Ice-Template Crosslinked PVA Aerogels Modified with Tannic Acid and Sodium Alginate.

With the commitment to reducing environmental impact, bio-based and biodegradable aerogels may be one approach when looking for greener solutions with similar attributes to current foam-like materials. This study aimed to enhance the mechanical, thermal, and flame-retardant behavior of poly(vinyl alcohol) (PVA) aerogels by adding sodium alginate (SA) and tannic acid (TA). Aerogels were obtained by freeze-drying and post-ion crosslinking through calcium chloride (CaCl2) and boric acid (H3BO3) solutions. The incorporation of TA and SA enhanced the PVA aerogel's mechanical properties, as shown by their high compressive specific moduli, reaching up to a six-fold increase after crosslinking and drying. The PVA/TA/SA aerogels presented a thermal conductivity of 0.043 to 0.046 W/m·K, while crosslinked ones showed higher values (0.049 to 0.060 W/m·K). Under TGA pyrolytic conditions, char layer formation reduced the thermal degradation rate of samples. After crosslinking, a seven-fold decrease in the thermal degradation rate was observed, confirming the high thermal stability of the formed foams. Regarding flammability, aerogels were tested through cone calorimetry. PVA/TA/SA aerogels showed a significant drop in the main parameters, such as the heat release rate (HRR) and the fire growth (FIGRA). The ion crosslinking resulted in a further reduction, confirming the improvement in the fire resistance of the modified compositions.

Aortic stiffness and related complications after endovascular repair of blunt thoracic aortic injury in young patients.

Background: This study aimed to evaluate the changes in aortic stiffness in young patients undergoing thoracic endovascular aortic repair (TEVAR) after blunt thoracic aortic injury (TBAI) and to examine the associated cardiovascular complications during follow-up. Patients and methods: We included survivors of TBAI who underwent stent graft placement between November 2009 and November 2019 and gave their consent to participate. Patients with relevant cardiovascular risk factors, comorbidities with potential impact on arterial stiffness, and prior aortic surgical or endovascular interventions were excluded. Fourteen TEVAR patients prospectively underwent clinical and noninvasive examinations and morphological imaging (mean time of follow-up and duration of implanted stent graft: 5.3 ± 1.8 years; mean age: 35.1 ± 8.7 years) and were compared to 14 healthy controls (matched for sex, age, height, and body mass index) in order to evaluate aortic stiffness. During the follow-up examinations, we assessed the pulse wave velocity (PWV; m/s) and development of arterial hypertension or heart failure, as indicated by N-terminal pro-brain natriuretic peptide (NT-proBNP; pg/mL) levels and performed echocardiography. Results: A significant increase in PWV values was recorded in the TEVAR group (median = 10.1; interquartile range [IQR] = 8.9-11.6) compared to the healthy controls (median = 7.3; IQR = 6.7-8.4), with an increase in the rank mean PWV (+ 3.8; Mann-Whitney U test p < .001). NT-proBNP levels of patients after TEVAR did not vary significantly compared to those of healthy controls (Mann-Whitney U test, p = .154). After TEVAR, five patients developed arterial hypertension during the follow-up, and three of them exhibited diastolic dysfunction. Conclusions: In young patients, TEVAR after TBAI may cause adverse cardiovascular complications due to increased aortic stiffness; therefore, screening for arterial hypertension during follow-up is recommended.

PLA/PA Bio-Blends: Induced Morphology by Extrusion.

The effect of processing conditions on the final morphology of Poly(Lactic Acid) (PLA) with bio-based Polyamide 10.10 (PA) 70/30 blends is analyzed in this paper. Two types of PLA were used: Commercial (neat PLA) and a rheologically modified PLA (PLAREx), with higher melt elasticity produced by reactive extrusion. To evaluate the ability of in situ micro-fibrillation (f) of PA phase during blend compounding by twin-screw extrusion, two processing parameters were varied: i) Screw speed rotation (rpm); and ii) take-up velocity, to induce a hot stretching with different Draw Ratios (DR). The potential ability of PA-f in both bio-blends was evaluated by the viscosity (p) and elasticity (k') ratios determined from the rheological tests of pristine polymers. When PLAREx was used, the requirements for PA-f was fulfilled in the shear rate range observed at the extrusion die. Scanning electron microscopy (SEM) observations revealed that, unlike neat PLA, PLAREx promoted PA-f without hot stretching and the aspect ratio increased as DR increased. For neat PLA-based blends, PA-f was promoted during the hot stretching stage. DMTA analysis revealed that the use of PLAREx PLAREx resulted in a better mechanical performance in the rubbery region (T > Tg PLA-phase) due to the PA-f morphology obtained.

