A Low-Cost IoT Based Buildings Management System (BMS) Using Arduino Mega 2560 And Raspberry Pi 4 For Smart Monitoring and Automation

This work presents an internet of things (IoT) based building management system (BMS) for monitoring, control, and energy management in buildings to provide an efficient way of energy utilization. Existing systems mainly provide monitoring of different parameters with limited controlling/automation functions. Existing solutions also do not provide automatic decision-making, advanced safety management, and resource tracking. However, the proposed system provides a comprehensive way of monitoring, controlling, and automatic decision making regarding different environmental and electrical parameters in buildings, i.e., temperature, humidity, dust, volt, etc., by using a low-cost wireless sensor network (WSN). The architecture of the proposed system consists of five layers and uses analog sensors which are connected to Arduino Mega 2560 microcontrollers for data collecting, NodeMCUs ESP8266 for wireless communication, Raspberry Pi4 microcomputers for decision making, and nod-RED dashboard which runs locally on a Raspberry Pi 4to provide a friendly end-user interface. The system also uses the Message Queuing Telemetry Transport (MQTT) communication protocol through Wi-Fi and completely relies on the local devices in the architecture and does not need cloud computing services. The proposed system provides two different kinds of automation, i.e., safety automation for the safety of different devices with advanced features, and energy automation. The proposed system is also able to provide humidity control inside a room and to track and count the available resources in any facility. The proposed system is low cost, scalable, and can be used in any building. Simulation results show that the proposed system is highly efficient

Role of TGF-ß in cancers : from pancreatic adenocarcinoma to rhabdomyosarcoma, characterization of a multifacet cytokine

Le TGF-β est une cytokine impliquée dans de multiples processus physiologiques. Elle joue notamment un rôle clé dans la régulation de processus développementaux et dans l’homéostasie tissulaire. Le TGF-β agit principalement sur le fonctionnement cellulaire en activant une cascade de signalisation dépendante des effecteurs SMAD, et qui aboutit à la régulation transcriptionnelle de gènes cibles. In fine, le TGF-β peut modifier l’état de différenciation cellulaire, la survie, la prolifération ou la migration des cellules. Des altérations de la voie du TGF-β sont impliquées dans de nombreuses pathologies, et notamment dans les cancers. Il a été établi que cette cytokine joue un rôle complexe au cours du processus tumoral, pouvant être considérée comme un suppresseur de tumeur ou un oncogène selon le contexte cellulaire. Au cours de mon doctorat, j’ai challengé deux questions relatives à l’implication du TGF-β dans les cancers. J’ai tout d’abord étudié le rôle de cette cytokine dans le processus d’invasion péri-neurale dans les adénocarcinomes pancréatiques, qui restent à ce jour une impasse thérapeutique majeure. Les résultats obtenus suggèrent que le TGF-β puisse jouer un rôle clé dans le dialogue entre les cellules tumorales et les cellules gliales/neuronales. J’ai également initié la caractérisation d’une protéine matricielle supposée réguler la séquestration du TGF-β, pour définir l’implication d’altérationsde la biodisponibilité de cette cytokine dans la survenue de rhabdomyosarcomes, des cancers du lignage musculaire fréquents chez les enfants et les adolescents. Les résultats obtenus illustrent la complexité du rôle du TGF-β dans différents cancers et la nécessité de poursuivre la caractérisation de son implication dans l’étiologie moléculaire des cancersTGF-β is a cytokine involved in multiple physiological processes. In particular, it plays a key role in the regulation of developmental processes and in tissue homeostasis. TGF-β mainly acts on cell function by activating a SMAD-dependent signaling cascade, which results in the transcriptional regulation of target genes. At the end, TGF-β can modify the state of cell differentiation, survival, proliferation or migration of cells. Alterations in TGF-β pathway are involved in many pathologies, including cancers. It has been established that this cytokine plays a complex role during the tumor process, since it can be considered as a tumor suppressor or an oncogene depending on the cellular context. During my Ph.D., I challenged two questions about the involvement of TGF-β in cancers. I first studied the role of this cytokine in the process of peri-neural invasion in pancreatic adenocarcinoma, which remain a major therapeutic dead end. The results obtained suggest that TGF-β can play a key role in the dialogue between tumor cells and glial/neuronal cells. I also initiated the characterization of a matrix protein supposed to regulate the sequestration of TGF-β, to define the implication of alterations of the bioavailability of this cytokine in the occurrence of rhabdomyosarcoma, cancers of the muscular lineage frequent in the children and teens. The results obtained illustrate the complexity of the role of TGF-β in different cancers and the need to further characterize its involvement in the molecular etiology of cancer

Prothrombin complex concentrate and fatal thrombotic adverse events: A complication to keep in mind.

