UW Neurological Surgery Recent PubMed Publications

The Cost of Nurse-Midwifery Care: Use of Interventions, Resources, and Associated Costs in the Hospital Setting.

Womens Health Issues. 2017 Jul - Aug;27(4):434-440

Authors: Altman MR, Murphy SM, Fitzgerald CE, Andersen HF, Daratha KB

Abstract
INTRODUCTION: Obstetrical care often involves multiple expensive, and often elective, interventions that may increase costs to patients, payers, and the health care system with little effect on patient outcomes. The objectives of this study were to examine the following hospital related outcomes: 1) use of labor and birth interventions, 2) inpatient duration of stay, and 3) total direct health care costs for patients attended by a certified nurse-midwife (CNM) compared with those attended by an obstetrician-gynecologist (OB-GYN), within an environment of safe and high-quality care.
MATERIAL AND METHODS: Electronic health records for 1,441 medically low-risk women who gave birth at a hospital located in the U.S. Pacific Northwest between January and September 2013 were sampled. Multilevel regression and generalized linear models were used for analysis.
RESULTS: Reduced use of selected labor and birth interventions (cesarean delivery, vacuum-assisted delivery, epidural anesthesia, labor induction, and cervical ripening), reduced maternal duration of stay, and reduced overall costs associated with CNM-led care relative to OB-GYN-led care were observed for medically low-risk women in a hospital setting. Maternal and neonatal outcomes were comparable across groups.
CONCLUSIONS: This study supports consideration of increased use of CNMs as providers for the care of women at low risk for complications to decrease costs for the health care system. The use of CNMs to the fullest extent within state-regulated scopes of practice could result in more efficient use of hospital resources.

PMID: 28215984 [PubMed - indexed for MEDLINE]

How early media exposure may affect cognitive function: A review of results from observations in humans and experiments in mice.

Proc Natl Acad Sci U S A. 2018 10 02;115(40):9851-9858

Authors: Christakis DA, Ramirez JSB, Ferguson SM, Ravinder S, Ramirez JM

Abstract
Attention deficit hyperactivity disorder (ADHD) is now among the most commonly diagnosed chronic psychological dysfunctions of childhood. By varying estimates, it has increased by 30% in the past 20 years. Environmental factors that might explain this increase have been explored. One such factor may be audiovisual media exposure during early childhood. Observational studies in humans have linked exposure to fast-paced television in the first 3 years of life with subsequent attentional deficits in later childhood. Although longitudinal and well controlled, the observational nature of these studies precludes definitive conclusions regarding a causal relationship. As experimental studies in humans are neither ethical nor practical, mouse models of excessive sensory stimulation (ESS) during childhood, akin to the enrichment studies that have previously shown benefits of stimulation in rodents, have been developed. Experimental studies using this model have corroborated that ESS leads to cognitive and behavioral deficits, some of which may be potentially detrimental. Given the ubiquity of media during childhood, these findings in humansand rodents perhaps have important implications for public health.

PMID: 30275319 [PubMed - indexed for MEDLINE]

Surgical management of superior petrosal sinus dural arteriovenous fistulae with dominant internal carotid artery supply.

Interv Neuroradiol. 2018 Jun;24(3):331-338

Authors: Stapleton CJ, Patel AP, Walcott BP, Torok CM, Koch MJ, Leslie-Mazwi TM, Rabinov JD, Butler WE, Patel AB

Abstract
Background While technological advances have improved the efficacy of endovascular techniques for tentorial dural arteriovenous fistulae (DAVF), superior petrosal sinus (SPS) DAVF with dominant internal carotid artery (ICA) supply frequently require surgical intervention to achieve a definitive cure. Methods To compare the angiographic and clinical outcomes of endovascular and surgical interventions in patients with SPS DAVF, the records of all patients with tentorial DAVF from August 2010 to November 2015 were reviewed. Results Within this cohort, eight patients with nine SPS DAVF were eligible for evaluation. Five DAVF were initially treated with endovascular embolization, while four underwent surgical occlusion without embolization. Of the SPS DAVF treated with embolization, two (40%) remained occluded on follow-up, while the remaining three (60%) persisted/recurred and required surgical intervention for definitive closure. Of the four SPS DAVF treated with primary surgical occlusion, all four (100%) remained closed on follow-up. In addition, of the three SPS DAVF that persisted/recurred following embolization and required subsequent surgical closure, all three (100%) remained occluded on follow-up. Two (100%) SPS DAVF that were successfully treated with embolization had major or minor external carotid artery supply, while the three (100%) persistent lesions had major ICA supply via the meningohypophyseal trunk (MHT). Three (75%) of the four SPS DAVF treated with primary surgical occlusion had dominant MHT supply. Conclusion Complete endovascular closure of SPS DAVF with dominant ICA supply via the MHT may be difficult to achieve, while upfront surgical intervention is associated with a high rate of complete occlusion.

