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lördag 28 februari 2015

Leusiinipitoinen toistojakso transmembraaniproteiinissa (LRRTM) tärkeä LTP:ssä . AMPAR rekrytointi, neurexiinit

  Leucine-rich repeat transmembrane proteins are essential for maintenance of long-term potentiation.
Neuron. 2013 Aug 7;79(3):439-46. doi: 10.1016/j.neuron.2013.06.007.
Tiivistelmä

Leusiinipitoisia  (L)   toistoja (LRR)   sisältävät  transmembraani (TM)  proteiinit ovat synaptisia soluadheesiomolekyylejä (CAM), jotka triggeröivät excitatorisen  synaptisen kokoontumisen viljellyissä neuroneissa ja vaikuttavat synaptiseen funktioon in vivo, mutta  niitten osuus synaptisessa plastisuudessa on tuntematon.
 shRNAvälitteisesti  sammutettu LRRTM1 ja LRRTM2  vastasyntyneen hiiren CA1 pyramidaalisoluissa vaikuttti LTP- blokeerautumisen akuuteissa hippokampileikkeissä.
Mutta kun lisättiin LRRTM2 molekyyliä solujen ulkotilaan, se oli riiittävä pitkäaikaispotentioitumiseen (LTP),  ehkä sen takia että se välitti sitoutumista neurexiineihin  (Nrxs)
Kun on tutkittu endogeenisten  AMPA-reseptoreitten ilmestymistä neuronisolun opintaan viljellyissä neuroneissa, on saatu viitettä siitä, että LRRTM- proteiinit pitävät yllä  AMPAreseptoreitten  esilletuomista  synapsipintaan  LTP-induktion jälkeen. ( AMPAreseptorin rekrytointi synapsipintaan)
LRRTM proteiineja vaaditaan myös kypsien synapsien LTP:ssä aikuisen CA1- pyramidaalineuroneissa, mikä viittaa siihen, että se LTP- blokki, mikä aiheutui  neonataalisten synapsien LRRTM1 ja LRRTM2  proteiinien vaimennuksesta,   ei johdu synapsikypsymisen viasta.

Abstract

Leucine-rich repeat transmembrane proteins (LRRTMs) are synaptic cell adhesion molecules that trigger excitatory synapse assembly in cultured neurons and influence synaptic function in vivo, but their role in synaptic plasticity is unknown.
 shRNA-mediated knockdown (KD) of LRRTM1 and LRRTM2 in vivo in CA1 pyramidal neurons of newborn mice blocked long-term potentiation (LTP) in acute hippocampal slices. 
Molecular replacement experiments revealed that the LRRTM2 extracellular domain is sufficient for LTP, probably because it mediates binding to neurexins (Nrxs).
 Examination of surface expression of endogenous AMPA receptors (AMPARs) in cultured neurons suggests that LRRTMs maintain newly delivered AMPARs at synapses after LTP induction. LRRTMs are also required for LTP of mature synapses on adult CA1 pyramidal neurons, indicating that the block of LTP in neonatal synapses by LRRTM1 and LRRTM2 KD is not due to impairment of synapse maturation.
Suomennosta 28.2. 2015

Muistin perusmuodostumisesta uusi väitöskirja (LTP)

VÄITÖSKIRJA, jossa on alettu arvioida ja punnita uudelleen LTP-teoriaa muistiaineksen  indusoitumisesta, konsolidoitumisesta ja stabiloitumsesta ja  suhteesta protiinisynteesiin   muistin  keskisessä  aivorakenteessa hippokampissa.

 Abbas, Abdul-Karim

Re-evaluation of the hypothesis that LTP has two temporal phases and that the late phase is protein synthesis-dependent



19-feb-2015
University of Gothenburg. Sahlgrenska Academy
Institute of Neuroscience and Physiology. Department of Physiology
I. Abbas, Abdul-Karim, Dozmorov, Mikhail, Li, Rui, Huang, Fen-Sheng, Hellberg, Fredrik, Danielson, Jonas, Tian, Ye, Ekström, Jörgen, Sandberg, Mats, Wigström, Holger. Persistent LTP without triggered protein synthesis. Neuroscience Research 2007 Jan;63(1):59-65.
VISA ARTIKEL

