bluuebunny/crossref_metadata_2025_split huggingface dataset:
Predictors of a Non-home Discharge Destination Following Spinal Fusion for Adolescent Idiopathic Scoliosis (AIS)
Authors: Malik Azeem Tariq , Kim Jeffery , Yu Elizabeth , Khan Safdar N. 
Published: September 2018

Study Design.
Retrospective cohort study.

Objective.
Analyze risk factors associated with a non-home discharge following spinal fusions in adolescent idiopathic scoliosis (AIS).

Summary of Background Data.
Current evidence is limited with regard to which patient-level and provider/hospital-level factors predict a non-home discharge disposition following spinal fusions in AIS. Identifying these factors can allow providers to identify which patients would ultimately require facility care and can be discharged early to these facilities to reduce hospital costs.

Methods.
The 2012 to 2016 American College of Surgeons—National Surgical Quality Improvement Program Pediatric database was queried using Current Procedural Terminology codes for posterior spinal fusions (22800, 22802, and 22804) and anterior spinal fusions (22808, 22810, and 22812). Patients were categorized into those receiving a posterior-only fusion, anterior-only fusion, and combined anterior-posterior fusion. Only patients aged 10 to 18 undergoing corrective surgery for idiopathic scoliosis were included in the study.

Results.
Out of a total of 8452 patients—90 (1.1%) were discharged to a destination other than home (skilled-care facility, separate acute care unit, and/or rehabilitation unit). Following multivariate analysis, children with a body mass index of 20 to 30 (P = 0.002) or >30 (P = 0.003), structural pulmonary abnormality (P = 0.030), past history of childhood cancer (P = 0.018), an ASA grade >II (P<0.001), undergoing a revision surgery versus a primary surgery (P = 0.039), a length of stay >4 days (P<0.001), and the occurrence of a predischarge complication (P = 0.003) were independent predictors associated with a non-home discharge disposition.

Conclusion.
In the current era of evolving health-care in which there is an increased focus toward decreasing costs, providers should consider utilizing these data to preoperatively identify patients who can be discharged to facility, and tailor an appropriate postoperative course of care aimed at expediting discharge processes to curb the financial burden of a prolonged length of stay.

Level of Evidence: 3
INNER MACULAR CHANGES AFTER VITRECTOMY WITH INTERNAL LIMITING MEMBRANE PEELING FOR RHEGMATOGENOUS RETINAL DETACHMENT
Authors: Fukukita Hiroshi , Ito Yasuki , Iwase Takeshi , Kaneko Hiroki , Yasuda Shunsuke , Kataoka Keiko , Terasaki Hiroko 
Published: September 2018

Purpose:
The internal limiting membrane (ILM), the innermost basement membrane of the retina, is peeled occasionally during vitreous surgery. This study aimed to investigate the effect of ILM loss on the retina.

Methods:
We used optical coherence tomography to retrospectively evaluate retinal changes in 26 eyes (11 ILM-peeled and 15 ILM-unpeeled eyes) of 26 patients after vitrectomy for retinal detachment. In addition, we studied six eyes of three patients with Alport syndrome, in which ILM is genetically impaired.

Results:
We observed significant inner retinal displacement of the foveal pit toward the optic disk with inner retinal thickening in the nasal area (fellow, 191.9 ± 24.3 μm vs. affected, 210.3 ± 31.4 μm; P = 0.048), inner retinal thinning in the temporal area (fellow, 174.3 ± 18.3 μm vs. affected, 142.2 ± 23.6 μm; P < 0.001), foveal thickening (ILM-unpeeled, 217.0 ± 39.4 μm vs. ILM-peeled, 302.0 ± 86.2 μm; P = 0.006), inner retinal dimples predominantly in the temporal area, and deviation between the foveal pit and foveal bulge. Eyes with Alport syndrome exhibited similar findings.

Conclusion:
Internal limiting membrane loss seems to cause characteristic inner retinal changes of the macula in both congenital and acquired conditions.
First Report on Detection of Dengue Virus in the Donor Cornea
Authors: Janani Madhuravasal Krishnan , Durgadevi Parthasarathy , Padmapriya Jayavel , Malathi Jambulingam , Kulandai Lily Therese , Rao Madhavan Hajib Narahari 
Published: September 2018

Background:
Dengue fever is the most prevalent form of flavivirus infection in humans. We have investigated whether corneoscleral tissue of the donor affected by dengue virus (DENV) harbors the virus.

