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Object detectors often experience a drop in performance when new environmental conditions are insufficiently represented in the training data. This paper studies how to automatically fine-tune a pre-existing object detector while exploring and acquiring images in a new environment without relying on human intervention, i.e., in a self-supervised fashion. In our setting, an agent initially explores the environment using a pre-trained off-the-shelf detector to locate objects and associate pseudo-labels. By assuming that pseudo-labels for the same object must be consistent across different views, we devise a novel mechanism for producing refined predictions from the consensus among observations. Our approach improves the off-the-shelf object detector by 2.66% in terms of mAP and outperforms the current state of the art without relying on ground-truth annotations., Comment: This article is a conference paper related to arXiv:2302.03566 and is currently under review

The growth in knowledge of the pathogenesis, molecular background, and immunohistochemical profile of neuroendocrine neoplasms (NENs) has led not only to an increased awareness of these diseases but also to several changes of the nomenclature. In particular, the concept and terminology of high-grade (grade 3) NENs and mixed neoplasms have changed considerably over the last 20 years, creating some confusion among pathologists and clinicians. The aim of this review is to elucidate the diagnostic criteria, including the most important differential diagnoses of high-grade NENs and mixed neuroendocrine/non-neuroendocrine neoplasms (MiNENs). The role of the Ki67 labelling index and morphology, used to define grade 3 NENs of the digestive system and lungs, is also discussed. The evolution of the concepts and terminology of MiNENs is revised, including the most important differential diagnoses.

Pancreatic neuroendocrine carcinomas (NECs) are rare and very aggressive neoplasms with dismal prognosis, especially when metastatic or with negative prognostic factors, such as vascular invasion. To the best of our knowledge, no case of pancreatic NEC with mismatch repair deficiency has been reported to date. We describe a 62-year-old patient who underwent pancreaticoduodenectomy for a NEC located in the pancreatic head, with peripancreatic lymph node metastases. Tumor necrosis was prominent and the Ki67 proliferative index was 60%. One year after the diagnosis, the patient experienced recurrence with a left supraclavicular lymph node metastasis, which was surgically removed, followed by standard cisplatin-etoposide chemotherapy. Neoplastic cells showed combined loss of expression of MLH1 and PMS2 in both primary tumor and lymph node metastasis. Microsatellite instability (MSI) test using a mononucleotide repeats pentaplex PCR (BAT-25, BAT-26, NR-21, NR-22, and NR-24) revealed minimal mononucleotide shifts showing deletion of less than 3 bp at NR-21, BAT-26, NR-24, and NR-22 loci. MLH1 methylation analysis revealed absence of the gene promoter methylation. BRAF and KRAS mutations were not detected. In gut, NECs' mismatch repair deficiency phenotype has been reported in about 10% of cases, and it represents an independent factor of more favorable outcome. Likewise, our patient is currently alive with a follow-up of more than 12 years after pancreaticoduodenectomy, by itself an unexpected finding for such an aggressive neoplasm.

The molecular alterations of pancreatic acinar cell carcinomas (ACCs) and mixed acinar-neuroendocrine carcinomas (MANECs) are not completely understood, and the possible role of c-MYC amplification in tumor development, progression, and prognosis is not known. We have investigated c-MYC gene amplification in a series of 35 ACCs and 4 MANECs to evaluate its frequency and a possible prognostic role. Gene amplification was investigated using interphasic fluorescence in situ hybridization analysis simultaneously hybridizing c-MYC and the centromere of chromosome 8 probes. Protein expression was immunohistochemically investigated using a specific monoclonal anti-c-myc antibody. Twenty cases had clones with different polysomies of chromosome 8 in absence of c-MYC amplification, and 5 cases had one amplified clone and other clones with chromosome 8 polysomy, while the remaining 14 cases were diploid for chromosome 8 and lacked c-MYC amplification. All MANECs showed c-MYC amplification and/or polysomy which were observed in 54% pure ACCs. Six cases (15.3%) showed nuclear immunoreactivity for c-myc, but only 4/39 cases showed simultaneous c-MYC amplification/polysomy and nuclear protein expression. c-myc immunoreactivity as well as c-MYC amplification and/or chromosome 8 polysomy was not statistically associated with prognosis. Our study demonstrates that a subset of ACCs shows c-MYC alterations including gene amplification and chromosome 8 polysomy. Although they are not associated with a different prognostic signature, the fact that these alterations are present in all MANECs suggests a role in the acinar-neuroendocrine differentiation possibly involved in the pathogenesis of MANECs.

