Developing a Cost-Effective Surgical Scheduling System Applying Lean Thinking and Toyota's Methods for Surgery-Related Big Data for Improved Data Use in Hospitals: User-Centered Design Approach.

BACKGROUND: Surgical scheduling is pivotal in managing daily surgical sequences, impacting patient experience and hospital resources significantly. With operating rooms costing approximately US $36 per minute, efficient scheduling is vital. However, global practices in surgical scheduling vary, largely due to challenges in predicting individual surgeon times for diverse patient conditions. Inspired by the Toyota Production System's efficiency in addressing similar logistical challenges, we applied its principles as detailed in the book "Lean Thinking" by Womack and Jones, which identifies processes that do not meet customer needs as wasteful. This insight is critical in health care, where waste can compromise patient safety and medical quality. OBJECTIVE: This study aims to use lean thinking and Toyota methods to develop a more efficient surgical scheduling system that better aligns with user needs without additional financial burdens. METHODS: We implemented the 5 principles of the Toyota system: specifying value, identifying the value stream, enabling flow, establishing pull, and pursuing perfection. Value was defined in terms of meeting the customer's needs, which in this context involved developing a responsive and efficient scheduling system. Our approach included 2 subsystems: one handling presurgery patient data and another for intraoperative and postoperative data. We identified inefficiencies in the presurgery data subsystem and responded by creating a comprehensive value stream map of the surgical process. We developed 2 Excel (Microsoft Corporation) macros using Visual Basic for Applications. The first calculated average surgery times from intra- or postoperative historic data, while the second estimated surgery durations and generated concise, visually engaging scheduling reports from presurgery data. We assessed the effectiveness of the new system by comparing task completion times and user satisfaction between the old and new systems. RESULTS: The implementation of the revised scheduling system significantly reduced the overall scheduling time from 301 seconds to 261 seconds (P=.02), with significant time reductions in the revised process from 99 seconds to 62 seconds (P<.001). Despite these improvements, approximately 21% of nurses preferred the older system for its familiarity. The new system protects patient data privacy and streamlines schedule dissemination through a secure LINE group (LY Corp), ensuring seamless flow. The design of the system allows for real-time updates and has been effectively monitoring surgical durations daily for over 3 years. The "pull" principle was demonstrated when an unplanned software issue prompted immediate, user-led troubleshooting, enhancing system reliability. Continuous improvement efforts are ongoing, except for the preoperative patient confirmation step, which requires further enhancement to ensure optimal patient safety. CONCLUSIONS: Lean principles and Toyota's methods, combined with computer programming, can revitalize surgical scheduling processes. They offer effective solutions for surgical scheduling challenges and enable the creation of a novel surgical scheduling system without incurring additional costs.

Association of Autonomic Symptom Burden with Sudden Sensorineural Hearing Loss.

OBJECTIVE: To investigate the autonomic symptom burden in patients with sudden sensorineural hearing loss (SSNHL) and its association with the severity and prognosis. STUDY DESIGN: Observational prospective study. SETTING: Tertiary academic medical center. METHODS: Patients diagnosed with SSNHL at a single medical center completed the COMPASS 31 questionnaire, which assesses dysautonomia across 6 domains with 31 questions. A total COMPASS 31 score was calculated by summing the scores from each weighted domain. The treatment outcome was evaluated by the percentage of recovery, calculated as the hearing gain in pure tone average (PTA) after treatment divided by the pretreatment PTA difference between the 2 ears. We defined poor recovery as a percentage of recovery <80%. RESULTS: A total of 63 SSNHL patients were included. The mean COMPASS 31 score was 23.4 (SD 14). Patients with poor recovery had significantly higher COMPASS 31 scores than those with good recovery (mean 26.4 [SD 14.4] vs 16.9 [SD 10.4]; 95% confidence interval [CI] 2-17). There was a negative association between COMPASS 31 score and both hearing gain (r = -.323, 95% CI -0.082 to -0.529) and percentage of recovery (r = -.365, 95% CI -0.129 to -0.562). Multivariate analyses of independent factors indicate that patients with higher COMPASS 31 scores had a greater risk for poor recovery (OR 1.06 [95% CI 1.003-1.117]). CONCLUSION: This study highlights the association between autonomic symptom burden and poor hearing outcomes in SSNHL patients. The findings underscore the importance of evaluating autonomic function during the treatment of SSNHL.

