PALEORADIOLOGICAL STUDY ON TWO INFANTS DATED TO THE 17th AND 18th CENTURIES

During an excavation campaign in the Church of the Conversion of Saint Paul in Roccapelago (North Italy), a hidden crypt was discovered, which yielded the remains of more than 400 individuals. The crypt was used as a cemetery by the inhabitants of the village of Roccapelago between the 16th and 18th centuries. Along the north side of the crypt, an area apparently separated from the rest of the burials was found, bordered by stones, where several burials of newborns and infants were concentrated. From here, five fabric rolls containing bones were recovered, and it was decided not to carry out destructive analyses, allocating the two best examples to a thorough radiological investigation to try to define the type of burial and the complete biological profile of the infant. The two rolls, subjects of this study, can be dated archaeologically between the 17th and 18th centuries. CT analysis shows a varied group of bones with a fairly good state of conservation. The paleoradiological study carried out had the primary objective of avoiding the destruction of the two rolls, ensuring their conservation; but at the same time, providing essential data to understand their nature, defining the biological profile and the type of deposition

Registration of ultrasound volumes based on Euclidean distance transform

During neurosurgical operations, surgeons can decide to acquire intraoperative data to better proceed with the removal of a tumor. A valid option is given by ultrasound (US) imaging, which can be easily obtained at subsequent surgical stages, giving therefore multiple updates of the resection cavity. To improve the efficacy of the intraoperative guidance, neurosurgeons may benefit from having a direct correspondence between anatomical structures identified at different US acquisitions. In this context, the commonly available neuronavigation systems already provide registration methods, which however are not enough accurate to overcome the anatomical changes happening during resection. Therefore, our aim with this work is to improve the registration of intraoperative US volumes. In the proposed methodology, first a distance mapping of automatically segmented anatomical structures is computed and then the transformed images are utilized in the registration step. Our solution is tested on a public dataset of 17 cases, where the average landmark registration error between volumes acquired at the beginning and at the end of neurosurgical procedures is reduced from 3.55mm to 1.27mm

A Block-Based Union-Find Algorithm to Label Connected Components on GPUs

In this paper, we introduce a novel GPU-based Connected Components Labeling algorithm: the Block-based Union Find. The proposed strategy significantly improves an existing GPU algorithm, taking advantage of a block-based approach. Experimental results on real cases and synthetically generated datasets demonstrate the superiority of the new proposal with respect to state-of-the-art

Modulation of the JAK/ERK/STAT signaling in melanocortin-induced inhibition of local and systemic responses to myocardial ischemia/reperfusion

The janus kinases (JAK), extracellular signal-regulated kinases (ERK) and signal transducers and activators of transcription (STAT) pathways have been shown to play a cardioprotective role. We previously gave evidence that melanocortins afford cardioprotection in conditions of myocardial ischemia/reperfusion. Here we aimed to investigate the influence of melanocortins on the JAK/ERK/STAT signaling in cardiac and systemic responses to prolonged myocardial ischemia/reperfusion. Ischemia was produced in rats by ligature of the left anterior descending coronary artery for 30 min. At the end of the 2-h reperfusion, western blot analysis of the cardioprotective transcription factors pJAK2, pERK1/2, pTyr-STAT3 and pSer-STAT3, the inflammatory mediator tumor necrosis factor-α (TNF-α), the pro-apoptotic factors BAX and c-jun N-terminal kinases (pJNK), the anti-apoptotic protein Bcl-XL, as well as of the cardioprotective enzyme heme oxygenase-1 (HO-1), was performed in the left ventricle and spleen. Intravenous treatment, during coronary artery occlusion, with the melanocortin analogs [Nle4, D-Phe7]α-melanocyte-stimulating hormone (NDP-α-MSH) and adrenocorticotropic hormone 1-24 [ACTH-(1-24)], induced a left ventricle up-regulation of pJAK2, pERK1/2 and pTyr-STAT3 (JAK-dependent), and a reduction in pJNK and TNF-α levels; these effects of NDP-α-MSH and ACTH-(1-24) were associated with over-expression of the pro-survival proteins HO-1 and Bcl-XL, and marked decrease of the myocardial infarct size. Melanocortin treatment did not affect left ventricle pSer-STAT3 (ERK1/2-dependent) and BAX levels. In the spleen, NDP-α-MSH and ACTH-(1-24) induced similar effects on the expression of the above transcription factors/proteins, except for pERK1/2 (down-regulated) and HO-1 (unaffected). Blockade of JAK and ERK pathways with AG490 and U0126, respectively, abrogated the myocardial infarct size reduction by NDP-α-MSH. These results indicate that melanocortins inhibit local and systemic inflammatory and apoptotic cascades triggered by prolonged myocardial ischemia/reperfusion, with consequent reduction in myocardium infarct size, seemingly via activation of the JAK/STAT signaling and with modulation of an ERK (STAT unrelated) signaling pathw

