Cone-beam Computed Tomography Analysis of the Root Canal Morphology of Mandibular Incisors Using Two Classification Systems in a Spanish Subpopulation: A Cross-Sectional Study.

OBJECTIVE: This study evaluated the root and canal morphology in permanent mandibular incisors teeth using cone-beam computer tomography imaging in a Spanish subpopulation, and compared these findings with ipsilateral (similarity) and contralateral (symmetry) incisors. In addition, the position of canal splitting was measured. METHODS: A total of 229 datasets comprising four mandibular teeth each (n=916 incisors) were analysed using Vertucci and Ahmed et al. classifications, and, the similarity and symmetry were calculated. The distance from the cemento-enamel junction (CEJ), and the most coronal canal divergence was measured (if present). The role of sex was also assessed. The Cochran Q Test, LOGIS PROC in SUDAAN, Chi-square, and Kappa were used for the different comparisons. A p-value of less than 0.05 was considered significant. RESULTS: All incisors were single-rooted and no significant differences regarding root canal morphology were found according to the sex of the subjects included in the database. The most common morphology was Vertucci type I/Ahmed et al. 1MI1(65.3% for central and 66.8% for lateral incisors respectively), followed by type III/1MI1-2-1 (31% for central and 30.6% for lateral incisors). 1.8% of the samples were considered as non-classifiable with Vertucci but were classified with codes using the Ahmed et al. system. Similarity values were 74.7% for the left side, and 74.2% for the right side, whereas symmetry values were 90% for central and 84.3% for lateral incisors. In the presence of divergences, the main (SD) distances from the CEJ were for type II/1MI1-2-1 3.8+-0.8 (centrals) 4.0+-0.7 mm (laterals); for type V/1MI1-2 this value ranged between 6.0+-1.8 and 5.5+-1.5 mm, whereas values for 1MI1-2-3-2-1 were 1.8 and 2.1 mm. No significant differences were found when the position of the most coronal divergence was compared between lateral and central incisors for the different morphologies. CONCLUSION: A high prevalence of Vertucci I/Ahmed et al. 1MI1 configuration was present in mandibular incisors from Spanish individuals. Similarity and symmetry were common, particularly for central incisors. The position of the coronal splitting of the canals varied according to the root canal morphology.

Traumatic brain injury extending to the striatum alters autonomic thermoregulation and hypothalamic monoamines in recovering rats.

The brain cortex is the structure that is typically injured in traumatic brain injury (TBI) and is anatomically connected with other brain regions, including the striatum and hypothalamus, which are associated in part with motor function and the regulation of body temperature, respectively. We investigated whether a TBI extending to the striatum could affect peripheral and core temperatures as an indicator of autonomic thermoregulatory function. Moreover, it is unknown whether thermal modulation is accompanied by hypothalamic and cortical monoamine changes in rats with motor function recovery. The animals were allocated into three groups: the sham group (sham), a TBI group with a cortical contusion alone (TBI alone), and a TBI group with an injury extending to the dorsal striatum (TBI + striatal injury). Body temperature and motor deficits were evaluated for 20 days post-injury. On the 3rd and 20th days, rats were euthanized to measure the serotonin (5-HT), noradrenaline (NA), and dopamine (DA) levels using high-performance liquid chromatography (HPLC). We observed that TBI with an injury extending to the dorsal striatum increased core and peripheral temperatures. These changes were accompanied by a sustained motor deficit lasting for 14 days. Furthermore, there were notable increases in NA and 5-HT levels in the brain cortex and hypothalamus both 3 and 20 days after injury. In contrast, rats with TBI alone showed no changes in peripheral temperatures and achieved motor function recovery by the 7th day post-injury. In conclusion, our results suggest that TBI with an injury extending to the dorsal striatum elevates both core and peripheral temperatures, causing a delay in functional recovery and increasing hypothalamic monoamine levels. The aftereffects can be attributed to the injury site and changes to the autonomic thermoregulatory functions.

Protective effects of macrophage-specific integrin α5 in myocardial infarction are associated with accentuated angiogenesis.

