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RATIONAL: While previous studies have assessed the clinical or economic value of specific technologies, the economic value of improving sensitivity for malignancy for lung cancer diagnoses broadly across technologies is unclear. OBJECTIVE: To identify the economic value of improving sensitivity of bronchoscopy biopsy for the diagnosis of lung cancer. METHODS: A decision analytic model was developed to quantify the economic value of increased sensitivity for malignancy for bronchoscopy biopsy of peripheral pulmonary lesions. Primary clinical outcomes included time-to-diagnosis and survival. Economic outcomes included (i) net monetary benefit (NMB), defined as the health benefits measured in quality-adjusted life year (QALY) times willingness to pay ($100,000/QALY) net of changes in medical costs, and (ii) incremental cost-effectiveness ratio (ICER). A decision tree modeling framework-with two Markov module branches-was developed. The two Markov modules corresponded to cancer patients who were (i) diagnosed and treated or (ii) undiagnosed and remained untreated. Outcomes were measured from a US payer perspective over 30 years. RESULTS: Improving sensitivity for malignancy by 10 percentage points decreased average time-to-diagnosis for lung cancer patients by 0.85 months (4 weeks) and increased survival by 0.36 years (19 weeks), due to faster treatment initiation. Overall health outcomes improved by 0.20 QALYs per patient. Cost increased by $6,727 per patient primarily through increased treatment costs among those diagnosed with cancer. Increasing sensitivity for malignancy by 10 percentage points improved NMB by $8,729 over 30 years (ICER of $34,052), driven largely by improved sensitivity to early-stage cancer (stage-specific NMB: I/II: $19,805; III: $2,101; IV: -$1,438). Forty-two percent of overall NMB ($3,668) accrued within 5 years of biopsy. The relationship between change in sensitivity and NMB was approximately linear (1% vs. 10% sensitivity improvement corresponded to NMB of $885 vs $8,729). The model was most sensitive to cancer treatment efficacy and follow-up time after a negative result. CONCLUSION: Increasing sensitivity of malignancy by 10 percentage points resulted in a $8,729 improvement in net economic value. Health systems can use this information when making decisions regarding the value of new bronchoscopy technologies. This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives License 4.0 ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ).
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Electrochemical advanced oxidation is an appealing point-of-use groundwater treatment option for removing pollutants such as 1,4-dioxane, which is difficult to remove by using conventional separation-based techniques. This study addresses a critical challenge in employing electrochemical cells in practical groundwater treatmentâelectrode stability over long-term operation. This study aims to simulate realistic environmental scenarios by significantly extending the experimental time scale, testing a flow-through cell in addition to a batch reactor, and employing an electrolyte with a conductivity equivalent to that of groundwater. We first constructed a robust titanium suboxide nanotube mesh electrode that is utilized as both anode and cathode. We then implemented a pulsed electrolysis strategy in which reactive oxygen species are generated during the anodic cycle, and the electrode is regenerated during the cathodic cycle. Under optimized conditions, single-pass treatment through the cell (effective area: 2 cm2) achieved a remarkable 65-70% removal efficiency for 1,4-dioxane in the synthetic groundwater for over 100 h continuous operation at a low current density of 5 mA cm-2 and a water flux of 6 L m-2 h-1. The electrochemical cell and pulse treatment scheme developed in this study presents a critical advancement toward practical groundwater treatment technology.
