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Primary immunodeficiency diseases (PID) is a congenital disease caused by single gene germline mutation related to the immune system. PID patients have immune dysregulation, and are susceptible to infectious diseases, autoimmune diseases, autoimmune diseases, allergic diseases, and malignant tumors. The first symptom of some PID patients is atopic disease, therefore they go to the department of allergy, department of pediatrics and other relevant departments. How to identify and diagnose PID in allergic patients, to reduce diagnosis delay and prevent disease aggravation are the abilities that allergists, pediatricians, and doctors in other relevant departments need to master. This article summarizes the warning signs of PID in allergic patients and the mechanism of allergy combined with PID, and then summarizes the common types of PID in allergic patients, the evaluation, treatment and prevention in patients with PID and allergy.原发性免疫缺陷病（primary immunodeficiency diseases，PID）是由免疫系统相关的单基因胚系突变导致的先天性疾病。PID患者存在免疫过程失调，对感染性疾病、自身免疫病、自身炎症性疾病、过敏性疾病和恶性肿瘤的易感性增加。部分PID患者以可疑过敏表现（如湿疹样皮损）为首发症状，或因严重的过敏性疾病就诊于变态反应科。如何在有可疑表现的过敏患者中识别并诊断出PID、减少诊断延误、预防疾病加重，是变态反应科、儿科及相关临床科室医生需要掌握的能力。本文总结归纳过敏患者中提示PID的警示征象和过敏合并PID的机制，同时概述过敏患者中常见的PID类型、PID伴发过敏患者的评估、治疗及预防。.

患儿 女，7岁，因“发热6 d，腹痛、呕吐3 d”于2021年7月就诊于安徽省儿童医院儿童重症医学科。患儿以发热、腹痛、呕吐及休克为主要临床表现。血新型布尼亚病毒核酸检测阳性，心电图示三度房室传导阻滞，床旁超声心动图示弥漫性室壁运动减低伴全心增大。诊断为暴发性心肌炎，予液体复苏、肾上腺素应用、营养心肌、利尿及丙种球蛋白冲击，并紧急植入临时心脏起搏器。临时起搏器安装术后48 h患儿自主心律恢复，术后第5天自主心律稳定，拔除起搏器，术后第14天顺利出院。出院后随访，患儿超声心动图未见异常。.

Ambient fine particulate matters (PM大气细颗粒物（PM

Deep U-Net Neural Network from the paper "Approximating Three-dimensional (3-D) Transport of Atmospheric Pollutants via Deep Learning" in Pytorch is built for replacing and accelerating the transport procedure in the chemical transport models. The dataset consisted of meteorological field, emission inventory, and concentrations of pollutant. Meteorological field was estimated by the Weather Research and Forecasting (WRF) model with the initial conditions and observation dataset from the National Centers for Environmental Prediction (NCEP). Emission inventory was derived from the Multi-resolution Emission Inventory for China (MEIC v1.3, 0.25° × 0.25°, 2016,http://www.meicmodel.org) and interpolated to the required 12 km *12 km horizontal resolution. A 3-D CTM numerical model of the Community Multiscale Air Quality (CMAQ) (https://github.com/USEPA/CMAQ/tree/5.3.1) was selected to simulate the concentration evolution with the meteorological field and emission inventory, as well as the benchmark for computation efficiency comparison for the deep learning surrogate.The retrieved training and validation datasets are too large (>1T) to be uploaded for share. Anyone who is interested in them is welcomed to contact the corresponding author for a point-to-point transfer. Full Changelog: https://github.com/junzheXu/DL_3-DTransport/commits/v0.0.0

先天性结核病是一种罕见、诊断困难且病死率高的严重结核病。本组3例确诊患儿发病年龄分别为7、20、7日龄，以发热为主要临床表现，结核病变均在肺部，胸部CT可见结节影、实变及淋巴结肿大等，胃液或肺泡灌洗液涂片检出抗酸杆菌，培养为结核分枝杆菌复合群且对利福平、异烟肼敏感，采用利福平、异烟肼二联抗结核治疗，疗程3~10个月，均临床痊愈，随访3年，3例患儿均生长发育良好。.

