Med Sci Monit Research Articles

Optical topography recording of cortical activity during high frequency yoga breathing and breath awareness Comment to: Non-invasive assessment of hemispheric language dominance by optical topography during a brief passive listening test: A pilot study Stefano Bembich, Sergio Demarini, Andrea Clarici, Stefano Massaccesi, Domenico Grasso Med Sci Monit 2011; 17(12): CR692-697

Optical topography recording of cortical activity during high frequency yoga breathing and breath awareness Comment to: Non-invasive assessment of hemispheric language dominance by optical topography during a brief passive listening test: A pilot study Stefano Bembich, Sergio Demarini, Andrea Clarici, Stefano Massaccesi, Domenico Grasso Med Sci Monit 2011; 17(12): CR692-697

Cerebral venous thrombosis associated with homozygous factor V Leiden mutation in a 15-year-old girl of Tunisian origin

Cerebral venous thrombosis (CVT) is a rare disease. It has numerous and complex etiologies. Inherited or acquired prothrombotic states play a key role in the development of this disease, such as factor V G1691A mutation (FV Leiden). A 15-year-old girl presented to the Department of Neurology with a complaint of severe headache with visual blurring. The diagnosis of CVT was not initially suspected because of the patient's condition on presentation. An MRI showed thrombosis in the superior sagittal sinus, confirming venous stroke. Anticardiolipin and antiphospholipid antibodies were assessed. In addition, inherited prothrombotic defects, such as protein C, protein S, and antithrombin deficiencies, and genetic mutations for FV Leiden, prothrombin gene G20210A (FII G20210A), and methyltetrahydrofolate reductase C677T (MTHFR C677T) were studied. All results were unremarkable except for the unique homozygous FV Leiden mutation, which likely contributed to this prothrombotic situation. This study highlights the fact that FV Leiden may play a significant role in the onset of CVT in young patients.

Lower serum apelin levels in women with polycystic ovary syndrome

We tested differences in serum apelin levels between women with polycystic ovary syndrome (PCOS) and those with a healthy regular menstrual cycle, finding that apelin levels were higher in normal women and that apelin was positively correlated with apolipoprotein A levels.

Efficacy of pharmacological treatment and genetic characterization in early diagnosed patients affected by long QT syndrome with impaired AV conduction

cardiac autonomic control in patients with subclinical and overt hyperthyroidism. Eur J Endocrinol 2001;145:691–6. [15] Biondi B. Should we treat all subjects with subclinical thyroid disease the same way? Eur J Endocrinol Sep 2008;159(3):343–5 Electronic publication 2008 Jul 22. [16] Haentjens P, Van Meerhaeghe A, Poppe K, Velkeniers B. Subclinical thyroid dysfunction and mortality: an estimate of relative and absolute excess all-cause mortality based on time-to-event data from cohort studies. Eur J Endocrinol Sep 2008;159(3):329–41 Electronic publication 2008 May 29. [17] Patane S, Marte F, Di Bella G, Turiano G. Acute myocardial infarction and subclinical hyperthyroidism without significant coronary stenoses. Int J Cardiol 2009 May 29;134(3):e135–7 [Electronic Publication ahead of print 2008 Jun 24]. [18] Patane S, Marte F. Paroxysmal atrial fibrillation during acute myocardial infarction associated with subclinical hyperthyroidism, severe three vessels coronary artery disease and elevation of prostate-specific antigen after Turp. Int J Cardiol 2010;138:e28–30. [19] Patane S, Marte F. Paroxysmal ventricular tachycardia and paroxysmal atrial fibrillation associated with subclinical hyperthyroidism, chronic renal failure and elevation of prostate-specific antigen during acute myocardial infarction. Int J Cardiol 2010 Feb 4;138(3):e44–6 [Electronic Publication ahead of print 2008 Aug 21]. [20] Patane S, Marte F. Atrial fibrillation associated with subclinical hyperthyroidism. Int J Cardiol 2009 May 29;134(3):e155–8 [Electronic Publication ahead of print 2009 Jan 29]. [21] Patane S, Marte F. Intermittent changing axis deviationwith intermittent left anterior hemiblock during atrial flutter with subclinical hyperthyroidism. Int J Cardiol 2009 Jun 26;135(2):e37–9 [Electronic Publication ahead of print 2008 Jan 24]. [22] Patane S, Marte F. Changing axis deviation and paroxysmal atrial flutter associated with subclinical hyperthyroidism. Int J Cardiol 2010 Oct 8;144(2):e31–3 [Electronic Publication ahead of print 2009 Jan 26]. [23] Erem C. Blood coagulation, fibrinolytic activity and lipid profile in subclinical thyroid disease: subclinical hyperthyroidism increases plasma factor X activity. Clin Endocrinol (Oxf) Mar 2006;64(3):323–9. [24] Coban E, Aydemir M, Yazicioglu G, Ozdogan M. Endothelial dysfunction in subjects with subclinical hyperthyroidism. J Endocrinol Invest Mar 2006;29(3):197–200. [25] Coban E, Aydemir M. Levels of plasma fibrinogen and D-dimer in subjects with subclinical hyperthyroidism. Med Sci Monit Jan 2008;14(1):CR42–46. [26] Patane S, Marte F. Atrial fibrillation and acute myocardial infarction without significant coronary stenoses associated with subclinical hyperthyroidism and erythrocytosis. Int J Cardiol 2010 Nov 5;145(1):e36–9 [Electronic Publication ahead of print 2009 Jan 30]. [27] Patane S, Marte F, Curro A, Cimino C. Recurrent acute pulmonary embolism and paroxysmal atrial fibrillation associated with subclinical hyperthyroidism. Int J Cardiol 2010 Jul 9;142(2):e25–6 [Electronic Publication ahead of print 2009 Jan 9]. [28] Coats AJ. Ethical authorship and publishing. Int J Cardiol 2009;131:149–50.

