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Background: Micronized acellular dermal matrix (mADM) can induce tissue regeneration and repair, and filling. Objectives: The efficacy and safety of (mADM) were evaluated in the treatment of atrophic acne scar. Methods: In this single‐blinded, self‐controlled, split‐face study, 16 patients (48 scar sites) were divided into treatment group (24 scar sites) and control group (24 scar sites). One side of the affected area was treated with mADM combined with platelet rich plasma (PRP) injection as the treatment group; the other side of the affected area was treated with PRP injection as the control group. The efficacy was evaluated by the Acne scar assessment scale (ASAS) and Acne Scar Weight Rating Scale (ECCA) 3 months after treatment. Results: After 3‐month treatment in 16 patients, the atrophic acne scars in both groups were all improved. The ASAS score and ECCA weight score in the treatment group was significantly lower than that in the control group (2.50 ± 0.51 vs. 3.62 ± 0.77 and 14.17 ± 10.18 vs. 31.88 ± 13.25; p < 0.001). Limitations: Short‐term 3‐month treatment period. Small sample size limits generalizability of results. Conclusion: The curative effect of mADM combined with PRP is significantly better than that of PRP alone. [ABSTRACT FROM AUTHOR]

This article discusses the case of a male infant who developed ALK-positive histiocytosis, a rare histiocytic proliferative disorder. The infant initially experienced jaundice, which resolved but then reoccurred along with other symptoms such as anemia and skin blemishes. Laboratory investigations and histological examination confirmed the diagnosis of ALK-positive histiocytosis. However, in a rare occurrence, the infant's lesions completely disappeared without any intervention during follow-up. The article highlights the variability in clinical presentation and the need for individualized treatment approaches for ALK-positive histiocytosis. [Extracted from the article]

Introduction: The role of bone marrow mesenchymal stem cells-derived exosomes (BMSCs-exo) in skin photoaging was explored in human dermal fibroblasts (HDFs). The underlying mechanism was further explored. Methods: HDFs were exposed to UVB irradiation to establish the cell photodamage models. The cell viability and levels of oxidative stress-related factors were tested. ELISA was done to detect TNF-α, IL-6, and IL-1β concentrations. Western blot was applied for protein examination. Results: UVB treatment led to the inhibition of cell viability. But after BMSCs-exo addition, the inhibitory effect was returned in a dose manner. UVB exposure contributed to the increase of reactive oxygen species and LDH and the downregulation of superoxide dismutase. In addition, excessive secretion of TNF-α, IL-6, and IL-1β was also detected in cells exposed to UVB. However, BMSCs-exo addition eliminated the effects of UVB on oxidative stress and inflammation in HDFs. BMSCs-exo inhibited matrix metalloproteinases MMP-1 and MMP-3 expression but promoted collagen I expression. UVB radiation activated the MAPK/AP-1 signaling, manifested as the increase of p-p38, c-Jun, and c-Fos protein levels, which were reversed by BMSCs-exo. As a p38 agonist, anisomycin counteracted the effect of BMSCs-exo on HDF's viability, oxidative stress, and inflammation. Conclusion: BMSCs-exo protected HDFs against UVB-induced inhibition of cell viability and the activation of cell oxidative stress and inflammation, which might be related to the inhibition of the MAPK/AP-1 signaling pathway. [ABSTRACT FROM AUTHOR]

Background: Mesenchymal stem cells‐derived exosome (MSCs‐exo) was identified to reduce photoaging. The purpose of this study was to investigate the potential role of microRNA (miR)‐29b‐3p derived from bone marrow MSCs‐exo (BMSCs‐exo) in photoaging. Methods: Exosomes were isolated from BMSCs and verified by Western blot. A photoaging cell model was constructed by UVB irradiation of human dermal fibroblasts (HDFs). Quantitative real‐time PCR (RT‐qPCR) was performed to detect the mRNA levels of miR‐29b‐3p, collagen type I and matrix metalloproteinases (MMPs). CCK‐8, Transwell and flow cytometry were applicated to examine cell viability, migration and apoptosis. Commercial kits are used to measure levels of oxidative stress indicators. Finally, a dual‐luciferase reporter assay was applied to validate the target of miR‐29b‐3p. Results: Extracted exosomes were positive for HSP70 and CD9. Survival of HDFs increased in an exosome concentration‐dependent manner. UVB irradiation inhibited miR‐29b‐3p levels compared with controls, but BMSCs‐exo treatment restored miR‐29b‐3p levels (p <.05). Additionally, BMSCs‐exo‐miR‐29b‐3p reversed the inhibition of HDFs migration and oxidative stress by UVB irradiation, as well as the promotion of apoptosis. However, this reversal was attenuated by the suppression of miR‐29b‐3p (p <.05). Furthermore, BMSCs‐exo‐miR‐29b‐3p also inhibited the degradation of collagen type I and the production of MMPs in photoaging, and they were also eliminated by the reduced miR‐29b‐3p. Finally, MMP‐2 was the target gene of miR‐29b‐3p. Conclusion: Our study presented a novel role for BMSCs‐exo‐miR‐29b‐3p in improving skin photoaging function, and these findings may provide new insights into the targeted treatment of skin photoaging. [ABSTRACT FROM AUTHOR]

To evaluate the efficacy and safety of 755 nm Q-Switched alexandrite laser for Hori's nevus in a large cohort of Chinese women. We retrospectively analyzed the efficacy and safety of 755 nm Q-Switched alexandrite laser for Hori's nevus. Reduction in pigment was evaluated using a 4-score method. A total of 482 patients, aged 16 to 52 years, were included in this analysis. Patients were treated with 755 nm Q-Switched alexandrite laser at fluence levels of 5–8 J/cm2 for 2–4 treatment sessions. Following the treatments, 53% of patients showed over 75% reductions in pigment while 50–75% reductions in pigment were observed in 28% of patients. The rest displayed less than 50% improvements. Efficacy was positively correlated with the number of treatment sessions (p < 0.0001). Adverse reactions were temporary, mild erythema, and edema. A small portion of patients (15%) had hyperpigmentation, which disappeared within 2–6 months. 755 nm Q-Switched alexandrite laser is safe and has moderate benefits for Hori's nevus. Because its efficacy is positively correlated with the number of treatment sessions, increase in treatment sessions possibly could achieve a better outcome. [ABSTRACT FROM AUTHOR]