Telbivudine-Induced Myopathy: Clinical Features, Histopathological Characteristics, and Risk Factors.

BACKGROUND AND PURPOSE: Oral nucleos(t)ide analogs (NAs) are the mainstay treatment for chronic hepatitis B (CHB). Myotoxicity is an important extrahepatic effect related to NA treatment. Telbivudine is the NA for CHB that is frequently associated with muscle-related side effects. The risk factors for telbivudine-induced myopathy (TIM) are not yet clear. METHODS: This study characterized the clinical, magnetic resonance images (MRI), and pathological features of 12 TIM cases. A group of telbivudine-tolerant (TT) patients with CHB who received regular telbivudine treatment during the same period without the occurrence of myopathy was collected. Demographic and clinical factors were compared between the patients with TIM and the TT controls. Factors independently associated with TIM were identified using logistic regression analysis. RESULTS: The patients with TIM (males/females: 7/5, mean age: 57 years) developed myopathy after using telbivudine for a median period of 19.5 months. Muscle histopathology revealed abnormal proliferation, subsarcolemmal or sarcoplasmic accumulations, and ultrastructural defects of mitochondria. When compared with TT cases, patients with TIM had a lower estimated glomerular filtration rate and were more frequently positive for hepatitis B e antigen (HBeAg). CONCLUSIONS: Mitochondrial abnormalities are characteristic histopathological features, and impaired renal function and HBeAg positivity are risk factors for TIM. Telbivudine-induced mitochondrial dysfunction and immune activation related to mitochondrial damage and HBeAg serostatus changes may underlie TIM. Constant clinical surveillance of myopathy during telbivudine treatment is needed due to the significant latency of its development. Dose adjustment for impaired renal function does not eliminate the risk of TIM occurrence.

Applicability of Oculomotor Tests for Predicting Central Vestibular Disorder Using Principal Component Analysis.

The videonystagmography oculomotor test battery is considered useful method for diagnosing vertigo. However, its role in diagnosing central vestibular disorder has not been clarified due to variations in interpretation. Patients (n = 103) with vertigo or dizziness symptoms undergoing the oculomotor tests and brain MRI within 1 month were analyzed. Two otology specialists retrospectively interpreted the oculomotor tests, and three neurology and neuroradiology specialists determined whether central lesions were present on brain MRI. Multivariable logistic regression analysis was performed to determine the factors contributing to discordant interpretation between oculomotor tests and brain MRI. Oculomotor tests predicting central lesions were assessed using principal component analysis. The intra- and inter-rater reliability in oculomotor test interpretation was moderate to good. Age > 60 years and multiple comorbidities were significant predictors of a discordant interpretation between MRI and oculomotor tests. Positive neurological symptoms and a higher oculomotor index (according to saccade (vertical axis), smooth pursuit (horizontal axis), and gaze-evoked nystagmus (horizontal/vertical axes) tests) significantly predicted central vestibular disorder in vertigo patients. Caution is required when interpreting the results of the oculomotor test battery for diagnosis of central lesions in older patients, as well as in those with multiple comorbidities.

Superior training efficacy of beginning movement load training for the baseball throwers.

