scholarly journals Effects of 3-isobutyryl-2-isopropylpyrazolo-(1,5-a)-pyridine(Ibudilast) on hypoxic injury in fetal rat cortical cells.

Nosotchu ◽  
1994 ◽  
Vol 16 (5) ◽  
pp. 354-359
Author(s):  
Takayuki Sakaki ◽  
Kazuo Yamada ◽  
Hideo Otsuki ◽  
Takamichi Yuguchi ◽  
Toru Hayakawa
Keyword(s):  
Cortical Cells ◽  
Hypoxic Injury ◽  
Fetal Rat

scholarly journals Effects of 5-bromodeoxyuridine on the ACTH-dependent mitochondrial biogenesis in cortical cells of fetal rat adrenals in tissue culture.

1976 ◽  
Vol 71 (3) ◽  
pp. 951-956 ◽  
Author(s):  
A I Kahri ◽  
M Salmenperä ◽  
A Saure
Keyword(s):  
Tissue Culture ◽  
Mitochondrial Dna ◽  
Dna Synthesis ◽  
Nuclear Dna ◽  
Acth Stimulation ◽  
Cortical Cells ◽  
Proliferative Phase ◽  
Fetal Rat ◽  
Rat Adrenals ◽  
Mitochondrial Dna Synthesis

Cortical cells of fetal rat adrenals in tissue culture were treated with 5-bromodeoxyuridine (BrdU) during their proliferative phase and during ACTH stimulation when nuclear DNA synthesis has almost ceased. Pretreatment with 0.5 mug/ml/day of BrdU inhibited the ACTH-induced differentiation of cortical cells as well as the secretion of corticosterone and 18-OH-deoxycorticosterone (18-OHDOC). When nuclear DNA synthesis was suppressed and mitochondrial DNA synthesis was stimulated by ACTH BrdU addition (30 mug/ml/day) permitted normal untrastructural differentiation of cortical cells, except that the development of mitochondrial inner membranes was inhibited. Simultaneously mitochondrial inner membranes was inhibited. Simultaneously mitochondrial 11beta- and 18-hydroxylations were strongly inhibited while cytoplasmic 21-hydroxylation was not affected.

Involvement of VIP on BDNF-induced somatostatin gene expression in cultured fetal rat cerebral cortical cells

2001 ◽  
Vol 94 (1-2) ◽  
pp. 59-66 ◽  
Author(s):  
Gemma Villuendas ◽  
Franco Sánchez-Franco ◽  
Nuria Palacios ◽  
Miriam Fernández ◽  
Lucinda Cacicedo
Keyword(s):  
Gene Expression ◽  
Cortical Cells ◽  
Fetal Rat

scholarly journals Prostaglandin E1 Induces c-Fos and Myc Proteins and Protects Rat Hippocampal Cells against Hypoxic Injury

1994 ◽  
Vol 14 (1) ◽  
pp. 150-155 ◽  
Author(s):  
Hideo Otsuki ◽  
Kazuo Yamada ◽  
Takamichi Yuguchi ◽  
Mamoru Taneda ◽  
Toru Hayakawa
Keyword(s):  
Hippocampal Neurons ◽  
Culture Medium ◽  
Quantitative Measure ◽  
Serum Free Medium ◽  
Free Medium ◽  
Hypoxic Injury ◽  
Hypoxia Group ◽  
Ldh Activity ◽  
Hippocampal Cell ◽  
Fetal Rat

We investigated the effects of prostaglandin (PG) E1 on the hypoxic injury of fetal rat hippocampal cells. Primary hippocampal cell cultures (embryonic day 18) were established and maintained. After 72 h in culture, PGE1 was added to the serum-free medium at a final concentration of 10−5-10−9 M. Cultures were divided into two groups: The normoxia group was in culture for another 48 h, and the hypoxia group was exposed to 24 h of hypoxia followed by continuation of culture for another 24 h. As a quantitative measure of cell death, lactate dehydrogenase (LDH) activity was estimated in the culture medium. The LDH activity, released by the hypoxic insult, was significantly smaller with PGE1 treatment at 10−6, 10−7, and 10−8 M (p < 0.01) and 10−9 M (p < 0.05) compared with the control. No differences in the LDH activities were observed in the normoxia group. Glial culture was not affected by the hypoxia. Western blot analysis showed an increased induction of 62-kDa c-Fos and 58, 60, and 66 kDa Myc proteins in rat hippocampal cells with 10−7 M PGE1 treatment. We conclude that PGE1 at concentrations of 10−6-10−9 M protects rat hippocampal neurons against hypoxic insult.

