Fructose Consumption Affects Placental Production of H2S: Impact on Preeclampsia-Related Parameters.

H2S, a gasotransmitter that can be produced both via the transsulfuration pathway and non-enzymatically, plays a key role in vasodilation and angiogenesis during pregnancy. In fact, the involvement of H2S production on plasma levels of sFLT1, PGF, and other molecules related to preeclampsia has been demonstrated. Interestingly, we have found that maternal fructose intake (a common component of the Western diet) affects tissular H2S production. However, its consumption is allowed during pregnancy. Thus, (1) to study whether maternal fructose intake affects placental production of H2S in the offspring, when pregnant; and (2) to study if fructose consumption during pregnancy can increase the risk of preeclampsia, pregnant rats from fructose-fed mothers (10% w/v) subjected (FF) or not (FC) to a fructose supplementation were studied and compared to pregnant control rats (CC). Placental gene expression, H2S production, plasma sFLT1, and PGF were determined. Descendants of fructose-fed mothers (FC) presented an increase in H2S production. However, if they consumed fructose during their own gestation (FF), this effect was reversed so that the increase disappeared. Curiously, placental synthesis of H2S was mainly non-enzymatic. Related to this, placental expression of Cys dioxygenase, an enzyme involved in Cys catabolism (a molecule required for non-enzymatic H2S synthesis), was significantly decreased in FC rats. Related to preeclampsia, gene expression of sFLT1 (a molecule with antiangiogenic properties) was augmented in both FF and FC dams, although these differences were not reflected in their plasma levels. Furthermore, placental expression of PGF (a molecule with angiogenic properties) was decreased in both FC and FF dams, becoming significantly diminished in plasma of FC versus control dams. Both fructose consumption and maternal fructose intake induce changes in molecules that contribute to increasing the risk of preeclampsia, and these effects are not always mediated by changes in H2S production.

Benefits of Using Magnetic Resonance Imaging During Breast Tissue Expansion: Literature Review and Case Series.

Breast cancer results in up to 1.6 million new candidates for yearly breast reconstruction (BR) surgery. Two-stage breast reconstruction surgery with the use of a tissue expander (TE) is a common approach to reconstructing the breast after mastectomy. However, a common disadvantage encountered with the traditional breast TE is the magnetic injection port, which has been reported to cause injuries in patients undergoing magnetic resonance (MR) imaging. Therefore this type of breast TE is labeled "MR unsafe." Recent technological advances have incorporated radio-frequency identification (RFID) technology in the TE to allow for the location of the injection port without magnetic components, resulting in an MR-conditional TE. This paper aims to review the information regarding the safety profile of TEs with magnetic ports and to gather distinct clinical scenarios in which an MR-conditional TE benefits the patient during the BR process. A literature review ranging from 2018 to 2022 was performed with the search terms: "tissue expander" OR "breast tissue expander" AND "magnetic resonance imaging" OR "MRI." Additionally, a case series was collected from each of the authors' practices. The literature search yielded 13 recent peer-reviewed papers, and 6 distinct clinical scenarios were compiled and discussed. Most clinicians find MRI examinations to be the state-of-art diagnostic imaging modality. However, due to the preexisting risks associated with TEs with magnetic ports, the MRI labeling classification should be considered when deciding which TE is the most appropriate for the patient requiring MRI examinations.

Maternal fructose boosts the effects of a Western-type diet increasing SARS-COV-2 cell entry factors in male offspring.

Fructose-rich beverages and foods consumption correlates with the epidemic rise in cardiovascular disease, diabetes and obesity. Severity of COVID-19 has been related to these metabolic diseases. Fructose-rich foods could place people at an increased risk for severe COVID-19. We investigated whether maternal fructose intake in offspring affects hepatic and ileal gene expression of proteins that permit SARS-CoV2 entry to the cell. Carbohydrates were supplied to pregnant rats in drinking water. Adult and young male descendants subjected to water, liquid fructose alone or as a part of a Western diet, were studied. Maternal fructose reduced hepatic SARS-CoV2 entry factors expression in older offspring. On the contrary, maternal fructose boosted the Western diet-induced increase in viral entry factors expression in ileum of young descendants. Maternal fructose intake produced a fetal programming that increases hepatic viral protection and, in contrast, exacerbates fructose plus cholesterol-induced diminution in SARS-CoV2 protection in small intestine of progeny.

