Research priorities for improving cognitive and neuropsychological outcomes in hydrocephalus.

Hydrocephalus is a neurological disorder that impacts approximately 85 per 100,000 individuals worldwide and is associated with motor and cognitive impairments. While many advances in surgical interventions have helped substantially improve the survival rates and quality of life of those affected, there continues to be significant gaps in our understanding of the etiology of this heterogeneous condition as well as its specific neuropsychological and functional challenges across different phases of life. To address these limitations, the Hydrocephalus Association and Rudi Schulte Research Institute organized a workshop titled, "Improving Cognitive and Psychological Outcomes in Hydrocephalus", composed of top academics in the fields of hydrocephalus, cognition, and neuropsychology, as well as individuals with hydrocephalus or their caregivers.

Inpatient healthcare burden and variables influencing hydrocephalus-related admissions across the lifespan.

Objective: The aims of this study were to quantify inpatient healthcare costs, describe patient demographics, and analyze variables influencing costs for pediatric and adult hydrocephalus shunt-related admissions in the US.

Methods: A cross-sectional study was performed using the 2019 Healthcare Cost and Utilization Project Kids' Inpatient Database (KID) and National Inpatient Sample (NIS), nationally representative weighted data sets of hospital discharges for pediatric and adult patients, respectively. International Classification of Diseases, 10th Revision, Clinical Modification and Procedure Coding System (ICD-10-CM/PCS) code filters for data extraction were queried for admission information.

Transection injury differentially alters the proteome of the human sural nerve.

Regeneration after severe peripheral nerve injury is often poor. Knowledge of human nerve regeneration and the growth microenvironment is greatly lacking. We aimed to identify the regenerative proteins in human peripheral nerve by comparing the proteome before and after a transection injury.

Using a Transection Paradigm to Enhance the Repair Mechanisms of an Investigational Human Cell Therapy.

One promising strategy in cell therapies for Parkinson's disease (PD) is to harness a patient's own cells to provide neuroprotection in areas of the brain affected by neurodegeneration. No treatment exists to replace cells in the brain. Thus, our goal has been to support sick neurons and slow neurodegeneration by transplanting living repair tissue from the peripheral nervous system into the substantia nigra of those with PD.

Telehealth Sustainability in a Neurosurgery Department During the COVID-19 Pandemic.

Background: The COVID-19 pandemic has shifted the dynamics of health care and neurosurgical practice. Elective surgeries were suspended for 8 weeks in Kentucky. Our objective was to determine if telehealth (TH) visits could be sustained as an alternative to in-person visits.

Gait and Balance Changes with Investigational Peripheral Nerve Cell Therapy during Deep Brain Stimulation in People with Parkinson's Disease.

Background: The efficacy of deep brain stimulation (DBS) and dopaminergic therapy is known to decrease over time. Hence, a new investigational approach combines implanting autologous injury-activated peripheral nerve grafts (APNG) at the time of bilateral DBS surgery to the globus pallidus interna.

Objectives: In a study where APNG was unilaterally implanted into the substantia nigra, we explored the effects on clinical gait and balance assessments over two years in 14 individuals with Parkinson's disease.

Initial management of meningiomas: Analysis of the National Cancer Database.

Background: Meningiomas are the most common central nervous system tumor. We describe current trends in treatment and survival using the largest cancer dataset in the United States.

Methods: We analyzed the National Cancer Database from 2004 to 2014, for all patients with diagnosis of meningioma.

CDK5 Inhibition Resolves PKA/cAMP-Independent Activation of CREB1 Signaling in Glioma Stem Cells.

Cancer stem cells promote neoplastic growth, in part by deregulating asymmetric cell division and enhancing self-renewal. To uncover mechanisms and potential therapeutic targets in glioma stem cell (GSC) self-renewal, we performed a genetic suppressor screen for kinases to reverse the tumor phenotype of our Drosophila brain tumor model and identified dCdk5 as a critical regulator. CDK5, the human ortholog of dCdk5 (79% identity), is aberrantly activated in GBMs and tightly aligned with both chromosome 7 gains and stem cell markers affecting tumor-propagation.

