Objective:To investigate the anatomic origin of juvenile nasopharyngeal angiofibroma（JNA） through radiologic analysis of tumor invasion patterns, providing insights into tumor etiology and surgical recurrence prevention. Methods:This retrospective cohort study included primary JNA cases at the Department of Otorhinolaryngology, Eye and ENT Hospital of Fudan University from March 2015 to September 2024. All patients underwent preoperative high-resolution CT（HRCT） scans, and some underwent enhanced magnetic resonance imaging. The study retrospectively analyzed the patients' imaging data to examine tumor invasion into the pterygopalatine fossa and the vidian canal. These sites were categorized into non-invaded, partially invaded, and completely invaded for the pterygopalatine fossa and the vidian canal. The study analyzed the proportions of invasion at these sites to further speculate on the origin of JNA. Results:A total of 105 JNA patients were included in the study. Among them, 100% of the patients had complete tumor invasion in the pterygopalatine fossa. For the vidian canal, the proportions of complete invasion, partial invasion, and non-invasion were 54.3%, 27.6%, and 18.1%, respectively. As the staging of JNA tumors increased, the proportion of vidian canal invasion also increased. Conclusion:Our evidence suggests that the pterygopalatine fossa, rather than the vidian canal, might be the likely origin of JNA, which is enlightening for the study of the etiological mechanisms of JNA.
Humans ; Nasopharyngeal Neoplasms/pathology* ; Retrospective Studies ; Angiofibroma/pathology* ; Neoplasm Invasiveness ; Pterygopalatine Fossa/pathology* ; Female ; Magnetic Resonance Imaging ; Male ; Tomography, X-Ray Computed ; Adolescent

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective:To explore the therapeutic efficacy and prognostic factors of combined rituximab and intensive chemotherapy for sporadic adult Burkitt lymphoma (BL) .Methods:This retrospective study examined the clinical and survival data of 30 patients newly diagnosed with BL between July 2011 and February 2023 at the Blood Diseases Hospital. Kaplan-Meier method was used for survival analysis, and the log-rank test was used for univariate analysis of prognostic factors.Results:The median age of the 30 patients was 43 years (24 - 66 years), and the male to female ratio was 3: 2. Extranodal invasion was present in 80% of the patients, with involvement of the bone marrow in 53.3% and central nervous system in 10.0%. The Ann Arbor stage was Ⅲ and Ⅳ in 86.7%. According to the number of Burkitt Lymphoma International Prognostic Index (BL-IPI) risk factors, patients were classified as low risk (0) in 20.0%, intermediate risk (1) in 43.3%, and high risk (≥2) in 36.7%. All patients were treated with an induction regimen of rituximab combined with intensive chemotherapy, with objective and complete response rates of 80.0% and 76.7%, respectively. The median follow-up was 49 months (6-153 months), and the 5-year progression-free survival (PFS) and overall survival (OS) rates were both (76.7±7.7) %. All patients with limited stage ( n=4) achieved continuous complete remission (CCR). Patients who had high risk, advanced stage sensitive to induction therapy ( n=10) sequentially received first-line autologous hematopoietic stem cell transplantation (auto-HSCT) as consolidation therapy; 9 patients achieved CCR, whereas 1 patient with central nervous system invasion developed early disease progression and died. The BL-IPI low, intermediate, and high risk groups had respective 5-year PFS rates of (83.3±15.2) %, 100.0%, and (45.5±15.0) % ( P=0.0069) and OS rates of (83.3±15.2) %, 100.0%, and (45.5±15.0) % ( P=0.0075). The main adverse effects of induction therapy were myelosuppression and secondary infections, which were effectively managed by appropriate symptomatic treatment. Univariate analysis demonstrated that worse PFS was associated with BL-IPI score ≥2 ( HR=4.90, 95% CI 1.02-23.45, P=0.0329) ; extranodal invasion at ≥2 sites ( HR=12.62, 95% CI 2.59-61.62, P=0.0021) ; and failure to achieve first complete response (CR1) after induction therapy ( HR=31.86, 95% CI 4.19-242.20, P<0.0001) . Conclusions:Intensive immunochemotherapy regimens were effective and well-tolerated by adult patients with highly aggressive BL. Treatment efficacy was ideal in patients with limited-stage disease, whereas prognosis was unsatisfactory in patients with high-risk BL-IPI. Sequential first-line auto-HSCT consolidation therapy may further improve outcomes in patients with high-risk advanced-stage disease who are sensitive to induction therapy. BL-IPI score ≥2, extranodal invasion at ≥2 sites, and failure to achieve CR1 after induction therapy were adverse prognostic factors in adult patients with BL.

