Nonspecific orbital inflammation(NSOI)is an orbital inflammation that is not associated with an infection. Even though it's often considered the most common diagnosis in orbital biopsies, it's still an exclusionary diagnosis that means systemic illnesses and other possible causes have to be ruled out. Though it is always an excluded clinical diagnosis, acute orbital symptoms such discomfort, exophthalmos, periorbital edema, chemosis, diplopia, and vision impairment are commonly associated with NSOI. Clinical diagnosis and management of NSOI provide a substantial difficulty. There are presently no recognized diagnostic criteria or standard treatment strategy for NSOI, and the clinical symptoms and histological features show significant variation. This guide was formulated under the auspices of the Ocular Oncology Committee of the Opthalmology Branch of the Chinese Medical Doctor Association, Opthalmology Committee of International Association of Intelligent Medicine, Opthalmology Committee of International Association of Translational Medicine making a detailed summary of the definition, classification, diagnosis and treatment of the NSOI, with a view to aiding clinicians to improve diagnostic efficiency and formulate a better treatment plan for patients.

Objective:To study the expression of stomatin-like protein 2(STOML2)in oral squamous cell carcinoma(OSCC)tissue and the effects of STOML2 on the tumorigenicity of OSCC cells(OSCCCs)in vitro and in vivo,and the related mechanism.Methods:The protein expression of STOML2 in OSCC and adjacent tissues of 56 patients was detected.OSCCCs SCC-15 were divided into 2 groups.Stom12-siRNA plasmid was transfected into the cells of experimental group and Mock-siRNA plasmid was transfected into the cells of control group.The mRNA and protein expression of STOML2,CDK4 and P16 in the cells was detected by qPCR and Western blot respectively.The cell cycle of the cells was detected by flow cytometry,and the proliferation of the cells was detected by CCK8 asay.The tumorigenicity of the cells was detected by subcutaneous tumor model in nude mice.Results:The positive rate of STOML2 in OSCC and adjacent tissues was 92.86％(52/56)and 8.93％(5/56)respectively(P＜0.001).After siRNA transfection,STOML2 mRNA expression in SCC-15 cells of experimental group and control group was(0.43±0.09)and(1.23±0.19),STOML2 protein ex-pression was(0.52±0.11)and(0.94±0.17)respectively.CDK4 expression was(0.33±0.13)and(1.18±0.17),P16 expression was(0.93±0.12)and(0.29±0.03),respectively.In CCK8 assay the absorbance of SCC-15 cells in experimental group and control group was(1.11±0.24)and(2.19±0.28),in flow cytometry the percentage of cells in G2/M phase was 35.72％±5.33％and 18.65％±3.71％(P＜0.05),respectively.In vivo test showed that the volume(μm3)of subcutaneous transplanted tumor was 1 192.07 ±250.9 and 2 280.5±600.1,the weight(g)of mice was 0.65±0.30 and 1.62±0.40,respectively.Conclusion:STOML2 expression increases in OSCC,STOML2 affects the tumorigenic ability of OSCCCs in vitro and in vivo by regulating P16 related pathways.

Orbital disorders include conditions originating from the orbital bones, surrounding tissues, and post-orbital septum. They also include systemic ailments affecting the orbit. Different clinical symptoms make up the complex range of orbital disorders. Because these disorders mostly impact the orbital area instead of the intraocular compartment, there is little diagnostic usefulness for typical ophthalmic visual tests. As such, the primary instruments for diagnosing and evaluating orbital illnesses have become ophthalmic imaging modalities, including ocular ultrasonography(B-scan), computed tomography(CT), and magnetic resonance imaging(MRI). One way to improve the precision and promptness of diagnosing orbital diseases is to standardize the functioning of widely used imaging equipment and define the radiological features of orbital abnormalities. Such programs are crucial for the care of patients with orbital disorders since they considerably reduce the number of misdiagnoses and missed diagnoses in these individuals. The underlying concepts, operational techniques, and normal and pathological imaging findings associated with common diagnostic tools for orbital illnesses are all thoroughly reviewed in this guideline. The objective is to improve primary healthcare settings' diagnostic competence in the field of orbital pathology and to standardize procedures for diagnosing orbital disorders.