High frequency yoga breathing increases energy ­expenditure from carbohydrates Comment to: Assessment of sleep patterns, energy expenditure and circadian rhythms of skin temperature in patients with acute coronary syndrome Hadil Al Otair, Mustafa Al-shamiri, Mohammed Bahobail, Munir M. Sharif, Ahmed S. BaHammam Med Sci Monit, 2011; 17(7): CR397–403

High frequency yoga breathing increases energy ­expenditure from carbohydrates Comment to: Assessment of sleep patterns, energy expenditure and circadian rhythms of skin temperature in patients with acute coronary syndrome Hadil Al Otair, Mustafa Al-shamiri, Mohammed Bahobail, Munir M. Sharif, Ahmed S. BaHammam Med Sci Monit, 2011; 17(7): CR397–403

Paroxysmal nocturnal hemoglobinuria clones are not present in HIV positive patients

The existence of paroxysmal nocturnal hemoglobinuria (PNH) clones in aplastic anemia and myelodysplastic syndrome is well established (Dunn et al., Ann Intern Med 1999;131:401–408; Kaiafa et al., Ann Hematol 2008;87:257–262). Although decreased expression of CD55 and CD59 on lymphocytes has been described in human immunodeficiency virus (HIV) positive patients, to our knowledge, PNH clones have not been characterized in HIV. However, a recent study from Greece (Terpos et al., Med Sci Monit 2008;14:CR276–CR280) found a significant loss of glycophosphotidylinositol (GPI)-linked antigens CD55 and CD59 on red blood cells from HIV positive patients. Blood samples from patients with confirmed HIV infection were submitted to our flow cytometry laboratory for absolute CD4 count analysis. When a blood sample demonstrated an absolute CD4 count of less than 400, the excess blood sample was then tested for the expression level of the GPI-linked cell surface antigens on red blood cells (CD55 and CD59) and white blood cells (CD14 and CD24). In addition, we used fluorescent areolysin (FLAER) to evaluate the presence or absence of the GPI anchor directly on white blood cells. Samples from 73 HIV positive patients were evaluated for expression levels of CD14, CD24, CD55, CD59, and FLAER. No patient sample demonstrated a loss of CD55, or CD59 on the red blood cells, or a loss of CD14, CD24, or FLAER on the granulocytes and monocytes. While PNH clones have been described in other hematologic diseases, we did not find evidence of PNH clones in our examined HIV positive patient samples. © 2010 International Clinical Cytometry Society

Prevalence and molecular characterization of extended-spectrum β-lactamase-producing Klebsiella pneumoniae in Riyadh, Saudi Arabia

BACKGROUND AND OBJECTIVES:Reports on extended-spectrum β-lactamases (ESBL) production by Enterobacteriaceae, and especially in Klebsiella pneumoniae, are few in Saudi Arabia. Therefore, we determined the prevalence of ESBL in K pneumoniae from Riyadh and characterized the predominant β-lactamase gene in these isolates.METHODS:A total of 400 K pneumoniae samples were isolated from two hospitals in Riyadh during 2007 and screened for production of ESBL using ESBL-E-strips and combined disk methods. PCR assay was used to detect blaTEM, blaSHV, and blaCTX-M genes.RESULTS:Phenotypic characterization identified a high ESBL rate of 55% of K pneumoniae isolates. ESBL-producing K pneumoniae were PCR positive for SHV, TEM and CTX-M β-lactamase genes with prevalences 97.3%, 84.1% and 34.1%, respectively. Within the CTX-M family, two groups of enzymes, CTX-M-1 and CTX-M-9-like genes were found with prevalences of 60% and 40%, respectively.CONCLUSIONS:This study confirms the high rate of ESBL in K pneumoniae clinical isolates in hospitals in Riyadh. This study demonstrates the worldwide spread of blaCTX-M genes. This first report of the presence of the blaCTX-M gene in clincial isolates in Saudi Arabia is evidence of the continuing worldwide spread of this gene.

