[Hyper- or normobaric oxygen therapy to treat migraine and cluster headache pain. Cochrane review].
Schmerz. 2008 Apr;22(2):129-32, 134-6. PMID: 17885769
A Schnabel, M Bennet, F Schuster, N Roewer, P Kranke
Klinik und Poliklinik für Anästhesiologie und operative Intensivmedizin, Universitätsklinikum Münster, Münster, Germany.
BACKGROUND: The aim of this systematic review was to assess the benefits and harms of supplemental oxygen (HBOT/NBOT) for treating and preventing migraine and cluster headaches.
MATERIAL AND METHODS: All randomized trials comparing the effect of supplemental oxygen on migraine or cluster headache with those that exclude supplemental oxygen were included in this review. The systematic search included all relevant sources according to the paradigms of the Cochrane Collaboration. Data were analyzed with RevMan 4.2.
RESULTS: Nine trials involving 201 participants satisfied the inclusion criteria. HBOT was effective in relieving an acute migraine and seemed to be sufficient in the treatment of an acute cluster attack. NBOT was effective in terminating acute cluster headache compared to sham treatment, but not in comparison to sublingual ergotamine. There was no evidence for any prophylactic effects. Serious adverse effects were not noted in the trials investigated.
CONCLUSIONS: There is some evidence that HBOT is effective for termination of acute migraine. NBOT was similarly effective in cluster headache, however with sparse data. Because of costs and poor availability HBOT cannot be regarded as a routine therapy. Further indications in the case of treatment failure using standard therapy need to be defined based on data of future clinical trials.
Article Published Date : Apr 01, 2008
Brain insulin response and peripheral metabolic changes in a Tau transgenic mouse model.
Neurobiol Dis. 2019 Jan 18;:
Authors: Leboucher A, Ahmed T, Caron E, Tailleux A, Raison S, Joly-Amado A, Marciniak E, Carvalho K, Hamdane M, Bantubungi K, Lancel S, Eddarkaoui S, Caillierez R, Vallez E, Staels B, Vieau D, Balschun D, Buee L, Blum D
Accumulation of hyper-phosphorylated and aggregated Tau proteins is a neuropathological hallmark of Alzheimer's Disease (AD) and Tauopathies. AD patient brains also exhibit insulin resistance. Whereas, under normal physiological conditions insulin signaling in the brain mediates plasticity and memory formation, it can also regulate peripheral energy homeostasis. Thus, in AD, brain insulin resistance affects both cognitive and metabolic changes described in these patients. While a role of Aβ oligomers and APOE4 towards the development of brain insulin resistance emerged, contribution of Tau pathology has been largely overlooked. Our recent data demonstrated that one of the physiological function of Tau is to sustain brain insulin signaling. We postulated that under pathological conditions, hyper-phosphorylated/aggregated Tau is likely to lose this function and to favor the development of brain insulin resistance. This hypothesis was substantiated by observations from patient brains with pure Tauopathies. To address the potential link between Tau pathology and brain insulin resistance, we have evaluated the brain response to insulin in a transgenic mouse model of AD-like Tau pathology (THY-Tau22). Using electrophysiological and biochemical evaluations, we surprisingly observed that, at a time when Tau pathology and cognitive deficits are overt and obvious, the hippocampus of THY-Tau22 mice exhibits enhanced response to insulin. In addition, we demonstrated that the ability of i.c.v. insulin to promote body weight loss is enhanced in THY-Tau22 mice. In line with this, THY-Tau22 mice exhibited a lower body weight gain, hypoleptinemia and hypoinsulinemia and finally a metabolic resistance to high-fat diet. The present data highlight that the brain of transgenic Tau mice exhibit enhanced brain response to insulin. Whether these observations are ascribed to the development of Tau pathology, and therefore relevant to human Tauopathies, or unexpectedly results from the Tau transgene overexpression is debatable and discussed.
PMID: 30665005 [PubMed - as supplied by publisher]
An Arabidopsis berberine-bridge enzyme-like protein specifically oxidizes cellulose oligomers and plays a role in immunity.
Plant J. 2019 Jan 21;:
Authors: Locci F, Benedetti M, Pontiggia D, Citterico M, Caprari C, Mattei B, Cervone F, De Lorenzo G
The plant cell wall is the barrier that pathogens must overcome to cause a disease and to this purpose they secrete degrading enzymes of the various cell wall components. Due to the complexity of these components, several types of oligosaccharide fragments may be released during pathogenesis and some of these can act as Damage-Associated Molecular Pattern (DAMPs). Well-known DAMPs are the oligogalacturonides (OGs) released upon degradation of homogalacturonan and the products of the cellulose breakdown, i.e. the cellodextrins (CDs). We have previously reported that four Arabidopsis Berberine Bridge Enzyme-like (BBE-like) proteins (OGOX1-4) oxidize OGs and impair their elicitor activity. We show here that another Arabidopsis BBE-like protein, which is expressed coordinately with OGOX1 during immunity, specifically oxidizes CDs with a preference for cellotriose (CD3) and longer fragments (CD4-6). Oxidized CDs show a negligible elicitor activity and are less utilizable by the fungus Botrytis cinerea as a carbon source. The enzyme, named CELLOX (CELLODEXTRIN OXIDASE), is encoded by the gene At4g20860. Plants overexpressing CELLOX display an enhanced resistance to B. cinerea likely because oxidized CDs are a less valuable carbon source. Thus, the capacity of oxidizing and impairing the biological activity of the cell wall-derived oligosaccharides seems to be a general trait of the family of BBE-like proteins, which may serve for the homeostatic control of the level of DAMPs to prevent their hyper-accumulation. This article is protected by copyright. All rights reserved.
