Importance of Lactic Acid in Maintaining Vaginal Health: A Review of Vaginitis and Vaginosis Etiopathogenic Bases and a Proposal for a New Treatment

The most frequent cause of visits to the gynecologist in the western world is vaginal discomfort (vaginitis and vaginosis) whose origin lies in the uncontrolled proliferation of bacteria, such as haemophilus vaginalis or Candida-type fungi, normally considered as saprophytes. Such uncontrolled development of saprophytes is caused by some types of aggression against Döderlein bacilli and/or by a significant decrease in the amount of lactic acid (use of broad-spectrum antibiotics, douches with aggressive products, etc.). Consequently, as the vagina creates a progressively alkalinized and increasingly inadequate environment for the lactobacilli activity, a more favorable environment for the growth of saprophytes is created. The more alkaline the medium becomes, the lower the production of lactic acid. Therefore a vicious circle is created, resulting in the bacillus acidophilus near the lack of metabolism and the disappearance of lactic acid, hydrogen peroxide and bacteriocins. All of the above make it possible for saprophytic bacteria to proliferate and become pathogenic. So far, all vaginitis and vaginosis treatments have solely been focused on attacking the disproportionately developed bacteria but have not addressed the restoration of a vaginal acidic environment, i.e. the environment allowing the proliferation of lactic acid-producing bacillus acidophilus. This explains the high rate of relapse occurring after the treatment of these vaginal profiles. In this paper we propose a new treatment focused on the use of lactic acid to prevent recurrence after a vaginitis or vaginosis treatment.La causa más frecuente de visita al ginecólogo en el mundo occidental son las molestias vaginales (vaginitis y vaginosis) cuyo origen radica en la proliferación descontrolada de bacterias, como el haemophilus vaginalis o los hongos tipo Candida, normalmente considerados saprofitos. Este desarrollo descontrolado de saprofitos está provocado por algún tipo de agresión a los bacilos Döderlein y/o por una disminución importante de la cantidad de ácido láctico (uso de antibióticos de amplio espectro, duchas vaginales con productos agresivos, etc.). En consecuencia, a medida que la vagina crea un ambiente progresivamente alcalinizado y cada vez más inadecuado para la actividad de los lactobacilos, se crea un ambiente más favorable para el crecimiento de saprofitos. Cuanto más alcalino se vuelve el medio, menor es la producción de ácido láctico. Por lo tanto, se crea un círculo vicioso, dando como resultado el bacillus acidophilus cerca de la falta de metabolismo y la desaparición del ácido láctico, el peróxido de hidrógeno y las bacteriocinas. Todo lo anterior hace posible que las bacterias saprofitas proliferen y se vuelvan patógenas. Hasta ahora, todos los tratamientos de vaginitis y vaginosis se han centrado únicamente en atacar las bacterias desproporcionadamente desarrolladas, pero no han abordado la restauración de un ambiente vaginal ácido, es decir, el ambiente que permite la proliferación del bacilo acidófilo productor de ácido láctico. Esto explica la alta tasa de recidiva que se produce tras el tratamiento de estos perfiles vaginales. En este trabajo proponemos un nuevo tratamiento centrado en el uso de ácido láctico para prevenir la recurrencia tras un tratamiento de vaginitis o vaginosis. peróxido de hidrógeno y bacteriocinas. Todo lo anterior hace posible que las bacterias saprofitas proliferen y se vuelvan patógenas. Hasta ahora, todos los tratamientos de vaginitis y vaginosis se han centrado únicamente en atacar las bacterias desproporcionadamente desarrolladas, pero no han abordado la restauración de un ambiente vaginal ácido, es decir, el ambiente que permite la proliferación del bacilo acidófilo productor de ácido láctico. Esto explica la alta tasa de recidiva que se produce tras el tratamiento de estos perfiles vaginales. En este trabajo proponemos un nuevo tratamiento centrado en el uso de ácido láctico para prevenir la recurrencia tras un tratamiento de vaginitis o vaginosis. peróxido de hidrógeno y bacteriocinas. Todo lo anterior hace posible que las bacterias saprofitas proliferen y se vuelvan patógenas. Hasta ahora, todos los tratamientos de vaginitis y vaginosis se han centrado únicamente en atacar las bacterias desproporcionadamente desarrolladas, pero no han abordado la restauración de un ambiente vaginal ácido, es decir, el ambiente que permite la proliferación del bacilo acidófilo productor de ácido láctico. Esto explica la alta tasa de recidiva que se produce tras el tratamiento de estos perfiles vaginales. En este trabajo proponemos un nuevo tratamiento centrado en el uso de ácido láctico para prevenir la recurrencia tras un tratamiento de vaginitis o vaginosis. todos los tratamientos de vaginitis y vaginosis se han centrado únicamente en atacar las bacterias desarrolladas desproporcionadamente, pero no han abordado la restauración de un entorno vaginal ácido, es decir, el entorno que permite la proliferación del bacillus acidophilus productor de ácido láctico. Esto explica la alta tasa de recidiva que se produce tras el tratamiento de estos perfiles vaginales. En este trabajo proponemos un nuevo tratamiento centrado en el uso de ácido láctico para prevenir la recurrencia tras un tratamiento de vaginitis o vaginosis. todos los tratamientos de vaginitis y vaginosis se han centrado únicamente en atacar las bacterias desarrolladas desproporcionadamente, pero no han abordado la restauración de un entorno vaginal ácido, es decir, el entorno que permite la proliferación del bacillus acidophilus productor de ácido láctico. Esto explica la alta tasa de recidiva que se produce tras el tratamiento de estos perfiles vaginales. En este trabajo proponemos un nuevo tratamiento centrado en el uso de ácido láctico para prevenir la recurrencia tras un tratamiento de vaginitis o vaginosis