Objective This study aims to explore the correlation between the grade of testicular tissue damage and clinical features which is used to evaluate the viability of testicular tissue after the orchidopexy for testicular torsion.Methods We conducted a retrospective,multicenter analysis of pathological specimens obtained from patients who under-went unilateral orchiectomy due to testicular torsion.Tissue viability was reassessed by the Mikuz grading scale.The corre-lations among tissue viability,duration of torsion symptoms,the angle of torsion,preoperative Doppler ultrasound image and intraoperative testicular resuscitation methods were analyzed.Results Eighty-five pathological specimens were en-rolled from 4 medical centers.The age range was 18 years(IQR 14-33),with a median torsion angle of 480°(IQR 180°-1080°).The interval from the torsion onset to surgical intervention was 18 hours(IQR 9-84).In the subgroup analysis of different torsion durations,the distribution of Grade I injuries was as follows.The subgroup within 12 hours ac-counted for 37.5％.The subgroup between 12 to 24 hours accounted for 14.28％.And the subgroup between 24 to 48 hours ac-counted for 6.45％.The subgroup exceeding 48 hours only accounted for 3.13％.Four patients received orchiectomy due to pre-operative ultrasound image indicating necrosis,correlating with Mikuz grade 3 tissue damage.The decision was made based on the failure of color recovery of affected testis in 57 cases,revealing 12.28％with grade 1 and 35.89％with grade Ⅱ damage.Twenty-four cases were identified as an Arda score of 3,with 4.16％showing grade 1 and 20.83％showing grade Ⅱ Mikuz damage.The method of Arda's grading could be used to determine the vitality of testicular tissue more accurately compared to the post-resusci-tation color observation method(P=0.032).Conclusion Pathological reassessment provides a precise determination of tis-sue viability in the affected testis.In some instances,the testicular tissue damage can be found potentially reversible.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective To explore the effect of plasma-activated gas(PAG)in promoting wound healing.Methods The pro-healing effect of PAG was explored by testing the effectiveness of PAG in promoting cell proliferation and healing of infected wounds.Cell proliferation assay:five different cells(i.e.,HSF,IHSMC,WPMY-1,HaCaT,and HFF)in logarithmic growth phase were inoculated into culture plates.After the cells grew adherently to the wall,the different cells were each grouped experimentally using a suitable time gradient.After the cells were treated with PAG for different time,their activity was detected by CCK-8 method.Animal infected wound healing assay:a wound of about 1.5 cm × 1.5 cm in size was created on the back of SD rats with sterile tweezers and scissors,and then the wound was infected with P.Aeruginosa with A600nm=6.5.After the infection was completed,the wounds were treated with PAG at regular intervals,and the experiment groups were subdivided according to the different treatment durations.Wound healing photographs and changes in relative wound area were used as indicators of healing performance.Results Cell proliferation assay:PAG treatment was effective in promoting cell proliferation for a reasonable period of time,while overdose led to cell death.Therefore,the dose of cells treated with plasma activation gas was defined as=W/N(J/cell),where W is the work consumed by the activation gas device during the treatment process and N is the number of cells.The three indexes(starting dose,optimal dose and safe dose range)were used to characterize the proliferative effect of PAG.Animal infected wound healing assay:the experimental groups all showed accelerated wound healing,so the optimal treatment time was used to characterize the pro-healing effect of PAG.The sterilization mode played a primary role,with an optimal treatment time of 2 min,and the pro-healing mode played a secondary role.The treatment conditions with the best overall healing effect were 2 min for the sterilization mode and 1 min for the pro-healing mode.Conclusion PAG has the effect of promoting cell proliferation and infected wound healing,and indicators can be summarized to quantitatively describe its effect,which is conducive to further standardization of PAG research and clinical utility.