Search

Humans have greatly benefited from their relationship with donkeys. Different roles that donkeys play in high- and low-income countries are two sides of the same coin. Their draft power is indispensable in low-income countries, and by contrast, their milk in Europe is fetching a premium. New productive niches are controversially being explored, for example, donkey meat and skin (ejiao); both are considered premium products and have increased value of donkeys in many developing regions of the world. New advances in human medicine are starting to consider possibilities of donkey serum and heart valves. Scientists and channels that they use to spread their knowledge directly influence public interest and implementation of welfare practices in domestic species, indirectly affecting their survival. The study's aim was to trace historical registry of www.sciendirect.com directory from 1896 to 2018 to assess trends followed by articles dealing with donkeys. Publications with 22 themes and 114 publications (91 JCR indexed journals) from 56 countries were included. JCR impact index was scored to study influence of publications dealing with donkeys. Chi-square test tested six variables, randomly influenced by the rest. Cramer's V measured strength of association between variables. Statistically significant differences were observed between almost every combination of variables except for year and JCR impact, year and area/topic and country of the corresponding author, and area/topic of submission. JCR impact and journal influences the area of the articles that are published. As some countries are more specialized in certain themes concerning donkey-related sciences, they are more likely to publish.

Juan-Antonio Riesco-Miranda,1,2 Segismundo Solano-Reina,3 Carlos Rábade-Castedo,4 José-Ignacio de Granda-Orive,5 Esther Pastor-Esplá,6 Marcos García-Rueda,7 Francisco-Javier Callejas-Gonzalez,8 Ángel Azpeitia-Anadón,9 Silvia Mas,10 Carlos-Andrés Jiménez-Ruiz11 1Servicio de Neumología, Hospital Universitario de Cáceres, Cáceres, Spain; 2CIBERES, Madrid, Spain; 3Servicio de Neumología, Hospital General Universitario Gregorio Marañón, Madrid, Spain; 4Servicio de Neumología, Hospital Clínico Universitario de Santiago de Compostela, Santiago de Compostela, Spain; 5Servicio de Neumología, Hospital Universitario Doce de Octubre, Universidad Complutense de Madrid, Madrid, Spain; 6Servicio de Neumología, Hospital Universitario San Juan de Alicante, Alicante, Spain; 7Servicio de Neumología, Hospital Universitario Carlos Haya, Málaga, Spain; 8Servicio de Neumología, Complejo Hospitalario Universitario de Albacete, Albacete, Spain; 9Departamento Médico Labs, Esteve S.A, Barcelona, Spain; 10Universidad Pompeu Fabra, Barcelona, Spain; 11Unidad Especializada de Tabaquismo, Hospital Clínico Universitario, Madrid, SpainCorrespondence: Silvia MasUniversitat Pompeu Fabra, Campus Poble Nou, Roc Boronat 138, Barcelona, 08018, SpainEmail silviamas.md@gmail.comPurpose: Smokers attending smoking cessation units (SCUs) may offer a unique opportunity for early recognition of undiagnosed chronic obstructive pulmonary disease (COPD). We aimed at assessing the impact of SCUs on the early diagnosis of COPD and describing the clinical and smoking profile of newly-diagnosed COPD cases at SCUs certified by the Spanish Society of Respiratory Diseases and Thoracic Surgery (SEPAR).Patients and Methods: A multicenter cross-sectional observational cohort study (DIPREPOQ study) was performed in eight SEPAR-certified SCUs in Spain. Adult current smokers with no previously diagnosed respiratory disease and having one o more respiratory symptoms were included. Lung functional tests were performed and previously undiagnosed COPD cases were identified and characterized based on national guidelines.Results: Out of 401 individuals newly attending the SCUs, 252 participants were included and 73 (28.9%) met the definition of previously undiagnosed COPD. A characterization of patients with COPD being newly recognized in SCUs showed: age (mean±SD) 61± 9 years; men 59%; active work status 53.1%; functional class I/II dyspnea 82.8%, GOLD state mild/moderate/severe 57%/31%/12%; non-exacerbators 90%, CAT 14± 4; emphysema in X-rays 40%. Most common co-morbidities were cardiovascular and psychiatric (anxiety and depression) ones. Usual smoking history included a lengthy smoking history (41± 9 years) and a current consumption of 24± 9 cigarettes/day.Conclusions and Implications: Consistently certified SCUs can have a substantial contribution to early diagnosis of COPD. A typical profile of newly detected cases is reported, with most patients being men at their early sixties, with mild symptoms and with high and lengthy smoking history. Our study reports a high usefulness of lung functional tests to detect undiagnosed COPD in appropriately selected participants attending SCUs at a large national scale, using a standardized methodology. This is likely to be facilitated by the certification of SCUs using well-defined requirements by national scientific societies.Keywords: health consequences, smoking, chronic obstructive pulmonary disease, smoking cessation unit

