Beneficial bacteria stimulate host immune cells to counteract dietary and genetic predisposition to mammary cancer in mice

Recent studies suggest health benefits including protection from cancer after eating fermented foods such as probiotic yogurt, though the mechanisms are not well understood. Here we tested mechanistic hypotheses using two different animal models: the first model studied development of mammary cancer when eating a Westernized diet, and the second studied animals with a genetic predilection to breast cancer. For the first model, outbred Swiss mice were fed a Westernized chow putting them at increased risk for development of mammary tumors. In this Westernized diet model, mammary carcinogenesis was inhibited by routine exposure to Lactobacillus reuteri ATCC-PTA-6475 in drinking water. The second model was FVB strain erbB2 (HER2) mutant mice, genetically susceptible to mammary tumors mimicking breast cancers in humans, being fed a regular (non-Westernized) chow diet. We found that oral supplement with these purified lactic acid bacteria alone was sufficient to inhibit features of mammary neoplasia in both models. The protective mechanism was determined to be microbially-triggered CD4+CD25+ lymphocytes. When isolated and transplanted into other subjects, these L. reuteri-stimulated lymphocytes were sufficient to convey transplantable anti-cancer protection in the cell recipient animals. These data demonstrate that host immune responses to environmental microbes significantly impact and inhibit cancer progression in distal tissues such as mammary glands, even in genetically susceptible mice. This leads us to conclude that consuming fermentative microbes such as L. reuteri may offer a tractable public health approach to help counteract the accumulated dietary and genetic carcinogenic events integral in the Westernized diet and lifestyle.National Institutes of Health (U.S.) (Grant P30-ES002109)National Institutes of Health (U.S.) (Grant RO1CA108854)National Institutes of Health (U.S.) (Grant U01 CA164337

Dietary Microbes Modulate Transgenerational Cancer Risk

Environmental factors are suspected in the increase of obesity and cancer in industrialized countries but are poorly understood. Here, we used animal models to test how future generations may be affected by Westernized diets. We discover long-term consequences of grandmothers' in utero dietary exposures, leading to high rates of obesity and frequent cancers of lung and liver in two subsequent generations of mice. Transgenerational effects were transplantable using diet-associated bacteria communities alone. Consequently, feeding of beneficial microbes was sufficient to lower transgenerational risk for cancer and obesity regardless of diet history. Targeting microbes may be a highly effective population-based approach to lower risk for cancer.National Institutes of Health (U.S.) (RO1CA108854)National Institutes of Health (U.S.) (U01 CA164337)National Institutes of Health (U.S.) (P30-ES002109

Gut bacteria require neutrophils to promote mammary tumorigenesis

Recent studies suggest that gastrointestinal tract microbiota modulate cancer development in distant non-intestinal tissues. Here we tested mechanistic hypotheses using a targeted pathogenic gut microbial infection animal model with a predilection to breast cancer. FVB-Tg(C3-1-TAg)cJeg/JegJ female mice were infected by gastric gavage with Helicobacter hepaticus at three-months-of-age putting them at increased risk for mammary tumor development. Tumorigenesis was multifocal and characterized by extensive infiltrates of myeloperoxidase-positive neutrophils otherwise implicated in cancer progression in humans and animal models. To test whether neutrophils were important in etiopathogenesis in this bacteria-triggered model system, we next systemically depleted mice of neutrophils using thrice weekly intraperitoneal injections with anti-Ly-6G antibody. We found that antibody depletion entirely inhibited tumor development in this H. hepaticus-infected model. These data demonstrate that host neutrophil-associated immune responses to intestinal tract microbes significantly impact cancer progression in distal tissues such as mammary glands, and identify gut microbes as novel targets for extra-intestinal cancer therapy.National Institutes of Health (U.S.) (Grant U01 CA164337)National Institutes of Health (U.S.) (Grant T32 OD011141

MIOCARDIOPATÍA POR VENTRÍCULO NO COMPACTADO. ACERCA DE EVOLUCIÓN HISTÓRICA, DEFINICIONES Y GENERALIDADES DEL TEMA.

Nota: La modalidad de Artículo de revisión suele eximirse de la confección de resumen, según las Normas de Publicación de la Revista Cubana de Cardiología y Cirugía Cardiovascular

Miocardiopatía por Ventrículo no compactado. Acerca de su asociación a otras entidades extracardiacas, alternativas terapéuticas, factores pronósticos.

La Miocardiopatía por ventrículo no compactado (MVNC) considerada actualmente una mitocondriopatía, está asociada, en la mayoría de los casos, con una enfermedad del músculo cardiaco o esquelético hereditaria o con anomalías cromosómicas. En dependencia del estudio, más de dos tercios de los pacientes con MVNC también presentan una enfermedad neuromuscular (ENM). Una relación causal entre las ENM y la MVNC es probable, aunque la relación exacta y la asociación patonogmónica permanecen esquivas

Ventricular Cardiomyopathy not compact. About the diagnosis, complementary examinations and diagnostic errors.

