High-fat hyperphagia in neurotrophin-4 deficient mice reveals potential role of vagal intestinal sensory innervation in long-term controls of food intake

2006 ◽  
Vol 400 (3) ◽  
pp. 240-245 ◽  
Author(s):  
Mardi S. Byerly ◽  
Edward A. Fox
Keyword(s):  
Food Intake ◽  
Potential Role ◽  
Sensory Innervation ◽  
High Fat ◽  
Deficient Mice

scholarly journals Control of appetite, blood glucose, and blood pressure during melanocortin-4 receptor activation in normoglycemic and diabetic NPY-deficient mice

2018 ◽  
Vol 314 (4) ◽  
pp. R533-R539 ◽  
Author(s):  
Alexandre A. da Silva ◽  
J. Nathan Freeman ◽  
John E. Hall ◽  
Jussara M. do Carmo
Keyword(s):  
Food Intake ◽  
Recovery Period ◽  
Receptor Activation ◽  
Metabolic Functions ◽  
Melanocortin 4 Receptor ◽  
The Central Nervous System ◽  
Deficient Mice ◽  
Antidiabetic Effects

Although central melanocortin 4 receptor (MC4R) blockade abolishes the central nervous system (CNS)-mediated anorexogenic, antidiabetic, and cardiovascular actions of leptin, chronic MC4R stimulation fails to completely mimic the effects of leptin. Because neuropeptide Y (NPY) and MC4R exert opposite effects on cardiovascular and metabolic functions, we tested the role of NPY in offsetting the long-term actions of MC4R activation. Wild-type (WT) and NPY-deficient (NPY−/−) mice were implanted with telemetry probes for measuring mean arterial pressure (MAP) and heart rate (HR) 24 h/day. After the mice recovered from surgery and stable baseline measurements, the MC3/4R agonist melanotan II (MTII, 120 μg·kg−1·day−1 iv) was infused for 7 days followed by a recovery period. No major differences between groups were observed at baseline except for slightly higher food intake and HR in NPY−/− mice (4.3 ± 0.2 vs. 3.4 ± 0.2 g/day and 567 ± 14 vs. 522 ± 13 beats/min). Chronic MTII infusion reduced food intake in both groups while causing transient increases in MAP and HR only in WT mice (peaks of 11 ± 3 mmHg and 126 ± 13 beats/min). To examine whether NPY deficiency would amplify the antidiabetic effects of MC4R activation, diabetes was induced with streptozotocin (STZ) 1 wk before baseline measurements were taken, and the same experimental protocol was followed. In WT and NPY−/− mice, STZ-induced diabetes led to similar hyperphagia, hyperglycemia, and weight loss, which were not reversed by chronic MTII treatment. Our results demonstrate that chronic MC4R activation, even in NPY-deficient mice, does not mimic chronic antidiabetic, cardiovascular, or metabolic actions of leptin, and that NPY is not essential for hyperphagia or cardiovascular changes associated with diabetes.

Prevention of Cardiac Hypertrophy in Experimental Chronic Renal Failure by Long-Term ACE Inhibitor Administration: Potential Role of Lysosomal Proteinases

1995 ◽  
Vol 15 (2) ◽  
pp. 129-136 ◽  
Author(s):  
Hiroaki Suzuki ◽  
Liliana Schaefer ◽  
Hong Ling ◽  
Roland M. Schaefer ◽  
Jobst Dämmrich ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Cardiac Hypertrophy ◽  
Potential Role ◽  
Ace Inhibitor ◽  
Lysosomal Proteinases

scholarly journals Duodenal Dysbiosis and Relation to the Efficacy of Proton Pump Inhibitors in Functional Dyspepsia

2021 ◽  
Vol 22 (24) ◽  
pp. 13609
Author(s):  
Lucas Wauters ◽  
Raúl Y. Tito ◽  
Matthias Ceulemans ◽  
Maarten Lambaerts ◽  
Alison Accarie ◽  
...  
Keyword(s):  
Functional Dyspepsia ◽  
Proton Pump Inhibitors ◽  
Proton Pump ◽  
Potential Role ◽  
Short Term ◽  
Beneficial Effects ◽  
Rrna Sequencing ◽  
Before And After

