Propolis Extract In Postharvest Conservation Of Solo Papaya Cv. 'golden'

The high perishability of papaya (Carica papaya L.) reduces the lifespan as well as limits marketing. Coating fruit is an alternative process to aid food preservation. The objective of this study was to evaluate the effects of propolis extract coating on physicochemical characteristics of papaya stored at room temperature. Solo papayas cv. 'Golden' were randomly divided into five postharvest treatments: three forms of dip-coating (70% alcohol, hydroalcoholic extract of propolis at 2.5%, and hydroalcoholic extract of propolis at 5%) and two controls (one uncoated and one with refrigerated uncoated fruit). Each four days, weight loss, fruit firmness, soluble solids (SS), titratable acidity (TA), SS/ TA ratio, and hydrogen potential (pH) were evaluated throughout 12 days of storage. A sensory analysis was performed on the fourth day of storage, being appraised by untrained tasters through acceptance testing. Refrigerated, 2.5% propolis, and 5% propolis treatments promoted the lowest weight losses. Flesh firmness of 5% propolis treatment was superior to that of control, alcohol, and 2.5% propolis treatments. Moreover, 5% propolis treatment achieved a great SS, differing only from alcohol treatment. Both TA and SS/TA had no variations among treatments, but along storage time. Flesh pH of refrigerated papaya showed significant differences in relation to other treatments. Also, refrigerated fruit presented chilling injury symptoms. Propolis-coated papaya showed sensory acceptability similar to those of the other treatments on the 4th day of storage. Therefore, propolis coating renders Solo papaya cv. 'Golden' a promising alternative to control fruit weight losses and firmness.3764039405

Raman Spectroscopy of Amino Acid Crystals

In this chapter, we investigate the Raman spectra of proteinogenic amino acid crystals. Amino acids are fundamental organic molecules that compose polypeptides (a linear chain of amino acids) and proteins (folded polypeptides with specific functions) found in all living beings. Surprisingly, the number of these basic molecules is not more than 22 (20 of them commonly known as the standard amino acids, plus pyrrolysine and selenocysteine). They are defined as a molecule formed by an NH2 group, a COOH group, a lateral chain (the R group), and a hydrogen atom, all of them connected to a single carbon, the α-carbon. Interestingly, α-amino acids show chirality, i.e., they present different distributions of group of atoms around the α-carbon, being defined as l- and d-form. For amino acids and proteins found in the living beings, the l-form is the dominant form, although some exceptions have been discovered in the last decades. In this chapter, we present the Raman spectra of all standard amino acids and discuss the different kinds of vibrations found, comparing them. As complementary part of the work, we present results on vibrational properties of some amino acids using Raman spectroscopy when subjected to specific conditions, with variation in temperature or pressure. Finally, we present some perspectives as the investigation of purines, a group of molecules associated with the DNA molecule

The DNA damage response is developmentally regulated in the African trypanosome

Genomes are affected by a wide range of damage, which has resulted in the evolution of a number of widely conserved DNA repair pathways. Most of these repair reactions have been described in the African trypanosome Trypanosoma brucei, which is a genetically tractable eukaryotic microbe and important human and animal parasite, but little work has considered how the DNA damage response operates throughout the T. brucei life cycle. Using quantitative PCR we have assessed damage induction and repair in both the nuclear and mitochondrial genomes of the parasite. We show differing kinetics of repair for three forms of DNA damage, and dramatic differences in repair between replicative life cycle forms found in the testse fly midgut and the mammal. We find that mammal-infective T. brucei cells repair oxidative and crosslink-induced DNA damage more efficiently than tsetse-infective cells and, moreover, very distinct patterns of induction and repair of DNA alkylating damage in the two life cycle forms. We also reveal robust repair of DNA lesions in the highly unusual T. brucei mitochondrial genome (the kinetoplast). By examining mutants we show that nuclear alkylation damage is repaired by the concerted action of two repair pathways, and that Rad51 acts in kinetoplast repair. Finally, we correlate repair with cell cycle arrest and cell growth, revealing that induced DNA damage has strikingly differing effects on the two life cycle stages, with distinct timing of alkylation-induced cell cycle arrest and higher levels of damage induced death in mammal-infective cells. Our data reveal that T. brucei regulates the DNA damage response during its life cycle, a capacity that may be shared by many microbial pathogens that exist in variant environments during growth and transmission

An Improved Description of the Dielectric Breakdown in Oxides Based on a Generalized Weibull distribution

In this work, we address modal parameter fluctuations in statistical distributions describing charge-to-breakdown $(Q_{BD})$ and/or time-to-breakdown $(t_{BD})$ during the dielectric breakdown regime of ultra-thin oxides, which are of high interest for the advancement of electronic technology. We reobtain a generalized Weibull distribution ($q$-Weibull), which properly describes $(t_{BD})$ data when oxide thickness fluctuations are present, in order to improve reliability assessment of ultra-thin oxides by time-to-breakdown $(t_{BD})$ extrapolation and area scaling. The incorporation of fluctuations allows a physical interpretation of the $q$-Weibull distribution in connection with the Tsallis statistics. In support to our results, we analyze $t_{BD}$ data of SiO$_2$-based MOS devices obtained experimentally and theoretically through a percolation model, demonstrating an advantageous description of the dielectric breakdown by the $q$-Weibull distribution.Comment: 5 pages, 3 figure

