Search

In this work we develop an adaptive scheme for quantization of subband or transform coded frames in a typical video sequence coder. Using a generalized Gaussian model for the subband or transform coefficients, we present a procedure to determine the optimum dead-zone quantizer for a given entropy of the quantizer output symbols. We find that, at low bit rates, the dead-zone quantizer offers better performance than the uniform quantizer. The model is used to develop an adaptive procedure to update the quantizer parameters on the basis of the state of a channel buffer with constant output rate and variable input rate. We compare the accuracy of the generalized Gaussian model in predicting the actual bit rate to that achievable using the simpler and more common Laplacian model. Experimental results show that the generalized Gaussian model has superior performance than the Laplacian model, and that it can be effectively used in a practical scheme for buffer control. Index Terms - Buffer control, statistical modeling, subband coding, transform coding.

The reports of intraductal papillary mucinous tumors (IPMT) of the pancreas are increasingly more frequent in the literature. The diagnosis by means of cross-sectional imaging of these tumors is not easy, especially in the early stages, when they can mimic an inflammatory disease of the pancreas. Prompt identification of the disease is nevertheless extremely important, especially in the case of tumors originating from the collateral branches, since its recognition can modify the management of the patient, in some cases obviating recourse to surgery. [ABSTRACT FROM AUTHOR]

Presents a study which develop an adaptive scheme for quantization of subband or transform coded frames in a typical video sequence coder. Quantizer output entropy and distortion; Entropy and distortion in subband or discrete cosine transform (DCT) coding schemes; Application to buffer control; Conclusions.

Histone posttranslational modifications (PTMs) have crucial roles in a multitude of cellular processes, and their aberrant levels have been linked with numerous diseases, including cancer. Although histone PTM investigations have focused so far on methylations and acetylations, alternative long-chain acylations emerged as new dimension, as they are linked to cellular metabolic states and affect gene expression through mechanisms distinct from those regulated by acetylation. Mass spectrometry is the most powerful, comprehensive, and unbiased method to study histone PTMs. However, typical mass spectrometry-based protocols for histone PTM analysis do not allow the identification of naturally occurring propionylation and butyrylation. Here, we present improved state-of-the-art sample preparation and analysis protocols to quantitate these classes of modifications. After testing different derivatization methods coupled to protease digestion, we profiled common histone PTMs and histone acylations in seven mouse tissues and human normal and tumor breast clinical samples, obtaining a map of propionylations and butyrylations found in different tissue contexts. A quantitative histone PTM analysis also revealed a contribution of histone acylations in discriminating different tissues, also upon perturbation with antibiotics, and breast cancer samples from the normal counterpart. Our results show that profiling only classical modifications is limiting and highlight the importance of using sample preparation methods that allow the analysis of the widest possible spectrum of histone modifications, paving the way for deeper insights into their functional significance in cellular processes and disease states., Competing Interests: Conflicts of interest A. V. and M. C. are PhD students within the European School of Molecular Medicine (SEMM). The other authors declare no competing interests., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Patients with estrogen receptor-positive breast cancer receive adjuvant endocrine therapies (ET) that delay relapse by targeting clinically undetectable micrometastatic deposits. Yet, up to 50% of patients relapse even decades after surgery through unknown mechanisms likely involving dormancy. To investigate genetic and transcriptional changes underlying tumor awakening, we analyzed late relapse patients and longitudinally profiled a rare cohort treated with long-term neoadjuvant ETs until progression. Next, we developed an in vitro evolutionary study to record the adaptive strategies of individual lineages in unperturbed parallel experiments. Our data demonstrate that ETs induce nongenetic cell state transitions into dormancy in a stochastic subset of cells via epigenetic reprogramming. Single lineages with divergent phenotypes awaken unpredictably in the absence of recurrent genetic alterations. Targeting the dormant epigenome shows promising activity against adapting cancer cells. Overall, this study uncovers the contribution of epigenetic adaptation to the evolution of resistance to ETs., Significance: This study advances the understanding of therapy-induced dormancy with potential clinical implications for breast cancer. Estrogen receptor-positive breast cancer cells adapt to endocrine treatment by entering a dormant state characterized by strong heterochromatinization with no recurrent genetic changes. Targeting the epigenetic rewiring impairs the adaptation of cancer cells to ETs. See related commentary by Llinas-Bertran et al., p. 704. This article is featured in Selected Articles from This Issue, p. 695., (©2024 The Authors; Published by the American Association for Cancer Research.)