Background: Long non-coding RNA (lncRNA) has been testified to influence the initiation and evolution of sundry carcinomas. Recently, lncRNA FOXD2 adjacent opposite strand RNA 1 (FOXD2-AS1) has been found to display vital regulating functions in various cancers. Methods: qRT-PCR was used to verify the dysregulation of FOXD2-AS1 expression in CCA cells and tissues, and the correlation of FOXD2-AS1 expression with clinicopathological characteristics was investigated. The viability, migration, and invasion of CCA cells were verified through CCK-8 assay, colony formation experiment, wound healing assay, and transwell assay. The regulatory networks of FOXD2-AS1 were analyzed by Bioinformatic prediction and dual-luciferase reporter assay. Results: We discovered that FOXD2-AS1 was significantly upregulated in CCA and its up-regulation was closely correlated with terminal TNM stage, lymph node metastasis and poor survival in the current research. In addition, it was revealed that FOXD2-AS1 was an independent prognostic factor. Functional tests uncovered that the cell viability, migration, and invasion could be restrained through downregulating the expression of FOXD2-AS1, while FOXD2-AS1 overexpression could facilitate the cell viability, migration, and invasion. Mechanistically, FOXD2-AS1 was founded to interact directly with miR-760 and the oncogene E2F3 was the downstream target of miR-760 through bioinformatic prediction and dual-luciferase reporter assays. Finally, we testified that FOXD2-AS1 could competitively sponge miR-760 and further upregulated the E2F3 expression to play a vital part in cholangiocarcinoma. Conclusions: This research revealed that lncRNA FOXD2-AS1 could enhance CCA malignant progression through regulating the miR-760/E2F3 axis and was expected to be a prognostic biomarker and therapeutic target for cholangiocarcinoma. [ABSTRACT FROM AUTHOR]

Background: Serum Cystatin S (CST4), a secretory protein that inhibits cellular matrix degradation, significantly influences the tumor microenvironment and tumor progression. However, the prognostic value of serum CST4 in gastric cancer (GC) remains unclear. This study aims to explore serum CST4's utility in GC prognostic assessment. Methods: A cohort of 334 patients with GC who underwent radical gastrectomy was assessed. Preoperative serum CST4 levels were measured alongside traditional tumor markers, correlating with clinical data and patient outcomes. The cohort was divided into training and test sets at a ratio of 3:1 for Cox regression analyses, which identified CST4 as an independent risk factor for overall survival (OS) and disease-free survival (DFS). A prognostic model was developed, validated with calibration curves, and its predictive value was evaluated using receiver operating characteristic (ROC) curves. In addition, CST4 expression was correlated with immune cell infiltration using data from The Cancer Genome Atlas (TCGA). Patients were stratified by median CST4 levels, and Kaplan-Meier curves for OS and DFS were plotted. Results: Cystatin S was confirmed as an independent risk factor for OS and DFS. Integrating CST4 with traditional markers and TNM pathological staging significantly enhanced the predictive value for prognosis. Cystatin S's impact on tumor progression is likely mediated through modulation of the immune microenvironment, including immune suppression and evasion. Conclusion: Cystatin S is an effective biomarker for GC prognostic assessment, assisting in the evaluation of prognosis and the selection of treatment strategies for patients with GC. [ABSTRACT FROM AUTHOR]

Background: Becker's nevus is a common skin disorder. Lasers and light instruments are the major modalities for the treatment of Becker's nevus, but the outcomes were mixed. Objective: To evaluate the efficacy of the intense pulsed light for Becker's nevus in a large Chinese cohort. Methods: We retrospectively analyzed the efficacy of the intense pulsed light for Becker's nevus in a single center. Results: A total of 45 patients, including 26 males and 19 females (male to female ratio = 1.4), aged 5‐42 years, were included in this analysis. Twenty‐seven patients (60%) were with hypertrichosis. Treatments with intense pulsed light resulted in over 75% improvements in pigmentation and hair density in 1 and 2 cases, respectively. One patient displayed 51%‐75% reductions in hair density. The rest displayed ≤50% improvements in pigmentation and hair density. Recurrence occurred in all cases within 6 months after the last treatment. Adverse reactions were temporary and mild hypopigmentation, hyperpigmentation, hypertrophic scar, pain, and erythema. Conclusion: Intense pulsed light does not exhibit long‐term benefits for Becker's nevus. Further studies in the large cohort are still required to validate the present results. Moreover, whether changes in the treatment parameters can improve the efficacy of intense pulsed light remains to be explored. [ABSTRACT FROM AUTHOR]

Background: Cholangiocarcinoma (CCA) is a mortal cancer with high mortality, whereas the function and mechanism of occurrence and progression of CCA are still mysterious. Long non-coding RNAs (lncRNAs) could function as important regulators in carcinogenesis and cancer progression. Growing evidences have indicated that the novel lncRNA linc00473 plays an important role in cancer progression and metastasis. However, its function and molecular mechanism in CCA remain unknown. Methods: The linc00473 expression in CCA tissues and cell lines was analyzed using qRT-PCR. Gain- and loss-of-function experiments were conducted to investigate the biological functions of linc00473 both in vitro and in vivo. Insights into the underlying mechanisms of competitive endogenous RNAs (ceRNAs) were determined by bioinformatics analysis, dual-luciferase reporter assays, qRT-PCR arrays, RNA immunoprecipitation (RIP) and rescue experiments. Results: Linc00473 was highly expressed in CCA tissues and cell lines. Linc00473 knockdown inhibited CCA growth and metastasis. Furthermore, linc00473 acted as miR-506 sponge and regulated its target gene DDX5 expression. Rescue assays verified that linc00473 modulated the tumorigenesis of CCA by regulating miR-506. Conclusions: The data indicated that linc00473 played an oncogenic role in CCA growth and metastasis, and could serve as a novel molecular target for treating CCA. [ABSTRACT FROM AUTHOR]

Objective To evaluate the effectiveness of preemptive multimodal analgesiain elderly patients undergoing laparoscopic colorectal surgery. Methods A prospective randomized controlled study was conducted in the Department of Gastrointestinal Surgery of the Second Hospital of Hebei Medical University from January 2022 to December 2022. A total of 133 patients were included according to the criteria and randomly divided into preemptive analgesia (PRA) group (test group, 67patients) and postoperative analgesia (POA) group (control group, 66patients). Results The Visual Analog Scale (VAS)scores of PRA group 24 h, 48 h, and 72 h after operation were lower than those of POA group, and the difference was statistically significant, P < 0.001.The incidences of postoperative gastrointestinal dysfunction (POGD) and postoperative delirium (POD)in PRA group were 13.43% and 8.98%, respectively, which were significantly lower than those in POA group (31.82% and 24.24%), P < 0.05. The levels of IL-6 and IL-10 in PRA group after the operation were 17.54 ± 2.13 ng/L and 15.57 ± 1.71 ng/L respectively, which were lower than those in POA group (25.45 ± 2.95 ng/L and 23.45 ± 1.88 ng/L), P < 0.05. The level of acetylcholinesterase(AchE) was 56.34 ± 5.62 nmol/L in the POA group, which was significantly higher than that in the POA group (49.59 ± 5.52 nmol/L), P < 0.001. Conclusion Preemptive multimodal analgesia can reduce the incidence of POGD and POD in elderly patients undergoing laparoscopic gastrocolic surgery, improve the recovery process of postoperative gastrointestinal function, increase the concentrations of propionic acid and butyric acid in short chain fatty acids (SCFAs) and the number of beneficial intestinal bacteria. [ABSTRACT FROM AUTHOR]