PMID: 30664296 [PubMed - as supplied by publisher]
Alterations in cardiovascular function in an experimental model of lung fibrosis and pulmonary hypertension.
Exp Physiol. 2019 Jan 21;:
Authors: Darwiche T, Collum SD, Bi W, Reynolds JO, Wilson C, Wareing N, Hernandez AM, Mertens TCJ, Zhou Z, Pandit LM, Karmouty-Quintana H
NEW FINDINGS: We have evaluated changes in cardiovascular physiology using echo in an experimental model of lung fibrosis. Remarkably, we report changes in cardiovascular function as early as day 7, concomitant with evidence of vascular remodeling. We also report that isolated pulmonary arteries were hyper-contractile to a thromboxane A2 agonist. These findings are significant since the development of pulmonary hypertension is one of the most significant predictors of mortality in patients with lung fibrosis where there are no available therapies and a lack of animal models.
ABSTRACT: Group III Pulmonary hypertension is observed in patients chronic lung diseases such as Chronic Obstructive Pulmonary Disease (COPD) or Idiopathic Pulmonary Fibrosis (IPF). Pulmonary Hypertension (PH) develops as a result of extensive pulmonary vascular remodeling and resultant changes in vascular tone that can lead to right ventricle hypertrophy. This eventually leads to right heart failure which is the leading indicator of mortality in patients with IPF. Treatments for Group III PH are not available, in part due to a lack of viable animal models. Here we have evaluated the cardiovascular changes in a model of lung fibrosis and PH. Data obtained from this study indicated that structural alterations in the right heart such as right ventricle wall hypertrophy occurred as early as day 21, where similar increases in right ventricle chamber size were seen between days 21-28. These structural changes correlated with decreases in the systolic function of the right ventricle and right ventricular cardiac output, which also occurred between the same time points. Characterization of pulmonary artery dynamics also highlighted that PH may be occurring as early as day 21 indicated by reductions in the velocity time integral; however, PH onsets at least from day 28 indicated by the significant reduction in pulmonary acceleration time values. In addition, we report hyperactivity of BLM-exposed pulmonary arteries to a thromboxane A2 receptor (Tbxa2r) agonist. Interestingly, although Tbxa2r expression levels did not change in the lung, altered expression was seen in the heart. This article is protected by copyright. All rights reserved.
PMID: 30663834 [PubMed - as supplied by publisher]
A New Promising Treatment Strategy for Carbon Monoxide Poisoning: High Flow Nasal Cannula Oxygen Therapy.
Med Sci Monit. 2019 Jan 21;25:605-609
Authors: Tomruk O, Karaman K, Erdur B, Armagan HH, Beceren NG, Oskay A, Bircan HA
BACKGROUND High-flow nasal cannula (HFNC) is an alternative to conventional normobaric oxygen therapy (NBO) for hypoxemic patients. Since nothing is known about its effect on carbon monoxide (CO) poisoning, we hypothesized that HFNC might be a useful device in the treatment of CO poisoning victims. MATERIAL AND METHODS We retrospectively reviewed the medical records of patients who were admitted consecutively to the emergency department with CO intoxication. Patients were divided into 2 groups: patients treated with HFNC and patients treated with conventional face mask (CFM). Demographic data, pretreatment, and control (after 1 hour) arterial blood gas analyses values of the patients were evaluated. RESULTS Sixty-eight patients (mean age 35.8±18.7 years) were included in this study. NBO was given via HFNC to 38 patients (55.9%), and via CFM to 30 patients (44.1%). The demographic characteristics and pretreatment values of carboxy-hemoglobin (COHb) were similar in the 2 groups. The mean COHb value of the HFNC group at the first hour was found significantly lower than the CFM group: 9.5±4.7 and 12.0±5.1, respectively (P=0.041). Improvement of COHb level was significantly higher in the HFNC group compared to the CFM group: 12.5±4.5 versus 6.7±3.7, respectively (P=0.001). CONCLUSIONS HFNC was superior than CFM in alleviating COHb levels in the victims of CO poisoning. We believe that using HFNC will increase patient comfort by shortening the duration of treatment in emergency department settings, especially in patients who have mild clinical findings of CO poisoning.
PMID: 30663634 [PubMed - in process]
Symptomatic os trigonum in national level javelin thrower: a case report.
J Can Chiropr Assoc. 2018 Dec;62(3):202-210
Authors: Bell S, Borody C
Introduction: Os trigonum syndrome is a relatively uncommon condition, resulting from compression of a congenital bony anomaly (os trigonum) and adjacent soft tissues during repetitive hyper-plantarflexion. This condition is currently well-described in ballet, soccer, and running athletes, but few cases exist describing os trigonum syndrome in overhead athletes.
Case Presentation: A 22-year-old national level male javelin athlete presented with a recalcitrant history of posterior ankle pain following a hyper-plantarflexion mechanism. Imaging demonstrated a symptomatic os trigonum and inflammation of surrounding soft tissues. Re-aggravation following a conservative trial of care led to orthopaedic referral. Surgical excision of the os trigonum was performed with an open posterolateral approach. The athlete returned to competition three months later with no recurrence of symptoms.
Summary: This case discusses the clinical presentation, imaging, and management of a symptomatic os trigonum and related pathologies in a javelin thrower.
PMID: 30662075 [PubMed]
Introduction: Antibody-Mediated Therapy Special Issue Part 2.
Int Immunol. 2017 12 30;29(11):487-489
Authors: Nakamura A, Tsumoto K, Takai T
PMID: 29300959 [PubMed - indexed for MEDLINE]