Macrophages sense changes in the extracellular matrix environment through the integrins and play a central role in regulation of the reparative response after myocardial infarction. Here we show that macrophage integrin α5 protects the infarcted heart from adverse remodeling and that the protective actions are associated with acquisition of an angiogenic macrophage phenotype. We demonstrate that myeloid cell- and macrophage-specific integrin α5 knockout mice have accentuated adverse post-infarction remodeling, accompanied by reduced angiogenesis in the infarct and border zone. Single cell RNA-sequencing identifies an angiogenic infarct macrophage population with high Itga5 expression. The angiogenic effects of integrin α5 in macrophages involve upregulation of Vascular Endothelial Growth Factor A. RNA-sequencing of the macrophage transcriptome in vivo and in vitro followed by bioinformatic analysis identifies several intracellular kinases as potential downstream targets of integrin α5. Neutralization assays demonstrate that the angiogenic actions of integrin α5-stimulated macrophages involve activation of Focal Adhesion Kinase and Phosphoinositide 3 Kinase cascades.

Metal Contents in Feathers from Birds (Rhynchopsitta terrisi, and Columba livia) with Different Ecological Niches.

The metal contaminants can be utilized as an ecological tool to analyze niche partition in birds. As environmental contamination biological indicators, essential (Zn, Cu, and Cr) and non-essential (Pb and Cd) metals in the flight feathers of the Maroon-fronted Parrot and Pigeon with different ecological niches were assessed. The feathers of the parrot were gathered at a national park (Parque Nacional Cumbres de Monterrey) and the feathers of pigeons were collected at an urban site, that is, the city of Monterrey, Mexico. An atomic absorption spectrophotometer was used to establish the concentration of metals in the feathers. Zn, Cu, Cr, Pb, and Cd were detected in the two studied samples. The results obtained in this study exhibited an increase in metal concentrations in pigeon feathers with respect to parrot feathers. In conclusion, employing parrot and pigeon feathers comprises an important tool to track trace-metal occurrence in the environment and metal accumulation in birds. This information is crucial to possess in order to minimize exposure to essential metals in species of wild birds with different ecological niches.

Cardiac Pericytes Acquire a Fibrogenic Phenotype and Contribute to Vascular Maturation After Myocardial Infarction.

BACKGROUND: Pericytes have been implicated in tissue repair, remodeling, and fibrosis. Although the mammalian heart contains abundant pericytes, their fate and involvement in myocardial disease remains unknown. METHODS: We used NG2Dsred;PDGFRαEGFP pericyte:fibroblast dual reporter mice and inducible NG2CreER mice to study the fate and phenotypic modulation of pericytes in myocardial infarction. The transcriptomic profile of pericyte-derived cells was studied using polymerase chain reaction arrays and single-cell RNA sequencing. The role of transforming growth factor-ß (TGF-ß) signaling in regulation of pericyte phenotype was investigated in vivo using pericyte-specific TGF-ß receptor 2 knockout mice and in vitro using cultured human placental pericytes. RESULTS: In normal hearts, neuron/glial antigen 2 (NG2) and platelet-derived growth factor receptor α (PDGFRα) identified distinct nonoverlapping populations of pericytes and fibroblasts, respectively. After infarction, a population of cells expressing both pericyte and fibroblast markers emerged. Lineage tracing demonstrated that in the infarcted region, a subpopulation of pericytes exhibited transient expression of fibroblast markers. Pericyte-derived cells accounted for ~4% of PDGFRα+ infarct fibroblasts during the proliferative phase of repair. Pericyte-derived fibroblasts were overactive, expressing higher levels of extracellular matrix genes, integrins, matricellular proteins, and growth factors, when compared with fibroblasts from other cellular sources. Another subset of pericytes contributed to infarct angiogenesis by forming a mural cell coat, stabilizing infarct neovessels. Single-cell RNA sequencing showed that NG2 lineage cells diversify after infarction and exhibit increased expression of matrix genes, and a cluster with high expression of fibroblast identity markers emerges. Trajectory analysis suggested that diversification of infarct pericytes may be driven by proliferating cells. In vitro and in vivo studies identified TGF-ß as a potentially causative mediator in fibrogenic activation of infarct pericytes. However, pericyte-specific TGF-ß receptor 2 disruption had no significant effects on infarct myofibroblast infiltration and collagen deposition. Pericyte-specific TGF-ß signaling was involved in vascular maturation, mediating formation of a mural cell coat investing infarct neovessels and protecting from dilative remodeling. CONCLUSIONS: In the healing infarct, cardiac pericytes upregulate expression of fibrosis-associated genes, exhibiting matrix-synthetic and matrix-remodeling profiles. A fraction of infarct pericytes exhibits expression of fibroblast identity markers. Pericyte-specific TGF-ß signaling plays a central role in maturation of the infarct vasculature and protects from adverse dilative remodeling, but it does not modulate fibrotic remodeling.