FOXO4 has essential roles in cellular metabolism and prevents cartilage degeneration in osteoarthritis (OA). Here we aim to provide evidence that deacetylated-FOXO4 stabilizes chondrocyte (CH) extracellular matrix (ECM) related to SOX9 activation.We used Chromatin immunoprecipitation (ChIP) and Dual-Luciferase reporter assay to verify that the FOXO4 protein activates SOX9 by binding to its promoter. We cultured human CHs with IL-1β to cause degeneration and supplied Sirt1 protein to deacetylate FOXO4. To confirm the function of FOXO4 and SOX9 during CHs degeneration, we also used the FOXO4 and SOX9 silenced CHs by siRNA transfection as a comparison. Western blot assay was used to analyze the protein level of Sirt1, SOX9, and the acetylated condition of FOXO4. Besides, RT-PCR was used to measure the mRNA level of collagen I/II/X, aggrecan, MMP-13, and ADAMTS-5 for determining the ECM states.FOXO4 protein transcriptionally activates SOX9 expression by binding to its promoter. Under the IL-1β stimulation, FOXO4 acetyl-lysine rate increased, and the SOX9 protein expression decreased, which was alleviated after the supplement of exogenic Sirt1 protein. Meanwhile, Sirt1 overexpression increased the collagen II and aggrecan and reduced the collagen I, collagen X, MMP-13, and ADAMTS-5 mRNA expression. However, the silencing of FOXO4 abolished the Sirt1 induced SOX9 expression and weakened the ECM production stability. Additionally, SOX9 silencing also alleviated the effect of the Sirt1 supplement on the degenerated CHs, though the FOXO4 was highly deacetylated.FOXO4 acetylation aggravates during the degeneration of CHs, and the deacetylation of FOXO4 by Sirt1 could activate the SOX9 expression and result in maintaining the ECM stability of cartilage.

Triple negative breast cancer (TNBC) is an aggressive subtype of breast cancer (BC) with poor prognosis. Identification of reliable biomarkers for predicting prognosis of TNBC contributes significantly to improve the clinical outcome and disease management. Long non-coding RNAs (LncRNAs) have been demonstrated to play a critical role in tumorigenesis of TNBC. In this study, we aimed to investigate the prognostic significance of serum exosomal lncRNA small ubiquitin-like modifier 1 pseudogene 3 (SUMO1P3) in TNBC.The expression level and clinical significance of tissue lncRNA SUMO1P3 in BC were analyzed using the public The Cancer Genome Atlas (TCGA) dataset. Then,A. Na-er, Y.-Y. Xu, Y.-H. Liu, Y.-J. Gan the serum exosomal lncRNA SUMO1P3 levels were examined in patients with TNBC, patients with non-TNBC, patients with benign breast disease and healthy controls using the quantitative real-time PCR. The potential clinical significance of serum exosomal lncRNA SUMO1P3 was further evaluated.Based on the TCGA data, tissue lncRNA SUMO1P3 was upregulated in BC tissues, and its upregulation was significantly correlated with poor survival. Our findings showed that the expression level of serum exosomal lncRNA SUMO1P3 was significantly higher in patients with TNBC compared to patients with non-TNBC, patients with benign breast disease and healthy controls. In addition, serum exosomal lncRNA SUMO1P3 was closely correlated with lymphovascular invasion, lymph node metastasis and histological grade. The serum exosomal lncRNA SUMO1P3 levels were markedly decreased in chemosensitive cases, while not in the chemoresistance cases. Moreover, patients in the high serum exosomal lncRNA SUMO1P3 group had worse overall survival than the patients in the low serum exosomal lncRNA SUMO1P3 group. The multivariate analysis showed that serum exosomal lncRNA SUMO1P3 was an independent prognostic factor for TNBC.Collectively, serum exosomal lncRNA SUMO1P3 might be a reliable and robust prognostic biomarker for TNBC.