II. Abbas, Abdul-Karim, Huang, Fen-Sheng, Li, Rui, Ekström, Jörgen, Wigström, Holger. Emetine treatment masks initial LTP without affecting long-term stability. Brain Research 2011 Dec 2;1426:18-29.
VISA ARTIKEL

III. Abbas, Abdul-Karim. Evidence for constitutive protein synthesis in hippocampal LTP stabilization. Neuroscience 2013 Aug 29;246:301-11.
VISA ARTIKEL

IV. Abbas, Abdul-Karim, Villers, Agnés, Ris, Laurence. Temporal phases of Long-term potentiation (LTP): myth or fact? Review in the Neurosciences 2015 (In Press).

978-91-628-9302-6
http://hdl.handle.net/2077/37535

Abstraktin suomennos:
  • Muistiainekertymän pitkäaikaispotentioituminen (LTP) on aktiivisuudesta riippuvaa lisääntymistä synaptisessa tehossa- ja tätä on eniten tutkittu hippokampista ja sitä on pidetty solusubstraattina, joka vastaa oppimista ja muistia.
     Jos uskotaan, että LTP:n ajallinen kestävyys on analogista hippokampista riippuvan muistimateriaalin pitkäaikaispysymiselle, tulee välttämättömäksi ymmärtää LTP:n stabilisoitumisen taustalla olevat mekanismiit.
Long-term potentiation (LTP) is an activity-dependent increase in synaptic efficacy that is most studied in the hippocampus and that is considered a cellular substrate for learning and memory. Accepting the belief that the durability (persistence in time) of LTP is analogical to long-standing store of hippocampus-dependent memories warrants the necessity for understanding the mechanisms underlying LTP stabilization.
  • Vaikka suurin osa neurologian alan tiedemiehistä olettaakin, että LTP-induktio, muistinmuodostuminen,  liipaisee esiin valkuaisainesynteesiä, joka toimii välineenä muistiaineksen jatkokonsolidoitumisessa, ei kuitenkaan ole selvä asia sellaisten oletettujen proteiinien olemassaolokaan eikä mekanismi, jolla ne vaikuttaisivat LTP:n konsolidoitumisen.
Although the great majority of neuroscientists assume that LTP induction, akin to the formation of memories triggers the synthesis of proteins that are instrumental for subsequent consolidation neither the identity of such presumed proteins nor the mechanisms by which they act to consolidate LTP are clear.
  • Tähän ajatteluun perustuen on LTP:ssä tapana ajallisesti  erottaa  varhaisvaihe, varhainen LTP ( early , E-LTP), mikä katsotaan proteiinisynteesistä riippumattomaksi sekä myöhäisvaihe ( late, L-LTP) , joka taas on katsottu  proteiinisynteesistä riippuvaiseksi. Kuitenkin useat behavioristiset ja elektrofysiologiset löydöt herättävät epäilyjä täman käsityksen oikeudesta.
Based on this notion LTP is distinguished temporally into an early phase (E-LTP), which is protein synthesis-independent and a late phase (L-LTP), which is protein synthesis-dependent. However, several behavioral and electrophysiological findings cast doubts on this notion.
  • Tässä käsilläolevassa väitöskirjassa tutkija on selvittänyt proteiinisynteesin estäjien (PSI) vaikutusta LTP:n stabiloitumiseen hippokampileikkeissä, joita oli valmistettu nuorilta koe-eläimiltä. He käsittelivät leikkeet proteiinisynteesi-inhibiittoreilla (PSI) ja tutkivat niitä siitä aikaikkunasta, mikä vastaa sellaista LTP:n indusoitumisvaihetta, mitä kirjallisuudessa on aiemminkin käytetty, ja he havaitsivat, että proteiinsynteesinestäjät (PSI) eivät pystyneetkään blokeeraamaan myöhäistä LTP-vaihetta (L-LTP), mikä tulos taas oli ristiriidassa aiemmin julkaistun tiedon kanssa.
In the present thesis I have examined the effect of protein synthesis inhibitors (PSIs) on the stabilization of LTP in hippocampal slices obtained from young rats. Treating hippocampal slices with PSIs using a temporal window relative to the induction of LTP that has previously been used in the literature failed to block L-LTP, a result in contrast with published data.
  • Kuitenkin esikäsittely pitkäaikaisesti vaikuttavalla PSI -aineella emetiinillä pystyi blokeeraamaan LTP:n LTP:hen korreloitumattomalla mekanismilla, koska aine osoitti huonontavaa tehoa perustason vasteeseen. Ja päinvastoin – jos proteiinikirjoa hippokampileikkeestä oli poistettu pitkäkestoisella PSI-esikäsittelyllä käyttäen sykloheximidi-nimistä ainetta, LTP:n stabiloituminen huononi.
However, long-lasting pretreatment with the PSI emetine blocked LTP by LTP-unrelated mechanism as the drug showed deteriorating effect on the baseline response. In contrast, depleting the protein repertoire in the slice by long-lasting pretreatment with the PSI cycloheximide deteriorated the stabilization of LTP.
  • Lisäksi proteiinien hajoamisen kiihdyttäminen käyttämällä vetyperoksidia LTP:n induktion jälkeen johti LTP:n häviämiseen. Sykloheximidin lisääminen indusoi LTP:n stabiloitumisessa edelleen huononemista. Nämä ristiriitaiset löydöt on äskettäinn toistettu useissa laboratorioissa.