Cholangiocarcinoma (CCA) is one of the most fatal cancers in humans, with a gradually increasing incidence worldwide. The efficient diagnostic and therapeutic measures for CCA to reduce mortality are urgently needed. Long noncoding RNAs (lncRNAs) may provide the potential diagnostic and therapeutic option for suppressing the CCA development. LncRNAs are a type of non‐protein‐coding RNAs, which are larger than 200 nucleotides in length. Increasing evidence reveals that lncRNAs exhibit critical roles in the carcinogenesis and development of CCA. Deregulation of lncRNAs impacts the proliferation, migration, invasion, and antiapoptosis of CCA cells by multiple sophisticated mechanisms. Consequently, lncRNAs likely represent promising biomarkers or intervention targets of CCA. In this review, we summarize current studies regarding the biological functions and regulatory mechanisms of diverse lncRNAs in CCA. [ABSTRACT FROM AUTHOR]

Objectives Long non-coding RNAs (lncRNAs), a group of transcripts with length greater than 200 nucleotides, have been involved in multiple pathophysiological processes of the human body, especially in tumorigenesis and progression of cancers. The aberrant expression of lncRNAs processes crucial functions involved in proliferation, apoptosis and metastatic capacity of cancers. Recent studies have revealed that small nucleolar RNA host gene 1 (SNHG1), a long non-coding RNA transcribed from UHG, was located in chromosome 11. Aberrant expression of SNHG1 has been demonstrated to be associated with various sites of cancers such as glioma, esophageal cancer, gastric cancer and many others, and its deregulation could be related to survival and prognosis of cancer patients. Pertinent to clinical practice, SNHG1 might act as a prognostic biomarker for tumors and might even serve as potential target for therapy. In this review, we summarized current researches concerning the role of SNHG1 in tumor progression and discussed its mechanisms involved. Materials and methods In this review, we summarized and figured out recent studies concerning the expression and biological mechanisms of SNHG1in tumor development. The related studies were obtained through a systematic search of PubMed, Embase and Cochrane Library. Results SNHG1 was a valuable cancer-related lncRNA that the expression level was up-regulation in a variety of malignancies, including glioma, esophageal cancer, lung cancer, gastric cancer, hepatocellular carcinoma, colorectal carcinoma, prostate cancer, cervical cancer, osteosarcoma, neuroblastoma, nasopharyngeal carcinoma. The aberrant expressions of SNHG1 have shown to contribute to proliferation, migration, and invasion of cancer cells. Conclusions SNHG1 represents promising novel biomarkers for various cancer types and have a great potential to be effectively used in clinical practice in the near future. [ABSTRACT FROM AUTHOR]

—In this paper, we investigate a microfluidic based sensing device for cell membrane permeability measurements in real time with applications in rapid assessment of red blood cell (RBC) quality at the individual cell level. The microfluidic chip was designed with unique abilities to line up the RBCs in the centerline of the microchannel using positive dielectrophoresis (p-DEP) forces, rapid mixing of RBCs with various media (e.g. containing permeating or nonpermeating solutes) injected from different inlets to achieve high mixing efficiency. The chip detects the impedance values of the RBCs within 0.19 s from the start of mixing with other media, at ten electrodes along the length of the channel and enables time series measurements of volume change of individual cell caused by cell osmosis in anisosmotic fluids over a 0.8 s postmixing timespan. This technique enables estimating water permeability of individual cell accurately. Here we first present confirmation of a linear voltage-diameter relationship in polystyrene bead standards. Next, we show that under equilibrium conditions, the voltage-volume relationship in rat red blood cells (RBCs) is linear, corresponding to previously published Boyle van 't Hoff plots. Using rat cells as a model for human, we present the first measurement of water permeability in individual red blood cells and confirm that these data align with previously published population level values for human RBC. Finally, we present preliminary evidence for possible application of our device to identify individual RBCs infected with Plasmodium falciparum malaria parasites. Future developments using this device will address the use of whole blood with non-homogenous cell populations, a task currently performed by clinical Coulter counters. [Display omitted] • Rapid identification of individual red blood cells infected with P. falciparum malaria parasites. • RBC membrane permeability was measured in individual cells. • The microfluidic sensor was calibrated and validated for sizing cells and beads. • RBCs were measured in 0.19 s after mixing with anisosmotic media from separate inlets at 5 electrodes over 1.3 s. • The focusing electrode pair lined up the RBCs in the centerline of the channel using p-Dep forces. [ABSTRACT FROM AUTHOR]

Spatial and temporal abnormalities in the frequency and amplitude of the cytosolic calcium oscillations can impact the normal physiological functions of neuronal cells. Recent studies have shown that ketamine can affect the growth and development and even induce the apoptotic death of neurons. This study used isolated developing hippocampal neurons as its study subjects to observe the effect of ketamine on the intracellular calcium oscillations in developing hippocampal neurons and to further explore its underlying mechanism using Fluo-4-loaded laser scanning confocal microscopy. Using a semi-quantitative method to analyze the spontaneous calcium oscillatory activities, a typical type of calcium oscillation was observed in developing hippocampal neurons. In addition, the administration of NMDA (N-Methyl-D-aspartate) at a concentration of 100 µM increased the calcium oscillation amplitude. The administration of MK801 at a concentration of 40 µM inhibited the amplitude and frequency of the calcium oscillations. Our results demonstrated that an increase in the ketamine concentration, starting from 30 µM, gradually decreased the neuronal calcium oscillation amplitude. The inhibition of the calcium oscillation frequency by 300 µM ketamine was statistically significant, and the neuronal calcium oscillations were completely eliminated with the administration of 3,000 µM Ketamine. The administration of 100, 300, and 1,000 µM NMDA to the 1 mM ketamine-pretreated hippocampal neurons restored the frequency and amplitude of the calcium oscillations in a dose-dependent manner. In fact, a concentration of 1,000 µM NMDA completely reversed the decrease in the calcium oscillation frequency and amplitude that was induced by 1 mM ketamine. This study revealed that ketamine can inhibit the frequency and amplitude of the calcium oscillations in developing hippocampal neurons though the NMDAR (NMDA receptor) in a dose-dependent manner, which might highlight a possible underlying mechanism of ketamine toxicity on the rat hippocampal neurons during development. [ABSTRACT FROM AUTHOR]

Abstract: Ketamine, an N-methyl-d-aspartate (NMDA) receptor antagonist, is widely used as a general pediatric anesthetic. Recent studies suggest that ketamine enhances neuronal apoptosis in developing rodents and nonhuman primates. The main goal of this study is to determine whether ketamine causes hippocampal neurodegeneration and behavioral deficits in adulthood, and if so, whether the effects of ketamine are associated with protein kinase C-gamma (PKCγ), extracellular signal regulated kinase (ERK)1/2 and Bcl-2 expression. Starting from postnatal day 7, Sprague–Dawley rat pups randomly received daily ketamine treatment (25, 50 and 75mg/kg, ip) for three consecutive days. Twenty-four hours after the last treatment with ketamine, the rats were decapitated, and the hippocampi were isolated for detection of neuronal apoptosis by TUNEL. The protein expression levels of PKCγ, ERK1/2 and Bcl-2 in the hippocampi were measured by western blot analysis. At 2months of age, learning and memory abilities were tested by the Morris water maze. Ketamine increased the number of apoptotic cells in the CA1 region and dentate gyrus at a dose of 75mg/kg but not at lower doses of 25 and 50mg/kg. The dose of 75mg/kg of ketamine suppressed p-PKCγ, p-ERK1/2 and Bcl-2 expression but not t-PKCγ or t-ERK expression. Ketamine administered to the developing brains of P7 rats at a dose of 75mg/kg caused learning and memory impairments in adulthood. Therefore, these data demonstrate that ketamine at a dose of 75mg/kg in the developing brain results in hippocampal neurodegeneration and persistent learning and memory impairment, which is associated with the PKCγ-ERK signaling pathway. This article is part of a Special Issue entitled: Brain Integration. [Copyright &y& Elsevier]