Vascular dementia (VD) is a type of memory, cognition, and behavior disorder caused by ischemic stroke or hemorrhagic stroke. It is a common pathogenesis of dementia that is only second to Alzheimer's disease. Inflammation plays a key role in VD. Interleukin-1β (IL-1β) is a kind of pro-inflammatory cytokine, while its mechanism in VD occurrence and development is still unclear.The healthy male rats were randomly divided into three groups, including sham group, VD model group (established by bilateral common carotid artery ligation), and IL-1β group (treated by IL-1β monoclonal antibody intracerebroventricular injection on based on model group). Rat learning ability was evaluated by Morris water maze assay. IL-1β expression in brain tissue and peripheral blood was examined by using Real Time-PCR and enzyme-linked immunosorbent assay (ELISA), respectively. Hippocampus apoptosis was detected by caspase 3 activity detection kit. B-cell lymphoma-2 (Bcl-2) and p38 mitogen-activated protein kinase (MAPK) protein levels were assessed by Western blot assay.IL-1β expression was increased, caspase 3 activity was enhanced, Bcl-2 level was declined, and p-P38 phosphorylation was elevated in brain tissue and peripheral blood from VD model group compared to sham group (p0.05). IL-1β monoclonal antibody significantly reduced IL-1β expression, improved learning ability, attenuated caspase 3 activity, increased Bcl-2 level, and declined p-P38 expression in VD rats compared to model group (p0.05).IL-1β can delay VD occurrence and development through the P38-MAPK signaling pathway to regulate cell apoptosis and improve learning ability.

Long noncoding RNA (lncRNA) plays a vital role in the progression of various cancers. However, the potential mechanisms of NR2F1-AS1 in the tumorigenesis of neuroblastoma (NB) have not been determined.The expression levels of NR2F1-AS1, miR-493 and TRIM2 were detected by RT-qPCR. The downstream target genes of NR2F1-AS1 or miR-493 were predicted by bioinformatics analysis (http://starbase.sysu.edu.cn/), which was further indicated by Luciferase reporter and RNA immunoprecipitation (RIP) assays. CCK-8, transwell, and TUNEL assays were performed to determine the viability, migration, invasion and apoptosis of NB cells.NR2F1-AS1 was highly expressed and miR-493 was lowly expressed in NB tissues and cell lines. The high expression of NR2F1-AS1 was associated with poor prognosis in NB. NR2F1-AS1 knockdown inhibited proliferation, migration, and invasion, and accelerated apoptosis of NB cells. MiR-493 was a downstream target of NR2F1-AS1, and the silencing of miR-493 reversed NR2F1-AS1 knockdown-attenuated progression of NB. Moreover, TRIM2 was demonstrated to be directly targeted by miR-493, and the upregulation of TRIM2 could abolish the inhibitory effect of miR-493 overexpression on the progression of NB. Finally, it was found that NR2F1-AS1 regulated TRIM2 expression by sponging miR-493.The present study demonstrated that NR2F1-AS1 promoted the progression of NB through the miR-493/TRIM2 axis. This finding may provide new insight into the treatment of NB.

Crude mortality rate (CR) for lung cancer in Qidong increased from 11.50/10江苏省启东市肺癌粗死亡率从1972—1976年的11.50/10万上升至2012—2016年的76.61/10万，中国人口标化死亡率从1972—1976年的13.11/10万上升至2012—2016年的34.27/10万，世界人口标化死亡率从1972—1976年的13.40/10万上升至2012—2016年的34.30/10万。1972—2016年粗死亡率、中国人口标化死亡率、世界人口标化死亡率的平均年度变化百分比分别为4.87%（95%

The aim of this study was to investigate the expression level and potential molecular mechanism of microRNA-1324 in gastric cancer (GCa) to provide a new perspective for the diagnosis and treatment of GCa.The expression levels of microRNA-1324 and MECP2 in GCa tissues and cell lines were detected using quantitative Real Time Polymerase Chain Reaction (qRT-PCR). The influence of microRNA-1324 and MECP2 on the proliferation or invasiveness of GCa cells were investigated by cell counting kit-8 (CCK-8) and colony formation assay or transwell assay, respectively. Furthermore, the regulatory interplay between microRNA-1324 and MECP2 was verified via Dual-Luciferase reporting assay, qRT-PCR, and Western Blot.QRT-PCR results revealed that microRNA-1324 expression was remarkably down-regulated in GCa tissues and cell lines, while the expression of MECP2 was remarkably up-regulated. Subsequently, we confirmed that miR-1324 could target and bind to MECP2, as well as inhibit its expression. Inhibition of microRNA-1324 remarkably enhanced the proliferative capacity and invasiveness of GCa cells. However, opposite results were observed after inhibiting MECP2 expression. At the same time, flow cytometry revealed that inhibition of microRNA-1324 accelerated cell cycle but inhibited apoptosis. Conversely, opposite results were observed when MECP2 was down-regulated in vitro.MicroRNA-1324 was remarkably down-regulated in GCa tissues or cell lines. Meanwhile, it could inhibit MECP2 expression, and promote the proliferation and invasion of GCa cells, eventually participating in the occurrence and development of GCa.