Histone modifications commonly integrate environmental cues with cellular metabolic outputs by affecting gene expression. However, chromatin modifications such as acetylation do not always correlate with transcription, pointing towards an alternative role of histone modifications in cellular metabolism. Using an approach that integrates mass spectrometry-based histone modification mapping and metabolomics with stable isotope tracers, we demonstrate that elevated lipids in acetyltransferase-depleted hepatocytes result from carbon atoms derived from deacetylation of hyperacetylated histone H4 flowing towards fatty acids. Consistently, enhanced lipid synthesis in acetyltransferase-depleted hepatocytes is dependent on histone deacetylases and acetyl-CoA synthetase ACSS2, but not on the substrate specificity of the acetyltransferases. Furthermore, we show that during diet-induced lipid synthesis the levels of hyperacetylated histone H4 decrease in hepatocytes and in mouse liver. In addition, overexpression of acetyltransferases can reverse diet-induced lipogenesis by blocking lipid droplet accumulation and maintaining the levels of hyperacetylated histone H4. Overall, these findings highlight hyperacetylated histones as a metabolite reservoir that can directly contribute carbon to lipid synthesis, constituting a novel function of chromatin in cellular metabolism., (© 2024. The Author(s).)

Histone-modifying enzymes depend on the availability of cofactors, with acetyl-coenzyme A (CoA) being required for histone acetyltransferase (HAT) activity. The discovery that mitochondrial acyl-CoA-producing enzymes translocate to the nucleus suggests that high concentrations of locally synthesized metabolites may impact acylation of histones and other nuclear substrates, thereby controlling gene expression. Here, we show that 2-ketoacid dehydrogenases are stably associated with the Mediator complex, thus providing a local supply of acetyl-CoA and increasing the generation of hyper-acetylated histone tails. Nitric oxide (NO), which is produced in large amounts in lipopolysaccharide-stimulated macrophages, inhibited the activity of Mediator-associated 2-ketoacid dehydrogenases. Elevation of NO levels and the disruption of Mediator complex integrity both affected de novo histone acetylation within a shared set of genomic regions. Our findings indicate that the local supply of acetyl-CoA generated by 2-ketoacid dehydrogenases bound to Mediator is required to maximize acetylation of histone tails at sites of elevated HAT activity., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Aims: Point-of-care ultrasound (POCUS) is the acquisition and interpretation of ultrasound imaging at the bedside to solve specific clinical questions based on signs and symptoms of presentation. While several studies evaluated POCUS diagnostic accuracy for a variety of clinical pictures in the emergency department (ED), only a few data are available on POCUS diagnostic accuracy performed by physicians with different POCUS skills. The objective of this research was to evaluate the diagnostic accuracy of POCUS compared to standard diagnostic imaging in the ED., Materials and Methods: This was a retrospective study conducted in the ED of a third-level university hospital. Patients who underwent cardiac, thoracic, abdominal, or venous lower limb POCUS and a standard imaging examination between June 2021 and January 2022 were included., Results: 1047 patients were screened, and 844 patients included. A total of 933 POCUS was included (102, 12.09%, cardiac; 466, 55.21%, thoracic; 336, 39.8%, abdominal; 29, 3.44%, lower limb venous POCUS), accounting for 2029 examinations. POCUS demonstrated 96.6% (95% CI 95.72-97.34) accuracy, 47.73 (95% CI 33.64-67.72) +LR, 0.09 (95% CI 0.06-0.12) -LR. +LR was greater than 10 for all investigations but for hydronephrosis (5.8), and -LR never exceeded 0.4., Conclusions: POCUS exhibited high diagnostic accuracy for virtually all conditions when performed by emergency department physicians., (© 2023 The Authors. Journal of Clinical Ultrasound published by Wiley Periodicals LLC.)

