Segmental hypoplasia of the basilar artery: a case report and review of literature

The anomalies of the basilar artery are rare when compared with those ones pertaining to the circle of Willis vessels. Partial duplication or fenestration is rather common (0.6% to 1.8% in the angiographic descriptions); on the other hand, other anomalies, including complete duplication, hypoplasia and aplasia are exceptional. A rare case of segmental hypoplasia of the basilar artery in a 49-year-old man with transient vertebrobasilar (VB) ischemia, explored by magnetic resonance imaging (MRI) and digital angiography (DA), is reported. The embryology, the clinical relevance and the magnetic resonance findings of this arterial anomaly are discussed, with a review of other six reported cases. The appearance of a segmental aplasia was suggested in our case by MRI, and successively confirmed not only by time-of-flight MR-angiography (TOF-MRA) but also by DA. Only ultrathin-slice T2-weighted (w) images revealed the real finding of basilar artery (BA) hypoplasia; this sequence, not employed in previously reported cases, is mandatory to allowing a clear differential diagnosis between BA aplasia and hypoplasia. In conclusion, segmental hypo-aplasia of the BA is an exceptional embryological anomaly. This anomaly may be of clinical importance, and it should be considered among the potential causes of vertebrobasilar insufficiency in young adults. These cases should be investigated by MR and MRA; we stress the importance of ultrathin slice T2-weighted sequences in order to discriminate between aplasia and hypoplasia

“VEGF induces human endothelial progenitor cells proliferations by eliciting oscillations in intracellular Ca2+ concentration”

Endothelial progenitor cells (EPCs) traffic from the bone marrow to the site of tissue regeneration and sustain neo-vascularization after acute vascular injury and upon the angiogenic switch in solid tumors. Therefore, they represent a suitable tool for cell-based therapy in regenerative medicine and provide a novel promising target in the fight against cancer. The main stimulus responsible for EPC egression from the bone marrow and engraftment within neovessels is vascular endothelial growth factor (VEGF). Intracellular Ca2+ signals regulate numerous endothelial functions, such as proliferation, migration, and differentiation, and underpin VEGF effect on mature endothelium. We have recently shown that EPC growth is governed by a store-dependent Ca2+ entry (SOCE) pathway on the plasma membrane, which is activated by depletion of the inositol-1,4,5-trisphosphate (InsP3)-sensitive Ca2+ pools1. The present study aimed at investigating the nature and the role of VEGF-elicited Ca2+ signals in EPCs. All the putative SOCE mediators (i.e. TRPC1, TRPC4, Orai1 and Stim1) were present in EPCs. VEGF induced long lasting Ca2+ oscillations, however, removal of external Ca2+ (0Ca2+) and SOCE inhibition with BTP-2 reduced the number of Ca2+ spikes. Blockade of phospholipase C-? (PLC-?) with U73122 and emptying the InsP3-sensitive Ca2+ pools with cyclopiazonic acid (CPA) prevented the Ca2+ response to VEGF. Accordingly, the Ca2+ response to VEGF was inhibited by superfusing CPA during the ongoing oscillations. Notably, VEGF induced EPC was abrogated by SOCE inhibition with BTP-2. Similarly, VEGF promoted NF-kB translocation into the nucleus in a BTP-2-sensitive manner. Thus, VEGF causes an initial InsP3-dependent Ca2+ discharge followed by SOCE-mediated Ca2+ entry in cEPCs. SOCE, in turn, controls store refilling and induces cell proliferation by recruiting NF-kB

TIMPs and MMPs expression in nasal polyps

Nasal polyposis is a chronic inflammatory disease characterized by inflammatory invasion of nasal mucosa, changes in cells differentiation, thickness reduction and remodelling of basal membrane, hyperplasia of mucous glands, extracellular matrix deposition. MMPs shown a proteolytic activities towards several components of extracellular matrix, play an important role in connective tissue remodeling. MMPs are a proteins family including 25 isoforms of Ca2+ and Zn 2+ dependant endopeptidases. MMPs are inactive and can be activated by proteases removing some amino acids. Tissue inhibitors of matrix metalloproteinases (TIMPs) are natural inhibitors of MMPs. TIMPs inhibiting MMPs activation by MMPs/TIMPs complexes: TIMP-1 and TIMP-2 are soluble protein, inhibiting mainly MMP-9 and 2, TIMP-3 is mainly associated to ECM. The balance between MMP/TIMP is very critical in matrix remodeling and various physiological processes. Imbalances between these enzymes and inhibitors may cause pathological processes such as chronic inflammation, degenerative disease and tumour invasion. In our study we aimed at demonstrating MMP/TIMP imbalance in nasal polyposis, similar to other pathological processes. The complex structure of polyp formation is still unknown. In this research nasal polyp specimens were obtained from 96 patients with nasal polyposis during endoscopic sinus surgery. Bullous middle turbinates with normal appearing mucosa of fifteen non-smoker patients free of any allergic or infectious diseases of nose or sinuses were used as controls. Patients were divided in three groups: patients of group A have morphostructural polyps; patients of group B have syndromic polyps; patients of group C have allergic polyps. We investigate MMP-1, MMP-2, MMP-3, MMP-9, TIMP-1, TIMP-2, TIMP-3 expression in our specimens using immunoistochemistry, Western Blot Analysis and RT-PCR methods. Our results shown a interesting relashionship between MMPs/TIMPs imbalance and nasal polyps formation

Aerobic training workload affects human endothelial cells redox

Moderate aerobic exercise reduces oxidative stress, intense physical activity may produce the opposite result. At present, the effects of different exercise loads on oxidative stress markers and the response of human cells to different exercise volumes have not been fully elucidated. In this research human (Eahy-926) endothelial cells (ECs), exposed or not exposed to oxidative stress, were conditioned with sera from two groups of triathletes practising at different workloads. Although no differences in functional and hemodynamic variables were observed between the two groups of triathletes, significant changes in some markers for oxidative stress were found in their sera. Thiobarbituric acid reactive substances (TBARS) and superoxide dismutase (SOD) activity were similar, but triathletes practicing the sport at lower volume (T1) had higher serum Nitric Oxide (NO) and lower catalase activity than triathletes performing the training at greater load (T2). The ECs conditioned with serum from T1 (T1-ECs) showed higher survival and proliferation rates and lower senescence levels than the ECs supplemented with T2 (T2-ECs) serum both before and after oxidative stress induction. These effects depended on catalase as demonstrated via enzyme activity inhibition using 3-amino-1,2,4-triazole (ATZ). After oxidative stress induction, Sirt1 activity, a regulator of the oxidative stress response, was significantly increased in the T1-ECs but not in the T2-ECs. Moreover, the T1-ECs required less catalase activity than the T2-ECs to counteract an equal amount of TBARS after H2O2 administration. In conclusion, this study demonstrates that the beneficial effects of aerobic exercise are eliminated when the training is performed at a greater workload. Moreover, we suggest an oxidative stress marker, serum catalase activity, as a valid tool to use in the supervision of changes to exercise volume

Aerobic training workload affects human endothelial cells redox

Moderate aerobic exercise reduces oxidative stress, intense physical activity may produce the opposite result. At present, the effects of different exercise loads on oxidative stress markers and the response of human cells to different exercise volumes have not been fully elucidated. In this research human (Eahy-926) endothelial cells (ECs), exposed or not exposed to oxidative stress, were conditioned with sera from two groups of triathletes practising at different workloads. Although no differences in functional and hemodynamic variables were observed between the two groups of triathletes, significant changes in some markers for oxidative stress were found in their sera. Thiobarbituric acid reactive substances (TBARS) and superoxide dismutase (SOD) activity were similar, but triathletes practicing the sport at lower volume (T1) had higher serum Nitric Oxide (NO) and lower catalase activity than triathletes performing the training at greater load (T2). The ECs conditioned with serum from T1 (T1-ECs) showed higher survival and proliferation rates and lower senescence levels than the ECs supplemented with T2 (T2-ECs) serum both before and after oxidative stress induction. These effects depended on catalase as demonstrated via enzyme activity inhibition using 3-amino-1,2,4-triazole (ATZ). After oxidative stress induction, Sirt1 activity, a regulator of the oxidative stress response, was significantly increased in the T1-ECs but not in the T2-ECs. Moreover, the T1-ECs required less catalase activity than the T2-ECs to counteract an equal amount of TBARS after H2O2 administration. In conclusion, this study demonstrates that the beneficial effects of aerobic exercise are eliminated when the training is performed at a greater workload. Moreover, we suggest an oxidative stress marker, serum catalase activity, as a valid tool to use in the supervision of changes to exercise volume

