Post-stroke pure apraxia of speech – A rare experience

Apraxia of speech (AOS) is a motor speech disorder, most typically caused by stroke, which in its “pure” form (without other speech-language deficits) is very rare in clinical practice. Because some observable characteristics of AOS overlap with more common verbal communication neurologic syndromes (i.e. aphasia, dysarthria) distinguishing them may be difficult. The present study describes AOS in a 49-year-old right-handed male after left-hemispheric stroke. Analysis of his articulatory and prosodic abnormalities in the context of intact communicative abilities as well as description of symptoms dynamics over time provides valuable information for clinical diagnosis of this specific disorder and prognosis for its recovery. This in turn is the basis for the selection of appropriate rehabilitative interventions

Effects of Constant Magnetic Field on Electrodeposition of Co-W-Cu Alloy

The paper presents a study of the effect of constant magnetic field (CMF) on the basic processes of Co-W-Cu alloys electrodeposition. The alloys electrodeposited in the presence of CMF were more homogeneous and smooth than those obtained without CMF. The reason for these changes was the fact that the Lorentz force, generated in CMF, caused the magnetohydrodynamic (MHD) effect. Electrolyte motion under the influence of CMF caused an increase of cobalt and tungsten content with a simultaneous decrease of copper content in the alloy. The presence of the magnetic field during plating leads to significant greater corrosion resistance and smaller roughness

Polymorphism of the ACE gene and the risk of obstructive sleep apnoea

WSTĘP: Zespół obturacyjnego bezdechu w czasie snu (obturacyjny bezdech śródsenny, OBŚ) charakteryzuje się pojawianiem nawracających epizodów bezdechów lub spłyceń oddychania. Wśród genów kandydatów, wpływających na ryzyko wystąpienia OBŚ wymienia się geny, których polimorfizmy wpływają na rozwój chorób o podobnej patogenezie co OBŚ: APOE, geny dla leptyny i receptora leptyny, TNFA1, ADRB2 oraz ACE (gen dla enzymu konwertującego angiotensynę). Dotychczas opisano zależność pomiędzy polimorfizmem genu ACE a chorobami sercowo-naczyniowymi, a jego wpływ na zachorowanie na OBŚ jest dyskusyjny. Celem pracy było zbadanie wpływu polimorfizmu insercyjno/delecyjnego (I/D) genu ACE na ryzyko zachorowania na OBŚ.MATERIAŁ I METODY: Badaniem objęto grupę 55 chorych, którzy zgłaszali się w celu rozpoczęcia terapii CPAP. Grupę kontrolną stanowiło 50 osób, które nie zgłaszały zaburzeń snu. Rozpoznanie ustalano na podstawie wyniku polisomnografii (wg klasyfikacji AASM) i wartości punktowej Skali Senności Epworth. DNA izolowano z leukocytów krwi obwodowej za pomocą zestawu Qiagen DNA mini Kit. Polimorfizm genu ACE oceniano na podstawie długości fragmentów produktów reakcji PCR w żelu agarozowym.WYNIKI: Nie wykazano statystycznie istotnych różnic w rozkładzie poszczególnych genotypów genu ACE w grupie chorych z OBŚ i w grupie kontrolnej. Wykazano natomiast, że allel D występował istotnie rzadziej w grupie chorych na OBŚ niż w grupie kontrolnej (χ² = 4,25, p = 0,04). Ponadto, nosiciele allela I mieli trzykrotnie większe ryzyko wystąpienia OBŚ (HR = 2,748, 95% CI = 1,029–7,340, p < 0,05).WNIOSKI: Analiza polimorfizmu genu ACE może być przydatna w ocenie ryzyka wystąpienia OBŚ u osób klinicznie predysponowanych do rozwoju tej choroby.INTRODUCTION: Obstructive sleep apnoea/hypopnea syndrome (OSA) is characterized by obstruction of the upper airway during sleep, resulting in repetitive breathing pauses accompanied by oxygen desaturation and arousal from sleep. Among the candidate genes affecting the risk of OSA, genes whose polymorphisms influence the development of diseases with similar pathogenesis such as OSA could be listed: APOE, genes for leptin and leptin receptor, TNFA1, ADRB2 and ACE (gene for angiotensin-converting enzyme). Until now there has been a confirmed relationship between ACE gene polymorphism and cardiovascular diseases, but its effect on the incidence of OSA is debatable. The aim of this study was to investigate the effect of ACE gene insertion/deletion (I/D) polymorphism on the risk of OSA.MATERIAL AND METHODS: Fifty-five patients with confirmed diagnose of OSA and qualified to CPAP therapy entered the study. The control group included 50 subjects who did not complain of any sleep related symptoms. Diagnose of OSA was set on the basis of full overnight polysomnography together with Epworth Sleepiness Scale according to American Academy of Sleep Medicine guidelines. DNA was isolated from peripheral blood leukocytes with Qiagen DNA mini Kit. ACE gene polymorphism was determined in genomic DNA using allele specific polymerase chain reaction. Different sizes of PCR products were observed on agarose gel electrophoresis.RESULTS: There were non-significant differences in the frequency of ACE genotypes. However, allele D had significantly lower prevalence in the study group than in the control group. (χ² = 4.25 p = 0.04). Moreover, I allele carriers had a threefold greater risk of developing OSA (HR = 2.748, 95% CI = 1.029–7.340, p < 0.05).CONCLUSIONS: Analysis of ACE gene polymorphism might be useful to determine the risk of developing OSA in clinically predisposed patients