Novelties in Macrofungi of the Tropical Montane Cloud Forest in Mexico.

The tropical montane cloud forest in Mexico is the most diverse and threatened ecosystem. Mexican macrofungi numbers more than 1408 species. This study described four new species of Agaricomycetes (Bondarzewia, Gymnopilus, Serpula, Sparassis) based on molecular and morphological characteristics. Our results support that Mexico is among the most biodiverse countries in terms of macrofungi in the Neotropics.

Inhibidores de la Rho quinasa y su rol en la disfunción endotelial corneal / Rho Kinase Inhibitors and their Role in Corneal Endothelial Dysfunction

El endotelio corneal es su capa más interna y, a pesar de ser una monocapa de células, es capaz de preservar la transparencia del tejido con dos funciones fundamentales: de barrera y de bomba endotelial sodio-potasio (Na-K). Las células endoteliales tienen muy poca capacidad de regeneración, por lo que cualquier lesión endotelial es compensada por la expansión y migración de las células residuales adyacentes. La disfunción endotelial corneal se caracteriza por un edema de la córnea que puede llevar hasta el transplante de este tejido. Nuevas terapias farmacológicas con inhibidores de Rho-Kinasa y terapias basadas en ingeniería tisular se han propuesto recientemente. Se realizó una búsqueda automatizada sobre los principales avances en estas terapias utilizando la plataforma Infomed, específicamente la Biblioteca Virtual de Salud. La información se resumió en el informe final. Concluimos que existe un progreso significativo en el entendimiento de la patogénesis, y en el desarrollo de los nuevos tratamientos(AU)

The corneal endothelium is its innermost layer and, despite being a monolayer of cells, is able to preserve tissue transparency with two fundamental functions: barrier and endothelial sodium-potassium (Na-K) pump. Endothelial cells have very little regenerative capacity, so any endothelial injury is compensated by the expansion and migration of adjacent residual cells. Corneal endothelial dysfunction is characterized by corneal edema that can lead to corneal tissue transplantation. New pharmacologic therapies with Rho kinase inhibitors and tissue engineering-based therapies have recently been proposed. An automated search on the main advances in these therapies was performed using the Infomed platform, specifically the Virtual Health Library. The information was summarized in the final report. We conclude that there is significant progress in the understanding of pathogenesis, and in the development of new treatments(AU)

Differential effects of Smad2 and Smad3 in regulation of macrophage phenotype and function in the infarcted myocardium.

TGF-ßs regulate macrophage responses, by activating Smad2/3. We have previously demonstrated that macrophage-specific Smad3 stimulates phagocytosis and mediates anti-inflammatory macrophage transition in the infarcted heart. However, the role of macrophage Smad2 signaling in myocardial infarction remains unknown. We studied the role of macrophage-specific Smad2 signaling in healing mouse infarcts, and we explored the basis for the distinct effects of Smad2 and Smad3. In infarct macrophages, Smad3 activation preceded Smad2 activation. In contrast to the effects of Smad3 loss, myeloid cell-specific Smad2 disruption had no effects on mortality, ventricular dysfunction and adverse remodeling, after myocardial infarction. Macrophage Smad2 loss modestly, but transiently increased myofibroblast density in the infarct, but did not affect phagocytic removal of dead cells, macrophage infiltration, collagen deposition, and scar remodeling. In isolated macrophages, TGF-ß1, -ß2 and -ß3, activated both Smad2 and Smad3, whereas BMP6 triggered only Smad3 activation. Smad2 and Smad3 had similar patterns of nuclear translocation in response to TGF-ß1. RNA-sequencing showed that Smad3, and not Smad2, was the main mediator of transcriptional effects of TGF-ß on macrophages. Smad3 loss resulted in differential expression of genes associated with RAR/RXR signaling, cholesterol biosynthesis and lipid metabolism. In both isolated bone marrow-derived macrophages and in infarct macrophages, Smad3 mediated synthesis of Nr1d2 and Rara, two genes encoding nuclear receptors, that may be involved in regulation of their phagocytic and anti-inflammatory properties. In conclusion, the in vivo and in vitro effects of TGF-ß on macrophage function involve Smad3, and not Smad2.

