Objective: This study evaluated the relationship between IVD degeneration and the vertebral body FSF in dogs and compared these factors between chondrodystrophic (CD) and nonchondrodystrophic (NCD) dogs. Methods: IVD degeneration in dogs was classified morphologically using the Pfirrmann grade, and the vertebral body FSF was evaluated quantitatively. Results: The vertebral body FSF showed a statistically significant difference among the age groups. The vertebral body FSF was significantly higher in Pfirrmann grades 3–5 than in grades 1 and 2. The mean Pfirrmann grade of CD dogs was higher than that of NCD dogs in the four-to-six-year-old group. The mean vertebral body FSF of CD dogs was higher than that of NCD dogs in the group of seven years and above. Conclusions and Relevance: In dogs, the vertebral body FSF increased significantly with age and Pfirrmann grade. The CD dogs showed a higher degree of IVD degeneration at a younger age than the NCD dogs. CD dogs appeared to experience more severe fat deposition of the vertebral body in old age than NCD dogs. MRI examinations are helpful for evaluating IVD degeneration and vertebral body fat deposition.

Objective: This study evaluated the relationship between IVD degeneration and the vertebral body FSF in dogs and compared these factors between chondrodystrophic (CD) and nonchondrodystrophic (NCD) dogs. Methods: IVD degeneration in dogs was classified morphologically using the Pfirrmann grade, and the vertebral body FSF was evaluated quantitatively. Results: The vertebral body FSF showed a statistically significant difference among the age groups. The vertebral body FSF was significantly higher in Pfirrmann grades 3–5 than in grades 1 and 2. The mean Pfirrmann grade of CD dogs was higher than that of NCD dogs in the four-to-six-year-old group. The mean vertebral body FSF of CD dogs was higher than that of NCD dogs in the group of seven years and above. Conclusions and Relevance: In dogs, the vertebral body FSF increased significantly with age and Pfirrmann grade. The CD dogs showed a higher degree of IVD degeneration at a younger age than the NCD dogs. CD dogs appeared to experience more severe fat deposition of the vertebral body in old age than NCD dogs. MRI examinations are helpful for evaluating IVD degeneration and vertebral body fat deposition.

Objective: This study evaluated the relationship between IVD degeneration and the vertebral body FSF in dogs and compared these factors between chondrodystrophic (CD) and nonchondrodystrophic (NCD) dogs. Methods: IVD degeneration in dogs was classified morphologically using the Pfirrmann grade, and the vertebral body FSF was evaluated quantitatively. Results: The vertebral body FSF showed a statistically significant difference among the age groups. The vertebral body FSF was significantly higher in Pfirrmann grades 3–5 than in grades 1 and 2. The mean Pfirrmann grade of CD dogs was higher than that of NCD dogs in the four-to-six-year-old group. The mean vertebral body FSF of CD dogs was higher than that of NCD dogs in the group of seven years and above. Conclusions and Relevance: In dogs, the vertebral body FSF increased significantly with age and Pfirrmann grade. The CD dogs showed a higher degree of IVD degeneration at a younger age than the NCD dogs. CD dogs appeared to experience more severe fat deposition of the vertebral body in old age than NCD dogs. MRI examinations are helpful for evaluating IVD degeneration and vertebral body fat deposition.

Objective: This study evaluated the relationship between IVD degeneration and the vertebral body FSF in dogs and compared these factors between chondrodystrophic (CD) and nonchondrodystrophic (NCD) dogs. Methods: IVD degeneration in dogs was classified morphologically using the Pfirrmann grade, and the vertebral body FSF was evaluated quantitatively. Results: The vertebral body FSF showed a statistically significant difference among the age groups. The vertebral body FSF was significantly higher in Pfirrmann grades 3–5 than in grades 1 and 2. The mean Pfirrmann grade of CD dogs was higher than that of NCD dogs in the four-to-six-year-old group. The mean vertebral body FSF of CD dogs was higher than that of NCD dogs in the group of seven years and above. Conclusions and Relevance: In dogs, the vertebral body FSF increased significantly with age and Pfirrmann grade. The CD dogs showed a higher degree of IVD degeneration at a younger age than the NCD dogs. CD dogs appeared to experience more severe fat deposition of the vertebral body in old age than NCD dogs. MRI examinations are helpful for evaluating IVD degeneration and vertebral body fat deposition.

