[The principle and practice of vidian neurectomy].

The latest research findings on bidirectional regulation of neuro-immunity through traditional neural circuits shed new light on the theoretical basis of the role of vidian neurectomy (VN). This article aims to provide a comprehensive understanding of VN, including the history of VN, the principle of neuroimmuno-interaction, the applied anatomy of VN as well as the methods of transnasal endoscopic surgery. Additionally, we introduce the concept of the nose-brain axis, which was proposed based on the advancement in the area of neuro-immune interactions.

MicroRNA profiling in complete and partial hydatidiform moles.

INTRODUCTION: Hydatidiform mole is one of the gestational trophoblastic disease and comprises complete (CM) and partial moles (PM), which carries a risk of developing persistence disease, invasive mole or choriocarcinoma. MicroRNAs (miRNAs) have been discovered in various tissues, including neoplastic tissues. Its role in the pathogenesis of molar pregnancy or as biomarkers are still largely uncertain. The aim of this study is to identify the differentially expressed miRNAs in CM and PM. MATERIALS AND METHODS: Using next-generation sequencing, the miRNAs profiles of CM (n=3) and PM (n=3) moles, including placenta of non-molar abortus (n=3) as control were determined. The differentially expressed miRNAs between each group were analysed. Subsequently, bioinformatics analysis using miRDB and Targetscan was utilised to predict target genes. RESULTS: We found 10 differentially expressed miRNAs in CMs and PMs, compared to NMAs, namely miR- 518a-5p, miR-423-3p, miR-503-5p, miR-302a-3p, and miR-1323. The other 5 miRNAs were novel, not listed in the known database. The 3 differentially expressed miRNAs in CMs were predicted to commonly target ZTBT46 and FAM73B mRNAs. DISCUSSION: miR-518 was consistently observed to be downregulated in CM versus PM, and CM versus NMA. Further bioinformatic analysis to provide insight into the possible role of these miRNAs in the pathogenesis of HMs, progression of disease and as potential diagnostic biomarkers as well as therapeutic targets for HMs is needed.

MJP going green.

No abstract available.

Globus pharyngeus due to a lymphangiomatous polyp arising from the tonsil.

INTRODUCTION: Lymphangiomatous polyp of the tonsil is generally accepted as a hamartomatous lesion. Its differential diagnosis includes fibroepithelial polyp, squamous papilloma, angiofibroma, haemangioma, arteriovenous malformation, hamartoma and lymphangioma. CASE REPORT: A 33-year-old man presented with 2 months history of feeling of foreign body sensation in the throat. Examination revealed a nodular red coloured polyp on the left tonsil. Histologically, the polyp was covered by squamous epithelium and is composed of numerous vascular channels containing lymphocytes and eosinophilic material, in a fibrous stroma. Immunohistochemically, the endothelial cells were positive toward CD31 and D2-40. DISCUSSION: The characteristic histological features of a lymphangiomatous polyp are benign vascular proliferation with variable fibrous, adipose and lymphoid stromal components. Nested intraepithelial epidermotropism of lymphocytes can be observed. The vascular channels are typically thin-walled and contain eosinophilic proteinaceous material and lymphocytes. There is no reported incidence of recurrent or malignant transformation.

Eosinophilic/ T cell chorionic vasculitis.

No abstract available.

Pathogenic SCN2A variants cause early-stage dysfunction in patient-derived neurons.

