No abstract available.
Animals ; Dogs* ; Neurons*

BACKGROUND: In recent years, estrogen has also been shown to modulate the development and function of the brain, bur not exclusively in areas involved with sexual behavior. Among the most novel and fascinating effects of estrogen are those on cognitive function and memory process and their alterations during aging and neurodegenarative disease like Alzheimer. Estrogen receptors distributed not only in the hypothalamus but many different areas, like cerebral cortex, hippocampus, basal forebrain, midbrain, spinal cord, and the diverse action of estrogen is supported by this fact. Numerous studies suggest thai estrogen may be beneficial in preserving cognitive function, but it is not clear yet. PURPOSE: In this study, we perform the immunohistochemical staining in the hippocampus of normal aged rat, and show the distribution of estrogen receptor compared with the neonatal rat. METHODS: we have used antibodies against a estrogen receptor(ER)-alpha to determine their distribution in neonatal and aged SD rat hippocampus. RESULTS: In neonatal rat hippocampus, ER-alpha immunoreactivity was observed in the nucleus of Purkinje cells, whereas in aged rat hippocampus, ER-a immunoreactivity was found mainly in the cytoplasm of Purkinje cells. CONCLUSION: We showed the age related intracellular differential distribution of ER-alpha immunoreactivity in the rat hippocampus. But, further investigations are required to establish whether functional relations like cognitive ability exist with this different intracellular expression of ER-alpha immunoreactivity.
Aging ; Animals ; Antibodies ; Asian Continental Ancestry Group ; Brain ; Cerebral Cortex ; Cytoplasm ; Estrogens* ; Hippocampus* ; Humans ; Hypothalamus ; Memory ; Mesencephalon ; Prosencephalon ; Purkinje Cells ; Rats* ; Receptors, Estrogen ; Sexual Behavior ; Spinal Cord

Autophagy is a eukaryotic self-degradation system that plays a pivotal role in the maintenance of cellular homeostasis. Atg9 is the only transmembrane Atg protein required for autophagosome formation. Although the subcellular localization of the Atg9A has been examined, little is known about its precise cell and tissue distribution. In the present study, we used G93A mutation in superoxide dismutase 1 [SOD1(G93A)] mutant transgenic mice as an in vivo model of amyotrophic lateral sclerosis (ALS) and performed immunohistochemical studies to investigate the changes of Atg9A immunoreactivity in the central nervous system of these mice. Atg9A-immunoreactivity was detected in the spinal cord, cerebral cortex, hippocampal formation, thalamus and cerebellum of symptomatic SOD1(G93A) transgenic mice. By contrast, no Atg9A-immunoreactivity were observed in any brain and spinal cord region of wtSOD1, pre-symptomatic and early symptomatic mice, and the number and staining intensity of Atg9A-positive cells did not differ in SOD1(G93A) mice between 8 and 13 weeks of age. These results provide evidence that Atg9A-immunoreactivity were found in the central nervous system of SOD1(G93A) transgenic mice after clinical symptoms, suggesting a possible role in the pathologic process of ALS. However, the mechanisms underlying the increased immunoreactivity for Atg9A and the functional implications require elucidation.
Amyotrophic Lateral Sclerosis ; Animals ; Autophagy ; Brain ; Central Nervous System* ; Cerebellum ; Cerebral Cortex ; Hippocampus ; Homeostasis ; Mice ; Mice, Transgenic* ; Spinal Cord ; Superoxide Dismutase ; Thalamus ; Tissue Distribution