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BACKGROUND: Heart failure (HF) is among the leading causes of death in the United States. Further, patients hospitalized because of HF with comorbid diabetes mellitus (DM) are at a significantly increased risk of death and rehospitalization. Results from the SOLOIST-WHF trial show that sotagliflozin lowered rates of readmission among hospitalized patients with HF and comorbid DM. However, it is unclear what the economic impact of the use of sotagliflozin would be on hospitals and health systems, particularly in an age where provider reimbursement is increasingly tied to value. OBJECTIVE: To quantify the 1-year financial impact on US provider health systems of adopting sotagliflozin relative to standard of care (SoC) across different alternative payment models. METHODS: This study created a 3-part decision tree model to quantify the financial impact of using sotagliflozin to treat patients hospitalized with HF in a US hospital setting. The model first estimated the clinical and economic outcomes of health systems with current SoC (no sotagliflozin) to treat US patients hospitalized for HF with comorbid DM. Then, using the results from the SOLOIST trial, the changes in clinical and economic outcomes with sotagliflozin adoption were modeled. Finally, the differences in health care utilization between sotagliflozin and SoC arms were translated to differences in health system reimbursement in the context of 3 common alternative payment models (APMs) in addition to the baseline fee-for-service (FFS) model: FFS with the Hospital Readmissions Reduction Program, the Bundled Payments for Care Improvement-Advanced program, and Accountable Care Organizations. RESULTS: A typical community hospital would have 83.4 patients per year on average with an index HF hospitalization with comorbid DM. The model predicted that sotagliflozin would reduce the probability of hospitalization, emergency department visits, and deaths by 29.3%, 38.5%, and 17.8%, respectively, compared with SoC. For hospitals not participating in APM programs, sotagliflozin resulted in a net loss of $92.94 per person ($7,754 per health system). Conversely, when accounting for provider health system participation in APMs, sotagliflozin adoption increased financial returns by $4,720 per person ($305,604 per health system) under the Hospital Readmissions Reduction Program, $1,200 per person ($100,106 per health system) for the Bundled Payments for Care Improvement-Advanced program, and $1,078 per person ($31,029 per health system) for Accountable Care Organizations. Based on the national average composition of APM reimbursement, sotagliflozin adoption resulted in a $1,576 increase in margin per patient with HF ($105,454 per health system). CONCLUSIONS: Although sotagliflozin adoption reduced health system revenue in an FFS payment model, it led to a net positive financial impact after accounting for APM bonus payments.
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Glicosídeos , Insuficiência Cardíaca , Modelos Econômicos , Humanos , Insuficiência Cardíaca/tratamento farmacológico , Insuficiência Cardíaca/economia , Estados Unidos , Glicosídeos/uso terapêutico , Glicosídeos/economia , Inibidores do Transportador 2 de Sódio-Glicose/uso terapêutico , Inibidores do Transportador 2 de Sódio-Glicose/economia , Hospitalização/economia , Diabetes Mellitus/tratamento farmacológico , Diabetes Mellitus/economia , Mecanismo de Reembolso , Readmissão do Paciente/estatística & dados numéricos , Readmissão do Paciente/economiaRESUMO
Nitrate, a prevalent water pollutant, poses substantial public health concerns and environmental risks. Electrochemical reduction of nitrate (eNO3RR) has emerged as an effective alternative to conventional biological treatments. While extensive lab work has focused on designing efficient electrocatalysts, implementation of eNO3RR in practical wastewater settings requires careful consideration of the effects of various constituents in real wastewater. In this critical review, we examine the interference of ionic species commonly encountered in electrocatalytic systems and universally present in wastewater, such as halogen ions, alkali metal cations, and other divalent/trivalent ions (Ca2+, Mg2+, HCO3-/CO32-, SO42-, and PO43-). Notably, we categorize and discuss the interfering mechanisms into four groups: (1) loss of active catalytic sites caused by competitive adsorption and precipitation, (2) electrostatic interactions in the electric double layer (EDL), including ion pairs and the shielding effect, (3) effects on the selectivity of N intermediates and final products (N2 or NH3), and (4) complications by the hydrogen evolution reaction (HER) and localized pH on the cathode surface. Finally, we summarize the competition among different mechanisms and propose future directions for a deeper mechanistic understanding of ionic impacts on eNO3RR.
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Nitratos , Nitratos/química , Catálise , Íons , Águas Residuárias/química , Oxirredução , Poluentes Químicos da Água/químicaRESUMO
Reactive astrocytes are associated with neuroinflammation and cognitive decline in diverse neuropathologies; however, the underlying mechanisms are unclear. We used optogenetic and chemogenetic tools to identify the crucial roles of the hippocampal CA1 astrocytes in cognitive decline. Our results showed that repeated optogenetic stimulation of the hippocampal CA1 astrocytes induced cognitive impairment in mice and decreased synaptic long-term potentiation (LTP), which was accompanied by the appearance of inflammatory astrocytes. Mechanistic studies conducted using knockout animal models and hippocampal neuronal cultures showed that lipocalin-2 (LCN2), derived from reactive astrocytes, mediated neuroinflammation and induced cognitive impairment by decreasing the LTP through the reduction of neuronal NMDA receptors. Sustained chemogenetic stimulation of hippocampal astrocytes provided similar results. Conversely, these phenomena were attenuated by a metabolic inhibitor of astrocytes. Fiber photometry using GCaMP revealed a high level of hippocampal astrocyte activation in the neuroinflammation model. Our findings suggest that reactive astrocytes in the hippocampus are sufficient and required to induce cognitive decline through LCN2 release and synaptic modulation. This abnormal glial-neuron interaction may contribute to the pathogenesis of cognitive disturbances in neuroinflammation-associated brain conditions.
