Schwann cell transplantation and descending propriospinal regeneration after spinal cord injury

After spinal cord injury (SCI), poor ability of damaged axons of the central nervous system (CNS) to regenerate causes very limited functional recovery. Schwann cells (SCs) have been widely explored as promising donors for transplantation to promote axonal regeneration in the CNS including the spinal cord. Compared with other CNS axonal pathways, injured propriospinal tracts display the strongest regenerative response to SC transplantation. Even without providing additional neurotrophic factors, propriospinal axons can grow into the SC environment which is rarely seen in supraspinal tracts. Propriospinal tract has been found to respond to several important neurotrophic factors secreted by SCs. Therefore, the SC is considered to be one of the most promising candidates for cell-based therapies for SCI. Since many reviews have already appeared on topics of SC transplantation in SCI repair, this review will focus particularly on the rationale of SC transplantation in mediating descending propriospinal axonal regeneration as well as optimizing such regeneration by using different combinatorial strategies. This article is part of a Special Issue entitled SI: Spinal cord injury

Transcriptional and Epigenetic Regulation in Injury-Mediated Neuronal Dendritic Plasticity

Injury to the nervous system induces localized damage in neural structures and neuronal death through the primary insult, as well as delayed atrophy and impaired plasticity of the delicate dendritic fields necessary for interneuronal communication. Excitotoxicity and other secondary biochemical events contribute to morphological changes in neurons following injury. Evidence suggests that various transcription factors are involved in the dendritic response to injury and potential therapies. Transcription factors play critical roles in the intracellular regulation of neuronal morphological plasticity and dendritic growth and patterning. Mounting evidence supports a crucial role for epigenetic modifications via histone deacetylases, histone acetyltransferases, and DNA methyltransferases that modify gene expression in neuronal injury and repair processes. Gene regulation through epigenetic modification is of great interest in neurotrauma research, and an early picture is beginning to emerge concerning how injury triggers intracellular events that modulate such responses. This review provides an overview of injury-mediated influences on transcriptional regulation through epigenetic modification, the intracellular processes involved in the morphological consequences of such changes, and potential approaches to the therapeutic manipulation of neuronal epigenetics for regulating gene expression to facilitate growth and signaling through dendritic arborization following injury

(E)-2-(Cyclo­hexyl­methyl­ene)succinic acid

The title compound, C11H16O4, crystallizes with three molecules in the asymmetric unit. The cyclo­hexane ring adopts a chair conformation. Inter­molecular O—H⋯O hydrogen bonds are observed and these help to establish the crystal packing

Case report: The first account of undifferentiated sarcoma with epithelioid features originating in the pleura

Undifferentiated epithelioid sarcoma (USEF) is a rare subtype of undifferentiated soft tissue sarcoma that presents unique challenges in clinical diagnosis and treatment. Here, we report a case of USEF occurring in the pleura of a 51-year-old man for the first time. Thoracoscopic examination revealed widespread nodular changes, and pathological analysis confirmed the presence of numerous epithelioid atypical cells. Immunohistochemical (IHC) analysis demonstrated an undifferentiated phenotype with distinct characteristics: epithelial membrane antigen (foci +), vimentin (+), Ki-67 (+70% +), TTF-1 (+), P53 (mutant type +90%), INI-1 (+), and CK5/6 (small foci +). Immunohistochemical examination of the tumor showed that the tumor was an undifferentiated epithelioid sarcoma. High-throughput DNA sequencing revealed pivotal mutations, including a nonsense mutation in the NF1 gene (c.641A > G(p.H214R)). and critical TP53 missense mutation (c.641A > G(p.H214R)). This TP53 mutation, with a tumor mutation burden of 16.5 Muts/Mb, signifies a high level of genomic instability, likely contributing to the rapid progression and aggressiveness of the disease. Detection of the TP53 mutation provides essential insights, indicating the disease’s rapid progression and highlighting the potential for targeted therapies. Although the patient’s disease progressed extremely rapidly and he tragically died within a week, we discussed the results of IHC and DNA sequencing in detail and discussed his possible treatment options. Insights gained from this case will be critical in shaping future diagnostic and therapeutic paradigms for USEF, particularly in the context of TP53 mutations

Impact of Different Static Air-Gap Eccentricity Forms on Rotor UMP of Turbogenerator

