Stimulation of GHRH Neuron Axon Growth by Leptin and Impact of Nutrition during Suckling in Mice.

Nutrition during the early postnatal period can program the growth trajectory and adult size. Nutritionally regulated hormones are strongly suspected to be involved in this physiological regulation. Linear growth during the postnatal period is regulated by the neuroendocrine somatotropic axis, whose development is first controlled by GHRH neurons of the hypothalamus.

Role of Adipose Tissue microRNAs in the Onset of Metabolic Diseases and Implications in the Context of the DOHaD.

The worldwide epidemic of obesity is associated with numerous comorbid conditions, including metabolic diseases such as insulin resistance and diabetes, in particular. The situation is likely to worsen, as the increase in obesity rates among children will probably lead to an earlier onset and more severe course for metabolic diseases. The origin of this earlier development of obesity may lie in both behavior (changes in nutrition, physical activity, etc.

Association between metabolic disorders and seminal plasma miRNA levels: a pilot study.

Background: Excess weight and metabolic disorders have a negative impact on male reproductive functions. The mechanisms involved are numerous and complex and epigenetic mechanisms may also be involved, notably through the small non-coding RNAs. Among them, microRNAs (miRNAs) are of particular interest.

[Really Just a Side Effect of Capecitabine? Case Report from the Oncological and Neurological Consultation].

Really Just a Side Effect of Capecitabine? Case Report from the Oncological and Neurological Consultation A case of our oncology and neurology department is presented. A male patient developed sensory polyneuropathy and mild left-side hemiparesis while receiving neoadjuvant radiochemotherapy with capecitabine as treatment for rectal cancer. Polyneuropathy as a side effect of capecitabine was thought to be the culprit.

Role of miRNA in the Transmission of Metabolic Diseases Associated With Paternal Diet-Induced Obesity.

The concept of Developmental Origins of Health and Diseases (DOHaD) recognizes that an unfavorable maternal environment alters the developmental trajectory of the fetus and can lead to long-term risk of developing chronic noncommunicable diseases. More recently, the concept of a paternal transmission [Paternal Origins of Health and Diseases (POHaD)] has emerged stressing the impact of paternal overweight or obesity on offspring's health and development. While very few examples of paternal epigenetic inheritance of metabolic disorders have been evidenced in human, many experimental mouse models based on high-fat diet (HFD)-induced paternal obesity have been developed to breakdown molecular mechanisms involved in the process.

Massive Arteriovenous Malformation with Stroke-Like Presentation.

We report of a 75-year-old patient with stroke-like presentation, where cerebral imaging led to the diagnosis of a massive arteriovenous malformation (AVM) of the whole left hemisphere. We suggest considering AVM as a differential diagnosis in patients with symptoms of acute stroke despite age and, in the absence of contraindications, in this setting to obtain MRI or CT angiography of the brain.

Impact of insulin on primary arcuate neurons culture is dependent on early-postnatal nutritional status and neuronal subpopulation.

Nutrition plays a critical role in programming and shaping linear growth during early postnatal life through direct action on the development of the neuroendocrine somatotropic (GH/IGF-1) axis. IGF-1 is a key factor in modulating the programming of linear growth during this period. Notably, IGF-1 preferentially stimulates axonal growth of GHRH neurons in the arcuate nucleus of the hypothalamus (Arc), which is crucial for the proliferation of somatotroph progenitors in the pituitary, thus influencing later GH secretory capacity.

Regulation of growth: Epigenetic mechanisms?

Organism development is controlled by both genetic programs and the environment to insure a reproductive success as adults. Linear growth is an important part of the development and is mostly controlled by genetic factors. However, the variability of height in a given species does not seem to be specifically associated with SNP.

Sex-Specificity of Mineralocorticoid Target Gene Expression during Renal Development, and Long-Term Consequences.

Sex differences have been identified in various biological processes, including hypertension. The mineralocorticoid signaling pathway is an important contributor to early arterial hypertension, however its sex-specific expression has been scarcely studied, particularly with respect to the kidney. Basal systolic blood pressure (SBP) and heart rate (HR) were measured in adult male and female mice.

Correction: IGF-1 Induces GHRH Neuronal Axon Elongation during Early Postnatal Life in Mice.

[This corrects the article DOI: 10.1371/journal.pone.

IGF-1 Induces GHRH Neuronal Axon Elongation during Early Postnatal Life in Mice.

Nutrition during the perinatal period programs body growth. Growth hormone (GH) secretion from the pituitary regulates body growth and is controlled by Growth Hormone Releasing Hormone (GHRH) neurons located in the arcuate nucleus of the hypothalamus. We observed that dietary restriction during the early postnatal period (i.

Mild pituitary phenotype in 3- and 12-month-old Aip-deficient male mice.

Germline mutations in the aryl hydrocarbon receptor-interacting protein (AIP) gene predispose humans to pituitary adenomas, particularly of the somatotroph lineage. Mice with global heterozygous inactivation of Aip (Aip(+/-)) also develop pituitary adenomas but differ from AIP-mutated patients by the high penetrance of pituitary disease. The endocrine phenotype of these mice is unknown.