Schizophrenia is a disorder of higher order hierarchical processing

Schizophrenia is a mental disorder in which the patient manifests with auditory hallucinations, paranoid or bizarre delusions, and disorganized speech and thinking. It is associated with significant social dysfunction. There are many hypotheses regarding schizophrenia. Most of these focus on schizophrenia as a manifestation of abnormalities from genetic [Mulle JG. Genomic structural variation and schizophrenia. Curr Psychiatry Rep 2008;10(2):171-7], viral [Fruntes V, Limosin F. Schizophrenia and viral infection during neurodevelopment: a pathogenesis model? Med Sci Monit 2008;14(6):RA71-7], neurochemical [e.g. dopamine (Lewis DA, Akil M. Cortical dopamine in schizophrenia: strategies for postmortem studies. J Psychiatr Res 1997;31(2):175-95) or interactions between neurotransmitters (Duncan GE, Sheitman BB, Lieberman JA. An integrated view of pathophysiological models of schizophrenia. Brain Res Brain Res Rev 1999;29(2):250-64)] or brain structural [Kotrla KJ, Weinberger DR. Brain imaging in schizophrenia. Annu Rev Med 1995;46:113-22] origins. Most of these hypotheses do not account for how or why these presumed causes lead to the manifestations of schizophrenia. We argue that brain structure and function is compatible with a hierarchical processing structure that forms the basis for perception and thought in healthy humans. We propose that perturbations of the types listed above lead to disruption of higher levels of perception and hierarchical temporal processing by the brain and that this constitutes the core deficit in schizophrenia. We present evidence that this model explains many of the features of schizophrenia and we make a series of predictions about schizophrenia.

Cord Blood Mercury and Early Child Development: Effects of the World Trade Center

Cord Blood Mercury and Early Child Development: Effects of the World Trade Center

Melatonin: A Suitable Agent for Depression Associated with Stroke?

