No abstract available.
Animals ; Lung* ; Rats*

No abstract available.
Anencephaly* ; Humans

Apodemus agrarius has been used for experimental purpose to identify the route of infection and pathogenesis of Korean hemorrhagic fever. However, despite the increasing amount of information being published at present about the physiologic and ecologic characteristics of Apodemus, few data are available about the morphologic findings in the brain. This study was aimed to clarify the change of NADPH-d and neuropeptide Y (NPY) associated with aging of the Apodemus. The number of NADPH-d positive or negative NPY neurons in the cerebral cortex and striatum were compared between two age groups of Apodemus (4 months and 24 months) after the histochemical and immunohis-tochemical staining. 1. The number of NADPH-d positive NPY neurons in cerebral cortex or striatum were not different between the two age groups. 2. The number of NADPH-d negative NPY neurons in cerebral region or caudatoputamen striatum were not different between the two age groups. 3. Most of NADPH-d or NPY neurons were bipolar or multipolar neurons with complex and long dendrites in the control group. 4. The NADPH-d or NPY neurons in cerebral cortex were more tortous and shorter than control in the aged group. These findings demonstrate that NADPH-d positive NPY neurons and NPY neurons do not seem to be change of age in cerebral cortex or striatum of Apodemus agrarius.
Aging ; Animals ; Brain ; Cerebral Cortex* ; Dendrites ; Hemorrhagic Fever with Renal Syndrome ; Humans ; Murinae* ; Neurons* ; Neuropeptide Y* ; Neuropeptides* ; Nitric Oxide

Translocation of synaptic zinc may mediate neuronal death in pathological conditions. In this study, we examined the possible correlation between zinc translocation and heat shock protein (HSP)72 induction in rat brains following kainate seizures. Zinc accumulation, visualized by Timm's method, occurred in degenerating neurons in hippocampus, amygdala, and cortex 6~24 h after kainate injection. Immunohistochemistry with anti-HSP72 antibody revealed HSP induction largely in areas where zinc accumulation occurred. At the cellular level, however, most HSP72 immunoreac-tive neurons were found to be Timm (-) and morphologically intact. Present results suggest that intense zinc translocation may induce neuronal death before possible HSP induction. However, we could not rule out the possibility that sublethal zinc translocation, below the detection limit by Timm's method, may play a role in HSP72 induction.
Amygdala ; Animals ; Brain* ; Heat-Shock Proteins* ; Hippocampus ; Hot Temperature* ; Immunohistochemistry ; Kainic Acid* ; Limit of Detection ; Neurons ; Rats* ; Seizures* ; Zinc*

beta-amyloid peptide (Abeta) consisting of 40 to 42 amino acid is the principle constituent of senile plaques in Alzheimer's disease. Although, the hypothesis that deposition of AP triggers a cascade of events leading to the pathology of Alzheimer's disease has been widely accepted, direct evidence for triggering accumulation of phosphorylated tau in paired helical filament is rare. In this study, we examined neurotoxicity induced by 3 kinds of beta-amyloid peptides 1 ~28, 25~,35 and 1~40 to elucidate the way of mechanism trading to neuronal cell death caused by Abeta using cultured hippocampal neurons. For this purpose, we measured lactate dehydrogenase (LDH) in the culture media after treatment with Abeta combined with anti-oxidant drug, trolox, or not. By histochemical and TUNEL method, we studied the change of immunoreaction to anti-MAP-2 (microtubule associated protein -2, the main component of neuritis) and detected apoptotic cells, respectively, in the hippocampal neurons treated with Abeta. To investigate whether tau phosphorylation involve neurotoxicity induced by Abeta, we immunostained the neurons with anti-SMI-31 to recognize phosphorylated Ser 396/404 of tau. From our data, we suggested that Abeta1-40 and Abeta25-35 induced marked neurodegenerative changes, and the mechanism responsible for cell death caused by Abeta -neurotoxicity was associated with the apoptosis. Because Abeta-neurotoxicity was not inhibited by anti-oxidant, trolox, we suggested that anti-oxidant did not protect the neuronal cells against the damage induced by Abeta in ou. expo.imental envi.onment. Finally, we suggested that AP treatment did not potentiate the immunoreactivity to anti-phosphorylated tau antibody and we speculated that Abeta-neurotoxicity led hippocampal cells to apoptosis without tau phosphorylation.
Alzheimer Disease ; Apoptosis* ; Cell Death ; Culture Media ; In Situ Nick-End Labeling ; L-Lactate Dehydrogenase ; Neurons* ; Pathology ; Peptides* ; Phosphorylation* ; Plaque, Amyloid