BACKGROUND: Superior shoulder motion with rotator cuff activation are essential for the performance of the throwing athletes. The present study compared the novel beginning movement load training (BMLT) and popular throwers ten program regarding the training efficacy of baseball throwers. We hypothesized that the BMLT contributed the superior training efficacy than popular throwers ten program. METHODS: Forty adult baseball players were randomized into study group and control group equally. In study group, the cyclic shoulder motion was repeatedly operated 3 days in a week and lasted for 6 weeks using three different BMLT training machines. As for control group, three popular cyclic training in the throwers ten program were adopted for the shoulder trainings as the same protocol in study group. The evaluations before and after training included the static range of motion (ROM), the maximal voluntary isometric contraction (MVICs) of the target muscle (pectoralis major, middle deltoid and supraspinatus) and throwing velocity. RESULT: After 6-week course, study group had significant wider static ROM in saggital adduction (p = 0.002), coronal internal rotation (p = 0.018) and external rotation (p = 0.044) than in control group. The maximal voluntary isometric contraction (MVIC) ratio of middle deltoid/supraspinatus was significant lower in study group (Study:Control = 1.14 ± 0.76:3.56 ± 5.57, p = 0.049) which indicated the enhanced supraspinatus maximal contraction in the study group after training. In addition, the study group had significant improvement in throwing speed (117 ± 10 vs. 109 ± 10 km/h, p = 0.040). CONCLUSION: The BMLT contributed the superiority in range of motion, recruitment of supraspinatus and throwing velocity than the popular thrower's ten program. It could be a favourable training for the overhead activity.

Zonisamide Therapy Reduces Metabolic Consequences and Diminishes Nonalcoholic Fatty Liver Disease in Patients with Epilepsy.

Antiepileptic drugs that can reduce aberrant metabolism are beneficial for patients. Zonisamide (ZNS) is a chemical with antiepileptic and antioxidant activities. Here, we evaluate the efficacy of ZNS therapy on reducing obesity and decreasing risks of vascular diseases and hepatic steatosis. Clinical and metabolic indicators including body weight, body mass index (BMI), serum lipid profiles, glycated hemoglobin (HbA1c), homocysteine, and an inflammatory marker, high-sensitivity C-reactive protein (hs-CRP), were assessed at baseline and at the end of 12 and 24 weeks of treatment. Nonalcoholic fatty liver disease was evaluated using the hepatic steatosis index (HSI). A body weight reduction of ≥5% was observed in 24.6% and 32.8% of patients after 12 and 24 weeks of ZNS treatment, respectively. After adjusting for age, sex, time, and the corresponding dependent variable at baseline, the generalized estimating equation analysis revealed that the body weight, BMI, serum levels of HbA1c, triglycerides, hs-CRP, and the index for HSI were significantly declined. These results suggest that ZNS provides benefits in patients with obesity and metabolic syndrome at high vascular risk.

Autonomic Dysfunction Contributes to Impairment of Cerebral Autoregulation in Patients with Epilepsy.

Patients with epilepsy frequently experience autonomic dysfunction and impaired cerebral autoregulation. The present study investigates autonomic function and cerebral autoregulation in patients with epilepsy to determine whether these factors contribute to impaired autoregulation. A total of 81 patients with epilepsy and 45 healthy controls were evaluated, assessing their sudomotor, cardiovagal, and adrenergic functions using a battery of autonomic nervous system (ANS) function tests, including the deep breathing, Valsalva maneuver, head-up tilting, and Q-sweat tests. Cerebral autoregulation was measured by transcranial Doppler examination during the breath-holding test, the Valsalva maneuver, and the head-up tilting test. Autonomic functions were impaired during the interictal period in patients with epilepsy compared to healthy controls. The three indices of cerebral autoregulation-the breath-holding index (BHI), an autoregulation index calculated in phase II of the Valsalva maneuver (ASI), and cerebrovascular resistance measured in the second minute during the head-up tilting test (CVR2-min)-all decreased in patients with epilepsy. ANS dysfunction correlated significantly with impairment of cerebral autoregulation (measured by BHI, ASI, and CVR2-min), suggesting that the increased autonomic dysfunction in patients with epilepsy may augment the dysregulation of cerebral blood flow. Long-term epilepsy, a high frequency of seizures, and refractory epilepsy, particularly temporal lobe epilepsy, may contribute to advanced autonomic dysfunction and impaired cerebral autoregulation. These results have implications for therapeutic interventions that aim to correct central autonomic dysfunction and impairment of cerebral autoregulation, particularly in patients at high risk for sudden, unexplained death in epilepsy.

Peroxisome Proliferator-Activated Receptor γ Coactivator 1α Activates Vascular Endothelial Growth Factor That Protects Against Neuronal Cell Death Following Status Epilepticus through PI3K/AKT and MEK/ERK Signaling.

