bluuebunny/crossref_metadata_2025_split huggingface dataset:
Fusidic Acid: A Neglected Risk Factor for Statin-Associated Myopathy
Authors: Rönnqvist Josefine , Hallberg Pär , Yue Qun-Ying , Wadelius Mia 
Published: December 2018

Background: Statins are widely used lipid-lowering drugs used for the prevention of cardiovascular disease. Statins are known to cause myopathy, an adverse drug reaction with various clinical features rhabdomyolysis. Objective: To describe clinical characteristics of statin-treated individuals who experienced myopathy and identify risk factors of statin-associated myopathy. Methods: A retrospective study was conducted on cases of statin-associated myopathy reported to the Swedish Medical Products Agency. Clinical factors were compared between cases and statin-treated controls not diagnosed with myopathy. Statistical methods were univariate and multivariate logistic regression and results were presented as odds ratio (OR) with 95% confidence interval (CI). To correct for multiple comparisons, the cutoff for statistical significance was set to P < .0017. Results: In total, 47 cases of statin-associated myopathy were compared with 3871 treated controls. Rhabdomyolysis was diagnosed in 51% of the cases. Markers for cardiovascular disease were more common in cases than controls. Statistical analysis revealed the following independent risk factors for myopathy: high statin dose (OR = 1.54, calculated using the standard deviation 19.82, 95% CI = 1.32-1.80, P < .0001), and concomitant treatment with fusidic acid (OR = 1002, 95% CI = 54.55-18 410, P < .0001), cyclosporine (OR = 34.10, 95% CI = 4.43-262.45, P = .0007), and gemfibrozil (OR = 12.35, 95% CI = 2.38-64.10, P = .0028). Conclusions: The risk of myopathy increases with statin dose and cotreatment with cyclosporine and gemfibrozil. Concomitant fusidic acid has previously only been noted in a few case reports. Considering that use of fusidic acid may become more frequent, it is important to remind of this risk factor for statin-associated myopathy.
Patients’ Expectations for Longevity of Kidney Transplant
Authors: Gruttadauria Michelle , Dunn Colin , Lin Juan , Kaminetsky Joshua R. , Applebaum Kayla , Portal Daniella , Mohammed Omar , Rocca Juan , Greenstein Stuart 
Published: December 2018

Introduction: Prior to transplantation, the transplant team is responsible for transplant education and posttransplant expectations. The majority of outcomes research focuses on 1- and 3-year graft survival, with a lack of literature focused upon whether patients have a realistic understanding of how many years deceased donor kidneys can be expected to function after transplant. Objective: To determine whether potential kidney transplant patients’ expectations for how long a deceased donor kidney will function after transplantation differs from transplant surgeons, using quantitative analysis. Design: A cross-sectional survey was used with potential adult kidney transplant recipients and transplant surgeons. Patient surveys included demographics, quality-of-life questions, and questions of expectations of kidney function for deceased donor kidneys from the Kidney Donor Profile Index. The survey categorized donor organ risk as 0% to 20%, 21% to 85%, and 86% to 100%, and results were compared to responses from US Transplant Surgeons. Surgeons were contacted via e-mail using an online survey program. Results: Responses included 154 transplant surgeons and 172 patients. Surgeon and patient responses were compared using Fisher exact test, showing a significant difference in each of the donor organ categories. We found that 47% of patient respondents did not correctly interpret the Kidney Donor Profile Index continuum. Conclusion: In every organ donor category, patients had a significantly different expectation for how long a transplanted kidney will last after transplant when compared to transplant surgeons. More study is required to determine why 47% of patients did not correctly interpret the Kidney Donor Profile continuum.
Complications and Readmissions After Total Knee Replacement in Octogenarians and Nonagenarians
Authors: Yohe Nicholas , Funk August , Ciminero Matthew , Erez Orry , Saleh Ahmed 
Published: December 2018

