ABSTRACT
Introduction: AL amyloidosis can involve the gastrointestinal (GI) tract in a sporadic manner, affecting certain anatomical areas while sparing others. Case Presentation: Our patient with AL amyloidosis and confirmed colonic involvement was found to have new odynophagia, GI bleeding, and imaging findings that might suggest AL amyloidosis. However, negative pathology results from esophageal biopsies suggested the patient's new ulcerations were more likely a side effect of her autologous stem cell transplant (SCT) and chemotherapy meant to target amyloidosis, as opposed to an effect of amyloid infiltration itself. Conclusion: GI involvement of amyloidosis requires a high degree of clinical suspicion and should be considered in patients with systemic diseases affecting the kidney, heart, and GI tract; however, when satisfactory biopsies obtained from endoscopy results are negative, other causes should be considered.
ABSTRACT
Fetal alcohol spectrum disorders (FASD) constitute a wide range of disorders that arise from prenatal exposure to ethanol (EtOH). However, detailed reports regarding the adverse effects of prenatal EtOH exposure on neocortical morphology and its underlying pathogenic mechanisms are limited. In the present study, we aimed to characterize the anatomical abnormalities of neocortical development and their correlation with microglial properties and neuro-inflammation in a mouse model of FASD. We evaluated the development and maturation of the neocortex in ICR mice prenatally exposed to 25% (w/v) EtOH using histological and molecular analyses. Reduced proliferation and excessive cell death were observed in the dorsal telencephalon. Abnormal neuronal distribution, layer formation, and dopaminergic neuronal projections were observed in the neocortex. Disruption of microglial differentiation (M1/M2 microglial ratio) and abnormal expression of pro-inflammatory and neurotrophic factors were induced, and these abnormalities were ameliorated by co-treatment with an anti-inflammatory drug (pioglitazone). FASD model mice displayed histological abnormalities, microglial abnormalities, and neuro-inflammation in both the embryonic and newborn stages. Thus, anti-inflammatory therapeutics may provide a novel preventive approach for the treatment of FASD.
Subject(s)
Ethanol/adverse effects , Neocortex/drug effects , Neocortex/metabolism , Neurogenesis/drug effects , Prenatal Exposure Delayed Effects , Animals , Cell Proliferation/drug effects , Cell Survival/drug effects , Cytokines/metabolism , Dopaminergic Neurons/drug effects , Dopaminergic Neurons/metabolism , Female , Fetal Alcohol Spectrum Disorders/etiology , Fetal Alcohol Spectrum Disorders/metabolism , Fetal Alcohol Spectrum Disorders/pathology , Inflammation/etiology , Inflammation/metabolism , Inflammation/pathology , Inflammation Mediators/metabolism , Mice , Microglia/drug effects , Microglia/metabolism , Neocortex/pathology , Neurodevelopmental Disorders/etiology , Neurodevelopmental Disorders/metabolism , Neurodevelopmental Disorders/pathology , Neurons/drug effects , Neurons/metabolism , Pregnancy , Signal TransductionABSTRACT
BACKGROUND: Auditory hypersensitivity is one of the major complications in autism spectrum disorder. The aim of this study was to investigate whether the auditory brain center is affected in autism model rats. METHODS: Autism model rats were prepared by prenatal exposure to thalidomide on embryonic day 9 and 10 in pregnant rats. The superior olivary complex (SOC), a complex of auditory nuclei, was immunostained with anti-calbindin d28k antibody at postnatal day 50. RESULTS: In autism model rats, SOC immunoreactivity was markedly decreased. Strength of immunostaining of SOC auditory fibers was also weak in autism model rats. Surprisingly, the size of the medial nucleus of trapezoid body, a nucleus exerting inhibitory function in SOC, was significantly decreased in autism model rats. CONCLUSIONS: Auditory hypersensitivity may be, in part, due to impairment of inhibitory processing by the auditory brain center.
Subject(s)
Auditory Pathways/physiopathology , Auditory Perception/physiology , Autism Spectrum Disorder/complications , Autistic Disorder/complications , Hyperacusis/etiology , Superior Olivary Complex/physiopathology , Animals , Auditory Pathways/pathology , Autism Spectrum Disorder/chemically induced , Autism Spectrum Disorder/pathology , Autism Spectrum Disorder/physiopathology , Autistic Disorder/chemically induced , Autistic Disorder/pathology , Autistic Disorder/physiopathology , Hyperacusis/pathology , Hyperacusis/physiopathology , Male , Rats , Rats, Wistar , Superior Olivary Complex/pathology , ThalidomideABSTRACT
Increases in the yield of rice, a staple crop for more than half of the global population, are imperative to support rapid population growth. Grain weight is a major determining factor of yield. Here, we report the cloning and functional analysis of THOUSAND-GRAIN WEIGHT 6 (TGW6), a gene from the Indian landrace rice Kasalath. TGW6 encodes a novel protein with indole-3-acetic acid (IAA)-glucose hydrolase activity. In sink organs, the Nipponbare tgw6 allele affects the timing of the transition from the syncytial to the cellular phase by controlling IAA supply and limiting cell number and grain length. Most notably, loss of function of the Kasalath allele enhances grain weight through pleiotropic effects on source organs and leads to significant yield increases. Our findings suggest that TGW6 may be useful for further improvements in yield characteristics in most cultivars.
