bluuebunny/crossref_metadata_2025_split huggingface dataset:
Protective and Detrimental Effects of Sodium Sulfide and Hydrogen Sulfide in Murine Ventilator-induced Lung Injury
Authors: Francis Roland C. , Vaporidi Katerina , Bloch Kenneth D. , Ichinose Fumito , Zapol Warren M. 
Published: October 2011

Background
The antiinflammatory effects of hydrogen sulfide (H2S) and sodium sulfide (Na2S) treatment may prevent acute lung injury induced by high tidal volume (HVT) ventilation. However, lung protection may be limited by direct pulmonary toxicity associated with H2S inhalation. Therefore, the authors tested whether the inhalation of H2S or intravascular Na2S treatment can protect against ventilator-induced lung injury in mice.

Methods
Anesthetized mice continuously inhaled 0, 1, 5, or 60 ppm H2S or received a single bolus infusion of Na2S (0.55 mg/kg) or vehicle and were then subjected to HVT (40 ml/kg) ventilation lasting 4 h (n = 4-8 per group).

Results
HVT ventilation increased the concentrations of protein and interleukin-6 in bronchoalveolar lavage fluid, contributing to reduced respiratory compliance and impaired arterial oxygenation, and caused death from lung injury and pulmonary edema. Inhalation of 1 or 5 ppm H2S during HVT ventilation did not alter lung injury, but inhalation of 60 ppm H2S accelerated the development of ventilator-induced lung injury and enhanced the pulmonary expression of the chemoattractant CXCL-2 and the leukocyte adhesion molecules CD11b and L-selectin. In contrast, pretreatment with Na2S attenuated the expression of CXCL-2 and CD11b during HVT ventilation and reduced pulmonary edema. Moreover, Na2S enhanced the pulmonary expression of Nrf2-dependent antioxidant genes (NQO1, GPX2, and GST-A4) and prevented oxidative stress-induced depletion of glutathione in lung tissue.

Conclusions
The data suggest that systemic intravascular treatment with Na2S represents a novel therapeutic strategy to prevent both ventilator-induced lung injury and pulmonary glutathione depletion by activating Nrf2-dependent antioxidant gene transcription.
Neuroprotective Effect of Curcumin in an Experimental Rat Model of Subarachnoid Hemorrhage
Authors: Kuo Chang-Po , Lu Chueng-He , Wen Li-Li , Cherng Chen-Hwan , Wong Chih-Shung , Borel Cecil O. , Ju Da-Tong , Chen Chun-Mei , Wu Ching-Tang 
Published: October 2011

Background
Subarachnoid hemorrhage (SAH) causes a high mortality rate and morbidity. It was suggested that oxidant stress plays an important role in neuronal injury after SAH. Therefore, we assessed the effect of curcumin on reducing cerebral vasospasm and neurologic injury in a SAH model in rat.

Methods
A double-hemorrhage model was used to induce SAH in rats. Groups of animals were treated with intraperitoneal injection of 20 mg/kg curcumin (curcumin group, n = 24) or dimethyl sulfoxide (vehicle group, n = 33), normal saline (SAH group, n = 34) or normal saline (sham group, n = 22), 3 h after SAH induction and daily for 6 days. Glutamate was measured before SAH induction and once daily for 7 days. Glutamate transporter-1, wall thickness and the perimeter of the basilar artery, neurologic scores, neuronal degeneration, malondialdehyde, superoxide dismutase, and catalase activities were assessed.

Results
Changes of glutamate levels were lower in the curcumin group versus the SAH and vehicle groups, especially on day 1 (56 folds attenuation vs. vehicle). Correspondingly, glutamate transporter-1 was preserved after SAH in curcumin-treated rats. In the hippocampus and the cortex, malondialdehyde was attenuated (30% and 50%, respectively). Superoxide dismutase (35% and 64%) and catalase (34% and 38%) activities were increased in the curcumin rats compared with the SAH rats. Mortality rate (relative risk: 0.59), wall thickness (30%) and perimeter (31%) of the basilar artery, neuron degeneration scores (39%), and neurologic scores (31%) were improved in curcumin-treated rats.