Objective:To investigate effect of vitexin on macrophage polarization and its impact on tumor growth in a mouse model of prostate cancer.Methods:C57BL/6J male mice were used to establish RM-1 prostate cancer xenograft model.Mice were ran-domly divided into model group,vitexin-low,medium and high doses groups(40,80,160 mg/kg),and cisplatin group as positive control.After continuous administration for 16 days,mice were euthanized and tumor mass was measured.HE staining was performed to observe tumor morphology.Immunohistochemistry was used to detect Ki67 positive rate.Flow cytometry was conducted to measure expressions of CD86+CD11b and CD206+CD11b in tumor-associated macrophages.CCK8 assay was performed to assess cytotoxic effect of vitexin on RAW264.7 macrophages to determine suitable concentrations.RT-qPCR was used to measure mRNA expressions of M2 macrophage markers,including arginase-1(ARG-1),Fizz1 and Ym1.Results:Vitexin inhibited tumor volume and weight,induced tumor tissue necrosis,suppressed Ki67 protein expression,increased expression of CD86+CD11b+M1 macrophages,and inhibited CD206+CD11b+M2 macrophage expression in mouse tumor tissues in vivo.Vitexin at concentrations of 10～20 μmol/L showed no cyto-toxicity on RAW264.7 macrophages in vitro,and promoted expression of iNOS in IL-4-induced M2 macrophages while inhibiting CD206 expression,as well as suppressed mRNA expressions of ARG-1,Fizz1 and Ym1.Conclusion:Vitexin effectively inhibits tumor growth in a mouse model of prostate cancer,possibly by regulating M2 macrophages towards an M1 phenotype and exerting immunomodulatory effects.

Pleomorphic adenoma of the lacrimal gland (LGPA) is the most common epithelial lacrimal gland tumor, mainly occurring in the orbital lacrimal gland.The specific mechanism of its occurrence is unknown.The average onset age of LGPA is 39.5 years, and its clinical manifestations are usually lachrymal mass and exophthalmos, which are painless.If patients feel pain, malignant lesions should be considered.Imaging studies are of great value in the diagnosis of LGPA and can also be an important reference for the formulation of the surgical plan.To avoid capsule damage and tumor spillage, incisional biopsy isn't performed before surgery in LGPA.The treatment of LGPA is intact capsule excision.The risk of recurrence and malignant transformation is closely related to whether the tumor can be completely removed.This article reviews the clinical manifestation, histopathological changes, medical imaging changes, molecular mechanisms of tumor occurrence and development, malignant transformation mechanism, treatment and prognosis of LGPA in recent years from domestic and foreign research results, expecting to provide some references for the diagnosis and treatment of LGPA.

The role of glial scar after intracerebral hemorrhage(ICH)remains unclear.This study aimed to inves-tigate whether microglia-astrocyte interaction affects glial scar formation and explore the specific function of glial scar.We used a pharmacologic approach to induce microglial depletion during different ICH stages and examine how ablating microglia affects astrocytic scar formation.Spatial transcriptomics(ST)analysis was performed to explore the potential ligand-receptor pair in the modulation of microglia-astrocyte interaction and to verify the functional changes of astrocytic scars at different periods.During the early stage,sustained microglial depletion induced disorganized astrocytic scar,enhanced neutrophil infiltration,and impaired tissue repair.ST analysis indicated that microglia-derived insulin like growth factor 1(IGF1)modulated astrocytic scar formation via mechanistic target of rapamycin(mTOR)signaling activation.Moreover,repopulating microglia(RM)more strongly activated mTOR signaling,facilitating a more protective scar formation.The combination of IGF1 and osteopontin(OPN)was necessary and sufficient for RM function,rather than IGF1 or OPN alone.At the chronic stage of ICH,the overall net effect of astrocytic scar changed from protective to destructive and delayed microglial depletion could partly reverse this.The vital insight gleaned from our data is that sustained microglial depletion may not be a reasonable treatment strategy for early-stage ICH.Inversely,early-stage IGF1/OPN treatment combined with late-stage PLX3397 treatment is a promising therapeutic strategy.This prompts us to consider the complex temporal dynamics and overall net effect of microglia and astrocytes,and develop elaborate treatment strategies at precise time points after ICH.