Delayed and repeated intranasal delivery of bone marrow stromal cells increases regeneration and functional recovery after ischemic stroke in mice.

Background: Stroke is a leading cause of death and disability worldwide, yet there are limited treatments available. Intranasal administration is a novel non-invasive strategy to deliver cell therapy into the brain. Cells delivered via the intranasal route can migrate from the nasal mucosa to the ischemic infarct and show acute neuroprotection as well as functional benefits.

Transplantation of iPS cell-derived neural progenitors overexpressing SDF-1α increases regeneration and functional recovery after ischemic stroke.

Ischemic stroke is a leading cause of human death and disability while clinical treatments are limited. The adult brain possesses endogenous regenerative activities that may benefit tissue repair after stroke. Trophic factors such as stromal cell-derived factor 1 alpha (SDF-1α) are upregulated in the ischemic brain, which promote endogenous regeneration.

TRIM8 regulates stemness in glioblastoma through PIAS3-STAT3.

Glioblastoma (GBM) is the most malignant form of primary brain tumor, and GBM stem-like cells (GSCs) contribute to the rapid growth, therapeutic resistance, and clinical recurrence of these fatal tumors. STAT3 signaling supports the maintenance and proliferation of GSCs, yet regulatory mechanisms are not completely understood. Here, we report that tri-partite motif-containing protein 8 (TRIM8) activates STAT3 signaling to maintain stemness and self-renewing capabilities of GSCs.

Regeneration after stroke: Stem cell transplantation and trophic factors.

Stroke is a leading cause of death and disability worldwide. However, there is only one Food and Drug Administration-approved drug for the treatment of ischemic stroke, i.e.

iPSC Transplantation increases regeneration and functional recovery after ischemic stroke in neonatal rats.

Limited treatments are available for perinatal/neonatal stroke. Induced pluripotent stem cells (iPSCs) hold therapeutic promise for stroke treatment, but the benefits of iPSC transplantation in neonates are relatively unknown. We hypothesized that transplanted iPSC-derived neural progenitor cells (iPSC-NPCs) would increase regeneration after stroke.

Inflammation, vasospasm, and brain injury after subarachnoid hemorrhage.

Subarachnoid hemorrhage (SAH) can lead to devastating neurological outcomes, and there are few pharmacologic treatments available for treating this condition. Both animal and human studies provide evidence of inflammation being a driving force behind the pathology of SAH, leading to both direct brain injury and vasospasm, which in turn leads to ischemic brain injury. Several inflammatory mediators that are elevated after SAH have been studied in detail.

Erythropoietin attenuates inflammatory factors and cell death in neonatal rats with intracerebral hemorrhage.

Stroke affects infants at a rate of 26/100,000 live births each year. Of these strokes, approximately 6.7 are hemorrhagic strokes.

Selective inhibition of cyclooxygenase 2 induces p27kip1 and skp2 in oral squamous cell carcinoma.

It has been shown that inhibition of cyclooxygenase 2 (COX-2) may cause growth arrest and reduced tumour formation in some human cancers; however, the mechanism is not fully known. In this study, we used an oral squamous cell carcinoma cell line to study growth inhibition and changes in critical cell cycle-regulating proteins induced by the selective COX-2 inhibitor celecoxib. Using cell viability assay, we established the optimal in vitro inhibitory dose of celecoxib and showed that inhibition of COX-2 markedly induces the expression of p27kip1, p21, waf1, and the F-box protein skp2.

Cause-specific mortality among Michigan employees of a chemical company: 1940 to 1994.

We observed 42,076 men and 11,706 women first employed at the Michigan locations of The Dow Chemical Company between 1940 and 1994. Follow-up was 98% complete, and we identified 16,242 deaths. Significant deficits in standardized mortality ratios were observed for all causes, all malignant neoplasms, and more than a dozen other causes of death when compared with rates in the United States.