Pathogenic heterozygous variants in SCN2A, which encodes the neuronal sodium channel NaV1.2, cause different types of epilepsy or intellectual disability (ID)/autism without seizures. Previous studies using mouse models or heterologous systems suggest that NaV1.2 channel gain-of-function typically causes epilepsy, whereas loss-of-function leads to ID/autism. How altered channel biophysics translate into patient neurons remains unknown. Here, we investigated iPSC-derived early-stage cortical neurons from ID patients harboring diverse pathogenic SCN2A variants [p.(Leu611Valfs*35); p.(Arg937Cys); p.(Trp1716*)] and compared them with neurons from an epileptic encephalopathy (EE) patient [p.(Glu1803Gly)] and controls. ID neurons consistently expressed lower NaV1.2 protein levels. In neurons with the frameshift variant, NaV1.2 mRNA and protein levels were reduced by ~ 50%, suggesting nonsense-mediated decay and haploinsufficiency. In other ID neurons, only protein levels were reduced implying NaV1.2 instability. Electrophysiological analysis revealed decreased sodium current density and impaired action potential (AP) firing in ID neurons, consistent with reduced NaV1.2 levels. In contrast, epilepsy neurons displayed no change in NaV1.2 levels or sodium current density, but impaired sodium channel inactivation. Single-cell transcriptomics identified dysregulation of distinct molecular pathways including inhibition of oxidative phosphorylation in neurons with SCN2A haploinsufficiency and activation of calcium signaling and neurotransmission in epilepsy neurons. Together, our patient iPSC-derived neurons reveal characteristic sodium channel dysfunction consistent with biophysical changes previously observed in heterologous systems. Additionally, our model links the channel dysfunction in ID to reduced NaV1.2 levels and uncovers impaired AP firing in early-stage neurons. The altered molecular pathways may reflect a homeostatic response to NaV1.2 dysfunction and can guide further investigations.

Exploring the Associations between Alzheimer's Disease and GBM Mediated by Microglia Based on Network Analysis.

Previous studies have revealed that there existed epidemic associations between Alzheimer's disease (AD) and many types of tumors, however, the inner biological mechanism connecting these diseases was not clear currently. In this study, we explored the transcriptome associations between AD and glioblastoma multiforme (GBM) that both originate in the brain, using microglia as a bridge, from gene and network levels. Firstly, we extracted human scRNA sequencing datasets from Gene Expression Omnibus (GEO) database, and identified differentially expressed genes within microglia after cell annotation. It was observed that there were 11 common genes shared by AD and GBM dys-regulated genes. Next, we utilized DIAMOnD and Flow Centrality algorithms to identify microglia modules and mediating pathways connecting these two diseases based on global network topology. Among these candidate pathways, the mediating genes FURIN and BACE1 (from SPIKN5 to CSNK1A1) were not only related to the formation of amyloid beta plaques that accumulate in the brain of AD patients, but also involved in cancer biology. Furthermore, the biological explorations of mediating pathways connecting AD and GBM modules reveal inflammatory response, lipid metabolism disorder, and cell proliferation terms. Finally, novel signatures for early AD detection as well as risk models for glioma prognosis were identified based on mediating genes involved in these pathways. In conclusion, this study provided a novel network-based strategy for exploring microglia mediation between AD and GBM and identified candidate signatures for disease detection and prognosis.

Case report on postmortem fentanyl measurement after overdose with more than 67 fentanyl patches.

PURPOSE: Fentanyl is an analgesic that is frequently prescribed, which resulted in non-intentional as well as intentional misuse and deaths. Here, we present a postmortem case of a patient who clearly died of a fentanyl overdose due to an extensive number of fentanyl patches combined with oral intake of fentanyl and cocaine. We aimed to show how postmortem analysis can be used to interpret postmortem fentanyl concentrations in unique cases like the one we present. CASE DESCRIPTION: A 23-year-old male was found dead in his bedroom with 67 non-prescribed patches of fentanyl on his body. In the room, there also were fentanyl tablets of 100 µg and cocaine powder, which had possibly also been taken by the deceased. To confirm the cause of death, urine and subclavian blood were retrieved to perform a standard postmortem toxicology screening. The toxicological screening revealed the presence of several drugs, including cocaine, fentanyl, lidocaine and paracetamol. Further analysis of the quantitative postmortem values of fentanyl with ultra-performance liquid chromatography-tandem mass spectrometry revealed a fentanyl concentration of 57.9 µg/L. Considering several issues around postmortem drug analyses, this value seemed to be in line with concentrations found in previously reported postmortem cases. CONCLUSION: We were able to confirm the expected cause of death with an extensive toxicological screening in combination with the circumstantial evidence. We identified fentanyl as most important cause for the fatal outcome in this specific case and simultaneously contributed to the limited availability of knowledge on postmortem fentanyl concentrations.

Identifying the spatiotemporal organization of high-traffic events in a mobile communication system using event synchronization and complex networks.