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Astrócitos , Disfunção Cognitiva , Hipocampo , Lipocalina-2 , Potenciação de Longa Duração , Doenças Neuroinflamatórias , Neurônios , Animais , Astrócitos/metabolismo , Astrócitos/patologia , Disfunção Cognitiva/metabolismo , Disfunção Cognitiva/etiologia , Disfunção Cognitiva/patologia , Lipocalina-2/metabolismo , Lipocalina-2/genética , Camundongos , Hipocampo/metabolismo , Hipocampo/patologia , Doenças Neuroinflamatórias/patologia , Doenças Neuroinflamatórias/metabolismo , Neurônios/metabolismo , Neurônios/patologia , Camundongos Knockout , Masculino , Camundongos Endogâmicos C57BL , Receptores de N-Metil-D-Aspartato/metabolismo , Optogenética , Região CA1 Hipocampal/patologia , Região CA1 Hipocampal/metabolismo , Modelos Animais de DoençasRESUMO
Cellular senescence, a hallmark of aging, is pathogenically linked to the development of aging-related diseases. This study demonstrates that FRMD6, an upstream component of the Hippo/YAP signaling cascade, is a key regulator of senescence. Proteomic analysis revealed that FRMD6 is upregulated in senescent IMR90 fibroblasts under various senescence-inducing conditions. Silencing FRMD6 mitigated the senescence of IMR90 cells, suggesting its requirement in senescence. Conversely, the overexpression of FRMD6 alone induced senescence in cells and in lung tissue, establishing a causal link. The elevated FRMD6 levels correlated well with increased levels of the inhibitory phosphorylated YAP/TAZ. We identified cellular communication network factor 3 (CCN3), a key component of the senescence-associated secretory phenotype regulated by YAP, whose administration attenuated FRMD6-induced senescence in a dose-dependent manner. Mechanistically, FRMD6 interacted with and activated MST kinase, which led to YAP/TAZ inactivation. The expression of FRMD6 was regulated by the p53 and SMAD transcription factors in senescent cells. Accordingly, the expression of FRMD6 was upregulated by TGF-ß treatment that activates those transcription factors. In TGF-ß-treated IMR90 cells, FRMD6 mainly segregated with p21, a senescence marker, but rarely segregated with α-SMA, a myofibroblast marker, which suggests that FRMD6 has a role in directing cells towards senescence. Similarly, in TGF-ß-enriched environments, such as fibroblastic foci (FF) from patients with idiopathic pulmonary fibrosis, FRMD6 co-localized with p16 in FF lining cells, while it was rarely detected in α-SMA-positive myofibroblasts that are abundant in FF. In sum, this study identifies FRMD6 as a novel regulator of senescence and elucidates the contribution of the FRMD6-Hippo/YAP-CCN3 axis to senescence.
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Aim: To assesses the cost-effectiveness of sotagliflozin for the treatment of patients hospitalized with heart failure and comorbid diabetes. Materials & methods: A de novo cost-effectiveness model with a Markov structure was created for patients hospitalized for heart failure with comorbid diabetes. Outcomes of interest included hospital readmissions, emergency department visits and all-cause mortality measured over a 30-year time horizon. Baseline event frequencies were derived from published real-world data studies; sotagliflozin's efficacy was estimated from SOLOIST-WHF. Health benefits were calculated quality-adjusted life years (QALYs). Costs included pharmaceutical costs, rehospitalization, emergency room visits and adverse events. Economic value was measured using the incremental cost-effectiveness ratio (ICER). Results: Sotagliflozin use decreased annualized rehospitalization rates by 34.5% (0.228 vs 0.348, difference: -0.120), annualized emergency department visits by 40.0% (0.091 vs 0.153, difference: -0.061) and annualized mortality by 18.0% (0.298 vs 0.363, difference: -0.065) relative to standard of care, resulting in a net gain in QAYs of 0.425 for sotagliflozin versus standard of care. Incremental costs using sotagliflozin increased by $19,374 over a 30-year time horizon of the patient, driven largely by increased pharmaceutical cost. Estimated ICER for sotagliflozin relative to standard of care was $45,596 per QALY. Conclusion: Sotagliflozin is a cost-effective addition to standard of care for patients hospitalized with heart failure and comorbid diabetes.