Beyond the Glycaemic Control of Dapagliflozin: Microangiopathy and Non-classical Complications.

Dapagliflozin is a selective sodium-glucose cotransporter 2 inhibitor (SGLT2i) indicated for the treatment of type 2 diabetes mellitus (T2DM), heart failure (HF) with reduced ejection fraction (EF) and chronic kidney disease (CKD). In monotherapy or as an additive therapy, dapagliflozin aids glycaemic control, is associated with reductions in blood pressure and weight, and promotes a favourable lipid profile. In this review, we address the impact of dapagliflozin on cardiovascular risk factors and common microangiopathic complications such as kidney disease and retinopathy in patients with T2DM. Furthermore, we evaluate its potential beneficial effects on other less frequent complications of diabetes, such as macular oedema, cognitive impairment, non-alcoholic fatty liver disease and respiratory disorders during sleep. Moreover, the underuse of SGLT2i in clinical practice is discussed. Our goal is to help translate this evidence into clinical practice.

Lack of definitive presurgical pathological diagnosis is associated with inadequate surgical margins in breast-conserving surgery.

PURPOSE: To determine the impact of definitive presurgical diagnosis on surgical margins in breast-conserving surgery (BCS) for primary carcinomas; clinicopathological features were also analyzed. METHODS: This retrospective study included women who underwent BCS for primary carcinomas in 2016 and 2017. Definitive presurgical diagnosis was defined as having a presurgical core needle biopsy (CNB) and not being upstaged between biopsy and surgery. Biopsy data and imaging findings including breast density were retrieved. Inadequate surgical margins (IM) were defined per latest ASCO and ASTRO guidelines. Univariable and multivariable analyses were performed. RESULTS: 360 women (median age, 66) met inclusion criteria with 1 having 2 cancers. 82.5% (298/361) were invasive cancers while 17.5% (63/361) were ductal carcinoma in situ (DCIS). Most biopsies were US-guided (284/346, 82.0%), followed by mammographic (60/346, 17.3%), and MRI-guided (2/346, 0.6%). US and mammographic CNB yielded median samples of 2 and 4, respectively, with a 14G needle. 15 patients (4.2%) lacked presurgical CNB. The IM rate was 30.0%. In multivariable analysis, large invasive cancers (>20 mm), dense breasts, and DCIS were associated with IM (p = 0.029, p = 0.010, and p = 0.013, respectively). Most importantly, lack of definitive presurgical diagnosis was a risk factor for IM (OR, 2.35; 95% CI: 1.23-4.51, p = 0.010). In contrast, neither patient age (<50) nor aggressive features (e.g., LVI) were associated with IM. CONCLUSION: Lack of a definitive presurgical diagnosis was associated with a two-fold increase of IM in BCS; other risk factors were dense breasts, large invasive cancers, and DCIS.

Liquid carbohydrate intake modifies transsulfuration pathway both in pregnant rats and in their male descendants / La ingesta de carbohidratos en forma líquida modifica la ruta de la transulfuración tanto en ratas gestantes como en su descendencia macho

Introduction: Fructose, alone or in combination with glucose, has been used as a source of added sugars to manufacture sugary drinks and processed foods. High consumption of simple sugars, mainly fructose, has been demonstrated to be one of the causes of developing metabolic diseases. Maternal nutrition is a key factor in the health of the progeny when adult. However, ingestion of fructose-containing foods is still permitted during gestation. Hydrogen sulphide (H2S) is a gasotransmitter produced in the transsulfuration pathway with proved beneficial effects to combat metabolic diseases. Methods: Carbohydrates were supplied to pregnant rats in drinking water (10% wt/vol) throughout gestation, and the pregnant rats, their foetuses, and adult male descendants were studied. Later, adult male progeny from control, fructose- and glucose-fed mothers were subjected to liquid fructose, and were compared to the control group. Liver H2S production was determined. Results: This study shows that, in pregnancy, either a fructose-rich diet per se or situations that produce an impaired insulin sensitivity such as an excessive intake of glucose, decrease hepatic and placental production of H2S. Furthermore, this effect was also observed in the liver of male offspring (both in foetal and adult stages). Interestingly, when these adult descendants were subjected to a high fructose intake, decreases in H2S synthesis in liver and adipose tissue due to this fructose intake were maternal consumption dependent. Conclusions: Given H2S is a protective agent against diseases such as diabetes, obesity, cardiovascular diseases, and metabolic syndrome, the fact that carbohydrate consumption reduces H2S synthesis both in pregnancy and in their progeny could have clear and relevant clinical implications.(AU)