Becker naevus is a common skin disorder, characterised by localised pigmented patch with or without hypertrichosis. Its prevalence can be as high as 4% in young males.[1] Although gender-related differences in the prevalence of Becker naevus are known,[2] other gender-related characteristics are not well defined. More females developed Becker naevus in early childhood (67% vs. 44%, I P i = 0.0024), whilst more males developed Becker naevus in late childhood (45% vs. 21%, I P i = 0.0009) (Table). [Extracted from the article]

This paper reports a microfluidic lab-on-chip for dynamic particle sizing and real time individual cell membrane permeability measurements. To achieve this, the device measures the impedance change of individual cells or particles at up to ten time points after mixing with different media, e.g. dimethyl sulfoxide or DI water, from separate inlets. These measurements are enabled by ten gold electrode pairs spread across a 20 mm long microchannel. The device measures impedance values within 0.26 s after mixing with other media, has a detection throughput of 150 samples/second, measures impedance values at all ten electrodes at this rate, and allows tracking of individual cell volume changes caused by cell osmosis in anisosmotic fluids over a 1.3 s postmixing timespan, facilitating accurate individual cell estimates of water permeability. The design and testing were performed using yeast cells (Saccharomyces cerevisiae). The relationship between volume and impedance in both polystyrene calibration beads as well as the volume-osmolality relationship in yeast were demonstrated. Moreover, we present the first noninvasive and non-optically-based water permeability measurements in individual cells. [Display omitted] • We calibrated and validated lab-on-chip dynamic cell sizing and cell membrane permeability measurements in individual cells. • Volume-correlated impedance change of myriad individual yeast cells was rapidly measured after mixing with anisosmotic media. • Measurements were performed within 0.26 s after mixing with media from separate inlets at up to 10 electrodes over 1.3 s. [ABSTRACT FROM AUTHOR]

Hypoxia is a hallmark of the tumor microenvironment, and hypoxia regions are frequently found in gastrointestinal cancers, which are associated with worse patients' survival and therapy resistance. However, the potential mechanisms of hypoxic tumor microenvironment still need to be further elucidated, especially about the roles of long non-coding RNAs (lncRNAs) in hypoxic tumor regions. In recent years, a great mount of independent research showed that many lncRNAs were modulated by hypoxia, and these lncRNAs were named as "hypoxia-regulated lncRNAs". In this review, the recent developments in the expression, regulation and functions of hypoxia-regulated lncRNAs in gastrointestinal cancers were summarized. In this review, we summarized and figured out recent studies concerning the expression and biological mechanisms of hypoxia-regulated lncRNAs in gastrointestinal cancers. The related studies were obtained through a systematic search of PubMed, Embase and Cochrane Library. Hypoxia-regulated lncRNAs have various roles in the regulation of metabolism, autophagy, invasion and metastasis in the hypoxic microenvironment. More importantly, hypoxic-regulated lncRNAs have a variety of potential mechanisms in gastrointestinal tumors, including epigenetic, lncRNA-miRNA interaction, lncRNA-protein interactions. Hypoxia-regulated lncRNAs will undoubtedly be developed as targets and promote the progress in ideal therapies for gastrointestinal cancer patients. [ABSTRACT FROM AUTHOR]

Background: Long non-coding RNAs (lncRNAs), which are a portion of non-protein-coding RNAs (ncRNAs), have manifested a paramount role in the pathophysiology of human diseases, particularly in pathogenesis and progression of disease. Myocardial infarction associated transcript (MIAT), which was recently found to demonstrate aberrant expression in various diseases, such as myocardial infarction, schizophrenia, ischemic stroke, diabetic complications, age-related cataract and cancers, is a novel disease-related lncRNA. This work summarize current evidence regarding the biological functions and underlying mechanisms of lncRNA MIAT during disease development. Short conclusion: LncRNA MIAT likely represents a feasible cancer biomarker or therapeutic target. [ABSTRACT FROM AUTHOR]

Verruciform xanthoma (VX) is a rare, benign lesion characterized histopathologically by epithelial papillomatous hyperplasia, local hyperkeratosis with incomplete keratosis, infiltration of foam cells and inflammatory cells in the papillary dermis. Cutaneous malakoplakia (CM) is a rare, chronic, granulomatous disease characterized histopathologically by Michaelis-Gutmann bodies (MGB). (a) Scattered infiltrating foam cells or histiocytes confined to the papillary layer of dermis; (b) the superficial lesion showed scattered infiltrating foam cells or histiocytes confined to the papillary layer of dermis. [Extracted from the article]

Accumulation and spread of tau in Alzheimer's disease and other tauopathies occur in a prion-like manner. However, the mechanisms and downstream consequences of tau trafficking remain largely unknown. We hypothesized that tau traffics from neurons to microglia via extracellular vesicles (EVs), leading to IL-6 generation and cognitive impairment. We assessed mice and neurons treated with anesthetics sevoflurane and desflurane, and applied nanobeam-sensor technology, an ultrasensitive method, to measure tau/p-tau amounts. Sevoflurane, but not desflurane, increased tau or p-tau amounts in blood, neuron culture medium, or EVs. Sevoflurane increased p-tau amounts in brain interstitial fluid. Microglia from tau knockout mice took up tau and p-tau when treated with sevoflurane-conditioned neuron culture medium, leading to IL-6 generation. Tau phosphorylation inhibitor lithium and EVs generation inhibitor GW4869 attenuated tau trafficking. GW4869 mitigated sevoflurane-induced cognitive impairment in mice. Thus, tau trafficking could occur from neurons to microglia to generate IL-6, leading to cognitive impairment. Using their previously developed nanobeam-sensor technology to detect tau protein in the blood, Yuanlin Dong et al. find that the anaesthetic sevoflurane induces trafficking of tau from neurons to microglia in mice. They further see that microglia can take up tau, leading to Il-6 production, overall bringing new insights into the mechanism of sevoflurane-mediated cognitive impairment. [ABSTRACT FROM AUTHOR]

