Sindromul coronarian acut şi Infarctul miocardic acut: protocol clinic naţional PCN-81

IMSP Institutul de CardiologieAcest protocol a fost elaborat de grupul de lucru al Ministerului Sănătăţii al Republicii Moldova constituit din colaboratorii IMSP Institutul de Cardiologie. Protocolul clinic naţional este elaborat în conformitate cu ghidurile internaţionale actuale privind sindromul coronarian acut și infarctul miocardic şi poate servi drept bază pentru elaborarea protocoalelor instituţionale (extras din protocolul naţional aferent pentru instituţia dată, fără schimbarea structurii, numerotaţiei capitolelor, tabelelor, figurilor, casetelor etc.), în baza posibilităţilor reale ale fiecărei instituţii în anul curent. La recomandarea Ministerului Sănătăţii pentru monitorizarea protocoalelor instituţionale pot fi folosite formulare suplimentare, care nu sunt incluse în protocolul clinic naţional

Bolile aortei: protocol clinic naţional PCN-242

IMSP Institutul de Cardiologie, Departamentul Cardiochirurgie ISMP SCRAcest protocol a fost elaborat de grupul de lucru al Ministerului Sănătăţii al Republicii Moldova (MS RM), constituit din colaboratorii IMSP Institutul de Cardiologie în colaborare cu IMSP Spitalul Clinic Republican. Protocolul clinic naţional este elaborat în conformitate cu ghidurile internaţionale actuale privind bolile aortice (ESC, 2014) şi poate servi drept bază pentru elaborarea protocoalelor instituţionale (extras din protocolul naţional aferent pentru instituţia dată, fără schimbarea structurii, numerotaţiei capitolelor, tabelelor, figurilor, casetelor etc.), în baza posibilităţilor reale ale fiecărei instituţii în anul curent. La recomandarea Ministerului Sănătăţii pentru monitorizarea protocoalelor instituţionale pot fi folosite formulare suplimentare, care nu sunt incluse în protocolul clinic naţional

β1A Integrin Is a Master Regulator of Invadosome Organization and Function

Use of patterned surfaces, reverse genetics, and time-controlled photoinactivation showed that β1 but not β3 integrins are required for invadosome formation, self-assembly, and stabilization into a ring structure. The activation state of β1 as well as its phosphorylation by protein kinase C on Ser785 control these process and link to the degradative function

β1 Integrin Deficiency Results in Multiple Abnormalities of the Knee Joint*

The lack of β1 integrins on chondrocytes leads to severe chondrodysplasia associated with high mortality rate around birth. To assess the impact of β1 integrin-mediated cell-matrix interactions on the function of adult knee joints, we conditionally deleted the β1 integrin gene in early limb mesenchyme using the Prx1-cre transgene. Mutant mice developed short limbed dwarfism and had joint defects due to β1 integrin deficiency in articular regions. The articular cartilage (AC) was structurally disorganized, accompanied by accelerated terminal differentiation, altered shape, and disrupted actin cytoskeleton of the chondrocytes. Defects in chondrocyte proliferation, cytokinesis, and survival resulted in hypocellularity. However, no significant differences in cartilage erosion, in the expression of matrix-degrading proteases, or in the exposure of aggrecan and collagen II cleavage neoepitopes were observed between control and mutant AC. We found no evidence for disturbed activation of MAPKs (ERK1/2, p38, and JNK) in vivo. Furthermore, fibronectin fragment-stimulated ERK activation and MMP-13 expression were indistinguishable in control and mutant femoral head explants. The mutant synovium was hyperplastic and frequently underwent chondrogenic differentiation. β1-null synoviocytes showed increased proliferation and phospho-focal adhesion kinase expression. Taken together, deletion of β1 integrins in the limb bud results in multiple abnormalities of the knee joints; however, it does not accelerate AC destruction, perturb cartilage metabolism, or influence intracellular MAPK signaling pathways

The Membrane-targeted Alkylphosphocholine Erufosine Interferes with Survival Signals from the Extracellular Matrix

Integrin-dependent adhesion of tumor cells to extracellular matrix proteins provides anchorage-dependent protection from cell death. In the present investigation we aimed to understand whether and how the paradigmatic membrane-targeted synthetic phospholipid analog erufosine is relevant for tumor cell adhesion to extracellular matrix proteins, cell survival and migration. The antineoplastic action of erufosine was analyzed with glioblastoma and prostate cancer cells adhering to fibronectin or collagen I using proliferation, adhesion and migration assays. The composition of adhesion contacts containing activated beta 1 integrins was studied using immunofluorescence. The importance of beta 1 integrins for the observed effects was analyzed in fibroblasts proficient or deficient in beta 1 integrin expression. Adhesion to collagen I and fibronectin increased the death threshold in serum-deprived tumor cells. Moreover, beta 1 integrin-deficient cells were more sensitive to erufosine-treatment compared to beta 1 integrin proficient cells suggesting a role of beta 1 integrins for matrix-mediated death resistance. Most importantly, erufosine disturbed the maturation of the cell adhesion complexes containing paxillin, activated beta 1 integrins and phosphorylated FAK, leading to a reduction of survival signals and inhibition of tumor cell adhesion and migration. These findings suggest that membrane-targeted synthetic phospholipids analogs may be of value for counteracting matrix-mediated treatment resistance in combined treatment approaches with radiotherapy or chemotherapy

Early detection of aging cartilage and osteoarthritis in mice and patient samples using atomic force microscopy

The pathological changes in osteoarthritis-a degenerative joint disease prevalent among older people-start at the molecular scale and spread to the higher levels of the architecture of articular cartilage to cause progressive and irreversible structural and functional damage. At present, there are no treatments to cure or attenuate the degradation of cartilage. Early detection and the ability to monitor the progression of osteoarthritis are therefore important for developing effective therapies. Here, we show that indentation-type atomic force microscopy can monitor age-related morphological and biomechanical changes In the hips of normal and osteoarthritic mice. Early damage in the cartilage of osteoarthritic patients undergoing hip or knee replacements could similarly be detected using this method. Changes due to aging and osteoarthritis are clearly depicted at the nanometre scale well before morphological changes can be observed using current diagnostic methods. Indentation-type atomic force microscopy may potentially be developed into a minimally invasive arthroscopic tool to diagnose the early onset of osteoarthritis In situ