Thromboembolic events such as deep vein thrombosis and pulmonary embolism are well-known complications that can occur after prothrombin complex concentrate therapy. However, acute myocardial infarction is a very rare but potentially life-threatening complication that was exclusively described in patients with bleeding disorders who received chronic and recurrent concentrate infusions. We report the case of a 70 year-old male patient with cholangiocarcinoma who was admitted to our hospital with worsening fatigue and weakness. His stay was complicated by uncontrolled bleeding secondary to rivaroxaban use and advanced liver disease. By the end of the prothrombin complex concentrate infusion used to reverse his coagulopathy, patient developed ST-segment elevation myocardial infarction with cardiogenic shock and passed away. This is the first reported case of acute myocardial infarction that occurs in a patient without hemophilia and after the first prothrombin complex concentrate infusion

Antimicrobials from Venomous Animals: An Overview

International audienc

Is kidney function affecting the management of myocardial infarction? A retrospective cohort study in patients with normal kidney function, chronic kidney disease stage III–V, and ESRD

Marc Saad,1 Boutros Karam,1 Geovani Faddoul,2 Youssef El Douaihy,1 Harout Yacoub,1 Hassan Baydoun,3 Christine Boumitri,1 Iskandar Barakat,1 Chadi Saifan,4 Elie El-Charabaty,4 Suzanne El Sayegh4 1Department of Internal Medicine, Staten Island University Hospital, Staten Island, 2Department of Nephrology, Icahn School of Medicine, New York, NY, 3Department of Cardiology, Tulane University Medical Center, New Orleans, LA, 4Department of Nephrology, Staten Island University Hospital, Staten Island, NY, USA Abstract: Patients with chronic kidney disease (CKD) are three times more likely to have myocardial infarction (MI) and suffer from increased morbidity and higher mortality. Traditional and unique risk factors are prevalent and constitute challenges for the standard of care. However, CKD patients have been largely excluded from clinical trials and little evidence is available to guide evidence-based treatment of coronary artery disease in patients with CKD. Our objective was to assess whether a difference exists in the management of MI (ST-segment elevation myocardial infarction and non-ST-segment elevation myocardial infarction) among patients with normal kidney function, CKD stage III–V, and end-stage renal disease (ESRD) patients. We conducted a retrospective cohort study on patients admitted to Staten Island University Hospital for the diagnosis of MI between January 2005 and December 2012. Patients were assigned to one of three groups according to their kidney function: Data collected on the medical management and the use of statins, platelet inhibitors, beta-blockers, and angiotensin converting enzyme inhibitors/angiotensin receptor blockers were compared among the three cohorts, as well as medical interventions including: catheterization and coronary artery bypass graft (CABG) when indicated. Chi-square test was used to compare the proportions between nominal variables. Binary logistic analysis was used in order to determine associations between treatment modalities and comorbidities, and to account for possible confounding factors. Three hundred and thirty-four patients (mean age 67.2±13.9 years) were included. In terms of management, medical treatment was not different among the three groups. However, cardiac catheterization was performed less in ESRD when compared with no CKD and CKD stage III–V (45.6% vs 74% and 93.9%) (P<0.001). CABG was performed in comparable proportions in the three groups and CABG was not associated with the degree of CKD (P=0.078) in binary logistics regression. Cardiac catheterization on the other hand carried the strongest association among all studied variables (P<0.001). This association was maintained after adjusting for other comorbidities. The length of stay for the three cohorts (non-CKD, CKD stage III–V, and ESRD on hemodialysis) was 16, 17, and 15 days, respectively and was not statistically different. Many observations have reported discrimination of care for patients with CKD considered suboptimal candidates for aggressive management of their cardiac disease. In our study, medical therapy was achieved at high percentage and was comparable among groups of different kidney function. However, kidney disease seems to affect the management of patients with acute MI; percutaneous coronary angiography is not uniformly performed in patients with CKD and ESRD when compared with patients with normal kidney function. Keywords: myocardial infarction, chronic kidney disease, end-stage renal diseas

Schwann cells support oncogenic potential of pancreatic cancer cells through TGFβ signaling

International audiencePancreatic ductal adenocarcinoma (PDAC) is one of the solid tumors with the poorest prognosis. The stroma of this tumor is abundant and composed of extracellular matrix and stromal cells (including cancer-associated fibroblasts and immune cells). Nerve fibers invading this stroma represent a hallmark of PDAC, involved in neural remodeling, which participates in neuropathic pain, cancer cell dissemination and tumor relapse after surgery. Pancreatic cancer-associated neural remodeling is regulated through functional interplays mediated by physical and molecular interactions between cancer cells, nerve cells and surrounding Schwann cells, and other stromal cells. In the present study, we show that Schwann cells (glial cells supporting peripheral neurons) can enhance aggressiveness (migration, invasion, tumorigenicity) of pancreatic cancer cells in a transforming growth factor beta (TGFβ)-dependent manner. Indeed, we reveal that conditioned medium from Schwann cells contains high amounts of TGFβ able to activate the TGFβ-SMAD signaling pathway in cancer cells. We also observed in human PDAC samples that high levels of TGFβ signaling activation were positively correlated with perineural invasion. Secretome analyses by mass spectrometry of Schwann cells and pancreatic cancer cells cultured alone or in combination highlighted the central role of TGFβ in neuro-epithelial interactions, as illustrated by proteomic signatures related to cell adhesion and motility. Altogether, these results demonstrate that Schwann cells are a meaningful source of TGFβ in PDAC, which plays a crucial role in the acquisition of aggressive properties by pancreatic cancer cells

