The current challenge worldwide is the administration of anti-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccines. Even if rarely, severe vascular adverse reactions temporally related to vaccine administration have induced diffidence in the population at large. In particular, researchers worldwide are focusing on the so-called “thrombosis and thrombocytopenia after COVID-19 vaccination”. This study aims to establish a practical workflow to define the relationship between adverse events following immunization (AEFI) and COVID-19 vaccination, following the basic framework of the World Health Organization (WHO). Post-mortem investigation plays a pivotal role to support this causality relationship when death occurs. To demonstrate the usefulness and feasibility of the proposed workflow, we applied it to two exemplificative cases of suspected AEFI following COVID-19 vaccination. Based on the proposed model, we took into consideration any possible causality relationship between COVID-19 vaccine administration and AEFI. This led us to conclude that vaccination with ChAdOx1 nCov-19 may cause the rare development of immune thrombocytopenia mediated by platelet-activating antibodies against platelet factor 4 (PF4), which clinically mimics heparin-induced autoimmune thrombocytopenia. We suggest the adoption of the proposed methodology in order to confirm or rule out a causal relationship between vaccination and the occurrence of AEFI.

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J. Neurochem. (2010) 114, 761–771. Abstract The possibility to selectively remove noradrenergic neurons in the locus coeruleus/subcoeruleus (LC/SubC) complex by the immunotoxin anti‐dopamine‐β‐hydroxylase (DBH)‐saporin has offered a powerful tool to study the functional role of this projection system. In the present study, the anatomical consequences of selective lesions of the LC/SubC on descending noradrenergic projections during early postnatal development have been investigated following bilateral intraventricular injections of anti‐DBH‐saporin or 6‐hydroxydopamine to immature (4 day old) rats. Administration of increasing doses (0.25–1.0 μg) of the immunotoxin produced, about 5 weeks later, a dose‐dependent loss of DBH‐immunoreactive neurons in the LC/SubC complex (≈ 45–90%) paralleled by a similar reduction of noradrenergic innervation in the terminal territories in the lumbar spinal cord. Even at the highest dose used (1.0 μg) the immunotoxin did not produce any detectable effects on dopaminergic, adrenergic, serotonergic or cholinergic neuronal populations, which, by contrast, were markedly reduced after administration of 6‐hydroxydopamine. The ≈ 90% noradrenergic depletion induced by 0.5 and 1.0 μg of anti‐DBH‐saporin remained virtually unchanged at 40 weeks post‐lesion. Conversely, the ≈ 45% reduction of spinal innervation density estimated at 5 weeks in animals injected with the lowest dose (0.25 μg) of the immunotoxin was seen recovered up to near‐normal levels at 40 weeks, possibly as a result of the intrinsic plasticity of the developing noradrenergic system. A similar reinnervation in the lumbar spinal cord was also seen promoted by grafts of fetal LC tissue implanted at the postnatal day 8 (i.e. 4 days after the lesion with 0.5 μg of anti‐DBH‐saporin). In these animals, the number of surviving neurons in the grafts and the magnitude of the reinnervation, with fibers extending in both the grey and white matter for considerable distances, were seen higher than those reported in previous studies using adult recipients. This would suggest that the functional interactions between the grafted tissue and the host may recapitulate the events normally occurring during the ontogenesis of the coeruleo‐spinal projection system, and can therefore be developmentally regulated. Thus, the neonatal anti‐DBH‐saporin lesion model, with the possibility to produce graded noradrenergic depletions, holds promises as a most valuable tool to address issues of compensatory reinnervation and functional recovery in the severed CNS as well as to elucidate the mechanisms governing long‐distance axon growth from transplanted neural precursors.

Despite recent advances in the management of thyroid cancer, the survival rate of this tumor may still be improved. Therefore, the identification of biological and molecular features of indolent and aggressive disease would be critical to define clinically useful predictors of high-risk lesions. microRNAs (miRNAs) are small RNA molecules with regulatory function and marked tissue specificity that modulate multiple targets belonging to several pathways. They are frequently deregulated in cancer and constitute a new class of blood-based biomarkers useful for cancer detection and prognosis definition, including thyroid cancer. In this review, the role of miRNAs in thyroid cancer development is described. The most common miRNAs detected in thyroid cancer along with their clinical significance are also discussed. Further studies aimed to detect plasma-based miRNA biomarkers in thyroid cancer patients may provide further insight into the management of thyroid cancer.

Papillary thyroid carcinoma (PTC) is the most common histotype among the thyroid cancer types. Although PTC is a curable malignancy, many patients relapse after treatment. Thus, there is a need to identify novel factors involved in the pathogenesis of PTC that may be used as targets for new therapies. The MAPK pathway has been implicated in the pathogenesis of PTC. Therefore, in this review, we summarize the role of the BRAF V600E mutation in the development and progression of thyroid cancer. The cinical implication of this molecular abnormality is also discussed. It is evident that the detection of the BRAF V600E mutation is crucial in order to identify novel avenues for thyroid cancer treatment.