Structural studies of mesoporous ZrO2_{2}-CeO2_{2} and ZrO2_{2}-CeO2_{2}/SiO2_{2} mixed oxides for catalytical applications

In this work the synthesis of ZrO$_{2}$-CeO$_{2}$ and ZrO$_{2}$-CeO$_{2}$/SiO$_{2}$ were developed, based on the process to form ordered mesoporous materials such as SBA-15 silica. The triblock copolymer Pluronic P-123 was used as template, aiming to obtain crystalline single phase walls and larger specific surface area, for future applications in catalysis. SAXS and XRD results showed a relationship between ordered pores and the material crystallization. 90% of CeO$_{2}$ leaded to single phase homogeneous ceria-zirconia solid solution of cubic fluorite structure (Fm$\bar{3}$m). The SiO$_{2}$ addition improved structural and textural properties as well as the reduction behavior at lower temperatures, investigated by XANES measurements under H$_{2}$ atmosphere

Bimodal magnetic force microscopy with capacitive tip-sample distance control

A single-passage, bimodal magnetic force microscopy technique optimized for scanning samples with arbitrary topography is discussed. A double phase-locked loop (PLL) system is used to mechanically excite a high quality factor cantilever under vacuum conditions on its first mode and via an oscillatory tip-sample potential on its second mode. The obtained second mode oscillation amplitude is then used as a proxy for the tip-sample distance, and for the control thereof. With appropriate z-feedback parameters two data sets reflecting the magnetic tip-sample interaction and the sample topography are simultaneously obtained

Inequities in medically assisted reproduction: A scoping review

Introduction: Infertility affects one in five women in the United States and may do so regardless of race/ethnicity, socioeconomic status, geographic location, income, or educational status. These factors, however, may play a large role in access to infertility treatments, or medically assisted reproduction (MAR). This scoping review aimed to identify gaps in research pertaining to inequities in MAR, and propose suggestions for future research directions.Methods: This review was conducted following the guidance of the Joanna Briggs Institute methodology for scoping reviews. Searches were performed in July 2022 using MEDLINE (via PubMed) and Ovid Embase, identifying articles for screening. Articles that reported on MAR inequities, published between 2016–2021 in the United States, and written in English were included. Each article’s inequity findings were analyzed, extracted, and reported. The frequencies of the inequities investigated were recorded.Results: Ninety-six articles underwent full-text screening and 66 were included in our sample. Race/ethnicity was the most commonly reported inequity. The majority of the studies focused on MAR outcomes by race/ethnicity, and many found that historically marginalized populations had worse outcomes. Since the NIH’s classification of Sexual and Gender Minorities as a health disparity population in 2016, 15 articles within our sample investigated LGBTQ+ inequities in MAR. Historically marginalized populations were less likely to use MAR or seek infertility care and findings were similar among LGBTQ+ populations. The majority of studies found positive correlations with MAR use with income and education. The least commonly studied inequities in our sample were sex or gender and rural/under-resourced populations; findings showed that men and people from rural/under-resourced populations were less likely to access MAR. Studies that examined occupational status had varying findings.Conclusion: Our study identified research gaps regarding MAR within each of the inequities examined, though some gaps were more prominent than others. We suggest that future research be targeted toward: (1) standardizing and diversifying race/ethnicity reporting regarding MAR, (2) increasing access to infertility care for LGBTQ+ populations by providing more inclusive care, (3) increasing access to infertility care for men, and (4) increasing access to MAR for rural/under-represented populations by identifying logistic challenges

Why growth equals power - and why it shouldn't : constructing visions of China

When discussing the success of China's transition from socialism, there is a tendency to focus on growth figures as an indication of performance. Whilst these figures are indeed impressive, we should not confuse growth with development and assume that the former necessarily automatically generates the latter. Much has been done to reduce poverty in China, but the task is not as complete as some observers would suggest; particularly in terms of access to health, education and welfare, and also in dealing with relative (rather than absolute) depravation and poverty. Visions of China have been constructed that exaggerate Chinese development and power in the global system partly to serve political interests, but partly due to the failure to consider the relationship between growth and development, partly due to the failure to disaggregate who gets what in China, and partly due to the persistence of inter-national conceptions of globalised production, trade, and financial flows

Germline EPHB2 Receptor Variants in Familial Colorectal Cancer

Familial clustering of colorectal cancer occurs in 15–20% of cases, however recognized cancer syndromes explain only a small fraction of this disease. Thus, the genetic basis for the majority of hereditary colorectal cancer remains unknown. EPHB2 has recently been implicated as a candidate tumor suppressor gene in colorectal cancer. The aim of this study was to evaluate the contribution of EPHB2 to hereditary colorectal cancer. We screened for germline EPHB2 sequence variants in 116 population-based familial colorectal cancer cases by DNA sequencing. We then estimated the population frequencies and characterized the biological activities of the EPHB2 variants identified. Three novel nonsynonymous missense alterations were detected. Two of these variants (A438T and G787R) result in significant residue changes, while the third leads to a conservative substitution in the carboxy-terminal SAM domain (V945I). The former two variants were found once in the 116 cases, while the V945I variant was present in 2 cases. Genotyping of additional patients with colorectal cancer and control subjects revealed that A438T and G787R represent rare EPHB2 alleles. In vitro functional studies show that the G787R substitution, located in the kinase domain, causes impaired receptor kinase activity and is therefore pathogenic, whereas the A438T variant retains its receptor function and likely represents a neutral polymorphism. Tumor tissue from the G787R variant case manifested loss of heterozygosity, with loss of the wild-type allele, supporting a tumor suppressor role for EPHB2 in rare colorectal cancer cases. Rare germline EPHB2 variants may contribute to a small fraction of hereditary colorectal cancer