Background: Postoperative delirium (POD) is a common neurologic disorder among elderly patients after non-cardiac surgery, which leads to various negative outcomes. Sleep disorder is considered an important cause of POD. The objective of this study was to investigate whether the Chinese traditional five-element music intervention could reduce POD by improving sleep quality in elderly patients undergoing non-cardiac surgery. Methods: A total of 132 patients aged 65 to 90 years who underwent non-cardiac surgery were randomized to two groups: the intervention (n = 60) and the control group (n = 63). Patients in the intervention group were subjected to the Chinese traditional five-element music intervention during the perioperative, while patients in the control group had no music intervention. POD was evaluated using the Confusion Assessment Method (CAM) in the first 5 days after surgery. The Richards‒Campbell Sleep Questionnaire (RCSQ) was used to assess subjective sleep quality. The levels of nocturnal melatonin and cortisol in saliva were measured on the preoperative and the first 2 postoperative days. Results: The incidence of POD within 5 days was 27.0% in the control group and 11.7% in the intervention group. Preoperative PSQI and MMSE scores were associated with POD. The RCSQ scores on the first postoperative day were significantly decreased in the two groups compared to the preoperative day. Compared to the control group, the RCSQ scores showed a significant improvement in the intervention group on the first postoperative day. Compared to the control group, the level of saliva melatonin in the intervention group showed a significant increase on the first postoperative day. However, there was no statistical difference in cortisol levels between the two groups. Conclusions: Chinese traditional five-element music intervention decreased the incidence of POD in elderly patients who underwent noncardiac surgery via improving sleep quality, which may be associated with increased levels of melatonin. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the effects of dexmedetomidine on cerebral oxygen saturation [Sct(O2)] and postoperative cognitive function in elderly patients undergoing minimally invasive coronary artery bypass graft surgery.Sixty elderly patients who received minimally invasive coronary artery bypass graft surgery were randomly equally divided into dexmedetomidine group (group D) and control group (group N). The patients in group D were pumped with 1 μg/kg dexmedetomidine for 15 min before incision, followed by continuous pumping at 0.3–0.5 μg/(kg·h) till the end of the operation. The patients in group N received same dose of normal saline during the operation. Sct(O2) was monitored at pre-induction (T0), post-induction (T1), 30 min (T2) after single-lung ventilation, and after surgery (T3). Mini-mental state examination (MMSE) was used to assess the cognitive function at 1 day before, 72 hour and 7 days after surgery.Sct(O2) level in group D was significantly higher than that in group N at T2 (P < 0.05). Sct(O2) level was statistically lower at T2 than that at T0, T1 and T3 in the same group N (P < 0.05). At 72 h and 7d after operation, the incidence of cognitive dysfunction in group D was markedly lower than that in group N (P < 0.05), the MMSE score in group D was markedly higher than those in group N, but was significantly lower than that before surgery (P < 0.05).Dexmedetomidine can alleviate the decrease of Sct(O2) during single-lung ventilation, improve postoperative cognitive function, and reduce the incidence of POCD in elderly patients with minimally invasive coronary artery bypass surgery. [ABSTRACT FROM AUTHOR]

Becker's nevus is a common pigmented dermatosis, usually featured by ipsilateral pigmented patch with hypertrichosis. Becker's nevus is often treated with various types of lasers although other regimens are available. However, clinical outcomes appear inconsistent among studies. To summarize the clinical outcomes of Becker's nevus treated with lasers via literature review. A variety of lasers had been used alone or in combination to treat Becker's nevus. Laser wavelengths used for Becker's nevus ranged from 504 to 10,600 nm, while the number of treatment varied from 1 to 12 sessions. The clinical outcomes were mixed although combination of lasers with different wavelengths appeared to achieve a better efficacy. Adverse effects were usually mild to moderate erythema. While lasers are relatively safe, their efficacy for Becker's nevus is moderate. It seems that combination therapy could improve the outcome. However, trials in larger group of patients are required to validate the efficacy of each type of lasers for Becker's nevus. [ABSTRACT FROM AUTHOR]

Propofol (2, 6-diisopropylphenol) is the commonly used intravenous sedative-hypnotic agent. Accumulating evidence shows that propofol affects cancer development by direct and indirect ways. In this review, we will provide an overview of the effects of propofol on cancer development and chemotherapy, with a special focus on the underlying molecular mechanisms involved. Propofol regulates both microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), and serves as a regulator of different signaling pathways including hypoxia-inducible factor-1α (HIF-1α), mitogen-activated protein kinase (MAPK), nuclear factor-kappaB (NF-κB), and nuclear factor E2-related factor-2 (Nrf2) pathways. In addition, propofol modulates host immune function. Possible correlation between propofol and cancer should be verified in further studies, including animal trials and prospective clinical studies. [ABSTRACT FROM AUTHOR]

CD177 is considered to represent neutrophils. We analyzed mRNA expression level of CD177 and clinical follow-up survey of PDAC to estimate overall survival (OS) from Gene Expression Omnibus (GEO) dataset (GSE21501, containing samples from 102 PDAC patients) by R2 platform ( http://r2.amc.nl ). We also analyzed correlated genes of CD177 by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis to predict the potential relationship between neutrophils and prognosis of PDAC. We then performed hematoxylin and eosin (H&E) staining and immunohistochemical staining of surgical specimens to verify infiltration of neutrophils in PDAC tissues. After analyzing mRNA expression data and clinical follow-up survey provided in the GEO dataset (GSE21501, containing samples from 102 PDAC patients) and clinicopathological data of 23 PDAC patients, we demonstrated that CD177 was correlated with poor prognosis. The univariate Kaplan–Meier survival analysis revealed that OS was inversely associated with increased expression of CD177 (P = 0.012). Expression of phosphodiesterase (PDE)4D was positively related to CD177 in gene correlation analysis (R = 0.413, P < 0.001) by R2 platform. H&E staining and immunohistochemistry of CD177 in 23 PDAC surgical samples showed accumulation of neutrophils in the stroma and blood vessels around the cancer cells. In addition, immunohistochemical staining showed that CD177 was highly expressed in the stroma and blood vessels around tumor tissues of PDAC, which was similar to H&E staining. Expression of CD177 can be used to represent infiltration of neutrophils, which may have potential prognostic value in PDAC. [ABSTRACT FROM AUTHOR]

[Display omitted] • Complex changes in white matter myelin occur after repeated esketamine exposure. • Rats receiving high esketamine doses exhibit long-term behavioural deficits. • This study facilitates further studies on narcotic drug neurotoxicity in rats. Esketamine is commonly used for sedation or general anaesthesia in infants and young children. However, repeated esketamine administration during periods of rapid brain growth and development may result in various pathophysiological and cognitive changes. Therefore, this study aimed to investigate the influence of recurrent esketamine exposure on long-term behavioural and white matter consequences. Seven-day-old (P7) male rats were allocated to control, high-, and low-dose groups. Behavioural paradigm assessment was conducted at P25–29. Diffusion tensor imaging revealed long-term effects on water diffusivity in the splenium and cingulum white matter of the corpus callosum at P30. Subsequent two-dimensional structure-tensor analysis of brain tissue sections stained with Luxol fast blue (LFB) showed marked changes in the white matter microstructure in rats after multiple exposures to varying esketamine doses. High-dose esketamine significantly reduced activity time and total distance in the open-field experiment. High-dose esketamine exposure might lead to impaired short-term memory in rats. Additionally, the high-dose group showed prolonged immobility time during the forced swimming test. On the balance beam, the high-dose group displayed more right turns and right-foot slips and lower time spent on the rotating bar, indicating motor defects, than did the other groups. Diffusion tensor imaging demonstrated a decreased water molecule diffusion ability in the corpus callosum in the high-dose group. LFB staining indicated microstructural differences in the white matter of animals in the high-dose group. These findings suggest that behavioural deficits in high-dose esketamine-treated rats are at least partially attributed to changes in the white matter microstructure. [ABSTRACT FROM AUTHOR]

