and necroptosis in the kidneys. Finally, kahweol reduced inflammatory cytokine production and immune cell accumulation together with suppression of nuclear factor kappa-B pathway and downregulation of vascular adhesion molecules. Together, these results suggest that kahweol ameliorates cisplatin-induced renal injury via its pleiotropic effects and might be a potential preventive option against cisplatin-induced nephrotoxicity.

Emerging evidence suggests that epigenetic mechanisms such as histone modification are crucially involved in the pathophysiology of acute kidney injury (AKI). The histone acetyltransferase p300 regulates several biological processes through the acetylation of histones or transcription factors. However, the role of p300 in cisplatin-induced AKI remains poorly understood. Therefore, we investigated the effects of garcinol, a potent p300 inhibitor, on cisplatin-induced AKI and explored the mechanisms. Administration of garcinol significantly reversed the upregulation of p300 and increased acetylation of histone H3, along with amelioration of renal dysfunction and histopathological injury in the kidneys of cisplatin-injected mice. Garcinol also attenuated oxidative stress and reduced expression of pro-oxidant enzymes. In addition, garcinol reduced the elevated production of cytokines and chemokines and suppressed immune cell accumulation together with downregulation of vascular adhesion molecules. These beneficial effects of garcinol were associated with a reduction in acetylation of the p65 subunit of nuclear factor kappa-B. Further, garcinol significantly inhibited apoptosis and caspase-3 activation, with a decrease in p53 acetylation in cisplatin-injected mice. Taken together, we demonstrated that the inhibition of p300 by garcinol ameliorated cisplatin-induced renal injury, presumably through epigenetic mechanisms. These results suggest that garcinol might be a potential preventive agent for cisplatin-induced AKI.

In this retrospective multicentre cohort study that included 27 COVID-19 patients who underwent tracheostomy, the mean time between intubation and tracheostomy was 15.8 days and the negative conversion time of COVID-19 was 43.1 days. Eleven patients (40.7%) died of COVID-19 and the use of percutaneous dilatation tracheostomy was significantly associated with in-hospital death. Timely tracheostomy could be performed in COVID-19 patients, regardless of duration of intubation or positivity of COVID-19 test, with an open surgical tracheostomy as a preferable technique.

Inflammation and oxidative stress plays an essential role in the pathophysiology of sepsis-associated acute kidney injury (AKI). SPA0355, a thiourea analogue, has been shown to display beneficial effects against a variety of inflammatory diseases arising from its anti-inflammatory and anti-oxidant properties. However, the potential protective effects of SPA0355 against lipopolysaccharide (LPS)-induced AKI have not been explored. The aim of this study was to evaluate the effects of SPA0355 on LPS-induced AKI and investigate its underlying mechanisms. We found that renal dysfunction and histological abnormalities after LPS injection were significantly ameliorated by SPA0355. The compound also reduced renal expression of tubular injury markers. Mechanistically, SPA0355 significantly suppressed plasma and tissue levels of inflammatory cytokines and immune cell infiltration with inhibition of nuclear factor kappa-B p65 signaling. In addition, elevated levels of 4-hydroxynonenal and malondialdehyde after LPS injection were significantly decreased by SPA0355. The compound also regulated expression of pro-oxidant and antioxidant enzymes after LPS injection. Moreover, SPA0355 attenuated LPS-induced tubular cell apoptosis via inhibition of p53 signaling pathway. Altogether, these results suggest that SPA0355 protects against LPS-induced AKI through suppressing inflammation, oxidative stress, and tubular cell apoptosis and might be a potential preventive option for the disease.

