Association of depressive symptom severity and suicidal ideation with health-related quality of life among stroke survivors, NHANES 2005-2018.

Stroke, a critical health issue in the US, not only has physical repercussions but also potentially affects the health-related quality of life (HRQoL) through neuropsychiatric outcomes like depressive symptoms and suicidal thoughts. This study utilized a nationally representative sample of 1302 US stroke survivors (age ≥ 20) from the US National Health and Nutrition Examination Survey (2005-2018) to assessed relationships between QoL via the CDC HRQOL-4 and evaluated depressive symptoms and suicidal ideation using the Patient Health Questionnaire-9 (PHQ-9). Participants (mean age: 64.4; 56.0 % female) showed that 40.7 % had at least mild depressive symptoms, and 18.8 % exhibited major depressive symptoms. Suicidal ideation was reported by 8.1 %. After sociodemographic and health condition adjustments, mild and major depressive symptoms, along with suicidal ideation, were associated with poorer general health status and more physically and mentally unhealthy days and activity limitation days. A dose-response relationship between PHQ-9 scores and HRQoL outcomes was evident (All P for trend <0.001). Stroke survivors with suicidal ideation also experienced more physically and mentally unhealthy days and activity limitation days. Depressive symptoms and suicidal ideation are associated with reduced HRQoL among US stroke survivors, underscoring the importance of thorough neuropsychiatric evaluations and interventions to bolster stroke survivors' well-being.

L4-to-L4 nerve root transfer for hindlimb hemiplegia after hypertensive intracerebral hemorrhage.

There is no effective treatment for hemiplegia after hypertensive intracerebral hemorrhage. Considering that the branches of L4 nerve roots in the lumbar plexus root control the movement of the lower extremity anterior and posterior muscles, we investigated a potential method of nerve repair using the L4 nerve roots. Rat models of hindlimb hemiplegia after a hypertensive intracerebral hemorrhage were established by injecting autogenous blood into the posterior limb of internal capsule. The L4 nerve root on the healthy side of model rats was transferred and then anastomosed with the L4 nerve root on the affected side to drive the extensor and flexor muscles of the hindlimbs. We investigated whether this method can restore the flexible movement of the hindlimbs of paralyzed rats after hypertensive intracerebral hemorrhage. In a beam-walking test and ladder rung walking task, model rats exhibited an initial high number of slips, but improved in accuracy on the paretic side over time. At 17 weeks after surgery, rats gained approximately 58.2% accuracy from baseline performance and performed ankle motions on the paretic side. At 9 weeks after surgery, a retrograde tracing test showed a large number of fluoro-gold-labeled motoneurons in the left anterior horn of the spinal cord that supports the L4-to-L4 nerve roots. In addition, histological and ultramicrostructural findings showed axon regeneration of motoneurons in the anterior horn of the spinal cord. Electromyography and paw print analysis showed that denervated hindlimb muscles regained reliable innervation and walking coordination improved. These findings suggest that the L4-to-L4 nerve root transfer method for the treatment of hindlimb hemiplegia after hypertensive intracerebral hemorrhage can improve the locomotion of hindlimb major joints, particularly of the distal ankle. Findings from study support that the L4-to-L4 nerve root transfer method can effectively repair the hindlimb hemiplegia after hypertensive intracerebral hemorrhage. All animal experiments were approved by the Animal Ethics Committee of the First Affiliated Hospital of Nanjing Medical University (No. IACUC-1906009) in June 2019.

Efficacy evaluation of personalized coaptation in neurotization for motor deficit after peripheral nerve injury: A systematic review and meta-analysis.

