Eggs are sources of protein, fats and micronutrients that play an important role in basic nutrition. However, eggs are traditionally associated with adverse factors in human health, mainly due to their cholesterol content. Nowadays, however, it is known that the response of cholesterol in human serum levels to dietary cholesterol consumption depends on several factors, such as ethnicity, genetic makeup, hormonal factors and the nutritional status of the consumer. Additionally, in recent decades, there has been an increasing demand for functional foods, which is expected to continue to increase in the future, owing to their capacity to decrease the risks of some diseases and socio-demographic factors such as the increase in life expectancy. This work offers a brief overview of the advantages and disadvantages of egg consumption and the potential market of functional eggs, and it explores the possibilities of the development of functional eggs by technological methods.
Germ-line mutations in the tumor suppressor gene Brca1 confer increased susceptibility to breast and ovarian cancers. BRCA1 is a 1863-amino acid protein with roles in transcriptional regulation and the cellular responses to DNA damage. Given its function in these nuclear processes, the subcellular localization of BRCA1 is an important issue and has been the object of recent controversy. BRCA1 contains two nuclear localization signals and is most frequently detected in the cell nucleus by immunofluorescence microscopy. In this study, we show that BRCA1 is a nuclear-cytoplasmic shuttling protein, capable of both entering and exiting the nucleus. We identified a functional Rev-type nuclear export sequence ( 81 QLVEELLKIICAFQLDTGL) near the amino terminus of BRCA1 that facilitates export via the CRM1/exportin pathway. Mutational inactivation of this nuclear export sequence, or treatment of cells with the CRM1-specific export inhibitor leptomycin B, induced nuclear accumulation of ectopic full-length BRCA1. Moreover, overexpression of the CRM1 export receptor resulted in decreased nuclear localization of endogenous BRCA1. The unexpected ability of BRCA1 to shuttle between nucleus and cytoplasm may have implications for the regulation and function of this tumor suppressor.Approximately 50% of inherited breast cancers and up to 90% of the familial cases of breast and ovarian cancer are linked to germ-line mutations of the tumor suppressor gene Brca1, the first susceptibility gene linked to these malignancies (1, 2). Although the biological basis for its tumor suppressive function is not yet clearly understood, mounting evidence suggests that Brca1 is a type of "caretaker" gene, whose inactivation renders cells prone to the accumulation of genetic abnormalities (reviewed in Ref.3). The increased mutation rate because of loss of BRCA1 may in turn induce alterations in other cancer-related genes and thereby lead to tumor formation.The human Brca1 gene encodes a 1863-amino acid protein involved in a variety of cellular processes. These include transcriptional activation (4, 5) and, supporting its proposed role as a caretaker, the cellular response to DNA damage (6). BRCA1 contains a carboxyl-terminal tandem of BRCT BRCA1 carboxyl-terminus repeats (7), a motif shared by several proteins involved in DNA repair and cell cycle checkpoint regulation (8). Apart from the BRCT motifs, BRCA1 homology to other known proteins is limited to an amino-terminal RING finger domain (9), which mediates protein-protein interactions, and two nuclear localization signals (NLSs), 1 which facilitate nuclear import of BRCA1 (10 -12).Full-length BRCA1 is predominantly located within the nucleus (13-15), but there are BRCA1 splice variants, such as the commonly expressed isoforms BRCA1⌬11b (11) or BRCA1⌬672-4095 (12), that lack the NLSs and are localized to the cytoplasm. Given the role of BRCA1 in critical nuclear processes, its localization within the cell is an important issue. In this regard, a series of conflicting reports on BRCA1 mislocaliza...
Increased local and systemic CRP-related MMP activation might provide a link between inflammation and plaque vulnerability.
SnO 2 nanoribbons with exposed (1 0 1 h) and (0 1 0) surfaces have recently been demonstrated to be highly effective NO 2 sensors even at room temperature. The sensing mechanism is examined here through first principles density functional theory (DFT) calculations. We show that the most stable adsorbed species involve an unexpected NO 3 group doubly bonded to Sn centers. Significant electron transfer to the adatoms explains an orders-of-magnitude drop in electrical conductance. X-ray absorption spectroscopy indicates predominantly NO 3 species on the surface, and computed binding energies are consistent with adsorbate stability up to 700 K. Nanoribbon responses to O 2 and CO sensing are also investigated.