Status epilepticus may cause molecular and cellular events, leading to hippocampal neuronal cell death. Peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α) is an important regulator of vascular endothelial growth factor (VEGF) and VEGF receptor 2 (VEGFR2), also known as fetal liver kinase receptor 1 (Flk-1). Resveratrol is an activator of PGC-1α. It has been suggested to provide neuroprotective effects in epilepsy, stroke, and neurodegenerative diseases. In the present study, we used microinjection of kainic acid into the left hippocampal CA3 region in Sprague Dawley rats to induce bilateral prolonged seizure activity. Upregulating the PGC-1α pathway will increase VEGF/VEGFR2 (Flk-1) signaling and further activate some survival signaling that includes the mitogen activated protein kinase kinase (MEK)/mitogen activated protein kinase (ERK) and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathways and offer neuroprotection as a consequence of apoptosis in the hippocampal neurons following status epilepticus. Otherwise, downregulation of PGC-1α by siRNA against pgc-1α will inhibit VEGF/VEGFR2 (Flk-1) signaling and suppress pro-survival PI3K/AKT and MEK/ERK pathways that are also accompanied by hippocampal CA3 neuronal cell apoptosis. These results may indicate that the PGC-1α induced VEGF/VEGFR2 pathway may trigger the neuronal survival signaling, and the PI3K/AKT and MEK/ERK signaling pathways. Thus, the axis of PGC-1α/VEGF/VEGFR2 (Flk-1) and the triggering of downstream PI3K/AKT and MEK/ERK signaling could be considered an endogenous neuroprotective effect against apoptosis in the hippocampus following status epilepticus.

Circulating MicroRNAs from Serum Exosomes May Serve as a Putative Biomarker in the Diagnosis and Treatment of Patients with Focal Cortical Dysplasia.

Focal cortical dysplasia (FCD) is a congenital malformation of cortical development where the cortical neurons located in the brain area fail to migrate in the proper formation. Epilepsy, particularly medically refractory epilepsy, is the most common clinical presentation for all types of FCD. This study aimed to explore the expression change of circulating miRNAs in patients with FCD from serum exosomes. A total of nine patients with FCD and four healthy volunteers were enrolled in this study. The serum exosomes were isolated from the peripheral blood of the subjects. Transmission electron microscopy (TEM) was used to identify the exosomes. Both exosomal markers and neuronal markers were detected by Western blotting analysis to prove that we could obtain central nervous system-derived exosomes from the circulation. The expression profiles of circulating exosomal miRNAs were assessed using next-generation sequencing analysis (NGS). We obtained a total of 107 miRNAs with dominant fold change (>2-fold) from both the annotated 5p-arm and 3p-arm of 2780 mature miRNAs. Based on the integrated platform of HMDD v3.2, miRway DB and DIANA-miRPath v3.0 online tools, and confirmed by MiRBase analysis, four potentially predicted miRNAs from serum exosomes in patients with FCD were identified, including miR194-2-5p, miR15a-5p, miR-132-3p, and miR-145-5p. All four miRNAs presented upregulated expression in patients with FCD compared with controls. Through Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and pathway category of four target miRNAs, we found eight possible signaling pathways that may be related to FCD. Among them, we suggest that the mTOR signaling pathway, PI3K-Akt signaling pathway, p53 signaling pathway, and cell cycle regulation and TGF-beta signaling pathway are high-risk pathways that play a crucial role in the pathogenesis of FCD and refractory epilepsy. Our results suggest that the circulating miRNAs from exosomes may provide a potential biomarker for diagnostic, prognostic, and therapeutic adjuncts in patients with FCD and refractory epilepsy.

Impairment in dynein-mediated nuclear translocation by BICD2 C-terminal truncation leads to neuronal migration defect and human brain malformation.

