Research progress on the inhibition of oxidative stress by teriparatide in spinal cord injury.

Spinal cord injury (SCI) is currently a highly disabling disease, which poses serious harm to patients and their families. Due to the fact that primary SCI is caused by direct external force, current research on SCI mainly focuses on the treatment and prevention of secondary SCI. Oxidative stress is one of the important pathogenic mechanisms of SCI, and intervention of oxidative stress may be a potential treatment option for SCI. Teriparatide is a drug that regulates bone metabolism, and recent studies have found that it has the ability to counteract oxidative stress and is closely related to SCI. This article summarizes the main pathological mechanisms of oxidative stress in SCI, as well as the relationship between them with teriparatide, and explores the therapeutic potential of teriparatide in SCI.

Teriparatide: an innovative and promising strategy for protecting the blood-spinal cord barrier following spinal cord injury.

The blood-spinal cord barrier (BSCB) is disrupted within minutes of spinal cord injury, leading to increased permeability and secondary spinal cord injury, resulting in more severe neurological damage. The preservation of blood-spinal cord barrier following spinal cord injury plays a crucial role in determining the prognosis. Teriparatide, widely used in clinical treatment for osteoporosis and promoting fracture healing, has been found in our previous study to have the effect of inhibiting the expression of MMP9 and alleviating blood-brain barrier disruption after ischemic stroke, thereby improving neurological damage symptoms. However, there are limited research on whether it has the potential to improve the prognosis of spinal cord injury. This article summarizes the main pathological mechanisms of blood-spinal cord barrier disruption after spinal cord injury and its relationship with Teriparatide, and explores the therapeutic potential of Teriparatide in improving the prognosis of spinal cord injury by reducing blood-spinal cord barrier disruption.

Teriparatide induces angiogenesis in ischemic cerebral infarction zones of rats through AC/PKA signaling and reduces ischemia-reperfusion injury.

Teriparatide is a commonly used drug indicated for the treatment of osteoporosis in postmenopausal women. Teriparatide can also upregulate Ang-1 expression through the AC/PKA signaling pathway to promote angiogenesis. At present, promoting angiogenesis is a promising but unrealized strategy for the treatment of ischemic cerebral infarction. However, there are few studies on the application of teriparatide in the treatment of cerebral infarction. We used teriparatide to treat ischemic cerebral infarction in rats and obtained three major findings. First, teriparatide can promote angiogenesis, reduce cerebral infarct size, and increase cerebral perfusion by upregulating Ang-1 expression. Second, teriparatide can promote the expression of HO1, SOD2 and inhibit the production of pro-inflammatory cytokines IL-1ß, IL-6 by upregulating Nrf2 expression. Third, we further found that teriparatide can mitigate blood-brain barrier disruption and brain edema by downregulating the expressions of MMP9, Ang-2 and AQP4. Our results indicate that teriparatide is neuroprotective through multiple mechanisms of action that include promoting angiogenesis, inhibiting oxidative stress and neuroinflammation, protecting blood-brain barrier, and reducing brain edema.

An Integrative Pan-Cancer Analysis of PBK in Human Tumors.

Background: PDZ binding kinase (PBK) is a serine/threonine kinase, which belongs to the mitogen-activated protein kinase kinase (MAPKK) family. It has been shown to be a critical gene in the regulation of mitosis and tumorigenesis, but the role of PBK in various cancers remains unclear. In this study, we systematically explored the prognostic and predictive value of PBK expression in 33 cancer types. Methods: Public databases including the cBioPortal database, GDSC database, GTEx database, CCLE database, and TCGA database were used to detect the PBK expression and its association with the prognosis, clinicopathologic stage, TMB, MSI, immune microenvironment, immune checkpoints, immune cell infiltration, enrichment pathways, and IC50 across pan-cancer. The statistical analyses and visualization were conducted using R software. Results: PBK expression is relatively high in most cancers compared to their normal counterparts, and this gene is barely expressed in normal tissues. High expression of PBK is significantly associated with poor prognosis and clinicopathologic stages I, II, and III in different cancers. Furthermore, PBK expression is strongly associated with TMB in 23 cancer types and associated with MSI in nine cancer types. Moreover, the correlation analysis of the microenvironment and immune cells indicated that PBK is negatively correlated with the immune infiltration levels but positively correlated with the infiltration levels of M0 and M1 macrophages, T cells CD4 memory activated, and T cells follicular helper. GSEA analysis revealed that the biological function or pathways relevant to the cell cycle and mitosis were frequently enriched at the level of high expression of PBK. Conclusion: These results revealed the oncogenic role of PBK, which is significantly upregulated in various cancers and indicated poor prognosis and immune infiltration in multiple cancers. It also suggested that PBK may serve as a biomarker in multiple tumor progress and patient survival.

One-stage posterior approach for treating multilevel noncontiguous thoracic and lumbar spinal tuberculosis.

OBJECTIVES: Multilevel noncontiguous thoracic and lumbar spinal tuberculosis (MNST) is a relatively rare entity. The objective of this retrospective study was to investigate whether a technique involving a one-stage posterior debridement and decompression, combined with an intervertebral fusion and posterior instrumentation, is effective for treating MNST. METHODS: Thirteen patients, with an average age of 40.69 (18-67) years, who had MNST and were surgically treated in our department from January 2008 to October 2013, were reviewed. RESULTS: The average follow-up time was 37.54 ± 10.49 (19-58) months. The mean Cobb angle range was 15.69° ± 00A09.09° (-3° to 33°). The mean erythrocyte sedimentation rate (ESR) was 47.69 ± 9.30 mm/h (range 30-62 mm/h) before the operation. Neurological deficits were evaluated using the Frankel grade system. The mean Cobb angle decreased to 6.92° ± 3.93° postoperatively. Three months after the operation, the Cobb angle was 7.54° ± 4.35°, and the average ESR was 10.38 ± 4.54 mm/h that was normal for all cases in this retrospective observational study. Solid fusion was achieved in all cases. No severe complications occurred. CONCLUSIONS: The study demonstrated that a one-stage posterior debridement and decompression, combined with an intervertebral fusion and posterior instrumentation, was effective for treating MNST.