Objective To investigate the mRNA expression and methylation status of IL-13 receptor(IL-13R)α1 gene in peripheral T lymphocytes of patients with systemic lupus erythematosus(SLE).Methods Venous blood samples were obtained from 10 SLE patients(5 in active phase,5 in inactive phase)and 6 normal human controls.CD4+ and CD8+ T cells were isolated from these samples via magnetic activated cell sorting(MACS).Real-time quantitative PCR was used to test the mRNA expression of IL-13Rα1 gene,and methylation specific PCR to detect the methylation status.Results The expression level of IL-13Rα1 mRNA was 2.224±0.251,1.712±0.132.and 1.104±0.044 in CD4+ T cells of active SLE patients,inactive SLE patients and controls,respectively;the difference between the three groups was statistically significant(all P＜0.05).The expression level of IL-13Rα1 mRNA in CD8+T cells was significantly higher in active SLE patients than that in the normal controls(1.672±0.142 vs 1.238±0.106,P＜0.05),while no difference was noted between inactive and active SLE patients or normal controls.The methylation index of IL-13Rα1 gene was 0.454±0.023.0.635±0.065.0.844±0.097 in CD4+T cells of active SLE patients,inactive SLE patients and normal controls,respectively,and the difference between the three groups was significant(all P＜0.05),while no significant difference was observed in the methylation index in CD8+T cells among these groups(P＞0.05).The IL-13Rα1 mRNA expression in CD4+T and CD8+T cells was positively correlated with SLE disease activity index(SLEDAI)score(r=0.79,0.76,P=0.007,0.02 respectively).A negative correlation was found between the methylation level Of IL-13Rα1 in CD4+T cells and SLEDAI score(r=-0.89.P＜0.0 1).as well as between the IL-13Rα1 mRNA expression and its methylation level(r=-0.84,P＜0.0 1).Conclusion The development of SLE may be related to the overexpression of IL-13Rα1 gene induced by DNA hypomethylation in T cells.

Leiomyomas are benign tumors that arise from smooth muscle cells and rarely involve the male genitourinary system. We reported a case of a patient who underwent radical orchiectomy for epididymal tumor. The postoperative pathological diagnosis was epididymal leiomyoma, and there was no recurrence after 9 months of follow-up.

Inflammatory myofibroblastic tumor (IMT) is a mesenchymal neoplasm. Although this desease may occur in any site of body, the ureter is occasionally involved. Its clinical manifestations and imaging lack specificity. The diagnosis depends on pathological results. The main treatment is surgical resection. Recurrence and metastasis seem to be rare. A rare case of ureteral IMT managed with segmental ureterectomy and ureterostomy under general anesthesia was reported.

Neurons in the primary auditory area (AUDp) innervate multiple brain regions with long-range projections while receiving informative inputs for diverse functions. However, the brain-wide connections of these neurons have not been comprehensively investigated. Here, we simultaneously applied virus-based anterograde and retrograde tracing, labeled the connections of excitatory and inhibitory neurons in the mouse AUDp, and acquired whole-brain information using a dual-channel fluorescence micro-optical sectioning tomography system. Quantified results showed that the two types of neurons received inputs with similar patterns but sent heterogeneous projections to downstream regions. In the isocortex, functionally different areas consistently sent feedback-dominated projections to these neurons, with concomitant laterally-dominated projections from the sensory and limbic cortices to inhibitory neurons. In subcortical regions, the dorsal and medial parts of the non-lemniscal auditory thalamus (AT) were reciprocally connected to the AUDp, while the ventral part contained the most fibers of passage from the excitatory neurons and barely sent projections back, indicating the regional heterogeneity of the AUDp-AT circuit. Our results reveal details of the whole-brain network and provide new insights for further physiological and functional studies of the AUDp.

The transgender children and adolescents （TCAs） face serious social dilemmas in the process of gender identity and expression， which hinders this group from seeking reasonable and equal rights to survival and development. From the perspective of equal rights and the theoretical framework of social dilemma， by interviewing TCAs who seek help from medical social workers in a hospital’s multi-disciplinary transgender clinic， this paper revealed that under the traditional system of “binary gender”， TCAs lacked social inclusiveness and infrastructure， which led to the two major social dilemmas of “social traps” and “social barriers” encountered by this group in the process of gender expression and gender identity. Specifically， the social gender selection of TCAs often leads to collective irrational reactions and gender punishment， preventing their legal and effective medical services. To this end， the research team used critical methodology to construct a joint disciplinary diagnosis and treatment path for TCAs with the participation of medical social workers， as well as verified that the path has significant intervention effects in rationalizing the needs of TCAs and their families， alleviating their psychological pressure and social adaptation problems in the process of gender identity， fostering a diverse dialogue environment in their families， as well as enhancing their self-efficacy and social participation， to provide assistahce to the TCAs groups in social difficulties， assisting their rights and interests be included in the child-friendly indicator system， and improving the whole society’s tolerance and understanding for TCAs group.

Many people affected by fragile X syndrome (FXS) and autism spectrum disorders have sensory processing deficits, such as hypersensitivity to auditory, tactile, and visual stimuli. Like FXS in humans, loss of Fmr1 in rodents also cause sensory, behavioral, and cognitive deficits. However, the neural mechanisms underlying sensory impairment, especially vision impairment, remain unclear. It remains elusive whether the visual processing deficits originate from corrupted inputs, impaired perception in the primary sensory cortex, or altered integration in the higher cortex, and there is no effective treatment. In this study, we used a genetic knockout mouse model (Fmr1^KO), in vivo imaging, and behavioral measurements to show that the loss of Fmr1 impaired signal processing in the primary visual cortex (V1). Specifically, Fmr1^KO mice showed enhanced responses to low-intensity stimuli but normal responses to high-intensity stimuli. This abnormality was accompanied by enhancements in local network connectivity in V1 microcircuits and increased dendritic complexity of V1 neurons. These effects were ameliorated by the acute application of GABA_A receptor activators, which enhanced the activity of inhibitory neurons, or by reintroducing Fmr1 gene expression in knockout V1 neurons in both juvenile and young-adult mice. Overall, V1 plays an important role in the visual abnormalities of Fmr1^KO mice and it could be possible to rescue the sensory disturbances in developed FXS and autism patients.
Animals ; Disease Models, Animal ; Fragile X Mental Retardation Protein/metabolism* ; Fragile X Syndrome/metabolism* ; Humans ; Mice ; Mice, Knockout ; Neurons/metabolism*