Objective:To explore the safety and effectiveness of medium-frequency electrotherapy for increasing the volume of the latissimus dorsi muscle.Methods:Fifteen adult New Zealand white rabbits were randomly divided into three groups, namely group A, group B, and group C, with 5 rabbits in each group. This was a self-control study, with the right latissimus dorsi muscle as the experimental group and the left latissimus dorsi muscle as the control group. The three groups corresponded to three different current intensity levels: 7.062 mA for group A (6th gear), 10.593 mA for group B (9th gear), and 14.124 mA for group C (12th gear). After the 12th, 24th, and 36th sessions of the experiment, ultrasonography was used to collect the thickness of the latissimus dorsi muscle. After the 36th electrostimulation, the latissimus dorsi muscle samples were collected to measure their in vivo muscle thickness and wet weight and were then sent for HE and MASSON staining.Results:After the 12th, 24th, and 36th electrostimulation sessions, ultrasonographic sampling in groups A and B showed an increase in the thickness of the right latissimus dorsi muscle compared to the left; for example, the thickness on the right of group B increased by 37.8%. The wet weight data collected after the 36th electrostimulation in groups A and B showed an increase in the right latissimus dorsi muscle compared to the left; for example, the wet weight on the right of group B increased by 5.04%.Conclusions:Different electrostimulation modes of medium-frequency therapy technology can induce muscle fiber thickening or atrophy. In this experiment, the 9th gear (10.593 mA) of medium-frequency therapy technology may be a suitable choice for inducing muscle fiber thickening, and the 12th gear (14.124 mA) may be a suitable choice for inducing skeletal muscle thinning.

Focal cortical dysplasia (FCD) is one of the most common causes of drug-resistant epilepsy. Dysmorphic neurons are the major histopathological feature of type II FCD, but their role in seizure genesis in FCD is unclear. Here we performed whole-cell patch-clamp recording and morphological reconstruction of cortical principal neurons in postsurgical brain tissue from drug-resistant epilepsy patients. Quantitative analyses revealed distinct morphological and electrophysiological characteristics of the upper layer dysmorphic neurons in type II FCD, including an enlarged soma, aberrant dendritic arbors, increased current injection for rheobase action potential firing, and reduced action potential firing frequency. Intriguingly, the upper layer dysmorphic neurons received decreased glutamatergic and increased GABAergic synaptic inputs that were coupled with upregulation of the Na⁺-K⁺-Cl^- cotransporter. In addition, we found a depolarizing shift of the GABA reversal potential in the CamKII-cre::PTEN^flox/flox mouse model of drug-resistant epilepsy, suggesting that enhanced GABAergic inputs might depolarize dysmorphic neurons. Thus, imbalance of synaptic excitation and inhibition of dysmorphic neurons may contribute to seizure genesis in type II FCD.
Animals ; Drug Resistant Epilepsy/surgery* ; Epilepsy/pathology* ; Malformations of Cortical Development/pathology* ; Malformations of Cortical Development, Group I ; Mice ; Neurons/pathology* ; Seizures/pathology*