Postoperative cognitive dysfunction (POCD) is a common complication in patients who undergo anesthesia in different types of surgeries. Emerging evidence implicates elevated beta-amyloid (Aβ) in the pathogenesis of POCD. Meanwhile, Dexmedetomidine (DEX) has recently shown promise in reducing POCD incidence. This study aimed to elucidate the role of Aβ in inducing endothelial permeability in cerebral microvascular endothelial cells and the underlying mechanisms and testing the effects of DEX. We demonstrated that Aβ 1–42 , the prevalent Aβ form related to POCD, is cytotoxic to HBMECs, increasing transendothelial permeability and inducing mitochondrial dysfunction, as evidenced by elevated mitochondrial reactive oxygen species (ROS) and decreased ATP production and mitochondrial membrane potential. Furthermore, Aβ 1–42 was shown to inhibit Sirt3, exacerbating mitochondrial dysfunction. Conversely, DEX was found to prevent Aβ 1–42 -induced mitochondrial dysfunction and permeability increases and preserved tight junction proteins in HBMECs.These findings suggest that DEX, as a Sirt3 activator, may offer a pharmacological strategy to mitigate Aβ 1–42 -related cerebral microvascular endothelial cell dysfunction and preserve cognitive function post-surgery. • Aβ 1–42 inhibits Sirt3 expression and activity, worsening mitochondrial dysfunction in HBMECs. • Dexmedetomidine treatment inhibits Aβ 1–42 -induced mitochondrial dysfunction in HBMECs. • Sirt3 mediates Dexmedetomidine-prevented permeability increases in HBMECs. [ABSTRACT FROM AUTHOR]

The article describes the case of a 45-year-old Chinese male patient with a history of asymptomatic macules on the head and face area which was diagnosed as cutaneous plasmacytosis. The results of histopathology and immunohistopathological study confirmed the diagnosis, which led physicians to prescribe prednisone, thalidomide and tacrolimus. A discussion on the history and clinical features of cutaneous plasmacytosis is offered.

Background: Tracheal injury could cause intratracheal scar hyperplasia which in turn causes benign tracheal stenosis (TS). With the increasing use of mechanical ventilation and ventilator, the incidence of TS is increasing. However, the molecular mechanisms of TS have not been elucidated. It is significant to further explore the molecular mechanisms of TS. Methods: The repeatability of public data was verified. Differently expressed genes (DEGs) and most significant genes were identified between TS and normal samples. Enrichment analysis of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were analyzed. The comparative toxicogenomics database were analyzed. TS patients were recruited and RT‐qPCR were performed to verify the most significant genes. Results: There exist strong correlations among samples of TS and normal group. There was a total of 194 DEGs, including 61 downregulated DEGs and 133 upregulated DEGs. GO were significantly enriched in mitotic nuclear division, cell cycle, and cell division. Analysis of KEGG indicated that the top pathways were cell cycle, and p53 pathway. MKI67(OMIM:176741), CCNB1(OMIM:123836), and CCNB2(OMIM:602755) were identified as the most significant genes of TS, and validated by the clinical samples. Conclusion: Bioinformatics methods might be useful method to explore the mechanisms of TS. In addition, MKI67, CCNB1, and CCNB2 might be the most significant genes of TS. [ABSTRACT FROM AUTHOR]

Abstract LncRNAs are a group of noncoding RNAs that are >200 nucleotides in length. These RNAs have no significant protein-coding potential due to the lack of obvious open reading frames. To date, accumulating evidence has demonstrated that dysregulation of lncRNAs exhibits indispensable roles in the pathological processes of human cancers. These RNAs function as either oncogenes or tumor suppressor genes to regulate proliferation, migration and invasion of cancer cells. GHET1, a prominent oncogenic lncRNA, is highly expressed in diverse malignancies. Furthermore, GHET1 performs key functions in carcinogenesis and progression, suggesting that GHET1 is expected to be a prospective biomarker or therapeutic target for cancers. In this review, we provide a summary of the current evidence concerning the biological functions, underlying mechanisms and clinical significance of GHET1 during tumor development. Highlights • GHET1 is overexpressed in diverse malignancies. • Increased GHET1 expression is correlated with poor prognosis and clinicopathological characteristics. • Upregulated GHET1 contributes to the proliferation, invasion and migration of various cancer cells. • The regulatory mechanisms of GHET1 are sophisticated in tumors. • GHET1 likely represents a viable biomarker and therapeutic target for the diagnosis and treatment of cancers. [ABSTRACT FROM AUTHOR]

The safety of anesthetics on the developing brain has caused concern. Ketamine, an N-methyl-D-aspartate receptor antagonist, is widely used as a general pediatric anesthetic. Recent studies suggested that ketamine alters the plasticity of dendritic spines in the developing brain and may be an important contributing factor to learning and cognitive impairment. However, the underlying molecular mechanism remains poorly understood. Therefore, the aim of the present study was to investigate the effect of ketamine on the plasticity of dendritic spines in cultured hippocampal neurons and the potential underlying mechanisms. After 5 days in vitro, rat hippocampal neurons were exposed to different concentrations (100, 300 and 500 µM) of ketamine for 6 h. Ketamine decreased the number and length of dendritic spines in a dose-dependent manner. Ketamine at a concentration of 300 µM caused an upregulation of transforming protein RhoA (RhoA) and Rho-associated kinase (ROCK) protein. These effects were inhibited by the ROCK inhibitor Y27632. These results suggested that ketamine induces loss and shortening of dendritic spines in hippocampal neurons via activation of the RhoA/ROCK signaling pathway. [ABSTRACT FROM AUTHOR]