Acinar-to-Ductal Metaplasia Induced by Transforming Growth Factor Beta Facilitates KRASG12D-driven Pancreatic TumorigenesisSummary

Background & Aims: Transforming growth factor beta (TGFβ) acts either as a tumor suppressor or as an oncogene, depending on the cellular context and time of activation. TGFβ activates the canonical SMAD pathway through its interaction with the serine/threonine kinase type I and II heterotetrameric receptors. Previous studies investigating TGFβ-mediated signaling in the pancreas relied either on loss-of-function approaches or on ligand overexpression, and its effects on acinar cells have so far remained elusive. Methods: We developed a transgenic mouse model allowing tamoxifen-inducible and Cre-mediated conditional activation of a constitutively active type I TGFβ receptor (TβRICA) in the pancreatic acinar compartment. Results: We observed that TβRICA expression induced acinar-to-ductal metaplasia (ADM) reprogramming, eventually facilitating the onset of KRASG12D-induced pre-cancerous pancreatic intraepithelial neoplasia. This phenotype was characterized by the cellular activation of apoptosis and dedifferentiation, two hallmarks of ADM, whereas at the molecular level, we evidenced a modulation in the expression of transcription factors such as Hnf1β, Sox9, and Hes1. Conclusions: We demonstrate that TGFβ pathway activation plays a crucial role in pancreatic tumor initiation through its capacity to induce ADM, providing a favorable environment for KRASG12D-dependent carcinogenesis. Such findings are highly relevant for the development of early detection markers and of potentially novel treatments for pancreatic cancer patients. Keywords: Pancreas, Cancer, TGFβ, Acinar-to-Ductal Metaplasia, KRASG12

Global variation in postoperative mortality and complications after cancer surgery: a multicentre, prospective cohort study in 82 countries

© 2021 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC-ND 4.0 licenseBackground: 80% of individuals with cancer will require a surgical procedure, yet little comparative data exist on early outcomes in low-income and middle-income countries (LMICs). We compared postoperative outcomes in breast, colorectal, and gastric cancer surgery in hospitals worldwide, focusing on the effect of disease stage and complications on postoperative mortality. Methods: This was a multicentre, international prospective cohort study of consecutive adult patients undergoing surgery for primary breast, colorectal, or gastric cancer requiring a skin incision done under general or neuraxial anaesthesia. The primary outcome was death or major complication within 30 days of surgery. Multilevel logistic regression determined relationships within three-level nested models of patients within hospitals and countries. Hospital-level infrastructure effects were explored with three-way mediation analyses. This study was registered with ClinicalTrials.gov, NCT03471494. Findings: Between April 1, 2018, and Jan 31, 2019, we enrolled 15 958 patients from 428 hospitals in 82 countries (high income 9106 patients, 31 countries; upper-middle income 2721 patients, 23 countries; or lower-middle income 4131 patients, 28 countries). Patients in LMICs presented with more advanced disease compared with patients in high-income countries. 30-day mortality was higher for gastric cancer in low-income or lower-middle-income countries (adjusted odds ratio 3·72, 95% CI 1·70–8·16) and for colorectal cancer in low-income or lower-middle-income countries (4·59, 2·39–8·80) and upper-middle-income countries (2·06, 1·11–3·83). No difference in 30-day mortality was seen in breast cancer. The proportion of patients who died after a major complication was greatest in low-income or lower-middle-income countries (6·15, 3·26–11·59) and upper-middle-income countries (3·89, 2·08–7·29). Postoperative death after complications was partly explained by patient factors (60%) and partly by hospital or country (40%). The absence of consistently available postoperative care facilities was associated with seven to 10 more deaths per 100 major complications in LMICs. Cancer stage alone explained little of the early variation in mortality or postoperative complications. Interpretation: Higher levels of mortality after cancer surgery in LMICs was not fully explained by later presentation of disease. The capacity to rescue patients from surgical complications is a tangible opportunity for meaningful intervention. Early death after cancer surgery might be reduced by policies focusing on strengthening perioperative care systems to detect and intervene in common complications. Funding: National Institute for Health Research Global Health Research Unit