• Clinical and Experimental Pediatrics
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• v.52 no.3
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• pp.289-294
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• 2009

Purpose : To assess the usefulness of magnetic resonance imaging (MRI), karyotyping, brainstem auditory evoked potential (BAEP), electroencephalogram (EEG), tandem mass screening test, and newborn metabolic screening test in children with language delay for diagnosing underlying diseases. Methods : From January 2000 to June 2007, a retrospective chart review was performed for 122 children with language delay who visited the Child Neurology Clinic at Yeungnam University Hospital and who underwent neuropsychologic tests and other diagnostic evaluations for underlying diseases. They were grouped into phenomenological diagnostic categories, and test results were analyzed according to the underlying diseases. Results : Of 122 patients, 47 (38.5%) had mental retardation, 40 (32.8%) had developmental language disorders, 23 (18.9 %) had borderline IQ, and 12 (9.8%) had autism spectrum disorder. In 26 (21.3%) cases, the causes or relevant clinical findings to explain language delay were found. Eight (10.4%) of 77 MRIs, 6 (8.0%) of 75 EEGs, and 4 (5%) of 80 BAEPs showed abnormal results. Results directly attributed to diagnosing underlying diseases were 2 hearing defects in BAEPs and 1 bilateral perisylvian cortical dysplasia in MRIs. No abnormal results were found in karyotyping, tandem mass screening tests, and new-born screening tests. Conclusion : Commonly used tests to diagnose the cause of language delay are not very effective and should only be used selectively, according to patient characteristics. However, despite the low diagnostic yields from these tests, because many patients show abnormal results, these tests are useful when conducted in complete evaluation.

• Korean Journal of Plant Resources
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• v.29 no.1
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• pp.1-10
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• 2016

Obesity is a pro-inflammatory state that contributes to the development of metabolic disorders such as hyperlipidemia, insulin resistance, type 2 diabetes, non-alcoholic fatty liver, and cardiovascular disease. In this study, we evaluated the inhibition of adipogenesis in 3T3-L1 cells and in high-fat diet (HFD)-induced obese mice by Peucedanum japonicum Thunberg L. water extract (PJT). Lipid accumulation measurement indicates that PJT markedly inhibited adipogenesis in a dose-dependent manner. RT-PCR results demonstrated that the mRNA expression of adipogenic transcription factors such as peroxisome proliferator-activated receptor-γ (PPARγ) and CCAAT/enhancer binding protein-α (C/EBPα) in 3T3-L1 cells were significantly down-regulated by PJT treatment. Oral administration of PJT (100, 300, and 500 ㎎/㎏, b.w/daily for 4 weeks) was conducted in high-fat diet induced obese mice and C57BL/6 mice. The PJT-administered group of HFD-induced mice had a lower body weight gain, along with decreased serum levels of glucose, triglycerides, and total cholesterol compared with the control mice, however, the HDL-cholesterol/total cholesterol ratio was increased. Furthermore, the elevated mRNA expression levels of adipogenesis related genes in the white adipose tissue of obese mice were significantly suppressed by PJT. These results indicate that PJT exhibits anti-obesity effects in obese mice by decreasing in serum lipid levels and lipogenesis related gene.

• Journal of Life Science
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• v.29 no.6
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• pp.747-753
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• 2019

Cognitive decline is characterized by reduced long-/short-term memory and attention span, and increased depression and anxiety. Such decline is associated with various degenerative brain disorders, especially Alzheimer's disease (AD) and Parkinson's disease (PD). The increases in elderly populations suffering from cognitive decline create social problems and impose economic burdens, and also pose safety threats; all of these problems have been extensively researched over the past several decades. Possible causes of cognitive decline include metabolic and hormone imbalance, infection, medication abuse, and neuronal changes associated with aging. However, no treatment for cognitive decline is available. In neurodegenerative diseases, changes in the gut microbiota and gut metabolites can alter molecular expression and neurobehavioral symptoms. Changes in the gut microbiota affect memory loss in AD via the downregulation of NMDA receptor expression and increased glutamate levels. Furthermore, the use of probiotics resulted in neurological improvement in an AD model. PD and gut microbiota dysbiosis are linked directly. This interrelationship affected the development of constipation, a secondary symptom in PD. In a PD model, the administration of probiotics prevented neuron death by increasing butyrate levels. Dysfunction of the blood-brain barrier (BBB) has been identified in AD and PD. Increased BBB permeability is also associated with gut microbiota dysbiosis, which led to the destruction of microtubules via systemic inflammation. Notably, metabolites of the gut microbiota may trigger either the development or attenuation of neurodegenerative disease. Here, we discuss the correlation between cognitive decline and the gut microbiota.