The recent introduction of robots to everyday scenarios has revealed new opportunities for collaboration and social interaction between robots and people. However, high level interaction will require semantic understanding of the environment. In this paper, we advocate that co-existence of assistive robots and humans can be leveraged to enhance the semantic understanding of the shared environment, and improve situation awareness. We propose a probabilistic framework that combines human activity sensor data generated by smart wearables with low level localisation data generated by robots. Based on this low level information and leveraging colocation events between a user and a robot, it can reason about semantic information and track humans and robots across different rooms. The proposed system relies on two-way sharing of information between the robot and the user. In the first phase, user activities indicative of room utility are inferred from consumer wearable devices and shared with the robot, enabling it to gradually build a semantic map of the environment. This will enable natural language interaction and high-level tasks for both assistive and co-working robots. In a second phase, via colocation events, the robot is able to share semantic information with the user, by labelling raw user data with semantic information about room type. Over time, the labelled data is used for training an Hidden Markov Model for room-level localisation, effectively making the user independent from the robot.

Angiogenesis, a process related to tumor growth and malignancy, is stimulated by several growth factors. Among these is vascular endothelial growth factor (VEGF), which acts on endothelial cells by binding with 2 specific receptors, VEGFR1 and VEGFR2. Recent studies have demonstrated that VEGF expression is correlated with microvessel density (MVD) and tumor progression. Digestive endocrine tumors are heterogeneous neoplasms exhibiting variable biological aggressiveness and behavior that often are not predictable on morphologic grounds alone. The aims of this study were to evaluate the expression of VEGF, VEGFR1, and VEGFR2 in digestive endocrine tumors and to examine its correlation with MVD and malignancy. A total of 84 specimens from endocrine neoplasms and normal gut and pancreatic tissue were immunohistochemically studied using specific antibodies directed against VEGF, VEGFR1, VEGFR2, endothelial antigens, and gastroenteropancreatic hormones. Ultrastructural immunocytochemistry was performed to identify the cellular localization of VEGF and the VEGFRs. In normal tissues, VEGF immunoreactivity was detected in G cells and PP cells. Ultrastructurally, VEGF was localized within secretory granules. The VEGFRs were not significantly expressed by normal endocrine cells. VEGF-immunoreactive (IR) cells were detected in 40 of 83 tumors, mainly G cell and enterochromaffin cell neoplasms. VEGFR1-IR cells were found in 44 of 82 tumors, and VEGFR2-IR cells were found in 55 of 82 tumors, with no predilection for any specific tumor type. The expression of VEGF and its receptors did not correlate with MVD or malignancy. These results suggest that in normal tissues, endothelial functions may be regulated by VEGF produced by some endocrine cells and that a VEGF/VEGFR binding mechanism may be involved in tumorigenesis, but not in tumor progression and aggressiveness. HUM PATHOL 34:18-27. Copyright 2003, Elsevier Science (USA). All rights reserved.