The role of endogenous Smad7 in regulating macrophage phenotype following myocardial infarction.

Smad7 restrains TGF-ß responses, and has been suggested to exert both pro- and anti-inflammatory actions that may involve effects on macrophages. Myocardial infarction triggers a macrophage-driven inflammatory response that not only plays a central role in cardiac repair, but also contributes to adverse remodeling and fibrosis. We hypothesized that macrophage Smad7 expression may regulate inflammation and fibrosis in the infarcted heart through suppression of TGF-ß responses, or via TGF-independent actions. In a mouse model of myocardial infarction, infiltration with Smad7+ macrophages peaked 7 days after coronary occlusion. Myeloid cell-specific Smad7 loss in mice had no effects on homeostatic functions and did not affect baseline macrophage gene expression. RNA-seq predicted that Smad7 may promote TREM1-mediated inflammation in infarct macrophages. However, these alterations in the transcriptional profile of macrophages were associated with a modest and transient reduction in infarct myofibroblast infiltration, and did not affect dysfunction, chamber dilation, scar remodeling, collagen deposition, and macrophage recruitment. In vitro, RNA-seq and PCR arrays showed that TGF-ß has profound effects on macrophage profile, attenuating pro-inflammatory cytokine/chemokine expression, modulating synthesis of matrix remodeling genes, inducing genes associated with sphingosine-1 phosphate activation and integrin signaling, and inhibiting cholesterol biosynthesis genes. However, Smad7 loss did not significantly affect TGF-ß-mediated macrophage responses, modulating synthesis of only a small fraction of TGF-ß-induced genes, including Itga5, Olfml3, and Fabp7. Our findings suggest a limited role for macrophage Smad7 in regulation of post-infarction inflammation and repair, and demonstrate that the anti-inflammatory effects of TGF-ß in macrophages are not restrained by endogenous Smad7 induction.

Efficacy and safety of discontinuing antibiotic treatment for uncomplicated respiratory tract infections when deemed unnecessary. A multicentre, randomized clinical trial in primary care.

OBJECTIVES: To determine the benefits and harms of discontinuing unnecessary antibiotic therapy for uncomplicated respiratory tract infections (RTI) when antibiotics are considered no longer necessary. METHODS: Multicentre, open-label, randomized controlled clinical trial in primary care centres from 2017 to 2020 (ClinicalTrials.gov, NCT02900820). Adults with RTIs-acute rhinosinusitis, sore throat, influenza or acute bronchitis-who had previously taken any dose of antibiotic for less than 3 days, which physicians no longer deemed necessary were recruited. The patients were randomly assigned in a 1:1 ratio to discontinuing antibiotic therapy or the usual strategy of continuing antibiotic treatment. The primary outcome was the duration of severe symptoms (number of days scoring 5 or 6 on a six-item Likert scale). Secondary outcomes included days with symptoms, moderate symptoms (scores of 3 or 4), antibiotics taken, adverse events, patient satisfaction and complications within the first 3 months. RESULTS: A total of 467 patients were randomized, out of which 409 were considered valid for the analysis. The mean (SD) duration of severe symptoms was 3.0 (1.5) days for the patients assigned to discontinuation and 2.8 (1.3) days for those allocated to the control group (mean difference 0.2 days; 95% CI -0.1 to 0.4 days). Patients randomized to the discontinuation group used fewer antibiotics after the baseline visit (52/207 (25.1%) versus 182/202 (90.1%); p 0.001). Patients assigned to antibiotic continuation presented a relative risk of adverse events of 1.47 (95% CI 0.80-2.71), but the need for further health-care contact in the following 3 months was slightly lower (RR 0.61; 95% CI 0.28-1.37). CONCLUSIONS: Discontinuing antibiotic treatment for uncomplicated RTIs when clinicians consider it unnecessary is safe and notably reduces antibiotic consumption.

Smad7 effects on TGF-ß and ErbB2 restrain myofibroblast activation and protect from postinfarction heart failure.