Additionally, acceleration of protein degradation using hydrogen peroxide after the induction of LTP resulted in decay of LTP. Addition of cycloheximide induced additive decay of LTP stabilization. These contradictory findings have recently been replicated by other laboratories.
  • Tässä väitöskirjassaan tutkija esittää oman työmallinsa, jonka tarkoituksena on selittää näitä ristiriitaisia löytöjä proteiininsynteesinestäjistä (PSI) ja LTP.stä. Mallissa myönnetään, että proteiinien turnover-prosessin kinetiikan tunteminen LTP:n indusoitumisen ajalta saattaa antaa ennusteen LTP:n jatkostabilisoitumisesta. Tämä voisi selittää sen suureen vaihtelevaisuuden, mitä ilmenee proteiinisynteesistä oletetusti  riippumattoman E-LTP - vaiheen ajallisessa kestossa.
  • Tämä malli saa tukea sellaisistakin kokeista, joissa käytettiin erään proteosomi-inhibiittorin (MG-115) matalaa pitoisuutta kohentamaan heikolla induktiolla indusoidun LTP:n stabiliteettia.
In this thesis I present a working model that aims to explain the discrepant findings regarding PSI and LTP. The model concedes that knowing the kinetics of protein turnover during the induction of LTP may provide a prediction for the subsequent stabilization of LTP.
This can explain the wide variability in the time course of the presumed protein-synthesis independent E-LTP. The model gains support from experiments in which a low concentration of the proteasome inhibitor MG-115 improved the stability of LTP induced by a weak induction protocol.
  • Yhteenvetona väitöskirjan tekija mainitsee tulostensa viittaavan siihen , että (1) on virheellistä dikotomiaa jakaa LTP ajallisesti varhaiseen (E-LTP) ja myöhäiseen (L-LTP) faasiin ja että (2) proteiinin hajoamistahdilla voitaisiin selvittää, pystyykö proteiininsynteesin estäjät vaikuttamaan jotakin LTP:n stabilisoitumiseen vai eivätkö pysty.
In summary, my results suggest that 1) the temporal distinction of LTP into E- and L-LTP is a false dichotomy and 2) the rate of protein degradation may explain whether PSIs would, or would not, have an effect on LTP stabilization.

Suomennos  abstraktista 28.2. 2015. Väitöstilaisuus on edessäpäin Göteborgin Yliopiston Sahlgrenskan Akatemiassa. 