Conclusions
Curcumin in multiple doses is effective against glutamate neurotoxicity and oxidative stress and improves the mortality rate in rats with SAH.
Neonatal Desflurane Exposure Induces More Robust Neuroapoptosis than Do Isoflurane and Sevoflurane and Impairs Working Memory
Authors: Kodama Mitsuyoshi , Satoh Yasushi , Otsubo Yukiko , Araki Yoshiyuki , Yonamine Ryuji , Masui Kenichi , Kazama Tomiei 
Published: October 2011

Background
In animal models, neonatal exposure to volatile anesthetics induces neuroapoptosis, leading to memory deficits in adulthood. However, effects of neonatal exposure to desflurane are largely unknown.

Methods
Six-day-old C57BL/6 mice were exposed to equivalent doses of desflurane, sevoflurane, or isoflurane for 3 or 6 h. Minimum alveolar concentration was determined by the tail-clamp method as a function of anesthesia duration. Apoptosis was evaluated by immunohistochemical staining for activated caspase-3, and by TUNEL. Western blot analysis for cleaved poly-(adenosine diphosphate-ribose) polymerase was performed to examine apoptosis comparatively. The open-field, elevated plus-maze, Y-maze, and fear conditioning tests were performed to evaluate general activity, anxiety-related behavior, working memory, and long-term memory, respectively.

Results
Minimum alveolar concentrations at 1 h were determined to be 11.5% for desflurane, 3.8% for sevoflurane, and 2.7% for isoflurane in 6-day-old mice. Neonatal exposure to desflurane (8%) induced neuroapoptosis with an anatomic pattern similar to that of sevoflurane or isoflurane; however, desflurane induced significantly greater levels of neuroapoptosis than almost equivalent doses of sevoflurane (3%) or isoflurane (2%). In adulthood, mice treated with these anesthetics had impaired long-term memory, whereas no significant anomalies were detected in the open-field and the elevated plus-maze tests. Although performance in a working memory task was normal in mice exposed neonatally to sevoflurane or isoflurane, mice exposed to desflurane had significantly impaired working memory.

Conclusions
In an animal model, neonatal desflurane exposure induced more neuroapoptosis than did sevoflurane or isoflurane and impaired working memory, suggesting that desflurane is more neurotoxic than sevoflurane or isoflurane.
Evolution of the Inflammatory and Fibroproliferative Responses during Resolution and Repair after Ventilator-induced Lung Injury in the Rat
Authors: Curley Gerard F. , Contreras Maya , Higgins Brendan , O'Kane Cecilia , McAuley Daniel F. , O'Toole Daniel , Laffey John G. 
Published: October 2011

Background
The time course and mechanisms of resolution and repair, and the potential for fibrosis following ventilation-induced lung injury (VILI), are unclear. We sought to examine the pattern of inflammation, injury, repair, and fibrosis following VILI.

Methods
Sixty anesthetized rats were subject to high-stretch; low-stretch, or sham ventilation, and randomly allocated to undergo periods of recovery of 6, 24, 48, and 96 h, and 7 and 14 days. Animals were then reanesthetized, and the extent of lung injury, inflammation, and repair determined.

Results
No injury was seen following low-stretch or sham ventilation. VILI caused severe lung injury, maximal at 24 h, but largely resolved by 96 h. Arterial oxygen tension decreased from a mean (SD) of 144.8 (4.1) mmHg to 96.2 (10.3) mmHg 6 h after VILI, before gradually recovering to 131.2 (14.3) mmHg at 96 h. VILI induced an early neutrophilic alveolitis and a later lymphocytic alveolitis, followed by a monocyte/macrophage infiltration. Alveolar tumor necrosis factor-α, interleukin-1β, and transforming growth factor-β1 concentrations peaked at 6 h and returned to baseline within 24 h, while interleukin-10 remained increased for 48 h. VILI generated a marked but transient fibroproliferative response, which restored normal lung architecture. There was no evidence of fibrosis at 7 and 14 days.

Conclusions
High-stretch ventilation caused severe lung injury, activating a transient inflammatory and fibroproliferative repair response, which restored normal lung architecture without evidence of fibrosis.
Intraoperative Acceleromyography Monitoring Reduces Symptoms of Muscle Weakness and Improves Quality of Recovery in the Early Postoperative Period
Authors: Murphy Glenn S. , Szokol Joseph W. , Avram Michael J. , Greenberg Steven B. , Marymont Jesse H. , Vender Jeffery S. , Gray Jayla , Landry Elizabeth , Gupta Dhanesh K. 
Published: October 2011

Background
The subjective experience of residual neuromuscular blockade after emergence from anesthesia has not been examined systematically during postanesthesia care unit (PACU) stays. The authors hypothesized that acceleromyography monitoring would diminish unpleasant symptoms of residual paresis during recovery from anesthesia by reducing the percentage of patients with train-of-four ratios less than 0.9.