The aim of this study was to investigate the role of microRNA-593-5p (miR-593-5p) in the development of lung adenocarcinoma (LA).The expression level of miR-593-5p in LA tissues and cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Luciferase reporter gene assay and Western blot were performed to evaluate the interaction between miR-593-5p and intercellular cell adhesion molecule-1 (ICAM-1). Furthermore, the effects of the miR-593-5p/ICAM-1 axis on A549 cells were determined by MTS, colony formation assay, and transwell assay, respectively.MiR-593-5p was significantly downregulated in both clinical samples and cell lines. The bioinformatics analysis predicted that miR-593-5p could complementarily bind to the 3'-UTR of ICAM-1. Luciferase reporter gene assay confirmed that ICAM-1 was the direct target of miR-593-5p. Western blot results demonstrated that miR-593-5p could effectively reduce the protein expression of ICAM-1 in cells. In vitro experiments indicated that the proliferation and migration of A549 cells were significantly inhibited by miR-593-5p transfection. However, the overexpression of ICAM-1 could effectively reverse the inhibitory effects of miR-593-5p in vitro. These results indicated that the inhibitory effects of miR-593-5p on LA were achieved by regulating ICAM-1 expression.MiR-593-5p/ICAM-1 axis might be a potential therapeutic target for the diagnosis and treatment of LA.

Gastric cancer (GC) is one of the most ordinary malignant tumors. Recent studies have revealed that circular RNAs (circRNAs) play an important role in the progression of tumorigenesis. In this research, circ-SMAD7 was selected to identify how it functions in the progression of GC.Circ-SMAD7 expression in paired GC patients' tissue samples and cell lines was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). The role of circ-SMAD7 in the metastasis of GC was detected through wound healing assay and transwell assay. Western blot assay and RT-qPCR were used to discover the function of circ-SMAD7 in epithelial-to-mesenchymal transition (EMT) process. Furthermore, tumor metastasis assay was also performed in vivo.In this study, RT-qPCR results showed that circ-SMAD7 expression was significantly lower in GC tissues compared to that in adjacent ones. Cell migration and invasion of GC were inhibited via upregulation of circ-SMAD7. Moreover, the results of further experiments revealed that the EMT-related proteins were regulated via upregulation of circ-SMAD7 in GC. Furthermore, tumor metastasis of GC was inhibited via upregulation of circ-SMAD7 in nude mice.These results indicate that upregulation of circ-SMAD7 inhibits GC cell migration and invasion via reversing the EMT process.

We analyze photonic scattering on a trimer with PT symmetry, where the photon propagates in an array of cavities. In the system, a passive and an active cavity couple to another cavity without loss and gain simultaneously, which is in the middle of the cavity array. Such three cavities can be regarded as the scattering target coupling to the unlimited number of cavities from two directions respectively. Our approach is to use the Schrodinger equation to calculate the reflection coefficient and transmission coefficient, and then let photonic transmission spreads from gain or loss cavity. It shows that the scattering of the photon is closely associated with the PT symmetric characteristic of the dynamics of the system. The atom’s modulation on the photonic transmission is also investigated. We found that the scattering center can behave as a photonic switch, which could be used potentially to control the photonic transmission.