Introduction: From 2000 to 2010, the cohort of patients aged 85 to 94 years had the fastest growth rate increasing in size by approximately 30%. The need for total knee arthroplasty (TKA) continues to increase with a larger percentage of patients older than 80 years requiring TKA. The purpose of our study was to examine the rate and risks of 30-day complications and unplanned readmission in patients older than 80 years. Materials and Methods: The National Surgical Quality Improvement Project database for the years 2008 to 2014 was queried for patients older than 80 years undergoing TKA. The risks of major complications, minor complications, bleeding occurrences, unplanned readmissions, and deaths over a 30-day period were examined using univariate and multivariate analyses. Results: Overall, 12 026 patients were included for analysis. In all, 422 (3.5%) experienced a major complication, 2316 (19.3%) experienced a minor complication, 2074 (17.2%) had a bleeding occurrence requiring transfusion, and 566 (4.7%) experienced an unplanned readmission. Thirty-eight (0.3%) deaths were recorded. There were no significant risk factors for major complications. Patients with an American Society of Anesthesiologists (ASA) >2 (odds ratio [OR]: 1.43 [1.239-1.651]), patients older than 84 years (OR: 1.240 [1.072-1.434]), and patients receiving general anesthesia (OR: 1.191 [1.035-1.370]) had increased risks of minor complications. Patients with a body mass index >30 (OR: 0.640 [0.532-0.770]) and men (OR: 0.815 [0.706-0.941]) had reduced rates of minor complications. Increased risk of unplanned readmission occurred in patients with chronic obstructive pulmonary disease (OR: 1.694 [1.007-2.850]) and congestive heart failure (OR: 3.030 [1.121-8.192]). Increased risk of death was seen in patients with an ASA >2 (OR: 8.9 [1.144-69.82]). Discussion/Conclusion: Elderly patients undergoing TKA have high complication and readmission rates. Surgeons should convey these increased risk factors and rates of complications in elective TKAs to their elderly patients and work with primary care physicians to mitigate these risks.
Axillary Nerve Position in Humeral Avulsions of the Glenohumeral Ligament
Authors: Bokor Desmond J. , Raniga Sumit , Graham Petra L. 
Published: December 2018

Background: The axillary nerve is at risk during repair of a humeral avulsion of the glenohumeral ligament (HAGL). Purpose: To measure the distance between the axillary nerve and the free edge of a HAGL lesion on preoperative magnetic resonance imaging (MRI) and compare these findings to the actual intraoperative distance measured during open HAGL repair. Study Design: Case series; Level of evidence, 4. Methods: A total of 25 patients with anterior instability were diagnosed as having a HAGL lesion on MRI and proceeded to open repair. The proximity of the axillary nerve to the free edge of the HAGL lesion was measured intraoperatively at the 6-o’clock position relative to the glenoid face. Preoperative MRI was then used to measure the distance between the axillary nerve and the free edge of the HAGL lesion at the same position. Distances were compared using paired t tests and Bland-Altman analyses. Results: The axillary nerve lay, on average, 5.60 ± 2.51 mm from the free edge of the HAGL lesion at the 6-o’clock position on preoperative MRI, while the mean actual intraoperative distance during open HAGL repair was 4.84 ± 2.56 mm, although this difference was not significant ( P = .154). In 52% (13/25) of patients, the actual intraoperative distance of the axillary nerve to the free edge of the HAGL lesion was overestimated by preoperative MRI. In 36% (9/25), this overestimation of distance was greater than 2 mm. Conclusion: The observed overestimations, although not significant in this study, suggest a smaller safety margin than might be expected and hence a substantially higher risk for potential damage. We recommend that shoulder surgeons exercise caution in placing capsular sutures in the lateral edge when contemplating arthroscopic repair of HAGL lesions, as the proximity of the nerve to the free edge of the HAGL tear is small enough to be injured by arthroscopic suture-passing instruments.
Bilateral Choroidal Osteomas in Rosai-Dorfman Disease
Authors: Storey Philip P. , de Koo Lisa Olmos , Berry Jesse 
Published: December 2018

