72 research outputs found
Alignment of the Verbesina alternifolia plastomes assembled with Illumina and Nanopore reads
No full textAlignment of the Verbesina alternifolia plastomes assembled with Illumina and Nanopore read
Nanopore draft references for Armeria
No full textChloroplast genome and ribosomal DNA (nrDNA) draft references for Armeria maritima (Mill.) Willd. sample (herbarium voucher GOET065227) obteined using Nanopore read
Nitric oxide in the injured spinal cord: Synthases cross-talk, oxidative stress and inflammation
No full textNitric oxide (NO) is a unique informational molecule involved in a variety of physiological processes in the central nervous system (CNS). It has been demonstrated that it can exert both protective and detrimental effects in several disease states of the CNS, including spinal cord injury (SCI). The effects of NO on the spinal cord depend on several factors such as: concentration of produced NO, activity of different synthase isoforrns, cellular source of production and time of release. Basically, it has been shown that low NO concentrations may play a role in physiologic processes, whereas large amounts of NO may be detrimental by increasing oxidative stress. However, this does not explain all the discrepancies evidenced studying the effects of NO in SCI models. The analysis of the different synthase isoforms, of their temporal profile of activation and cellular source has shed light on this topic. Two post-injury time intervals can be defined with reference to the NO production: immediately after injury and several hours-to-days later. The initial immediate peak of NO production after injury is due to the up-regulation of the neuronal NO synthase (nNOS) in resident spinal cord cells. The late peak is due primarily to the activity of inducible NOS (iNOS) produced by inflammatory infiltrating cells. High NO levels produced by up-regulated nNOS and NOS are neurotoxic; the down-regulation of nNOS corresponds temporally to the expression of NOS. On the bases of those evidence, therapeutic approaches should be aimed: (1) to reduce the NO-elicited damage by inhibition of specific synthases according to the temporal profile of activation; (2) by maintaining physiologic amount of NO to keep the induction of iNOS expression suppressed and avoiding ischemia/reperfusion injuries; (3) by using scavengers of oxygen and nitrogen reactive species or using inhibitors of the specific kinases. (C) 2007 Elsevier B.V. All rights reserved
Isolation, genomic and proteomic characterization of fibroblastic and epithelial limbal stem cells and evaluation of their multilineage differentiation capability.
Full text linkABSTRACT
BACKGROUND: The limbus of the eye, located at the junction of the cornea and conjunctiva of the ocular surface, represents a unique stem cell niche in human body. A critical advantage of limbal cells is that they are easily accessible with a well established and minimally invasive procedure. Several groups have reported the gene expression profile of limbal and corneal epithelial cells that has significantly contributed to the understanding of several cellular pathways and intrinsic factors that underpin the phenotypic difference between the two cell types [1-3]. However the gene expression profile of the human limbal epithelial and limbal stromal cultured cells obtained from the native limbal tissue has not been addressed until now. The lack of specific molecular markers for the identification of the multipotent limbal subpopulation limited the investigation of their differentiation capability. SSEA4 (stage specific embryonic antigen) is recognized marker of pluripotent stem cells, such as embryonic stem cells, and not of multipotent stem cells. Actually, the researcher are agreed that SSEA4 expression is lost from stem cells as they start to differentiate. It is generally agreed that the LESC are characterized by special location in the limbus, clonality, cytokeratin profile, transformation-related protein 63 (p63) delta isomers, and ATP-binding cassette sub-family G member 2 (ABCG2) expression [4-5]. Fibroblast (f)-LSCs represent a multipotent stem cell population characterized as CD105+, CD73+, CD90+, CD34+ and CD45- as well as by their self-renewal and multi-lineage differentiation capability [6-7].
AIM: To identify the better protocol of isolation and expansion for LESC and f-LSCs to obtain two purified and distinct subpopulations for molecular and proteomic characterization to evaluate their multilineage differentiation capability.
MATERIAL AND METHODS: Cytofluorimetric analisys; sphere formation assay; qRT PCR and proteomic assays; multilineage differentiation assays were performed.
RESULTS: Both f-LSC and LESC populations expressed SSEA4 (principal staminal marker) 98.63 ± 3.5%; vs 78.32 ± 2.8%, respectively (at 2PD) and ABCG2 (limbal specific marker).
The f-LSC genomic expression profile in comparison to LESC didn’t show significant differences and both cell populations kept a stem genomic expression profiles since 24 PD. f-LSC kept an high SSEA4 positive expression (98.63 ± 3.5%; 90.36 ± 1.4%; 2PD-14PD) whereas LESC showed a CK15+/ΔNp63+ pattern and a reduced expression of SSEA4 (78.32 ± 2.8% vs 13.90± 4.6 %; 2PD-14PD).
f-LSC, but not LESC, were differentiated into pancreatic β-cell phenotype (insulin-producing beta-like cells). Furthermore, both f-LSC and LESC achieved terminal osteoblastic and adipose differentiation. By contrast, the specific for committed LESC towards definitive epithelial phenotype cytokeratin profile, reduced LESC multilineage differentiation skill.
CONCLUSIONS: The identification of genetic profiles and novel molecular markers characteristic of specific cellular phenotypes is likely to assist in better defining the stages of progression from unspecialized cells to cell types of interest. Yet, translation of these promising basic science discoveries into successful cell replacement therapy in human subjects is likely to require sophisticated methods for assessing genetic and phenotypic stability
Lamina terminalis fenestration
No full textChohan et al.3 (Chohan MO, Carlson AP,
Hart BL, et al: Lack of functional patency of the lamina
terminalis after fenestration following clipping of anterior
circulation aneurysms. Clinical article. J Neurosurg
119:629–633, September 2013). In their study, the authors
injected, on postoperative Day 1 following clipping of
anterior circulation aneurysms, an iodine-based contrast
agent intraventricularly to assess, with CT imaging, the
flow into the basal cisterns through a fenestrated lamina
terminalis. They concluded that fenestration of the lamina
terminalis (FLT) did not result in functional patency of
the lamina terminalis when performed as part of surgical
clipping for ruptured aneurysms.