PMID: 29433364 [PubMed - indexed for MEDLINE]

Impeding DNA Break Repair Enables Oocyte Quality Control.

Mol Cell. 2018 10 18;72(2):211-221.e3

Authors: Qiao H, Rao HBDP, Yun Y, Sandhu S, Fong JH, Sapre M, Nguyen M, Tham A, Van BW, Chng TYH, Lee A, Hunter N

Abstract
Oocyte quality control culls eggs with defects in meiosis. In mouse, oocyte death can be triggered by defects in chromosome synapsis and recombination, which involve repair of DNA double-strand breaks (DSBs) between homologous chromosomes. We show that RNF212, a SUMO ligase required for crossing over, also mediates oocyte quality control. Both physiological apoptosis and wholesale oocyte elimination in meiotic mutants require RNF212. RNF212 sensitizes oocytes to DSB-induced apoptosis within a narrow window as chromosomes desynapse and cells transition into quiescence. Analysis of DNA damage during this transition implies that RNF212 impedes DSB repair. Consistently, RNF212 is required for HORMAD1, a negative regulator of inter-sister recombination, to associate with desynapsing chromosomes. We infer that oocytes impede repair of residual DSBs to retain a "memory" of meiotic defects that enables quality-control processes. These results define the logic of oocyte quality control and suggest RNF212 variants may influence transmission of defective genomes.

PMID: 30270110 [PubMed - indexed for MEDLINE]

A truncating mutation in EPOR leads to hypo-responsiveness to erythropoietin with normal haemoglobin.

Commun Biol. 2018;1:49

Authors: Oskarsson GR, Kristjansson RP, Lee AL, Sveinbjornsson G, Magnusson MK, Ivarsdottir EV, Benonisdottir S, Oddsson A, Davidsson OB, Saemundsdottir J, Halldorsson GH, Arthur J, Arnadottir GA, Masson G, Jensson BO, Holm H, Olafsson I, Onundarson PT, Gudbjartsson DF, Norddahl GL, Thorsteinsdottir U, Sulem P, Stefansson K

Abstract
The cytokine erythropoietin (EPO), signalling through the EPO receptor (EPO-R), is essential for the formation of red blood cells. We performed a genome-wide association study (GWAS) testing 32.5 million sequence variants for association with serum EPO levels in a set of 4187 individuals. We detect an association between a rare and well imputed stop-gained variant rs370865377[A] (p.Gln82Ter) in EPOR, carried by 1 in 550 Icelanders, and increased serum EPO levels (MAF = 0.09%, Effect = 1.47 SD, P = 3.3 × 10-7). We validated these findings by measuring serum EPO levels in 34 additional pairs of carriers and matched controls and found carriers to have 3.23-fold higher EPO levels than controls (P = 1.7 × 10-6; P combined = 1.6 × 10-11). In contrast to previously reported EPOR mutations, p.Gln82Ter does not associate with haemoglobin levels (Effect = -0.045 SD, P = 0.32, N = 273,160), probably due to a compensatory EPO upregulation in response to EPO-R hypo-responsiveness.

PMID: 30271932 [PubMed]

Alzheimer's disease (AD) therapeutics - 2: Beyond amyloid - Re-defining AD and its causality to discover effective therapeutics.