La miocardiopatía no compactada (MVNC) es una entidad primaria de origen genético, caracterizada por anomalías en la morfología de la pared ventricular, provocada aparentemente por una alteración en la morfogénesis endomiocárdica durante el desarrollo embrionario, evidenciándose la presencia y persistencia de trabeculaciones acompañadas de recesos intertrabeculares que son perfundidos desde la cavidad ventricular, estos espacios lacunares intertrabeculares no tienen conexión con el árbol coronario. Su pronóstico está determinado por el grado de disfunción ventricular izquierda, la gravedad de las arritmias emergentes y por la ocurrencia de eventos tromboembólicos, síntomas estos que caracterizan la clínica de esta entidad. Los criterios diagnósticos validados incluyen los aportes del ecocardiograma, la resonancia magnética y se suma actualmente la tomografía axial computarizada. Existen entidades cardiacas que aunque comparten algunas características morfológicas de la estructura miocárdica, no cumplen con todos los criterios diagnósticos de la misma.La non-compaction cardiomyopathie (MVNC) est une entité génétique primaire caractérisée par des anomalies dans la morphologie de la paroi ventriculaire, apparemment causée par une perturbation dans la morphogenèse endomyocardique cours du développement embryonnaire, ce qui démontre la présence et la persistance de trabéculations accompagné par des évidements intertrabéculaires qui sont perfusé de la cavité ventriculaire, ces espaces lacunaires intertrabéculaires ont aucun lien avec l'arbre coronarien. Son pronostic vital est déterminé par le degré de dysfonction ventriculaire gauche, la gravité des arythmies et la survenue d'événements thromboemboliques émergents, tels symptômes qui caractérisent cette entité clinique. Critères diagnostiques validés comprennent les contributions de échocardiogramme, résonance magnétique et totalise actuellement tomodensitométrie. Il existe des entités de cœur, mais partagent certaines caractéristiques morphologiques de la structure du myocarde, ne répondent pas à tous les critères de diagnostic pour elle.A cardiomiopatia não compactada (mVNC) é uma entidade genética primária caracterizada por anormalidades na morfologia da parede ventricular, aparentemente, causada por um distúrbio na morfogénese endomyocardial durante o desenvolvimento embrionário, demonstrando a presença e persistência de trabéculas acompanhada por recessos intertrabecular que são perfundidos a partir da cavidade ventricular, esses espaços lacunares intertrabecular têm nenhuma conexão com a árvore coronariana. Sua prognóstico é determinada pelo grau de disfunção ventricular esquerda, arritmias e gravidade da ocorrência de acontecimentos tromboembólicos emergentes, tais sintomas que caracterizam esta entidade clínica. Critérios de diagnóstico validados incluem as contribuições de ecocardiograma, ressonância magnética e, atualmente, totaliza tomografia computadorizada. Há entidades cardíacos, mas compartilham algumas características morfológicas da estrutura do miocárdio, não preenchem todos os critérios diagnósticos para ele.The non-compaction cardiomyopathy (MVNC) is a primary genetic entity characterized by abnormalities in the morphology of the ventricular wall, apparently caused by a disturbance in endomyocardial morphogenesis during embryonic development, demonstrating the presence and persistence of trabeculations accompanied by recesses intertrabecular that are perfused from the ventricular cavity, these spaces lacunar intertrabecular have no connection to the coronary tree. His prognosis is determined by the degree of left ventricular dysfunction, severity of arrhythmias and emerging occurrence of thromboembolic events, such symptoms that characterize this clinical entity. Validated diagnostic criteria include the contributions of echocardiogram, magnetic resonance and currently totals computed tomography. There are heart entities but share some morphological characteristics of myocardial structure, do not meet all the diagnostic criteria for it

Ventricular Cardiomyopathy not compact. About his association with other extracardiac entities, alternative therapies and prognostic factors