In April, 2004, a 62-year-old man with epistaxis, rhinorrhea, and sensation of nasal obstruction attended an appointment at the ear, nose, and throat department that found a solid mass of the right nasal cavity with no clinical evidence of lymph-node or distant metastases as confi rmed by CT and MRI (fi gure 1A). Biopsy of the mass revealed a proliferation of undiff erentiated cells with scant cytoplasm, hyper chromatic nuclei, and high mitotic rate, which formed infi ltrating nests in the stroma of the nasal mucosa (fi gure 2A). Tumour cells showed immuno reactivity for cytokeratin AE1/AE3, synaptophysin, neuron-specifi c enolase (fi gure 2B), CD56, and p53, but not for CD45. The histological features and the immunophenotype were suggestive of a poorly diff erentiated neuroendocrine small-cell carcinoma of the nasal cavity. The patient underwent somatostatin-receptor scintigraphy, which showed tracer uptake in the nasal region only. Blood concentrations of neuron-specifi c enolase, chromogranin A, carcinoembryonic antigen, and Cyfra 21-1 were unremarkable. The patient was treated with carboplatin (area under curve=6) on day 1 and etoposide (100 mg/m) on days 1–3 for seven cycles from May to October, 2004. In October, 2004, CT and MRI showed partial reduction of the mass (fi gure 1B). The patient sub sequently underwent transcranial-endoscopic endo nasal resection of the neoplasm with partial removal of the ethmoid and inferior conchae, the nasal septum, the fl oor and the lateral walls of the right nasal cavity, and the right maxillary sinus. Histologically, the tumour showed two main components. The predominant component was represented by clusters of mature synaptophysin and CD56-positive ganglion cells dispersed in a schwannianlike glial fi brillary acidic protein (GFAP)-positive background (fi gure 2C). Ganglion cells also stained positively for somatostain-receptor 2A (fi gure 2D). The second component was characterised by a proliferation of malignant cells, with abundant eosinophilic cytoplasm strongly positive for actin and desmin (fi gures 2E and 2F). This component was consistent with a rhabdomyosarcoma. The proliferation of undiff erentiated cells seen in the nasal biopsy done during the fi rst clinical investigation was not clearly identifi ed. Only scattered malignant cells that were immunoreactive for cytokeratin AE1/AE3 were seen in the surgically resected tumour tissue. The occurrence of a rhabdomyosarcoma associated with ganglio neuromatous and undiff erentiated components led us to diagnose a malignant ectomesenchymoma. Postsurgical adjuvant treatment with concurrent chemotherapy (weekly cisplatin [45 mg total] and radiotherapy [50 Gy total]) to the right nasal cavity was given from March to April, 2005. The patient was still alive at last follow-up in September, 2006, and had complete remission of the tumour, which was confi rmed both radiologically (fi gure 1C) and histologically. Malignant ectomesenchymoma is a rare multiphenotypic soft-tissue tumour with both mesenchymal and neuroectodermal components. It is believed to arise from pluripotential migratory neural crest cells (ectomesenchym) that can diff erentiate into neuroectodermal and mesenchymal tissues. The mesenchymal component usually consists of rhabdomyoblastic elements, although other malignant mesenchymal components have also been described. Neuroectodermal elements are mainly represented by ganglion cells and neuroma-like structures. About 50 cases have been reported in studies published in English. This neoplasm most frequently aff ects children, although a few cases in Lancet Oncol 2007; 8: 358–60

Metastasis in a tracheostomy site occurs rarely, usually from head and neck primary tumors. Breast cancer relapse to a tracheostomy has not been described to date.A 71-year-old women presented with symptoms typical of central airway obstruction, 10 years after mastectomy for breast cancer. Fifteen months before admission, when cancer follow-up was negative, she also had surgery for cerebral aneurysm and a tracheostomy. On admission, CT showed a solid mass infiltrating the tracheostomy tract and projecting into the airway. Tracheal obstruction palliation was achieved by laser resection of the endotracheal growth and stenting. Histology documented breast cancer metastasis.Tracheostomy site metastasis was the presenting sign of late-onset relapse of breast cancer. This case supports the concept of surgery-driven interruption of micrometastatic cancer dormancy, in that the initial recurrence developed in a tracheostomy that was surgically created several years after resection of the primary tumor.

Fused deposition modelling is one of the most widely used additive manufacturing techniques and the diffusion of 3D printers has increased in popularity even further in recent times. Since high precision is required in 3D printing, a good control over the extrusion process is necessary. In this regard, a crucial phenomenon to be accounted for is the die or extrudate swell, i.e., the enlargement of the cross-section of the strand when coming out of the printer nozzle. While this phenomenon has been studied in large scale extruders, it has not yet been investigated in depth for 3D printing processes. In this work, the die swell phenomenon observed in a printed PLA filament is studied by experiments and fluid dynamic simulations. A novel, easy-to-use, accurate and fast procedure for measuring the value of the die swell ratio during the printing process is developed, accounting for typical errors related to a non-constant strand diameter and possible oscillations of the filament with respect to the extrusion direction. As the printing velocity is increased, a linearly increasing swelling ratio is observed at low printing speeds. The trend flattens at moderate speed values. A sudden increase is found at high printing velocities. The swelling ratio measured with the proposed technique is compared with the results of multi-mode viscoelastic simulations at different temperatures. A fair agreement between the experimental measurements and the numerical predictions is found for printing velocities that are typically employed in commercial 3D printers, supporting the reliability of the developed procedure.