The colorimetric sensor is a facile, cost-effective, and non-power-operated green energy material for gas detection. In this study, the colorimetric sensing property of a meta-aramid/dye 3 nanofiber sensor for ammonia (NH3) gas detection was investigated. This colorimetric sensor was prepared using various dye 3 concentrations via electrospinning. Morphological, thermal, structural, and mechanical analyses of the sensor were carried out by field-emission scanning electron microscopy, thermogravimetric analysis, Fourier-transform infrared spectroscopy, and a universal testing machine, respectively. A homemade computer color matching machine connected with a gas flow device characterized the response of the meta-aramid/dye 3 nanofiber colorimetric sensor to various exposure levels of NH3 gas. From the results, we confirmed that this colorimetric green energy sensor could detect ammonia gas in the concentration of 1&ndash, 10 ppm with a sensing response time of 10 s at room temperature. After washing with laundry detergent for 30 min, the colorimetric sensors still exhibited sensing property and reversibility.

Sepsis-associated acute kidney injury (AKI) is a leading cause of death in hospitalized patients worldwide. Despite decades of effort, there is no effective treatment for preventing the serious medical condition. Bee venom has long been used to treat a variety of inflammatory diseases. However, whether bee venom has protective effects against lipopolysaccharide (LPS)-induced AKI has not been explored. The aim of this study was to evaluate the effects of bee venom on LPS-induced AKI. The administration of bee venom alleviated renal dysfunction and structural injury in LPS-treated mice. Increased renal levels of tubular injury markers after LPS treatment were also suppressed by bee venom. Mechanistically, bee venom significantly reduced plasma and tissue levels of inflammatory cytokines and immune cell infiltration into damaged kidneys. In addition, mice treated with bee venom exhibited reduced renal expression of lipid peroxidation markers after LPS injection. Moreover, bee venom attenuated tubular cell apoptosis in the kidneys of LPS-treated mice. In conclusion, these results suggest that bee venom attenuates LPS-induced renal dysfunction and structural injury via the suppression of inflammation, oxidative stress, and tubular cell apoptosis, and might be a useful therapeutic option for preventing endotoxemia-related AKI.

Spasticity is a frequently observed symptom in patients with neurological impairments. Spastic movements of their upper and lower limbs are periodically measured to evaluate functional outcomes of physical rehabilitation, and they are quantified by clinical outcome measures such as the modified Ashworth scale (MAS). This study proposes a method to determine the severity of elbow spasticity, by analyzing the acceleration and rotation attributes collected from the elbow of the affected side of patients and machine-learning algorithms to classify the degree of spastic movement, this approach is comparable to assigning an MAS score. We collected inertial data from participants using a wearable device incorporating inertial measurement units during a passive stretch test. Machine-learning algorithms&mdash, including decision tree, random forests (RFs), support vector machine, linear discriminant analysis, and multilayer perceptrons&mdash, were evaluated in combinations of two segmentation techniques and feature sets. A RF performed well, achieving up to 95.4% accuracy. This work not only successfully demonstrates how wearable technology and machine learning can be used to generate a clinically meaningful index but also offers rehabilitation patients an opportunity to monitor the degree of spasticity, even in nonhealthcare institutions where the help of clinical professionals is unavailable.

Background Different adiponectin isoforms appear to be differentially involved in the pathogenesis of various diseases. The purpose of this study was to generate monoclonal antibodies (mAbs) specific to different adiponectin isoforms and investigate whether these mAbs have potential as therapeutic agents for such diseases. Methods Hybridoma cells producing monoclonal antibodies were generated and screened using enzyme-linked immunosorbent assay and Western blotting for the production of mAbs recognizing human adiponectin isoforms. Results The mAb from hybridoma clone KH7–41 recognized both the middle molecular weight (MMW) (hexamer) and low molecular weight (LMW) (trimer) isoforms of adiponectin in human serum, whereas the KH7–33 mAb detected only MMW (hexamer) adiponectin. The KH4–8 clone recognized both the high molecular weight (HMW) (multimer) and MMW adiponectin isoforms. However, in mouse and rat sera, the abovementioned antibodies recognized only the MMW isomer. These mAbs also recognized adiponectin in various human tissues, such as lung, kidney, and adipose tissues, although the three mAbs had different staining intensities. The mAb from clone KH4–8 effectively inhibited increases in interleukin-6 (IL-6) and IL-8 expression in recombinant adiponectin-stimulated human osteoblasts and human umbilical vein endothelial cells. Also, the mAbs KH7–33 and KH4–8 significantly ameliorated rheumatic symptoms in a collagen-induced arthritis mouse model. This result suggests that these mAb treatments may ameliorate adiponectin-mediated inflammatory response. Conclusions mAbs against human adiponectin isomers can potentially be developed as therapeutic antibodies to target specific detrimental isoforms of adiponectin while maintaining the functions of beneficial isoforms. Electronic supplementary material The online version of this article (10.1186/s13075-018-1736-3) contains supplementary material, which is available to authorized users.