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Análise Custo-Benefício , Glicosídeos , Insuficiência Cardíaca , Cadeias de Markov , Anos de Vida Ajustados por Qualidade de Vida , Inibidores do Transportador 2 de Sódio-Glicose , Humanos , Insuficiência Cardíaca/tratamento farmacológico , Insuficiência Cardíaca/economia , Insuficiência Cardíaca/mortalidade , Glicosídeos/uso terapêutico , Glicosídeos/economia , Inibidores do Transportador 2 de Sódio-Glicose/uso terapêutico , Inibidores do Transportador 2 de Sódio-Glicose/economia , Readmissão do Paciente/estatística & dados numéricos , Readmissão do Paciente/economia , Feminino , Masculino , Hospitalização/economia , Hospitalização/estatística & dados numéricos , Diabetes Mellitus Tipo 2/tratamento farmacológico , Diabetes Mellitus Tipo 2/economia , Diabetes Mellitus Tipo 2/complicações , Idoso , Serviço Hospitalar de Emergência/economia , Serviço Hospitalar de Emergência/estatística & dados numéricosRESUMO
Background: Mild cognitive impairment (MCI) is an intermediary condition between typical cognitive decline that occurs owing to aging and dementia. It is necessary to implement an intervention to slow the progression from MCI to Alzheimer's disease. This manuscript reports the protocol for a clinical trial on the effect of acupuncture in patients with MCI. Methods: The trial will be a randomized, prospective, parallel-arm, active-controlled trial. Sixty-four patients with MCI will be randomized to the Rehacom or acupuncture group (n = 32 each). The participants in the acupuncture group will receive electroacupuncture at GV24 (Shenting) and GV20 (Baihui) and acupuncture at EX-HN1 (Sishencong) once (30 min) a day, twice per week for 12 weeks. The patients in the Rehacom group will receive computerized cognitive rehabilitation using RehaCom software once (30 min) daily, twice weekly for 12 weeks. The primary outcome measure is the change in the Montreal Cognitive Assessment Scale score. The secondary outcome measures are the Geriatric Depression Scale, Alzheimer's Disease Assessment Scale-Korean version-cognitive subscale-3 scores, and European Quality of Life Five Dimensions Five Level Scale. The safety outcomes will include the incidence of adverse events, blood pressure, blood chemistry parameters, and pulse rate. The efficacy outcome will be assessed at baseline and at six weeks, 13 weeks, and 24 weeks after baseline. Discussion: The findings of this protocol will provide information regarding the effects of acupuncture on MCI. Clinical trial registration: https://cris.nih.go.kr/cris/search/detailSearch.do?search_lang=E&focus=reset_12&search_page=M&pageSize=10&page=undefined&seq=25579&status=5&seq_group=25579, KCT0008861.
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Avian pathogenic Escherichia coli (APEC) causes enormous economic losses and is a primary contributor to the emergence of multidrug resistance (MDR)-related problems in the poultry industry. Bacteriophage (phage) therapy has been successful in controlling MDR, but phage-resistant variants have rapidly emerged through the horizontal transmission of diverse phage defense systems carried on mobile genetic elements. Consequently, while multiple phage cocktails are recommended for phage therapy, there is a growing need to explore simpler and more cost-effective phage treatment alternatives. In this study, we characterized two novel O78-specific APEC phages, φWAO78-1 and φHAO78-1, in terms of their morphology, genome, physicochemical stability and growth kinetics. Additionally, we assessed the susceptibility of thirty-two O78 APEC strains to these phages. We analyzed the roles of highly susceptible cells in intestinal settlement and fecal shedding (susceptible cell-assisted intestinal settlement and shedding, SAIS) of phages in chickens via coinoculation with phages. Furthermore, we evaluated a new strategy, susceptible cell-assisted resistant cell killing (SARK), by comparing phage susceptibility between resistant cells alone and a mixture of resistant and highly susceptible cells in vitro. As expected, high proportions of O78 APEC strains had already acquired multiple phage defense systems, exhibiting considerable resistance to φWAO78-1 and φHAO78-1. Coinoculation of highly susceptible cells with phages prolonged phage shedding in feces, and the coexistence of susceptible cells markedly increased the phage susceptibility of resistant cells. Therefore, the SAIS and SARK strategies were demonstrated to be promising both in vivo and in vitro.