fredag 27 februari 2015

CSF Rhinorrhea, perustava tieto

Liquorrhea , Likvorvuoto nenästä ( tai korvasta Otorrhea) Riskit


Cerebrospinal fluid rhinorrhoea Cerebrospinal fluid rhinorrhoea: diagnosis and management
Allan Abuabara DDS, Specialist in Dental and Maxillofacial Radiology, Health Division, Joinville City Hall, Joinville, Santa Catarina, Brazil
Correspondence:
Dr. Abuabara Rua Quintino Bocaiúva, 102, apto 206, Joinville, SC, Brazil. 89204-300;
E-mail: allan.abuabara@gmail.com
Received: 25-07-2006 Accepted: 30-01-2007
Abuabara A. Cerebrospinal fluid rhinorrhoea: diagnosis and manage-ment
.Med Oral Patol Oral Cir Bucal 2007;12:E397-400.
© Medicina Oral S. L. C.I.F. B 96689336 - ISSN 1698-6946

Abstract

A cerebrospinal fluid (CSF) rhinorrhoea occurs when there is a fistula between the dura and the skull base and discharge of CSF from the nose. CSF rhinorrhea or liquorrhoea commonly occurs following head trauma (fronto-basal skull fractures), as a result of intracranial surgery, or destruction lesions. A spinal fluid leak from the intracranial space to the nasal respiratory tract is potentially very serious because of the risk of an ascending infection which could produce
fulminant meningitis.

This article reviewed the causes, diagnosis and treatment of CSF leakage. A PUBMED search of the National Library of Medicine was conducted.
CSF leak most commonly occurs following trauma and the majority of cases presenting within the first three months. CSF rhinorrhoea have significantly greater incidence of periorbital haematoma. This suggests that patients with head injuries and features of periorbital haematoma are at greater risk of unobserved dural tear and delayed CSF leakage.
In the presence of a skull base fracture on computed tomography and a clinical CSF leak, there is no need for a further confirmatory test. In cases where a confirmatory test is needed, the beta-2 transferrin assay is the test of choice because of its high sensitivity and specificity.
A greater proportion of the CSF leaks in the patients resolved spontaneously. CSF fistulae persisting for > 7 days had a significantly increased risk of developing meningitis. Treatment decisions should be dictated by the severity of neurological decline during the emergency period and the presence/absence of associated intracranial lesions. The timing for surgery and CSF drainage procedures must be decided with great care and with a clear strategy.

Key words:
Liquorrhoea, rhinorrhoea, cerebrospinal fluid, head injury.
Indexed in:-Index Medicus / MEDLINE / PubMed-EMBASE, Excerpta Medica-SCOPUS-Indice Médico Español-IBECS CONCEPt

Surgical management of multiple traumatized patients with head trauma is highly individualized and depends on a number of factors including etiology, intracranial pressure,concomitant injuries, patient age and the possibility of an interdisciplinary procedure. Severe head and neck trauma are often connected with fractures of the frontal skull base or nasoethmoido-orbital complex and cerebrospinal fluid (CSF) leakage (1).
CSF leak is an escape of the fluid that surrounds the brain and spinal cord, from the cavities within the brain or central canal in the spinal cord. A CSFrhinorrhoea occurs when there is a fistula between the dura and the skull base and discharge of CSF from the nose. A spinal fluid leak from the intracranial space to the nasal respiratory tract is potentially very serious because of the risk of an ascending infection which could produce fulminant meningitis (2). CSF leaks have been associated with abouta 10% risk of developing meningitis per year (3).

CSF rhinorrhea commonly occurs following head trauma (fronto-basal skull fractures) or as a result of intracranial surgery.
Others conditions include paranasal sinuses along with osteomyelitis of the adjacent bone, congenital anomalies of the brain and its coverings such as meningoceles or meningoencephaloceles, and destruction lesions along the skull base (4). Pituitary tumors cause erosion of the sella turcica floor and are frequently associated with CSFrhinorrhea (5).