Introducción: La fructosa, sola o en combinación con glucosa, se usa como fuente de azúcares añadidos para elaborar bebidas azucaradas y comidas procesadas. El elevado consumo de azúcares simples, sobre todo fructosa, se ha mostrado como una de las causas del desarrollo de enfermedades metabólicas. La nutrición materna es un factor clave en la salud de la descendencia adulta. Sin embargo, el consumo de alimentos que contienen fructosa está todavía permitido durante la gestación. El sulfuro de hidrógeno (H2S) es un gasotransmisor producido en la ruta de la transulfuración con probados beneficios para luchar contra las enfermedades metabólicas. Métodos: Los carbohidratos se suministraron a las ratas gestantes en el agua de bebida (10% p/v) a lo largo de la gestación, y se estudiaron las ratas preñadas, sus fetos y los descendientes macho adultos. Posteriormente, a la progenie macho adulta procedente de madres control, alimentadas con fructosa o bien con glucosa, se le administró fructosa líquida y se comparó con un grupo control. Se determinó la producción hepática de H2S. Resultados: Este estudio muestra cómo en la gestación, una dieta rica en fructosa per se o situaciones en las que se produce una empeorada sensibilidad a la insulina tal como un consumo excesivo de glucosa, disminuyen la producción hepática y placentaria de H2S. Más aún, este efecto también fue observado en el hígado de la descendencia macho (tanto en el estado fetal como en la edad adulta). Es destacable que, cuando esta descendencia adulta era sometida a una ingesta elevada de fructosa, las disminuciones en la síntesis de H2S en el hígado y el tejido adiposo debidas a dicho consumo eran dependientes del consumo materno...(AU)

Liquid carbohydrate intake modifies transsulfuration pathway both in pregnant rats and in their male descendants.

INTRODUCTION: Fructose, alone or in combination with glucose, has been used as a source of added sugars to manufacture sugary drinks and processed foods. High consumption of simple sugars, mainly fructose, has been demonstrated to be one of the causes of developing metabolic diseases. Maternal nutrition is a key factor in the health of the progeny when adult. However, ingestion of fructose-containing foods is still permitted during gestation. Hydrogen sulphide (H2S) is a gasotransmitter produced in the transsulfuration pathway with proved beneficial effects to combat metabolic diseases. METHODS: Carbohydrates were supplied to pregnant rats in drinking water (10% wt/vol) throughout gestation, and the pregnant rats, their foetuses, and adult male descendants were studied. Later, adult male progeny from control, fructose- and glucose-fed mothers were subjected to liquid fructose, and were compared to the control group. Liver H2S production was determined. RESULTS: This study shows that, in pregnancy, either a fructose-rich diet per se or situations that produce an impaired insulin sensitivity such as an excessive intake of glucose, decrease hepatic and placental production of H2S. Furthermore, this effect was also observed in the liver of male offspring (both in foetal and adult stages). Interestingly, when these adult descendants were subjected to a high fructose intake, decreases in H2S synthesis in liver and adipose tissue due to this fructose intake were maternal consumption dependent. CONCLUSIONS: Given H2S is a protective agent against diseases such as diabetes, obesity, cardiovascular diseases, and metabolic syndrome, the fact that carbohydrate consumption reduces H2S synthesis both in pregnancy and in their progeny could have clear and relevant clinical implications.

Maternal Fructose Intake Increases Liver H2 S Synthesis but Exarcebates its Fructose-Induced Decrease in Female Progeny.