A 76-year-old man was incidentally found on a CT scan to have lymphadenopathy and bilateral kidney enlargement suggestive of infiltrative renal disease. He was largely asymptomatic but had bilateral salivary and lacrimal gland enlargement. A grossly elevated serum IgG (>70 g/L) with concomitant suppression of other immunoglobulins, a small IgG restriction, and a parotid biopsy revealing lymphoplasmacytic infiltrate with slight kappa light chain excess all suggested a lymphoproliferative disorder (LPD). The diagnostic workup was further confounded by a normal serum IgG4 concentration. Moreover, bone marrow and renal biopsies did not reveal evidence of LPD. Discussion with the laboratory not only clarified that the markedly increased total IgG could not be accounted for by the small IgG restriction, but also identified a discrepancy in the IgG4 measurement. Repeat analysis of a follow-up sample revealed an elevated IgG4 of 5.94 (reference interval: 0.039–0.864) g/L, which prompted a repeat parotid biopsy that showed predominant IgG4+ lymphocytic infiltrates. Despite the deluding presentations, a final diagnosis of IgG4-related disease (IgG4-RD) was made based on elevated serum IgG4 concentrations and histopathological findings. This case highlights the importance of recognizing limitations of laboratory testing and the benefit of close communications among clinical subspecialties and the laboratory.

Peroxisome proliferator-activated receptor γ (PPARγ) regulates fatty acid storage and glucose metabolism. Recently, PPARγ has been reported to be involved in cancer. The present study reported a PPARγ consensus binding site (AGGTCA) in the ptprf promoter and identified a strong association between PPARγ and PTPRF expression, as well as their tumor suppressor roles in a v-Ha-Ras-induced model of breast cancer.The prognostic potential of PPARγ was assessed with a KM analysis of raw data from 3,951 breast cancer patients. The expression of PPARγ and PTPRF in the rat breast cancer cell lines was detected by Western blot and qPCR. The impact of PPARγ on cancer cell migration, invasion, and growth was confirmed using cell migration assay, transwell cell invasion assay, tri-dimensional soft agar culture, respectively. The binding of PPARγ with the ptprf promoter was then examined using electrophoretic mobility shift assay. The inhibitory effect of PPARγ on tumor growth was then examined in mouse tumor model in vivo.It was identified that PPARγ expression is lost in the aggressive v-Ha-Ras-induced breast cancer cell line FE1.2 but highly expressed in less malignant FE1.3 cells. Exogenous expression of PPARγ in FE1.2 cells (FE1.2-PPARγhi) resulted in a marked inhibition of proliferation compared with that in FE1.2-Vector control group. FE1.2-PPARγhi cells also exhibited reduced migration, invasion, and colony formation abilities compared with those of the controls. The PPARγ agonist rosiglitazone also suppressed the malignant properties of FE1.2 cells. Protein tyrosine phosphatase receptor F (PTPRF), a downstream target of PPARγ, was markedly induced in FE1.2-PPARγhi cells. A PPARγ consensus binding site (AGGTCA) was identified in the ptprf promoter, and an electrophoretic mobility shift assay confirmed that PPARγ bind to this promoter. Similar to the effect of vector-mediated overexpression of PPARγ, ectopic overexpression of PTPRF in FE1.2 cells led to reduced proliferation. Furthermore, a PPARγ antagonist (GW9662) and PTP inhibitor (NSC87877) abrogated the suppressive function of PPARγ and PTPRF in FE1.2 cells, respectively. PPARγ overexpression or activation suppressed the progression and distant organ metastasis of breast cancer cells in a NOD/SCID mouse model.These results suggest that PPARγ inhibits tumor cell proliferation, at least in part, through direct regulation of the ptprf gene and that PPARγ is a potential target for breast cancer treatment.