Biochem Pharmacol. 2018 12;158:376-401

Authors: Mullane K, Williams M

Abstract
Compounds targeted for the treatment of Alzheimer's Disease (AD) have consistently failed in clinical trials despite evidence for target engagement and pharmacodynamic activity. This questions the relevance of compounds acting at current AD drug targets - the majority of which reflect the seminal amyloid and, to a far lesser extent, tau hypotheses - and limitations in understanding AD causality as distinct from general dementia. The preeminence of amyloid and tau led to many alternative approaches to AD therapeutics being ignored or underfunded to the extent that their causal versus contributory role in AD remains unknown. These include: neuronal network dysfunction; cerebrovascular disease; chronic, local or systemic inflammation involving the innate immune system; infectious agents including herpes virus and prion proteins; neurotoxic protein accumulation associated with sleep deprivation, circadian rhythm and glymphatic/meningeal lymphatic system and blood-brain-barrier dysfunction; metabolic related diseases including diabetes, obesity hypertension and hypocholesterolemia; mitochondrial dysfunction and environmental factors. As AD has become increasingly recognized as a multifactorial syndrome, a single treatment paradigm is unlikely to work in all patients. However, the biomarkers required to diagnose patients and parse them into mechanism/disease-based sub-groups remain rudimentary and unvalidated as do non-amyloid, non-tau translational animal models. The social and economic impact of AD is also discussed in the context of new FDA regulatory draft guidance and a proposed biomarker-based Framework (re)-defining AD and its stages as part of the larger landscape of treating dementia via the 2013 G8 initiative to identify a disease-modifying therapy for dementia/AD by 2025.

PMID: 30273552 [PubMed - indexed for MEDLINE]

Alzheimer's disease (AD) therapeutics - 1: Repeated clinical failures continue to question the amyloid hypothesis of AD and the current understanding of AD causality.

Biochem Pharmacol. 2018 12;158:359-375

Authors: Mullane K, Williams M

Abstract
Deposits of amyloid plaques and neurofibrillary tangles of aggregated tau in the brain represent key hallmarks of the neurodegenerative disorder, Alzheimer's Disease (AD) and form the basis of the major hypotheses of AD causality. To date, therapeutics that reduce brain amyloid in AD patients have demonstrated no effect in reversing the associated decline in cognition or function indicating that the amyloid hypothesis is either incorrect or that there is a point when the disease becomes independent of Aβ production or is refractory to any type of therapeutic intervention. The clinical failures of inhibitors of tau aggregation, neurotransmitter modulators and drugs repurposed from AD-associated disease indications tend to support this latter viewpoint. Current understanding of AD causality is thus incomplete, a situation that has been compounded by a debate on whether AD is a singularly distinct form of dementia and by the dogmatic promotion of hypotheses over actual clinical data. The latter has repeatedly led to compounds lacking efficacy in Phase II trials being advanced into Phase III where their lack of efficacy is routinely recapitulated. This Commentary, the first of two, discusses amyloid and tau as putative drug targets for AD in the context of the prevalence and economic and social impact of this insidious neurodegenerative disease.

PMID: 30273553 [PubMed - indexed for MEDLINE]

Outcome after myocardial infarction without obstructive coronary artery disease.

Heart. 2019 04;105(7):524-530

Authors: Williams MJA, Barr PR, Lee M, Poppe KK, Kerr AJ

Abstract
OBJECTIVE: The medium-term outcome and cause of death in patients with myocardial infarction with non-obstructive coronary arteries (MINOCA) is not well characterised. The aim of this study was to compare mortality and rates of recurrent events in post myocardial infarction (MI) patients with obstructive coronary artery disease (CAD) and in patients with MINOCA compared with an age and sex-matched cohort without cardiovascular disease (CVD).
METHODS: We performed a national cohort study of consecutive patients undergoing coronary angiography for MI during 2 years between 2013 and 2015 from the All New Zealand Acute Coronary Syndrome-Quality Improvement (ANZACS QI) registry. MI patient registry data were linked anonymously to national hospitalisation and mortality records. Age and sex matched patients without known CVD formed the comparison group.
RESULTS: Of the 8305 patients with MI, 897 (10.8%) were classified as MINOCA. Compared with those without known CVD, the adjusted HRs for the primary outcome (all-cause death or recurrent non-fatal MI) were 7.81 (95% CI 6.64 to 9.19, p<0.0001) in those with obstructive CAD and 4.64 (95% CI 3.54 to 6.10, p<0.0001) in those with MINOCA. Kaplan-Meier all-cause mortality at 2 years was 7.9% for those with obstructive CAD, with nearly half being CVD deaths (3.6% CVD deaths and 4.5% non-CVD deaths, respectively). In contrast, MINOCA all-cause mortality was 4.9% with non-CVD death (4.5%) predominating.
CONCLUSIONS: MINOCA is common and has an adverse outcome rate approximately half than that of those with obstructive CAD. The predominant contributor to mortality is non-CVD death. The rate of events in MINOCA is significantly greater than the population without CVD.