In mobile communication systems, congestion is related to high-traffic events (HTEs) that occur in the coverage areas of base stations. Understanding, recognizing, and predicting these HTEs and researching their occurrence rules provides theoretical and decision-making support for preventing system congestion. Communication sectors are regarded as nodes, and if HTEs occur synchronously among sectors, then the corresponding nodes are connected. The total number of synchronous HTEs determines the edge weights. The mobile-communication spatiotemporal data are mapped to a weighted network, with the occurrence locations of HTEs as the basic elements. Network analysis provides a structure for representing the interaction of HTEs. By analyzing the topological features of the event synchronization network, the associations among the occurrence times of HTEs can be mined. We find that the event synchronization network is a small-world network, the cumulative strength distribution is exponential, and the edge weight obeys a power law. Moreover, the node clustering coefficient is negatively correlated with the node degree. A congestion coefficient based on several topological parameters is proposed, and the system congestion is visualized. The congestion coefficient contains information about the synchronous occurrence of HTEs between a sector and its neighbors and information about the synchronous occurrence of HTEs among its neighbors. For the mobile communication system considered in this study, the congestion coefficient of a large number of sectors is small and the risk of system congestion is low.

Medical record archives in the era of digitalisation.

No abstract available.

Guidelines on retention of pathology records and materials (Version 2/2022).

No abstract available.

[Clinical application analysis of a method for locating scalp projection of intracranial lesions based on neuroimaging].

Objective: To explore the feasibility of a method based on neuroimaging and surface markers for locating scalp projection of intracranial lesions. Methods: The clinical data of 46 patients who were used 'double-circle method' for locating scalp projection of intracranial lesions at Department of Neurosurgery,the First Affiliated Hospital of Xiamen University from January to June 2021 were retrospective analyzed. All patients with 2 electrodes(artificial fiducials) randomly attached to scalp had been examed thin-layer brain CT. The distances from the center of each fiducial to the root of the nose and tragus were measured through the images. A compass was used to draw two arcs with the root of nose and the tragus as the center and the pre-measured distance as the radius on patient's scalp. Then two arcs' intersection on the scalp was the fiducial. The method was named 'double-circle method'. Two neurosurgeons were arranged to perform fiducial identification with double-circle method, and record the error between the result and the actual fiducial point.Independent sample t test was used for data comparison, and Kappa test was used to analysis the inter-group consistency. Results: Ninety-two fiducial points of 46 patients were collected. Time consuming of doctor A was (8.1±2.3) minutes(range:5 to 15 minutes)and doctor B was (8.9±3.5) minutes(range:4 to 17 minutes).The positioning error from the doctor A was (4.4±2.4)mm(range:0 to 12 mm) and doctor B was(4.2±2.6) mm(range:0 to 14 mm)(t=-0.575,P=0.567),the difference was not statistically significant. The Kappa value of the consistency test of error between two doctors was 0.517(P=0.001).The consistency was moderate.Eight patients used 'double-circle method' and neuronavigation for locating scalp projection of intracranial lesions at the same time. The diameter of the lesions was (3.8±0.9)cm (range: 2.6 to 5.1 cm), and the positioning error of the 'double-circle method' and navigation was (4.0±1.9) mm(range: 1 to 6 mm), and all patients were confirmed to be accurately located during surgery. Conclusion: 'Double-circle method' is a simple,convenient and accurate way in locating intracranial lesions and has certain clinical significance.

[Diagnosis and treatment of periprosthetic fracture after medial unicompartmental knee arthroplasty].

Unicompartmental knee arthroplasty (UKA) is an effective treatment for end-stage anteromedial osteoarthritis of the knee. Medial tibial plateau fracture or femoral condyle fracture may occur after UKA, and its treatment is very challenging. The causes leading to this complication include: surgical technique errors, such as the weakening of posterior cortical strength of the tibial platform during operation, the reduction of bone mass due to too much tibial osteotomy, and the stress concentration in the bone bed due to bad alignment of the prosthesis, etc. Prosthesis design factors, such as press-fit fixation design of cementless UKA prosthesis, and multiple nail holes fixation for tibial osteotomy guide, etc. And the morphology of tibial plateau, such as tibial platform in Asian people with narrow and small shap and medial overhanging condyles. Correct selection of patients, strict surgical principles and standardized surgical techniques are the keys to prevent periprosthetic fractures during and after medial UKA. After the diagnosis is confirmed, the treatment choice mainly depends on the fracture pattern and the stability of the prosthesis.

[Role of personalized 3D printing in brain protection after decompressive craniectomy].