Bimetallic nanostructures with non-random metal atoms distribution are very important for various applications. To synthesize such structures via benign wet chemistry approach remains challenging. This paper reports a synthesis of a Au/Pd alloy nanostructure through the galvanic replacement reaction between Pd ultrathin nanowires (2.4 +/- 0.2 nm in width, over 30 nm in length) and AuCl3 in toluene. Both morphological and structural changes were monitored during the reaction up to 10 h. Continuous changes of chemical composition and crystalline structure from Pd nanowires to Pd68Au32 and Pd45Au55 alloys, and to Au nanoparticles were observed. More interestingly, by using combined techniques such as high-resolution transmission electron microscopy (HRTEM), X-ray diffraction (XRD), energy dispersive X-ray spectrometry (EDS), UV-vis absorption, and extended X-ray absorption fine structure (EXAFS) spectroscopy, we found the formation of Pd68Au32 non-random alloy with Au-rich core and Pd-rich shell, and random Pd45Au55 alloy with uniformly mixed Pd and Au atom inside the nanoparticles, respectively. Density functional theory (DFT) calculations indicated that alkylamine will strongly stabilize Pd to the surface, resulting in diffusion of Au atoms into the core region to form a non-random alloy. We believe such benign synthetic techniques can also enable the large scale preparation of various types of non-random alloys for several technically important catalysis applications.
IntroductionMatrix metalloproteinases (MMPs) play a role in infectious diseases through extracellular matrix (ECM) degradation, which favors the migration of immune cells from the bloodstream to sites of inflammation. Although higher levels of MMP-9 and tissue inhibitor of matrix metalloproteinases-1 (TIMP-1) have been found in small series of patients with sepsis, MMP-10 levels have not been studied in this setting. The objective of this study was to determine the predictive value of MMP-9, MMP-10, and TIMP-1 on clinical severity and mortality in a large series of patients with severe sepsis.MethodsThis was a multicenter, observational, and prospective study carried out in six Spanish Intensive Care Units. We included 192 (125 surviving and 67 nonsurviving) patients with severe sepsis and 50 age- and sex-matched healthy controls in the study. Serum levels of MMP-9, MMP-10, TIMP-1, tumor necrosis factor (TNF)-alpha, and interleukin (IL)-10 were measured in patients with severe sepsis at the time of diagnosis and in healthy controls.ResultsSepsis patients had higher levels of MMP-10 and TIMP-1, higher MMP-10/TIMP-1 ratios, and lower MMP-9/TIMP-1 ratios than did healthy controls (P < 0.001). An association was found between MMP-9, MMP-10, TIMP-1, and MMP-9/TIMP-1 ratios and parameters of sepsis severity, assessed by the SOFA score, the APACHE-II score, lactic acid, platelet count, and markers of coagulopathy. Nonsurviving sepsis patients had lower levels of MMP-9 (P = 0.037), higher levels of TIMP-1 (P < 0.001), lower MMP-9/TIMP-1 ratio (P = 0.003), higher levels of IL-10 (P < 0.001), and lower TNF-α/IL-10 ratio than did surviving patients. An association was found between MMP-9, MMP-10, and TIMP-1 levels, and TNF-α and IL-10 levels. The risk of death in sepsis patients with TIMP-1 values greater than 531 ng/ml was 80% higher than that in patients with lower values (RR = 1.80; 95% CI = 1.13 to 2.87;P = 0.01; sensitivity = 0.73; specificity = 0.45).ConclusionsThe novel findings of our study on patients with severe sepsis (to our knowledge, the largest series reporting data about MMP levels in sepsis) are that reduced MMP-9/TIMP-1 ratios and increased MMP-10 levels may be of great pathophysiologic significance in terms of severity and mortality, and that TIMP-1 levels may represent a biomarker to predict the clinical outcome of patients with sepsis.
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