PMID: 30269079 [PubMed - indexed for MEDLINE]

Referral frequency, attrition rate, and outcomes of germline testing in patients with pancreatic adenocarcinoma.

Fam Cancer. 2019 04;18(2):241-251

Authors: Walker EJ, Carnevale J, Pedley C, Blanco A, Chan S, Collisson EA, Tempero MA, Ko AH

Abstract
Hereditary predisposition is estimated to account for 10% of all pancreatic cancer cases. However, referral patterns and clinical workflow for germline testing in this disease differ significantly by institution, and many at-risk patients may not undergo appropriate counseling and testing. We undertook an analysis of patients diagnosed with pancreatic cancer (PDAC) who were referred to the Clinical Genetics program of a high-volume academic center over a 3-year period to assess referral frequency, evaluate the yield of germline testing in this selected patient cohort, and elucidate the reasons individuals did not undergo recommended germline testing. Medical records of patients with PDAC referred for genetic counseling between January 2015 and October 2017 were reviewed for demographic, medical/family history, and disease-specific data. If testing did not occur, reasons were documented. Genetic test results were categorized as negative, variants of unknown significance, or established pathogenic mutations. Descriptive statistics included means with standard deviations; associations were analyzed with t test and Fisher's exact test. 32% (137 of 432) of PDAC patients were referred for genetic counseling, but only 64% attended their appointment and 60% ultimately underwent germline testing. Common reasons for attrition included worsening disease severity, lack of patient follow-up, insurance concerns, and logistic/travel challenges. Pathogenic germline mutations were detected in 20% (16 of 82) of patients tested, distributed across races/ethnicities, and significantly associated with younger age and positive family history of breast cancer. PDAC patients frequently do not undergo genetic counseling/germline testing despite appropriate referrals, highlighting a need to develop streamlined processes to engage more patients in testing, especially those with high-risk features.

PMID: 30267352 [PubMed - indexed for MEDLINE]

A clinical decision rule to predict intracranial hypertension in severe traumatic brain injury.

J Neurosurg. 2018 09 28;131(2):612-619

Authors: Alali AS, Temkin N, Barber J, Pridgeon J, Chaddock K, Dikmen S, Hendrickson P, Videtta W, Lujan S, Petroni G, Guadagnoli N, Urbina Z, Chesnut RM

Abstract
OBJECTIVE: While existing guidelines support the treatment of intracranial hypertension in severe traumatic brain injury (TBI), it is unclear when to suspect and initiate treatment for high intracranial pressure (ICP). The objective of this study was to derive a clinical decision rule that accurately predicts intracranial hypertension.
METHODS: Using Delphi methods, the authors identified a set of potential predictors of intracranial hypertension and a clinical decision rule a priori by consensus among a group of 43 neurosurgeons and intensivists who have extensive experience managing severe TBI without ICP monitoring. To validate these predictors, the authors used data from a Latin American trial (n = 150; BEST TRIP). To report on the performance of the rule, they calculated sensitivity, specificity, and positive and negative predictive values with 95% confidence intervals. In a secondary analysis, the rule was validated using data from a North American trial (n = 131; COBRIT).
RESULTS: The final predictors and the clinical decision rule were approved by 97% of participants in the consensus working group. The predictors are divided into major and minor criteria. High ICP would be considered suspected in the presence of 1 major or ≥ 2 minor criteria. Major criteria are: compressed cisterns (CT classification of Marshall diffuse injury [DI] III), midline shift > 5 mm (Marshall DI IV), or nonevacuated mass lesion. Minor criteria are: Glasgow Coma Scale (GCS) motor score ≤ 4, pupillary asymmetry, abnormal pupillary reactivity, or Marshall DI II. The area under the curve for the logistic regression model that contains all the predictors was 0.86. When high ICP was defined as > 22 mm Hg, the decision rule performed with a sensitivity of 93.9% (95% CI 85.0%-98.3%), a specificity of 42.3% (95% CI 31.7%-53.6%), a positive predictive value of 55.5% (95% CI 50.7%-60.2%), and a negative predictive value of 90% (95% CI 77.1%-96.0%). The sensitivity of the clinical decision rule improved with higher ICP cutoffs up to a sensitivity of 100% when intracranial hypertension was defined as ICP > 30 mm Hg. Similar results were found in the North American cohort.
CONCLUSIONS: A simple clinical decision rule based on a combination of clinical and imaging findings was found to be highly sensitive in distinguishing patients with severe TBI who would suffer intracranial hypertension. It could be used to identify patients who require ICP monitoring in high-resource settings or start ICP-lowering treatment in environments where resource limitations preclude invasive monitoring.Clinical trial registration no.: NCT02059941 (clinicaltrials.gov).

