The effect of titanium alloy modified with a-C:N:H and a-SICX_{X}NY_{Y}(H) coatings on adhesion and immune response of human osteoblast-like MG-63 cells

The study was conducted in order to determine the effects of modified titanium alloy (Ti-6Al-4V) surfaces on the biological response of a human osteoblast-like cell line. MG-63 cells were cultured on disk-shaped Ti-alloys: unmodified, and covered with a-C:N:H or a-SiCxNy(H) layers. Interactions between materials and cells were examined through determination of cells adhesion and secretion of cytokines involved in the development of immune response

Ocena stężenia adipokin u dzieci z mukowiscydozą

Introduction: Patients with CF present numerous pathological conditions such as malnutrition, depletion of fat-free mass, metabolic disturbances (abnormal glucose metabolism, increased insulin resistance, chronic energy deficit, local and chronic inflammation), which could affect or be associated with altered adipokines concentration Material and Methods: We aimed in this study to investigate the levels of selected adipokines such as resistin, apelin, adiponectin to demonstrate their application as possible markers of inflammation. Results: Serum level of resistin was higher (p < 0.001) and adiponectin - lower (p=0.02) in CF children than in healthy children. There was no difference in serum apelin level between two examined groups. However, values of adiponectin/BMI and apelin/BMI ratios in CF did not differ significantly from controls. Higher values of resistin/BMI ratio in CF in comparison to controls were observed Serum resistin/adiponectin ratio was significantly higher in CF patients than in controls (p < 0.0001). Resistin/BMI ratio correlated negatively with FEV1 (R:-48,p < 0.043). Serum resistin/adiponectin ratio correlated negatively with FEV1/FVC (R:-49, p=0.04), Adipokines showed no correlation with BMI and BMI-SDS, glucose, total cholesterol, and LDL-, HDL-cholesterol, triglyceride serum levels. Spirometric parameters FEV1, FVC, VC correlated negatively with serum glucose levels (R: -0.55, p < 0.018; R: -0.65 p < 0.0025; R:-0.76, p < 0.0008 respectively). FEV1 and FVC correlated positively with BMI-SDS (R:0.58, p < 0.01; R:0.5, p < 0.036, respectively). Conclusions: A significant increase in resistin concentration expressed also as resistin/BMI, and resistin/adiponectin ratios, observed in children with CF may suggests that this adipokine is involved in the inflammatory process underlying the disease and is related to worse spirometric parameters describing airways obstruction.Wstęp: Pacjenci z mukowiscydozą (CF) ujawniają liczne stany patologiczne, takie jak niedożywienie, zmniejszenie beztłuszczowej masy ciała, zaburzenia metaboliczne m.in. nieprawidłowy metabolizm glukozy, zwiększoną insulinooporność, przewlekły deficyt energetyczny, miejscowe i przewlekłe stany zapalne, które mogą wpływać lub być związane ze zmianami stężenia adipokin. Materiał i metody: Celem aktualnego badania było oznaczenie stężenia wybranych adipokin, takich jak rezystyna, apelina, adiponektyna w celu wykazania możliwości ich zastosowania jako markerów stanu zapalnego. Wyniki: Stężenie rezystyny w surowicy było wyższe (p &lt; 0.001) a adiponektyny — niższe (p = 0,02) u dzieci z CF niż u zdrowych dzieci. Nie stwierdzono różnicy w stężeniu apeliny w surowicy krwi pomiędzy tymi dwoma badanymi grupami. Wartości wskaźników adiponektyna/BMI i apelina/BMI u dzieci z CF nie różniły się jednakże znacząco od stwierdzanych w grupie kontrolnej. Obserwowano wyższe wartości wskaźnika rezystyna/BMI w CF w porównaniu z grupą kontrolną Wskaźnik rezystyna/adiponektyna w surowicy był znacząco wyższy u pacjentów z CF niż u osób z grupy kontrolnej (p &lt; 0.0001). Stosunek rezystyna/BMI korelował negatywnie z FEV1 (R: –48, p &lt; 0.043). Stosunek rezystyna/adiponektyna w surowicy korelował negatywnie z FEV1 / FVC (R: –49, p = 0,04). Stężenie adipokin w surowicy nie wykazało korelacji z BMI i BMI-SDS, stężeniem glukozy, cholesterolu całkowitego, stężeniem cholesterolu LDL i HDL, stężeniem triglicerydów. Parametry spirometryczne FEV1, FVC, VC korelowały negatywnie ze stężeniem glukozy w surowicy (R: –0,55, p &lt; 0.018, R: –0,65 p &lt; 0.0025, R: –0,76, p &lt; 0.0008). FEV1 i FVC wykazywały dodatnią korelację z BMI-SDS (R: 0,58, p &lt; 0,01, R: 0,5, p &lt; 0.036). Wnioski: Znaczne zwiększenie stężenia rezystyny wyrażone również jako wskaźnik rezystyna /BMI oraz stosunek rezystyna/adi­ponektyna, obserwowane u dzieci z CF może sugerować, że ta adipokina jest zaangażowana w proces zapalny leżący u podstaw choroby i jest związana z pogorszeniem parametrów spirometrycznych opisujących niedrożność dróg oddechowych