During brain development, the nucleus of migrating neurons follows the centrosome and translocates into the leading process. Defects in these migratory events, which affect neuronal migration, cause lissencephaly and other neurodevelopmental disorders. However, the mechanism of nuclear translocation remains elusive. Using whole exome sequencing (WES), we identified a novel nonsense BICD2 variant p.(Lys775Ter) (K775X) from a lissencephaly patient. Interestingly, most BICD2 missense variants have been associated with human spinal muscular atrophy (SMA) without obvious brain malformations. By in utero electroporation, we showed that BicD2 knockdown in mouse embryos inhibited neuronal migration. Surprisingly, we observed severe blockage of neuronal migration in cells overexpressing K775X but not in those expressing wild-type BicD2 or SMA-associated missense variants. The centrosome of the mutant was, on average, positioned farther away from the nucleus, indicating a failure in nuclear translocation without affecting the centrosome movement. Furthermore, BicD2 localized at the nuclear envelope (NE) through its interaction with NE protein Nesprin-2. K775X variant disrupted this interaction and further interrupted the NE recruitment of BicD2 and dynein. Remarkably, fusion of BicD2-K775X with NE-localizing domain KASH resumed neuronal migration. Our results underscore impaired nuclear translocation during neuronal migration as an important pathomechanism of lissencephaly.

Sirtuin 1 Regulates Mitochondrial Biogenesis and Provides an Endogenous Neuroprotective Mechanism Against Seizure-Induced Neuronal Cell Death in the Hippocampus Following Status Epilepticus.

Status epilepticus may decrease mitochondrial biogenesis, resulting in neuronal cell death occurring in the hippocampus. Sirtuin 1 (SIRT1) functionally interacts with peroxisome proliferator-activated receptors and γ coactivator 1α (PGC-1α), which play a crucial role in the regulation of mitochondrial biogenesis. In Sprague-Dawley rats, kainic acid was microinjected unilaterally into the hippocampal CA3 subfield to induce bilateral seizure activity. SIRT1, PGC-1α, and other key proteins involving mitochondrial biogenesis and the amount of mitochondrial DNA were investigated. SIRT1 antisense oligodeoxynucleotide was used to evaluate the relationship between SIRT1 and mitochondrial biogenesis, as well as the mitochondrial function, oxidative stress, and neuronal cell survival. Increased SIRT1, PGC-1α, and mitochondrial biogenesis machinery were found in the hippocampus following experimental status epilepticus. Downregulation of SIRT1 decreased PGC-1α expression and mitochondrial biogenesis machinery, increased Complex I dysfunction, augmented the level of oxidized proteins, raised activated caspase-3 expression, and promoted neuronal cell damage in the hippocampus. The results suggest that the SIRT1 signaling pathway may play a pivotal role in mitochondrial biogenesis, and could be considered an endogenous neuroprotective mechanism counteracting seizure-induced neuronal cell damage following status epilepticus.

Resveratrol Promotes Mitochondrial Biogenesis and Protects against Seizure-Induced Neuronal Cell Damage in the Hippocampus Following Status Epilepticus by Activation of the PGC-1α Signaling Pathway.

Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) is known to regulate mitochondrial biogenesis. Resveratrol is present in a variety of plants, including the skin of grapes, blueberries, raspberries, mulberries, and peanuts. It has been shown to offer protective effects against a number of cardiovascular and neurodegenerative diseases, stroke, and epilepsy. This study examined the neuroprotective effect of resveratrol on mitochondrial biogenesis in the hippocampus following experimental status epilepticus. Kainic acid was microinjected into left hippocampal CA3 in Sprague Dawley rats to induce bilateral prolonged seizure activity. PGC-1α expression and related mitochondrial biogenesis were investigated. Amounts of nuclear respiratory factor 1 (NRF1), mitochondrial transcription factor A (Tfam), cytochrome c oxidase 1 (COX1), and mitochondrial DNA (mtDNA) were measured to evaluate the extent of mitochondrial biogenesis. Increased PGC-1α and mitochondrial biogenesis machinery after prolonged seizure were found in CA3. Resveratrol increased expression of PGC-1α, NRF1, and Tfam, NRF1 binding activity, COX1 level, and mtDNA amount. In addition, resveratrol reduced activated caspase-3 activity and attenuated neuronal cell damage in the hippocampus following status epilepticus. These results suggest that resveratrol plays a pivotal role in the mitochondrial biogenesis machinery that may provide a protective mechanism counteracting seizure-induced neuronal damage by activation of the PGC-1α signaling pathway.