Purpose: The purpose of this case report is to describe a case of bilateral choroidal osteomas in Rosai-Dorfman disease, a rare pseudolymphomatous disorder. Methods: A case report was conducted. Results: A middle-aged man with biopsy-proven Rosai-Dorfman disease presented with chronic poor vision of the left eye. Clinical examination showed bilateral white lesions with scalloped edges, and optical coherence tomography revealed hyporeflective choroidal lesions. Ultrasonography confirmed the lesions as choroidal osteomas. The patient was observed and remains stable after 9 months of follow-up. Conclusions: Bilateral choroidal osteomas in the setting of Rosai-Dorfman disease are an uncommon finding. While the best treatment for the disease remains unclear, observation is a reasonable option for stable patients.
Targeting Sirt-1 controls GVHD by inhibiting T-cell allo-response and promoting Treg stability in mice
Authors: Daenthanasanmak Anusara , Iamsawat Supinya , Chakraborty Paramita , Nguyen Hung D. , Bastian David , Liu Chen , Mehrotra Shikhar , Yu Xue-Zhong 
Published: December 2018

Abstract
Graft-versus-host disease (GVHD) remains one of the major complications after allogeneic bone marrow transplantation (allo-BMT). Sirtuin-1 (Sirt-1) plays a crucial role in various biological processes including cellular senescence, metabolism, and inflammatory responses. Sirt-1 deacetylation regulates different transcription factors that are important for modulating immune responses. In the current study, we addressed the role of Sirt-1 in GVHD induction by employing Sirt-1 conditional knockout mice as well as a pharmacological Sirt-1 inhibitor. Using major histocompatibility complex (MHC)–mismatched and MHC-matched murine BMT models, we found that Sirt-1−/− T cells had a reduced ability to induce acute GVHD (aGVHD) via enhanced p53 acetylation. Sirt-1-deficient T cells also promoted induced regulatory T cell (iTreg) differentiation and inhibited interferon-γ production after allo-BMT. Sirt-1 deletion in iTregs increased Foxp3 stability and restrained iTreg conversion into pathogenic T cells. Furthermore, we found that administration with a Sirt-1 inhibitor, Ex-527, significantly improved recipient survival and clinical scores, with no signs of tumor relapse. These results indicate that Sirt-1 inhibition can attenuate GVHD while preserving the graft-versus-leukemia effect. Consistently, Sirt-1-deficient T cells also displayed a remarkably reduced ability to induce chronic GVHD (cGVHD). Mechanistic studies revealed that Sirt-1 deficiency in T cells enhanced splenic B-cell reconstitution and reduced follicular T helper cell development. Sirt-1 deficiency in T cells modulated donor B-cell responses reducing both B-cell activation and plasma cell differentiation. In addition, therapeutic Sirt-1 inhibition could both prevent cGVHD and reduce established cGVHD. In conclusion, Sirt-1 is a promising therapeutic target for the control of aGVHD and cGVHD pathogenesis and possesses high potential for clinical application.
Cerebral Edema and Elevated Intracranial Pressure
Authors: Koenig Matthew A. 
Published: December 2018

ABSTRACT

PURPOSE OF REVIEW
This article reviews the management of cerebral edema, elevated intracranial pressure (ICP), and cerebral herniation syndromes in neurocritical care.

RECENT FINDINGS
While corticosteroids may be effective in reducing vasogenic edema around brain tumors, they are contraindicated in traumatic cerebral edema. Mannitol and hypertonic saline use should be tailored to patient characteristics including intravascular volume status. In patients with traumatic brain injury who are comatose, elevated ICP should be managed with an algorithmic, multitiered treatment protocol to maintain an ICP of 22 mm Hg or less. Third-line ICP treatments include anesthetic agents, induced hypothermia, and decompressive craniectomy. Recent clinical trials have demonstrated that induced hypothermia and decompressive craniectomy are ineffective as early neuroprotective strategies and should be reserved for third-line management of refractory ICP elevation in severe traumatic brain injury. Monitoring for cerebral herniation should include bedside pupillometry in supratentorial space-occupying lesions and recognition of upward herniation in patients with posterior fossa lesions.