Repair of the infarcted heart requires TGF-ß/Smad3 signaling in cardiac myofibroblasts. However, TGF-ß-driven myofibroblast activation needs to be tightly regulated in order to prevent excessive fibrosis and adverse remodeling that may precipitate heart failure. We hypothesized that induction of the inhibitory Smad, Smad7, may restrain infarct myofibroblast activation, and we examined the molecular mechanisms of Smad7 actions. In a mouse model of nonreperfused infarction, Smad3 activation triggered Smad7 synthesis in α-SMA+ infarct myofibroblasts, but not in α-SMA-PDGFRα+ fibroblasts. Myofibroblast-specific Smad7 loss increased heart failure-related mortality, worsened dysfunction, and accentuated fibrosis in the infarct border zone and in the papillary muscles. Smad7 attenuated myofibroblast activation and reduced synthesis of structural and matricellular extracellular matrix proteins. Smad7 effects on TGF-ß cascades involved deactivation of Smad2/3 and non-Smad pathways, without any effects on TGF-ß receptor activity. Unbiased transcriptomic and proteomic analysis identified receptor tyrosine kinase signaling as a major target of Smad7. Smad7 interacted with ErbB2 in a TGF-ß-independent manner and restrained ErbB1/ErbB2 activation, suppressing fibroblast expression of fibrogenic proteases, integrins, and CD44. Smad7 induction in myofibroblasts serves as an endogenous TGF-ß-induced negative feedback mechanism that inhibits postinfarction fibrosis by restraining Smad-dependent and Smad-independent TGF-ß responses, and by suppressing TGF-ß-independent fibrogenic actions of ErbB2.

Isolation methods of large and small extracellular vesicles derived from cardiovascular progenitors: A comparative study.

Since the discovery of the beneficial therapeutical effects of extracellular vesicles (EVs), these agents have been attracting great interest as next-generation therapies. EVs are nanosized membrane bodies secreted by all types of cells that mediate cell-cell communication. Although the classification of different subpopulations of EVs can be complex, they are broadly divided into microvesicles and exosomes based on their biogenesis and in large and small EVs based on their size. As this is an emerging field, current investigations are focused on basic aspects such as the more convenient method for EV isolation. In the present paper, we used cardiac progenitor cells (CPCs) to study and compare different cell culture conditions for EV isolation as well as two of the most commonly employed purification methods: ultracentrifugation (UC) and size-exclusion chromatography (SEC). Large and small EVs were separately analysed. We found that serum starvation of cells during the EV collecting period led to a dramatic decrease in EV secretion and major cell death. Regarding the isolation method, our findings suggest that UC and SEC gave similar EV recovery rates. Separation of large and small EV-enriched subpopulations was efficiently achieved with both purification protocols although certain difference in sample heterogeneity was observed. Noteworthy, while calnexin was abundant in large EVs, ALIX and CD63 were mainly found in small EVs. Finally, when the functionality of EVs was assessed on primary culture of adult murine cardiac fibroblasts, we found that EVs were taken up by these cells, which resulted in a pronounced reduction in the proliferative and migratory capacity of the cells. Specifically, a tendency towards a larger effect of SEC-related EVs was observed. No differences could be found between large and small EVs. Altogether, these results contribute to establish the basis for the use of EVs as therapeutic platforms, in particular in regenerative fields.

Type 1 diabetes and subcutaneous insulin resistance syndrome treated with pancreas transplantation.

We present a case of subcutaneous insulin resistance syndrome, a rare entity, consisting of subcutaneous and intramuscular insulin resistance, with normal or almost normal sensitivity to insulin when administered intravenously. Its cause is unknown and its treatment is challenging. Our patient required a pancreas transplant.

Presentamos un caso de síndrome de resistencia subcutánea a la insulina, entidad infrecuente, que consiste en resistencia a la insulina por vía subcutánea e intramuscular, con sensibilidad normal o casi normal a la insulina cuando se aplica por vía intravenosa. Se desconoce su causa y su tratamiento es un desafío. Nuestra paciente requirió trasplante de páncreas.

