Processing and structural characterization of Si-based carbothermal derivatives of rice husk

Abstract: The processing and structural characterization of Si-based carbothermal derivatives of rice husk (RH) was investigated. RH, an agro-waste, was used as starting material in a single-stage processing route to produce Si-based refractory compounds via carbothermal treatment. The processing was carried out at different temperatures windows (900–1,900°C) at 10°C/min heating range in a controlled atmosphere. The functional groups of the reaction products were analyzed using Fourier transform infrared spectroscopy. The crystalline and amorphous phases were identified by X-ray diffractometer (XRD), while the morphological features were examined by scanning electron microscopy. It was observed that the major functional groups present after carbothermal treatment of RH are OH− (hydroxyl), Si–O–Si (siloxane), and Si–C groups. However, polytypes of silicon carbide (SiC) such as 3C-SiC (C = cubic), hexagonal symmetry 6H-SiC, and mixes of 3C-SiC, 2H-SiC, and 4H-SiC were various polytypes of SiC observed for different processing temperatures adopted. The SiC made up between 63 and 74 wt.% of the crystalline phases was identified by XRD from the process. Hence, the carbothermal treatment explored

A Scoping Review of Interventions to Address Financial Toxicity in Pediatric and Adult Patients and Survivors of Cancer

ABSTRACT Background Financial toxicity (FT) is a common and significant challenge for people with cancer, impacting immediate clinical outcomes such as treatment adherence, as well as long‐term outcomes such as quality of life and mortality. Multiple studies have tested interventions to address FT and develop recommendations for their implementation. Methods In this scoping review, we analyzed thirty‐six studies across 35,405 participants examining institution‐based interventions for FT in both pediatric and adult patients and survivors of cancer in the U.S. Results Common interventions included: financial navigation (n = 15), direct financial/medical assistance (n = 8), financial counseling or coaching (n = 5), and cost conversations prompters or encounter decision aids for treatment and cost (n = 5). Outcome measures varied widely, including the COmprehensive Score for financial Toxicity (COST), the Medical Expenditure Panel Survey (MEPS), total out‐of‐pocket costs or savings, and mental/psychological quality‐of‐life measured by the Patient‐Reported Outcomes Measurement Information System (PROMIS). Many interventions showed promising results on improving FT, including financial assistance (e.g., free medication, copay assistance), treatment and insurance decision aids, and financial counseling. These strategies improved FT‐related metrics, including patient out‐of‐pocket costs, care‐related financial burden, health insurance knowledge, quality of life, and even overall survival. There was no dominant intervention method, with both low‐ and high‐resource options proving effective. Discussion Future research should seek to understand causal relationships between interventions and FT through robust study designs, such as randomized controlled trials with longitudinal follow‐up, and evaluate interventions' implementation potential. There is also a need for standardized metrics for evaluating and reporting FT to better compare different interventions' success

Translating Cancer Risk Prediction Models into Personalized Cancer Risk Assessment Tools: Stumbling Blocks and Strategies for Success

Abstract Cancer risk prediction models such as those published in Cancer Epidemiology, Biomarkers, and Prevention are a cornerstone of precision medicine and public health efforts to improve population health outcomes by tailoring preventive strategies and therapeutic treatments to the people who are most likely to benefit. However, there are several barriers to the effective translation, dissemination, and implementation of cancer risk prediction models into clinical and public health practice. In this commentary, we discuss two broad categories of barriers. Specifically, we assert that the successful use of risk-stratified cancer prevention and treatment strategies is particularly unlikely if risk prediction models are translated into risk assessment tools that (i) are difficult for the public to understand or (ii) are not structured in a way to engender the public's confidence that the results are accurate. We explain what aspects of a risk assessment tool's design and content may impede understanding and acceptance by the public. We also describe strategies for translating a cancer risk prediction model into a cancer risk assessment tool that is accessible, meaningful, and useful for the public and in clinical practice.</jats:p

