Primary anaplastic lymphoma kinase-positive large B-cell lymphoma of the left bulbar conjunctiva: A case report.

BACKGROUND: Anaplastic lymphoma kinase (ALK)-positive large B-cell lymphoma (LBCL) is an aggressive and rare variant of diffuse LBCL. Herein, we report an uncommon case of stage IE extranodal ALK-positive LBCL initially originating in the bulbar conjunctiva. CASE SUMMARY: A 63-year-old woman presented with a mass in the left bulbar conjunctiva that had persisted for six months, accompanied by swelling and pain that had persisted for 3 d. Eye examination revealed an 8 mm slightly elevated pink mass in the lower conjunctival sac of the left eye. Microscopically, the tumor was composed of large immunoblastic and plasmablastic large lymphoid cells with scattered anaplastic or multinucleated large cells. Immunophenotypically, the neoplastic cells were positive for ALK, CD10, CD138, Kappa, MUM1, BOB.1, OCT-2, CD4, CD45, EMA, CD79a, CD38, and AE1/AE3, and negative for CD20, PAX5, Lambda, BCL6, CD30 and all other T-cell antigens. The results of gene rearrangement tests showed monoclonal IGH/IGK/IGL and TCRD rearrangements. Fluorescence in situ hybridization studies did not reveal any BCL2, BCL6 or MYC rearrangements. Furthermore, Epstein-Barr virus was not detected by in situ hybridization in the lesions. Based on the histopathological and imaging examinations, the neoplasm was classified as stage IE ALK-positive LBCL. No further treatments were administered. At the 6, 15, and 21 mo postoperative follow-up visits, the patient was in good condition, without obvious discomfort. This case represents the first example of primary extranodal ALK-positive LBCL presenting as a bulbar conjunctival mass, which is extremely rare and shares morphological and immunohistochemical features with a variety of other neoplasms that can result in misdiagnosis. CONCLUSION: Awareness of the condition presented in this case report is necessary for early and accurate diagnosis and appropriate treatment.

Non-alcoholic fatty liver disease increases the risk of cardiovascular disease in young adults and children: a systematic review and meta-analysis of cohort studies.

Background and aims: It is uncertain if there is a link between non-alcoholic fatty liver disease (NAFLD) and cardiovascular diseases (CVD) in young adults and children. To evaluate the potential link between these two conditions, we conducted a systematic review and meta-analysis of cohort studies. Methods: A comprehensive search was conducted in PubMed, Web of Science and Embase in order to locate all relevant cohort studies published until August 2023. Random effects meta-analyses were conducted using the generic inverse variance method, with additional subgroup and sensitivity analyses. The Newcastle-Ottawa Scale was employed to evaluate the methodological quality. Results: Four cohort studies (eleven datasets) involving 10,668,189 participants were included in this meta-analysis. This meta-analysis demonstrated that NAFLD increases the risk of CVD in young adults and children (HR = 1.63, 95% CI: 1.46-1.82, P < 0.00001). Further subgroup analyses showed that individuals with NAFLD were at a heightened risk of coronary heart disease (CHD) (HR = 3.10, 95% CI: 2.01-4.77, P < 0.00001), myocardial infarction (MI) (HR = 1.69, 95% CI: 1.61-1.78, P < 0.00001), atrial fibrillation (AF) (HR = 2.00, 95% CI: 1.12-3.57, P = 0.02), congestive heart failure (CHF) (HR = 3.89, 95% CI: 1.20-12.61, P = 0.02), and stroke (HR = 1.47, 95% CI: 1.39-1.55, P < 0.00001). The results of subgroup analyses based on the study location, NAFLD definition, and follow-up time also showed consistency with the overall results. Sensitivity analyses showed that our results were robust. All of the included studies were judged to be of medium to high quality. Conclusion: Current evidence reveals that NAFLD is linked to an increased risk of major CVD (including CHD, MI, AF, CHF and stroke) in young adults and children. Further research is needed to strengthen this association and provide stronger evidence for primary prevention of CVD in young adults and children with NAFLD. Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/, PROSPERO registration number: CRD42023457817.