Serum Levels of Brain-Derived Neurotrophic Factor and Insulin-Like Growth Factor 1 Are Associated With Autonomic Dysfunction and Impaired Cerebral Autoregulation in Patients With Epilepsy.

Background: Brain-derived neurotrophic factor (BDNF) and insulin-like growth factor 1 (IGF-1) may regulate the autonomic nervous system (ANS) in epilepsy. The present study investigated the role of IGF-1 and BDNF in the regulation of autonomic functions and cerebral autoregulation in patients with epilepsy. Methods: A total of 57 patients with focal epilepsy and 35 healthy controls were evaluated and their sudomotor, cardiovagal, and adrenergic functions were assessed using a battery of ANS function tests, including the deep breathing, Valsalva maneuver, head-up tilting, and Q-sweat tests. Cerebral autoregulation was measured by transcranial doppler during the breath-holding test and the Valsalva maneuver. Interictal serum levels of BDNF and IGF-1 were measured with enzyme-linked immunosorbent assay kits. Results: During interictal period, reduced serum levels of BDNF and IGF-1, impaired autonomic functions, and decreased cerebral autoregulation were noted in patients with epilepsy compared with healthy controls. Reduced serum levels of BDNF correlated with age, adrenergic and sudomotor function, overall autonomic dysfunction, and the autoregulation index calculated in Phase II of the Valsalva maneuver, and showed associations with focal to bilateral tonic-clonic seizures. Reduced serum levels of IGF-1 were found to correlate with age and cardiovagal function, a parameter of cerebral autoregulation (the breath-hold index). Patients with a longer history of epilepsy, higher seizure frequency, and temporal lobe epilepsy had lower serum levels of IGF-1. Conclusions: Long-term epilepsy and severe epilepsy, particularly temporal lobe epilepsy, may perturb BDNF and IGF-1 signaling in the central autonomic system, contributing to the autonomic dysfunction and impaired cerebral autoregulation observed in patients with focal epilepsy.

Identification of rare paired box 3 variant in strabismus by whole exome sequencing.

AIM: To identify the potentially pathogenic gene variants that contributes to the etiology of strabismus. METHODS: A Chinese pedigree with strabismus was collected and the exomes of two affected individuals were sequenced using the next-generation sequencing technology. The resulting variants from exome sequencing were filtered by subsequent bioinformatics methods and the candidate mutation was verified as heterozygous in the affected proposita and her mother by sanger sequencing. RESULTS: Whole exome sequencing and filtering identified a nonsynonymous mutation c.434G-T transition in paired box 3 (PAX3) in the two affected individuals, which were predicted to be deleterious by more than 4 bioinformatics programs. This altered amino acid residue was located in the conserved PAX domain of PAX3. This gene encodes a member of the PAX family of transcription factors, which play critical roles during fetal development. Mutations in PAX3 were associated with Waardenburg syndrome with strabismus. CONCLUSION: Our results report that the c.434G-T mutation (p.R145L) in PAX3 may contribute to strabismus, expanding our understanding of the causally relevant genes for this disorder.

Higher neutrophil counts and neutrophil-to-lymphocyte ratio predict prognostic outcomes in patients after non-atrial fibrillation-caused ischemic stroke.