Theoretical analysis and numerical FEM calculations, together with segmental experiment studies, are used to study the impact of the static air-gap eccentricity forms on the rotor unbalanced magnetic pull (UMP) of turbogenerator. The universal expression of the magnetic flux density under different forms of SAGE is firstly deduced, based on which the detailed UMP formulas for the normal condition and three SAGE cases are obtained, respectively. Then the exciting characteristics of the UMP for each SAGE form to generate vibrations are analyzed. Finally, numerical FEM calculations and segmental experiments are carried out to investigate the effect of SAGE forms on the rotor UMP, taking the SDF-9 type non-salient-pole fault simulating generator as the object. It is shown that, no matter what kind of SAGE occurs, amplitude increments at each even harmonic component of the UMP and the rotor vibration, especially the 2nd harmonic component, will be brought in. Meanwhile, the UMP keeps directing to the very position where the minimum radial air-gap is. Among the different SAGE forms, the rotor offset has the most sensitive effect on the rotor UMP and vibration, while the stator ellipse deformation has the weakest impact

AAV-KLF7 Promotes Descending Propriospinal Neuron Axonal Plasticity after Spinal Cord Injury

DPSN axons mediate and maintain a variety of normal spinal functions. Unsurprisingly, DPSN tracts have been shown to mediate functional recovery following SCI. KLF7 could contribute to CST axon plasticity after spinal cord injury. In the present study, we assessed whether KLF7 could effectively promote DPSN axon regeneration and synapse formation following SCI. An AAV-KLF7 construct was used to overexpress KLF7. In vitro, KLF7 and target proteins were successfully elevated and axonal outgrowth was enhanced. In vivo, young adult C57BL/6 mice received a T10 contusion followed by an AAV-KLF7 injection at the T7–9 levels above the lesion. Five weeks later, overexpression of KLF7 was expressed in DPSN. KLF7 and KLF7 target genes (NGF, TrkA, GAP43, and P0) were detectably increased in the injured spinal cord. Myelin sparring at the lesion site, DPSN axonal regeneration and synapse formation, muscle weight, motor endplate morphology, and functional parameters were all additionally improved by KLF7 treatment. Our findings suggest that KLF7 promotes DPSN axonal plasticity and the formation of synapses with motor neurons at the caudal spinal cord, leading to improved functional recovery and further supporting the potential of AAV-KLF7 as a therapeutic agent for spinal cord injury

荆州区农村人口初发糖尿病胰岛功能的现状跟踪调查*

Objective: To study the change of islet function in patients with incipient diabetic characteristics through incipient diabetic tracking observation of the islet function in patients of Jingzhou area. Methods: Selection of 1220 cases of patients with diabetes mellitus in Jingzhou area as research object at the beginning, 12 months follow-up, the clinic after 3 months, 6 months and 12 months, all patients to detect blood sugar change, c-peptide release quantity, calculate insulin secretion index (HOMA -β) and insulin resistance index (HOMA IR), summarizes the characteristic of islet function in patients with changes. Results: ① The patients restored to basic standard blood sugar in 3 months by drug treatment, and the patient's blood glucose levels not seen obvious fluctuation after 6 months and 12 months; ② During follow-up, patients with diabetes sustained c-peptide release quantity reduction, and in three months after treatment, c-peptide release decreased obviously, and see a doctor at 6 months and 12 months after the comparison, the difference was statistically significant (P < 0.05). ③ During follow-up, insulin capacity was decreasing among patients with diabetes, within three months after the doctor had the greatest reduction, the difference was statistically significant (P < 0.05); ④ During follow-up, island hormone decreasing index, insulin resistance index continued to rise among patients with diabetes, and 6 months and 12 months, the most significant variations in 3 months (P < 0.05). Conclusion: With the extension of course, the pancreatic islet function in patients with early onset diabetes decreased gradually. It could be proved that there is a significant correlation between the two and especially seen in obvious function decline of pancreatic islets among the patients within 3 months.目的  通过对荆州区初发糖尿病患者的胰岛功能进行跟踪观察，探讨发现初发糖尿病患者胰岛功能的变化特点。方法  选取荆州区1220例初发糖尿病患者作为观察对象，跟踪随访12个月，在就诊后的3个月、6个月及12个月时，全部患者检测血糖变化、Ｃ-肽释放量，计算胰岛素分泌指数（HOMA-β）及胰岛素抵抗指数（HOMA-IR），观察总结患者的胰岛功能变化特点。结果  （1）通过药物治疗，患者血糖在3个月时基本达标，6个月及12个月时，患者的血糖水平未见明显波动；（2）随访期间，糖尿病患者Ｃ-肽释放量持续降低，且在就诊后3个月内，Ｃ-肽释放量下降明显，与就诊后6个月时及12个月时比较，差异有统计学意义（P＜0.05）。（3）随访期间，糖尿病患者胰岛素放量持续降低，就诊后3个月内下降最明显，差异有统计学意义（P＜0.05）；（4）随访期间，糖尿病患者胰岛素分泌指数持续降低，胰岛素抵抗指数持续升高，且与6个月时和12个月时比较，3个月时变化幅度最为显著（P＜0.05）。结论  随着病程的延长，初发糖尿病患者胰岛功能逐渐降低，二者具有显著相关性，且3个月内患者的胰岛功能下降最为显著