La hipertrabeculación/no-compactación del ventrículo izquierdo (LVHT) está asociada, en la mayoría de los casos, con una enfermedad del músculo cardiaco o esquelético hereditaria o con anomalías cromosómicas. En dependencia del estudio, más de dos tercios de los pacientes con LVHT también presentan una enfermedad neuromuscular (NMD). Las NMD asociadas con LVHT con mayor frecuencia son el syndrome de Barth, las enfermedades mitocondriales, zaspopatía, y las distrofias miotónicas. Las NMD que solo están presentes con la LVHT ocasionalmente son la distrobrevinopatía, laminopatías, distrofinopatías, deficiencia de miodelinato de aminasa, miositis corporal de inclusión hereditaria, y la neuropatía CMT1A. Una relación causal entre las NMD y la LVHT es probable, aunque la relación exacta y la asociación patomecánica permanecen esquivas. La relación patogénica cercana está apoyada por el hecho que el fenómeno de LVHT adquirida ocurre predominantemente en las NMD. Una remisión consecuente de los pacientes con LVHT al neurólogo, la remisión consecuente de los pacientes con NMD al cardiólogo, e investigaciones familiares pueden ayudar a clarificar asuntos no resueltos aún concernientes a la patogénesis, el curso y el pronóstico de la LVHT.Hipertrabeculação / não-compactação do ventrículo esquerdo (LVHT) está associada, na maioria dos casos, uma doença do coração ou anomalias cromossómicas ou músculo esquelético hereditárias. Dependendo do estudo, mais de dois terços das pacientes com LVHT também têm uma doença neuromuscular (NMD). O LVHT NMD associado com mais frequência são a síndrome de Barth, doenças mitocondriais, zaspopatía, e distrofia miotônica. O NMD que só estão presentes com LVHT são ocasionalmente distrobrevinopatía, laminopatias, distrofinopatias, miodelinato de deficiência deaminase, hereditária miosite de corpos de inclusão, e CMT1A neuropatia. A relação causal entre NMD e LVHT é provável, mas a relação de parceria e exatas pathomechanics ainda imperceptíveis. A relação próxima patogênico é apoiada pelo fato de que o fenômeno da LVHT adquirida ocorre predominantemente na NMD. Uma referência consistente de pacientes com LVHT o neurologista, o posterior encaminhamento de pacientes com cardiologista NMD, e pesquisa da família pode ajudar a esclarecer questões ainda não resolvidas relativas a patogênese, curso e prognóstico da LVHT.Hypertrabeculation / non-compaction du ventricule gauche (LVHT) est associé, dans la plupart des cas, une maladie du cœur ou squelettiques anomalies chromosomiques héréditaires ou musculaire. Selon l'étude, plus de deux tiers des patients atteints LVHT ont aussi une maladie neuromusculaire (NMD). Le LVHT NMD associé avec le plus fréquemment sont les syndrome de Barth, les maladies mitochondriales, zaspopatía, et la dystrophie myotonique. Le NMD qui ne sont présents avec LVHT sont occasionnellement distrobrevinopatía, laminopathies, dystrophinopathies, miodelinato de la carence en désaminase, héréditaire myosite à corps d'inclusion, et CMT1A neuropathie. Une relation causale entre la NMD et LVHT est probable, mais la relation et de partenariat exactes pathomécanique reste insaisissable. La relation proche pathogène est étayée par le fait que le phénomène de LVHT acquis se produit principalement dans le NMD. Un renvoi cohérente des patients atteints de LVHT le neurologue, le renvoi ultérieur des patients atteints de cardiologue NMD, et la recherche de la famille peut aider à clarifier les questions encore en suspens concernant la pathogénèse, le déroulement et le pronostic de LVHT.Hypertrabeculation / non-compaction of the left ventricle (LVHT) is associated, in most cases, a disease of the heart or skeletal hereditary chromosomal abnormalities or muscle. Depending on the study, more than two thirds of patients with LVHT also have a neuromuscular disease (NMD). The NMD LVHT associated with most frequently are the Barth syndrome, mitochondrial diseases, zaspopatía, and myotonic dystrophy. The NMD that are only present with LVHT are occasionally distrobrevinopatía, laminopathies, dystrophinopathies, miodelinato of deaminase deficiency, hereditary inclusion body myositis, and CMT1A neuropathy. A causal relationship between NMD and LVHT is likely, but the exact relationship and partnership pathomechanics remain elusive. The nearby pathogenic relationship is supported by the fact that the phenomenon of acquired LVHT occurs predominantly in the NMD. A consistent referral of patients with LVHT the neurologist, the subsequent referral of patients with NMD cardiologist, and family research can help clarify matters still unresolved concerning the pathogenesis, course and prognosis of LVHT

Miocardiopatía por Ventrículo no compactado. Acerca de su asociación a otras entidades extracardiacas, alternativas terapéuticas, factores pronósticos.