GHIA (Grupo de Herramientas Interactivas Avanzadas)

Es este documento se resumen las principales líneas actuales de investigación del grupo GHIA en lo que a informática educativa se refiere, así como su contexto y proyectos de futuro.This document summarizes the main research areas of GHIA regarding computer based learning, as well as its context and future work.En el momento actual, agradecemos su apoyo a los proyectos ASIES (TIN2010-17344) y Go-Lite (TIN2011-24139), financiados por el Ministerio de Educación, y al proyecto e-Madrid (S2009/TIC-1650), financiado por la Comunidad Autónoma de Madrid

Mortality from gastrointestinal congenital anomalies at 264 hospitals in 74 low-income, middle-income, and high-income countries: a multicentre, international, prospective cohort study

Summary Background Congenital anomalies are the fifth leading cause of mortality in children younger than 5 years globally. Many gastrointestinal congenital anomalies are fatal without timely access to neonatal surgical care, but few studies have been done on these conditions in low-income and middle-income countries (LMICs). We compared outcomes of the seven most common gastrointestinal congenital anomalies in low-income, middle-income, and high-income countries globally, and identified factors associated with mortality. Methods We did a multicentre, international prospective cohort study of patients younger than 16 years, presenting to hospital for the first time with oesophageal atresia, congenital diaphragmatic hernia, intestinal atresia, gastroschisis, exomphalos, anorectal malformation, and Hirschsprung’s disease. Recruitment was of consecutive patients for a minimum of 1 month between October, 2018, and April, 2019. We collected data on patient demographics, clinical status, interventions, and outcomes using the REDCap platform. Patients were followed up for 30 days after primary intervention, or 30 days after admission if they did not receive an intervention. The primary outcome was all-cause, in-hospital mortality for all conditions combined and each condition individually, stratified by country income status. We did a complete case analysis. Findings We included 3849 patients with 3975 study conditions (560 with oesophageal atresia, 448 with congenital diaphragmatic hernia, 681 with intestinal atresia, 453 with gastroschisis, 325 with exomphalos, 991 with anorectal malformation, and 517 with Hirschsprung’s disease) from 264 hospitals (89 in high-income countries, 166 in middleincome countries, and nine in low-income countries) in 74 countries. Of the 3849 patients, 2231 (58·0%) were male. Median gestational age at birth was 38 weeks (IQR 36–39) and median bodyweight at presentation was 2·8 kg (2·3–3·3). Mortality among all patients was 37 (39·8%) of 93 in low-income countries, 583 (20·4%) of 2860 in middle-income countries, and 50 (5·6%) of 896 in high-income countries (p<0·0001 between all country income groups). Gastroschisis had the greatest difference in mortality between country income strata (nine [90·0%] of ten in lowincome countries, 97 [31·9%] of 304 in middle-income countries, and two [1·4%] of 139 in high-income countries; p≤0·0001 between all country income groups). Factors significantly associated with higher mortality for all patients combined included country income status (low-income vs high-income countries, risk ratio 2·78 [95% CI 1·88–4·11], p<0·0001; middle-income vs high-income countries, 2·11 [1·59–2·79], p<0·0001), sepsis at presentation (1·20 [1·04–1·40], p=0·016), higher American Society of Anesthesiologists (ASA) score at primary intervention (ASA 4–5 vs ASA 1–2, 1·82 [1·40–2·35], p<0·0001; ASA 3 vs ASA 1–2, 1·58, [1·30–1·92], p<0·0001]), surgical safety checklist not used (1·39 [1·02–1·90], p=0·035), and ventilation or parenteral nutrition unavailable when needed (ventilation 1·96, [1·41–2·71], p=0·0001; parenteral nutrition 1·35, [1·05–1·74], p=0·018). Administration of parenteral nutrition (0·61, [0·47–0·79], p=0·0002) and use of a peripherally inserted central catheter (0·65 [0·50–0·86], p=0·0024) or percutaneous central line (0·69 [0·48–1·00], p=0·049) were associated with lower mortality. Interpretation Unacceptable differences in mortality exist for gastrointestinal congenital anomalies between lowincome, middle-income, and high-income countries. Improving access to quality neonatal surgical care in LMICs will be vital to achieve Sustainable Development Goal 3.2 of ending preventable deaths in neonates and children younger than 5 years by 2030