Bernardino Alcazar-Navarrete,1,2 Antonia Fuster,3 Patricia García Sidro,4 Juan Luis García Rivero,5 Beatriz Abascal-Bolado,6 Abel Pallarés-Sanmartín,7 Eduardo Márquez,2,8 Agustin Valido-Morales,9 Ana Boldova Loscertales,10 Francisco Javier Callejas-Gonzalez,11 Marta Palop,12 Juan Antonio Riesco,2,13 Rafael Golpe,14 Juan Jose Soler-Cataluña,2,15 Marc Miravitlles2,16 1AIG De Medicina. Hospital De Alta Resolución De Loja. Agencia Sanitaria Hospital De Poniente, Loja, Granada, Spain; 2CIBERES. Instituto De Salud Carlos III, Madrid, Spain; 3Servicio De Neumología. Hospital Universitario De Son Llatzer, Palma De Mallorca, Spain; 4Servicio De Neumología. Hospital De La Plana, Castellón, Spain; 5Servicio De Neumología. Hospital De Laredo, Laredo, Spain; 6Servicio De Neumología. Hospital Universitario Marqués De Valdecilla, Santander, Spain; 7Servicio De Neumología. Hospital Universitario Alvaro Cunqueiro, Vigo, Spain; 8Unidad Médico-Quirúrgica De Enfermedades Respiratorias. Hospital Virgen Del Rocío, Sevilla, Spain; 9UGC De Neumología. HU Virgen Macarena, Sevilla, Spain; 10Servicio De Neumología. Hospital Royo Villanova, Zaragoza, Spain; 11Servicio De Neumología. Complejo Hospitalario Universitario De Albacete, Albacete, Spain; 12Servicio De Neumología. Hospital De Sagunto, Sagunto, Spain; 13Servicio De Neumología. Hospital San Pedro De Alcántara, Cáceres, Spain; 14Servicio De Neumología. Hospital Universitario Lucus Augusti, Lugo, Spain; 15Servicio De Neumología. Hospital Arnau De Villanova- Lliria, Valencia, Spain; 16Servicio De Neumología. Hospital Universitari Vall De Hebron/Vall d’Hebron Institut De Recerca, Barcelona, SpainCorrespondence: Bernardino Alcazar-NavarreteHospital De Alta Resolución De Loja. Agencia Sanitaria Hospital De Poniente. Avda Tierno Galván s/n, Loja 18300, Granada, SpainEmail balcazar@telefonica.netBackground: The concept of clinical control has been proposed as an instrument for evaluating patients with COPD. However, the possible association between clinical control, reduced symptom severity and HRQoL has yet to be confirmed.Methods: This multicentre, prospective and observational study was carried out in 15 pulmonology clinics in Spain. The patients were followed up for six months, with a baseline visit (V0), followed by visits at three months (V1) and six months (V2). Clinical control was determined at V1, with the application of both clinical criteria and the COPD assessment test (CAT). All patients reported their symptoms by a validated symptom diary (E-RS) using a portable device, and their HRQoL was assessed using the EQ5D questionnaire. The relationship between clinical control and E-RS and HRQoL during follow-up was assessed with t-test.Results: A total of 126 patients were screened. After application of the inclusion/exclusion criteria, 93 were finally included (mean age 66 ± 8 years, 84.9% male), with a mean FEV1 predicted of 49.8% ± 16.5%. Of these patients, 44 (47.3%) achieved clinical control at V1, according to CAT criteria, and 50 (53.8%), according to clinical criteria. The E-RS scores differed between controlled and uncontrolled patients at all time points, both according to CAT (mean differences of − 4.6, − 5.6 and − 6.2 units at V0, V1 and V2, respectively, p< 0.005 for all comparisons) and to clinical criteria (mean differences of − 3.3, − 5-6 and − 4.99 units, respectively, p< 0.005 for all comparisons). The controlled patients also presented a significantly better HRQoL, measured by the EQ5D questionnaire (mean difference 0.13 and 0.10 at V2 by CAT or clinical criteria, respectively, p< 0.05).Conclusion: Clinical control in patients with COPD, whether measured by CAT or by clinical criteria, is associated with a lower symptom load and a better HRQoL.Keywords: control, symptoms, quality of life, impact, COPD