Transient ischemic attack (TIA) is a neurologic emergency characterized by cerebral ischemia eliciting a temporary focal neurological deficit. Many clinical prediction scores have been proposed to assess the risk of stroke after TIA; however, studies on their clinical validity and comparisons among them are scarce. The objective is to compare the accuracy of ABCD 2 , ABCD 2 -I, and OTTAWA scores in the prediction of a stroke at 7, 90 days, and 1 year in patients presenting with TIA. Single-centre, retrospective study including patients with TIA admitted to the Emergency Department of our third-level, University Hospital, between 2018 and 2019. Five hundred three patients were included. Thirty-nine (7.7%) had a stroke within 1 year from the TIA: 9 (1.7%) and 24 (4.7%) within 7 and 90 days, respectively. ABCD 2 , ABCD 2 -I, and OTTAWA scores were significantly higher in patients who developed a stroke. AUROCs ranged from 0.66 to 0.75, without statistically significant differences at each time-point. Considering the best cut-off of each score, only ABCD 2  > 3 showed a sensitivity of 100% only in the prediction of stroke within 7 days. Among clinical items of each score, duration of symptoms, previous TIA, hemiparesis, speech disturbance, gait disturbance, previous cerebral ischemic lesions, and known carotid artery disease were independent predictors of stroke. Clinical scores have moderate prognostic accuracy for stroke after TIA. Considering the independent predictors for stroke, our study indicates the need to continue research and prompts the development of new tools on predictive scores for TIA., (© 2022. The Author(s).)

Minimal lesions of the small bowel are mucosal changes characterized by an increased number of intraepithelial lymphocytes (with or without crypt hyperplasia) and normal villous architecture. Such changes are associated with a wide spectrum of conditions, ranging from food intolerances to infections, and from drugs to immune diseases, with different clinical profiles and manifestations, which complicates the formulation of a differential diagnosis. Patient history, symptom evaluation, and histopathology are the diagnostic features needed to establish a correct diagnosis. Physicians should assist pathologists in formulating a precise morphological evaluation by taking well-oriented small intestinal biopsies and collecting informative clinical findings that inform histopathology. In this current clinical controversy, the authors provide the reader with an appraisal of the small intestine minimal lesions through a careful analysis of the major conditions (e.g., celiac disease and other non-celiac disorders) responsible for such changes and their differential diagnosis. Also, we acknowledge that some of the diseases detailed in this article may progress from an early minimal lesion to overt mucosal atrophy. Thus, the timing of the diagnosis is of paramount importance.

Purpose: To compare the Entrance Surface Dose (ESD) for a normal patient, measured on three types of dedicated digital equipment for chest radiography: an amorphous selenium system, a CR (Computed Radiography) system, and a system for direct radiography (DR) based on an amorphous silicon active matrix (a-Si) connected to a CsI(T1) detector., Materials and Methods: The ESD values were measured with different dosimeters placed in the air parallel to the detector plane, and at a distance equal to the thickness of a normal-build patient. The measurements were taken with the radiological parameters (Posterior-Anterior projection (PA) and Lateral projection (L)) used in diagnostic practice to obtain high-quality diagnostic radiographic images. The measurements taken with the DR equipment were repeated after the manufacturer added a 0.2 mm-thick Cu filter. The ESD values obtained by this series of measurements were reported as mean and standard deviation values (M+/-SD)., Results: With the PA projection, the doses measured for the different devices were the following: amorphous selenium system 0.12+/-0.06 mGy, CR system 0.3+/-0.05 mGy, DR system 0.05+/-0.02 mGy. With the L projection: amorphous selenium system 0.40+/-0.13 mGy, CR system 0.9+/-0.17 mGy, and DR system 0.21+/-0.15 mGy., Conclusions: The use of digital systems allows a significant reduction of the patient dose. In particularly the Direct Radiography system, based on a CsI/a-Si detector, administers the lowest patient dose.

This study is aimed at evaluating which pre-operative findings at CT are prevailingly associated with histologically malignant appearance of mucinous cystic tumor (MCT) of the pancreas. The CT examinations of 52 female patients affected with pathologically proved MCT were retrospectively evaluated by two radiologists, blinded to the histopathological assessment of the biologic behavior (either benign or malignant). A multivariate logistic regression analysis was performed in order to identify the most important features associated with the malignant nature of MCT. Calcifications in the wall and/or in the septa, thick wall, and septations resulted in the most important features associated with malignancy. The simultaneous presence of all these radiological signs constitutes an almost "certain" marker of malignancy, being the risk equal to 0.95, whereas the simultaneous presence of at least two of them entails a risk of malignancy ranging from 0.56 to 0.74, according to the type of morphological features. On the other hand, the absence of the mentioned radiological features entails a negligible risk of malignancy (0.02). Mucinous cystic tumors characterized by multilocular macrocystic architecture, with thick wall and calcifications in the wall and/or the septa, present the highest risk of malignancy, and advocate prompt surgical intervention. When those signs are absent, the probability of malignancy is lower. In this case a non-operative management is possible.