Purpose:
To identify the risk for viral transmission through corneal transplants in areas where DENV circulates.

Methods:
Excised corneoscleral tissue from a cadaver with a history of viral hemorrhagic fever was analyzed using reverse transcriptase-polymerase chain reaction for the presence of DENV and chikungunya virus (CHIV).

Results:
DENV was detected in RNA extracted from the donor corneoscleral rim. Further genotyping of the viral isolate from the virus-infected cell harvest revealed DENV type 3 as the causative agent. CHIV was not detected.

Conclusions:
The data presented in this study recommend the implementation of polymerase chain reaction for detection of DENV and CHIV to analyze excised corneoscleral tissue of a donor with viral hemorrhagic fever.
Role of pvdE Pyoverdine Synthesis in Pseudomonas aeruginosa Keratitis
Authors: Suzuki Takashi , Okamoto Sayuri , Oka Naoko , Hayashi Naoki , Gotoh Naomasa , Shiraishi Atsushi 
Published: September 2018

Purpose:

Pseudomonas aeruginosa produces pyoverdine, encoded by the pvdE gene, for high-affinity iron uptake from transferrin and lactoferrin. This study investigated the contribution of pyoverdine to P. aeruginosa keratitis pathogenesis using in vitro and in vivo models.

Methods:
The P. aeruginosa strains examined were parental strain PAO1 and isogenic mutant strain pvdE (ΔpvdE) defective in pyoverdine. Bacterial growth in vitro was determined by PAO1 and ΔpvdE optical densities in Luria–Bertani (LB) broth. PAO1 or ΔpvdE (108 colony-forming units/mL) was inoculated onto cultured human corneal epithelial cells (HCECs) for 1 hour. The monolayers were examined for bacterial adhesion and invasion. In addition, the corneas of C57BL/6 mice were infected with PAO1 or ΔpvdE. Corneal virulence was evaluated by determining clinical scores and bacterial counts during infection.

Results:
The growth of PAO1 and ΔpvdE in LB broth was similar. Although adhesion of ΔpvdE onto HCECs was significantly increased compared with PAO1, the invasive capacity of ΔpvdE was significantly decreased. Clinical scores and bacterial numbers were significantly lower in ΔpvdE-infected eyes compared with PAO1-infected eyes at 6, 24, and 48 hours (P < 0.001). ΔpvdE was not detected in mouse corneas and did not induce corneal opacity at 6, 24, or 48 hours.

Conclusions:
ΔpvdE lost invasive ability toward HCECs. Moreover, ΔpvdE did not cause keratitis in vivo. Thus, pvdE pyoverdine synthesis has critical roles in proliferation and invasion on ocular surfaces and could be a target for prevention of P. aeruginosa keratitis.
Fuchs Endothelial Corneal Dystrophy and Mitochondria
Authors: Miyai Takashi 
Published: September 2018

Abstract:
Fuchs endothelial corneal dystrophy (FECD) is a bilateral progressive corneal endothelial disease characterized by guttae, which present as partial Descemet membrane thickening, inducing corneal edema at the final stage. Oxidative stress has been reported to play an important role in the pathogenesis of FECD. The electron transport chain and oxidative phosphorylation (oxphos) system in mitochondria are the main sources of endogenous oxidative stress, arising from superoxide generation through premature electron leakage to oxygen. In FECD, corneal endothelial cells have altered mitochondria with mitochondrial DNA damage, decreased oxphos proteins, and lower mitochondrial membrane potential. Mitochondrial dynamics and mitophagy comprise the organelle-level mitochondrial quality control system. Mitochondrial dynamics includes fusion and fission processes. When mitochondria are severely damaged, fission becomes the dominant process to remove damaged mitochondria. Mitophagy is a selective autophagy pathway that removes damaged mitochondria, and is triggered by mitochondrial membrane potential depolarization. In the FECD corneal endothelium, mitochondria have a fission-dominant morphology and low density through mitophagy upregulation because of quality control processes against altered mitochondria.
Congenital Corneal Opacities Associated With Trisomy 8 Mosaicism Syndrome
Authors: Welsh Christopher , Khalili Sina , Hazrati Lili-Naz , Mireskandari Kamiar 
Published: September 2018

Purpose:
To describe the clinical, anterior segment optical coherence tomography (OCT) and histopathological features of 2 infants with congenital corneal opacities (CCOs) and undiagnosed trisomy 8 mosaicism syndrome (T8mS).