PMID: 30265194 [PubMed - indexed for MEDLINE]

Internal decompression of the acutely contused spinal cord: Differential effects of irrigation only versus biodegradable scaffold implantation.

Biomaterials. 2018 12;185:284-300

Authors: Guest JD, Moore SW, Aimetti AA, Kutikov AB, Santamaria AJ, Hofstetter CP, Ropper AE, Theodore N, Ulich TR, Layer RT

Abstract
Severe spinal cord injury leads to hemorrhage, edema and elevated tissue pressures that propagate ischemia. Liquefactive necrosis of damaged tissue eventually results in chronic cavities due to a wound healing process lacking adhesive contractile cells. Biomaterials can potently influence wound healing responses. Internal decompression (ID) refers to pial opening, allowing spontaneous extrusion and irrigation of fluid necrotic debris relieving pressure and resulting in a space for biomaterial scaffold insertion. After thoracic contusions, rats were randomized to: contusion only, contusion + ID and contusion + ID + PLGA-PLL scaffold implantation, to test for neuroprotection and endogenous repair over 3 months. ID alone reduced inflammatory activity, cavity volume, and increased tissue sparing. Scaffold biodegradation produced delayed ingrowth of inflammatory and other cells resulting in endogenously derived laminin-rich tissue, marked reduction in cavitation and presence of tissue remodeling macrophages. Extensive recruitment of Schwann cells into adjacent spared white matter occurred, greatest in scaffold-implanted animals. Despite tissue preservation with myelin repair, no groups differed significantly in open field locomotion. However, across all rats, spared epicenter tissue and locomotor outcomes were correlated. Scaffold-implanted animals showed no obvious toxicity. To study the clinical feasibility, timing and indications for scaffold implantation, Göttingen minipigs underwent ID and were implanted with scaffolds 4, 6, and 24 h after T10 contusion. High intra-spinal tissue pressures fell to pre-injury levels after ID and scaffold implantation. Extrusion of necrotic debris left sufficient space for a sized scaffold. These results provided the preclinical rationale for a current clinical study of biomaterial scaffold implantation into the human injured spinal cord.

PMID: 30265898 [PubMed - indexed for MEDLINE]

cIMPACT-NOW update 3: recommended diagnostic criteria for "Diffuse astrocytic glioma, IDH-wildtype, with molecular features of glioblastoma, WHO grade IV".

Acta Neuropathol. 2018 11;136(5):805-810

Authors: Brat DJ, Aldape K, Colman H, Holland EC, Louis DN, Jenkins RB, Kleinschmidt-DeMasters BK, Perry A, Reifenberger G, Stupp R, von Deimling A, Weller M

Abstract

PMID: 30259105 [PubMed - indexed for MEDLINE]

Sparse recurrent excitatory connectivity in the microcircuit of the adult mouse and human cortex.

Elife. 2018 Sep 26;7:

Authors: Seeman SC, Campagnola L, Davoudian PA, Hoggarth A, Hage TA, Bosma-Moody A, Baker CA, Lee JH, Mihalas S, Teeter C, Ko AL, Ojemann JG, Gwinn RP, Silbergeld DL, Cobbs C, Phillips J, Lein E, Murphy G, Koch C, Zeng H, Jarsky T

Abstract
Generating a comprehensive description of cortical networks requires a large-scale, systematic approach. To that end, we have begun a pipeline project using multipatch electrophysiology, supplemented with two-photon optogenetics, to characterize connectivity and synaptic signaling between classes of neurons in adult mouse primary visual cortex (V1) and human cortex. We focus on producing results detailed enough for the generation of computational models and enabling comparison with future studies. Here, we report our examination of intralaminar connectivity within each of several classes of excitatory neurons. We find that connections are sparse but present among all excitatory cell classes and layers we sampled, and that most mouse synapses exhibited short-term depression with similar dynamics. Synaptic signaling between a subset of layer 2/3 neurons, however, exhibited facilitation. These results contribute to a body of evidence describing recurrent excitatory connectivity as a conserved feature of cortical microcircuits.