OBJECTIVE: To develop an in vitro model analogous to the environment of traumatic spinal cord injury (SCI), the authors evaluated change of astrogliosis following treatments with kainate and/or scratch, and degree of neurite outgrowth after treatment with a kainate inhibitor. METHODS: Astrocytes were obtained from the rat spinal cord. Then, 99% of the cells were confirmed to be GFAP-positive astrocytes. For chemical injury, the cells were treated with kainate at different concentrations (10, 50 or 100 µM). For mechanical injury, two kinds of uniform scratches were made using a plastic pipette tip by removing strips of cells. For combined injury (S/K), scratch and kainate were provided. Cord neurons from rat embryos were plated onto culture plates immediately after the three kinds of injuries and some cultures were treated with a kainate inhibitor. RESULTS: Astro-gliosis (glial fibrillary acidic protein [GFAP], vimentin, chondroitin sulfate proteoglycan [CSPG], rho-associated protein kinase [ROCK], and ephrin type-A receptor 4 [EphA4]) was most prominent after treatment with 50 µM kainate and extensive scratch injury in terms of single arm (p<0.001) and in the S/K-induced injury model in view of single or combination (p<0.001). Neurite outgrowth in the seeded spinal cord (β-III tubulin) was the least in the S/K-induced injury model (p<0.001) and this inhibition was reversed by the kainate inhibitor (p<0.001). CONCLUSION: The current in vitro model combining scratch and kainate induced glial scarring and inhibitory molecules and restricted neurite outgrowth very strongly than either the mechanically or chemically-induced injury model; hence, it may be a useful tool for research on SCI.
Animals ; Arm ; Astrocytes ; Chondroitin Sulfate Proteoglycans ; Cicatrix* ; Embryonic Structures ; In Vitro Techniques ; Kainic Acid* ; Neurites ; Neuroglia ; Neurons ; Plastics ; Protein Kinases ; Rats ; Spinal Cord Injuries ; Spinal Cord* ; Vimentin

Nitric oxide (NO) is a short lived membrane permeable gas, a recently identified neuronal messenger molecule, and implicated in several activity-dependent forms of synaptic plasticity. The histochemical staining of NADPH-diaphorase (NADPH-d) provides a simple method to select populations of neurons containing nitric oxide synthase (NOS), throughout the brain. The NADPH-d positive neurons, uniquely resistant to toxic insults and neurodegenerative diseases, have been colocalized with neurons in the brain and peripheral tissue containing NOS. Apodemus agrarius has been used for experimental purpose to identify the route of infection and pathogenesis of korean hemorrhagic fever. However, despite of the increasing publication at present about the physiologic and ecologic characteristics of Apodemus, a few data are available about the morphologic findings in the brain. In this study we used NADPH-d histochemistry to evaluate the distribution of neurons, contain NOS, on the postnatal development in cerebral cortex and striatum of the Apodemus agrarius. In the cerebral cortex of Apodemus agrarius, NADPH-d positive neurons were observed in all cortical layers, but were concentrated in V-VI layer. NADPH-d positive neurons of forebrain were more dense than other cortical regions. At 1 week after birth, NADPH-d positive neurons had short processes and immature features. In contrast, at 12 weeks after birth, NADPH-d positive neurons had longer and more complex processes than that of earlier ages. In the striatum, NADPH-d positive neurons were intensely stained, predominantly medium-sized neurons. They had multipolar or bipolar dendritic branches which belong to fusiform or stellate cell types in all groups. In addition, at 4 and 12 weeks after birth, NADPH-d positive neurons had long and complex fiber network. The number of NADPH-d positive neurons in the striatum was relatively decreased during postnatal development. However, the length and complexity of their processes were relatively increased after birth. Present results showed postnatal maturation patterns such as morphological features of NADPH-d positive neurons. These findings suggest that NADPH-d positive neurons will be reach adult level after 4 weeks of postnatal age. Therefore, this report provide the morphological evidence supporting the hypothesis that NO may be play a role in regulation of neuronal development and synaptic plasticity during postnatal development of Apodemus agrarius.
Adult ; Animals ; Brain ; Cerebral Cortex* ; Hemorrhagic Fever with Renal Syndrome ; Humans ; Membranes ; Murinae* ; Neurodegenerative Diseases ; Neurons* ; Nitric Oxide ; Nitric Oxide Synthase ; Parturition ; Plastics ; Prosencephalon ; Publications