SCOPE: Fructose intake from added sugars correlates with the epidemic rise in metabolic syndrome and cardiovascular diseases (CVD). However, consumption of beverages containing fructose is allowed during gestation. Homocysteine (Hcy) is a well-known risk factor for CVD while hydrogen sulfide (H2 S), a product of its metabolism, has been proved to exert opposite effects to Hcy. METHODS AND RESULTS: First, it is investigated whether maternal fructose intake produces subsequent changes in Hcy metabolism and H2 S synthesis of the progeny. Carbohydrates are supplied to pregnant rats in drinking water (10% wt/vol) throughout gestation. Adult female descendants from fructose-fed, control or glucose-fed mothers are studied. Females from fructose-fed mothers have elevated homocysteinemia, hepatic H2 S production, cystathionine γ-lyase (CSE) (the key enzyme in H2 S synthesis) expression and plasma H2 S, versus the other two groups. Second, it is studied how adult female progeny from control (C/F), fructose- (F/F), and glucose-fed (G/F) mothers responded to liquid fructose and compared them to the control group (C/C). Interestingly, hepatic CSE expression and H2 S synthesis are diminished by fructose intake, this effect being more pronounced in F/F females. CONCLUSION: Maternal fructose intake produces a fetal programming that increases hepatic H2 S production and, in contrast, exacerbates its fructose-induced drop in female progeny.

Deep brain stimulation for aggressiveness: long-term follow-up and tractography study of the stimulated brain areas.

OBJECTIVE: Initial studies applying deep brain stimulation (DBS) of the posteromedial hypothalamus (PMH) to patients with pathological aggressiveness have yielded encouraging results. However, the anatomical structures involved in its therapeutic effect have not been precisely identified. The authors' objective was to describe the long-term outcome in their 7-patient series, and the tractography analysis of the volumes of tissue activated in 2 of the responders. METHODS: This was a retrospective study of 7 subjects with pathological aggressiveness. The findings on MRI with diffusion tensor imaging (DTI) in 2 of the responders were analyzed. The authors generated volumes of tissue activated according to the parameters used, and selected those volumes as regions of interest to delineate the tracts affected by stimulation. RESULTS: The series consisted of 5 men and 2 women. Of the 7 patients, 5 significantly improved with stimulation. The PMH, ventral tegmental area, dorsal longitudinal fasciculus, and medial forebrain bundle seem to be involved in the stimulation field. CONCLUSIONS: In this series, 5 of 7 medication-resistant patients with severe aggressiveness who were treated with bilateral PMH DBS showed a significant long-lasting improvement. The PMH, ventral tegmental area, dorsal longitudinal fasciculus, and medial forebrain bundle seem to be in the stimulation field and might be responsible for the therapeutic effect of DBS.

Effects of Maternal Fructose Intake on Perinatal ER-Stress: A Defective XBP1s Nuclear Translocation Affects the ER-stress Resolution.

Endoplasmic reticulum (ER) homeostasis is crucial to appropriate cell functioning, and when disturbed, a safeguard system called unfolded protein response (UPR) is activated. Fructose consumption modifies ER homeostasis and has been related to metabolic syndrome. However, fructose sweetened beverages intake is allowed during gestation. Therefore, we investigate whether maternal fructose intake affects the ER status and induces UPR. Thus, administrating liquid fructose (10% w/v) to pregnant rats partially activated the ER-stress in maternal and fetal liver and placenta. In fact, a fructose-induced increase in the levels of pIRE1 (phosphorylated inositol requiring enzyme-1) and its downstream effector, X-box binding protein-1 spliced form (XBP1s), was observed. XBP1s is a key transcription factor, however, XBP1s nuclear translocation and the expression of its target genes were reduced in the liver of the carbohydrate-fed mothers, and specifically diminished in the fetal liver and placenta in the fructose-fed mothers. These XBP1s target genes belong to the ER-associated protein degradation (ERAD) system, used to buffer ER-stress and to restore ER-homeostasis. It is known that XBP1s needs to form a complex with diverse proteins to migrate into the nucleus. Since methylglyoxal (MGO) content, a precursor of advanced glycation endproducts (AGE), was augmented in the three tissues in the fructose-fed mothers and has been related to interfere with the functioning of many proteins, the role of MGO in XBP1s migration should not be discarded. In conclusion, maternal fructose intake produces ER-stress, but without XBP1s nuclear migration. Therefore, a complete activation of UPR that would resolve ER-stress is lacking. A state of fructose-induced oxidative stress is probably involved.

Maternal fructose induces gender-dependent changes in both LXRα promoter methylation and cholesterol metabolism in progeny.