Deleting IGF-1 receptor from forebrain neurons confers neuroprotection during stroke and upregulates endocrine somatotropin.

Insulin-like growth factors control numerous processes, namely somatic growth, metabolism and stress resistance, connecting this pathway to aging and age-related diseases. Insulin-like growth factor signaling also impacts on neurogenesis, neuronal survival and structural plasticity. Recent reports demonstrated that diminished insulin-like growth factor signaling confers increased stress resistance in brain and other tissues.

Impact of admission glucose and diabetes on recanalization and outcome after intra-arterial thrombolysis for ischaemic stroke.

Background: Stroke patients with diabetes and admission hyperglycaemia have worse outcomes than non-diabetics, with or without intravenous thrombolysis. Poor vessel recanalization was reported in diabetics treated with intravenous thrombolysis.

Aims: This study aimed to determine the impact of admission glucose and diabetes on recanalization and outcome after intra-arterial thrombolysis.

Diffusion-weighted MRI helps predict outcome in basilar artery occlusion patients treated with intra-arterial thrombolysis.

Background: Intra-arterial thrombolysis (IAT) can improve clinical outcome in patients with acute basilar artery occlusion (BAO). The purpose of this study was to determine whether the severity of neurological symptoms, the extent of early ischemic damage on pretreatment diffusion-weighted MRI (DWI), and the lesion progression or regression on post-treatment MRI can predict functional outcome in patients with BAO treated with IAT.

Methods: Thirty-six BAO patients (13 women, 23 men; mean age 60 years) treated with IAT within 12 h of symptom onset were studied.

Exploring endocrine GH pattern in mice using rank plot analysis and random blood samples.

GH plays important pleiotropic roles in development, growth, metabolism, and aging of vertebrate species. Mouse mutants with altered GH signaling have been increasingly instrumental in studying somatotropic pathophysiology. However, the pulsatile characteristics of GH secretion are difficult to study in mice because catheterization is cumbersome and long-term serial sampling is limited by small body size and blood volume.

Epigenetics and parental effects.

Parental effects are a major source of phenotypic plasticity and may influence offspring phenotype in concert with environmental demands. Studies of "environmental epigenetics" suggest that (1) DNA methylation states are variable and that both demethylation and remethylation occur in post-mitotic cells, and (2) that remodeling of DNA methylation can occur in response to environmentally driven intracellular signaling pathways. Studies of mother-offspring interactions in rodents suggest that parental signals influence the DNA methylation, leading to stable changes in gene expression.

Enriching stress research.

Enriched environments are known to boost physical and mental health in rodents and humans. Now, Cao et al. (2010) report that environmental enrichment also suppresses tumor growth in mice by stimulating the hypothalamus to produce brain-derived neurotrophic factor that acts on the sympathetic nervous system to reduce leptin production in white fat tissue.

Allogeneic hematopoietic SCT as treatment option for patients with mitochondrial neurogastrointestinal encephalomyopathy (MNGIE): a consensus conference proposal for a standardized approach.

Allogeneic hematopoietic SCT (HSCT) has been proposed as a treatment for patients with mitochondrial neurogastrointestinal encephalomyopathy (MNGIE). HSCT has been performed in nine patients using different protocols with varying success. Based on this preliminary experience, participants of the first consensus conference propose a common approach to allogeneic HSCT in MNGIE.

What is a minor stroke?

Background And Purpose: The term "minor stroke" is often used; however a consensus definition is lacking. We explored the relationship of 6 "minor stroke" definitions and outcome and tested their validity in subgroups of patients.

Methods: A total of 760 consecutive patients with acute ischemic strokes were classified according to the following definitions: A, score < or = 1 on every National Institutes of Health Stroke Scale (NIHSS) item and normal consciousness; B, lacunar-like syndrome; C, motor deficits with or without sensory deficits; D, NIHSS < or = 9 excluding those with aphasia, neglect, or decreased consciousness; E, NIHSS < or = 9; and F, NIHSS < or = 3.

A novel dominant mutation of the Nav1.4 alpha-subunit domain I leading to sodium channel myotonia.

Background: Mutations in SCN4A may lead to myotonia.

Methods: Presentation of a large family with myotonia, including molecular studies and patch clamp experiments using human embryonic kidney 293 cells expressing wild-type and mutated channels.

Results: In a large family with historic data on seven generations and a clear phenotype, including myotonia at movement onset, with worsening by cold temperature, pregnancy, mental stress, and especially after rest after intense physical activity, but without weakness, the phenotype was linked with the muscle sodium channel gene (SCN4A) locus, in which a novel p.

Brain IGF-1 receptors control mammalian growth and lifespan through a neuroendocrine mechanism.

Mutations that decrease insulin-like growth factor (IGF) and growth hormone signaling limit body size and prolong lifespan in mice. In vertebrates, these somatotropic hormones are controlled by the neuroendocrine brain. Hormone-like regulations discovered in nematodes and flies suggest that IGF signals in the nervous system can determine lifespan, but it is unknown whether this applies to higher organisms.