This article reviewed the causes, diagnosis and treatment of CSF leakage. A PUBMED search of the National Library of Medicine was conducted. EPIDEMIOLOGY CSF rhinorrhea can be divided in traumatic and non-trau-matic: the traumatic group can be divided in accidental and iatrogenic. The non-traumatic group is associated to braintumors (intracranial and extracranial tumors, cholesteatoma, or tuberculoma are know to erode the bone directly) (6), skull base congenital defects and meningoceles or meningoencephalocles (7).
CSF leak most commonly occurs following trauma (80-90% of cases) and the majority of cases presenting within the first three months. Other etiologies include: postoperative defect (10 %), spontaneous leak (3-4 %), tumor, and inflammation (8). Usually the fracture involves some portion of the anterior cranial fossa floor with the leaks occurring through the cribriform plate or ethmoid sinus roof into the nose.
Another frequently seen anterior fossa fracture site is the posterior wall of the frontal sinus through which CSF can escape into the nose via the nasofrontal duct.
Less common are middle cranial fossa fractures that can cause leakage to the nose via the sphenoid sinus or eustachian tube (2).
Nontraumatic cerebrospinal fluid fistulae tend to occur less frequently, and most of them are related to diseases that cause increased intracranial pressure or local skull destruction. Such conditions include hydrocephalus, tumors, osteomyelitis of the skull and brain cysts.
Congenital defects of the skull can also serve as the source of fistulae, usually occurring in the anterior cranial fossa (2).
Fain et al. (9) presented a classification of trauma to the cranial base, based on observation in 80 cases. There were five types.
Type I: involves only the anterior wall of the frontal sinus.
Type II: involves the face (craniofacial disjunction of the Lefort II type or crush face) and extend upward to the cranial base and, in occurrence, to the anterior wall of the frontal sinus, because of the facial retrusion.
Type III: involves frontal part of the skull and extend down to the cranial base.
Type IV: is a combination of types II and III.
Type V: involves only ethmoidal or sphenoidal bones.
CSF leak is unfrequent in types II, and transitionnal, if it occurs; but it often occurs in types III, IV and V which include in every case a dural tear. Correct diagnosis facilitates treatment. Fractures of types I and II can be fully treated by maxillo-facial surgeons, whereas for types III, IV, and V,
they need the help of a neuro-surgeon.

CLINICAL PICTURE  AND PATHOGENESIS

CSF rhinorrhea after intracranial or intranasal surgery is a known potential complication with significant morbidity and mortality. Accurate identification of the site of CSF leakage is necessary for a successful surgical repair. The most reliable methods of distinguishing between a traumatic
or neoplastic lesion and a spontaneous CSF rhinorrhea are high-resolution computed tomography (CT) and magnetic resonance (MR) tomography (10). MR imaging is reserved for defining the nature of soft tissue i.e. inflammatory tissue, meningoencephalocele or tumor (11). In MR images we can find brain herniation into the ethmoid or frontal sinuses (12). CT with or without intrathecal contrast and preoperative nasal endoscopy are frequently used to preoperatively localize the site of the leak (13).

CSF rhinorrhoea have significantly greater incidence of periorbital haematoma. This suggests that patients with head injuries and features of periorbital haematoma are at greater risk of unobserved dural tear and delayed CSF leakage. Frontal and ethmoid fractures in particular are also associated with CSF leakage (14). Radiographic exams like simple skull X rays are quite ineffective. However it can demonstrate indirect signs like fractures and pneumoencephalus (7). Various combinations of planar tomography and CT, contrast-enhanced CT cisternography, and radionuclide cisternography, and, more recently, MR cisternography have been used in the diagnosis of CSF leak. Radionuclide
cisternography and contrast-enhanced CT cisternography techniques require injections into the intrathecal space, most often via lumbar puncture. Although cisternography has minimal inherent risks, such as infection and lumbar CSF leak, it significantly increases expense and adds
patient discomfort. Radionuclide studies do not provide precise anatomic localization of CSF leaks (15). Stone et al. (15) suggest that high-resolution CT is a useful screening examination for the initial workup of CSF rhinorrhea or otorrhea. When the clinical and imaging findings coincide,
further evaluation using CT cisternography and radionuclide cisternography is often unnecessary. Computerized cisternography and radionuclide cisternography should be used if MR imaging is contraindicated or if a clinically and biologically proven CSF fistulae is not visualized by CT or
MR imaging (8). Diagnosis through nasal inspection and performance of laboratory tests of the fluid can be conducted. In some cases, there is contamination of the material with blood or
other secretions, so the test with beta-2 transferrine becomes mandatory (7). Beta-2 transferrin is a carbohydrate-free (desialated) isoform of transferrin, which is almost exclusively found in the CSF (16) and blood or nasal secretion does not disturb the test (17). Beta-2 transferrin is not present in blood, nasal mucus, tears or mucosal discharge.
This protein was first described by Irjala et al in 1979 (18). Intense research over the last decade has validated its characteristics and value in clinical use as a specific CSF marker
(19). Beta-2 transferrin was reported to have a sensitivity of near 100% and a specificity of about 95% in a large retrospective study (20).
Detection of glucose in the sample fluid using Glucostix test strips has been a traditional method for detection of the presence of CSF in nasal and ear discharge. Glucose detection using Glucostix test strips is not recommended as a confirmatory test due to its lack of specificity and
sensitivity (19). Interpretation of the results is confounded by various factors such as contamination from glucose-containing fluid (tears, nasal mucus, blood in nasal mucus) or
relatively low CSF glucose levels (meningitis) (19). Studies have shown (21) that glucose can be detected in airways secretions from people with diabetes mellitus, stress hyperglycaemia and people with nasal epithelial inflammation due to viral colds.
In the presence of a skull base fracture on CT and a clinical CSF leak, there is no need for a further confirmatory test.