We have some remarks and criticisms regarding this
article, which leads to clear-cut conclusions
Anti-Inflammatory Action of Heterogeneous Nuclear Ribonucleoprotein A2/B1 in Patients with Autoimmune Endocrine Disorders
Full text linkOur previous studies documented that human fibroblast-limbal stem cells (f-LSCs) possess immunosuppressive capabilities, playing a role in regulating T-cell activity. This study highlights the molecular activities by which human f-LSCs can attenuate the inflammatory responses of self-reactive peripheral blood mononuclear cells (PBMCs) collected from patients with autoimmune endocrine diseases (AEDs). Anti-CD3 activated PBMCs from twenty healthy donors and fifty-two patients with AEDs were cocultured on f-LSC monolayer. 2D-DIGE proteomic experiments, mass spectrometry sequencing and functional in vitro assays were assessed in cocultured PBMCs. We identified the downmodulation of several human heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNP A2/B1) isoforms in healthy and AED activated PBMCs upon f-LSC interaction. The reduction of hnRNPA2/B1 protein expression largely affected the cycling ki67+, CD25+, PD-1+ reactive cells and the double marked CD8+/hnRNPA2B1+ T cell subset. Anti-PD1 blocking experiments evoked hnRNPA2/B1 overexpression, attributing putative activation function to the protein. hnRNPA2/B2 transient silencing inverted immunopolarization of the self-reactive PBMCs from AEDs toward a M2/Th2-type background. Pharmacological inhibition and co-immunoprecipitation experiments demonstrated the involvement of NF-ĸB in hnRNPA2/B activity and turnover. Our data indicate cardinal involvement of hnRNP A2/B1 protein in peripheral mechanisms of tolerance restoration and attenuation of inflammation, identifying a novel immunoplayer potentially targetable in all AEDs
Espressione del Tumor Necrosis Factor Receptor-Associated Factor 1 e 2 (TRAF 1& 2) e regolazione dell'attivazione di NF-kB TNF-indotta e meccanismi anti-apoptotici nei glomi cerebrali
No full textComplications in Anterior Cranial Fossa Surgery
No full textA variety of neurosurgical disorders affect the anterior cranial base
and require an anterior cranial fossa approach. As neurosurgeons,
we usually deal with the treatment of benign neoplasms, in particular
meningiomas. Nonetheless, other common neurosurgical
pathologies include traumatic injuries, craniofacial malformations
(i.e., hypertelorism, craniosynostosis), cerebrospinal fluid (CSF)
fistulas, and vascular lesions (i.e., arterio-venous fistulas). Although
surgery of benign lesions of the anterior cranial fossa is a relatively
common procedure, tumors like meningiomas can reach huge sizes
and encase vital neurovascular structures, making surgery in the
area a real challenge.
Furthermore, the anterior cranial base is also involved by
malignant tumors. With some notable exceptions (leukemia,
lymphoma, myeloma, metastases), malignant neoplasms are
treated surgically but require adjuvant radiation or chemotherapy.
Malignant lesions are generally challenging lesions that require a
multidisciplinary approach to achieve an en bloc resection with
margins of uninvolved tissue after broad circumferential exposure
whenever possible.1 Indications for surgical treatment of malignant
tumors are influenced by the extent of the lesion taken together with
clinical data, including age and performance. Surgical morbidity
must be weighed against the anticipated natural course of the lesion
and results of nonsurgical treatments, when applicable.
Here we briefly describe the transcranial approaches to the
anterior cranial fossa and discuss complications commonly encountered
in anterior cranial fossa surgery and their avoidance
Espressione del telomeric Repeat Binding Factor-1 (TRF-1) nei tumori cerebrali della serie astrogliale: possibili implicazioni clinico-terapeutiche
No full textExpression of telomeric repeat binding factor-1 in astroglial bran tumors
No full textOBJECTIVE: In human somatic cells, telomeres shorten with successive cell divisions, resulting in progressive genomic instability, altered gene expression, and cell death. Recently, telomere-specific deoxyribonucleic acid-binding proteins, such as telomeric repeat binding factor-1 (TRF1), have been proposed as candidates for the role of molecules regulating telomerase activity, and they have been suggested to play key roles in the maintenance of telomere function. The present study was designed to assess TRF1 expression in human astroglial brain tumors and to speculate on the clinical implications of its expression.
METHODS: Twenty flash-frozen surgical specimens obtained from adult patients who underwent craniotomy for microsurgical tumor resection, histologically verified as World Health Organization Grade II to IV astrocytomas, were used. Expression of TRF1 in astrocytomas of different grades was studied by means of both immunohistochemical and Western blotting analysis. The correlation between the extent of TRF1 expression and histological grading, performance status, and length of survival of patients underwent statistical analyses.
RESULTS: TRF1 was expressed in all tumor samples. The level of its expression was variable, decreasing from low-grade through high-grade astrocytomas (P = 0.0032). TRF1 expression correlated with the patient's length of survival (P < 0.001) and performance status (P < 0.001) and proved to be an independent indicator of length of survival.
CONCLUSION: Our findings suggest that the loss of TRF1 expression capability, as a result of down-regulation of TRF1 expression in malignant gliomas cells, may play a role in the malignant progression of astroglial brain tumors
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