Atopic dermatitis (AD) is a chronic skin inflammatory disease characterized by recurrent eczema and itching. It is caused by a poorly controlled immune response and damage to the skin barrier. Purified bee venom (BV) is a natural toxin produced by honeybees (Apis mellifera L.), and is well known for its anti‑inflammatory, analgesic and anti‑cancer effects against various types of disease. However, treatment strategies based on anti‑inflammatory properties have not been adequately studied in AD. Thus, the present study examined the progression of AD‑like skin lesions induced by ovalbumin (OVA) and the mechanism of action of BV. BV, administered by intraperitoneal inoculation, was observed to reduce the symptoms of AD, in addition to the serum immunoglobulin E levels, according to dorsal skin thickness and histopathologic analysis. The treatment also inhibited the infiltration of eosinophils and mast cells. These results suggested that it is possible to develop novel AD alternative therapy using BV by effectively suppressing allergic skin inflammation in AD.

Urine-derived stem cells (USCs) are considered as a promising cell source capable of neuronal differentiation. In addition, specific growth factors and extracellular matrix are essential for enhancing their neuronal differentiation efficiency. In this study, we investigated the possibility of neuronal differentiation of USCs and the role of laminin and platelet-derived growth factor BB (PDGF-BB) as promoting factors. USCs were isolated from fresh urine of healthy donors. Cultured USCs were adherent to the plate and their morphology was similar to the cobblestone. In addition, they showed chromosome stability, rapid proliferation rate, colony forming capacity, and mesenchymal stem cell characteristics. For inducing the neuronal differentiation, USCs were cultured for 14 days in neuronal differentiation media supplemented with/without laminin and/or PDGF-BB. To identify the expression of neuronal markers, RT-PCR, flow cytometry analysis and immunocytochemistry were used. After neuronal induction, the cells showed neuron-like morphological change and high expression level of neuronal markers. In addition, laminin and PDGF-BB respectively promoted the neuronal differentiation of USCs and the combination of laminin and PDGF-BB showed a synergistic effect for the neuronal differentiation of USCs. In conclusion, USCs are noteworthy cell source in the field of neuronal regeneration and laminin and PDGF-BB promote their neuronal differentiation efficiency.

Atopic dermatitis (AD) is an inflammatory skin disease characterized by intense pruritus and relapsable eczematous lesions. The hallmarks of AD are defects in the epidermal barrier and immunoglobulin E (IgE)-mediated sensitization to several environmental allergens, as well as an immune disorder mediated by an imbalance toward T-helper-2 response. Melittin, a major component of bee venom, has been studied in various inflammatory diseases. However, the beneficial effects of melittin on mouse with AD-like symptoms have not been explored. Therefore, we investigated the anti-allergic effects of melittin. AD was induced by ovalbumin (OVA) patch. After agent treatment, skin tissues and sera were extracted from the sacrificed mice were used to demonstrate the effects of melittin through various molecular biological methods. The results showed that OVA-induced skin thickening and inflammatory infiltration were decreased in the melittin-treated group. Melittin prevented OVA-induced filaggrin deficiency and imbalanced inflammatory mediators. Furthermore, melittin inhibited IL-4/IL-13-induced filaggrin downregulation through the blockade of STAT3 activation in human keratinocytes. In summary, this study has shown that melittin ameliorated OVA-induced AD-like symptoms from various perspectives. The findings of this study may be the first evidence of the anti-inflammatory effects of melittin on OVA-induced AD.