Neurotransmitter regulation of somatostatin secretion by fetal rat cerebral cortical cells in culture

1993 ◽  
Vol 16 (9) ◽  
pp. 661-668 ◽  
Author(s):  
M. T. de los Frailes ◽  
L. Cacicedo ◽  
M. J. Lorenzo ◽  
R. M. Tolón ◽  
G. Fernández ◽  
...  
Keyword(s):  
Cortical Cells ◽  
Cells In Culture ◽  
Somatostatin Secretion ◽  
Fetal Rat

Ultrastructural Cytopiasmic Changes of Adrenal Cortex During Pregnancy

1969 ◽  
Vol 27 ◽  
pp. 298-299
Author(s):  
T. M. Murad ◽  
Karen Israel ◽  
Jack C. Geer
Keyword(s):  
Adrenal Gland ◽  
Steroid Hormones ◽  
Adrenal Cortex ◽  
Lipid Droplets ◽  
Plasma Cholesterol ◽  
Adrenal Steroids ◽  
Dynamic Changes ◽  
Cortical Cells ◽  
Acetyl Coenzyme A ◽  
Adrenal Cortical Cells

Adrenal steroids are normally synthesized from acetyl coenzyme A via cholesterol. Cholesterol is also shown to enter the adrenal gland and to be localized in the lipid droplets of the adrenal cortical cells. Both pregnenolone and progesterone act as intermediates in the conversion of cholesterol into steroid hormones. During pregnancy an increased level of plasma cholesterol is known to be associated with an increase of the adrenal corticoid and progesterone. The present study is designed to demonstrate whether the adrenal cortical cells show any dynamic changes during pregnancy.

Effects of Steroids on Fetal Rat Liver

1969 ◽  
Vol 27 ◽  
pp. 350-351
Author(s):  
F. G. Zaki
Keyword(s):  
Liver Injury ◽  
Rat Liver ◽  
Fetal Liver ◽  
Dosage Level ◽  
Maternal Plasma ◽  
Methyl Prednisolone ◽  
Fetal Rat ◽  
Toxic Agents ◽  
Fetal Rat Liver ◽  
Neonatal Liver

Fetal and neonatal liver injury induced by agents circulating in maternal plasma, even though well recognized, its morphological manifestations are not yet established. As part of our studies of fetal and neonatal liver injury induced by maternal nutritional disorders, metabolic impairment and toxic agents, the effects of two anti-inflammatory steroids have been recently inves tigated.Triamcinolone and methyl prednisolone were injected each in a group of rats during pregnancy at a-dosage level of 2 mgm three times a week. Fetal liver was studied at 18 days of gestation. Litter size and weight markedly decreased than those of control rats. Stillbirths and resorption were of higher incidence in the triamcinolone group than in those given the prednisolone.

Temporal and spatial interrelationships of confronting cisternae to nuclear envelope

1992 ◽  
Vol 50 (1) ◽  
pp. 930-931
Author(s):  
John R. Palisano
Keyword(s):  
Endoplasmic Reticulum ◽  
Nuclear Envelope ◽  
Tumor Cells ◽  
Hela Cells ◽  
Microscopic Investigation ◽  
Electron Microscopic Investigation ◽  
Serial Sections ◽  
Electron Microscopic ◽  
Fetal Rat ◽  
Temporal And Spatial

Although confronting cistemae (CC) have been observed in a variety of tumor cells and normal fetal rat, mouse, and human epithelial tissues, little is known about their origin or role in mitotic cells. While several investigators have suggested that CC arise from nuclear envelope (NE) folding back on itself during prophase, others have suggested that CC arise when fragments of NE pair with endoplasmic reticulum. An electron microscopic investigation of 0.25 um thick serial sections was undertaken to examine the origin of CC in HeLa cells.

"STEROID-CELL" ANTIBODY IN ENDOCRINE DISEASES

1974 ◽  
Vol 76 (4) ◽  
pp. 729-740 ◽  
Author(s):  
Peter Kamp ◽  
Per Platz ◽  
Jørn Nerup
Keyword(s):  
Leydig Cells ◽  
Addison’S Disease ◽  
Addison's Disease ◽  
Hormone Production ◽  
Cortical Cells ◽  
Endocrine Diseases ◽  
Cell Antibody ◽  
Indirect Immunofluorescence Technique ◽  
Males And Females ◽  
Adrenal Cortical Cells

ABSTRACT By means of an indirect immunofluorescence technique, sera from 116 patients with Addison's disease, an equal number of age and sex matched controls and 97 patients with other endocrine diseases were examined for the occurrence of antibody to steroid-producing cells in ovary, testis and adrenal cortex. Fluorescent staining was observed in the theca cells of growing follicles, the theca lutein cells, testicular Leydig cells and adrenal cortical cells, i. e. cells which contain enzyme systems used in steroid hormone production. The "steroid-cell" antibody was present in 24 % of the patients with idiopathic Addison's disease, equally frequent in males and females, and in 17 % of the patients with tuberculous Addison's disease, but was rarely found in controls, including patients with other endocrine diseases. Female hypergonadotrophic hypogonadism made an exception, since the "steroid-cell" antibody was found in about half the cases with this condition.

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