Abstract Objectives Long non-coding RNAs (lncRNAs) are a type Table of endogenous RNA longer than 200 nucleotides in length, and this kind of RNAs lack or possess limited ability of coding proteins. A large number of studies have demonstrated that lncRNAs could take part in massive biological processes, such as transcriptional activation and interference, cellular differentiation, proliferation, migration, invasion and apoptosis. The abnormal expression of lncRNAs has been clarified to play extremely important roles in various diseases, especially in human cancers. LncRNA actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) is a newly recognized cancer-related lncRNA deriving from the antisense strand of DNA at the AFAP1 coding gene locus. A slew of new studies suggest that AFAP1-AS1 is involved in many kinds of malignant tumors. Moreover, in recent years, the dysregulated expression of AFAP1-AS1 has been confirmed to be associated with oncogenesis and tumor progression. Evidence has increasingly shown that AFAP1-AS1 could probably serve as a novel potential molecular biomarker in tumor diagnosis and therapeutic target in tumor treatment. In this review, we sum up present stage new hottest research issues in respect of the biological functions and molecular mechanisms of AFAP1-AS1 in occurrence and progression of human tumors. Materials and methods In this review, we summarize the recent researches about the expression and molecular biological mechanisms of lncRNA AFAP1-AS1 in tumor development. Existing relevant studies are acquired and analyzed by searching Pubmed, BioMedNet, GEO database and Academic Search Elit systematically. Results Long non-coding RNA AFAP1-AS1 is an important tumor-associated lncRNA and its aberrant expression has been found in many malignancies so far, including pancreatic ductal adenocarcinoma, cholangiocarcinoma, gallbladder cancer, hepatocellular carcinoma, gastric cancer, colorectal cancer, esophageal cancer, nasopharyngeal carcinoma, lung cancer, ovarian cancer, breast cancer, retinoblastoma, laryngeal cancer, tongue squamous cell carcinoma and thyroid cancer. In addition, the dysregulated expression of AFAP1-AS1 is related to carcinogensis, overall survival (OS), disease-free survival (DFS), progression-free survival (PFS) and tumor progression containing lymph node metastasis, distant metastasis, histological grade, tumor size and tumor stage. Conclusions A series of studies provide detailed information to understand lncRNA AFAP1-AS1 role in various human cancers. LncRNA AFAP1-AS1 is an oncogene in tumors that have been studied so far, and it may act as a useful tumor biomarker and therapeutic target. [ABSTRACT FROM AUTHOR]

Ketamine, a non-competitive N -methyl d -aspartate (NMDA) receptor antagonist, is widely used in pediatric clinical practice. However, prolonged exposure to ketamine results in widespread anesthetic neurotoxicity and long-term neurocognitive deficits. The molecular mechanisms that underlie this important event are poorly understood. We investigated effects of anesthetic ketamine on neuroapoptosis and further explored role of NMDA receptors in ketamine-induced neurotoxicity. Here we demonstrate that ketamine induces activation of cell cycle entry, resulting in cycle–related neuronal apoptosis. On the other hand, ketamine administration alters early and late apoptosis of cultured hippocampus neurons by inhibiting PKC/ERK pathway, whereas excitatory NMDA receptor activation reverses these effects. Ketamine-induced neurotoxicity blocked by NMDA is mediated through activation of PKC/ERK pathway in developing hippocampal neurons. [ABSTRACT FROM AUTHOR]

SOX2 overlapping transcript (Sox2ot), a long noncoding RNA (lncRNA), was initially found a close concomitant expression pattern of SOX2 gene . Multiple studies have demonstrated that the relatively upregulated Sox2ot could be observed in different types of cancer tissues and effectively promotes cell proliferation, invasion, and tumorigenesis in vitro. In the present study, we aimed to detect the crucial prognostic role of Sox2ot in cholangiocarcinoma (CCA) patients' clinicopathologic features and evaluated the correlation between Sox2ot expression and CCA patients overall survival. 58 CCA patients who underwent surgical treatment were recruited for the investigation. Sox2ot expression levels estimated by the quantitative real-time PCR (qRT-PCR) showed that both clinical tissues and cell lines possessed the overexpressed states and the upregulation of Sox2ot significantly associated with lymph node invasion ( p = 0.0308), TNM stage ( p = 0.0072) and postoperative recurrence ( p = 0.0019). The Kaplan-Meier curve showed a strong association between Sox2ot and overall survival (OS) and multivariate analysis confirmed this finding. Furthermore, the proliferation, migration and invasion assays were carried out with RBE and QBC939 cell lines and the knockdown of Sox2ot in all experiments could remarkably decrease malignant biological behaviors. Taken together, lncRNA Sox2ot indicates an unfavorable prognostic biomarker and potential therapeutics target for CCA patients. [ABSTRACT FROM AUTHOR]

• LXA4 ameliorated surgery-induced cognitive decline. • LXA4 mitigated neuroinflammation and microglia activation after surgery. • LXA4 inhibited M1 polarization and promoted M2 polarization of BV2 microglia. • LXA4 mitigated LPS-induced inflammation and oxidative stress. • The effects of LXA4 on LPS-stimulated BV2 microglia was blocked by SIRT1 selective inhibitor EX-527. Perioperative neurocognitive disorder (PND) is a common complication that increases morbidity and mortality in elderly patients undergoing surgery. Abnormal microglia activation causes neuroinflammation and contributes to the development of PND. Growing evidence shows that lipoxin A4 (LXA4), a lipid mediator, possesses potent anti-inflammatory activities. In this study, we investigated whether LXA4 exerted a protective effect against surgery-induced neurocognitive deficits and explored the underlying mechanisms. Mice were subjected to laparotomy under sevoflurane anesthesia to establish an animal model of PND. LXA4 (15 μg/kg/d, ip) was administered three days prior surgery. We showed that LXA4 significantly alleviated surgery-induced cognitive impairments, attenuated neuroinflammation and microglial activation in hippocampus. In BV2 microglial cells treated with LPS (100 ng/mL), pre-application of LXA4 (100 nΜ) significantly inhibited M1 polarization and promoted M2 polarization, and decreased the levels of pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) and increased the levels of anti-inflammatory cytokine (IL-10). LXA4 also mitigated LPS-regulated expression of HO-1, NOX2, and SOD1, elevated SOD activity, and attenuated ROS production. Furthermore, we revealed that LXA4 increased the expression of SIRT1 and decreased the protein level of acetylated NF-κB p65. SIRT1 inhibitor EX-527 abolished the anti-inflammatory and antioxidant response effects of LXA4 in BV2 microglial cells. Hence, LXA4 is a potential therapeutic agent for surgery-induced neuroinflammation, oxidative stress, and cognitive deficit, and the effect of LXA4 is probably mediated by the activation of the SIRT1/NF-κB signaling pathway in microglia. [ABSTRACT FROM AUTHOR]

Ketamine, the widely used intravenous anesthetic, has been reported to cause neurotoxicity and disturbs normal neurogenesis. However, the efficacy of current treatment strategies targeting ketamine's neurotoxicity remains limited. Lipoxin A4 methyl ester (LXA4 ME) is relatively stable lipoxin analog, which serves an important role in protecting against early brain injury. The purpose of this study was to investigate the protective effect of LXA4 ME on ketamine-caused cytotoxicity in SH-SY5Y cells, as well as the underlying mechanisms. Cell viability, apoptosis and endoplasmic reticulum stress (ER stress) were detected by adopting experimental techniques including CCK-8 assay, flow cytometry, western blotting and transmission electron microscope. Furthermore, examining the expression of leptin and its receptor (LepRb), we also measured the levels of activation of the leptin signaling pathway. Our results showed that LXA4 ME intervention promoted the cell viability, inhibited cell apoptosis, and reduced the expression of ER stress related protein and morphological changes induced by ketamine. In addition, inhibition of leptin signaling pathway caused by ketamine could be reversed by LXA4 ME. However, as the specific inhibitor of leptin pathway, leptin antagonist triple mutant human recombinant (leptin tA) attenuated the cytoprotective effect of LXA4 ME against ketamine-induced neurotoxicity. In conclusion, our findings demonstrated LXA4 ME could exert a neuroprotective effect on ketamine-induced neuronal injury via activation of the leptin signaling pathway. • Ketamine could induce decrease of cell viability, apoptosis, ER stress and inactivation of leptin pathway. • LXA4 ME intervention reduced the damage effects of ketamine on SH-SY5Y cells. • LXA4 ME could exert a protective effect on ketamine-induced neuronal injury via activation of the leptin signaling pathway. [ABSTRACT FROM AUTHOR]

