9 research outputs found
THE ROLE OF BROCA’S AREA IN SYNTAX: A TMS STUDY ON WRITTEN GREEK LANGUAGE
A number of recent papers have addressed the potential of transcranial magnetic stimulation (TMS) to interfere with linguistic processes or speech production. In this paper we present an experiment with TMS to clarify the role of Broca’s area in syntactic processing. An experimental paradigm contrasted sentences that require syntactic and semantic decisions on written Greek language. We found a clue of selective priming effects on syntactic decisions but not on semantic decisions. Our results provide evidence of the involvement of Broca’s area in syntax
F TACHEODISPERSION. A NEW NEUROPHYSIOLOGICAL METHOD FOR THE INVESTIGATION OF PERIPHERAL NERVE DISORDERS
F WAVE IS A LATE, EVOKED MUSCLE RESPONSE PRODUCED BY RECURRENT DISCHARGES OF ANTIDROMICALLY ACTIVATED MOTOR NEURONES. IN F TACHEODISPERSION, THE NEW NEUROPHYSIOLOGICAL METHOD APPLIED IN THIS STUDY, A SIGNIFICANT NUMBER OF CONSECUTIVELYRECORDED F WAVES ARE USED TO ESTIMATE THE DISTRIBUTION OF CONDUCTION VELOCITIES (FCV)OF INDIVIDUAL OF SMALL GROUPS OF MOTOR NERVE FIBRES. WE STUDIED 39 HEALTHY SUBJECTS AND 52 PATIENTS WITH POLYNEUROPATHY. ANALYSIS OF F TACHEODISPERSION IN THE HEALTHY VOLUNTEERS SUGGESTED AN AGE RELATED SLOWING OF FCVMAX FCVMIN FCV MEAN WHICH WAS MORE PROMINENT IN THE PERONEAL THAN THE ULNAR. PATIENT'S NERVES WERE DIVIDED INTO 4 GROUPS. F TACHEODISPERSION IN THE FIRST GROUP (NORMAL CONVENTIONAL MEASUREMENTS) SHOWED MILD SHIFT OF FCV TOWARDS THE LOWER NORMAL LIMIT. (ABSTRACT TRUNCATED)ΤO F ΚΥΜΑ ΕΙΝΑΙ ΕΝΑ ΚΑΘΥΣΤΕΡΗΜΕΝΟ ΠΡΟΚΛΗΤΟ ΜΥΙΚΟΔΥΝΑΜΙΚΟ ΠΟΥ ΠΑΡΑΓΕΤΑΙ ΑΠΟ ΠΑΛΙΝΔΡΟΜΕΣ ΕΚΦΟΡΤΙΣΕΙΣ ΚΙΝΗΤΙΚΩΝ ΚΥΤΤΑΡΩΝ ΤΩΝ ΠΡΟΣΘΙΩΝ ΚΕΡΑΤΩΝ ΤΟΥ ΝΩΤΙΑΙΟΥ ΜΥΕΛΟΥ ΜΕΤΑ ΑΠΟ ΠΕΡΙΦΕΡΙΚΟ ΕΡΕΘΙΣΜΟ ΤΩΝ ΝΕΥΡΑΞΟΝΩΝ ΤΟΥΣ. ΕΝΑΣ ΣΤΑΤΙΣΤΙΚΩΣ ΣΗΜΑΝΤΙΚΟΣ ΑΡΙΘΜΟΣ F ΚΥΜΑΤΩΝ ΧΡΗΣΙΜΟΠΟΙΕΙΤΑΙ ΣΤΗ ΜΕΘΟΔΟ ΤΗΣ F ΤΑΧΕΟΔΙΑΣΠΟΡΑΣ, ΤΗ ΝΕΑ ΝΕΥΡΟΦΥΣΙΟΛΟΓΙΚΗ ΜΕΘΟΔΟ ΠΟΥ ΕΦΑΡΜΟΖΕΤΑΙ ΣΤΗΝ ΕΡΓΑΣΙΑ ΑΥΤΗ, ΓΙΑ ΤΟΝ ΥΠΟΛΟΓΙΣΜΟΤΗΣ ΚΑΤΑΝΟΜΗΣ ΤΩΝ ΤΑΧΥΤΗΤΩΝ ΑΓΩΓΗΣ ΜΕΜΟΝΩΜΕΝΩΝ Η ΜΙΚΡΩΝ ΟΜΑΔΩΝ ΚΙΝΗΤΙΚΩΝ ΝΕΥΡΙΚΩΝ ΙΝΩΝ. ΣΤΗ ΜΕΛΕΤΗ 39 ΥΓΙΗ ΑΤΟΜΑ ΚΑΙ 52 ΑΣΘΕΝΕΙΣ ΕΞΕΤΑΣΤΗΚΑΝ. ΣΤΑ ΥΓΙΗ ΑΤΟΜΑ ΔΙΑΠΙΣΤΩΘΗΚΕ ΜΙΑ ΜΕΙΩΣΗ ΤΟΥ ΣΥΝΟΛΟΥ ΤΩΝ ΤΑΧΥΤΗΤΩΝ ΜΕ ΤΗΝ ΠΑΡΟΔΟ ΤΗΣ ΗΛΙΚΙΑΣ Η ΟΠΟΙΑ ΕΙΝΑΙ ΠΙΟ ΕΜΦΑΝΗΣ ΣΤΟ ΠΕΡΟΝΙΑΙΟ ΠΑΡΑ ΣΤΟ ΩΛΕΝΙΟ. ΑΝΑΓΝΩΡΙΣΤΗΚΑΝ 4 ΚΑΤΗΓΟΡΙΕΣ ΝΕΥΡΩΝ ΣΤΟΥΣ ΑΣΘΕΝΕΙΣ ΑΝΑΛΟΓΑ ΜΕ ΤΑ ΕΥΡΗΜΑΤΑ ΤΩΝ ΣΥΜΒΑΤΙΚΩΝ ΗΛΕΚΤΡΟΦΥΣΙΟΛΟΓΙΚΩΝ ΜΕΤΡΗΣΕΩΝ. ΣΤΗΝ ΠΡΩΤΗ ΚΑΤΗΓΟΡΙΑ (ΦΥΣΙΟΛΟΓΙΚΕΣ ΣΥΜΒΑΤΙΚΕΣ ΜΕΤΡΗΣΕΙΣ) ΠΑΡΑΤΗΡΗΘΗΚΕ ΗΠΙΑ ΜΕΙΩΣΗ ΤΗΣ ΜΕΓΙΣΤΗΣ ΚΑΙ ΕΛΑΧΙΣΤΗΣ ΤΑΧΥΤΗΤΑΣ ΠΟΥ ΕΚΤΙΜΗΘΗΚΑΝ ΜΕ F ΤΑΧΕΟΔΙΑΣΠΟΡΑ (F-TXΜΕΓ. F-TXΜΙΚ.) (ΠΕΡΙΚΟΠΗ ΠΕΡΙΛΗΨΗΣ
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Is the G2019S LRRK2 mutation common in all southern European populations?
Mutations in the leucine-rich repeat kinase 2 (
LRRK2) gene, especially the G2019S mutation, have been identified as a common cause of Parkinson’s disease in southern European and other Mediterranean populations (Iberians, Ashkenazi Jews and North African Arabs). Owing to the geographic and historic vicinity of Greece with areas of high prevalence of
LRRK2 mutations we studied the frequency of the G2019S mutation in a well characterized cohort of familial and sporadic Parkinson’s disease patients of Greek origin from mainland Greece. The prevalence of the
LRRK2 R1441C mutation and the G2385R Asian polymorphism was also determined. We identified no patients with any of the studied mutations/polymorphisms. Very low prevalence of the
LRRK2 G2019S mutation has been reported in other southern European populations.
