An immunohistochemical study of the diagnostic value of TREM-1 as marker for fatal sepsis cases

Triggering receptor expressed on myeloid cells-1 (TREM-1) is produced and up-regulated by exposure of myeloid cells to lipopolysaccharides or other components of either bacterial or fungal origin, which causes it to be strongly expressed on phagocytes that accumulate in inflamed areas. Because TREM-1 participates in septic shock and in amplifying the inflammatory response to bacterial and fungal infections, we believe it could be an immunohistochemical marker for postmortem diagnosis of sepsis. We tested the anti-TREM-1 antibody in 28 cases of death by septic shock and divided them into two groups. The diagnosis was made according to the criteria of the Surviving Sepsis Campaign. In all cases, blood cultures were positive. The first group was comprised subjects that presented high ante-mortem serum procalcitonin and the soluble form of TREM-1 (s-TREM-1) values. The second group comprised subjects in which s-TREM-1 was not measured ante-mortem. We used samples of brain, heart, lung, liver and kidney for each case to test the anti-TREM-1 antibody. A semiquantitative evaluation of the immunohistochemical findings was made. In lung samples, we found immunostaining in the cells of the monocyte line in 24 of 28 cases, which suggests that TREM-1 is produced principally by cells of the monocyte line. In liver tissue, we found low TREM-staining in the hepatocyte cytoplasm, duct epithelium, the portal-biliary space and blood vessel. In kidney tissue samples, we found the TREM-1 antibody immunostaining in glomeruli and renal tubules. We also found TREM-1 staining in the lumen of blood vessels. Immunohistochemical staining using the anti-TREM-1 antibody can be useful for postmortem diagnosis of sepsis

mTOR-related cell-clearing systems in epileptic seizures, an update

Recent evidence suggests that autophagy impairment is implicated in the epileptogenic mechanisms downstream of mTOR hyperactivation. This holds true for a variety of genetic and acquired epileptic syndromes besides malformations of cortical development which are classically known as mTORopathies. Autophagy suppression is sufficient to induce epilepsy in experimental models, while rescuing autophagy prevents epileptogenesis, improves behavioral alterations, and provides neuroprotection in seizure-induced neuronal damage. The implication of autophagy in epileptogenesis and maturation phenomena related to seizure activity is supported by evidence indicating that autophagy is involved in the molecular mechanisms which are implicated in epilepsy. In general, mTOR-dependent autophagy regulates the proliferation and migration of inter-/neuronal cortical progenitors, synapse development, vesicular release, synaptic plasticity, and importantly, synaptic clustering of GABAA receptors and subsequent excitatory/inhibitory balance in the brain. Similar to autophagy, the ubiquitin–proteasome system is regulated downstream of mTOR, and it is implicated in epileptogenesis. Thus, mTOR-dependent cell-clearing systems are now taking center stage in the field of epilepsy. In the present review, we discuss such evidence in a variety of seizure-related disorders and models. This is expected to provide a deeper insight into the molecular mechanisms underlying seizure activit

Analytical solution of the equation of motion for a rigid domain wall in a magnetic material with perpendicular anisotropy

This paper reports the solution of the equation of motion for a domain wall in a magnetic material which exhibits high magneto-crystalline anisotropy. Starting from the Landau-Lifschitz-Gilbert equation for field-induced motion, we solve the equation to give an analytical expression, which specifies the domain wall position as a function of time. Taking parameters from a Co/Pt multilayer system, we find good quantitative agreement between calculated and experimentally determined wall velocities, and show that high field uniform wall motion occurs when wall rigidity is assumed.Comment: 4 pages, 4 figure

Radiological and surgical aspects of polymorphous low-grade neuroepithelial tumor of the young (PLNTY)

Background: Polymorphous low-grade neuroepithelial tumor of the young (PLNTY) is a low-grade epilepsy-associated tumor recently introduced in WHO 2021 classification. Since it has been recognized as an independent nosological entity, PLNTY has been mainly studied from a genetic and molecular perspective, not recognizing unique characteristic clinical and radiological features. Methods: A systematic literature research has been conducted aiming to identify all relevant studies about the radiological, clinical and surgical features of PLNTY. We described a representative case of a 45-year-old man treated with awake-surgery with confirmed diagnosis of PLNTY, reporting the radiological and surgical characteristics through imaging and intra-operative video. We performed a statistical meta-analysis attempting to assess the presence of relationships between surgical and radiologic tumor characteristics and clinical outcome and type of surgery. Results: A total of 16 studies were included in the systematic review. The final cohort was composed of 51 patients. Extent of resection (EOR) and outcome are not significantly associated with the different genetic profiling (p = 1), the presence of cystic intralesional component, calcification (p = 0.85), contrast-enhancing and lesion boundaries (p = 0.82). No significant correlation there is between EOR and remission or better control of epilepsy-related symptoms (p = 0.38). The contrast enhancement in the tumor is significantly associated with recurrence or poor control of epileptic symptoms (p = 0.07). Conclusions: In PLNTYs, contrast enhancement seems to impact prognosis, recurrence, and seizure control much more than radiological features, genetic features and type of resection of the tumor

