Characterization of kaolinite-cetyltrimethylammonium chloride intercalation complex synthesized through eco-friend kaolinite-urea pre-intercalation complex

Because of its suitability for producing kaolinite nanoscrolls, the kaolinite-cetyltrimethylammonium chloride intercalation complex is of interest in the research area of kaolinite nanocomposites. Experimental and molecular simulation analyses are used to investigate this intercalation complex, revealing its real structure formed through partially methoxy-modified kaolinite. Cost-efficient homogenization method is applied to synthesize the eco-friend kaolinite-urea pre-intercalation complex, which was found to be favorable to intercalate cetyltrimethylammonium chloride into the interlayer space of kaolinite. The influence of the pre-intercalated urea molecules, the partial modification of kaolinite structure with methoxy groups, and the presence of methanol molecules in the interlayer space of kaolinite on the intercalation of cetyltrimethylammonium chloride is characterized experimentally by X-ray diffraction, thermal analysis, Fourier transform infrared spectroscopy, and electron microscopy. The kaolinite-cetyltrimethylammonium chloride complex is identified at the basal spacing of 3.82 nm with the chemical formula of Al2Si2O5(OH)3.7(OCH3)0.3(CTAC)1.6(Me)1.6. Our molecular simulations predict methanol-containing structures between methoxy-functionalized kaolinite layers with diffuse guest molecular arrangements

Az angiotenzin konvertáló enzim gátlók szerepe a pneumónia megelőzésében

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Polyploid Adipose Stem Cells Shift the Balance of IGF1/IGFBP2 to Promote the Growth of Breast Cancer

Background: The close proximity of adipose tissue and mammary epithelium predispose involvement of adipose cells in breast cancer development. Adipose-tissue stem cells (ASCs) contribute to tumor stroma and promote growth of cancer cells. In our previous study, we have shown that murine ASCs, which undergo polyploidization during their prolonged in vitro culturing, enhanced the proliferation of 4T1 murine breast cancer cells in IGF1 dependent manner. Aims: In the present study, our aim was to clarify the regulation of ASC-derived IGF1. Methods: 4T1 murine breast carcinoma cells were co-transplanted with visceral fat-derived ASCs (vASC) or with the polyploid ASC.B6 cell line into female BALB/c mice and tumor growth and lung metastasis were monitored. The conditioned media of vASCs and ASC.B6 cells were subjected to LC-MS/MS analysis and the production of IGFBP2 was verified by Western blotting. The regulatory effect was examined by adding recombinant IGFBP2 to the co-culture of ASC.B6 and 4T1. Akt/protein kinase B (PKB) activation was detected by Western blotting. Results: Polyploid ASCs promoted the tumor growth and metastasis more potently than vASCs with normal karyotype. vASCs produced the IGF1 regulator IGFBP2, which inhibited proliferation of 4T1 cells. Downregulation of IGFBP2 by polyploidization of ASCs and enhanced secretion of IGF1 allowed survival signaling in 4T1 cells, leading to Akt phosphorylation. Conclusions: Our results implicate that ASCs in the tumor microenvironment actively regulate the growth of breast cancer cells through the IGF/IGFBP system

Lisinoprillel kapcsolatos evidenciák összefoglalása

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P-298: Screening of adolescent hypertension, and evaluation of target organ damages. Results from the Debrecen hypertension study

We performed a cross-sectional, population-based survey in Debrecen. All high school attending youths (a total sample of 10359, average age was 16.2±1.0 years) participated in the study. Following a 10 minute rest, 3 repeated BP measurements were taken by a validated OMRON M4 devices. Subjects completed a demographic and lifestyle survey as well. The 50th, 90th and 95th percentile value of the BP were defined by dividing the adolescent population into age-, gender- and height-specific subgroups. In comparison with US guidelines, in our sample, the systolic BP of boys in the different subgroups was 6 to 11 mmHg higher, while this difference was less marked for girls (1 to 5 mmHg). There were no marked differences in diastolic BP. With the help of a multiplex regression model we analyzed factors influencing BP. At systolic BP gender (β=0.373) and BMI(β=0.261) had a largest relative weight, while age (β=0.043), father's hypertension (β=0.042) and mother's hypertension (β=0.38) had a smaller, but also significant importance. BMI (β=0.264), gender (β=0.097), age (β=0.052), father's HTN (β=0.041) and mother's HTN (β=0.038) were predictive of diastolic BP. Adjusted R2 was 0.281 at systolic, and 0.181 at diastolic BP. Systolic and/or diastolic BP exceeded the age, gender and height adjusted 90th percentile of 1614 (15.84%) adolescents. Performing 2x3 extra measurements on this sample, 2.34% of the subjects had confirmed HTN. Target organ damage was observed in numerous cases: left ventricular hypertrophy in 13%, retinopathy in 12% and microalbuminuria in 10% of hypertensives. IMT in the common carotid artery was higher in hypertensive adolescents (means±SD: 0.55±0.11 mm) than in healthy control subjects (0.48±0.08 mm, p<0.001). Similar to this, a higher LVMI was measured in hypertensive (102.7±30.5 g/m2), than in healthy teenagers (91.1±25.2 g/m2, p<0.01). The screening of high blood pressure is important in adolescence also, because of the prevalence and the target organ damages. Early diagnosis of hypertension and follow-up may lead to the prevention of target organ damage