La Miocardiopatía por ventrículo no compactado (MVNC) considerada actualmente una mitocondriopatía, está asociada, en la mayoría de los casos, con una enfermedad del músculo cardiaco o esquelético hereditaria o con anomalías cromosómicas. En dependencia del estudio, más de dos tercios de los pacientes con MVNC también presentan una enfermedad neuromuscular (ENM). Una relación causal entre las ENM y la MVNC es probable, aunque la relación exacta y la asociación patonogmónica permanecen esquivas

Ventricular Cardiomyopathy not compact. About his association with other extracardiac entities, alternative therapies and prognostic factors

La hipertrabeculación/no-compactación del ventrículo izquierdo (LVHT) está asociada, en la mayoría de los casos, con una enfermedad del músculo cardiaco o esquelético hereditaria o con anomalías cromosómicas. En dependencia del estudio, más de dos tercios de los pacientes con LVHT también presentan una enfermedad neuromuscular (NMD). Las NMD asociadas con LVHT con mayor frecuencia son el syndrome de Barth, las enfermedades mitocondriales, zaspopatía, y las distrofias miotónicas. Las NMD que solo están presentes con la LVHT ocasionalmente son la distrobrevinopatía, laminopatías, distrofinopatías, deficiencia de miodelinato de aminasa, miositis corporal de inclusión hereditaria, y la neuropatía CMT1A. Una relación causal entre las NMD y la LVHT es probable, aunque la relación exacta y la asociación patomecánica permanecen esquivas. La relación patogénica cercana está apoyada por el hecho que el fenómeno de LVHT adquirida ocurre predominantemente en las NMD. Una remisión consecuente de los pacientes con LVHT al neurólogo, la remisión consecuente de los pacientes con NMD al cardiólogo, e investigaciones familiares pueden ayudar a clarificar asuntos no resueltos aún concernientes a la patogénesis, el curso y el pronóstico de la LVHT.Hipertrabeculação / não-compactação do ventrículo esquerdo (LVHT) está associada, na maioria dos casos, uma doença do coração ou anomalias cromossómicas ou músculo esquelético hereditárias. Dependendo do estudo, mais de dois terços das pacientes com LVHT também têm uma doença neuromuscular (NMD). O LVHT NMD associado com mais frequência são a síndrome de Barth, doenças mitocondriais, zaspopatía, e distrofia miotônica. O NMD que só estão presentes com LVHT são ocasionalmente distrobrevinopatía, laminopatias, distrofinopatias, miodelinato de deficiência deaminase, hereditária miosite de corpos de inclusão, e CMT1A neuropatia. A relação causal entre NMD e LVHT é provável, mas a relação de parceria e exatas pathomechanics ainda imperceptíveis. A relação próxima patogênico é apoiada pelo fato de que o fenômeno da LVHT adquirida ocorre predominantemente na NMD. Uma referência consistente de pacientes com LVHT o neurologista, o posterior encaminhamento de pacientes com cardiologista NMD, e pesquisa da família pode ajudar a esclarecer questões ainda não resolvidas relativas a patogênese, curso e prognóstico da LVHT.Hypertrabeculation / non-compaction du ventricule gauche (LVHT) est associé, dans la plupart des cas, une maladie du cœur ou squelettiques anomalies chromosomiques héréditaires ou musculaire. Selon l'étude, plus de deux tiers des patients atteints LVHT ont aussi une maladie neuromusculaire (NMD). Le LVHT NMD associé avec le plus fréquemment sont les syndrome de Barth, les maladies mitochondriales, zaspopatía, et la dystrophie myotonique. Le NMD qui ne sont présents avec LVHT sont occasionnellement distrobrevinopatía, laminopathies, dystrophinopathies, miodelinato de la carence en désaminase, héréditaire myosite à corps d'inclusion, et CMT1A neuropathie. Une relation causale entre la NMD et LVHT est probable, mais la relation et de partenariat exactes pathomécanique reste insaisissable. La relation proche pathogène est étayée par le fait que le phénomène de LVHT acquis se produit principalement dans le NMD. Un renvoi cohérente des patients atteints de LVHT le neurologue, le renvoi ultérieur des patients atteints de cardiologue NMD, et la recherche de la famille peut aider à clarifier les questions encore en suspens concernant la pathogénèse, le déroulement et le pronostic de LVHT.Hypertrabeculation / non-compaction of the left ventricle (LVHT) is associated, in most cases, a disease of the heart or skeletal hereditary chromosomal abnormalities or muscle. Depending on the study, more than two thirds of patients with LVHT also have a neuromuscular disease (NMD). The NMD LVHT associated with most frequently are the Barth syndrome, mitochondrial diseases, zaspopatía, and myotonic dystrophy. The NMD that are only present with LVHT are occasionally distrobrevinopatía, laminopathies, dystrophinopathies, miodelinato of deaminase deficiency, hereditary inclusion body myositis, and CMT1A neuropathy. A causal relationship between NMD and LVHT is likely, but the exact relationship and partnership pathomechanics remain elusive. The nearby pathogenic relationship is supported by the fact that the phenomenon of acquired LVHT occurs predominantly in the NMD. A consistent referral of patients with LVHT the neurologist, the subsequent referral of patients with NMD cardiologist, and family research can help clarify matters still unresolved concerning the pathogenesis, course and prognosis of LVHT