Role of chymase in cigarette smoke-induced pulmonary artery remodeling and pulmonary hypertension in hamsters

<p>Abstract</p> <p>Background</p> <p>Cigarette smoking is an important risk factor for pulmonary arterial hypertension (PAH) in chronic obstructive pulmonary disease (COPD). Chymase has been shown to function in the enzymatic production of angiotensin II (AngII) and the activation of transforming growth factor (TGF)-β1 in the cardiovascular system. The aim of this study was to determine the potential role of chymase in cigarette smoke-induced pulmonary artery remodeling and PAH.</p> <p>Methods</p> <p>Hamsters were exposed to cigarette smoke; after 4 months, lung morphology and tissue biochemical changes were examined using immunohistochemistry, Western blotting, radioimmunoassay and reverse-transcription polymerase chain reaction.</p> <p>Results</p> <p>Our results show that chronic cigarette smoke exposure significantly induced elevation of right ventricular systolic pressures (RVSP) and medial hypertrophy of pulmonary arterioles in hamsters, concurrent with an increase of chymase activity and synthesis in the lung. Elevated Ang II levels and enhanced TGF-β1/Smad signaling activation were also observed in smoke-exposed lungs. Chymase inhibition with chymostatin reduced the cigarette smoke-induced increase in chymase activity and Ang II concentration in the lung, and attenuated the RVSP elevation and the remodeling of pulmonary arterioles. Chymostatin did not affect angiotensin converting enzyme (ACE) activity in hamster lungs.</p> <p>Conclusions</p> <p>These results suggest that chronic cigarette smoke exposure can increase chymase activity and expression in hamster lungs. The capability of activated chymase to induce Ang II formation and TGF-β1 signaling may be part of the mechanism for smoking-induced pulmonary vascular remodeling. Thus, our study implies that blockade of chymase might provide benefits to PAH smokers.</p

Frequency of CDH1 germline mutations in gastric carcinoma coming from high- and low-risk areas: metanalysis and systematic review of the literature

<p>Abstract</p> <p>Background</p> <p>The frequency of E-cadherin germline mutations in countries with different incidence rates for gastric carcinoma has not been well established. The goal of this study was to assess the worldwide frequency of <it>CDH1 </it>germline mutations in gastric cancers coming from low- and high-risk areas.</p> <p>Methods</p> <p>English articles using MEDLINE access (from 1998 to 2011). Search terms included <it>CDH1</it>, E-cadherin, germline mutation, gastric cancer, hereditary, familial and diffuse histotype.</p> <p>The study included all E-cadherin germline mutations identified in gastric cancer patients; somatic mutations and germline mutations reported in other tumors were excluded.</p> <p>The method of this study was scheduled in accordance with the "PRISMA statement for reporting systematic reviews and meta-analyses". Countries were classified as low- or middle/high risk-areas for gastric carcinoma incidence. Statistical analysis was performed to correlate the <it>CDH1 </it>mutation frequency with gastric cancer incidence areas.</p> <p>Results</p> <p>A total of 122 E-cadherin germline mutations have been identified; the majority (87.5%) occurred in gastric cancers coming from low-risk areas. In high-risk areas, we identified 16 mutations in which missense mutations were predominant. (68.8%). We verified a significant association between the mutation frequency and the gastric cancer risk area (<it>p </it>< 0.001: overall identified mutations in low- vs. middle/high-risk areas).</p> <p>Conclusions</p> <p>E-cadherin genetic screenings performed in low-risk areas for gastric cancer identified a higher frequency of <it>CDH1 </it>germline mutations. This data could open new approaches in the gastric cancer prevention test; before proposing a proband candidate for the <it>CDH1 </it>genetic screening, geographic variability, alongside the family history should be considered.</p

Nature meets nurture: molecular genetics of gastric cancer

The immensity of genes and molecules implicated in gastric carcinogenesis is overwhelming and the relevant importance of some of these molecules is too often unclear. This review serves to bring us up-to-date with the latest findings as well as to look at the larger picture in terms of how to tackle the problem of solving this multi-piece puzzle. In this review, the environmental nurturing of intestinal cancer is discussed, beginning with epidemiology (known causative factors for inducing molecular change), an update of H. pylori research, including the role of inflammation and stem cells in premalignant lesions. The role of E-cadherin in the nature (genotype) of diffuse gastric cancer is highlighted, and finally the ever growing discipline of SNP analysis (including IL1B) is discussed