Autophagy is a eukaryotic self-degradation system that plays a pivotal role in the maintenance of cellular homeostasis. Atg9 is the only transmembrane Atg protein required for autophagosome formation. Although the subcellular localization of the Atg9A has been examined, little is known about its precise cell and tissue distribution. In the present study, we used G93A mutation in superoxide dismutase 1 [SOD1(G93A)] mutant transgenic mice as an in vivo model of amyotrophic lateral sclerosis (ALS) and performed immunohistochemical studies to investigate the changes of Atg9A immunoreactivity in the central nervous system of these mice. Atg9A-immunoreactivity was detected in the spinal cord, cerebral cortex, hippocampal formation, thalamus and cerebellum of symptomatic SOD1(G93A) transgenic mice. By contrast, no Atg9A-immunoreactivity were observed in any brain and spinal cord region of wtSOD1, pre-symptomatic and early symptomatic mice, and the number and staining intensity of Atg9A-positive cells did not differ in SOD1(G93A) mice between 8 and 13 weeks of age. These results provide evidence that Atg9A-immunoreactivity were found in the central nervous system of SOD1(G93A) transgenic mice after clinical symptoms, suggesting a possible role in the pathologic process of ALS. However, the mechanisms underlying the increased immunoreactivity for Atg9A and the functional implications require elucidation.
Amyotrophic Lateral Sclerosis ; Animals ; Autophagy ; Brain ; Central Nervous System* ; Cerebellum ; Cerebral Cortex ; Hippocampus ; Homeostasis ; Mice ; Mice, Transgenic* ; Spinal Cord ; Superoxide Dismutase ; Thalamus ; Tissue Distribution

Duchenne Muscular dystrophy(DMD) is a debilitating X-linked muscle disease and dyskophin is a muscle membrane protein, which is recently discovered through reverse genetics by Kunkel et al(1987). We evaluate the dystrophin distribution by irnmunohistochemical staining with anti Torpedo dyskophin antibody in the muscle biopsy materials from 11 clinically and pathologically diagnosed Duchenne type muscular dyskophy and 23 controls of other neuromuscular disorders or normal amputed legs. Normal staining of dystrophin were found in all the muscle preparation from 23 controls. In 10 of 11 pahents with Duchenne type muscular dyskophy diagnosed clinically and pathologically, reaction to anti-Torpedo dystrophin antibody was absent or markedly deficient. However, in one subject with definite DMD clinically, the immunostaining showed normal dense staining. He was a 5-year-old boy who was presented with abdominal pain and general muscle weakness, and his final diagnosis were choledocal cyst and Duchenne muscular dyskophy. Therefore it could be concluded that the immunohistochemical staining with anti-Torpedo dystrophin antibody should prove helpful in delineatior of myopathies that overlap clinically with Duchenne type progressive muscular dyskophies and it shows prornise as an accurate tool for the diagnosis of DMD and for the evaluation of therapeutic effects.
Abdominal Pain ; Biopsy ; Child, Preschool ; Diagnosis ; Dystrophin* ; Humans ; Leg ; Male ; Membrane Proteins ; Muscle Weakness ; Muscular Diseases ; Muscular Dystrophies* ; Reverse Genetics ; Torpedo

No abstract available.
Animals ; Brain* ; Mice*

Asymmetrical distribution of the vasoactive intestinal polypeptide (VIP)-immunoreactive neurons in the hippocam-pal formation of rat nd iv/iv mouse was detected by the immunocytochemical method. The animals were divided into 3 groups and group I was subdivided into 4 groups according to sex and handedness determined by the paw-preference test : group I (male right-handedness (MR), male left-handedness (ML), female right-handedness (FR), female left-handedness (FL)), group II (female rats ovariectomized in neonatal period), group III (iv/iv mouse, situs solitus & inversus). The number of VIP-immunoreactive neurons were counted under the light microscope and the following results were obtained. 1. In MR of group I, the area containing the higher density of VIP neurons in the left hippocampal formation than the right were the CA1, CA3, dentate gyrus and subiculum. In ML, the area containing the higher density of VIP neurons in the left cortex were the level 2 of dentate gyrus, and the area exhibiting higher density in the right cortex were level 1, 3 of dentate gyrus. 2. The asymmetrical distributional pattern of VIP in ovariectomized rat (group II) was similar to male subgroups in group I. 3. In group III, there was no asymmetrical distribution of VIP-immunoreactive neurons. Above results show that asymmetrical distribution of VIP neurons are prominent in the right handedness or male groups, and the sexually dimorphic pattern of VIP is related directly or indirectly to gonadal steroids, but there seems to be no relationship between iv gene and asymmetrical distribution of VIP neurons in cerebral cortex.
Animals ; Cerebral Cortex ; Dentate Gyrus ; Female ; Functional Laterality* ; Gonads* ; Hippocampus* ; Humans ; Immunohistochemistry ; Male ; Mice ; Neurons* ; Ovariectomy ; Rats* ; Steroids* ; Vasoactive Intestinal Peptide*