Fructose consumption from added sugars correlates with the epidemic rise in obesity, metabolic syndrome and cardiovascular diseases. However, consumption of beverages containing fructose is allowed during gestation. We have investigated whether maternal fructose intake produces subsequent changes in cholesterol metabolism of progeny. Carbohydrates were supplied to pregnant rats in drinking water (10% w/v solution) throughout gestation. Adult male and female descendants from fructose-fed, control or glucose-fed mothers were studied. Male offspring from fructose-fed mothers had elevated plasma HDL-cholesterol levels, whereas female progeny from fructose-fed mothers presented lower levels of non-HDL cholesterol vs. the other two groups. Liver X-receptor (LXR), an important regulator of cholesterol metabolism, and its target genes such as scavenger receptor B1, ATP-binding cassette (ABC)G5 and cholesterol 7-alpha hydroxylase showed decreased gene expression in males from fructose-fed mothers and the opposite in the female progeny. Moreover, the expression of a number of LXRα target genes related to lipogenesis paralleled to that for LXRα expression. In accordance with this, LXRα gene promoter methylation was increased in males from fructose-fed mothers and decreased in the corresponding group of females. Surprisingly, plasma folic acid levels, an important methyl-group donor, were augmented in males from fructose-fed mothers and diminished in female offspring. Maternal fructose intake produces a fetal programming that influences, in a gender-dependent manner, the transcription factor LXRα epigenetically, and both hepatic mRNA gene expression and plasma parameters of cholesterol metabolism in adult progeny. Changes in the LXRα promoter methylation might be related to the availability of the methyl donor folate.

Histological changes secondary to wire coil placement in breast tissue and lymph nodes.

We describe the histological and immunohistochemical features of the changes produced by spiral coil localization wires in the breast parenchyma and lymph nodes of a total of 100 patients undergoing surgery for different breast lesions. Coil wires produced cystic lesions containing a hyaline, mucous-like, PAS-negative fluid. Cavities were lined by cells of variable morphology ranging from synovial-like cells (with a conspicuous epithelial appearance) to mononuclear or multinucleate histiocytic cells that expressed CD68, but were negative for keratins. CD3-positive/CD8-positive T lymphocytes predominated in the inflammatory reaction. Pathologists should be aware of these changes in order to differentiate coil-related lesions from other granulomatous or epithelial lesions, including mucocele-like and ductal carcinoma in situ lesions.

A case-control study to assess the effectiveness of pertussis vaccination during pregnancy on newborns, Valencian community, Spain, 1 March 2015 to 29 February 2016.

In the Valencian Community (Spain), the programme of maternal pertussis vaccination during pregnancy started in January 2015. The objective of this study was to estimate in this region the vaccine effectiveness (VE) in protecting newborns against laboratory-confirmed pertussis infection. A matched case-control study was undertaken in the period between 1 March 2015 and 29 February 2016. Twenty-two cases and 66 controls (+/- 15 days of age difference) were included in the study. Cases were non-vaccinated infants < 3 months of age at disease onset testing positive for pertussis by real-time PCR. For every case three unvaccinated controls were selected. Odds ratios (OR) were calculated by multiple conditional logistic regression for association between maternal vaccination and infant pertussis. Other children in the household, as well as mother- and environmental covariates were taken into account. The VE was calculated as 1 - OR. Mothers of five cases (23%) and of 41 controls (62%) were vaccinated during pregnancy. The adjusted VE was 90.9% (95% confidence interval (CI): 56.6 to 98.1). The only covariate in the final model was breastfeeding (protective effect). Our study provides evidence in favour of pertussis vaccination programmes for pregnant women in order to prevent whooping cough in infants aged less than 3 months.

Fructose during pregnancy provokes fetal oxidative stress: The key role of the placental heme oxygenase-1.

SCOPE: One of the features of metabolic syndrome caused by liquid fructose intake is an impairment of redox status. We have investigated whether maternal fructose ingestion modifies the redox status in pregnant rats and their fetuses. METHODS AND RESULTS: Fructose (10% wt/vol) in the drinking water of rats throughout gestation, leads to maternal hepatic oxidative stress. However, this change was also observed in glucose-fed rats and, in fact, both carbohydrates produced a decrease in antioxidant enzyme activity. Surprisingly, mothers fed carbohydrates displayed low plasma lipid oxidation. In contrast, fetuses from fructose-fed mothers showed elevated levels of plasma lipoperoxides versus fetuses from control or glucose-fed mothers. Interestingly, a clearly augmented oxidative stress was observed in placenta of fructose-fed mothers, accompanied by a lower expression of the transcription factor Nuclear factor-erythroid 2-related factor-2 (Nrf2) and its target gene, heme oxygenase-1 (HO-1), a potent antioxidant molecule. Moreover, histone deacetylase 3 (HDAC3) that has been proposed to upregulate HO-1 expression by stabilizing Nrf2, exhibited a diminished expression in placenta of fructose-supplemented mothers. CONCLUSIONS: Maternal fructose intake provoked an imbalanced redox status in placenta and a clear diminution of HO-1 expression, which could be responsible for the augmented oxidative stress found in their fetuses.

