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BACKGROUND: Betalains are presently gaining popularity as pigments for use as natural colorants and/or bioactive compounds in functional foods. Quinoa (Chenopodium quinoa Willd.) has been recognized as an extremely nutritious grain and has recently been found to be a novel and good betalain source. Microencapsulation has been studied as a protected‐delivery procedure to stabilize betalains. There are no studies about microencapsulation of betacyanins extracted from quinoa using spray‐drying technology. RESULTS: Optimal microencapsulation was obtained at a drying temperature of 165 °C, a rotameter air flow rate of 47 mm (940 L h−1) and 10% w/w maltodextrin, which produced good encapsulation yield (58.1%) and efficiency (100%). Optimized maltodextrin–betacyanin microcapsules (diameter 4.4 μm) have low moisture (1.64 ± 0.08%) and water activity (0.127 ± 0.006), a betacyanin content of 0.1995 ± 0.0017 g kg−1 and saponin content <0.080 mg kg−1. The oxygen consumption rate by betacyanin was −4.373 × 10−5 bar min−1 at 80 °C and −6.67 × 10−5 bar min−1 at 90 °C, which was accompanied by fading of the color. CONCLUSION: Microencapsulated betacyanin was optimized by response surface methodology, and its stability was measured under accelerated conditions by oxygen consumption. Microencapsulations contain betacyanin and low saponin concentration, which might confer unique health‐promoting properties. © 2018 Society of Chemical Industry [ABSTRACT FROM AUTHOR]

Melanomas are heterogeneous and aggressive tumors, and one of the worse in prognosis. Melanoma subtypes follow distinct pathways until terminal oncogenic transformation. Here, we have evaluated a series of molecules that exhibit potent cytotoxic effects over the murine and human melanoma cell lines B16F10 and MalMe-3M, respectively, both ex vivo and in animals carrying these melanoma cells. Ex vivo mechanistic studies on molecular targets involved in melanoma growth, migration and viability were evaluated in cultured cells treated with these drugs which exhibited potent proapoptotic and cytotoxic effects and reduced cell migration. These drugs altered the Wnt/β-catenin pathway, which is important for the oncogenic phenotype of melanoma cells. In in vivo experiments, male C57BL/6 or nude mice were injected with melanoma cells that rapidly expanded in these animals and, in some cases were able to form metastasis in lungs. Treatment with anti-tumor drugs derived from benzylamine and 2-thiophenemethylamine (F10503LO1 and related compounds) significantly attenuated tumor growth, impaired cell migration, and reduced the metastatic activity. Several protocols of administration were applied, all of them leading to significant reduction in the tumor size and enhanced animal survival. Tumor cells carrying a luciferase transgene allowed a time-dependent study on the progression of the tumor. Molecular analysis of the pathways modified by F10503LO1 and related compounds defined the main relevant targets for tumor regression: the activation of pro-apoptotic and anti-proliferative routes. These data might provide the proof-of-principle and rationale for its further clinical evaluation. [ABSTRACT FROM AUTHOR]

Friedreich's ataxia (FA) is a severe disorder with autosomal recessive inheritance that is caused by the abnormal expansion of GAA repeat in intron 1 of FRDA gen. This alteration leads to a partial silencing of frataxin transcription, causing a multisystem disorder disease that includes neurological and non-neurological damage. Recent studies have proven the effectiveness of neurotrophic factors in a number of neurodegenerative diseases. Therefore, we intend to determine if liver growth factor (LGF),which has a demonstrated antioxidant and neuroprotective capability, could be a useful therapy for FA. To investigate the potential therapeutic activity of LGF we used transgenic mice of the FXNtm1MknTg (FXN)YG8Pook strain. In these mice, intraperitoneal administration of LGF (1.6 µg/mouse) exerted a neuroprotective effect on neurons of the lumbar spinal cord and improved cardiac hypertrophy. Both events could be the consequence of the increment in frataxin expression induced by LGF in spinal cord (1.34-fold) and heart (1.2-fold). LGF also upregulated by 2.6-fold mitochondrial chain complex IV expression in spinal cord, while in skeletal muscle it reduced the relation oxidized glutathione/reduced glutathione. Since LGF partially restores motor coordination, we propose LGF as a novel factor that may be useful in the treatment of FA. [ABSTRACT FROM AUTHOR]