Fungos associados a sementes de quinoa (Chenopodium quinoa wield).

bitstream/item/90616/1/1738.pd

Elastic Scattering and Total Reaction Cross Section for the 6He + 27Al System

The elastic scattering of the radioactive halo nucleus 6He on 27Al target was measured at four energies close to the Coulomb barrier using the RIBRAS (Radioactive Ion Beams in Brazil) facility. The Sao Paulo Potential(SPP) was used and its diffuseness and imaginary strength were adjusted to fit the elastic scattering angular distributions. Reaction cross-sections were extracted from the optical model fits. The reduced reaction cross-sections of 6He on 27Al are similar to those for stable, weakly bound projectiles as {6,7}Li, 9Be and larger than stable, tightly bound projectile as 16O on 27Al.Comment: 7 pages, 1 table, 3 figure

Spectra of complex networks

We propose a general approach to the description of spectra of complex networks. For the spectra of networks with uncorrelated vertices (and a local tree-like structure), exact equations are derived. These equations are generalized to the case of networks with correlations between neighboring vertices. The tail of the density of eigenvalues $\rho(\lambda)$ at large $|\lambda|$ is related to the behavior of the vertex degree distribution $P(k)$ at large $k$. In particular, as $P(k) \sim k^{-\gamma}$, $\rho(\lambda) \sim |\lambda|^{1-2\gamma}$. We propose a simple approximation, which enables us to calculate spectra of various graphs analytically. We analyse spectra of various complex networks and discuss the role of vertices of low degree. We show that spectra of locally tree-like random graphs may serve as a starting point in the analysis of spectral properties of real-world networks, e.g., of the Internet.Comment: 10 pages, 4 figure

SALO, a novel classical pathway complement inhibitor from saliva of the sand fly Lutzomyia longipalpis.

Blood-feeding insects inject potent salivary components including complement inhibitors into their host's skin to acquire a blood meal. Sand fly saliva was shown to inhibit the classical pathway of complement; however, the molecular identity of the inhibitor remains unknown. Here, we identified SALO as the classical pathway complement inhibitor. SALO, an 11 kDa protein, has no homology to proteins of any other organism apart from New World sand flies. rSALO anti-complement activity has the same chromatographic properties as the Lu. longipalpis salivary gland homogenate (SGH)counterparts and anti-rSALO antibodies blocked the classical pathway complement activity of rSALO and SGH. Both rSALO and SGH inhibited C4b deposition and cleavage of C4. rSALO, however, did not inhibit the protease activity of C1s nor the enzymatic activity of factor Xa, uPA, thrombin, kallikrein, trypsin and plasmin. Importantly, rSALO did not inhibit the alternative or the lectin pathway of complement. In conclusion our data shows that SALO is a specific classical pathway complement inhibitor present in the saliva of Lu. longipalpis. Importantly, due to its small size and specificity, SALO may offer a therapeutic alternative for complement classical pathway-mediated pathogenic effects in human diseases

APOBEC Mutagenesis Inhibits Breast Cancer Growth through Induction of T cell-Mediated Antitumor Immune Responses

The APOBEC family of cytidine deaminases is one of the most common endogenous sources of mutations in human cancer. Genomic studies of tumors have found that APOBEC mutational signatures are enriched in theHER2 subtype of breast cancer and are associated with immunotherapy response in diverse cancer types. However, the direct consequences of APOBEC mutagenesis on the tumor immune microenvironment have not been thoroughly investigated. To address this, we developed syngeneic murine mammary tumor models with inducible expression of APOBEC3B. We found that APOBEC activity induced antitumor adaptive immune responses and CD4 T cell-mediated, antigen-specific tumor growth inhibition. Although polyclonal APOBEC tumors had a moderate growth defect, clonal APOBEC tumors were almost completely rejected, suggesting that APOBEC-mediated genetic heterogeneity limits antitumor adaptive immune responses. Consistent with the observed immune infiltration in APOBEC tumors, APOBEC activity sensitized HER2-driven breast tumors to anti- CTLA-4 checkpoint inhibition and led to a complete response to combination anti-CTLA-4 and anti-HER2 therapy. In human breast cancers, the relationship between APOBEC mutagenesis and immunogenicity varied by breast cancer subtype and the frequency of subclonal mutations. This work provides a mechanistic basis for the sensitivity of APOBEC tumors to checkpoint inhibitors and suggests a rationale for using APOBEC mutational signatures and clonality as biomarkers predicting immunotherapy response in HER2-positive (HER2 ) breast cancers