Methods:
This is a retrospective case report documenting ocular and systemic findings, imaging, pathology and management of 2 patients with T8mS.

Results:
An 11-month-old white male infant and a 4-week-old Asian female were initially seen for unilateral and bilateral CCOs, respectively. Corneal examination revealed para-axial anterior stromal opacities with blood vessels. Superficial irregular opacities were seen on OCT, and specular microscopy revealed normal endothelial cell morphology. One eye required superficial keratectomy to clear the visual axis and developed steroid-induced glaucoma in the early postoperative period, successfully treated with goniotomy. Both patients had hyperopia, anisometropia, and amblyopia, which was managed with glasses and patching. Cytogenetic testing (through microarray and fluorescence in situ hybridization) later diagnosed T8mS in both cases.

Conclusions:
T8mS should be considered in the differential diagnosis for superficial CCOs with blood vessels. Anterior segment OCT can guide management and cytogenetics performed to confirm diagnosis. Systemic associations and, in particular, risk of acute myeloid leukemia and myelodysplastic syndromes warrant prompt diagnosis of this condition.
Exploring the transcriptome of resident spinal microglia after collagen antibody–induced arthritis
Authors: Fernandez-Zafra Teresa , Gao Tianle , Jurczak Alexandra , Sandor Katalin , Hore Zoe , Agalave Nilesh M. , Su Jie , Estelius Johanna , Lampa Jon , Hokfelt Tomas , Wiesenfeld-Hallin Zsuzsanna , Xu Xiaojun , Denk Franziska , Svensson Camilla I. 
Published: September 2018

Abstract
Recent studies have suggested a sexually dimorphic role of spinal glial cells in the maintenance of mechanical hypersensitivity in rodent models of chronic pain. We have used the collagen antibody–induced arthritis (CAIA) mouse model to examine differences between males and females in the context of spinal regulation of arthritis-induced pain. We have focused on the late phase of this model when joint inflammation has resolved, but mechanical hypersensitivity persists. Although the intensity of substance P, calcitonin gene–related peptide, and galanin immunoreactivity in the spinal cord was not different from controls, the intensity of microglia (Iba-1) and astrocyte (glial fibrillary acidic protein) markers was elevated in both males and females. Intrathecal administration of the glial inhibitors minocycline and pentoxifylline reversed mechanical thresholds in male, but not in female mice. We isolated resident microglia from the lumbar dorsal horns and observed a significantly lower number of microglial cells in females by flow cytometry analysis. However, although genome-wide RNA sequencing results pointed to several transcriptional differences between male and female microglia, no convincing differences were identified between control and CAIA groups. Taken together, these findings suggest that there are subtle sex differences in microglial expression profiles independent of arthritis. Our experiments failed to identify the underlying mRNA correlates of microglial actions in the late phase of the CAIA model. It is likely that transcriptional changes are either subtle and highly localised and therefore difficult to identify with bulk isolation techniques or that other factors, such as changes in protein expression or epigenetic modifications, are at play.
Targeting the Nav1.8 ion channel engenders sex-specific responses in lysophosphatidic acid–induced joint neuropathy
Authors: O'Brien Melissa S. , Philpott Holly T.A. , McDougall Jason J. 
Published: September 2018