In the present study, we investigated influences of glycogen synthase kinase (GSK) 3beta on the development and/or progression of amyotrophic lateral sclerosis (ALS). We used transgenic mice expressing a human Cu/Zn superoxide dismutase mutant (SOD1G93A) as an in vivo model of ALS and examined expressional changes of GSK3beta immunohistochemically in the spinal cord, brain stem and cerebellum. With these experiments we demonstrate that the neurons in these regions of symptomatic SOD1G93A transgenic mice showed increased GSK3beta immunoreactivities compared with wild-type SOD1 transgenic mice. In contrast to symptomatic SOD1G93A transgenic mice, few GSK3beta immunoreactivity changes were detected in 8w- and 13w-old presymptomatic SOD1G93A transgenic mice. These data suggest the possibility that GSK3 functions as a modulating factor of apoptosis-related alterations in ALS and that GSK3beta exert differential functions in the development and/or progression of ALS. But the exact functional significances of these changes require further elucidation.
Amyotrophic Lateral Sclerosis ; Animals ; Brain Stem ; Central Nervous System* ; Cerebellum ; Glycogen Synthase Kinases* ; Glycogen Synthase* ; Glycogen* ; Humans ; Mice ; Mice, Transgenic* ; Neurons ; Spinal Cord ; Superoxide Dismutase

The first author of the article has duely admitted that he is mainly responsible for the misconduct.

BACKGROUND: Human umbilical cord blood-derived mesenchymal stem cells (hUCB-MSCs) may have multiple therapeutic applications for cell based therapy including the treatment of pulmonary artery hypertension (PAH). As low survival rates and potential tumorigenicity of implanted cells could undermine the mesenchymal stem cell (MSC) cell-based therapy, we chose to investigate the use of conditioned medium (CM) from a culture of MSC cells as a feasible alternative. METHODS: CM was prepared by culturing hUCB-MSCs in three-dimensional spheroids. In a rat model of PAH induced by monocrotaline, we infused CM or the control unconditioned culture media via the tail-vein of 6-week-old Sprague-Dawley rats. RESULTS: Compared with the control unconditioned media, CM infusion reduced the ventricular pressure, the right ventricle/(left ventricle+interventricular septum) ratio, and maintained respiratory function in the treated animals. Also, the number of interleukin 1alpha (IL-1alpha), chemokine (C-C motif) ligand 5 (CCL5), and tissue inhibitor of metalloproteinase 1 (TIMP-1)-positive cells increased in lung samples and the number of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling technique (TUNEL)-positive cells decreased significantly in the CM treated animals. CONCLUSIONS: From our in vivo data in the rat model, the observed decreases in the TUNEL staining suggest a potential therapeutic benefit of the CM in ameliorating PAH-mediated lung tissue damage. Increased IL-1alpha, CCL5, and TIMP-1 levels may play important roles in this regard.
Animals ; Apoptosis ; Culture Media ; Culture Media, Conditioned ; Deoxyuridine ; Fetal Blood* ; Gene Expression ; Humans ; Hypertension* ; In Situ Nick-End Labeling ; Interleukin-1alpha ; Lung ; Mesenchymal Stromal Cells ; Models, Animal ; Monocrotaline ; Pulmonary Artery ; Rats* ; Rats, Sprague-Dawley ; Survival Rate ; Tissue Inhibitor of Metalloproteinase-1 ; Umbilical Cord* ; Ventricular Pressure