PMID: 30256194 [PubMed - in process]

Semi-autonomous image-guided brain tumour resection using an integrated robotic system: A bench-top study.

Int J Med Robot. 2018 Feb;14(1):

Authors: Hu D, Gong Y, Seibel EJ, Sekhar LN, Hannaford B

Abstract
BACKGROUND: Complete brain tumour resection is an extremely critical factor for patients' survival rate and long-term quality of life. This paper introduces a prototype medical robotic system that aims to automatically detect and clean up brain tumour residues after the removal of tumour bulk through conventional surgery.
METHODS: We focus on the development of an integrated surgical robotic system for image-guided robotic brain surgery. The Behavior Tree framework is explored to coordinate cross-platform medical subtasks.
RESULTS: The integrated system was tested on a simulated laboratory platform. Results and performance indicate the feasibility of supervised semi-automation for residual brain tumour ablation in a simulated surgical cavity with sub-millimetre accuracy. The modularity in the control architecture allows straightforward integration of further medical devices.
CONCLUSIONS: This work presents a semi-automated laboratory setup, simulating an intraoperative robotic neurosurgical procedure with real-time endoscopic image guidance and provides a foundation for the future transition from engineering approaches to clinical application.

PMID: 29105281 [PubMed - indexed for MEDLINE]

Evaluating a Targeted Bedside Measure of Cerebral Perfusion in a Nonhuman Primate Model of Neonatal Hypoxic-Ischemic Encephalopathy.

J Ultrasound Med. 2018 Apr;37(4):913-920

Authors: Peeples ES, Ezeokeke CK, Juul SE, Mourad PD

Abstract
OBJECTIVES: To compare ultrasound-derived resistive indices (RIs) obtained at the level of the thalamus via fast Doppler ultrasound with traditional anterior cerebral artery measures in a model of neonatal hypoxic-ischemic encephalopathy and to correlate each with clinical outcomes.
METHODS: Nine nonhuman primate neonates underwent no umbilical cord occlusion (n = 3), umbilical cord occlusion without hypothermia (n = 3), or umbilical cord occlusion with hypothermia (n = 3). The RI was measured in the anterior cerebral artery and thalamus on days 0, 1, and 4 of life. Magnetic resonance imaging with spectroscopy was performed on day 4.
RESULTS: Mean thalamus and anterior cerebral artery RI values in the first 36 hours of life were statistically different in neonates who died (+0.13; P = .019) or developed cerebral palsy (-0.08; P = .003). Thalamic RI values showed stronger associations with serum and spectroscopic lactate values than those in the anterior cerebral artery. The umbilical cord occlusion-with-hypothermia group showed a significant increase in the RI in the thalamus but not the anterior cerebral artery.
CONCLUSIONS: Resistive index measurements in the thalamus may eventually supplement other bedside measures for predicting outcomes in the HIE population, but further studies need to differentiate the effect of hypothermia from illness severity on thalamic perfusion.

PMID: 28960438 [PubMed - indexed for MEDLINE]

Would the control of invasive alien plants reduce malaria transmission? A review.

Parasit Vectors. 2018 02 01;11(1):76

Authors: Stone CM, Witt ABR, Walsh GC, Foster WA, Murphy ST

Abstract
Vector control has been the most effective preventive measure against malaria and other vector-borne diseases. However, due to concerns such as insecticide resistance and budget shortfalls, an integrated control approach will be required to ensure sustainable, long-term effectiveness. An integrated management strategy should entail some aspects of environmental management, relying on coordination between various scientific disciplines. Here, we review one such environmental control tactic: invasive alien plant management. This covers salient plant-mosquito interactions for both terrestrial and aquatic invasive plants and how these affect a vector's ability to transmit malaria. Invasive plants tend to have longer flowering durations, more vigorous growth, and their spread can result in an increase in biomass, particularly in areas where previously little vegetation existed. Some invasive alien plants provide shelter or resting sites for adult mosquitoes and are also attractive nectar-producing hosts, enhancing their vectorial capacity. We conclude that these plants may increase malaria transmission rates in certain environments, though many questions still need to be answered, to determine how often this conclusion holds. However, in the case of aquatic invasive plants, available evidence suggests that the management of these plants would contribute to malaria control. We also examine and review the opportunities for large-scale invasive alien plant management, including options for biological control. Finally, we highlight the research priorities that must be addressed in order to ensure that integrated vector and invasive alien plant management operate in a synergistic fashion.