The global burden of disease study (GBD) provides valuable information for evaluating population health in terms of disease burden. This study collected and reviewed GBD data in Korea for the year 1990 and 2013. The burdens of cancer, cardiovascular disease, communicable disease, and injuries have decreased remarkably, thereby greatly diminishing the overall disease burden on Korea. Meanwhile, the burdens due to non-fatal chronic diseases such as neuropsychiatric and musculoskeletal disease became major burden contributors. Responding to this circumstance presents a complex challenge to the Korean health system and Korean health policy.
Cardiovascular Diseases ; Chronic Disease ; Communicable Diseases ; Health Policy ; Korea* ; Musculoskeletal Diseases

The enteric protozoan parasite Entamoeba histolytica is the causative agent of human amebiasis. During infection, adherence of E. histolytica through Gal/GalNAc lectin on the surface of the amoeba can induce caspase-3-dependent or -independent host cell death. Phosphorylinositol 3-kinase (PI3K) and protein kinase C (PKC) in E. histolytica play an important function in the adhesion, killing, or phagocytosis of target cells. In this study, we examined the role of amoebic PI3K and PKC in amoeba-induced apoptotic cell death in Jurkat T cells. When Jurkat T cells were incubated with E. histolytica trophozoites, phosphatidylserine (PS) externalization and DNA fragmentation in Jurkat cells were markedly increased compared to those of cells incubated with medium alone. However, when amoebae were pretreated with a PI3K inhibitor, wortmannin before being incubated with E. histolytica, E. histolytica-induced PS externalization and DNA fragmentation in Jurkat cells were significantly reduced compared to results for amoebae pretreated with DMSO. In addition, pretreatment of amoebae with a PKC inhibitor, staurosporine strongly inhibited Jurkat T cell death. However, E. histolytica-induced cleavage of caspase-3, -6, and -7 were not inhibited by pretreatment of amoebae with wortmannin or staurosporin. In addition, we found that amoebic PI3K and PKC have an important role on amoeba adhesion to host compartment. These results suggest that amebic PI3K and PKC activation may play an important role in caspase-independent cell death in Entamoeba-induced apoptosis.
*Apoptosis ; Caspases/metabolism ; Entamoeba histolytica/*enzymology/*growth & development ; Humans ; Hydrolysis ; Jurkat Cells ; Phosphatidylinositol 3-Kinases/*metabolism ; Protein Kinase C/*metabolism ; T-Lymphocytes/*parasitology/*physiology

Entamoeba histolytica is a tissue-invasive protozoan parasite causing dysentery in humans. During infection of colonic tissues, amoebic trophozoites are able to kill host cells via apoptosis or necrosis, both of which trigger IL-8-mediated acute inflammatory responses. However, the signaling pathways involved in host cell death induced by E. histolytica have not yet been fully defined. In this study, we examined whether calpain plays a role in the cleavage of pro-survival transcription factors during cell death of colonic epithelial cells, induced by live E. histolytica trophozoites. Incubation with amoebic trophozoites induced activation of m-calpain in a time- and dose-dependent manner. Moreover, incubation with amoebae resulted in marked degradation of STAT proteins (STAT3 and STAT5) and NF-kappaB (p65) in Caco-2 cells. However, IkappaB, an inhibitor of NF-kappaB, was not cleaved in Caco-2 cells following adherence of E. histolytica. Entamoeba-induced cleavage of STAT proteins and NF-kappaB was partially inhibited by pretreatment of cells with a cell-permeable calpain inhibitor, calpeptin. In contrast, E. histolytica did not induce cleavage of caspase-3 in Caco-2 cells. Furthermore, pretreatment of Caco-2 cells with a calpain inhibitor, calpeptin (but not the pan-caspase inhibitor, z-VAD-fmk) or m-calpain siRNA partially reduced Entamoeba-induced DNA fragmentation in Caco-2 cells. These results suggest that calpain plays an important role in E. histolytica-induced degradation of NF-kappaB and STATs in colonic epithelial cells, which ultimately accelerates cell death.
Caco-2 Cells ; Calcium-Binding Proteins ; Calpain/genetics/metabolism ; Caspase 3/genetics/metabolism ; Caspases ; *Cell Death ; Colon/cytology ; Entamoeba histolytica/*physiology ; Epithelial Cells/cytology/parasitology ; Humans ; I-kappa B Proteins/metabolism ; Intestinal Mucosa/cytology ; NF-kappa B/genetics/*metabolism ; RNA Interference ; RNA, Small Interfering ; STAT3 Transcription Factor/genetics/*metabolism ; STAT5 Transcription Factor/genetics/*metabolism ; Signal Transduction