LRRK2 mutations appear to be limited in certain populations and differing ancestry and founder effects may explain the reported variability. Accurate estimations of the frequency and penetrance of different
LRRK2 mutations are essential for correct and cost-efficient use of genetic testing and proper genetic counseling of patients with Parkinson’s disease
Reconstituted HDL-apoE3 promotes endothelial cell migration through ID1 and its downstream kinases ERK1/2, AKT and p38 MAPK
Introduction: Atherosclerotic Coronary Artery Disease (ASCAD) is the
leading cause of mortality worldwide. Novel therapeutic approaches
aiming to improve the atheroprotective functions of High Density
Lipoprotein (HDL) include the use of reconstituted HDL forms containing
human apolipoprotein A-I (rHDL-apoA-I). Given the strong
atheroprotective properties of apolipoprotein E3 (apoE3), rHDL-apoE3 may
represent an attractive yet largely unexplored therapeutic agent.
Objective: To evaluate the atheroprotective potential of rHDL-apoE3
starting with the unbiased assessment of global transcriptome effects
and focusing on endothelial cell (EC) migration as a critical process in
reendothelial ization and atherosclerosis prevention. The cellular,
molecular and functional effects of rHDL-apoE3 on EC
migration-associated pathways were assessed, as well as the potential
translatability of these findings in vivo.
Methods: Human Aortic ECs (HAEC) were treated with rHDL-apoE3 and total
RNA was analyzed by whole genome miaoarrays. Expression and
phosphorylation changes of key EC migration-associated molecules were
validated by qRT-PCR and Western blot analysis in primary HAEC, Human
Coronary Artery ECs (HCAEC) and the human EA.hy926 EC line. The capacity
of rHDL-apoE3 to stimulate EC migration was assessed by wound healing
and transwell migration assays. The contribution of MEK1/2, PI3K and the
transcription factor ID1 in rHDL-apoE3-induced EC migration and
activation of EC migration-related effectors was assessed using specific
inhibitors (PD98059: MEK1/2, LY294002: PI3K) and siRNA-mediated gene
silencing, respectively. The capacity of rHDL-apoE3 to improve vascular
permeability and hypercholesterolemia in vivo was tested in a mouse
model of hypercholesterolemia (apoE KO mice) using Evans Blue assays and
lipid/lipoprotein analysis in the serum, respectively.
Results: rHDL-apoE3 induced significant expression changes in 198 genes
of HAEC mainly involved in reendothelialization and
atherosclerosis-associated functions. The most pronounced effect was
observed for EC migration, with 42/198 genes being involved in the
following EC migration-related pathways: 1) MEK/ERK, 2)
PI3K/AKT/eNOS-MMP2/9, 3) RHO-GTPases, 4) integrin. rHDL-apoE3 induced
changes in 24 representative transcripts of these pathways in HAEC,
increasing the expression of their key proteins PIK3CG, EFNB2, ID1 and
FLT1 in HCAEC and EA.hy926 cells. In addition, rHDL-apoE3 stimulated
migration of HCAEC and EA.hy926 cells, and the migration was markedly
attenuated in the presence of PD98059 or LY294002. rHDL-apoE3 also
increased the phosphorylation of ERK1/2, AKT, eNOS and p38 MAPK in these
cells, while PD98059 and LY294002 inhibited rHDL-apoE3-induced
phosphorylation of ERK1/2, AKT and p38 MAPK, respectively. LY had no
effect on rHDL-apoE3-mediated eNOS phosphorylation. ID1 siRNA markedly
decreased EA.hy926 cell migration by inhibiting rHDL-apoE3-triggered
ERK1/2 and AKT phosphorylation. Finally, administration of a single dose
of rHDL-apoE3 in apoE KO mice markedly improved vascular permeability as
demonstrated by the reduced concentration of Evans Blue dye in tissues
such as the stomach, the tongue and the urinary bladder and ameliorated
hypercholesterolemia.
Conclusions: rHDL-apoE3 significantly enhanced EC migration in vitro,
predominantly via overexpression of ID1 and subsequent activation of
MEK1/2 and P13K, and their downstream targets ERK1/2, AKT and p38 MAPK,
respectively, and improved vascular permeability in vivo. These novel
insights into the rHDL-apoE3 functions suggest a potential clinical use
to promote re-endothelialization and retard development of
atherosclerosis. (C) 2021 Elsevier Inc. All rights reserved