Simultaneous Embeddings with Few Bends and Crossings

A simultaneous embedding with fixed edges (SEFE) of two planar graphs $R$ and $B$ is a pair of plane drawings of $R$ and $B$ that coincide when restricted to the common vertices and edges of $R$ and $B$. We show that whenever $R$ and $B$ admit a SEFE, they also admit a SEFE in which every edge is a polygonal curve with few bends and every pair of edges has few crossings. Specifically: (1) if $R$ and $B$ are trees then one bend per edge and four crossings per edge pair suffice (and one bend per edge is sometimes necessary), (2) if $R$ is a planar graph and $B$ is a tree then six bends per edge and eight crossings per edge pair suffice, and (3) if $R$ and $B$ are planar graphs then six bends per edge and sixteen crossings per edge pair suffice. Our results improve on a paper by Grilli et al. (GD'14), which proves that nine bends per edge suffice, and on a paper by Chan et al. (GD'14), which proves that twenty-four crossings per edge pair suffice.Comment: Full version of the paper "Simultaneous Embeddings with Few Bends and Crossings" accepted at GD '1

On a Tree and a Path with no Geometric Simultaneous Embedding

Two graphs $G_1=(V,E_1)$ and $G_2=(V,E_2)$ admit a geometric simultaneous embedding if there exists a set of points P and a bijection M: P -> V that induce planar straight-line embeddings both for $G_1$ and for $G_2$. While it is known that two caterpillars always admit a geometric simultaneous embedding and that two trees not always admit one, the question about a tree and a path is still open and is often regarded as the most prominent open problem in this area. We answer this question in the negative by providing a counterexample. Additionally, since the counterexample uses disjoint edge sets for the two graphs, we also negatively answer another open question, that is, whether it is possible to simultaneously embed two edge-disjoint trees. As a final result, we study the same problem when some constraints on the tree are imposed. Namely, we show that a tree of depth 2 and a path always admit a geometric simultaneous embedding. In fact, such a strong constraint is not so far from closing the gap with the instances not admitting any solution, as the tree used in our counterexample has depth 4.Comment: 42 pages, 33 figure

Cerebrovascular complications and infective endocarditis. impact of available evidence on clinical outcome

Infective endocarditis (IE) is a life-threatening disease. Its epidemiological profile has substantially changed in recent years although 1-year mortality is still high. Despite advances in medical therapy and surgical technique, there is still uncertainty on the best management and on the timing of surgical intervention. The objective of this review is to produce further insight intothe short- and long-term outcomes of patients with IE, with a focus on those presenting cerebrovascular complications

Paclitaxel in endovascular devices. Identikit of a “serial killer”?

Recent developments in the management of peripheral artery disease have been momentous, and a key advance has been the introduction of drug-coated balloons, which capitalise on the mechanical effects of angioplasty balloons, and on the pharmacologic effects of anti-restenotic drugs [1,2]. Indeed, single reports from randomized trials and pooled estimates from meta-analyses have clearly showed that paclitaxel-coated balloons reduce the risk of restenosis and repeat revascularization, while improving patency, limb salvage, and freedom from claudication

MTOR modulates intercellular signals for enlargement and infiltration in glioblastoma multiforme

Recently, exosomal release has been related to the acquisition of a malignant phenotype in glioblastoma cancer stem cells (GSCs). Remarkably, intriguing reports demonstrate that GSC-derived extracellular vesicles (EVs) contribute to glioblastoma multiforme (GBM) tumorigenesis via multiple pathways by regulating tumor growth, infiltration, and immune invasion. In fact, GSCs release tumor-promoting macrovesicles that can disseminate as paracrine factors to induce phenotypic alterations in glioma-associated parenchymal cells. In this way, GBM can actively recruit different stromal cells, which, in turn, may participate in tumor microenvironment (TME) remodeling and, thus, alter tumor progression. Vice versa, parenchymal cells can transfer their protein and genetic contents to GSCs by EVs; thus, promoting GSCs tumorigenicity. Moreover, GBM was shown to hijack EV-mediated cell-to-cell communication for self-maintenance. The present review examines the role of the mammalian Target of Rapamycin (mTOR) pathway in altering EVs/exosome-based cell-to-cell communication, thus modulating GBM infiltration and volume growth. In fact, exosomes have been implicated in GSC niche maintenance trough the modulation of GSCs stem cell-like properties, thus, affecting GBM infiltration and relapse. The present manuscript will focus on how EVs, and mostly exosomes, may act on GSCs and neighbor non tumorigenic stromal cells to modify their expression and translational profile, while making the TME surrounding the GSC niche more favorable for GBM growth and infiltration. Novel insights into the mTOR-dependent mechanisms regulating EV-mediated intercellular communication within GBM TME hold promising directions for future therapeutic applications

Post-mortem diagnosis of intravascular large B-cell lymphoma

Intravascular large B-cell lymphoma (IVLBCL) is a rare (<1%), typically aggressive extranodal variant of mature non-Hodgkin B-cell lymphoma. IVLBCL is characterized by malignant lymphoid cells lodged within blood vessels, particularly capillary channels. Herein, we present a case of a 50-year-old man with a history of myeloradiculitis (∼1 year) and paraparesis requiring hospitalization. During the course of his hospital stay, computed tomography (CT), magnetic resonance imaging, CT-positron emission tomography, and biopsy failed to establish a diagnosis. The patient died 2 months later from bilateral pneumonia. Postmortem examination was undertaken to determine the cause of death. Histologic sections of the patient’s brain, heart, lung, and liver showed aggregates of highly atypical cells bearing enlarged, pleomorphic, and hyperchromatic nuclei. Strong intravascular positivity for CD45 and CD20 markers indicated the cells were of B-cell origin, supporting a diagnosis of IVLBCL