The Role of Hippocampal Structural Synaptic Plasticity in Repetitive Transcranial Magnetic Stimulation to Improve Cognitive Function in Male SAMP8 Mice.

BACKGROUND: Repetitive transcranial magnetic stimulation (rTMS) has been used to improve cognitive function, but the stimulation protocols are variable and the underlying mechanism is unclear. Therefore, we intend to examine whether 5Hz rTMS with 30% maximum output could improve cognitive functions in senescence-accelerated-prone mouse 8 (SAMP8) through changing synaptic plasticity. METHODS: SAMP8 and senescence-accelerated-prone mouse/resistant 1 (SAMR1) (7-month old male) were randomly divided into 3 groups: SMAP8 rTMS group (P8-rTMS), SMAP8 sham-rTMS group (P8-sham), and SAMR1 sham-rTMS group (R1-sham). The P8-rTMS group was treated daily with 5Hz rTMS with 30% maximum output for 14 consecutive days, whereas the other two groups were controls without rTMS stimulation. Morris water maze (MWM) experiment was performed after rTMS or sham treatment to assess the effect of rTMS on cognitive function. Reverse transcription polymerase chain reaction and Western blot assays were used to detect the mRNA and protein expression of presynaptic Synapsin (SYN) and postsynaptic density 95 (PSD95) in the hippocampus of these mice. RESULTS: The mean escape latency of the P8-rTMS group was significantly shorter than that of the P8-sham group. The number of platform crossings of the P8-rTMS group was significantly higher than that of the P8-sham group. rTMS significantly upregulated the protein and mRNA expression of SYN and PSD95 in the hippocampus of p8-rTMS mice compared to those of P8 sham mice. CONCLUSION: 5Hz rTMS with 30% maximum output enhances learning and memory in the SAMP8 mice. This improvement may be associated with the increased expression of synaptic structure proteins SYN and PSD95 in the hippocampus.

Marrow mesenchymal stem cell transplantation with sodium alginate gel for repair of spinal cord injury in mice / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the effects of sodium alginate gels on marrow mesenchymal stem cell transplantation for repair of spinal cord injury (SCI) in mice.</p><p><b>METHODS</b>In the present study, effects of different sterilization methods and concentrations of sodium alginate gels were examined. Marrow mesenchymal stem cells (mMSCs) were isolated from mice and cultured. Cells were cultured with sodium alginate gels and MTT assay was applied to determine the cell viability. Mice spinal cord injury was induced by spinal cord transection. mMSCs were transplanted into the cavity of injured spinal cord with sodium alginate gels. The effects of sodium alginate gel were assessed by BMS scales and immunofluorescence staining for NF-200.</p><p><b>RESULTS</b>Compared with liquid form, solid form sodium alginate gel prepared with high pressure vapor sterilization had a better effect on cell viability. SCI mice treated with 10 % sodium alginate gel and mMSCs achieved higher score in BMS scale as well as higher expression of NF-200 compared with the untreated SCI group.</p><p><b>CONCLUSION</b>Sodium alginate gel prepared with solid form sterilization induces mMSCs proliferation and thus can be used as the carrier of stem cell in treatment of SCI.</p>

Somatostatin mRNA expression in hippocampus of diabetic rats model / 中国医学科学院学报

<p><b>OBJECTIVE</b>To investigate the relationship between diabetes and somatostatin (SOM).</p><p><b>METHODS</b>We established a streptozocin-induced diabetic rats model and studied the changes of SOM mRNA in hippocampi of diabetic and normal rats by using in situ hybridication and computer image analysis. We studied the mechanism of chronic diabetes encephalopathy by observing the changes of somatostatin mRNA in the hippocampus of diabetic rats was studied.</p><p><b>RESULT</b>The number, light density and average area of positive cells in dentate gyrus area of hippocampus in diabetes model were reduced significantly as compared with normal rats (P < 0.01).</p><p><b>CONCLUSION</b>A decline in SOM mRNA expression may play a role in chronic diabetes encephalopathy because of SOM effect in brain.</p>