Influence of opioid peptides on human neutrophil apoptosis and activation in vitro.

BACKGROUND: It has been shown that cells of the immune system release opioid peptides and possess receptors for them. The concentrations of opioid peptides in the peripheral circulation rapidly increase during inflammation and acute stress response. AIMS: The effect of opioid peptides Met-enkephalin (M-ENK) and beta-endorphin (beta-END) on the oxidative metabolism of normal human neutrophils and their death by apoptosis in vitro was investigated. METHODS: Isolated from peripheral blood, neutrophils were incubated in the presence or absence of 10(-6) to 10(-10) M of M-ENK and beta-END for 12 and 18 h. Apoptosis of neutrophils was determined in vitro by flow cytometric analysis of cellular DNA content and Annexin V-FITC protein binding to the cell surface. The MTT-reduction assay was employed to estimate the oxidative metabolism of neutrophils. RESULTS: Treatment with M-ENK caused a significant increase in apoptotic cells after 18 h of culture: *0 M (control) versus 10(-10) M, p < or = 0.02; **10(-10) M versus 10(-10) M, p < or = 0.02. Treatment with beta-END caused a significant increase in apoptotic cells after 12 h of culture: 0 M versus 10(-8) M, p < or = 0.03; **0 M versus 10(-10) M, p < or = 0.04. We found the significant increase in MTT reduction by neutrophils in the presence of M-ENK and beta-END both before and after the culture. However, the ability of neutrophils to reduce the MTT salt to formazan decreased significantly after the culture. CONCLUSIONS: We observed that the in vitro effect of opioid peptides on the neutrophil survival and their functional state was time and dose dependent. The presence of antioxidants in the culture medium modifies neutrophil survival

Guzy ośrodkowego układu nerwowego u dzieci - trudności diagnostyczne

Nowotwory ośrodkowego układu nerwowego (OUN) są najczęstszymi guzami litymi u dzieci. Dzieli się je na guzy mózgu i guzy rdzenia kręgowego. Symptomatologia kliniczna zależy od lokalizacji guza i jego budowy histologicznej. Czas trwania objawów wiąże się też z wiekiem dziecka i umiejętnością postrzegania przez rodziców i lekarza pierwszego kontaktu wczesnych sygnałów guza OUN. Rokowanie u dzieci z rozpoznaniem guzów OUN jest gorsze niż w przypadku większości pozostałych nowotworów dziecięcych. Wczesna diagnoza i doszczętny lub subtotalny zabieg neurochirurgiczny poprawiają rokowanie. Forum Medycyny Rodzinnej 2011, tom 5, nr 1, 69-7

Trimethyl-3-meth­oxy-4-oxo-5-triphenyl­phospho­ranyl­idene­cyclo­pent-1-ene-1,2,3-tricarboxyl­ate