Back to table of contents Previous article Next article LETTERFull AccessMelatonin: A Suitable Agent for Depression Associated with Stroke?Ertugrul Cam Ph.D.,Burak Yulug M.D.,Nurettin Cengiz Ph.D.,Ester Poelkin Ph.D.,Dogan Isýk M.D.,Mustafa Bakar Ph.D.,Erol Ozan M.D.,Ertugrul Kilic Ph.D.,Ertugrul Cam Ph.D.Search for more papers by this author,Burak Yulug M.D.Search for more papers by this author,Nurettin Cengiz Ph.D.Search for more papers by this author,Ester Poelkin Ph.D.Search for more papers by this author,Dogan Isýk M.D.Search for more papers by this author,Mustafa Bakar Ph.D.Search for more papers by this author,Erol Ozan M.D.Search for more papers by this author,Ertugrul Kilic Ph.D.Search for more papers by this author,Published Online:1 Oct 2008AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: It is widely known that occurrence of poststroke mood disorders, especially depression, is one of the most frequent complications of stroke. 1 It affects approximately 20%–40% of all patients and the definitive treatment of this clinical picture includes various antidepressant agents. 1 The evidence about the antidepressant-like activity of melatonin and melatonin agonists is rapidly increasing. 2 – 7 However melatonin is also an important agent in sleep disturbances, which are shown to be associated with stroke. 8 In light of these findings we wanted to evaluate whether this novel antidepressant agent also has neuroprotective effect on cerebral ischemia. To examine this matter we evaluated the neuroprotective effect of melatonin in a relevant model for stroke in humans. Thus we administered the indole prophylactically for 4 weeks before the middle cerebral artery thread occlusions and evaluated the effects of melatonin treatment on ischemic brain injury 24 hours after reperfusion. Reproducibility of cerebral ischemia was controlled by Laser Doppler Flowmetry, and the neuroprotection was evaluated by infarct volume measurements ( Figure 1 ). Melatonin significantly reduced the infarct size ( Figure 1 ) (mean 1.12±0.5 mm 3 compared to 2.62±0.5 mm 3 ) when given prophylactically (p<0.05). This study was interesting with regard to poststroke depression by which a mood stabilizer with neuroprotective property would be preferable. Additionally, this finding supports that melatonin may be a suitable agent for patients with stroke and sleep disturbances, not only with its inhibiting effect on ischemic neuronal injury, but also with its improving effect on sleep disturbances. This can in turn provide additional support for the restorative process after brain injury. FIGURE 1. Infarct Volumes of Mice Subjected to Transient Cerebral IschemiaMelatonin led to a decrease in infarct size in treated animals. *Significantly different from vehicle-treated control animals (p≤0.05).However, further experiments to evaluate the long-term clinical applicability of such neuroprotective effects of melatonin in poststroke depression patients with MRI and spectroscopy studies would be the logical future steps to be taken in the field of psychiatric research.Department of Anatomy, University of Zurich, SwitzerlandDepartment of Psychiatry, University of Bern, SwitzerlandDepartment of Histology, University of 100.Yil, Van, TurkeyDepartment of Neurology, University of Göttingen, Göttingen, GermanyDepartment of Psychiatry, Dokuz Eylül University, İzmir, TurkeyDepartment of Neurology, Uludag UniversityDepartment of Psychiatry, Atatürk University, ErzurumDepartment of Physiology, University of Yeditepe, Istanbul, TurkeyReferences1 . Whyte EM, Mulsant BH: Poststroke depression: epidemiology, pathophysiology and biological treatment. Biol Psychiatry 2002; 52:253–264Google Scholar2 . Bertaina-Anglade V, la Rochelle CD, Boyer PA, et al: Antidepressant-like effects of agomelatine (S 20098) in the learned helplessness model. Behav Pharmacol 2006; 17:703–713Google Scholar3 . Ergün Y, Ergün UG, Orhan FO, et al: Co-administration of a nitric oxide synthase inhibitor and melatonin exerts an additive antidepressant-like effect in the mouse forced swim test. Med Sci Monit 2006; 12:BR307–312Google Scholar4 . Sumaya IC, Masana MI, Dubocovich ML: The antidepressant-like effect of the melatonin receptor ligand luzindole in mice during forced swimming requires expression of MT2 but not MT1 melatonin receptors. J Pineal Res 2005; 39:170–177Google Scholar5 . Barden N, Shink E, Labbé M, et al: Antidepressant action of agomelatine (S 20098) in a transgenic mouse model. Prog Neuropsychopharmacol Biol Psychiatry 2005; 29:908–916Google Scholar6 . Loiseau F, Le Bihan C, Hamon M, et al: Antidepressant-like effects of agomelatine, melatonin, and the NK1 receptor antagonist GR205171 in impulsive-related behaviour in rats. Psychopharmacology (Berl) 2005; 182:24–32Google Scholar7 . Mantovani M, Pértile R, Calixto JB, et al: Melatonin exerts an antidepressant-like effect in the tail suspension test in mice: evidence for involvement of N -methyl- D -aspartate receptors and the L-arginine-nitric oxide pathway. Neurosci Lett 2003; 343:1–4 Google Scholar8 . Kunz D, Mahlberg R, Muller C, et al: Melatonin in patients with reduced REM sleep duration: two randomized controlled trials. J Clin Endocrinol Metab 2004; 89:128–134Google Scholar FiguresReferencesCited byDetailsCited ByNone Volume 20Issue 4 Fall, 2008Pages 498-500 Metrics PDF download History Published online 1 October 2008 Published in print 1 October 2008

The Many Possible Benefits of Natriuretic Peptides After Myocardial Infarction

Natriuretic peptides (NPs) are well-known markers of the ventricular hypertrophic response, as documented in many studies performed either in animals or with cultured cardiomyocytes. In recent years, evidence has been mounting that NPs are in fact negative regulators of the hypertrophic response, as reviewed recently.1 In this light, NPs appear as endogenous cardioprotective agents of which expression increases in reaction to myocardial pathological conditions, but it is still unclear to which extent these agents may actually decrease mortality. In this issue of Hypertension , Nakanashi et al2 show that when myocardial infarction (MI) is induced by permanent occlusion of the coronary artery, mortality by heart failure is increased in knockout mice with inactivation of the gene coding for the NP receptor guanylyl cyclase-A (GC-A). Beyond these short-term effects, inactivation of GC-A also worsens post-MI chronic ventricular remodeling. Although the present study does not show whether these chronic remodeling processes also increase mortality at a later stage, the remodeling is accompanied by ventricular enlargement and decreased fractional shortening, both of which usually associate with poor prognosis. The importance of these data is enhanced by the fact that increasing numbers of studies are investigating the utility of recombinant NPs in humans.3 However, several questions remain concerning the particular modes of action of NPs. One issue concerns the question of whether NPs work via peripheral mechanisms or via a direct action on the myocardium. Importantly, congestive heart failure is accompanied by volume expansion, and the present article shows that the natriuresis and diuresis are decreased in GC-A knockout animals during the 4 days that follow MI, thus possibly contributing to increased heart failure during …