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https://www.selleckchem.com/products/eidd-1931.html HCC in non-CE and four-CE except in equilibrium phase (r = 0.42, 0.44, 0.35, and 0.33; all P  less then  .05), and very strong correlations for liver in all phases (r = 0.86, 0.83, 0.85, 0.87, and 0.84; all P  less then  .05). Those correlation coefficients were significantly higher for liver for each phase (all P  less then  .05). FVFDECT did not differ significantly across scan phases regarding HCC or liver (P = .076 and 0.56). Bland-Altman analysis showed fixed bias in all phases between non- and four-CE FVFDECT in HCC and liver.As compared with liver, correlations between FVF measured by DECT-based MMD and FF measured by CSI were weak in HCC in all phases. FVF is reproducible across all scan phases in HCC and liver. The MMD algorithm requires modification for HCC fat quantification given the heterogeneous components of HCC. Simultaneous occurrence of anti-glomerular basement membrane (anti-GBM) disease and thin basement membrane nephropathy (TBMN), both of which invade the type IV collagen subunits, is very rare. Here, we present the case of a 20-year-old male patient diagnosed with both anti-GBM disease and TBMN upon presenting dyspnea and hemoptysis. No laboratory abnormalities, except arterial hypoxemia (PaO275.4 mmHg) and microscopic hematuria, were present. Chest computed tomography revealed bilateral infiltrations in the lower lung fields; thus, administration of empirical antibiotics was initiated. Gross hemoptysis persisted nonetheless, and bronchoscopy revealed diffuse pulmonary hemorrhage with no endobronchial lesions. Broncho-alveolar lavage excluded bacterial pneumonia, tuberculosis, and fungal infection. Enzyme-linked immunosorbent assay of his serum was positive for anti-GBM antibody (95.1 U/mL). Human leukocyte antigen (HLA) test was positive for both HLA-DR15/-DR04. Other than diffuse thinning of the GBM (a research is needed to elucidate the pathogenesis and long-term outcome of the comorbidity

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