Proton pump inhibitors (PPI) may improve symptoms in functional dyspepsia (FD) through duodenal eosinophil-reducing effects. However, the contribution of the microbiome to FD symptoms and its interaction with PPI remains elusive. Aseptic duodenal brushings and biopsies were performed before and after PPI intake (4 weeks Pantoprazole 40 mg daily, FD-starters and controls) or withdrawal (2 months, FD-stoppers) for 16S-rRNA sequencing. Between- and within-group changes in genera or diversity and associations with symptoms or duodenal factors were analyzed. In total, 30 controls, 28 FD-starters and 19 FD-stoppers were followed. Mucus-associated Porphyromonas was lower in FD-starters vs. controls and correlated with symptoms in FD and duodenal eosinophils in both groups, while Streptococcus correlated with eosinophils in controls. Although clinical and eosinophil-reducing effects of PPI therapy were unrelated to microbiota changes in FD-starters, increased Streptococcus was associated with duodenal PPI effects in controls and remained higher despite withdrawal of long-term PPI therapy in FD-stoppers. Thus, duodenal microbiome analysis demonstrated differential mucus-associated genera, with a potential role of Porphyromonas in FD pathophysiology. While beneficial effects of short-term PPI therapy were not associated with microbial changes in FD-starters, increased Streptococcus and its association with PPIeffects in controls suggest a role for duodenal dysbiosis after long-term PPI therapy.

scholarly journals Neuroinflammation and Its Impact on the Pathogenesis of COVID-19

2021 ◽  
Vol 8 ◽  
Author(s):  
Mohammed M. Almutairi ◽  
Farzane Sivandzade ◽  
Thamer H. Albekairi ◽  
Faleh Alqahtani ◽  
Luca Cucullo
Keyword(s):  
Immune System ◽  
Molecular Mechanisms ◽  
Potential Role ◽  
Immune Cell ◽  
Clinical Manifestations ◽  
Cell Infiltration ◽  
Cellular Mechanisms ◽  
Cytokine Levels

Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The clinical manifestations of COVID-19 include dry cough, difficult breathing, fever, fatigue, and may lead to pneumonia and respiratory failure. There are significant gaps in the current understanding of whether SARS-CoV-2 attacks the CNS directly or through activation of the peripheral immune system and immune cell infiltration. Although the modality of neurological impairments associated with COVID-19 has not been thoroughly investigated, the latest studies have observed that SARS-CoV-2 induces neuroinflammation and may have severe long-term consequences. Here we review the literature on possible cellular and molecular mechanisms of SARS-CoV-2 induced-neuroinflammation. Activation of the innate immune system is associated with increased cytokine levels, chemokines, and free radicals in the SARS-CoV-2-induced pathogenic response at the blood-brain barrier (BBB). BBB disruption allows immune/inflammatory cell infiltration into the CNS activating immune resident cells (such as microglia and astrocytes). This review highlights the molecular and cellular mechanisms involved in COVID-19-induced neuroinflammation, which may lead to neuronal death. A better understanding of these mechanisms will help gain substantial knowledge about the potential role of SARS-CoV-2 in neurological changes and plan possible therapeutic intervention strategies.

scholarly journals Case Report: Clostridium neonatale Bacteremia in a Preterm Neonate With Necrotizing Enterocolitis

2021 ◽  
Vol 9 ◽  
Author(s):  
Nadim Cassir ◽  
Isabelle Grandvuillemin ◽  
Manon Boxberger ◽  
Priscilla Jardot ◽  
Farid Boubred ◽  
...  
Keyword(s):  
Necrotizing Enterocolitis ◽  
Potential Role ◽  
Preterm Neonate ◽  
Gastrointestinal Disorder ◽  
Etiologic Agent ◽  
Preterm Neonates ◽  
Environmental Cleaning ◽  
Life Threatening

Necrotizing enterocolitis is a life-threatening acquired gastrointestinal disorder among preterm neonates and is associated with a high mortality rate and long-term neurodevelopmental morbidity. No etiologic agent has been definitively established; nonetheless, the most implicated bacteria include members of the Clostridium genus. We reported here on a case of Clostridium neonatale bacteremia in a preterm neonate with necrotizing enterocolitis, providing more information regarding the potential role of this bacterium in pathogenesis of necrotizing enterocolitis. We emphasized the sporulating form of C. neonatale that confers resistance to disinfectants usually applied for the hospital environmental cleaning. Further works are needed to establish the causal relationship between the occurrence of NEC and the isolation of C. neonatale, with promising perspectives in terms of diagnostic and therapeutic management.

Radiotherapy after Prostatectomy

2002 ◽  
Vol 88 (6) ◽  
pp. 445-452 ◽  
Author(s):  
Giuseppe Sanguineti ◽  
Paola Franzone ◽  
Laura Culp ◽  
Michela Marcenaro ◽  
Salvina Barra ◽  
...  
Keyword(s):  
High Risk ◽  
Radical Prostatectomy ◽  
Adjuvant Radiotherapy ◽  
Potential Role ◽  
Specific Antigen ◽  
Salvage Treatment ◽  
Salvage Radiotherapy ◽  
Risk Of Failure