Neuroendocrine neoplasms (NENs) of the major and minor ampulla are rare diseases with clinico-pathologic features distinct from non-ampullary-duodenal NENs. However, they have been often combined and the knowledge on prognostic factors specific to ampullary NENs (Amp-NENs) is limited. The aim of this study was to identify factors associated with metastatic potential and patient prognosis in Amp-NENs. We clinically and histologically investigated an international series of 119 Amp-NENs, comprising 93 ampullary neuroendocrine tumors (Amp-NETs) and 26 neuroendocrine carcinomas (Amp-NECs). Somatostatin-producing tubulo-acinar NET represented the predominant Amp-NET histologic subtype (58 cases, 62%, 12 associated with type 1 neurofibromatosis). Compared to Amp-NETs, Amp-NECs arose in significantly older patients and showed a larger tumor size, a more frequent small vessel invasion, a deeper level of invasion and a higher rate of distant metastasis, and, importantly, a tremendously worse disease-specific patient survival. In Amp-NETs, the WHO grade proved to be a strong predictor of disease-specific survival (hazard ratio: 12.61, p 60 years, small vessel invasion, pancreatic invasion, and distant metastasis at diagnosis. Although nodal metastatic disease was not associated with survival by itself, patients with > 3 metastatic lymph nodes showed a worse outcome in comparison with the remaining Amp-NET cases with lymphadenectomy. Tumor epicenter in the major ampulla, small vessel invasion, and tumor size > 16 mm were independent predictors of nodal metastases in Amp-NETs. In conclusion, we identified prognostic factors, which may eventually help guide treatment decisions in Amp-NENs.

Carboxyl ester lipase (CEL) is an enzyme that hydrolyzes a wide variety of lipid substrates, including ceramides, which are known to show inhibitory regulation of pituitary hormone secretion in experimental models. Because no studies on CEL expression in human pituitary and pituitary adenomas have been reported in the literature, we investigated CEL expression in 10 normal pituitary glands and 86 well-characterized pituitary adenomas [12 FSH/LH cell, 17 α-subunit/null cell, 6 TSH cell, 21 ACTH cell, 11 prolactin (PRL) cell, and 19 GH cell adenomas] using IHC, immunoelectron microscopy, Western blotting, and quantitative RT-PCR. In normal adenohypophysis, CEL was localized in GH, ACTH, and TSH cells. In adenomas, it was mainly found in functioning GH, ACTH, and TSH tumors, whereas its expression was poor in the corresponding silent adenomas and was lacking in FSH/LH cell, null cell, and PRL cell adenomas. Ultrastructurally, CEL was localized in secretory granules close to their membranes. This is the first study demonstrating CEL expression in normal human pituitary glands and in functioning GH, ACTH, and TSH adenomas. Considering that CEL hydrolyzes ceramides, inactivating their inhibitory function on pituitary hormone secretion, our findings suggest a possible role of CEL in the regulation of hormone secretion in both normal and adenomatous pituitary cells. (J Histochem Cytochem 58:881–889, 2010)

Currently used histopathologic criteria for the diagnosis of pancreatic endocrine tumors are still under discussion as far as to their capacity to identify prognostically different tumor subsets, which are potentially helpful for patient management. A recently developed TNM staging system and a variety of proposed histologic and clinicopathologic parameters still need to be fully validated. One hundred fifty-five pancreatic endocrine tumors encompassing all the main histologic types and stages, operated with intention to cure and then followed tip for a median 126 months, were carefully investigated histologically to identify prognostically informative parameters at univariable, bivariable, and multivariable analysis. Ki67 index, mitotic rate, neuroinvasion with or without vascular, peritumoral or stromal infiltrative patterns, as well as tumor size, and association with endocrine syndromes other than insulinoma proved effective in predicting recurrence and disease-specific death among well-differentiated tumors. Poorly differentiated histologic features, more than 10 mitoses/10 high power fields, and necrosis were helpful in the identification of high-grade cancers with an invariably poor prognosis. The TNM system proved to be highly predictive of patient outcome and easy to combine with histologic and clinicopathologic parameters to classify pancreatic endocrine tumors into groups of increasing malignant potential. (c) 2009 Elsevier Inc. All rights reserved.