Liquid fructose in pregnancy exacerbates fructose-induced dyslipidemia in adult female offspring.

Fructose intake from added sugars correlates with the epidemic rise in metabolic syndrome and related events. Nevertheless, consumption of beverages sweetened with fructose is not regulated in gestation. Previously, we found that maternal fructose intake produces in the progeny, when fetuses, impaired leptin signaling and hepatic steatosis and then impaired insulin signaling and hypoadiponectinemia in adult male rats. Interestingly, adult females from fructose-fed mothers did not exhibit any of these disturbances. However, we think that, actually, these animals keep a programmed phenotype hidden. Fed 240-day-old female progeny from control, fructose- and glucose-fed mothers were subjected for 3weeks to a fructose supplementation period (10% wt/vol in drinking water). Fructose intake provoked elevations in insulinemia and adiponectinemia in the female progeny independently of their maternal diet. In accordance, the hepatic mRNA levels of several insulin-responsive genes were similarly affected in the progeny after fructose intake. Interestingly, adult progeny of fructose-fed mothers displayed, in response to the fructose feeding, augmented plasma triglyceride and NEFA levels and hepatic steatosis versus the other two groups. In agreement, the expression and activity for carbohydrate response element binding protein (ChREBP), a lipogenic transcription factor, were higher after the fructose period in female descendants from fructose-fed mothers than in the other groups. Furthermore, liver fructokinase expression that has been indicated as one of those responsible for the deleterious effects of fructose ingestion was preferentially augmented in that group. Maternal fructose intake does influence the adult female offspring's response to liquid fructose and so exacerbates fructose-induced dyslipidemia and hepatic steatosis.

Fructose only in pregnancy provokes hyperinsulinemia, hypoadiponectinemia, and impaired insulin signaling in adult male, but not female, progeny.

PURPOSE: Fructose intake from added sugars correlates with the epidemic rise in metabolic syndrome and cardiovascular diseases. However, consumption of beverages containing fructose is allowed during gestation. Recently, we found that an intake of fructose (10 % wt/vol) throughout gestation produces impaired fetal leptin signaling and hepatic steatosis. Therefore, we have investigated whether fructose intake during pregnancy produces subsequent changes in the progeny, when adult. METHODS: Fed 261-day-old male and female descendants from fructose-fed, control or glucose-fed mothers were used. Plasma was used to analyze glucose, insulin, leptin, and adiponectin. Hepatic expression of proteins related to insulin signaling was determined. RESULTS: Fructose intake throughout pregnancy did not produce alterations in the body weight of the progeny. Adult male progeny of fructose-fed mothers had elevated levels of insulin without a parallel increase in phosphorylation of protein kinase B. However, they displayed an augmented serine phosphorylation of insulin receptor substrate-2, indicating reduced insulin signal transduction. In agreement, adiponectin levels, which have been positively related to insulin sensitivity, were lower in male descendants from fructose-fed mothers than in the other two groups. Furthermore, mRNA levels for insulin-responsive genes were not affected (phosphoenolpyruvate carboxykinase, glucose-6-phosphatase) or they were decreased (sterol response element-binding protein-1c) in the livers of male progeny from fructose-supplemented rats. On the contrary, adult female rats from fructose-fed mothers did not exhibit any of these disturbances. CONCLUSION: Maternal fructose, but not glucose, intake confined to the prenatal stage provokes impaired insulin signal transduction, hyperinsulinemia, and hypoadiponectinemia in adult male, but not female, progeny.

Maternal fructose intake induces insulin resistance and oxidative stress in male, but not female, offspring.