Methods
One hundred fifty-five patients were randomized to receive intraoperative acceleromyography monitoring (acceleromyography group) or conventional qualitative train-of-four monitoring (control group). Neuromuscular management was standardized, and extubation was performed when defined criteria were achieved. Immediately upon a patient's arrival to the PACU, the patient's train-of-four ratios were measured using acceleromyography, and a standardized examination was used to assess 16 symptoms and 11 signs of residual paresis. This examination was repeated 20, 40, and 60 min after PACU admission.

Results
The incidence of residual blockade (train-of-four ratios less than 0.9) was reduced in the acceleromyography group (14.5% vs. 50.0% control group, with the 99% confidence interval for this 35.5% difference being 16.4-52.6%, P &lt; 0.0001). Generalized linear models revealed the acceleromyography group had less overall weakness (graded on a 0-10 scale) and fewer symptoms of muscle weakness across all time points (P &lt; 0.0001 for both analyses), but the number of signs of muscle weakness was small from the time of arrival in the PACU and did not differ between the groups at any time.

Conclusion
Acceleromyography monitoring reduces the incidence of residual blockade and associated unpleasant symptoms of muscle weakness in the PACU and improves the overall quality of recovery.
Clinical and Radiological Mid-Term Outcomes of Lumbar Single-Level Total Disc Replacement
Authors: Scott-Young Matthew N. , Lee Matthew J. , Nielsen David E. A. , Magno Carly L. , Kimlin Kristy R. , Mitchell Evan O. 
Published: October 2011

Study Design.
Prospective single-center case cohort study.

Objective.
Evaluation of clinical and radiographic outcomes of a consecutive 122-patient cohort with discogenic back pain, at 2- to 10-year follow-up periods, treated by a single surgeon, with CHARITÉ Artificial Disc (DePuy Spine, Raynham, MA).

Summary of Background Data.
Minimum 2-year clinical and radiographic level 1 data for the first lumbar artificial disc, the CHARITÉ Artificial Disc (DePuy Spine), have recently been published, demonstrating sustained clinical benefit of the device for the treatment of degenerative disc disease.

Methods.
Patients were assessed preoperatively using clinical outcome measures, including visual analog scale (VAS) score back and leg, Oswestry Disability Index (ODI), 36-Item Short Form Health Survey (SF-36), and Roland-Morris Questionnaires (RMDQ), and further assessed postoperatively, 3-, 6-, 12-months, and yearly thereafter.

Results.
Average follow-up was 44.9 ± 23.3 months (n = 122). The median age at surgery was 43.0 ± 9.0 years. Preoperative diagnosis included degenerative disc disease in 118 (96.7%) and internal disc disruption in 4 (3.3%). Surgery was performed at L5–S1 in 96 (77.9%) patients and at L4–L5 in 27 (22.1%). Statistically significant clinical improvements from baseline were observed on VAS (back and leg), ODI, SF-36 PCS, SF-36 MCS, and RMDQ 3 months onward. Back VAS scores decreased from 78.2 ± 21.3 preoperatively to 21.9 ± 27.8 by final follow-up. ODI scores decreased from 51.1 ± 17.3 to 16.2 ± 17.9 at last follow-up. The RMDQ scores also decreased from 16.7 ± 4.7 to 4.2 ± 5.8. SF-36 PCS and MCS increased from 25.7 ± 11.0 to 46.4 ± 10.3 for PCS and from 35.5 ± 17.4 to 51.6 ± 10.8 for MCS. Patient satisfaction surveys indicated that 90.56% patients rated their satisfaction with the surgery as “excellent” or “good” at 2 years. Range of motion averaged 8.6 ± 3.5 (median = 8.0°) at the last follow-up time point.

Conclusion.
Outcomes verify the clinical efficacy of total disc replacement for treatment of discogenic back pain with or without radiculopathy. The outcomes instruments demonstrated statistically significant improvements 3 months onward.