Introduction: Residual pleural cavities are pleural spaces caused by a lack of pulmonary reexpansion mainly secondary to pleural infections or thoracic surgeries. If they can not be solved with first line treatments (thoracic drainage, fibrinolytics or surgical decortication), these can become cronic and complicate. Material and Methods: Retrospective descriptive study of patients with complicated residual pleural cavities at the Thoracic Surgery Service of the “Complejo Hospitalario Universitario de Albacete” from November 2004 to May 2015. Results: Sixty-three patients were diagnosed, showing that incidence was more frequent in men (n=57; 90.5%). 16.27% of the surgeries treated within this period were secondary to this pathology. The infectious pathology was the most frequent (n = 35; 55.6%), whereas within the postoperative group, it was pneumonectomy (n = 8; 42.1%), with 190.7 days in average from surgical intervention to the diagnosis. In 43 patients (68.3%), the pleural fluid culture was positive. In 17 patients (27%), it was associated with a bronchopleural fistula. From the 63 patients, 16 (25.4%) received a single surgical treatment (25.4%), while 47 (74.6%) required more than one treatment. In 39 cases (61.9%), the complicated pleural cavity was resolved, whereas in 24 (38.1%) patients it wasn’t. Conclusions: Despite it being a rare pathology, it is still present today, mainly as a post-surgical or infectious complication. To date, the treatments described haven’t exhibited high efficacy.

Type 2 diabetes mellitus is associated with alterations in bile acid (BA) signaling. The aim of our study was to test whether pancreatic β-cells contribute to BA-dependent regulation of glucose homeostasis. Experiments were performed with islets from wild-type, farnesoid X receptor (FXR) knockout (KO), and β-cell ATP-dependent K(+) (K(ATP)) channel gene SUR1 (ABCC8) KO mice, respectively. Sodium taurochenodeoxycholate (TCDC) increased glucose-induced insulin secretion. This effect was mimicked by the FXR agonist GW4064 and suppressed by the FXR antagonist guggulsterone. TCDC and GW4064 stimulated the electrical activity of β-cells and enhanced cytosolic Ca(2+) concentration ([Ca(2+)](c)). These effects were blunted by guggulsterone. Sodium ursodeoxycholate, which has a much lower affinity to FXR than TCDC, had no effect on [Ca(2+)](c) and insulin secretion. FXR activation by TCDC is suggested to inhibit K(ATP) current. The decline in K(ATP) channel activity by TCDC was only observed in β-cells with intact metabolism and was reversed by guggulsterone. TCDC did not alter insulin secretion in islets of SUR1-KO or FXR-KO mice. TCDC did not change islet cell apoptosis. This is the first study showing an acute action of BA on β-cell function. The effect is mediated by FXR by nongenomic elements, suggesting a novel link between FXR activation and K(ATP) channel inhibition. [ABSTRACT FROM AUTHOR]