Objective: To explore the application value of personalized three-dimensional (3D) printed protective cap in brain protection after decompressive craniectomy (DC). Methods: Fourty-five patients who underwent DC from January 2021 to October 2021 were selected, including 26 males and 19 females, aged 5-73 (50±13) years old. The brain CT data were imported into 3D Slicer software to rebuild the protective cap through 3D printing. The cap was worn on the head of the patient, thereby preventing secondary braindamage. The follow-up results were compared with 53 patients without protective capduring the same period. Results: There were no statistically significant differences in age, skull defect location and follow-up time between the two groups (all P>0.05).Among 45 patients, 47 brain protective caps (2 cases with bilateral skull defects) were successfully designed. The time for image post-processingand 3D printing was (21.2±6.0) min and (62.4±8.3) min, respectively. There were 6 cases of low compliance, 9 cases of moderate compliance, 32 cases of high compliance, respectively. Six cases with low conformity were redesigned and printed, 2 of 9 cases with moderate conformity were redesigned and printed, and the remaining 7 cases reached high compliance after grinding and packaging. In the current study, 45 patients with brain protective caps were followed up for 3 months, and no secondary brain injury occurred. However, among 53 patients without brain protective caps during the same period, 4 patients had secondary accidental brain compression. The incidence of injury was 7.5 %, and the difference was statistically significant (P<0.001). Conclusion: Brain protective cap designed based on cranial CT and 3D printing can be used in patients with skull defects to protect the brain tissue from secondary crush damage and has certain clinical value.

Antibiotic use reduces efficacy of tyrosine kinase inhibitors in patients with advanced melanoma and non-small-cell lung cancer.

BACKGROUND: Antibiotic (ABX) use can reduce the efficacy of immune checkpoint inhibitors and chemotherapeutics. The effect for patients treated with targeted therapies, namely, small-molecule tyrosine kinase inhibitors (TKIs), is less known. PATIENTS AND METHODS: Retrospective data were analysed for TKI-treated patients with advanced melanoma and non-small-cell lung cancer (NSCLC) between January 2015 and April 2017 at The Christie NHS Foundation Trust. Data on demographics, disease burden, lactate dehydrogenase (LDH) level, presence of brain metastases, ECOG performance status (PS) and ABX use were collected. Progression-free survival (PFS) and overall survival (OS) were compared between the ABX+ group (ABX within 2 weeks of TKI initiation-6 weeks after) and the ABX- group (no ABX during the same period). RESULTS: A total of 168 patients were included; 89 (53%) with NSCLC and 79 (47%) with melanoma. 55- (33%) patients received ABX. On univariable analysis, ABX+ patients demonstrated shorter PFS (208 versus 357 days; P = 0.008) and OS (294 versus 438 days; P = 0.024). Increased age, poorer PS and higher LDH were associated with shorter PFS and OS. On multivariable analysis, ABX use was independently associated with shorter PFS [hazard ratio (HR) 1.57, 95% confidence interval (CI) 1.05-2.34, P = 0.028] and OS (HR 2.19, 95% CI 1.44-3.32, P = 0.0002). The negative impact of ABX on OS was particularly pronounced for patients with PS of ≥2 (HR 3.82, 95% CI 1.18-12.36, P = 0.025). CONCLUSION: For patients treated with TKIs, ABX use is independently associated with reduced PFS and OS and judicious use is warranted, particularly in patients with poorer PS.

The prevalence of neovascularity in rotator cuff tendinopathy: comparing conventional Doppler with superb microvascular imaging.