Abstract
Joint neuropathic pain occurs in a subset of arthritis patients, and lysophosphatidic acid (LPA) has been implicated as a mediator of joint neuropathy. The mechanism by which LPA promotes neuropathic pain is unknown but may be related to altered signalling of the voltage-gated sodium channel Nav1.8 located on nociceptors. Because arthritis and neuropathic pain are more prevalent in females, this study aimed to explore potential sex differences in the development of LPA-induced joint neuropathy and whether Nav1.8 played a role in the associated neuropathic pain. Joint neuropathy was induced in male and female Wistar rats (179-284 g) by intra-articular injection of 50-µg LPA. Pain behaviour was assessed over 21 days using von Frey hair algesiometry. On day 21, electrophysiological recordings of joint primary afferents were conducted to measure peripheral sensitisation. Saphenous nerve morphology and expression of the nerve-damage marker ATF3 and Nav1.8 in ipsilateral dorsal root ganglions were compared on the basis of sex. The analgesic properties of the selective Nav1.8 antagonist A-803467 was determined in pain behaviour and electrophysiology experiments. Females developed more severe mechanical allodynia than males after LPA treatment. Lysophosphatidic acid caused more pronounced demyelination of the saphenous nerve in females, but no sex differences were observed in the expression of ATF3 or Nav1.8 in dorsal root ganglion neurones. Blockade of Nav1.8 channels with A-803467 resulted in a decrease in joint mechanosensitivity and secondary allodynia with females exhibiting a greater response. These findings suggest that LPA has sex-specific effects on joint neuropathy and Nav1.8 gating, which should be considered when treating neuropathic arthritis patients.
Contribution of dorsal root ganglion octamer transcription factor 1 to neuropathic pain after peripheral nerve injury
Authors: Yuan Jingjing , Wen Jing , Wu Shaogen , Mao Yuanyuan , Mo Kai , Li Zhisong , Su Songxue , Gu Hanwen , Ai Yanqiu , Bekker Alex , Zhang Wei , Tao Yuan-Xiang 
Published: September 2018

Abstract
Neuropathic pain genesis is related to gene alterations in the dorsal root ganglion (DRG) after peripheral nerve injury. Transcription factors control gene expression. In this study, we investigated whether octamer transcription factor 1 (OCT1), a transcription factor, contributed to neuropathic pain caused by chronic constriction injury (CCI) of the sciatic nerve. Chronic constriction injury produced a time-dependent increase in the level of OCT1 protein in the ipsilateral L4/5 DRG, but not in the spinal cord. Blocking this increase through microinjection of OCT1 siRNA into the ipsilateral L4/5 DRG attenuated the initiation and maintenance of CCI-induced mechanical allodynia, heat hyperalgesia, and cold allodynia and improved morphine analgesia after CCI, without affecting basal responses to acute mechanical, heat, and cold stimuli as well as locomotor functions. Mimicking this increase through microinjection of recombinant adeno-associated virus 5 harboring full-length OCT1 into the unilateral L4/5 DRG led to marked mechanical allodynia, heat hyperalgesia, and cold allodynia in naive rats. Mechanistically, OCT1 participated in CCI-induced increases in Dnmt3a mRNA and its protein and DNMT3a-mediated decreases in Oprm1 and Kcna2 mRNAs and their proteins in the injured DRG. These findings indicate that OCT1 may participate in neuropathic pain at least in part by transcriptionally activating Dnmt3a and subsequently epigenetic silencing of Oprm1 and Kcan2 in the DRG. OCT1 may serve as a potential target for therapeutic treatments against neuropathic pain.
Psychosocial Predictors of Adjustment to Disability Among Patients With Breast Cancer: A Cross-Sectional Descriptive Study
Authors: ZHANG Qingyue , XIAO Shan , YAN Ling , SUN Liyuan , WANG Yan , HUANG Mengqiu 
Published: September 2018

ABSTRACT

Background:
Acceptance of disability relates to the process of adaptation, which reflects how the values of a patient change over time to accept herself or himself as an intrinsically worthy person. Acceptance of disability (AOD) plays an important role in the adjustment of persons with physical disability to their environment. However, no studies on the level of AOD in patients with breast cancer are available in the literature.

Purpose:
The aim of this study was to explore the significant factors that influence disability acceptance in Chinese women with breast cancer.

Methods:
A cross-sectional study was conducted on 292 patients with breast cancer between January and April 2017. Participants were assessed using the Acceptance of Disability Scale-Revised, Medical Coping Modes Questionnaire, Sense of Coherence Scale, Social Relational Quality Scale, and general information questionnaire. Multiple regression analysis was used to determine the factors associated with the level of disability acceptance.

Results:
The mean score for AOD was 79.14 and ranged from 32 to 128. Multiple regression analysis indicated that family intimacy, friendships, confrontation, manageability, family commitment, marital status, surgery, and acceptance–resignation significantly affected disability acceptance, explaining 49.1% of the total variance in disability acceptance.