The title compound, C30H27O8P (2), was formed as one of two products {(1) [Krawczyk et al. (2010 ▶). Acta Cryst. E66 (cv2752)] and (2)} in the reaction of dimethyl acetyl­enedicarboxyl­ate with triphenyl­phosphine. The mol­ecule of (2) consists of a five-membered carbocyclic ring. The P atom is a part of a triphenylphosphoranylidene substituent. In contrast to (1), the five-membered ring of (2) is planar, the r.m.s. deviation being only 0.009 (2) Å

A novel role for Mms2 in the control of spontaneous mutagenesis and Pol3 abundance

Mms2 is a ubiquitin E2-variant protein with a very well-documented function in the tolerance pathway that protects both human and yeast cells from the lethal and mutagenic effects of DNA damage. Interestingly, a high expression level of human MMS2 is associated with poor survival prognosis in different cancer diseases. Here we have analyzed the physiological effects of Mms2 overproduction in yeast cells. We show that an increased level of this protein causes a spontaneous mutator effect independent of Ubc13, a cognate partner of Mms2 in the PCNA- polyubiquitinating complex responsible for the template switch. Instead, this new promutagenic role of Mms2 requires Ubc4 (E2) and two ubiquitin ligases of HECT and RING families, Rsp5 and Not4, respectively. We have established that the promutagenic activity of Mms2 is dependent on the activities of error-prone DNA polymerase ζ and Rev1. Additionally, it requires the ubiquitination of K164 in PCNA which facilitates recruitment of these translesion polymerases to the replication complex. Importantly, we have established also that the cellular abundance of Mms2 influences the cellular level of Pol3, the catalytic subunit of replicative DNA polymerase δ. Lack of Mms2 increases the Pol3 abundance, whereas in response to Mms2 overproduction the Pol3 level de- creases. We hypothesize that increased levels of spontaneous mutagenesis may result from the Mms2-induced reduction in Pol3 accumulation leading to increased participation of error-prone polymerase ζ in the replica- tion comple

The role of selected mechanisms of innate immunity in the pathogenesis of diabetes

Understanding the important role of the non-specific immune response in protecting the body against the development of numerous diseases has become partially possible after the discovery of several classes of pattern recognition receptors (PRR), such as Toll-like or NOD-like receptors. A group of cytoplasmic proteins called the inflammasome, which detect PAMP and DAMP through the PRR receptors, is able to activate pro-inflammatory cytokines and trigger an acute inflammatory reaction both in the extracellular and intracellular space. Low-grade systemic and local inflammation contributes to the development and progression of various conditions, including autoimmune and metabolic diseases, such as diabetes, metabolic syndrome and atherosclerosis, which until recently were not even considered inflammatory diseases. This review will discuss the role of innate immunity in the development of type 1 and type 2 diabetes, focusing on the role of specific innate immunity receptors and insulin resistance involved in these diseases pathogenesis

Tetra­methyl 1,1,2-triphenyl-2H-1λ5-phosphole-2,3,4,5-tetra­carboxyl­ate

The title compound, C30H27O8P (1), was formed as one of two products {(1) and (2) [Krawczyk et al. (2010 ▶). Acta Cryst. E66 (cv2753)]} in the reaction of dimethyl acetyl­enedicarboxyl­ate with triphenyl­phosphine. The mol­ecule of (1) consists of a five-membered ring, in which the P atom is incorporated. One of the phenyl groups of the triphenyl­phosphine migrated to a vicinal C atom during the reaction. The five-membered ring of (1) is corrugated [r.m.s. deviation = 0.0719 (8) Å], whereas that in compound (2) is planar, the r.m.s. deviation being only 0.009 (2) Å

SACROILIAC JOINT SYNDROME – DESCRIPTION OF PAIN ETIOLOGY

Numerous clinical studies have supported the thesis that sacroiliac (SI) joints constitute one of the causes of spinal pain radiating to the lower limb. The pathology of SI joint has been variously defined. The majority of definitions refer to the joint structure as the potential source of pain.As far as the etiology of SI joint dysfunction is concerned, it has not been disambiguated yet.Among the main causative factors, injuries and strains of the structures surrounding the joint are noted.Joint pathology usually manifests itself by pain occurring within the area of the joint.The causes of pain may be divided into two categories: intra-articular and extra-articular.Pain caused by the SI joint may be nociceptive or neural in nature, whereaspain pattern characteristic of the joint correlates with its innervation (S2 dorsal rami) and is consistent with the localisation of radicular pain to a large extent