The article discusses the highlights of the 24th International Symposium on Morphological Sciences held in Istanbul, Turkey on September 2-6, 2015. The Turkish Society of Anatomy and Clinical Anatomy (TSACA) served as host of the event. Medical photography in gross and clinical anatomy is cited as one of the workshops included in the Scientific Program. Swedish scientist Sten Grillner also presented a lecture on the evolutionary logics of networks.

The article presents the profiles of several speakers in the XXIV International Symposium on Morphological Sciences to be held Istanbul, Turkey on September 2-6, 2015 including Sten Grillner, Reha S. Erzurumlu and Alev Erisir. Grillner is professor at the Karolinska Institute and member of the U.S. National Academy of Science. Erzurumlu is an anatomy professor at University of Maryland School of Medicine, Baltimore. Erisir is assistant professor of psychology at the University of Virginia.

Type 2 diabetes has a complex pathology that involves a chronic inflammatory state. Emerging evidence suggests a link between the innate immune system receptor NOD1 (nucleotide-binding and oligomerization domain 1) and the pathogenesis of diabetes, in monocytes and hepatic and adipose tissues. The aim of the present study was to assess the role of NOD1 in the progression of diabetic cardiomyopathy. We have measured NOD1 protein in cardiac tissue from Type 2 diabetic (db) mice. Heart and isolated cardiomyocytes from db mice revealed a significant increase in NOD1, together with an up-regulation of nuclear factor κB (NF-κB) and increased apoptosis. Heart tissue also exhibited an enhanced expression of pro-inflammatory cytokines. Selective NOD1 activation with C12-D-glutamyl-m-diaminopimelic acid (iEDAP) resulted in an increased NF-κB activation and apoptosis, demonstrating the involvement of NOD1 both in wild-type and db mice. Moreover, HL-1 cardiomyocytes exposed to elevated concentrations of glucose plus palmitate displayed an enhanced NF-κB activity and apoptotic profile, which was prevented by silencing of NOD1 expression. To address this issue in human pathology, NOD1 expression was evaluated in myocardium obtained from patients with Type 2 diabetes (T2DMH) and from normoglycaemic individuals without cardiovascular histories (NH). We have found that NOD1 was expressed in both NH and T2DMH; however, NOD1 expression was significantly pronounced in T2DMH. Furthermore, both the pro-inflammatory cytokine tumour necrosis factor α (TNF-α) and the apoptosis mediator caspase-3 were up-regulated in T2DMH samples. Taken together, our results define an active role for NOD1 in the heightened inflammatory environment associated with both experimental and human diabetic cardiac disease. [ABSTRACT FROM AUTHOR]

Liver growth factor (LGF) is an endogenous albumin-bilirubin complex with antihypertensive effects in spontaneously hypertensive rats (SHR). We assessed the actions of LGF treatment on SHR mesenteric resistance and intramyocardial arteries (MRA and IMA, respectively), heart, and vascular smooth muscle cells (VSMC). SHR and Wistar-Kyoto (WKY) rats treated with vehicle or LGF (4.5 μg LGF/rat, 4 ip injections over 12 days) were used. Intra-arterial blood pressure was measured in anesthetized rats. The heart was weighted and paraffin-embedded. Proliferation, ploidy, and fibronectin deposition were studied in carotid artery-derived VSMC by immunocytochemistry. In MRA, we assessed: 1) geometry and mechanics by pressure myography; 2) function by wire myography; 3) collagen by sirius red staining and polarized light microscopy, and 4) elastin, cell density, nitric oxide (NO), and superoxide anion by confocal microscopy. Heart sections were used to assess cell density and collagen content in IMA. Left ventricular hypertrophy (LVH) regression was assessed by echocardiography. LGF reduced blood pressure only in SHR. LGF in vitro or as treatment normalized the alterations in proliferation and fibronectin in SHR-derived VSMC with no effect on WKY cells. In MRA, LGF treatment normalized collagen, elastin, and VSMC content and passive mechanical properties. In addition, it improved NO availability through reduction of superoxide anion. In IMA, LGF treatment normalized perivascular collagen and VSMC density, improving the wall-to-lumen ratio. Paired experiments demonstrated a partial regression of SHR LVH by LGF treatment. The effective cardiovascular antifibrotic and regenerative actions of LGF support its potential in the treatment of hypertension and its complications. [ABSTRACT FROM AUTHOR]