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Bacteriófagos , Infecções por Escherichia coli , Doenças das Aves Domésticas , Animais , Bacteriófagos/genética , Galinhas , Escherichia coli/genética , Colífagos , Morte Celular , Doenças das Aves Domésticas/terapiaRESUMO
The electrochemical upcycling of nitrate (NO3-) to ammonia (NH3) holds promise for synergizing both wastewater treatment and NH3 synthesis. Efficient stripping of gaseous products (NH3, H2, and N2) from electrocatalysts is crucial for continuous and stable electrochemical reactions. This study evaluated a layered electrocatalyst structure using copper (Cu) dendrites to enable a high curvature and hydrophobicity and achieve a stratified liquid contact at the gas-liquid interface of the electrocatalyst layer. As such, gaseous product desorption or displacement from electrocatalysts was enhanced due to the separation of a wetted reaction zone and a nonwetted zone for gas transfer. Consequently, this electrocatalyst structure yielded a 2.9-fold boost in per-active-site activity compared with that with a low curvature and high hydrophilic counterpart. Moreover, a NH3 Faradaic efficiency of 90.9 ± 2.3% was achieved with nearly 100% NO3- conversion. This high-curvature hydrophobic Cu dendrite was further integrated with a gas-extraction membrane, which demonstrated a comparable NH3 yield from the real reverse osmosis retentate brine.
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In recent years, there has been a substantial surge in the investigation of transition-metal dichalcogenides such as MoS2 as a promising electrochemical catalyst. Inspired by denitrification enzymes such as nitrate reductase and nitrite reductase, the electrochemical nitrate reduction catalyzed by MoS2 with varying local atomic structures is reported. It is demonstrated that the hydrothermally synthesized MoS2 containing sulfur vacancies behaves as promising catalysts for electrochemical denitrification. With copper doping at less than 9% atomic ratio, the selectivity of denitrification to dinitrogen in the products can be effectively improved. X-ray absorption characterizations suggest that two sulfur vacancies are associated with one copper dopant in the MoS2 skeleton. DFT calculation confirms that copper dopants replace three adjacent Mo atoms to form a trigonal defect-enriched region, introducing an exposed Mo reaction center that coordinates with Cu atom to increase N2 selectivity. Apart from the higher activity and selectivity, the Cu-doped MoS2 also demonstrates remarkably improved tolerance toward oxygen poisoning at high oxygen concentration. Finally, Cu-doped MoS2 based catalysts exhibit very low specific energy consumption during the electrochemical denitrification process, paving the way for potential scale-up operations.
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Peptidoglycan recognition protein 1 (PGLYRP1) is a pattern-recognition protein that mediates antibacterial actions and innate immune responses. Its expression and role in neuroinflammatory conditions remain unclear. We observed the upregulation of PGLYRP1 in inflamed human and mouse spinal cord and brain, with microglia being the primary cellular source. Experiments using a recombinant PGLYRP1 protein show that PGLYRP1 potentiates reactive gliosis, neuroinflammation, and consequent behavioral changes in multiple animal models of neuroinflammation. Furthermore, shRNA-mediated knockdown of Pglyrp1 gene expression attenuates this inflammatory response. In addition, we identify triggering receptor expressed on myeloid cell-1 (TREM1) as an interaction partner of PGLYRP1 and demonstrate that PGLYRP1 promotes neuroinflammation through the TREM1-Syk-Erk1/2-Stat3 axis in cultured glial cells. Taken together, our results reveal a role for microglial PGLYRP1 as a neuroinflammation mediator. Finally, we propose that PGLYRP1 is a potential biomarker and therapeutic target in various neuroinflammatory diseases.