Aims and background The role of radiotherapy after prostatectomy is controversial. This paper tries to give some guidelines for everyday practice through an analysis of literature data. Methods The potential role of radiotherapy in the adjuvant and salvage setting is discussed. We also report and interpret available literature data for both settings. Results As regards an increase in or detectable prostate-specific antigen (PSA) after radical prostatectomy, about 40–50% of patients are rendered bNED with local salvage radiotherapy, but only 10–50% are long-term (5 years) biochemically controlled. A timely salvage treatment is crucial to optimize control probability. As regards adjuvant radiotherapy for undetectable postoperative PSA in patients at high risk of failure as judged on pathology, results are more encouraging. Recent data report bNED rates ≥70% at 5 years. Conclusions Although results are far from satisfactory, salvage radiotherapy should be considered for every patient with an increased or detectable PSA after surgery. Adjuvant radiotherapy seems preferable to salvage radiotherapy for patients at high (>30%) risk of failure.

scholarly journals A Study on the Potential Role of Occlusal Fissure Fractures in the Etiopathogenesis of Equine Cheek Teeth Apical Infections

2019 ◽  
Vol 36 (3) ◽  
pp. 171-178 ◽  
Author(s):  
Katherina Y. Wellman ◽  
Padraic M. Dixon
Keyword(s):  
Computed Tomography ◽  
Methylene Blue ◽  
Potential Role ◽  
Histological Study ◽  
Extraction Process ◽  
Dental Tissue ◽  
Rule Out

Thirty-nine equine cheek teeth diagnosed as having anachoretic apical infections and also having occlusal fissure fractures, but without occlusal pulpar exposure, that had been orally extracted without causing occlusal damage and 10 control teeth were used in this study. The teeth were individually imaged by computed tomography, occlusally stained with methylene blue and visually reexamined, then sectioned subocclusally at 5 mm intervals until the fissure fractures could no longer be detected. A limited histological study was then performed on 7 apically infected and 5 control teeth. Standard computed tomography only detected 1 of 39 fissure fractures. Thirteen of the 39 stained teeth had subocclusal fissure fractures visually identified at approximately 6 mm beneath the surface, and in 9 of these 13 teeth the fissure fractures had deeper staining to a level immediately above or into a pulp horn, indicating a potential route for bacterial pulpitis. However, the current study cannot rule out the possibility that the extraction process, long-term formalin storage, or the processing of teeth may have allowed for deeper staining. Additionally, methylene blue may penetrate dental tissue more readily than bacteria can invade. Further studies on the potential role of fissure fractures in the etiopathogenesis of cheek teeth apical infection are warranted.

scholarly journals Impaired thrombin generation in Reelin-deficient mice: a potential role of plasma Reelin in hemostasis

2014 ◽  
Vol 12 (12) ◽  
pp. 2054-2064 ◽  
Author(s):  
W.-L. Tseng ◽  
T.-H. Chen ◽  
C.-C. Huang ◽  
Y.-H. Huang ◽  
C.-F. Yeh ◽  
...  
Keyword(s):  
Thrombin Generation ◽  
Potential Role ◽  
Deficient Mice

scholarly journals Potential Role of the Chemokine Macrophage Inflammatory Protein 1α in Human and Experimental Schistosomiasis

2005 ◽  
Vol 73 (4) ◽  
pp. 2515-2523 ◽  
Author(s):  
Adriano L. S. Souza ◽  
Ester Roffê ◽  
Vanessa Pinho ◽  
Danielle G. Souza ◽  
Adriana F. Silva ◽  
...  
Keyword(s):  
Potential Role ◽  
Severe Disease ◽  
Experimental Studies ◽  
Interleukin 4 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein ◽  
Deficient Mice

ABSTRACT In human schistosomiasis, the concentrations of the chemokine macrophage inflammatory protein 1α (MIP-1α/CCL3) is greater in the plasma of patients with clinical hepatosplenic disease. The objective of the present study was to confirm the ability of CCL3 to detect severe disease in patients classified by ultrasonography (US) and to evaluate the potential role of CCL3 in Schistosoma mansoni-infected mice. CCL3 was measured by enzyme-linked immunosorbent assay in the plasma of S. mansoni-infected patients. CCL3-deficient mice were infected with 25 cercariae, and various inflammatory and infectious indices were evaluated. The concentration of CCL3 was higher in the plasma of S. mansoni-infected than noninfected patients. Moreover, CCL3 was greater in those with US-defined hepatosplenic than with the intestinal form of the disease. In CCL3-deficient mice, the size of the granuloma and the liver eosinophil peroxidase activity and collagen content were diminished compared to wild-type mice. In CCL3-deficient mice, the worm burden after 14 weeks of infection, but not after 9 weeks, was consistently smaller. The in vitro response of mesenteric lymph node cells to antigen stimulation was characterized by lower levels of interleukin-4 (IL-4) and IL-10. CCL3 is a marker of disease severity in infected humans, and experimental studies in mice suggest that CCL3 may be a causative factor in the development of severe schistosomiasis.

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