Phenotypic and functional characterization of endothelial progenitor cells isolated from peripheral blood of renal cell carcinoma patients

Endothelial progenitor cells (EPCs) are mobilized from either bone marrow or arterial walls to restore blood perfusion to ischemic organs and establish the vascular network within growing tumors [1]. The Ca2+ machinery plays a key role in EPC activation and might serve a molecular target for novel therapies of highly angiogenic tumors, such as renal cell carcinoma (RCC) [1]. The Ca2+ toolkit is remodelled in EPCs isolated from RCC patients (RCC-EPCs) as respect to healthy donors [2]. The present study was undertaken to evaluate for the first time the functional properties of EPCs isolated from tumor patients by focusing on RCC-EPCs. We extended our analysis at microscopic level by monitoring the sub-cellular structure of RCC-EPCs relative to their Ca2+ signalling fingerprint. Our results showed a striking functional and ultrastructural difference between RCC-EPCs and their normal counterparts, which might be the basis for designing novel, more specific anti-angiogenic treatments

Ultrastructural and functional differences between normal and tumor endothelial progenitor cells

Endothelial progenitor cells (EPCs) may be released from bone marrow to sustain the angiogenic switch that promotes tumor growth and metastatization of several solid cancers (Moccia et al., 2014). It has long been thought that tumor endothelium represents a rather stable structure, devoid of the genetic heterogeneity featuring neoplastic cells; however, more recent studies showed that tumor endothelial cells (TECs) present with an altered gene expression profile that bestows massive morphological and functional differences on them as compared to normal cells (Aird, 2012). Similarly, circulating EPCs isolated from individuals suffering from metastatic renal cellular carcinoma (mRCC) undergo a significant remodelling of their Ca2+ machinery, which is a master regulator of both angiogenesis and vasculogenesis. The present study clearly indicate that EPCs isolated from RCC (RCC-EPCs) and breast carcinoma (BC-EPCs) patients display ultrastructural and functional differences as compared to normal cells (N-EPCs)

Pola Asuh Sebagai Prediktor Kontrol Diri

Each parents have their own way to raise their chidren, which is affecting on how each individual’s self control differs. The present research adresses this central assumption to know the correlation between parenting and individual’s self-control. There are 108 participants in this research, they are college students at Faculty of Psychology, Muhammadiyah University of Surakarta. The sampling technique used in this research is disproportional stratified random sampling. We used quantitative method with help of self-control scale dan parenting-perception scale as measuring tools. The collected data was analized by product moment correlation method with SPSS 16 for windows. Based on the result of the analized data, it shows 0,446 correlation coefficient value with 0,000 sig. (p) value, which means there is a very significant positive correlation between parenting and self-control. As for parenting’s contribution on self-control, determination coefficient’s value shows 19,9%. It means that there are 80,1% other factors which predisposing individual’s self-control

Phenotypic and functional characterization of endothelial progenitor cells isolated from peripheral blood of renal cell carcinoma patients

Endothelial progenitor cells (EPCs) are mobilized from either bone marrow or arterial walls to restore blood perfusion to ischemic organs and establish the vascular network within growing tumors [1]. The Ca2+ machinery plays a key role in EPC activation and might serve a molecular target for novel therapies of highly angiogenic tumors, such as renal cell carcinoma (RCC) [1]. The Ca2+ toolkit is remodelled in EPCs isolated from RCC patients (RCC-EPCs) as respect to healthy donors [2]. The present study was undertaken to evaluate for the first time the functional properties of EPCs isolated from tumor patients by focusing on RCC-EPCs. We extended our analysis at microscopic level by monitoring the sub-cellular structure of RCC-EPCs relative to their Ca2+ signalling fingerprint. Our results showed a striking functional and ultrastructural difference between RCC-EPCs and their normal counterparts, which might be the basis for designing novel, more specific anti-angiogenic treatments