In cases where a confirmatory test is needed, the beta-2 transferrin assay is the test of choice because of its high sensitivity and specificity (19).

MANAGEMEN AND PROGNOSIS
Most of CSF leaks close spontaneously within 7 to 10 days
(19, 22, 23). Although most trauma-related CSF leaks resolve without intervention, conservative treatment of CSF leaks may lead to bacterial meningitis, therefore surgical closure of leaks or defects at the skull base should be considered treatment of choice to prevent ascending meningitis
(24). CSF fistulae persisting for > 7 days had a significantly increased risk of developing meningitis (23). The goal of surgical therapy is repair of the dural defect contributing to the CSF leak (15). The surgical management of CSF leak has changed significantly after the introduction of functional endoscopic sinus surgery in the management of sinusitis.
The clear anatomical exposure of the roof of the nasal and the sinus cavities by the endoscope offers the surgeon an opportunity to identify the area of the CSF leak, which enables one to adequately plan the treatment (25).
It is currently accepted that endoscopic intranasal management of CSF rhinorrhea is the preferred method of surgical repair, with higher success rates and less morbidity than intracranial surgical repair in selected cases (13). Endonasal endoscopic approach can be preferred for the closure of uncomplicated CSF fistula, located at the anterior or posterior ethmoid roof and in the sphenoid sinus, due to its minimal postoperative morbidity. Uncomplicated CSF fistula, located at the posterior wall of frontal sinuses can be repaired extradurally with osteoplastic frontal sinusotomy.
Intracranial approaches should be reserved for more complicated CSF rhinorrhea which results from extensive comminuted fractures of the anterior cranial base and is accompanied
with intracranial complications (26). Anosmia is the most frequent permanent complication mentioned.
The value of antibiotic prophylaxis in patients with CSF leakage is debatable. In a literature review, Brodie (27) concluded that individually, each of the studies evaluated demonstrated no significant difference in the incidence of meningitis with prophylactic antibiotic therapy. The reason
for this is that inadequate numbers of patients were available at each institution. Pooling the data from the past 25 years revealed a statistically significant reduction in the incidence of meningitis with prophylactic antibiotic therapy. It is ethically justifiable to keep antibiotic prophylaxis in patients with CSF fistulae until other studies settle the question.

COMPLEMENTARY EXPLORATION
Post-traumatic CSF leaks are uncommon and will usually resolve without surgical intervention. Successful management in refractory cases often involves a combination of observation, CSF diversion, and/or extracranial and intracranial procedures (28). The factors that had a critical influence on outcome are level of consciousness on admission and presence of additional intracranial pathology associated with CSF leakage within cases of traumatic CSF fistulae
due to skull base fractures. Patients with CSF leaks that persist greater than 24 hours are at risk for meningitis, and maybe require surgical intervention. Prophylactic antibiotics may be effective and should be considered in this group of patients (29). Treatment decisions should be dictated by the
severity of neurological decline during the emergency period and the presence/absence of associated intracranial lesions.
The timing for surgery and CSF drainage procedures must be decided with great care and with a clear strategy (22)

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approach to manage extensive fractures of the frontal skull base. Laryngorhinootologie 2006;85:265-71.
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Muistiin 27..2. 2015