Emerging evidence suggests that the lack of PPARα enhances hepatic steatosis and inflammation in Ppara-null mice when fed a high-fat diet (HFD). Thus, the aim of this study was to determine whether Ppara-null mice are more susceptible to nonalcoholic steatohepatitis (NASH) than their wild-type (WT) counterparts following short-term feeding with a HFD. Age-matched male WT and Ppara-null mice were randomly assigned to consume ad libitum a standard Lieber-DeCarli liquid diet (STD) (35% energy from fat) or a HFD (71% energy from fat) for 3 wk. Liver histology, plasma transaminase levels, and indicators of oxidative/nitrosative stress and inflammatory cytokines were evaluated in all groups. Levels of lobular inflammation and the NASH activity score were greater in HFD-exposed Ppara-null mice than in the other 3 groups. Biochemical analysis revealed elevated levels of ethanol-inducible cytochrome P450 2E1 and TNFα accompanied by increased levels of malondialdehyde as well as oxidized and nitrated proteins in Ppara-null mice. Elevated oxidative stress and inflammation were associated with activation of c-Jun-N-terminal kinase and p38 kinase, resulting in increased hepatocyte apoptosis in Ppara-null mice fed a HFD. These results, with increased steatosis, oxidative stress, and inflammation observed in Ppara-null mice fed a HFD, demonstrate that inhibition of PPARα functions may increase susceptibility to high fat-induced NASH. [ABSTRACT FROM AUTHOR]

Background: The modulation of energetic homeostasis by pollutants has recently emerged as a potential contributor to the onset of metabolic disorders. Diethylhexyl phthalate (DEHP) is a widely used industrial plasticizer to which humans are widely exposed. Phthalates can activate the three peroxisome proliferator-activated receptor (PPAR) isotypes on cellular models and induce peroxisome proliferation in rodents. Objectives: In this study, we aimed to evaluate the systemic and metabolic consequences of DEHP exposure that have remained so far unexplored and to characterize the underlying molecular mechanisms of action. Methods: As a proof of concept and mechanism, genetically engineered mouse models of PPARs were exposed to high doses of DEHP, followed by metabolic and molecular analyses. Results: DEHP-treated mice were protected from diet-induced obesity via PPAR[alpha]-dependent activation of hepatic fatty acid catabolism, whereas the activity of neither PPAR[beta] nor PPAR[gamma] was affected. However, the lean phenotype observed in response to DEHP in wild-type mice was surprisingly abolished in PPAR[alpha]-humanized mice. These species differences are associated with a different pattern of coregulator recruitment. Conclusion: These results demonstrate that DEHP exerts species-specific metabolic actions that rely to a large extent on PPARa signaling and highlight the metabolic importance of the species-specific activation of PPARa by xenobiotic compounds. [ABSTRACT FROM AUTHOR]

The mechanisms underlying peroxisome proliferator-induced hepatocarcinogenesis are unclear but are mediated by the peroxisome proliferator-activated receptor α (PPARα). To determine the role of PPARα in the mechanisms of hepatocarcinogenesis, the effect of Wy-14,643 on expression patterns of acyl CoA oxidase (ACO) and proteins involved in cell proliferation in the PPARα-null mouse were evaluated. ACO, CDK-1, CDK-2, CDK-4, PCNA and c-myc proteins were significantly increased in wild-type mice fed Wy-14,643 for 5 weeks or 11 months, as compared with controls. This effect was not observed in Wy-14,643-treated PPARα-null mice. Expression patterns of cyclin B1, cyclin D, cyclin E and p53 were not different in any of the groups. mRNAs encoding CDK-1, CDK-4, cyclin D1 and c-myc were also increased in wild-type mice fed Wy-14,643 but not in PPARα-null mice. These results indicate that the increase in CDK-1, CDK-4 and c-myc may be caused by an increase in transcription that is mediated directly or indirectly by PPARα. Thus PPARα-dependent alterations in cell cycle regulatory proteins induced by peroxisome proliferators are likely to contribute to the hepatocarcinogenicity of peroxisome proliferators. [ABSTRACT FROM PUBLISHER]