Level of Evidence: N/A
The Charcot Joint: A Modern Neurologic Perspective
Authors: Chisholm Kara A , Gilchrist James M 
Published: October 2011

Abstract

The Charcot joint, or Charcot neuroarthropathy, is a syndrome that was described over 140 years ago but one with very little exposure in the neurologic literature. We present a case recently seen and then discuss the history, epidemiology, pathophysiology, clinical features, and diagnosis of acute and chronic Charcot joint disease with particular emphasis on the value and limitations of imaging. A diagnostic algorithm is proposed. We also review the therapeutic strategies available for acute and chronic Charcot joints with a treatment algorithm. This review is aimed at enhancing the awareness of neurologists regarding Charcot neuroarthropathy, because they are often the principal caregivers for patients with peripheral neuropathy. We hope to promote early detection of acute Charcot neuroarthropathy, thereby reducing or preventing the bony deformation of chronic Charcot neuroarthropathy.
Neuromuscular Diseases Associated With Chronic Hepatitis C Virus Infection
Authors: Stübgen Joerg-Patrick 
Published: October 2011

Abstract

Hepatitis C virus (HCV) infection is a growing international health problem, and more than 170 million people are chronic carriers. Up to 50% of HCV-positive patients develop at least one extrahepatic manifestation during the course of disease. To varying degrees of certainty, there is evidence of an association between chronic HCV infection and a variety of neuromuscular diseases. The pathogenesis of most extrahepatic diseases remains unclear but possibly includes HCV lymphotropism and/or HCV-induced autoantibodies. The therapeutic approach to HCV-associated autoimmune disorders entails eradication of HCV with one of the recombinant interferon-alpha preparations with or without additional immunosuppressive drugs.
Ocular Myasthenia Gravis in an Academic Neuro-Ophthalmology Clinic: Clinical Features and Therapeutic Response
Authors: Mittal Manoj Kumar , Barohn Richard J , Pasnoor Mamatha , McVey April , Herbelin Laura , Whittaker Thomas , Dimachkie Mazen 
Published: October 2011

Abstract

Objective:
The frequency of ocular myasthenia gravis (OMG) in patients referred to an academic neuro-ophthalmology clinic for suspected myasthenia gravis is not known. Our objective was to determine the frequency of ocular OMG in patients referred to an academic neuro-ophthalmologist and determine alternate diagnoses and response to therapy.

Methods:
We performed a retrospective chart review of patients presenting to the University of Kansas Neuro-Ophthalmology Clinic with suspected OMG over 9 years. We defined OMG as isolated ptosis/diplopia at initial presentation supported by at least one of the following abnormal tests: edrophonium test, ice test, Cogan lid twitch, fatigability on sustained upgaze, acetylcholine receptor binding antibody, greater than 10% decrement on repetitive stimulation, or abnormal single-fiber jitter. We also determined the cause of ptosis/diplopia if it was not the result of OMG. Patients who progressed from OMG to generalized disease were termed transformed myasthenia gravis (TMG).

Results:
One hundred thirty-eight patients were referred with mean age at presentation 58 ± 19 years. Myasthenia gravis was diagnosed in 101 patients; 95 had OMG; six had generalized MG. Diagnosis in the other 37 was cranial nerve palsies (nine), levator dehiscence (five), multiple sclerosis (two), blepharospasm (two), decompensated phorias (three), accommodation spasm (four), exophoria (three), skew deviation (two), Graves disease (one), hypertropia (one), myopathy (one), neurosarcoidosis (one), progressive supranuclear palsy (one), Miller Fisher variant of Guillain-Barre syndrome (one), and obstructive sleep apnea (one). Mean follow-up was 3.0 ± 2.8 years. Test sensitivity/specificity in OMG was fatigability on sustained upgaze 0.80/0.63; ice pack 0.80/0.25; Cogan lid twitch 0.59/1.00; edrophonium 0.88/0.50; acetylcholine receptor binding antibody 0.38/1.00; repetitive nerve stimulation 0.24/1.00; and single-fiber electromyography 0.90/1.00. Pyridostigmine was used without prednisone in 59 of 97 patients with OMG and 12 of 59 developed TMG. Prednisone was used in 38 patients; 21 of 38 (55%) met Myasthenia Gravis Foundation of America improvement status and none had TMG.