Selected State Policies and Associations With Alcohol Use Behaviors and Risky Driving Behaviors Among Youth: Findings from Monitoring the Future Study

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/134154/1/acer13041.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/134154/2/acer13041_am.pd

Right Ventricular Dysfunction in Systemic Sclerosis–Associated Pulmonary Arterial Hypertension

Background— Systemic sclerosis–associated pulmonary artery hypertension (SScPAH) has a worse prognosis compared with idiopathic pulmonary arterial hypertension (IPAH), with a median survival of 3 years after diagnosis often caused by right ventricular (RV) failure. We tested whether SScPAH or systemic sclerosis–related pulmonary hypertension with interstitial lung disease imposes a greater pulmonary vascular load than IPAH and leads to worse RV contractile function. Methods and Results— We analyzed pulmonary artery pressures and mean flow in 282 patients with pulmonary hypertension (166 SScPAH, 49 systemic sclerosis–related pulmonary hypertension with interstitial lung disease, and 67 IPAH). An inverse relation between pulmonary resistance and compliance was similar for all 3 groups, with a near constant resistance×compliance product. RV pressure–volume loops were measured in a subset, IPAH (n=5) and SScPAH (n=7), as well as SSc without PH (n=7) to derive contractile indexes (end-systolic elastance [E es ] and preload recruitable stroke work [M sw ]), measures of RV load (arterial elastance [E a ]), and RV pulmonary artery coupling (E es /E a ). RV afterload was similar in SScPAH and IPAH (pulmonary vascular resistance=7.0±4.5 versus 7.9±4.3 Wood units; E a =0.9±0.4 versus 1.2±0.5 mm Hg/mL; pulmonary arterial compliance=2.4±1.5 versus 1.7±1.1 mL/mm Hg; P &gt;0.3 for each). Although SScPAH did not have greater vascular stiffening compared with IPAH, RV contractility was more depressed (E es =0.8±0.3 versus 2.3±1.1, P &lt;0.01; M sw =21±11 versus 45±16, P =0.01), with differential RV-PA uncoupling (E es /E a =1.0±0.5 versus 2.1±1.0; P =0.03). This ratio was higher in SSc without PH (E es /E a =2.3±1.2; P =0.02 versus SScPAH). Conclusions— RV dysfunction is worse in SScPAH compared with IPAH at similar afterload, and may be because of intrinsic systolic function rather than enhanced pulmonary vascular resistive and pulsatile loading. </jats:sec

Serum Endostatin Is a Genetically Determined Predictor of Survival in Pulmonary Arterial Hypertension

Rationale: Pulmonary arterial hypertension (PAH) is a medically incurable disease resulting in death from right ventricular (RV) failure. Both pulmonary vascular and RV remodeling are linked to dynamic changes in the microvasculature. Therefore, we hypothesized that circulating angiostatic factors could be linked to outcomes and represent novel biomarkers of disease severity in PAH. Objectives: We sought to determine the relationship of a potent angiostatic factor, endostatin (ES), with disease severity and mortality in PAH. Furthermore, we assessed genetic predictors of ES expression and/or function and their association with outcomes in PAH. Methods: We measured levels of serum ES in two independent cohorts of patients with PAH. Contemporaneous clinical data included New York Heart Association functional class, 6-minute-walk distance, invasive hemodynamics, and laboratory chemistries. Measurements and Main Results: Serum ES correlated with poor functional status, decreased exercise tolerance, and invasive hemodynamics variables. Furthermore, serum ES was a strong predictor of mortality. A loss-of-function, missense variant in the gene encoding ES, Col18a1, was linked to lower circulating protein and was independently associated with reduced mortality. Conclusions: Our data link increased expression of ES to disease severity in PAH and demonstrate a significant relationship with adverse outcomes. Circulating ES levels can be genetically influenced, implicating ES as a genetically determined modifier of disease severity impacting on survival. These observations support serum ES as a potential biomarker in PAH with the capacity to predict poor outcomes. More importantly, this study implicates Col18a1/ES as a potential new therapeutic target in PAH