Type 1 diabetes and subcutaneous insulin resistance syndrome treated with pancreas transplantation / Diabetes tipo 1 y síndrome de resistencia subcutánea a la insulina tratada con trasplante de páncreas

Abstract We present a case of subcutaneous insulin resistance syndrome, a rare entity, consisting of subcutaneous and intramuscular insulin resistance, with normal or almost normal sensitivity to insulin when administered intravenously. Its cause is unknown and its treatment is challenging. Our patient required a pancreas transplant.

Resumen Presentamos un caso de síndrome de resistencia subcutánea a la insulina, entidad in frecuente, que consiste en resistencia a la insulina por vía subcutánea e intramuscular, con sensibilidad normal o casi normal a la insulina cuando se aplica por vía intravenosa. Se desconoce su causa y su tratamiento es un desafío. Nuestra paciente requirió trasplante de páncreas.

CTCF chromatin residence time controls three-dimensional genome organization, gene expression and DNA methylation in pluripotent cells.

The 11 zinc finger (ZF) protein CTCF regulates topologically associating domain formation and transcription through selective binding to thousands of genomic sites. Here, we replaced endogenous CTCF in mouse embryonic stem cells with green-fluorescent-protein-tagged wild-type or mutant proteins lacking individual ZFs to identify additional determinants of CTCF positioning and function. While ZF1 and ZF8-ZF11 are not essential for cell survival, ZF8 deletion strikingly increases the DNA binding off-rate of mutant CTCF, resulting in reduced CTCF chromatin residence time. Loss of ZF8 results in widespread weakening of topologically associating domains, aberrant gene expression and increased genome-wide DNA methylation. Thus, important chromatin-templated processes rely on accurate CTCF chromatin residence time, which we propose depends on local sequence and chromatin context as well as global CTCF protein concentration.

Augmented renal clearance. An unnoticed relevant event.

Augmented renal clearance (ARC) is a phenomenon that can lead to a therapeutic failure of those drugs of renal clearance. The purpose of the study was to ascertain the prevalence of ARC in the critically ill patient, to study the glomerular filtration rate (GFR) throughout the follow-up and analyze the concordance between the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) estimation formula and measured GFR. Observational, prospective, multicenter study. ARC was defined as a creatinine clearance greater than 130 ml/min/1.73 m2. Eighteen hospitals were recruited. GFR measurements carried out twice weekly during a 2-month follow-up period. A total of 561 patients were included. ARC was found to have a non-negligible prevalence of 30%. More even, up to 10.7% already had ARC at intensive care unit (ICU) admission. No specific pattern of GFR was found during the follow-up. Patients in the ARC group were younger 56.5 (53.5-58.5) versus 66 (63.5-68.5) years than in the non-ARC group, p < 0.001. ICU mortality was lower in the ARC group, 6.9% versus 14.5%, p = 0.003. There was no concordance between the estimation of GFR by the CKD-EPI formula and GFR calculated from the 4-h urine. ARC is found in up to 30% of ICU patients, so renal removal drugs could be under dosed by up to 30%. And ARC is already detected on admission in 10%. It is a dynamic phenomenon without an established pattern that usually occurs in younger patients that can last for several weeks. And the CKD-EPI formula does not work to estimate the real creatinine clearance of these patients.

Protein Profile and Simulated Digestive Behavior of Breast Milk from Overweight and Normal Weight Mothers.

Human milk proteins have shown to vary in concentration and distribution through lactation. However, while some regulatory components, such as hormones, have shown associations with regard to the mothers' body mass index, there is limited information on the possible influence of this condition on the whole protein distribution. The objective of this study was to evaluate the protein profile of human milk from normal weight and overweight or obese mothers to identify differences in protein expression in colostrum, transitional and mature milk. The mass spectrometry analysis showed the ability to class with a high degree of confidence the lactation state and the milk profile according to the mother's condition. Individual milk samples were subjected to a digestion in vitro model that takes into account the specificities of the gastrointestinal conditions of full-term newborn infants. The digestion products were compared with available data from the digestive contents in newborns. The behavior of the most abundant proteins and the overall peptide generation and survival, showed good correspondence with in vivo data.

Study of the phenolic compound profile and antioxidant activity of human milk from Spanish women at different stages of lactation: A comparison with infant formulas.

