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4mmol/L), while there were 26 in the second tertile (5.4-7.1mmol/L) and 50 in the third tertile (≥ 7.1mmol/L). The non-adjusted relationship between FBG and ICAS was positive. After controlling potential confounders, the association of FPG with ICAS remained positive, as well as in subgroups analysis, such as age, sex, hypertension, diabetes mellitus, hyperlipidaemia and COAD. AG-14361 mw The association remained unchanged after adjusted sex, age, hypertension, DM, uric acid, hyperlipidaemia, and CAOD (OR = 1.08, 95% CI = 1.02-1.15). The analyses also showed that the positive association was statistically significant (P < 0.05) among individuals without diabetes.
This study showed a positive relationship between FBG and ICAS, which suggests that clinicians may need to be simultaneously concerned about FBG and ICAS.
This study showed a positive relationship between FBG and ICAS, which suggests that clinicians may need to be simultaneously concerned about FBG and ICAS.
Reduced kidney function has been associated with worse clinical outcomes in patients with myeloproliferative neoplasms (MPN). Statins and angiotensin-converting enzyme inhibitors (ACE-i) have renoprotective properties and their pleiotropic effects might also affect the malignant MPN clone; however, whether concomitant use of statins and ACE‑i has apositive effect on estimated glomerular filtration rate (eGFR) in polycythemia vera (PV) patients is currently unknown.
This multicenter retrospective study investigated effects of statins and ACE‑i on 12-month eGFR dynamics in 75PV patients.
Of the patients 25 (33.3%) had a10% or more increase in eGFR at 12months. Univariately, statins (55.5% vs. 16.3%; p = 0.022), ACE‑i (61% vs. 24.6%; p = 0.004), male sex (54.3%, vs. 15%; p < 0.001) and the absence of chronic kidney disease (CKD, 45.5% vs. 16.1%; p = 0.008) were statistically significantly associated with an improvement in eGFR. ACE‑i (p = 0.008), CKD (p < 0.001), male sex (p = 0.004) and higher baseline eGFR (p = 0.007) remained statistically significantly associated with an improvement in eGFR in the multivariate logistic regression model also including statins, hydroxyurea, high-risk disease, cardiovascular risk factors, chronic heart failure and baseline hematocrit.
The ACE‑i might have renoprotective properties in PV. Further studies are needed to elucidate whether the use of these drugs could also affect other MPN-related outcomes.
The ACE‑i might have renoprotective properties in PV. Further studies are needed to elucidate whether the use of these drugs could also affect other MPN-related outcomes.The phase of the cell cycle determines numerous aspects of cancer cell behaviour including invasiveness, ability to migrate and responsiveness to cytotoxic drugs. To non-invasively monitor progression of cell cycle in vivo, a family of genetically encoded fluorescent indicators, FUCCI (fluorescent ubiquitination-based cell cycle indicator), has been developed. Existing versions of FUCCI are based on fluorescent proteins of two or more different colors fused to cell-cycle-dependent degradation motifs. Thus, FUCCI-expressing cells emit light of different colors in different phases providing a robust way to monitor cell cycle progression by fluorescence microscopy and flow cytometry but limiting the possibility to simultaneously visualize other markers. To overcome this limitation, we developed a single-color variant of FUCCI, called FUCCI-Red, which utilizes two red fluorescent proteins with distinct fluorescence lifetimes, mCherry and mKate2. Similarly to FUCCI, these proteins carry cell cycle-dependent degradation motifs to resolve G1 and S/G2/M phases. We showed utility of FUCCI-Red by visualizing cell cycle progression of cancer cells in 2D and 3D cultures and monitoring development of tumors in vivo by confocal and fluorescence lifetime imaging microscopy (FLIM). Single-channel registration and red-shifted spectra make FUCCI-Red sensor a promising instrument for multiparameter in vivo imaging applications, which was demonstrated by simultaneous detection of cellular metabolic state using endogenous fluorescence in the blue range.The opportunistic pathogen Pseudomonas aeruginosa has gained precedence over the years due to its ability to develop resistance to existing antibiotics, thereby necessitating alternative strategies to understand and combat the bacterium. Our previous work identified the interaction between the bacterial lectin LecA and its host cell glycosphingolipid receptor globotriaosylceramide (Gb3) as a crucial step for the engulfment of P. aeruginosa via the lipid zipper mechanism. In this study, we define the LecA-associated host cell membrane domain by pull-down and mass spectrometry analysis. We unraveled a predilection of LecA for binding to saturated, long fatty acyl chain-containing Gb3 species in the extracellular membrane leaflet and an induction of dynamic phosphatidylinositol (3,4,5)-trisphosphate (PIP3) clusters at the intracellular leaflet co-localizing with sites of LecA binding. We found flotillins and the GPI-anchored protein CD59 not only to be an integral part of the LecA-interacting membrane domain, but also majorly influencing bacterial invasion as depletion of either of these host cell proteins resulted in about 50% reduced invasiveness of the P. aeruginosa strain PAO1. In summary, we report that the LecA-Gb3 interaction at the extracellular leaflet induces the formation of a plasma membrane domain enriched in saturated Gb3 species, CD59, PIP3 and flotillin thereby facilitating efficient uptake of PAO1.
This study evaluates 18F-FDG PET/CT imaging characteristics of pathologically proven hepatocellular adenoma (HCA) subtypes.
This is a retrospective review of an institutional database (2011-2017) for subjects with a pathologic diagnosis of hepatic adenomas established within 6 months of a pre-treatment 18F-FDG PET/CT exam. An expert pathological review by a hepatopathologist was performed to confirm diagnosis and subtype HCA. A review of the 18F-FDG PET/CT exams was performed by two board-certified nuclear radiologists in consensus. Corresponding demographic and clinical data were obtained by electronic chart review.
Nine subjects were identified. An HCA subtype was established in seven subjects (4 HNF1A-mutated and 3 Inflammatory). The mean HCA lesion size was 2.8cm (range 0.6-6.2, SD 2.0) with a mean SUVmax of 5.9 (range 2.1-18.9, SD 5.1). The SUV values of HNF1A-mutated HCA were significantly higher than inflammatory HCA lesion SUVmax (5.3 ± 1.48 vs. 2.8 ± 0.59, p < 0.033), lesion-to-liver SUVmax ratio (1.
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