PMID: 29391041 [PubMed - indexed for MEDLINE]

Functional independence after acquired brain injury: Prospective effects of health self-efficacy and cognitive impairment.

Rehabil Psychol. 2018 Nov;63(4):595-603

Authors: Parker HA, Rapport LJ, Williams MW, Hanks RA, Lumley MA, Bogg T

Abstract
OBJECTIVE: To examine how health self-efficacy and cognitive impairment severity relate to functional independence after acquired brain injury (ABI).
DESIGN: Observational.
SETTING: Outpatient rehabilitation hospital.
PARTICIPANTS: Seventy-five adults with predominately stroke or traumatic brain injury who were beginning a course of occupational therapy.
MAIN MEASURES: Health self-efficacy was assessed with the Self-Rated Abilities for Health Practices. Cognitive functioning was assessed via a composite z score of neuropsychological tests. Trait affectivity was assessed with the Positive and Negative Affect Schedule. Functional independence was assessed with the Barthel Index and Lawton Instrumental Activities of Daily Living Scale.
RESULTS: Health self-efficacy correlated moderately with functional independence. A moderation threshold effect was detected that revealed for whom health self-efficacy predicted functional independence. Among participants with normal to mildly impaired cognition (>-2 z cognitive composite), health self-efficacy correlated positively with functional independence, which held after accounting for trait affectivity. In contrast, health self-efficacy was not correlated with functional independence among participants with greater impairment (<-2 z cognitive composite).
CONCLUSIONS: Health self-efficacy predicts functional independence and may serve as a protective factor after ABI among individuals with relatively intact cognition. However, health self-efficacy does not predict functional independence among individuals with moderate or severe cognitive impairment, possibly due to limited self-awareness. This study extends the literature linking health self-efficacy with rehabilitation outcomes and reinforces the need for promoting self-management in ABI. (PsycINFO Database Record (c) 2018 APA, all rights reserved).

PMID: 30247052 [PubMed - indexed for MEDLINE]

Criminal justice measures for economic data harmonization in substance use disorder research.

Health Justice. 2018 Sep 21;6(1):17

Authors: McCollister KE, Yang X, Murphy SM, Leff JA, Kronmal RA, Crane HM, Chandler RK, Taxman FS, Feaster DJ, Metsch LR, Cunningham WE, Altice FL, Schackman BR

Abstract
BACKGROUND: The consequences of substance use disorders (SUDs) are varied and broad, affecting many sectors of society and the economy. Economic evaluation translates these consequences into dollars to examine the net economic impact of interventions for SUD, and associated conditions such as HCV and HIV. The nexus between substance use and crime makes criminal justice outcomes particularly significant for estimating the economic impact of SUD interventions, and important for data harmonization.
METHODS: We compared baseline data collected in six NIDA-funded Seek, Test, Treat and Retain (STTR) intervention studies that enrolled HIV-infected/at-risk individuals with SUDs (total n = 3415). Criminal justice measures included contacts with the criminal justice system (e.g., arrests) and criminal offenses. The objective was to develop a list of recommended measures and methods supporting economic data harmonization opportunities in HIV and SUD research, with an initial focus on crime-related outcomes.
RESULTS: Criminal justice contacts and criminal offenses were highly variable across studies. When measures grouped by offense classifications were compared, consistencies across studies emerged. Most individuals report being arrested for property or public order crimes (> 50%); the most commonly reported offenses were prostitution/pimping, larceny/shoplifting, robbery, and household burglary.
CONCLUSIONS: We identified four measures that are feasible and appropriate for estimating the economic consequences of SUDs/HIV/HCV: number of arrests, number of convictions, days of incarceration, and times committing criminal offenses, by type of offense. To account for extreme variation, grouping crimes by offense classification or calculating monthly averages per event allows for more meaningful comparisons across studies.