Inflammation and Treatment-Resistant Depression from Clinical to Animal Study: A Possible Link?

The aim of this study was to investigate the relationship between treatment-resistant depression (TRD) and inflammation in humans and experimental models. For the human study, a retrospective cohort study was conducted with 206 participants; half were on antidepressants for major depressive disorder. The patients were divided into healthy and depressed groups. Inflammation was assessed based on the values of the main inflammatory biomarkers (CRP, WBC and ESR). For the animal experiments, 35 adult male Wistar rats were assigned to stressed and non-stressed groups. Inflammation and stress were induced using lipopolysaccharide and chronic unpredictable mild stress. A 10 mg/kg intraperitoneal injection of fluoxetine (FLX), a known antidepressant, was simultaneously administered daily for 4 weeks. Behavioral tests were performed. The plasma levels of inflammatory and stress biomarkers were measured and were significantly higher in the stressed and non-responsive groups in both studies. This study provides evidence of the link between inflammation and TRD. We further observed a possible link via the Phosphorylated Janus Kinase 2 and Phosphorylated Signal Transducer and Activator of Transcription 3 (P-JAK2/P-STAT3) signaling pathway and found that chronic stress and high inflammation hinder the antidepressant effects of FLX. Thus, non-response to antidepressants could be mitigated by treating inflammation to improve the antidepressant effect in patients with TRD

GHIA (Grupo de Herramientas Interactivas Avanzadas), UAM

Es este documento se resumen las principales líneas actuales de investigación del grupo GHIA en lo que a informática educativa se refiere, así como su contexto y proyectos de futuro.This document summarizes the main research areas of GHIA regarding computer based learning, as well as its context and future work

Neonatal Birthweight Spectrum: Maternal Risk Factors and Pregnancy Outcomes in Saudi Arabia

Background and Objectives: Low-birth-weight (LBW) neonates are at increased risk of morbidity and mortality which are inversely proportional to birth weight, while macrosomic babies are at risk of birth injuries and other related complications. Many maternal risk factors were associated with the extremes of birthweight. The objectives of this study are to investigate maternal risk factors for low and high birthweight and to report on the neonatal complications associated with abnormal birth weights. Materials and Methods: We conducted a retrospective analysis of medical records of deliveries ≥ 23 weeks. We classified the included participants according to birth weight into normal birth weight (NBW), LBW, very LBW (VLBW), and macrosomia. The following maternal risk factors were included, mother’s age, parity, maternal body mass index (BMI), maternal diabetes, and hypertension. The neonatal outcomes were APGAR scores Results: A total of 1855 were included in the study. There were 1638 neonates (88.3%) with NBW, 153 (8.2%) with LBW, 27 (1.5%) with VLBW, and 37 (2.0%) with macrosomia. LBW was associated with maternal hypertension (aOR = 3.5, 95% CI = 1.62–7.63), while increasing gestational age was less likely associated with LBW (aOR = 0.51, 95% CI = 0.46–0.57). Macrosomia was associated with maternal diabetes (aOR = 3.75, 95% CI = 1.67–8.41), in addition to maternal obesity (aOR = 3.18, 95% CI = 1.24–8.14). The odds of VLBW were reduced significantly with increasing gestational age (aOR = 0.41, 95% CI = 0.32–0.53). In total, 81.5% of VLBW neonates were admitted to the NICU, compared to 47.7% of LBW and 21.6% of those with macrosomia. RD was diagnosed in 59.3% of VLBW neonates, in 23% of LBW, in 2.7% of macrosomic and in 3% of normal-weight neonates. Hyperbilirubinemia was reported in 37.04%, 34.21%, 22.26%, and 18.92% of VLBW, LBW, NBW, and macrosomic newborns, respectively. Conclusions: Most neonates in this study had normal birthweights. Maternal hypertension and lower gestational age were associated with increased risk of LBW. Additionally, maternal obesity and diabetes increased the risk of macrosomia. Neonatal complications were predominantly concentrated in the LBW and VLBW, with a rising gradient as birthweight decreased. The main complications included respiratory distress and NICU admissions