BACKGROUND: We aimed to determine whether higher neutrophil counts (NC) and neutrophil-to-lymphocyte ratio (NLR) were independently predictive of worse in-hospital outcome in patients after acute ischemic stroke (IS). METHODS: A retrospective observational study with prospective manner of IS registration. Between April 2012 and August 2014, a total number of 1731 patients with post-IS were consecutively enrolled in the study. Blood samples were drawn upon admission. Primary endpoint was in-hospital mortality. Secondary endpoint was severe stroke (≥16 NIHSS). RESULTS: The NC progressively increased from mild (NIHSS ≤ 5) to moderate (NIHSS ≥ 6 < 16) and severe (NIHSS ≥ 16) stroke (p = 0.006). NLR was independently associated with in-hospital mortality (p = 0.002). Multiple stepwise linear regression analysis showed that NC (p = 0.001) and NLR (p = 0.002) were independently predictive of higher NIHSS. Multiple stepwise logistic regression analysis showed that NC was independently associated with severe stroke (p < 0.0001). The best discriminating factor for in-hospital mortality with respect to NLR was ≥3.20 (sensitivity 62.7%, specificity 60.3%, likelihood ratio: 12.2). Patients with NLR ≥3.20 had a 2.55-fold increased risk for in-hospital mortality (OR = 1.49-4.37) compared to patients with NLR <3.20. The best discriminating factor for severe stroke (≥16 NIHSS) with respect to NC was ≥74% (sensitivity 47.1%, specificity 74.0%, likelihood ratio: 29.0). Patients with NC >74% had a 2.54-fold increased risk of severe stroke (OR = 1.82-3.54) compared to patients with NC <74%. CONCLUSION: NLR was independently associated with in-hospital mortality and higher NC was independently predictive of severe stroke.

Diabetic Retinopathy Is Strongly Predictive of Cardiovascular Autonomic Neuropathy in Type 2 Diabetes.

A well-established, comprehensive, and simple test battery was used here to re-evaluate risk factors for cardiovascular autonomic neuropathy (CAN) in type 2 diabetes. One hundred and seventy-four patients with type 2 diabetes were evaluated through the methods of deep breathing and Valsalva maneuver for correlation with factors that might influence the presence and severity of CAN. The Composite Autonomic Scoring Scale (CASS) was used to grade the severity of autonomic impairment, and CAN was defined as a CASS score ≥2. Results showed that nephropathy, duration of diabetes, blood pressure, uric acid, and the presence of retinopathy and metabolic syndrome significantly correlated with the CASS score. Age may not be a risk factor for diabetic CAN. However, the effects of diabetes on CAN are more prominent in younger patients than in older ones. Diabetic retinopathy is the most significant risk factor predictive of the presence of CAN in patients with type 2 diabetes.

Association between oxidative stress and outcome in different subtypes of acute ischemic stroke.

OBJECTIVES: This study investigated serum thiobarbituric acid-reactive substances (TBARS) and free thiol levels in different subtypes of acute ischemic stroke (AIS) and evaluated their association with clinical outcomes. METHODS: This prospective study evaluated 100 AIS patients, including 75 with small-vessel and 25 with large-vessel diseases. Serum oxidative stress (TBARS) and antioxidant (thiol) were determined within 48 hours and days 7 and 30 after stroke. For comparison, 80 age- and sex-matched participants were evaluated as controls. RESULTS: Serum TBARS was significantly higher and free thiol was lower in stroke patients than in the controls on days 1 and 7 after AIS. The level of free thiol was significantly lower in the large-vessel disease than in the small-vessel disease on day 7 after stroke. Using the stepwise logistic regression model for potential variables, only stroke subtype, NIHSS score, and serum TBARS level were independently associated with three-month outcome. Higher TBARS and lower thiol levels in the acute phase of stroke were associated with poor outcome. CONCLUSIONS: Patients with large-vessel disease have higher oxidative stress but lower antioxidant defense compared to those with small-vessel disease after AIS. Serum TBARS level at the acute phase of stroke is a potential predictor for three-month outcome.

Statistical anomaly detection for individuals with cognitive impairments.

We study anomaly detection in a context that considers user trajectories as input and tries to identify anomalies for users following normal routes such as taking public transportation from the workplace to home or vice versa. Trajectories are modeled as a discrete-time series of axis-parallel constraints ("boxes") in the 2-D space. The anomaly can be estimated by considering two trajectories, where one trajectory is the current movement pattern and the other is a weighted trajectory collected from N norms. The proposed system was implemented and evaluated with eight individuals with cognitive impairments. The experimental results showed that recall was 95.0% and precision was 90.9% on average without false alarm suppression. False alarms and false negatives dropped when axis rotation was applied. The precision with axis rotation was 97.6% and the recall was 98.8%. The average time used for sending locations, running anomaly detection, and issuing warnings was in the range of 15.1-22.7 s. Our findings suggest that the ability to adapt anomaly detection devices for appropriate timing of self-alerts will be particularly important.