Learn-Morph-Infer: A new way of solving the inverse problem for brain tumor modeling

Current treatment planning of patients diagnosed with a brain tumor, such as glioma, could significantly benefit by accessing the spatial distribution of tumor cell concentration. Existing diagnostic modalities, e.g. magnetic resonance imaging (MRI), contrast sufficiently well areas of high cell density. In gliomas, however, they do not portray areas of low cell concentration, which can often serve as a source for the secondary appearance of the tumor after treatment. To estimate tumor cell densities beyond the visible boundaries of the lesion, numerical simulations of tumor growth could complement imaging information by providing estimates of full spatial distributions of tumor cells. Over recent years a corpus of literature on medical image-based tumor modeling was published. It includes different mathematical formalisms describing the forward tumor growth model. Alongside, various parametric inference schemes were developed to perform an efficient tumor model personalization, i.e. solving the inverse problem. However, the unifying drawback of all existing approaches is the time complexity of the model personalization which prohibits a potential integration of the modeling into clinical settings. In this work, we introduce a deep learning based methodology for inferring the patient-specific spatial distribution of brain tumors from T1Gd and FLAIR MRI medical scans. Coined as Learn-Morph-Infer, the method achieves real-time performance in the order of minutes on widely available hardware and the compute time is stable across tumor models of different complexity, such as reaction–diffusion and reaction–advection–diffusion models. We believe the proposed inverse solution approach not only bridges the way for clinical translation of brain tumor personalization but can also be adopted to other scientific and engineering domains

Melanocortins protect against brain damage and counteract cognitive decline in a transgenic mouse model of moderate Alzheimer\u5f3s disease.

We previously reported that melanocortins induce neuroprotection in experimental acute and chronic neurodegenerative conditions, including Alzheimer\u5f3s disease (AD) of mild severity. Here we investigated whether melanocortins afford neuroprotection and counteract cognitive decline in AD with a medium level of severity by using 24 week-old (at the start of the study) APPSwe transgenic mice (Tg2576). Saline-treated (days 1-50) control Tg2576 mice showed an impairment in spatial learning and memory, associated (at day 50, end of the study) with hippocampus at low levels of the synaptic activity-dependent gene Zif268, relevant brain changes such as cerebral cortex/hippocampus increased level of \u3b2-amyloid (A\u3b2) deposit, and neuronal loss, in comparison with wild-type animals. Treatment of Tg2576 mice (once daily at days 1-50) with a nanomolar dose of the melanocortin analog [Nle4,D-Phe7]\u3b1-melanocyte-stimulating hormone (NDP-\u3b1-MSH) reduced cerebral cortex/hippocampus level of A\u3b2 deposit, decreased neuronal loss, increased hippocampus Zif268 expression and improved cognitive functions, relative to saline-treated Tg2576 mice. Pharmacological blockade of melanocortin MC4 receptors with the MC4 receptor antagonist HS024 prevented all favorable effects of NDP-\u3b1-MSH. Our data indicate that MC4 receptor-stimulating melanocortins are able to counteract cognitive decline in experimental AD of medium severity through induction of neuroprotection and improvement of synaptic transmission. After further studies, these agents could gain a role as disease modifying therapeutics for AD