Karaglud6427
This article reports the first x-ray phase sensitive breast tomosynthesis (PBT) system that is aimed for direct translation to clinical practice for the diagnosis of breast cancer.
To report the preclinical evaluation and comparison of the newly built PBT system with a conventional digital breast tomosynthesis (DBT) system.
The PBT system is developed based on a comprehensive inline phase contrast theoretical model. The system consists of a polyenergetic microfocus x-ray source and a flat panel detector mounted on an arm that is attached to a rotating gantry. It acquires nine projections over a 15° angular span in a stop-and-shoot manner. A dedicated phase retrieval algorithm is integrated with a filtered back-projection method that reconstructs tomographic slices. The American College of Radiology (ACR) accreditation phantom, a contrast detail (CD) phantom and mastectomy tissue samples were imaged at the same glandular dose levels by both the PBT and a standard of care DBT system for image quality chary of breast cancer screening and diagnosis.
Lymphocyte transformation test (LTT) has been widely used to evaluate non-immediate drug hypersensitivity reactions (NIDHRs). However, the lack of standardization and the low sensitivity have limited its routine diagnostic use. The drug presentation by dendritic cells (DCs) and the assessment of proliferation on effector cells have shown promising results. Flow-cytometry-based methods can help apply these improvements. We aimed to assess the added value of using drug-primed-DCs and the determination of the proliferative response of different lymphocyte subpopulations in NIDHRs.
Patients with confirmed NIDHR were evaluated by both conventional (C-LTT) and with drug-primed-DCs LTT (dDC-LTT)analysing the proliferative response in T cells and other effector cell subpopulations by using the fluorescent molecule, carboxyfluorescein diacetate succinimidyl ester (CFSE).
The C-LTT showed a significantly lower sensitivity (29.4%) compared with dDC-LTT (61.8%), which was confirmed analysing each particular clinical entity SJS-TEN (62.5% vs 87.5%), MPE (15% vs 47.4%) and AGEP (33% vs 80%). When including the effector cell subpopulations involved in each clinical entity, CD3
+CD4
T
1 or CD3
+NK cells in SJS-TEN, CD3
+CD4
T
1+NK cells in MPE and CD3
+NK cells in AGEP, we could significantly increase the sensitivity of the in vitro test to 100%, 68.4% and 100%, respectively, with an overall sensitivity of 87% and 85% of specificity in NIDHR.
The use of a flow-cytometry-based test, DCs as drug presenting cells, and focusing on effector cell subpopulations for each clinical entity significantly improved the drug-specific proliferative response in NIDHRs with a unique cellular in vitro test.
The use of a flow-cytometry-based test, DCs as drug presenting cells, and focusing on effector cell subpopulations for each clinical entity significantly improved the drug-specific proliferative response in NIDHRs with a unique cellular in vitro test.
It is well established that both smokers and patients with COPD are at a significantly heightened risk of cardiovascular disease (CVD), although the mechanisms underpinning the onset and progression of co-morbid CVD are largely unknown. Here, we explored whether cigarette smoke (CS) exposure impairs vascular function in mice and given the well-known pathological role for oxidative stress in COPD, whether the antioxidant compound ebselen prevents CS-induced vascular dysfunction in mice.
Male BALB/c mice were exposed to either room air (sham) or CS generated from nine cigarettes per day, 5 days a week for 8 weeks. Mice were treated with ebselen (10 mg·kg
, oral gavage once daily) or vehicle (5% w/v CM cellulose in water) 1 h prior to the first CS exposure of the day. Upon killing, bronchoalveolar lavage fluid (BALF) was collected to assess pulmonary inflammation, and the thoracic aorta was excised to investigate vascular endothelial and smooth muscle dilator responses ex vivo.
CS exposure caused a significant increase in lung inflammation which was reduced by ebselen. CS also caused significant endothelial dysfunction in the thoracic aorta which was attributed to a down-regulation of eNOS expression and increased vascular oxidative stress. Ebselen abolished the aortic endothelial dysfunction seen in CS-exposed mice by reducing the oxidative burden and preserving eNOS expression.
Targeting CS-induced oxidative stress with ebselen may provide a novel means for treating the life-threatening pulmonary and cardiovascular manifestations associated with cigarette smoking and COPD.
Targeting CS-induced oxidative stress with ebselen may provide a novel means for treating the life-threatening pulmonary and cardiovascular manifestations associated with cigarette smoking and COPD.
Albuminuria is considered as a significant predictor of cardiovascular morbidity and mortality in patients with diabetes mellitus. The main purpose of this study was to determine the correlation between albuminuria and global left ventricular (LV) function in patients with type 2 diabetes (T2D).
This observational study was conducted on 80 consecutive asymptomatic patients with T2D and an LV ejection fraction ≥55%. Angiogenesis inhibitor The patients were divided into two groups depending on the presence or absence of albuminuria. Echocardiography-derived indices of the LV function were then compared between these groups.
The patients with albuminuria were older (mean ± SD 60.37 ± 9.05 vs 54.52 ± 10.26 years of age, P = .01) and had higher hemoglobin A1c (HbA1c) levels (8.45 ± 1.97 vs 7.25 ± 1.93 mg/dL, P = .012) than those without albuminuria. Among the echocardiographic variables, the patients with albuminuria had higher LV Tei-index (median [lower-upper quartile] 0.620 [0.455-0.824] vs 0.441 [0.336-0.586], P < .001), more prolonged early filling (E)-wave deceleration time (274.87 ± 75.97 vs 239.40 ± 61.35 ms, P = .032), increased interventricular septal wall thickness (1.11 ± 0.31 vs 0.95 ± 0.21 cm, P = .012), and lower mean early diastolic mitral annular velocity (7.57 ± 2.34 vs 8.68 ± 2.46 cm/s, P = .046) than those without albuminuria. Among risk factors, only albuminuria and HbA1c levels were associated with a significant increase in LV Tei-index (Beta = 0.426 and P < .001, Beta = 0.226 and P = .042, respectively).
The LV Tei-index was significantly higher in diabetic patients with than without albuminuria. Low HbA1c levels were correlated with a decrease in LV Tei-index.
The LV Tei-index was significantly higher in diabetic patients with than without albuminuria. Low HbA1c levels were correlated with a decrease in LV Tei-index.