In addition to the well-known role of the thyroid hormone receptors (TRs) in growth, development and metabolism, there is increasing evidence that they have profound effects on cell proliferation and malignant transformation. TRs repress transcriptional induction of cyclin D1 by the ras oncogene and block transformation and tumor formation by Ras-transformed fibroblasts in nude mice. Mutant receptors that do not bind coactivators are able to display these actions, whereas receptors defective in corepressors binding are unable to antagonize the responses to the ras oncogene. Furthermore, expression of TRβ1 in hepatocarcinoma and breast cancer cells abolishes anchorage-independent growth and migration, blocks responses to growth factors and represses expression of prometastatic genes, reducing tumor growth and strongly inhibiting invasiveness, extravasation and metastasis formation in euthyroid mice. By contrast, when cells are inoculated into hypothyroid host, tumor growth is retarded, but tumors are more invasive and metastatic growth is enhanced. Increased aggressiveness and tumor growth retardation was also observed with parental cells that do not express TRs, showing that changes secondary to hypothyroidism can modulate tumor progression and metastatic growth independently of the presence of TRs on the tumor cells. Finally, increased malignancy of skin tumors is found in mice lacking TRs, further demonstrating the role of these receptors as inhibitors of tumor progression and suggesting that they represent a potential therapeutic target in cancer. [ABSTRACT FROM AUTHOR]

The article presents abstracts on science topics which include enantiomer excesses of sugar derivatives in carbonaceous meteorites, horizontal gene transfer and transposon mutagenesis in hepatocellular carcinoma.

Maintenance of E-cadherin mediated cell–cell contacts is often required for the survival of epithelial cells and tissues. Here we report that oncogenic activation of H-Ras in murine keratinocytes can prevent cell death induced by immunological disruption of E-cadherin adhesion. A similar situation was observed in cells showing constitutive activation of the p110α catalytic subunit of class IA PI3K. This protective effect is associated with β-catenin-dependent transcription and with activation of survival factor Akt/PKB. In addition, we induced cell death by employing photodynamic therapy, using Zn-phthalocyanine as a photosensitizer that targets E-cadherin adhesion complexes. We have found that cell death based on this photodynamic action is also bypassed in cells showing constitutive activation of H-Ras and p110α. Taken together, these results indicate that H-Ras/PI3K/Akt signaling plays a key role in cell survival mediated by E-cadherin cell–cell contacts. J. Cell. Physiol. 219: 84–93, 2009. © 2008 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Liver growth factor (LGF), a mitogen for liver cells, reduces fibrosis in a rat model of cirrhosis. The present study assesses the possible vascular antifibrotic and antihypertensive effects of LGF treatment on spontaneously hypertensive rats (SHR). Methods: Six-month-old male SHR and normotensive Wistar Kyoto rats (WKY) were treated with LGF (4.5 μg LGF/rat i.p. twice a week for 2 weeks). Haemodynamic parameters were measured in anaesthetized rats. Vascular structure and function were studied in carotid arteries using optical and confocal microscopy, radioimmunoassay for desmosine, and isometric tension recording. Results: LGF reduced systolic and diastolic blood pressure only in SHR. When compared to those of untreated SHR, carotid arteries from LGF-treated SHR showed: 1) a 50% reduction in collagen area and an increase in vascular smooth muscle cell number in the media, 2) no difference in total elastin content, but an increase in size of fenestrae in the internal elastic lamina, and 3) enhanced relaxation to acetylcholine, sodium nitroprusside, and forskolin. These effects were specific for SHR, since no changes were observed in LGF-treated WKY. Conclusion: Short-term treatment with a low dose of LGF induced a large improvement in vascular structure and function and significantly reduced blood pressure in a rat model of essential hypertension. The present results could open future research to explore the vascular effects of this endogenous factor in order to determine its potential as an antifibrotic and antihypertensive agent in humans. [Copyright &y& Elsevier]

The article presents abstracts on chemistry topics which include wetting hysteresis, structure determination of helical filaments, and sexual selection indexes through simulations of diverse mating systems.