BACKGROUND AND OBJECTIVES: Elevated endothelin (ET)-1 level is strongly correlated with the pathogenesis of pulmonary arterial hypertension (PAH). Expression level of nicotinamide adenine dinucleotide phosphate oxidase (NOX) 4 is increased in the PAH patients. Ambrisentan, a selective endothelin receptor A (ERA) antagonist, is widely used in PAH therapy. The current study was undertaken to evaluate the effects of ambrisentan treatment in the monocrotaline (MCT)-induced PAH rat model. METHODS: Rats were categorized into control group (C), monocrotaline group (M) and ambrisentan group (Am). The M and Am were subcutaneously injected 60 mg/kg MCT at day 0, and in Am, ambrisentan was orally administered the day after MCT injection for 4 weeks. The right ventricle (RV) pressure was measured and pathological changes of the lung tissues were observed by Victoria blue staining. Protein expressions of ET-1, ERA, endothelial nitric oxide synthase (eNOS) and NOX4 were confirmed by western blot analysis. RESULTS: Ambrisentan treatment resulted in a recovery of the body weight and RV/left ventricle+septum at week 4. The RV pressure was lowered at weeks 2 and 4 after ambrisentan administration. Medial wall thickening of pulmonary arterioles and the number of intra-acinar arteries were also attenuated by ambrisentan at week 4. Protein expression levels of ET-1 and eNOS were recovered at weeks 2 and 4, and ERA levels recovered at week 4. CONCLUSIONS: Ambrisentan administration resulted in the recovery of ET-1, ERA and eNOS protein expression levels in the PAH model. However, the expression level of NOX4 remained unaffected after ambrisentan treatment.
Animals ; Arteries ; Arterioles ; Blotting, Western ; Body Weight ; Endothelin Receptor Antagonists ; Endothelins ; Gene Expression ; Heart Ventricles ; Humans ; Hypertension ; Hypertension, Pulmonary ; Lung ; Models, Animal ; Monocrotaline ; NADP ; NADPH Oxidase ; Nitric Oxide Synthase Type III ; Oxidoreductases ; Rats ; Receptors, Endothelin ; Victoria

BACKGROUND AND OBJECTIVES: Elevated endothelin (ET)-1 level is strongly correlated with the pathogenesis of pulmonary arterial hypertension (PAH). Expression level of nicotinamide adenine dinucleotide phosphate oxidase (NOX) 4 is increased in the PAH patients. Ambrisentan, a selective endothelin receptor A (ERA) antagonist, is widely used in PAH therapy. The current study was undertaken to evaluate the effects of ambrisentan treatment in the monocrotaline (MCT)-induced PAH rat model. METHODS: Rats were categorized into control group (C), monocrotaline group (M) and ambrisentan group (Am). The M and Am were subcutaneously injected 60 mg/kg MCT at day 0, and in Am, ambrisentan was orally administered the day after MCT injection for 4 weeks. The right ventricle (RV) pressure was measured and pathological changes of the lung tissues were observed by Victoria blue staining. Protein expressions of ET-1, ERA, endothelial nitric oxide synthase (eNOS) and NOX4 were confirmed by western blot analysis. RESULTS: Ambrisentan treatment resulted in a recovery of the body weight and RV/left ventricle+septum at week 4. The RV pressure was lowered at weeks 2 and 4 after ambrisentan administration. Medial wall thickening of pulmonary arterioles and the number of intra-acinar arteries were also attenuated by ambrisentan at week 4. Protein expression levels of ET-1 and eNOS were recovered at weeks 2 and 4, and ERA levels recovered at week 4. CONCLUSIONS Ambrisentan administration resulted in the recovery of ET-1, ERA and eNOS protein expression levels in the PAH model. However, the expression level of NOX4 remained unaffected after ambrisentan treatment.

OBJECTIVES: Although ginseng has been reported to protect neuronal cells and improve various cognitive functions, relationship between ginseng supplementation and response inhibition, one of the important cognitive domains has not been explored. In addition, effects of ginseng on in vivo human brain have not been investigated using the diffusion tensor imaging (DTI). The purpose of the current study is to investigate changes in intrusion errors and white matter microstructure after Korean Red Ginseng supplementation using standardized neuropsychological tests and DTI. METHODS: Fifty-one healthy participants were randomly allocated to the Korean Red Ginseng (n = 26) or placebo (n = 25) groups for 8 weeks. The California Verbal Learning Test was used to assess the number of intrusion errors. Intelligence quotient (IQ) was measured with the Korean Wechsler Adult Intelligence Scale. Depressive and anxiety symptoms were evaluated using Hamilton Depression Rating Scale, Hamilton Anxiety Rating Scale, and Hopkins Symptom Checklist-25. The fractional anisotropy (FA) was measured from the brain DTI data. RESULTS: After the 8-week intervention, Korean Red Ginseng supplementation significantly reduced intrusion errors after adjusting age, sex, IQ, and baseline score of the intrusion errors (p for interaction = 0.005). Change in FA values in the left anterior corona radiata was greater in the Korean Red Ginseng group compared to the placebo group (t = 4.29, p = 0.04). CONCLUSIONS: Korean Red Ginseng supplementation may be efficacious for improving response inhibition and white matter microstructure integrity in the prefrontal cortex.
Adult ; Anisotropy ; Anxiety ; Brain ; California ; Depression ; Diffusion Tensor Imaging ; Humans ; Intelligence ; Neurons ; Neuropsychological Tests ; Panax* ; Prefrontal Cortex ; Verbal Learning