AIMS: To determine the prevalence of neovascularity in the supraspinatus tendon of patients presenting with clinically painful unilateral rotator cuff tendinopathy (RCT) using conventional colour Doppler ultrasound (CDU), power Doppler ultrasound (PDU), and superb microvascular imaging (SMI). The association between Doppler findings and clinical scores was also assessed. METHODS: The bilateral supraspinatus of consecutive patients presented with unilateral RCT clinically were evaluated with grey-scale ultrasound (tendon thickening, heterogeneous echotexture, and hypoechogenicity), CDU, PDU, and SMI. The prevalence of neovascularity and grey-scale changes on duplex imaging techniques were analysed. The relationship between neovascularity on CDU, PDU, SMI, and pain/disability as determined using a visual analogue scale (VAS) and the Oxford Shoulder Score (OSS) were assessed. RESULTS: Fifty-nine patients (mean age 53 years, 39 women) were recruited. Of the symptomatic supraspinatus tendons, 42.4% (25/59) demonstrated neovascularity on SMI, compared to 6.8% (4/59) on PDU and 5.1% (3/59) on CDU. Of the asymptomatic supraspinatus tendons, 5.1% (3/59) depicted neovascularity on SMI but not on conventional Doppler techniques. SMI showed a significant correlation with the VAS (r2 = 0.560, p<0.001) and OSS (r2 = 0.62, p<0.001). PDU weakly correlated with the VAS and OSS (r2 = 0.312, p=0.016; r2 = 0.260, p=0.047, respectively) while CDU did not show a significant relationship. CONCLUSION: SMI is superior in demonstrating neovascularity and shows better correlation with pain and functional deficit compared to conventional Doppler in patients with painful RCT. SMI also showed vascularity to a lesser degree in the asymptomatic tendon. Further large-scale studies are needed to prove the diagnostic value of SMI in the assessment of RCT.

Lnc-AC145676.2.1-6-3 can influence STX3-induced abnormal autophagy by sponging hsa-miR-1292-3p in intestinal aGVHD.

OBJECTIVE: Intestinal acute graft-versus-host disease (aGVHD) is a serious complication of allogeneic hematopoietic stem cell transplantation (allo-HSCT). Abnormal autophagy levels in intestinal aGVHD have been confirmed in many studies. LncRNAs exert coregulatory functions and participate in a variety of intracellular regulatory processes. In this study, we investigated how lnc-AC145676.2.1-6-3 regulates dysregulated STX3-related autophagy in aGVHD. MATERIALS AND METHODS: First, we established a mouse model of aGVHD by transplanting a mononuclear cell suspension from Balb/c donor mice treated with 60Co X-rays into CB6F1 recipient mice. STX3-related indicators were analyzed by Western blotting (WB) and immunohistochemistry which confirmed that STX3 plays an important role in dysregulating autophagy in intestinal aGVHD. TNF-αinduced Caco-2 cells, which is an in vitro model of intestinal barrier dysfunction, were established to verify the effect of STX3. The direct interaction between the partners of lnc-AC145676.2.1-6-3-mediated hsa-miR-1292-3p and STX3 axis was evaluated by the Dual-Luciferase activity assay. We performed PCR, WB, and immunofluorescence in Caco-2 cells to determine whether the abnormal autophagy levels were influenced by lnc-AC145676.2.1-6-3. RESULTS: The results showed that lnc-AC145676.2.1-6-3 could significantly suppress the number of autophagic vacuoles, the LC3-II/I ratio, and beclin1 levels by increasing STX3 levels. CONCLUSIONS: Lnc-AC145676.2.1-6-3 may play an important role in intestinal aGVHD by targeting STX3.

Increased retention of tau PET ligand [18F]-AV1451 in Alzheimer's Disease Psychosis.

Psychosis in Alzheimer's disease (AD) represents a distinct disease subtype with a more rapid progression of illness evidenced by an increased velocity of cognitive decline and a hastened mortality. Previous biomarker and post-mortem studies have implicated tau neuropathology as a possible mediator of the accelerated decline in AD psychosis. Tau positron emission tomography (PET) neuroimaging provides the opportunity to evaluate tau pathology in-vivo, so that clinical symptomatology can be correlated with disease pathology. [18F]-AV1451 (Flortaucipir) is a PET ligand with high affinity for insoluble paired-helical filaments (PHFs) of hyperphosphorylated tau. In order to determine whether the development of psychosis and worsened prognosis in AD is associated with an increased burden of tau pathology that can be identified with tau imaging, we identified subjects within the Alzheimer's disease neuroimaging initiative (ADNI) who had [18F]-AV1451 imaging at baseline and became psychotic over the course of the study (N = 17) and matched them 1:3 for gender, age, and education to subjects who had [18F]-AV1451 imaging at baseline and did not become psychotic (N = 50). We compared baseline [18F]-AV1451 retention, in addition to cognitive and functional baseline and longitudinal change, in those who became psychotic over the course of participation in ADNI with those who did not. Results suggest that increases in tau pathology in frontal, medial temporal, and occipital cortices, visualized with [18F]-AV1451 binding, are associated with psychosis and a more rapid cognitive and functional decline.