SUMMARY
Although elevated ICP, cerebral edema, and cerebral herniation are interrelated, treatments should be based on the distinct pathophysiologic process. Focal lesions resulting in brain compression are primarily managed with surgical decompression, whereas global or multifocal brain injury requires a treatment protocol that includes medical and surgical interventions.
Coma and Brain Death
Authors: Rabinstein Alejandro A. 
Published: December 2018

ABSTRACT

PURPOSE OF REVIEW
This article discusses the diagnostic and therapeutic approach to patients who are comatose and reviews the current knowledge on prognosis from various causes of coma. This article also provides an overview of the principles for determination of brain death as well as advice on how to avoid common pitfalls.

RECENT FINDINGS
Technologic advances have refined our understanding of the physiology of consciousness and the spectrum of disorders of consciousness; they also promise to improve our prognostic accuracy. Yet the clinical principles for the evaluation and treatment of coma remain unaltered. The clinical standards for determination of death by neurologic criteria (ie, brain death) are also well established, although variabilities in local protocols and legal requirements remain a problem to be resolved.

SUMMARY
Effective evaluation of coma demands a systematic approach relying on clinical information to ensure rational use of laboratory and imaging tests. When the cause of coma is deemed irreversible in the setting of a catastrophic brain injury and no clinical evidence exists for brain and brainstem function, patients should be evaluated for the possibility of brain death by following the clinical criteria specified in the American Academy of Neurology guidelines.
Status Epilepticus, Refractory Status Epilepticus, and Super-refractory Status Epilepticus
Authors: Nelson Sarah E. , Varelas Panayiotis N. 
Published: December 2018

ABSTRACT

PURPOSE OF REVIEW
Status epilepticus, refractory status epilepticus, and super-refractory status epilepticus can be life-threatening conditions. This article presents an overview of the three conditions and discusses their management and outcomes.

RECENT FINDINGS
Status epilepticus was previously defined as lasting for 30 minutes or longer but now is more often defined as lasting 5 minutes or longer. A variety of potential causes exist for status epilepticus, refractory status epilepticus, and super-refractory status epilepticus, but all three ultimately involve changes at the cellular and molecular level. Management of patients with status epilepticus generally requires several studies, with EEG of utmost importance given the pathophysiologic changes that can occur during the course of status epilepticus. Status epilepticus is treated with benzodiazepines as first-line antiepileptic drugs, followed by phenytoin, valproic acid, or levetiracetam. If status epilepticus does not resolve, these are followed by an IV anesthetic and then alternative therapies based on limited data/evidence, such as repetitive transcranial magnetic stimulation, therapeutic hypothermia, immunomodulatory agents, and the ketogenic diet. Scores have been developed to help predict the outcome of status epilepticus. Neurologic injury and outcome seem to worsen as the duration of status epilepticus increases, with outcomes generally worse in super-refractory status epilepticus compared to status epilepticus and sometimes also to refractory status epilepticus.

SUMMARY
Status epilepticus can be a life-threatening condition associated with multiple complications, including death, and can progress to refractory status epilepticus and super-refractory status epilepticus. More studies are needed to delineate the best management of these three entities.
Management of Stroke in the Neurocritical Care Unit
Authors: Venkatasubba Rao Chethan P. , Suarez Jose I. 
Published: December 2018

ABSTRACT

PURPOSE OF REVIEW
This article provides updated information regarding the diagnosis and treatment (specifically critical care management) of acute ischemic stroke. This article also discusses the increased use of thrombolysis and thrombectomy in clinical practice.

RECENT FINDINGS
Stroke is the leading cause of disability in the United States. A significant proportion of patients with acute ischemic stroke require critical care management. Much has changed in the early evaluation and treatment of patients presenting with acute ischemic stroke. The introduction of embolectomy in large vessel occlusions for up to 24 hours post–symptom onset has resulted in one in every three eligible patients with acute ischemic stroke with the potential to lead an independent lifestyle. These patients increasingly require recognition of complications and initiation of appropriate interventions as well as earlier admission to dedicated neurocritical care units to ensure better outcomes.

SUMMARY
This article emphasizes issues related to the management of patients with acute ischemic stroke undergoing mechanical thrombectomy and thrombolysis and addresses the complex physiologic changes affecting neurologic and other organ systems.
Intracerebral Hemorrhage
Authors: Ziai Wendy C. , Carhuapoma J. Ricardo 
Published: December 2018

ABSTRACT

PURPOSE OF REVIEW
This article describes the advances in the management of spontaneous intracerebral hemorrhage in adults.