Human milk (HM) has been proven to have important and essential antioxidant properties to counteract infant susceptibility to oxidative stress. Phenolic compounds are secondary metabolites which come from plants and are potent natural antioxidants. The ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) method used in the present study allowed the quantification of 26 phenolic compounds (ten hydroxybenzoic acids, seven hydroxycinnamic acids, four flavonoids, three hydroxybenzaldehydes and two other polyphenols) in HM samples at different stages of lactation (colostrum, transitional milk and mature milk) and infant formulas (IF). Many of the phenolic compounds identified have been reported to be present in HM for the first time. The total phenolic compound content (TPC) was quantified using the Folin assay and the antioxidant activity (AC) was evaluated with the DPPH, ABTS and FRAP assays. Significant differences were evidenced between HM and IF. HM from mothers with an adherence to a Mediterranean diet contained twice as many individual phenolic compounds as infant formulas, with a higher proportion of hydroxybenzoic acids. Conversely, IF showed a higher proportion of hydroxycinnamic acids. Overall, the antioxidant activity of HM showed small variations during lactation.

Comparación de las características de la córnea entre individuos chinos y cubanos / Comparison between corneal features of Chinese and Cuban subjects

Objetivo: Comparar las características de la córnea entre individuos chinos y cubanos adultos sanos. Métodos: Se realizó un estudio observacional, descriptivo, transversal, en 120 ojos de individuos sanos (60 chinos y 60 cubanos), entre 18 y 29 años de edad, entre septiembre del año 2016 y diciembre de 2017 en el Instituto Cubano de Oftalmología "Ramón Pando Ferrer". Se evaluó la edad, el sexo, la queratometría, la paquimetría y las características del endotelio corneal. Resultados: Predominó el sexo femenino (53,3 por ciento en los cubanos y 66,6 por ciento en los chinos). La edad promedio fue de 24,4 años en ambos grupos. La queratometría promedio resultó mayor en el grupo de estudio de cubanos, con un valor de 44,7 y 44,6 dioptrías en ambos ojos, respectivamente. El espesor corneal fue de 607,3-629,9 en los cubanos y de 575,4-607,2 en los chinos. El coeficiente de variación, la desviación estándar y la densidad celular se diferenciaron mínimamente en ambos ojos para ambas nacionalidades, y resultaron superiores en los ojos izquierdos con un coeficiente de 32,0 (±11,0) en los chinos. La desviación estándar promedio fue de 112,0 (± 36,5) en ambos grupos y en el ojo derecho la densidad celular fue 2 857,1 (± 240,0 cél/mm2) en los chinos y 2 760,0 (± 367,2) en los cubanos. El average de los cubanos estuvo entre 369,0 y 380, y para los chinos entre 352,4 y 358,4 en los ojos derecho e izquierdo. Conclusiones: Existen diferencias significativas en los valores queratométricos. El espesor corneal resulta discretamente más reducido en los chinos. El coeficiente de variación, la densidad celular, el average y la desviación estándar no presentan diferencias estadísticamente significativas(AU)

Objective: Compare the corneal features of Chinese and Cuban healthy adult subjects. Methods: A cross-sectional observational descriptive study was conducted of 120 eyes of healthy 18-29 year old individuals (60 Chinese and 60 Cuban) from September 2016 to December 2017 at Ramón Pando Ferrer Cuban Institute of Ophthalmology. The variables analyzed were sex, keratometry, pachymetry and characteristics of the corneal endothelium. Results: Female sex prevailed (53.3 percent among Cuban and 66.6 percent among Chinese subjects). Mean age was 24.4 years in both groups. Mean keratometry was higher in the Cuban group, with values of 44.7 and 44.6 diopters for both eyes, respectively. Corneal thickness was 607.3-629.9 among Cuban and 575.4-607.2 among Chinese subjects. Variation coefficient, standard deviation and cell density were minimally different between the two eyes in both groups, and were higher in left eyes of Chinese subjects with a coefficient of 32.0 (±11.0). Mean standard deviation was 112.0 (± 36.5) in both groups, whereas right eye cell density was 2 857.1 (± 240.0 cell/mm2) among Chinese and 2 760.0 (± 367.2) among Cuban subjects. Average between right and left eyes ranged from 369.0 to 380 for the Cubans and from 352.4 to 358.4 for the Chinese. Conclusions: Significant differences were found between keratometric values. Corneal thickness was slightly lower among Chinese subjects. Variation coefficient, cell density, average and standard deviation did not show any statistically significant differences(AU)