[The effects of whole-body cryotherapy and melatonin supplementation on total antioxidative status and some antioxidative enzymes in multiple sclerosis patients].
Pol Merkur Lekarski. 2011 Sep ;31(183):150-3. PMID: 21991843
Elzbieta Miller, Małgorzata Mrowicka, Katarzyna Malinowska, Józef Kedziora, Ireneusz Majsterek
Oxidative stress is an important factor which contribute to the pathogenesis of lesions in multiple sclerosis (MS). Whole body cryotherapy (WBCT) is often used in treatment neurological and orthopedic diseases. THE AIM, MATERIAL AND METHODS: The aim of this study was to determinate the level of total antioxidative status (TAS) in plasma and activity of superoxide dismutase (SOD) and catalase (CAT) in erythrocytes of MS patients (n = 28) before and after 10 exposures of WBCT (-120 degrees C/3 minutes/day). 16 MS patients during 10 exposures of WBCT additionally were supplemented by 10 mg of melatonin. RESULTS: Increasing of TAS level in plasma as well as supplemented with melatonin and non-supplemented MS patients was observed after 10 exposures of WBCT Melatonin statistically significant increased activity of SOD and CAT in erythrocytes of MS patients treated with WBCT. CONCLUSIONS: Results of our study indicate significant increase of TAS level in plasma of MS patients of WBCT treatment. This indicate that WBCT might be a therapy which suppress oxidative stress in MS patients.
Article Published Date : Sep 01, 2011
Can subphysiological cold application be utilized in excessive dermal scarring prophylaxis and treatment?: A promising hypothetical perspective.
Med Hypotheses. 2016 Dec;97:4-6
Authors: Yağmur Ç, Sinan Engin M, Ogawa R
Excessive dermal scarring (EDS) is a wound healing complication, characterized by protruded erythematous and inelastic 'proliferative scar tissue' which is associated with increased and prolonged inflammation process within the wound microenvironment. As inflammation plays a key role in this process, methods to contain or attenuate excessive inflammation hold promise in treatment and prophylaxis of EDS conditions. While cold exposure is notorious as the causative agent a wide array of morbidities and fatalities, its tempered use is exploited in medicine for ablative and therapeutic applications. "Subphysiological cold" has been administered for its antiinflammatory effects which act via decreasing vascular permeability and downregulating proliferation of cells in the wound environment; this knowledge supports our hypothesis that "subphysiological cold application" can also be utilized in human EDS prophylaxis and treatment. In this study, we are reviewing the mechanisms of its both deleterious and therapeutic actions and suggesting another possible application for prevention and/or treatment of human EDS conditions.
PMID: 27876128 [PubMed - indexed for MEDLINE]
Neonatal hypoxic ischemic encephalopathy: an update on disease pathogenesis and treatment.
Expert Rev Neurother. 2017 May;17(5):449-459
Authors: Yıldız EP, Ekici B, Tatlı B
INTRODUCTION: Hypoxic ischemic encephalopathy (HIE) is the most important reason for morbidity and mortality in term-born infants. Understanding pathophysiology of the brain damage is essential for the early detection of patients with high risk for HIE and development of strategies for their treatments. Areas covered: This review discusses pathophysiology of the neonatal HIE and its treatment options, including hypothermia, melatonin, allopurinol, topiramate, erythropoietin, N-acetylcyctein, magnesium sulphate and xenon. Expert commentary: Several clinical studies have been performed in order to decrease the risk of brain injury due to difficulties in the early diagnosis and treatment, and to develop strategies for better long-term outcomes. Although currently standard treatment methods include therapeutic hypothermia for neonates with moderate to severe HIE, new supportive options are needed to enhance neuroprotective effects of the hypothermia, which should aim to reduce production of the free radicals and to have anti-inflammatory and anti-apoptotic actions.
PMID: 27830959 [PubMed - indexed for MEDLINE]