Objective:The vasculature and canal were located using radiography after the fresh osseous specimens were decalcified, after which the anatomic investigation of intraosseous vasculature was conducted based on the orientation of the canals.Methods:To investigate the basic dissected methods for intraosseous vasculature and the related clinical significance. Methods The materials were obtained from seven fresh knee joint specimens from patients with amputation due to car accidents, nine fresh knee joint specimens from patients with amputation due to oncological radical surgery, and 44 knee joint specimens from 24 cadavers. Among them, 22 were males (55%) and 18 were females (45%), 28 were left knees (46.7%) and 32 were right knees (53.3%). 10 were aged from 16-90 years old (from 8 donors) and 50 were aged from 15-85 years old (from 32 donors). The tributaries of middle genicular vein which penetrate into the proximal tibial epiphysis and metaphysis via our previously discovered and denominated "foramen of tibial intercondylar eminence (FTIE)" were dissected as an example. After obtaining the fresh knee joint specimen, angiography was performed to observe the continuous extraosseous and intraosseous blood vessels. The first group of specimens with the removal of cortical bone was reserved in formalin solution at 4 °C for 7 d, sequentially immersed in Ethylene Diamine Tetraacetic Acid (EDTA), the decalcification agent, for 30 d with replacement for each two days. Based on the CT scanning and three-dimensional reconstruction, the orientation of bony canal which enclosed the vasculature was exposed to guide the anatomic incision. The exquisite dissection was achieved with the help of ophthalmological microsurgical instruments. The anatomical dissection were intuitively observed, compared with the angiographic images, and verified by histological examinations. The second group of samples was decalcified with strong acid as another strategy, and the comparison between different groups was conducted. To estimate the advantages and disadvantages of the two decalcification and dissection methods, and the distribution and universality of specific intraosseous vasculatures and canals, the methods can be utilized to dissect the diameter of the intraosseous vessels. Based on the anatomical study of intraosseous vasculature, the mechanisms including etiology, recurrence and spread of bone tumors and epiphyseal injuries were analyzed to improve the therapeutic regimen.Results:The intraosseous tributaries of middle genicular vein which penetrate into the tibial intercondylar eminence from the articular cavity were dissected, these vessels extended to the tibial metaphysis from epiphysis through the epiphyseal line or senescent physes. The diameter of the vessel entering the FTIE was 1.2 mm, and the intraosseous vessels divided into several tinier tributaries with the diameter of 0.3 mm to cross the epiphyseal line or closed physeal plate and differentiated into capillaries in the distal regions, therefore was difficult to dissect directly. The histological examinations confirmed the authenticity of intraosseous vessels. Compared with the samples decalcified with strong acid, the blood vessels were obviously dissolved, and only a few residual epithelial cells were observed under the light microscope. Based on the anatomical study of intraosseous vessels, the treatment protocols for some related bone tumors and epiphyseal injuries were modified and satisfactory results were achieved.Conclusion:The methods can realize the ideal direct dissection for the intraosseous blood vessels with the outer diameter greater than or equal to 0.3 mm.

To address the increasing need for detecting and validating protein biomarkers in clinical specimens, mass spectrometry (MS)-based targeted proteomic techniques, including the selected reaction monitoring (SRM), parallel reaction monitoring (PRM), and massively parallel data-independent acquisition (DIA), have been developed. For optimal performance, they require the fragment ion spectra of targeted peptides as prior knowledge. In this report, we describe a MS pipe-line and spectral resource to support targeted proteomics studies for human tissue samples. To build the spectral resource, we integrated common open-source MS computational tools to assemble a freely accessible computational workflow based on Docker. We then applied the workflow to gen-erate DPHL, a comprehensive DIA pan-human library, from 1096 data-dependent acquisition (DDA) MS raw files for 16 types of cancer samples. This extensive spectral resource was then applied to a proteomic study of 17 prostate cancer (PCa) patients. Thereafter, PRM validation was applied to a larger study of 57 PCa patients and the differential expression of three proteins in prostate tumor was validated. As a second application, the DPHL spectral resource was applied to a study consisting of plasma samples from 19 diffuse large B cell lymphoma (DLBCL) patients and 18 healthy control subjects. Differentially expressed proteins between DLBCL patients and healthy control subjects were detected by DIA-MS and confirmed by PRM. These data demonstrate that the DPHL supports DIA and PRM MS pipelines for robust protein biomarker discovery. DPHL is freely accessible at https://www.iprox.org/page/project.html?id=IPX0001400000.