It has been reported that injection of Freund's complete adjuvant (FCA) into the hindpaw of a rat induces inflammatory responses with accompanying pain behaviors. Signs of pain behaviors observed in FCA-injected animals were reported to be similar to symptoms seen in patients with inflammatory pain. The nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) is a selective histochemical marker for the nitric oxide synthesizing enzyme, nitric oxide synthase (NOS). N (G)-nitro-L-arginine methyl ester (L-NAME) is a NOS inhibitor. In the present study, we examined if inflammaory pain causes increases in NADPH-diaphorase reactivities in neurons of the dorsal root ganglia (DRG). The results were as follows; 1. FCA-induced inflammation on a limb increased staining density (SD) of NADPH-d positive neurons in the ipsilateral side DRG. 2. Pretreatment of L-NAME did not changed SD of NADPH-d positive neurons on the inflammation of contralateral side DRG 3. Posttreatment of L-NAME decreased the inflammation induced SD of NADPH-d positive neurons. 4. n-NOS immunoreactivity did not match NADPH-d histochemical study, implying the constant level of enzyme itself. Inflammation pain on a hindlimb increased staining density of NADPH-diaphorase positive neuron in the DRG, which was decreased by L-NAME. L-NAME also decreased pain perception. This suggests a role of NO in the pain perception and/or modulation at the level of DRG.
Animals ; Diagnosis-Related Groups* ; Extremities ; Ganglia, Spinal ; Hindlimb ; Humans ; Inflammation ; NAD ; NADP ; Neurons ; NG-Nitroarginine Methyl Ester ; Nitric Oxide Synthase ; Nitric Oxide* ; Pain Perception ; Rats*

Background: Recent studies have demonstrated that the levels of adipocyte fatty acid-binding protein (A-FABP) are closely associated with diabetic kidney disease (DKD) in patients with type 2 diabetes mellitus (T2DM). This study aimed to examine the association between serum A-FABP level and rapid renal function decline in patients with T2DM and preserved renal function. Methods: This was a prospective observational study of 452 patients with T2DM and preserved renal function who had serial measurements of estimated glomerular filtration rate (eGFR). Rapid renal function decline was defined as an eGFR decline of >4% per year. The association between baseline serum A-FABP level and rapid renal function decline was investigated. Results: Over a median follow-up of 7 years, 82 participants (18.1%) experienced rapid renal function decline. Median A-FABP levels were significantly higher in patients with rapid renal function decline, compared to non-decliners (20.2 ng/mL vs. 17.2 ng/ mL, P=0.005). A higher baseline level of A-FABP was associated with a greater risk of developing rapid renal function decline, independent of age, sex, duration of diabetes, body mass index, systolic blood pressure, history of cardiovascular disease, baseline eGFR, urine albumin creatinine ratio, total cholesterol, glycosylated hemoglobin, high-sensitivity C-reactive protein and use of thiazolidinedione, insulin, angiotensin-converting-enzyme inhibitors and angiotensin II-receptor blockers and statin (odds ratio, 3.10; 95% confidence interval, 1.53 to 6.29; P=0.002). Conclusion A high level of serum A-FABP is associated with an increased risk of rapid renal function decline in patients with T2DM and preserved renal function. This suggests that A-FABP could play a role in the progression of DKD in the early stages.

Recent studies have demonstrated that the levels of adipocyte fatty acid-binding protein (A-FABP) are closely associated with diabetic kidney disease (DKD) in patients with type 2 diabetes mellitus (T2DM). This study aimed to examine the association between serum A-FABP level and rapid renal function decline in patients with T2DM and preserved renal function.