BACKGROUND AND PURPOSE: Vessel wall imaging can identify intracranial atherosclerotic plaque and give clues about its components. We aimed to investigate whether the plaque hyperintensity in the middle cerebral artery on T2-weighted vessel wall imaging is associated with ischemic stroke. MATERIALS AND METHODS: We retrospectively reviewed our institutional vessel wall MR imaging data base. Patients with an acute ischemic stroke within 7-day onset in the MCA territory were enrolled. Patients with stroke and stenotic MCA plaque (stenosis degree, ≥50%) were included for analysis. Ipsilateral MCA plaque was defined as symptomatic, and contralateral plaque, as asymptomatic. Plaque was manually delineated on T2-weighted vessel wall imaging. The plaque signal was normalized to the ipsilateral muscle signal. The thresholds and volume of normalized plaque signal were investigated using logistic regression and receiver operating characteristic analysis to determine the association between normalized plaque signal and stroke. RESULTS: One hundred eight stenotic MCAs were analyzed (from 88 patients, 66 men; mean age, 58 ± 15 years), including 72 symptomatic and 36 asymptomatic MCA plaques. Symptomatic MCA plaque showed larger plaque hyperintensity volume compared with asymptomatic MCA plaque. The logistic regression model incorporating stenosis degree, remodeling ratio, and normalized plaque signal 1.3–1.4 (OR, 6.25; 95% CI, 1.90–20.57) had a higher area under curve in differentiating symptomatic/asymptomatic MCA plaque, compared with a model with only stenosis degree and remodeling ratio (area under curve, 0.884 versus 0.806; P =.008). CONCLUSIONS: The MCA plaque hyperintensity on T2-weighted vessel wall imaging is independently associated with ischemic stroke and adds value to symptomatic MCA plaque classification. Measuring the normalized signal intensity may serve as a practical and integrative approach to the analysis of intracranial atherosclerotic plaque.

Triple-negative breast cancer (TNBC) is an aggressive type of breast cancer. Long noncoding RNAs (lncRNAs) have been reported to be involved in the development of TNBC. However, the role and mechanism of LINC01096 in TNBC are largely unclear. This work aims to investigate the effect of LINC01096 on cell viability, apoptosis, migration, and invasion of TNBC cells, as well as explore the interaction between LINC01096 and microRNA (miR)-3130-3p.Sixty TNBC patients were recruited. T47-D and BT-549 cells were cultured for experiments in vitro. The expression levels of LINC01096 and miR-3130-3p were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell viability, apoptosis, migration, and invasion were determined by MTT, flow cytometry, and trans-well assays. The target association between LINC01096 and miR-3130-3p was confirmed by the luciferase reporter assay.The expression of LINC01096 was enhanced in TNBC tissues and cells. High expression of LINC01096 predicted poor outcomes of patients with TNBC. Silence of LINC01096 led to the suppression of cell viability, migration, and invasion, as well as the promotion of apoptosis in TNBC cells. MiR-3130-3p was targeted by LINC01096 and lowly expressed in TNBC. Overexpression of miR-3130-3p repressed cell viability, migration, and invasion, while it induced apoptosis. However, the knockdown of miR-3130-3p induced the opposite effect. This was weakened by inhibiting LINC01096.Knockdown of LINC01096 inhibited cell viability, migration, and invasion; however, it promoted apoptosis in TNBC by up-regulating miR-3130-3p, indicating a novel target for the treatment of TNBC.

Metastatic melanoma, which is refractory to therapies, is one of the most aggressive types in skin cancers. microRNAs (miRNAs) have recently emerged as novel molecules which have therapeutic effects on melanoma. This study focused on the roles and mechanisms of miR-200a in melanoma progression.Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine the level of miR-200a expression in 46 pairs of melanoma tissues and para-cancerous specimens, and the relationship between miR-200a level and clinical features of melanoma patient prognosis was analyzed. MiR-200a expression in melanoma cells was further verified by qRT-PCR. In addition, we identified the biological target of miR-200a using TargetScan. To delineate the molecular mechanism underlying the tumor-suppressive roles of miR-200a in melanoma, Western blots were performed to determine the functions of miR-200a in PI3K/Akt pathway and EMT.QRT-PCR analysis demonstrated a prominent decrease of miR-200a in melanoma tissues, which was associated with the poor prognosis and malignant clinicopathologic features of melanoma patients. Moreover, functional assays indicated that miR-200a overexpression markedly repressed melanoma cell proliferation, invasion, and migration capacities. A luciferase reporter analysis showed that Golgi membrane protein 1 (GOLM1) was a functional target of miR-200a in melanoma cells. Western blot analysis revealed that miR-200a inhibited melanoma progression by regulating PI3K/Akt signaling pathway and epithelial-mesenchymal transition (EMT). It was also found that miR-200a upregulation markedly suppressed melanoma tumorigenesis in vivo. All these data showed that miR-200a served as a promising therapeutic target in melanoma patients.We provided evidence that miR-200a was down-regulated in melanoma and was implicated in melanoma progression via inhibiting GOLM1 expressions and regulating PI3K/Akt signaling pathway and EMT. Decreased levels of miR-200a were related to poor prognosis of melanoma patients. Findings of the present study provided a novel insight into understanding melanoma pathogenesis, suggesting that miR-200a may function as a promising and potential therapeutic biomarker for melanoma treatments.