Latino men who have sex with other men are disproportionately affected by AIDS/HIV. We describe sociodemographic and psychosocial characteristics of a probability sample of 744 unmarried Latino men, comparing men reporting at least one sexual encounter with another man (MSM; 5.5% of sample) with men reporting sex exclusively with women (MSW) or reporting they were not sexually active (NSA). MSM were significantly older, more acculturated, and more educated than others. MSM were more comfortable with sexuality and reported over twice as many sexual partners in the previous year as MSW. MSM always used condoms with 83% of their multiple partners, compared to 50% of MSW Homophobia and sexual discomfort among MSM may decrease self-efficacy to use condoms. [ABSTRACT FROM AUTHOR]

Our previous studies have shown that 2,3-epoxy-4-hydroxynonanal, a reactive epoxy aldehyde capable of forming etheno adducts with DNA bases, is mutagenic and tumorigenic (Carcinogenesis, 14, 2073). The epoxy aldehyde can be generated from trans-4-hydroxy-2-nonenal, a lipid peroxidation product of ω-6 polyunsaturated fatty acids, by autoxidation or by incubation with fatty acid hydroperoxides or hydrogen peroxides (Chem. Res. Toxicol., 9, 306). These are plausible in vivo pathways for the formation of 2,3-epoxy-4-hydroxynonanal. The possibility that 2,3-epoxy-4-hydroxynonanal is a tumorigen of endogenous oritin is suggested by recent observations that etheno bases are detected as background DNA lesions in untreated rodents and humans. A metabolic pathway critical for detoxification of 2,3-epoxy-4-hydroxynonanal involves the ring-opening by epoxide hydrolase, which abolishes its ability to form cyclic etheno DNA adducts. In this study we examined whether 2,3-epoxy-4-hydroxynonanal is a substrate of cDNA expressed human epoxide hydrolase. Human epoxide hydrolase was expressed in TK- 143 cells (thymidine kinase-deficient human embryoblast) infected with recombinant vaccinia virus encoding human epoxide hydrolase cDNA. Controls consisted of the cells infected with vaccinia virus in the absence of human epoxide hydrolase cDNA. No hydrolysis occurred when [2,3-3H]2,3-epoxy-4-hydroxynonanal was incubated at 37°C for 30 min at pH 7.4 with cells expressing human epoxide hydrolase as indicated by the presence of a pair of radioactive peaks in reverse-phase HPLC chromatography, which comigrated with the UV standards of the two diastereomers of the epoxy aldehyde. The identity of these compounds as the intact epoxy aldehyde was further supported by derivatization to the 2,4-dinitrophenylhydrazones followed by reversed phase HPLC analysis. Similar results were observed with the control cells or with the heat deactivated human epoxide hydrolase. The epoxide hydrolase activity in the expressed cells was demonstrated by their ability to convert benzo[a]pyrene-4,5-dihydroepoxide to benzo[a]pyrene-trans-4,5-dihydrodiol under the same conditions. These results clearly indicate that 2,3-epoxy-4-hydroxynonanal is not a substrate of human epoxide hydrolase, and, thus strengthen its possible endogenous role in the formation of promutagenic exocyclic etheno adducts in vivo. [ABSTRACT FROM PUBLISHER]

The effects of ligand activation of PPARbeta/delta were examined in the mouse mammary tumor cell line (C20). Expression of PPARbeta/delta was markedly lower in C20 cells as compared to the human non-tumorigenic mammary gland derived cell line (MCF10A) and mouse keratinocytes. Ligand activation of PPARbeta/delta in C20 cells caused upregulation of the PPARbeta/delta target gene angiopoietin-like 4 (Angptl4). Inhibition of C20 cell proliferation and clonogenicity was observed following treatment with GW0742 or GW501516, two highly specific PPARbeta/delta ligands. In addition, an increase in apoptosis was observed in C20 cells cultured with 10microM GW501516 that preceded the observed inhibition of cell proliferation. Results from this study show that proliferation of the C20 mouse mammary gland cancer cell line is inhibited by ligand activation of PPARbeta/delta due in part to increased apoptosis. [ABSTRACT FROM AUTHOR]