Conclusion:
The diagnosis of myasthenia gravis was confirmed in the majority of patients referred to our academic neuro-ophthalmology clinic, but 27% did not have myasthenia gravis. It is possible that prednisone treatment of OMG may prevent progression to TMG, but further study is required.
Handheld Office-Based Spirometry versus Laboratory Spirometry in Low-Risk Patients Undergoing Lung Resection
Authors: Puri Varun , Zoole Jennifer B. , Musick Joanne , Krupnick Alexander S. , Kreisel Daniel , Crabtree Traves D. , Patterson G. Alexander , Meyers Bryan F. 
Published: October 2011

Objective To compare handheld office spirometry with laboratory spirometry in evaluation of low-risk patients undergoing pulmonary resection. Methods Low-risk patients evaluated for lung resection were enrolled in a prospective study and underwent office and laboratory spirometry. Standard laboratory spirometry values were considered the gold standard. Values of forced expiratory volume in 1 second (FEV1) <1.5 L or FEV1% <60% were determined in advance to signal high risk. Results Thirty patients with mean age 64 ± 12 years and median Karnofsky performance status 100 (80–100) were evaluated. The mean FEV1-office spirometry and mean FEV1-laboratory spirometry were comparable (2.14 L vs 2.36 L) as were the mean FEV1%-office spirometry and FEV1%-laboratory spirometry (78% vs 85%). The differences were within limits established a priori. Laboratory spirometry identified 3 of 30 (10%) patients as high risk and office spirometry identified 5 of 30 (16%) patients as high risk, including the 3 patients identified by laboratory spirometry. The sensitivity of office spirometry for detecting high risk was 100% (3/3) and specificity was 93% (25/27). The negative predictive value of office spirometry was 100% (25/25). Office spirometry added a median of 1 minute to the office visit, whereas laboratory spirometry added 42 minutes. Eventually, 25 of 30 (83%) patients underwent lung resection. There were 12 lobar and 13 sublobar resections. One patient developed postoperative respiratory morbidity. This patient was high risk by office spirometry but not by laboratory spirometry. This patient was discharged on home oxygen. Conclusions Office spirometry FEV1 and FEV1% are clinically comparable to formal laboratory spirometry values. Office Spirometry saves time and possibly expense in the preoperative workup of patients evaluated for lung resection.
Safety of Percutaneous Endoscopic Gastrostomy in Medically Complicated Infants
Authors: Minar Philip , Garland Jeffery , Martinez Alfonso , Werlin Steven 
Published: October 2011

ABSTRACTBackground and Objective:Percutaneous endoscopic gastrostomy (PEG) tubes have been placed in children for more than 2 decades to provide nutrition to those unable to adequately and safely feed orally. Despite the well‐documented success of PEG placement in older children, there is only 1 published article documenting the safety of PEG placement in small infants. In all children, PEG studies demonstrate the major complication rate to vary from 0.5% to 17%. The objective of this study was to evaluate the incidence of acute complications of PEG placement in medically complicated infants with a weight of less than 6 kg.Patients and Methods:We reviewed the charts of all infants cared for in the neonatal intensive care unit of Wheaton Franciscan Health Care‐St Joseph's Regional Hospital, Milwaukee, WI, who received a PEG tube between January 2001 and June 30, 2008.Results:Forty infants with a mean gestational age of 29 weeks (range 23–41 weeks) with a mean weight of 3250 g (range 2100–5600 g) at time of PEG placement were included. The primary indication for most infants was dysphagia or inability to orally feed safely. A PEG was successfully placed in 38 of 40 (95%) infants. There was 1 major complication: a 38‐week infant with Prader‐Willi syndrome developed a pneumomediastinum caused by a tear at the upper esophageal sphincter. In a second infant the PEG bumper could not be passed beyond the upper esophageal sphincter. Sixteen infants had other surgical procedures performed at the time of PEG placement. For those infants only having a PEG placed, the mean procedure time was 10 minutes.Conclusions:PEG placement is both feasible and safe in small, medically complicated infants.
Long‐term Efficacy of Low‐dose Tricyclic Antidepressants for Children With Functional Gastrointestinal Disorders
Authors: Teitelbaum Jonathan E. , Arora Ruchi 
Published: October 2011

ABSTRACTObjective:The aim of the study was to determine the long‐term efficacy of the tricyclic antidepressant (TCA) drugs amitriptyline or imipramine in treating functional gastrointestinal disorders (FGIDs) in pediatric patients.Materials and Methods:A retrospective chart review of children with a diagnosis of irritable bowel syndrome, functional dyspepsia, and functional abdominal pain diagnosed on the basis of the Rome III criteria was performed. Charts were analyzed for response to the medication and the duration of the response.Results:A total of 98 patients took a TCA for an FGID. Of the 98 patients, 77 patients (78.6%) responded to the treatment for an average of 10.73 (range 1–45) months.Conclusions:TCAs are effective in treating FGIDs in pediatric patients for a long duration.