In order to evaluate the occurrence of a Leydig cell cycle related to the cycle of the seminiferous epithelium in man, the numbers of peritubular Leydig cells and surface area of these cells along 1 mm of tubular basement membrane at each stage of the cycle were calculated on histological sections of young adult testes. The Leydig cells that were located separated from the tubules (perivascular Leydig cells) were also classified according to the stage of the cycle shown by the nearest seminiferous tubule; the surface area and number of these cells were also calculated. The total surface area and numbers of Leydig cells (peritubular plus perivascular) along 1 mm of tubular basement membrane did not change during the cycle of the seminiferous epithelium. Both the surface area and the numbers of peritubular Leydig cells were greater in stages I and II of the cycle, when spermatozoa are released; they decreased in stages III and IV and increased again in stages V and VI, whereas the contrary occurred in perivascular Leydig cells. The average surface area of each Leydig cell type remained constant throughout the stages of the cycle. [ABSTRACT FROM AUTHOR]

Human testicular specimens were obtained from biopsies and autopsies covering the period from birth to adulthood. The number of testosterone-containing Leydig cells was determined using the peroxidase-anti-peroxidase method. This number decreased markedly from 3-6 months of age to the end of the first year of life and, up to 6 years of age, only a small number of testosterone-containing cells was found. From 6 years onwards the number of Leydig cells progressively increased. Ultrastructural examination revealed four types of Leydig cells: (1) fetal-type Leydig cells (from birth to 1 year of age) with round nuclei, abundant smooth endoplasmic reticulum and mitochondria with tubular cristae; (2) infantile-type Leydig cells (from birth to 8-10 years of age), showing a multilobated nucleus, moderately abundant smooth endoplasmic reticulum, some lipid droplets and mitochondria with parallel cristae; (3) prepubertal, partially differentiated Leydig cells (from 6 years of age onwards) with regularly-outlined round nuclei, abundant smooth endoplasmic reticulum, mitochondria with tubular cristae, and some lipid droplets and lipofuscin granules; and (4) mature adult Leydig cells (from 8-10 years of age onwards). The ultrastructure of the infantile-type Leydig cells and the lack of delay between the disappearance of the fetal-type Leydig cells and the appearance of infantile-type Leydig cells suggest that fetal-type Leydig cells give rise to the infantile-type Leydig cells. Before puberty, myofibroblast-like precursor cells differentiate into the prepubertal, partially differentiated Leydig cells, which complete their differentiation into the adult Leydig cells. [ABSTRACT FROM AUTHOR]

Presents the list of the members of the European Academy of Andrology.

FXR1 is an alternatively spliced gene that encodes RNA binding proteins (FXR1P) involved in muscle development. In contrast to other tissues, cardiac and skeletal muscle express two FXR1P isoforms that incorporate an additional exon-15. We report that recessive mutations in this particular exon of FXR1 cause congenital multi-minicore myopathy in humans and mice. Additionally, we show that while Myf5-dependent depletion of all FXR1P isoforms is neonatal lethal, mice carrying mutations in exon-15 display non-lethal myopathies which vary in severity depending on the specific effect of each mutation on the protein. FXR1P is a RNA binding protein involved in muscle development. Here, the authors show that mutations in FXR1 exon 15, which is alternatively spliced in muscle, cause multi-minicore myopathy in humans and in mouse models. [ABSTRACT FROM AUTHOR]

Reports on news briefs about the European Academy of Andrology (EAA) as of March 2001. Membership; Schedule of the second European Congress of Andrology; EAA Prize for 1999.