Objective. Fructose intake from added sugars correlates with the epidemic rise in metabolic syndrome and cardiovascular diseases. However, consumption of beverages containing fructose is allowed during gestation. Recently, we found that an intake of fructose (10% wt/vol) throughout gestation produces an impaired fetal leptin signalling. Therefore, we have investigated whether maternal fructose intake produces subsequent changes in their progeny. Methods. Blood samples from fed and 24 h fasted female and male 90-day-old rats born from fructose-fed, glucose-fed, or control mothers were used. Results. After fasting, HOMA-IR and ISI (estimates of insulin sensitivity) were worse in male descendents from fructose-fed mothers in comparison to the other two groups, and these findings were also accompanied by a higher leptinemia. Interestingly, plasma AOPP and uricemia (oxidative stress markers) were augmented in male rats from fructose-fed mothers compared to the animals from control or glucose-fed mothers. In contrast, female rats did not show any differences in leptinemia between the three groups. Further, insulin sensitivity was significantly improved in fasted female rats from carbohydrate-fed mothers. In addition, plasma AOPP levels tended to be diminished in female rats from carbohydrate-fed mothers. Conclusion. Maternal fructose intake induces insulin resistance, hyperleptinemia, and plasma oxidative stress in male, but not female, progeny.

[Reemergence of measles. Epidemic situation in the Valencian Community during the years 2011 and 2012]. / Reemergencia del sarampión. Situación epidémica en la Comunidad Valenciana durante los años 2011 y 2012.

Measles incidence declined until becomes a sporadic reporting and infrequent notification in the last decade. The reemergence of the disease reached 744 cases in 2012, a rate of 14.50×10(5) inhabitants. A classic design in Public Health Surveillance was performed: retrospective analysis of cumulative incidence and characteristics of the affected subjects. Those dates were in record linkage with Valencia Microbiology Network (RedMIVA). Finally, 976 cases of measles were confirmed in 2011-2012 epidemic period. Time-line distribution shows three waves with amplitude length on 12-15 weeks. Proportion of unvaccinated or unknown subjects came up to 85% of cases. 25 outbreaks were reported, 499 cases associated. In 7 of the 10 community outbreaks early cases were from Roma population unvaccinated. In the city of Valencia was applied post-exposure prophylaxis in 32 schools and was observed low coverage: between 63% and 77% in 8 schools and less than 50% in 4. Serum negative rate was 12.4% and we highlight the rate under 16 months: 44.8%. Cohorts of 20-59 years had negative rates between 13.5 to 5.9%. The origin of the epidemic was the importation of cases to a territory with inadequate immune protection against measles. Its impact and development was conditioned by previous immunization coverage, the social and ethnic pattern of different areas or quarters and the extensive application of post-exposure prophylaxis at school and family contacts of cases.

Reemergencia del sarampión. Situación epidémica en la Comunidad Valenciana durante los años 2011 y 2012 / Reemergence of measles. Epidemic situation in the Valencian Community during the years 2011 and 2012

La incidencia del sarampión descendió hasta llegar a ser una notificación esporádica e infrecuente en la última década. La reemergencia de la enfermedad alcanzó 744 casos en 2012, tasa de 14,50 × 105 habitantes. Se aplicó un diseño clásico en Vigilancia de Salud Pública: análisis retrospectivo de incidencia acumulada y características de los sujetos afectados. Se cruzaron los datos de encuesta con los de la Red Microbiológica Valenciana (RedMIVA). En total, 976 casos de sarampión fueron confirmados en el período epidémico 2011-2012. La distribución temporal muestra 3 ondas de amplitud constante: 12 a 15 semanas. La proporción de sujetos no vacunados y con estado vacunal desconocido alcanzó el 85% de los casos. Se documentaron 25 brotes, 499 casos asociados; en 7 de 10 brotes comunitarios, el inicio ocurrió en población de etnia gitana sin vacunar. En la ciudad de Valencia se aplicó profilaxis postexposición en 32 colegios, observándose bajas coberturas, entre el 63 y el 77%, en 8 centros e inferiores al 50% en 4. La tasa de serologías negativas fue del 12,4%, destacando los menores de 16 meses con el 44,8%. Las cohortes de 20 a 59 años presentaron tasas de negatividad del 13,5 al 5,9%. La epidemia tuvo su origen en la importación de casos a un territorio con insuficiente protección inmunitaria contra el sarampión. Su impacto y desarrollo estuvo condicionado por la cobertura vacunal previa, el patrón social y étnico de diferentes territorios y barrios, y la aplicación extensiva de profilaxis postexposición a contactos escolares y familiares de casos