Early postnatal anesthesia causes long-lasting learning and memory impairment in rodents, however, evidence for a specific neurotoxic effect on early synaptogenesis has not been demonstrated. Drebrin A is an actin binding protein whose localization in dendritic protrusions serves an important role in dendritic spine morphogenesis, and is a marker for early synaptogenesis. We therefore set out to investigate whether clinically-relevant concentrations of anesthetic sevoflurane, widely- used in infants and children, alters dendritic morphology in cultured fetal day 16 mouse hippocampal neurons. After 7 days in vitro, mouse hippocampal neurons were exposed to four hours of 3% sevoflurane in 95% air/5% CO2 or control condition (95% air/5% CO2). Neurons were fixed in 4% paraformaldehyde and stained with Alexa Fluor555-Phalloidin, and/or rabbit anti-mouse drebrin A/E antibodies which permitted subcellular localization of filamentous (F)-actin and/or drebrin immunoreactivity, respectively. Sevoflurane caused acute significant length-shortening in filopodia and thin dendritic spines in days-in-vitro 7 neurons, an effect which was completely rescued by co-incubating neurons with ten micromolar concentrations of the selective Rho kinase inhibitor Y27632. Filopodia and thin spine recovered in length two days after sevoflurane exposure. Yet cluster-type filopodia (a precursor to synaptic filopodia) were persistently significantly decreased in number on day-in-vitro 9, in part owing to preferential localization of drebrin immunoreactivity to dendritic shafts versus filopodial stalks. These data suggest that sevoflurane induces F-actin depolymerization leading to acute, reversible length-shortening in dendritic protrusions through a mechanism involving (in part) activation of RhoA/Rho kinase signaling and impairs localization of drebrin A to filopodia required for early excitatory synapse formation. [ABSTRACT FROM AUTHOR]

LINC00261 plays a vital role in tumorigenesis and metastasis of digestive system cancer. However, an influence of LINC00261 on cholangiocarcinoma has a little research. There, we investigated clinical role and molecular mechanisms of LINC00261 in cholangiocarcinoma. The qRT-PCR was performed for the detection of LINC00261 level in 50 paired specimens from CCA patients and six cell lines. Cell proliferation were explored by CCK-8 and colony formation assays in QBC939 and RBE cells after transfected with si-LINC00261 or si-NC. Then, AO/EB double fluorescence staining and flow cytometric assays were performed to assess cell apoptosis. Transwell and wound healing assays were selected to evaluate migratory and invasive property of cells. Protein levels, such as PCNA, Bax, Bcl-2, and several epithelial-to-mesenchymal transition markers, including E-cadherin, N-cadherin and Vimentin, were detected by western blot assays. Furthermore, we use a R2 platform to evaluate the correlation between LINC00261 and EMT makers and predict the overall survival and relapse-free survival for CCA patients by the expression of LINC00261/ EMT makers. LINC00261 was overexpressed in cancerous tissues and CCA cell lines compared with adjacent tissues and HIBEC, respectively. Up-regulation of LINC00261 was related to larger tumor size (p = 0.009), positive lymph node metastasis (p = 0.021), advanced TNM stages (p = 0.017) and higher postoperative recurrence (p = 0.009) for CCA patients. Additionally, univariate and multivariate analysis displayed that LINC00261 an independent prognostic factor in CCA patients. Knockdown of LINC00261 expression in RBE and QBC939 cell lines inhibited cell proliferation, migration and invasion property and increased cell apoptosis and the EMT progression. Moreover, there was a strong correlation between LINC00261 and E-cadherin (CDH1) (p < 0.05), and low expression of E-cadherin (CDH1) has a poor overall survival and relapse-free survival in CCA patients (p < 0.05). Overall, high level of LINC00261 in CCA predicts a poor prognosis, and promotes a metastasis via EMT process. Thus, LINC00261 could be a promising biomarker and therapeutic target for CCA, and in the high level of LINC00261 in CCA, E-cadherin or CDH1 might be an effective factor for tumor metastasis or poor prognosis. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented which discusses a case study of a 40-year-old man who was evaluated for asymptomatic verrucous plaques in the upper gingiva and diagnosed with multiple verruciform xanthomas following his bone marrow transplantation.

Cholangiocarcinoma (CCA) arising from the neoplastic transformation of cholangiocytes with increasing incidence in the worldwide. Unfortunately, a large amount of CCA patients lost their chance for surgery because it is hard to diagnose in the early stages. Long non-coding RNAs (lncRNAs) is closely associated with development and progression of various malignant tumors. Hox transcript antisense intergenic (HOTAIR), a negative prognostic factor for patients with gastric, liver and pancreatic carcinoma. Its transcription levels and functional roles in CCA is still unknown. Therefore, we aimed to explore the effect of HOTAIR in CCA including cell proliferation, apoptosis, migration, invasion and epithelial-to-mesenchymal transition (EMT). The results showed that HOTAIR was highly expressed both in CCA tissue samples and cell lines compared with corresponding normal bile duct tissues and Human intrahepatic biliary epithelial cells (HIBEC). Its overexpression was closely correlated with Tumor size, TNM stage and postoperative recurrence in CCA patients. Moreover, up-regulation of HOTAIR has correlation with prognosis in CCA patients. Knockdown of HOTAIR by siRNAs significantly decreased the migration and invasion but increased apoptosis of CCA cells in vitro. Overall, our study revealed that HOTAIR may play as a new potential therapeutic target and forecast poor prognosis for this fatal disease. [ABSTRACT FROM AUTHOR]

Background: Accumulating evidence has indicated that long non-coding RNAs (lncRNAs) behave as a novel class of transcription products during multiple cancer processes. However, the mechanisms responsible for their alteration in cholangiocarcinoma (CCA) are not fully understood. Methods: The expression of SPRY4-IT1 in CCA tissues and cell lines was determined by RT-qPCR, and the association between SPRY4-IT1 transcription and clinicopathologic features was analyzed. Luciferase reporter and chromatin immunoprecipitation (ChIP) assays were performed to explore whether SP1 could bind to the promoter region of SPRY4-IT1 and activate its transcription. The biological function of SPRY4-IT1 in CCA cells was evaluated both in vitro and in vivo. ChIP, RNA binding protein immunoprecipitation (RIP) and luciferase reporter assays were performed to determine the molecular mechanism of SPRY4-IT1 in cell proliferation, apoptosis and invasion. Results: SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally, SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Furthermore, SPRY4-IT1 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion; inducing cell apoptosis and reversing the epithelial-to-mesenchymal transition (EMT) process in CCA cells. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold. Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p. Conclusions: Our data illustrate how SPRY4-IT1 plays an oncogenic role in CCA and may offer a potential therapeutic target for treating CCA. [ABSTRACT FROM AUTHOR]