Avelumab use in Merkel cell carcinoma treatment

Avelumab is a programmed death-ligand 1 (PD-L1) blocking human IgG1 lambda monoclonal antibody. It was the first immunotherapy to be approved for the treatment of MCC. In March 2017, the FDA granted accelerated approval to avelumab for the treatment of adults and pediatric patients 12 years and older with metastatic Merkel cell carcinoma (MCC) irrespective of prior therapy. In July 2017, the European Medicines Agency (EMA) recommended the approval of avelumab as a monotherapy for the treatment of adult patients with metastatic Merkel cell carcinoma (mMCC). Approvals were based on the efficacy and safety demonstrated in JAVELIN Merkel 200 (NCT02155647), a multi-center, open-label, single-arm, phase II clinical trial [1]. Part A of the study consisted of patients treated in the second line with metastatic, chemotherapy-refractory MCC. Part B consisted of systemic treatment-naive patients who received avelumab as first-line treatment for metastatic or distally recurrent MCC. In the first line the ORR is 39.7%. Durable responses lasting at least 6 months were observed and the majority of responses are observed earlywith the median time to response of 6.1 week. PFS rate at 6 months and at 12 months are 41% and 31%, respectively. Median OS is 20.3 months. The OS rate at 1 year is 60%

Avelumab use in Merkel cell carcinoma treatment

Avelumab is a programmed death-ligand 1 (PD-L1) blocking human IgG1 lambda monoclonal antibody. It was the first immunotherapy to be approved for the treatment of MCC. In March 2017, the FDA granted accelerated approval to avelumab for the treatment of adults and pediatric patients 12 years and older with metastatic Merkel cell carcinoma (MCC) –irrespective of prior therapy. In July 2017, the European Medicines Agency (EMA) recommended the approval of avelumab as a monotherapy for the treatment of adult patients with metastatic Merkel cell carcinoma (mMCC). Approvals were based on the efficacy and safety demonstrated in JAVELIN Merkel 200 (NCT02155647), a multi-center, open-label, single-arm, phase II clinical trial [1]. Part A of the study consisted of patients treated in the second line with metastatic, chemotherapy-refractory MCC. Part B consisted of systemic treatment-naive patients who received avelumab as a first-line treatment for metastatic or distally recurrent MCC. In the first line the ORR is 39.7%. Durable responses lasting at least 6 months were observed and the majority of responses are observed early with the median time to response of 6.1 week. PFS rate at 6 and 12 months are 41% and 31%, respectively. Median OS is 20.3 months. The OS rate at 1 year is 60%