Measles incidence declined until becomes a sporadic reporting and infrequent notification in the last decade. The reemergence of the disease reached 744 cases in 2012, a rate of 14.50 × 105 inhabitants. A classic design in Public Health Surveillance was performed: retrospective analysis of cumulative incidence and characteristics of the affected subjects. Those dates were in record linkage with Valencia Microbiology Network (RedMIVA). Finally, 976 cases of measles were confirmed in 2011-2012 epidemic period. Time-line distribution shows three waves with amplitude length on 12-15 weeks. Proportion of unvaccinated or unknown subjects came up to 85% of cases. 25 outbreaks were reported, 499 cases associated. In 7 of the 10 community outbreaks early cases were from Roma population unvaccinated. In the city of Valencia was applied post-exposure prophylaxis in 32 schools and was observed low coverage: between 63% and 77% in 8 schools and less than 50% in 4. Serum negative rate was 12.4% and we highlight the rate under 16 months: 44.8%. Cohorts of 20- 59 years had negative rates between 13.5 to 5.9%. The origin of the epidemic was the importation of cases to a territory with inadequate immune protection against measles. Its impact and development was conditioned by previous immunization coverage, the social and ethnic pattern of different areas or quarters and the extensive application of post-exposure prophylaxis at school and family contacts of cases

Reemergencia del sarampión. Situación epidémica en la Comunidad Valenciana durante los años 2011 y 2012 / Reemergence of measles. Epidemic situation in the Valencian Community during the years 2011 and 2012

La incidencia del sarampión descendió hasta llegar a ser una notificación esporádica e infrecuente en la última década. La reemergencia de la enfermedad alcanzó 744 casos en 2012, tasa de 14,50 × 105habitantes.Se aplicó un diseño clásico en Vigilancia de Salud Pública: análisis retrospectivo de incidencia acumulada y características de los sujetos afectados. Se cruzaron los datos de encuesta con los de la Red Microbiológica Valenciana (RedMIVA).En total, 976 casos de sarampión fueron confirmados en el período epidémico 2011-2012. La distribución temporal muestra 3 ondas de amplitud constante: 12 a 15 semanas. La proporción de sujetos no vacunados y con estado vacunal desconocido alcanzó el 85% de los casos. Se documentaron 25 brotes, 499 casos asociados; en 7 de 10 brotes comunitarios, el inicio ocurrió en población de etnia gitana sin vacunar. En la ciudad de Valencia se aplicó profilaxis postexposición en 32 colegios, observándose bajas coberturas, entre el 63 y el 77%, en 8 centros e inferiores al 50% en 4. La tasa de serologías negativas fue del 12,4%, destacando los menores de 16 meses con el 44,8%. Las cohortes de 20 a 59 años presentaron tasas de negatividad del 13,5 al 5,9%.La epidemia tuvo su origen en la importación de casos a un territorio con insuficiente protección inmunitaria contra el sarampión. Su impacto y desarrollo estuvo condicionado por la cobertura vacunal previa, el patrón social y étnico de diferentes territorios y barrios, y la aplicación extensiva de profilaxis postexposición a contactos escolares y familiares de casos (AU)

Measles incidence declined until becomes a sporadic reporting and infrequent notification in the last decade. The reemergence of the disease reached 744 cases in 2012, a rate of 14.50 × 105 inhabitants. A classic design in Public Health Surveillance was performed: retrospective analysis of cumulative incidence and characteristics of the affected subjects. Those dates were in record linkage with Valencia Microbiology Network (RedMIVA).Finally, 976 cases of measles were confirmed in 2011-2012 epidemic period. Time-line distribution shows three waves with amplitude length on 12-15 weeks. Proportion of unvaccinated or unknown subjects came up to 85% of cases. 25 outbreaks were reported, 499 cases associated. In 7 of the 10 community outbreaks early cases were from Roma population unvaccinated. In the city of Valencia was applied post-exposure prophylaxis in 32 schools and was observed low coverage: between 63% and 77% in 8 schools and less than 50% in 4. Serum negative rate was 12.4% and we highlight the rate under 16 months: 44.8%. Cohorts of 20-59 years had negative rates between 13.5 to 5.9%.The origin of the epidemic was the importation of cases to a territory with inadequate immune protection against measles. Its impact and development was conditioned by previous immunization coverage, the social and ethnic pattern of different areas or quarters and the extensive application of post-exposure prophylaxis at school and family contacts of cases (AU)