To investigate the expression of lncRNA LACAT1 in oral squamous cell carcinoma (OSCC) tissues, and to further investigate its potential mechanism in OSCC as well as its relationship with clinicopathology and prognosis.Quantitative Real-time polymerase chain reaction (qRT-PCR) was used to analyze LACAT1 level in 78 pairs of OSCC tumor tissues and adjacent tissues, and the interplay between LACAT1 level and OSCC clinical indices along with patient's prognosis was analyzed. Further, the expression level of LACAT1 in OSCC cell line was verified by qRT-PCR. In addition, after LACAT1 knockdown model was constructed using lentivirus and transfected into OSCC cell lines, cell cloning assay and flow cytometry were used to analyze the impact of LACAT1 on biological functions of OSCC cells, and finally its association with microRNA-4301 was explored.In this experiment, qRT-PCR results revealed that LACAT1 level in OSCC tumor tissue specimens was significantly higher than that in paracancerous tissues. In addition, the pathology stage in patients with higher level of LACAT1 was also higher while the overall survival rate was lower. Compared with sh-NC group, the cell proliferation ability of sh-LACAT1 group was significantly decreased while cell apoptosis was oppositely increased. QRT-PCR results showed that microRNA-4301 level was significantly elevated in cells of sh-LACAT1 group, suggesting that the expression of above two molecules was negatively correlated. Meanwhile, cell reverse experiment also demonstrated that LACAT1 and microRNA-4301 can be mutually regulated, and thereby promote the malignant progression of OSCC.The LACAT1 level was found significantly increased in OSCC tissues and cells, which resulted in an advanced OSCC pathological stage and a poor prognosis of patients. In addition, it was found that LACAT1 may promote the malignant progression of OSCC by modulating microRNA-4301 activity.

Objectives The implementation of competency-based evaluations increases the emphasis on in-training assessment. The Consultation Letter Rating Scale (CLRS), published by the Royal College of Physicians and Surgeons of Canada, is a tool that assesses written-communication competencies. This multisite project evaluated the tool's validity, reliability, feasibility, and acceptability for use in postgraduate geriatric medicine training. Methods Geriatric medicine trainees provided consultation letters from the 2017-2018 academic year. Geriatricians reviewed a standardized module and completed the tool for all the deidentified letters. The reviewers recorded the time used to complete the tool for each letter and completed a survey on content validity. Trainees completed a survey on the tool's usefulness. Responses were reviewed independently by two authors for thematic content. The unweighted and the weighted κ were used to measure interrater reliability. Results A total of 10 of 11 (91%) eligible trainees each provided five letters that were reviewed independently by six geriatricians, leading to a total of 300 assessments. A very small portion (4% [N = 12]) of assessments was incomplete. An average of 4.82 minutes (standard deviation = 3.17) was used to complete the tool. There was high interrater agreement for overall scores, with a multiple-rater weighted κ of 83% (95% confidence interval = 76%-89%). The interrater agreement was lower for the individual components. Both raters and trainees found the comments more useful than the numerical ratings. Conclusions Our results support the use of the CLRS for facilitating feedback on the quality of consult letters to improve written-communication competencies among geriatric medicine trainees. J Am Geriatr Soc 67:2157-2160, 2019.

卡萨巴赫-梅里特综合征（KMS）是一种由巨大血管瘤导致的以血小板减少和消耗性凝血功能障碍为表现的疾病，多见于婴幼儿。本例报道为1例成人KMS患者，经长春地辛等治疗后症状得以改善，血小板和凝血功能未进一步恶化，可维持在一定水平。.