Conclusions/Implications for Practice:
The participants had a moderate level of disability acceptance. Disability acceptance is an important factor in the psychosocial adaptation to cancer. Healthcare staff should pay special attention to low scores for this factor and explore the potential of psychological interventions to effectively reduce the posttraumatic stress response, encourage the adoption of positive coping strategies, and hasten disability acceptance and return to society.
Unique Circulating MicroRNA Profiles in HIV Infection
Authors: Narla Venkata , Bhakta Nirav , Freedman Jane E. , Tanriverdi Kahraman , Maka Kristinalisa , Deeks Steven G. , Ganz Peter , Hsue Priscilla 
Published: September 2018

Objective:
MicroRNAs (miRNAs) are noncoding RNAs that regulate gene expression. We aimed to determine the association between extracellular miRNAs and HIV infection.

Design:
Single-center, cross-sectional study.

Methods:
We analyzed the expression of 192 plasma-derived miRNAs in 69 HIV-infected individuals and 24 uninfected controls using TaqMan miRNA assays and a high-throughput Real-Time PCR instrument (Fluidigm). False discovery rate (FDR) was applied.

Results:
HIV-infected individuals and controls were similar in age, sex, and traditional risk factors. Among those with HIV, 72.5% were on antiretroviral therapy (ARVs) and 64% had an undetectable viral load. Twenty-nine miRNAs were differentially expressed in the plasma of HIV-infected individuals compared with controls (P < 0.05, FDR < 0.15). Nineteen miRNAs were differentially expressed among HIV+ subjects on ARVs, HIV+ subjects not on ARVs, and HIV− subjects (P < 0.05 and FDR < 0.15). Thirty-four miRNAs were differentially expressed between HIV− subjects and elite controllers (ie, suppressed viral loads despite the absence of ARVs; P < 0.05 and FDR < 0.15). These 34 miRNAs included miRs-29c, 146b, 223, and 382, which were previously reported to have intracellular roles in HIV latency, as well as miRs-126, 145, and let-7, which were previously shown to be differentially expressed in coronary artery disease among uninfected individuals.

Conclusions:
We demonstrate a unique expression profile of 29 miRNAs in HIV+ subjects and 34 miRNAs in elite controllers as compared to HIV− subjects. These miRNA signatures may be useful in further elucidating mechanisms of viral and immunological control and may have diagnostic or prognostic value in HIV-associated coronary artery disease.
Brief Report: Hyperbilirubinemia Is Associated With a Decreased Risk of Carotid Atherosclerosis in HIV-Infected Patients on Virological Suppression
Authors: Muccini Camilla , Galli Laura , Poli Andrea , Carbone Alessia , Maillard Myriam , Giusti Maria Cristina , Spagnuolo Vincenzo , Bigoloni Alba , Guffanti Monica , Gianotti Nicola , Lazzarin Adriano , Castagna Antonella 
Published: September 2018

Objective:
To investigate the association between total, direct, and indirect bilirubin and the presence of carotid lesions in a large sample of HIV-1–infected patients on virological suppression.

Design:
Retrospective study on adult HIV-1–infected patients, with a carotid ultrasound (CUS) examination performed between January 2008 and August 2016, with HIV-RNA <50 copies per milliliter at CUS and without previous cardiovascular events.

Methods:
Intima media thickness was measured in 4 segments: carotid common artery and bifurcation on the left and right sides. Carotid lesion was defined as an intima media thickness ≥1.5 mm in ≥1 region at CUS. Patients were classified as: normal if all bilirubin values before CUS were below the upper normal limit and with hyperbilirubinemia if ≥1 bilirubin value above upper normal limit before CUS was recorded. Multivariate logistic regression was used to determine whether hyperbilirubinemia showed association with the presence of ≥1 carotid lesion, after adjusting for confounding factors.

Results:
Overall, 903 patients were evaluated, 511 with ≥1 and 392 without carotid lesions. At multivariate analysis, total [adjusted odds ratio (95% confidence interval) 0.57 (0.36 to 0.90), P = 0.016] and indirect hyperbilirubinemia before CUS [adjusted odds ratio (95% confidence interval) 0.62 (0.40 to 0.97), P = 0.036] were associated with a lower risk of carotid lesions in addition to younger age, negative hepatitis C virus antibodies, higher nadir CD4+, lower low-density lipoprotein cholesterol, higher high-density lipoprotein cholesterol, lower triglycerides, and no use of statin; no effect of atazanavir treatment on carotid lesions was detected.

Conclusions:
In HIV-1–treated patients, total or indirect hyperbilirubinemia was likely associated with the absence of carotid lesions.