Profile of the Immune and Inflammatory Response in Individuals With Prediabetes and Type 2 Diabetes.

OBJECTIVE: The inflammatory and immune systems are altered in type 2 diabetes. Here, the aim was to profile the immune and inflammatory response in subjects with prediabetes and diabetes in a large population-representative sample. RESEARCH DESIGN AND METHODS: In total, 15,010 individuals were analyzed from the population-based Gutenberg Health Study. Glucose status was classified according to HbA1c concentration and history of diagnosis. All samples were analyzed for white blood cells (WBCs), granulocytes, lymphocytes, monocytes, platelets, C-reactive protein (CRP), albumin, fibrinogen, and hematocrit. Interleukin-18 (IL-18), IL-1 receptor antagonist (IL-1RA), and neopterin concentrations were determined in a subcohort. RESULTS: In total, 7,584 men and 7,426 women were analyzed (range 35-74 years), with 1,425 and 1,299 having prediabetes and diabetes, respectively. Biomarkers showed varying dynamics from normoglycemic via subjects with prediabetes to subjects with diabetes: 1) gradual increase (WBCs, granulocytes, monocytes, IL-1RA, IL-18, and fibrinogen), 2) increase with subclinical disease only (lymphocytes and CRP), 3) increase from prediabetes to diabetes only (neopterin), and 4) no variation with glucose status (hematocrit). The strongest relative differences were found for CRP, IL-1RA, and fibrinogen concentrations. Several inflammatory and immune markers were associated with the glucose status independent from cardiovascular risk factors and comorbidities, varied with disease severity and the presence of disease-specific complications in the diabetes subcohort. CONCLUSIONS: The inflammatory and immune biomarker profile varies with the development and progression of type 2 diabetes. Markers of inflammation and immunity enable differentiation between the early preclinical and clinical phases of the disease, disease complications, and progression.

Differential response of p53 and p21 on HDAC inhibitor-mediated apoptosis in HCT116 colon cancer cells in vitro and in vivo.

We investigated the effect of a novel histone deacetylase inhibitor, A-423378.0, on the colon carcinoma cell line HCT116 and genetically modified derivatives lacking either p21(cip1/waf1) or p53. HCT116 cell lines were incubated with A-423378.0 at different concentrations for 3-120 h. Cell viability, proliferation and apoptosis rates were determined and verified by western blot, detection of mitochondrial membrane potential breakdown DeltaPsi(m), activation of caspases-3, -8 and cytokeratin 18 cleavage. A subcutaneous xenograft model was established in NMRI mice with daily intraperitoneal injections of 10 mg/kg for 14 days. All three HCT116 cell lines responded to A-423378.0 treatment in a dose- and time-dependent manner via induction of apoptosis as measured by breakdown of DeltaPsi(m) and BrdU incorporation. We identified that A-423378.0 induced the expression of TRAIL and TRAIL receptor, especially TRAIL-R2/hDR5, which was up-regulated in HCT116 cells after treatment with A-423378.0. In vivo, a growth inhibitory effect was observed with HDAC-I treatment, which was paralleled by a down-regulation of PCNA and a concomitant induction of apoptosis. Treatment of wild-type or knock-out HCT116 cells with A-423378.0 exerts potent anti-proliferative and pro-apoptotic effects in vitro and in vivo. A-423378.0 was able to induce apoptosis in both p21(WAF1) and p53 deficient tumour cells, which appeared to be mediated by the intrinsic cell death pathway. Interestingly, the effects of A-423378.0 on the extrinsic cell death pathway through activation of TRAIL and its signalling pathway indicate that A-423378.0 may be a potent new therapeutic compound for the treatment of advanced colorectal cancer.