RECENT FINDINGS
Therapeutic intervention in intracerebral hemorrhage has continued to focus on arresting hemorrhage expansion, with large randomized controlled trials addressing the effectiveness of rapidly lowering blood pressure, hemostatic therapy with platelet transfusion, and other clotting complexes and clot volume reduction both of intraventricular and parenchymal hematomas using minimally invasive techniques. Smaller studies targeting perihematomal edema and inflammation may also show promise.

SUMMARY
The management of spontaneous intracerebral hemorrhage, long relegated to the management and prevention of complications, is undergoing a recent evolution in large part owing to stereotactically guided clot evacuation techniques that have been shown to be safe and that may potentially improve outcomes.
Subarachnoid Hemorrhage
Authors: Muehlschlegel Susanne 
Published: December 2018

ABSTRACT

PURPOSE OF REVIEW
This article reviews the epidemiology, clinical presentation, diagnosis, and management of patients with aneurysmal subarachnoid hemorrhage (SAH). SAH is a type of hemorrhagic stroke and is a neurologic emergency with substantial morbidity and mortality. This article reviews the most common and potentially life-threatening neurologic and medical complications to promote their early recognition and prevent secondary brain injury.

RECENT FINDINGS
Over the past 30 years, the incidence of SAH has remained stable; yet, likely because of improved care in specialized neurocritical care units, discharge mortality has considerably decreased. Two consensus guidelines by the American Heart Association/American Stroke Association and the Neurocritical Care Society have outlined best practices for the management of patients with SAH. The most important recommendations include admission of patients to high-volume centers (defined as more than 35 SAH admissions per year) under the management of a multidisciplinary, specialized team; expeditious identification and treatment of the bleeding source with evaluation by a multidisciplinary team consisting of cerebrovascular neurosurgeons, neuroendovascular specialists, and neurointensivists; management of patients in a neurocritical care unit with enteral nimodipine, blood pressure control, euvolemia, and close monitoring for neurologic and medical complications; and treatment of symptomatic cerebral vasospasm/delayed cerebral ischemia with induced hypertension and endovascular therapies. This article also highlights new insights of SAH pathophysiology and provides updates in the management approach.

SUMMARY
SAH remains a neurologic emergency. Management of patients with SAH includes adherence to published guidelines, but some areas of SAH management remain understudied. Clinical trials are required to elucidate the role of these controversial management approaches in improving patient outcomes.
EGCG protects cardiomyocytes against hypoxia-reperfusion injury through inhibition of OMA1 activation
Authors: Nan Jinliang , Nan Cunjin , Ye Jian , Qian Lu , Geng Ya , Xing Dawei , Rahman Muhammad Saif Ur , Huang Mingyuan 
Published: December 2018

ABSTRACT
Mitochondria are important for energy production and cardiomyocyte homeostasis. OMA1, a metalloendopeptidase, initiates the proteolytic process of the fusion-allowing protein OPA1, to deteriorate mitochondrial structure and function. In this study, mouse embryonic fibroblasts (MEFs) and neonatal mouse cardiomyocytes (NMCMs) subjected to hypoxia-reperfusion injury (HRI) and/or H2O2 were used to mimic oxidative stress in the heart following ischemia-reperfusion injury (IRI). In vitro experiments demonstrated that HRI or stimulation with H2O2 induced self-cleavage of OMA1 and the subsequent conversion of OPA1 from its long form to its short form, leading to mitochondrial fragmentation, cytochrome c release and apoptosis. By using Molecular Operating Environment (MOE) software to simulate the binding interaction of 2295 phytochemicals against OMA1, epigallocatechin gallate (EGCG) and betanin were selected as candidates of OMA1 inhibitor. We found that EGCG directly interacted with OMA1 and potently inhibited self-cleavage of OMA1, leading to attenuated OPA1 cleavage. This study, therefore, suggests to use OMA1 inhibition induced by EGCG to treat cardiac IRI.