A véralvadás XIII-as faktora: strukturális és funkcionális vonatkozások, jelentősége különböző kórképekben = Blood coagulation FXIII: structural, functional aspects, its involvement in various pathological conditions

Új megállapításokat tettünk a FXIII plazmában történő aktivációjára, a két alegység (FXIII-A és FXIII-B) egymáshoz kapcsolódásának strukturális elemeire és a FXIIIa-glutamin szubsztrát kapcsolatra vonatkozóan. Új módszereket dolgoztunk ki a FXIII aktivitás mérésére, a FXIII-A intracelluláris detektálására. Utóbbi bevezetésre került a leukémiák diagnosztikájában. Immunoassay-t dolgoztunk ki az a2 plazmin inhibitor két izoformájának mennyiségi meghatározására. 10 FXIII-A hiányos betegen derítettük fel a háttérben álló mutációkat és ezek következményeit a fehérje strukturájára-funkciójára. Kísérletesen bizonyítottuk, hogy a plazma FXIII hiánya sebgyógyulási zavart okoz. Kimutattuk, hogy myocardiális infarctuson (MI) átesett nőkben emelkedett a plasma FXIII szintje és az emelkedett FXIII szint 2,5-3,0 szorosra fokozza az MI rizikóját, ami kizárólag nőkön érvényesül. 16 cikk metaanalízisiével a FXIII-A L34 allél szignifikáns védőhatását lehetett kimutatni a coronaria betegség ellen, a polimorfizmus a nagy rizikóju magyar populációban azonban csak emelkedett fibrinogén szint esetén védő hatású. A L/L homozigóták FXIII szintje MI-ben szignifikánsan alacsonyabb a vad típusúakénál. Csontvelő abláció után csökken, magas thrombocyta számmal járó myeloproliferatív betegségben emelkedik a FXIII szintje. Bronchoalveoláris mosófolyadékban kimutatható az alveoláris macrophagokból származó FXIII-A, chronicus bronchitisben ennek szintje emelkedik, s esetenként megjelenik a plazma FXIII is. | New results were reported on the activation of factor XIII (FXIII) in plasma, on the structural elements involved in the association of FXIII subunits (FXIII-A and FXIII-B) and on the interaction of activated FXIII (FXIIIa) with its glutamine substrate. Methods were developed for the determination of FXIII activity and the intracellular detection of FXIII-A by flow cytometry. The latter was introduced in the diagnostics of leukemias. Immunoassay was developed for the determination of the two isoforms of a2 plasmin inhibitor. The mutations causing FXIII-A deficiency were identified in 10 patients and their consequences were explored at the protein level. The involvement of FXIII in would healing was proven. It was shown that in women with the history of myocardial infarction (MI) FXIII level was elevated and elevated FXIII level represented a 2.5-3.0-fold increased risk of MI in women, but not in men. A protective effect of the FXIII-A L34 allele against MI was demonstrated by metaanalysis of 16 articles. In the Hungarian population this protective effect prevailed only at high fibrinogen level. FXIII level was decreased in L/L homozygotes with the history of MI. Bone marrow ablation decreased plasma FXIII level, while myeloproliferative diseases increased it. In the bronchoalveolar lavage fluid FXIII-A derived from alveolar macrophages was detected, in inflammatory bronchoalveolar diseases FXIII-A level increased and occasionally plasma FXIII was also be present

Licensing by Inflammatory Cytokines Abolishes Heterogeneity of Immunosuppressive Function of Mesenchymal Stem Cell Population

When mesenchymal stem cells (MSCs) are used for therapy of immunological pathologies, they get into an inflammatory environment, altering the effectiveness of the treatment. To establish the impact of environmental inflammatory factors on MSCs' immunofunction in the mirror of intrinsic heterogeneity of mouse MSC population, individual MSC clones were generated and characterized. Adipogenic but not osteogenic differentiation and pro-angiogenic activity of five independent MSC cell lines were similar. Regarding osteogenic differentiation, clones MSC3 and MSC6 exhibited poorer capacity than MSC2, MSC4, and MSC5. To study the immunosuppressive heterogeneity, in vitro and in vivo experiments have been carried out using T-cell proliferation assay and delayed-type hypersensitivity (DTH) response, respectively. A remarkable difference was found between the clones in their ability to inhibit T-cell proliferation in the following order: MSC2MSC5>MSC4>MSC3>>MSC6. Nevertheless, the differences between the immunosuppressive activities of the individual clones disappeared on pretreatment of the cells with pro-inflammatory cytokines, a procedure called licensing. Stimulation of all clones with IFN- and TNF- resulted in elevation of their inhibitory capability to a similar level. Nitric oxide (NO) and prostaglandin E2 (PGE2) were identified as major mediators of immunofunction of the MSC clones. The earlier findings were also supported by in vivo results. Without licensing, MSC2 inhibited DTH response, while MSC6 did not affect DTH response. In contrast, prestimulation of MSC6 with inflammatory cytokines resulted in strong suppression by this clone as well. Here, we have showed that MSC population is functionally heterogeneous in terms of immunosuppressive function; however, this variability is largely reduced under pro-inflammatory conditions