99mTc-sestamibi thigh SPECT/CT imaging for assessment of myopathy in cerebrotendinous xanthomatosis with histopathological and immunohistochemical correlation.

PURPOSE: The aim of this study was to determine the effectiveness of using Tc-sestamibi thigh SPECT/CT imaging for evaluating myopathy in cerebrotendinous xanthomatosis (CTX). PATIENTS AND METHODS: Four genetically proven CTX patients (Family I, Cases I-1 and I-2; Family II, Cases II-1 and II-2) were included. They all underwent muscle biopsies for histopathologic and ultrastructural studies. Immunohistochemical staining for vinculin expression was also performed. Tc-sestamibi thigh SPECT/CT imaging was conducted on all 4 CTX patients, and both visual interpretation and muscle-to-background (M/B) ratio count were applied for assessment. Correlation analysis of the imaging findings and results of the ultrastructural and immunohistochemical studies was done. RESULTS: In the Tc-sestamibi thigh SPECT/CT imaging study, all 4 CTX cases had abnormal scores of visual interpretation and M/B ratios. The ultrastructural features of the skeletal muscle of the 4 CTX cases showed mitochondrial and membrane system abnormalities, with increased depositions of metabolites. They also had abnormal increases in vinculin expression after immunohistochemical staining of the skeletal muscle. CONCLUSIONS: This is the first report on the use of Tc-sestamibi thigh SPECT/CT imaging to assess the mitochondrial status of CTX. The imaging findings may have a correlation with the ultrastructural and immunohistochemical findings on skeletal muscle. Although the Tc-sestamibi thigh SPECT/CT imaging is not specific for CTX, this noninvasive in vivo assessment can be an important tool for the detection and follow-up study of skeletal muscle involvement in CTX.

Non-cephalosporin-susceptible, glucose non-fermentative Gram-negative bacilli meningitis in post-neurosurgical adults: clinical characteristics and therapeutic outcome.

OBJECTIVE: The clinical and laboratory characteristics of non-cephalosporin-susceptible (non-CS) glucose non-fermentative Gram-negative (G(-)) infections in adults with postneurosurgical meningitis are rarely examined solely in the literature. METHODS: The data of 28 post-neurosurgical adults meningitis with glucose non-fermentative G(-) infections, collected during a study period of 5 years (2006-2010), were reviewed. The clinical and laboratory data between the non-cephalosporin-susceptible groups and the cephalosporin-susceptible groups were compared. RESULTS: A total of 30 G(-) strains were collected from the 28 enrolled cases. Among the implicated glucose non-fermentative G(-) strains, 18 strains, belonging to 17 cases, were non-CS. Among the 18 non-cephalosporin-susceptible strains, Acinetobacter spp. (39%, 7/18) was the most common, followed by Pseudomonas spp. (22%, 4/18), Stenotrophomonas maltophilia (22%, 4/18) and Elizabethkingia meningoseptica (11%, 2/18). With a comparative analysis, there were no significant difference between the non-cephalosporin-susceptible and cephalosporin-susceptible glucose non-fermentative G(-) groups. The clinical and laboratory data were also of no statistical significance between the fatal (n=4) and non-fatal (n=13) non-cephalosporin-susceptible groups. CONCLUSION: Sixty percent (18/30) of implicated glucose non-fermentative G(-) strains of post-NS meningitis in adults are non-cephalosporin-susceptible. Among the non-cephalosporin-susceptible glucose non-fermentative G(-) strains, Acinetobacter spp., Pseudomonas spp., S. maltophilia and E. meningoseptica are the commonly implicated pathogens, and their emergence in this specific group of meningitis has caused a therapeutic dilemma. The clinical manifestations of non-cephalosporin-susceptible glucose non-fermentative G(-) meningitis were not unique; therefore, only bacterial culture and antimicrobial susceptibility test are the methods for identification confirmation.