INTRODUCTION: Peripheral neurotization, recently as a promising approach, has taken effect in recovering motor function after damage to a peripheral nerve root. Neural anastomosis comprised of nerve conduit and neurorrhaphy participates in the nerve reconstruction. Current literature lacks evidence supporting an individualized coaptation for rescue of locomotor loss in rat subjects with paraplegia secondary to peripheral nerve injury (PNI). METHODS: This meta-analysis intends to qualify the specificity of gap-specific coaptation in treating a paralyzed limb following PNI. We used a highly sensitive search strategy to identify all published studies in multiple databases up to 1 May 2019. All identified trials were systematically evaluated using specific inclusion and exclusion criteria. Cochrane methodology was also applied to the results of this study. RESULTS: Twelve studies, including 349 rat subjects, met eligibility criteria. For a medium nerve defect (0.5-3.0 cm), nerve conduit was more likely than neurorrhaphy to precipitate axon regeneration and improve motor outcome of the hemiplegic limb (OR = 3.61, 95% CI = 1.80, 7.26, p < .0003) at 3-month follow-up, whereas neurorrhaphy might take its place in promoting limb motor function in a small nerve gap (<0.5 cm) (OR = 0.48, 95% CI = 0.22, 1.07, p < .007). For a small nerve defect, nerve conduit still demonstrated visible effectiveness in recovery of limb motion albeit poorer than neurorrhaphy (OR = 1.50, 95% CI = 0.92, 2.47, p < .05). CONCLUSION: Selective neurotization facilitates motor regeneration after nerve transection, and advisable choice of neural coaptation can maximize functional outcome on an individual basis.

HOXB13 promotes proliferation, migration, and invasion of glioblastoma through transcriptional upregulation of lncRNA HOXC-AS3.

HOXB13 exerts a close relation in several human cancers. This study explored the role of HOXB13 in glioblastoma (GBM), a brain tissue with the highest aggressive rate and mortality in adults. Through microarray and immunohistochemistry analyses, HOXB13 was highly expressed in GBM tissues. Furthermore, we showed that high-level expression of HOXB13 in GBM was associated with worse survival, suggesting that HOXB13 could be a prognostic marker for patients with GBM. GBM cells U87 and U251 overexpressing HOXB13 showed enhanced proliferation, migration, and invasion relative to the control cells, while knockdown of HOXB13 led to decreased cell proliferation, migration, and invasion abilities. In addition, dual-luciferase report assay, chromatin immunoprecipitation assay, and quantitative real-time polymerase chain reaction data showed that HOXB13 directly bound to HOXC-AS3 promoter. HOXC-AS3 was involved in HOXB13-induced proliferation, migration, and invasion of GBM cells. In summary, this study revealed the prognostic potential of HOXB13 in GBM. We believed that HOXB13/HOXC-AS3 signaling axis can be served as therapeutic targets for this highly aggressive cancer.

MicroRNA-940 inhibits glioma progression by blocking mitochondrial folate metabolism through targeting of MTHFD2.

The aggressiveness and recurrence of glioma are major obstacles for the treatment of this type of tumor. Further understanding of the molecular mechanisms of glioma is necessary to improve the efficacy of therapy. MicroRNAs have been widely studied in many human cancers. Here, we found that miR-940 was one of the primary downregulated miRNAs in clinical samples and glioma cell lines through bioinformatics analysis and qRT-PCR. Upregulating miR-940 expression significantly inhibited the proliferation and invasion and promoted apoptosis of U87 and U118 cells. In addition, experiments in vivo showed that upregulation of miR-940 expression inhibited xenograft growth. Methylenetetrahydrofolate dehydrogenase (MTHFD2), a dual-functional metabolic enzyme, is involved in the one-carbon metabolism of folate in mitochondria. We found MTHFD2 to be overexpressed in glioma tissues and our clinical samples by qRT-PCR and Western blot assays. Through TargetScan prediction and luciferase assays, we found that miR-940 directly targets MTHFD2. Upregulation of miR-940 expression inhibited the expression of MTHFD2 and led to intracellular one-carbon metabolism dysfunction. Furthermore, the antitumor effects of miR-940 could be attenuated by overexpression of MTHFD2. Together, the results of our study suggest that miR-940 may be a new therapeutic target for the treatment of glioma through targeting of MTHFD2.