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Microglia , Doenças Neuroinflamatórias , Animais , Camundongos , Humanos , Microglia/metabolismo , Receptor Gatilho 1 Expresso em Células Mieloides/metabolismo , Imunidade Inata , Inflamação/metabolismo , Citocinas/metabolismoRESUMO
Background and Objectives: The surge in breast-related surgeries in Korea underscores the critical need for an accurate early diagnosis of silicone breast implant-related issues. Complications such as BIA-ALCL and BIA-SCC add complexity to breast health concerns, necessitating vigilant monitoring. Despite advancements, discrepancies persist between ultrasonographic and pathologic classifications of silicone implant ruptures, highlighting a need for enhanced diagnostic tools. This study explores the reliability of ultrasonography in diagnosing silicone breast implant ruptures and determining the extent of silicone migration, specifically with a focus on guiding potential capsulectomy based on pathology. Materials and Methods: A comprehensive review of medical records encompassing 5557 breast implants across 2790 patients who underwent ultrasound-assisted examinations was conducted. Among the screened implants, 8.9% (249 cases) were diagnosed with silicone breast implant rupture through ultrasonography. Subsequently, 89 women underwent revisional surgery, involving capsulectomy. The pathological analysis of 111 periprosthetic capsules from these cases aimed to assess the extent of silicone migration, and the findings were juxtaposed with the existing ultrasonographic rupture classification. Results: The diagnostic agreement between preoperative sonography and postoperative findings reached 100% for silicone breast implant ruptures. All eighty prosthetic capsules exhibiting a snowstorm sign in ultrasonography demonstrated silicone migration to capsules upon pathologic findings. Conclusions: High-resolution ultrasonography emerged as a valuable and reliable imaging modality for diagnosing silicone breast implant ruptures, with a notable ability to ascertain the extent of free silicone migration to capsules. This diagnostic precision is pivotal in informing decisions about potential capsulectomy during revisional surgery. The study advocates for an update to the current binary ultrasonographic classification, suggesting a more nuanced categorization into three types (subcapsular, intracapsular, and extracapsular) based on pathology.
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Implantes de Mama , Feminino , Humanos , Implantes de Mama/efeitos adversos , Silicones/efeitos adversos , Sistemas Automatizados de Assistência Junto ao Leito , Reprodutibilidade dos Testes , Falha de Prótese , Ultrassonografia , Ruptura , Imageamento por Ressonância Magnética/métodosRESUMO
Use of single-atom catalysts (SACs) has become a popular strategy for tuning activity and selectivity toward specific pathways. However, conventional SAC synthesis methods require high temperatures and pressures, complicated procedures, and expensive equipment. Recently, underpotential deposition (UPD) has been investigated as a promising alternative, yielding high-loading SAC electrodes under ambient conditions and within minutes. Yet only few studies have employed UPD to synthesize SACs, and all have been limited to UPD of Cu. In this work, a flexible UPD approach for synthesis of mono- and bi-metallic Cu, Fe, Co, and Ni SACs directly on oxidized, commercially available carbon electrodes is reported. The UPD mechanism is investigated using in situ X-ray absorption spectroscopy and, finally, the catalytic performance of a UPD-synthesized Co SAC is assessed for electrochemical nitrate reduction to ammonia. The findings expand upon the usefulness and versatility of UPD for SAC synthesis, with hopes of enabling future research toward realization of fast, reliable, and fully electrified SAC synthesis processes.
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Citrus fruit yield is essential for market stability, as it allows businesses to plan for production and distribution. However, yield estimation is a complex and time-consuming process that often requires a large number of field samples to ensure representativeness. To address this challenge, we investigated the optimal altitude for unmanned aerial vehicle (UAV) imaging to estimate the yield of Citrus unshiu fruit. We captured images from five different altitudes (30 m, 50 m, 70 m, 90 m, and 110 m), and determined that a resolution of approximately 5 pixels/cm is necessary for reliable estimation of fruit size based on the average diameter of C. unshiu fruit (46.7 mm). Additionally, we found that histogram equalization of the images improved fruit count estimation compared to using untreated images. At the images from 30 m height, the normal image estimates fruit numbers as 73, 55, and 88. However, the histogram equalized image estimates 88, 71, 105. The actual number of fruits is 124, 88, and 141. Using a Vegetation Index such as IPCA showed a similar estimation value to histogram equalization, but I1 estimation represents a gap to actual yields. Our results provide a valuable database for future UAV field investigations of citrus fruit yield. Using flying platforms like UAVs can provide a step towards adopting this sort of model spanning ever greater regions at a cheap cost, with this system generating accurate results in this manner.
