SARS-CoV-2 infection predicts larger infarct volume in patients with acute ischemic stroke

Background and purpose: Acute ischemic stroke (AIS) is a fearful complication of Coronavirus Disease-2019 (COVID-19). Aims of this study were to compare clinical/radiological characteristics, endothelial and coagulation dysfunction between acute ischemic stroke (AIS) patients with and without COVID-19 and to investigate if and how the SARS-CoV-2 spike protein (SP) was implicated in triggering platelet activation. Methods: We enrolled AIS patients with COVID-19 within 12 h from onset and compared them with an age- and sex-matched cohort of AIS controls without COVID-19. Neuroimaging studies were performed within 24 h. Blood samples were collected in a subset of 10 patients. Results: Of 39 AIS patients, 22 had COVID-19 and 17 did not. Admission levels of Factor VIII and von Willebrand factor antigen were significantly higher in COVID-19 patients and positively correlated with the infarct volume. In multivariate linear regression analyses, COVID-19 was an independent predictor of infarct volume (B 20.318, Beta 0.576, 95%CI 6.077-34.559; p = 0.011). SP was found in serum of 2 of the 10 examined COVID-19 patients. Platelets from healthy donors showed a similar degree of procoagulant activation induced by COVID-19 and non-COVID-19 patients' sera. The anti-SP and anti-FcγRIIA blocking antibodies had no effect in modulating platelet activity in both groups. Conclusions: SARS-CoV-2 infection seems to play a major role in endothelium activation and infarct volume extension during AIS

TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A

Variants of UNC13A, a critical gene for synapse function, increase the risk of amyotrophic lateral sclerosis and frontotemporal dementia1-3, two related neurodegenerative diseases defined by mislocalization of the RNA-binding protein TDP-434,5. Here we show that TDP-43 depletion induces robust inclusion of a cryptic exon in UNC13A, resulting in nonsense-mediated decay and loss of UNC13A protein. Two common intronic UNC13A polymorphisms strongly associated with amyotrophic lateral sclerosis and frontotemporal dementia risk overlap with TDP-43 binding sites. These polymorphisms potentiate cryptic exon inclusion, both in cultured cells and in brains and spinal cords from patients with these conditions. Our findings, which demonstrate a genetic link between loss of nuclear TDP-43 function and disease, reveal the mechanism by which UNC13A variants exacerbate the effects of decreased TDP-43 function. They further provide a promising therapeutic target for TDP-43 proteinopathies

Global disparities in surgeons’ workloads, academic engagement and rest periods: the on-calL shIft fOr geNEral SurgeonS (LIONESS) study

: The workload of general surgeons is multifaceted, encompassing not only surgical procedures but also a myriad of other responsibilities. From April to May 2023, we conducted a CHERRIES-compliant internet-based survey analyzing clinical practice, academic engagement, and post-on-call rest. The questionnaire featured six sections with 35 questions. Statistical analysis used Chi-square tests, ANOVA, and logistic regression (SPSS® v. 28). The survey received a total of 1.046 responses (65.4%). Over 78.0% of responders came from Europe, 65.1% came from a general surgery unit; 92.8% of European and 87.5% of North American respondents were involved in research, compared to 71.7% in Africa. Europe led in publishing research studies (6.6 ± 8.6 yearly). Teaching involvement was high in North America (100%) and Africa (91.7%). Surgeons reported an average of 6.7 ± 4.9 on-call shifts per month, with European and North American surgeons experiencing 6.5 ± 4.9 and 7.8 ± 4.1 on-calls monthly, respectively. African surgeons had the highest on-call frequency (8.7 ± 6.1). Post-on-call, only 35.1% of respondents received a day off. Europeans were most likely (40%) to have a day off, while African surgeons were least likely (6.7%). On the adjusted multivariable analysis HDI (Human Development Index) (aOR 1.993) hospital capacity > 400 beds (aOR 2.423), working in a specialty surgery unit (aOR 2.087), and making the on-call in-house (aOR 5.446), significantly predicted the likelihood of having a day off after an on-call shift. Our study revealed critical insights into the disparities in workload, access to research, and professional opportunities for surgeons across different continents, underscored by the HDI

Cerebrovascular complications of COVID-19 and COVID-19 vaccination

The risk of stroke and cerebrovascular disease complicating infection with SARS-CoV-2 has been extensively reported since the onset of the pandemic. The striking efforts of many scientists in cooperation with regulators and governments worldwide have rapidly brought the development of a large landscape of vaccines against SARS-CoV-2. The novel DNA and mRNA vaccines have offered great flexibility in terms of antigen production and led to an unprecedented rapidity in effective and safe vaccine production. However, as mass vaccination has progressed, rare but catastrophic cases of thrombosis have occurred in association with thrombocytopenia and antibodies against PF4 (platelet factor 4). This catastrophic syndrome has been named vaccine-induced immune thrombotic thrombocytopenia. Rarely, ischemic stroke can be the symptom onset of vaccine-induced immune thrombotic thrombocytopenia or can complicate the course of the disease. In this review, we provide an overview of stroke and cerebrovascular disease as a complication of the SARS-CoV-2 infection and outline the main clinical and radiological characteristics of cerebrovascular complications of vaccinations, with a focus on vaccine-induced immune thrombotic thrombocytopenia. Based on the available data from the literature and from our experience, we propose a therapeutic protocol to manage this challenging condition. Finally, we highlight the overlapping pathophysiologic mechanisms of SARS-CoV-2 infection and vaccination leading to thrombosis

Neurological manifestations in COVID-19: how relevant is this association?