PMID: 30242561 [PubMed]

Vessel wall MRI characteristics of endovascularly treated aneurysms: association with angiographic vasospasm.

J Neurosurg. 2018 09 21;131(3):859-867

Authors: Mossa-Basha M, Huynh TJ, Hippe DS, Fata P, Morton RP, Levitt MR

Abstract
OBJECTIVE: The aim of this paper was to evaluate the association between intracranial vessel wall MRI enhancement characteristics and the development of angiographic vasospasm in endovascularly treated aneurysm patients.
METHODS: Consecutive cases of both ruptured and unruptured intracranial aneurysms that were treated endovascularly, followed by intracranial vessel wall MRI in the immediate postoperative period, were included. Two raters blinded to clinical data and follow-up imaging independently evaluated for the presence, pattern, and intensity of wall enhancement. Development of angiographic vasospasm was independently evaluated. Delayed cerebral ischemia; cerebral infarct; procedural details; and presence and grade of subarachnoid, parenchymal, and intraventricular hemorrhage were evaluated. Statistical associations were determined on a per-vessel segment and per-patient basis.
RESULTS: Twenty-nine patients with 30 treated aneurysms (8 unruptured and 22 ruptured) were included in this study. Interobserver agreement was substantial for the presence of enhancement (κ = 0.67) and nearly perfect for distribution (κ = 0.87) and intensity (κ = 0.84) of wall enhancement. Patients with ruptured aneurysms had a significantly greater number of enhancing segments than those with unruptured aneurysms (29.9% vs 7.2%; OR 5.5, 95% CI 2.2-13.7). For ruptured cases, wall enhancement was significantly associated with subsequent angiographic vasospasm while controlling for grade of hemorrhage (adjusted OR 3.9, 95% CI 1.7-9.4). Vessel segments affected by balloon, stent, or flow-diverter use demonstrated greater enhancement than those not affected (OR 22.7, 95% CI 5.3-97.2 for ruptured; and OR 12.9, 95% CI 3.3-49.8 for unruptured).
CONCLUSIONS: Vessel wall enhancement after endovascular treatment of ruptured aneurysms is associated with subsequent angiographic vasospasm.

PMID: 30239313 [PubMed - indexed for MEDLINE]

Heterozygosity of Chaperone Grp78 Reduces Intestinal Stem Cell Regeneration Potential and Protects against Adenoma Formation.

Cancer Res. 2018 11 01;78(21):6098-6106

Authors: van Lidth de Jeude JF, Spaan CN, Meijer BJ, Smit WL, Soeratram TTD, Wielenga MCB, Westendorp BF, Lee AS, Meisner S, Vermeulen JLM, Wildenberg ME, van den Brink GR, Muncan V, Heijmans J

Abstract
Deletion of endoplasmic reticulum resident chaperone Grp78 results in activation of the unfolded protein response and causes rapid depletion of the entire intestinal epithelium. Whether modest reduction of Grp78 may affect stem cell fate without compromising intestinal integrity remains unknown. Here, we employ a model of epithelial-specific, heterozygous Grp78 deletion by use of VillinCreERT2-Rosa26ZsGreen/LacZ-Grp78+/fl mice and organoids. We examine models of irradiation and tumorigenesis, both in vitro and in vivo Although we observed no phenotypic changes in Grp78 heterozygous mice, Grp78 heterozygous organoid growth was markedly reduced. Irradiation of Grp78 heterozygous mice resulted in less frequent regeneration of crypts compared with nonrecombined (wild-type) mice, exposing reduced capacity for self-renewal upon genotoxic insult. We crossed mice to Apc-mutant animals for adenoma studies and found that adenomagenesis in Apc heterozygous-Grp78 heterozygous mice was reduced compared with Apc heterozygous controls (1.43 vs. 3.33; P < 0.01). In conclusion, epithelium-specific Grp78 heterozygosity compromises epithelial fitness under conditions requiring expansive growth such as adenomagenesis or regeneration after γ-irradiation. These results suggest that Grp78 may be a therapeutic target in prevention of intestinal neoplasms without affecting normal tissue.Significance: Heterozygous disruption of chaperone protein Grp78 reduces tissue regeneration and expansive growth and protects from tumor formation without affecting intestinal homeostasis. Cancer Res; 78(21); 6098-106. ©2018 AACR.

PMID: 30232220 [PubMed - indexed for MEDLINE]