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Citrus , Dispositivos Aéreos não Tripulados , Diagnóstico por Imagem , Frutas , AltitudeRESUMO
OBJECTIVE: This study aimed to measure the value of increasing lung cancer screening rates for high-risk individuals and its impact on health disparities. METHODS: The model estimated changes in health economic outcomes if low-dose computed tomography screening increased from current to 100% compliance, following clinical guidelines. Current low-dose computed tomography screening rates were estimated by income, education, and race, using 2017-2019 Behavioral Risk Factor Surveillance System data. The model contained a decision tree module to segment the population by screening outcomes and a Markov chain module to estimate cancer progression over time. Model parameters included information on survival, quality of life, and costs related to cancer diagnosis, treatment, and adverse events. Distributional cost-effectiveness analysis estimated the net monetary value from reduced health disparities-measured using quality-adjusted life expectancy-across income, education, and race groups. Outcomes were assessed over 30 years. RESULTS: Lung cancer screening eligibility using US Preventive Services Task Force guidelines was higher for individuals with income <$15 000 (47.2%) and without a high-school education (46.1%) than individuals with income >$50 000 (16.6%) and with a college degree (13.5%), respectively. Increasing lung cancer screening to 100% compliance was cost-effective ($64 654 per quality-adjusted life-year) and produced economic value by up to $560 per person ($182.1 billion for United States overall). Up to 32.2% of the value was due to reductions in health disparities. CONCLUSIONS: Significant value in increasing lung cancer screening rates derived from reducing health disparities. Policy makers and clinicians may not be appropriately prioritizing cancer screening if value from reducing health disparities is unconsidered.
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Detecção Precoce de Câncer , Neoplasias Pulmonares , Humanos , Estados Unidos , Qualidade de Vida , Programas de Rastreamento , Neoplasias Pulmonares/diagnóstico por imagem , Neoplasias Pulmonares/epidemiologia , Análise Custo-Benefício , Tomografia Computadorizada por Raios X/métodos , Desigualdades de SaúdeRESUMO
Lipocalin-2, a neutrophil gelatinase-associated lipocalin, is a 25-kDa secreted protein implicated in a broad range of inflammatory diseases affecting the brain and periphery. It is a pleotropic protein expressed by various immune and nonimmune cells throughout the body. Importantly, the surge in lipocalin-2 levels in disease states has been associated with a myriad of undesirable effects, further exacerbating the ongoing pathological processes. In the brain, glial cells are the principal source of lipocalin-2, which plays a definitive role in determining their functional phenotypes. In different central nervous system pathologies, an increased expression of glial lipocalin-2 has been linked to neurotoxicity. Lipocalin-2 mediates a crosstalk between central and peripheral immune cells under neuroinflammatory conditions. One intriguing aspect is that elevated lipocalin-2 levels in peripheral disorders, such as cancer, metabolic conditions, and liver diseases, potentially incite an inflammatory activation of glial cells while disrupting neuronal functions. This review comprehensively summarizes the influence of lipocalin-2 on the exacerbation of neuroinflammation by regulating various cellular processes. Additionally, this review explores lipocalin-2 as a mediator of neuroimmune crosstalk in various central nervous system pathologies and highlights the role of lipocalin-2 in carrying inflammatory signals along the neuroimmune axis.
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Lipocalina-2 , Neuroimunomodulação , Lipocalina-2/metabolismo , Humanos , Animais , Doenças Neuroinflamatórias/imunologia , Doenças Neuroinflamatórias/metabolismo , Neuroglia/metabolismo , Neuroglia/imunologiaRESUMO
Prostate cancer (PCa) used to be one of the most common nondermatologic cancers in men that can be treated only with surgery. However, a revolutionary breakthrough came in the 1980s with the introduction of long-acting luteinizing hormone-releasing hormone (LHRH) agonists for the curative treatment of PCa. This paradigm shift contributed to the combined use of androgen deprivation therapy (ADT), chemotherapy, and radiotherapy for the treatment. The latest data highlight the use of treatment intensification (TI), i.e., combined use of radiotherapy (RT) and hormonal or drug treatments, for localized or locally advanced PCa. Indeed, the results of combined modality treatments have shown a reduction in disease-specific mortality and improved overall survival. Although TI seems promising, more research studies are warranted to confirm its efficacy. This review summarizes the latest available outcome results of pivotal trials and clinical studies on the efficacy of TI.