INTRODUCTION: Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) was first reported in December 2019 in an outbreak occurring in Wuhan, China and has spread rapidly all over the word causing a global pandemic with approximately 129 million confirmed cases and more than 2.8 million deaths worldwide as of April 2nd, 2021. With the increasing number of people affected by this disease, it has become early apparent that SARS-CoV-2 may also affect the nervous system. EVIDENCE ACQUISITION: A great number of case reports, case series and review, often incomplete and not-peer- reviewed, about the observation of neurological symptoms in coronavirus disease-19 (COVID-19) have been published to date. In this review, we have tried to summarize the most recent evidences about the main neurological syndrome as- sociated to the infection: delirium/confusion, encephalitis, Guillain-Barré Syndrome (GBS) and ischemic stroke. EVIDENCE SYNTHESIS: From the huge amount of literature published in the last year, it appears that the neurological involvement of nervous system in COVID-19 is a relatively rare event as compared to the lung damage, but it is one of the most frequent extra-pulmonary complications. A supposed direct invasion of the nervous system, a para-infectious or post-infectious immune-mediated disease, or simply post-systemic effects of the viral infection, have been proposed as the main mechanisms. CONCLUSIONS: Encephalopathy and stroke are the most serious and common syndromes associated with COVID-19, mostly related to the inflammatory and hypercoagulable status, whereas available data suggest a post-infectious immune mediated mechanism for SARS-CoV-2 related GBS. However, more extensive epidemiological and histopathological studies are warranted to confirm the casualty of this latter associatio

Evidence of SARS-CoV-2 spike protein on retrieved thrombi from COVID-19 patients

The pathophysiology of COVID-19-associated coagulopathy is complex and not fully understood. SARS-CoV-2 spike protein (SP) may activate platelets and interact with fibrin(ogen). We aimed to investigate whether isolated SP can be present in clots retrieved in COVID-19 patients with acute ischemic stroke (by mechanical thrombectomy) and myocardial infarction. In this pilot study, we could detect SP, but not nucleocapsid protein, on platelets of COVID-19 patients' thrombi. In addition, in all three COVID-19 thrombi analyzed for molecular biology, no SARS-CoV-2 RNA could be detected by real-time polymerase chain reaction. These data could support the hypothesis that free SP, besides the whole virus, may be the trigger of platelet activation and clot formation in COVID-19

Vaccine-induced immune thrombotic thrombocytopenia: a possible pathogenetic role of ChAdOx1 nCoV-19 vaccine encoded soluble SARS-CoV-2 spike protein

Not available

TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A.

Variants of UNC13A, a critical gene for synapse function, increase the risk of amyotrophic lateral sclerosis and frontotemporal dementia1-3, two related neurodegenerative diseases defined by mislocalization of the RNA-binding protein TDP-434,5. Here we show that TDP-43 depletion induces robust inclusion of a cryptic exon in UNC13A, resulting in nonsense-mediated decay and loss of UNC13A protein. Two common intronic UNC13A polymorphisms strongly associated with amyotrophic lateral sclerosis and frontotemporal dementia risk overlap with TDP-43 binding sites. These polymorphisms potentiate cryptic exon inclusion, both in cultured cells and in brains and spinal cords from patients with these conditions. Our findings, which demonstrate a genetic link between loss of nuclear TDP-43 function and disease, reveal the mechanism by which UNC13A variants exacerbate the effects of decreased TDP-43 function. They further provide a promising therapeutic target for TDP-43 proteinopathies

Molecular and morphological characterisation of the oldest Cucumis melo L. seeds found in the Western Mediterranean Basin

[EN] In 2008¿2009, a rescue excavation uncovered an intact Late Bronze Age well in Sa Osa, Sardinia (Italy). The structure yielded a large number of waterlogged plant remains, of which a group of melon seeds (Cucumis melo L.) were some of the most remarkable. These seeds represent the earliest recorded remains of this taxon in the Western Mediterranean and are some of the oldest ever recorded. The plant remains were preserved in anoxic conditions and were found in a perfect state of conservation, making them ideal candidates for morphometric and molecular characterisation. A total of 96 parameters, measured using an automatic image analysis system, were specifically designed to evaluate the morphological features of 15 preserved whole seeds. DNA extraction from archaeological samples followed a procedure specifically set up to avoid any kind of contamination. A 123-SNP genotyping platform that had been validated previously was used. The morphological and molecular data of the archaeological seeds were successfully compared with those of a set of 179 accessions, including landraces, of feral and wild melons from Europe, Africa, and Asia. Both analyses confirmed that these ancient seeds did not belong to a wild melon, but instead to a cultivated one. This primitive melon could have belonged to a group of ancestral non-sweet or semi-sweet forms of chate, flexuosus, or ameri varieties, showing similarities to North African and Central Asian accessions. This finding is coherent with the reportedly important role of cucumber-like melons in the species¿ diversification process and with the accepted role of the ameri group as the ancestors of the modern sweet varieties.Sabato, D.; Esteras Gómez, C.; Grillo, O.; Peña-Chocarro, L.; Leida, C.; Ucchesu, M.; Usai, A.... (2017). Molecular and morphological characterisation of the oldest Cucumis melo L. seeds found in the Western Mediterranean Basin. 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