[Tips for women in their forties].
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Aging↗
Biomedical subjects
G Schultz
Publications and source records attributed to G Schultz.
[Estrogen-effective isoflavones in Trifolium pratense (red clover). Distribution in superterranean parts of plants and occurrence as "bound" isoflavones].
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Animals↗
[Isoflavone glucoside formononetin-7-glucoside and biochanin A-7-glucoside in Trifolium pratense L].
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Flavonoids↗
Hepatic angiomyoma: CT and MRI findings.
Angiomyoma is a benign tumor that arises from soft muscular tissue within the blood vessel wall. This lesion has been found in different organs. The preferential location of these tumors is the lower extremity. We describe the rare case of a hepatic angiomyoma and present the radiologic findings of computed tomography and magnetic resonance imaging.
Angiomyoma↗
A nucleotide regulatory site for somatostatin inhibition of adenylate cyclase in S49 lymphoma cells.
The cyc- variants of S49 lymphoma cells have served as powerful tools for studying the components and mechanisms of hormone-induced adenylate cyclase stimulation, as these cells are deficient in the guanine nucleotide regulatory site (Ns) mediating hormone, guanine nucleotide, cholera toxin and fluoride-induced stimulations of the enzyme. Because of this deficiency, membranes of these cells have been used for reconstitution of the system by inserting the coupling component derived from other cell types. The hormone-sensitive adenylate cyclase is not only stimulated by hormones but can also be inhibited by a wide variety of hormones and neurotransmitters, and there is some evidence that hormonal inhibition may be mediated by a distinct guanine nucleotide regulatory site. Studies in cyc- cells lacking a functional Ns may therefore answer this unresolved, important question. We have recently observed that stable GTP analogues can inhibit cyc- adenylate cyclase stimulated by purified, preactivated Ns or forskolin, which can activate adenylate cyclase even in the absence of a functional Ns (ref. 10). The data indicated that these Ns-deficient cells contain an inhibitory guanine nucleotide site, Ni. To strengthen this concept, we investigated whether the cyc- adenylate cyclase can be inhibited by a hormone. We report here that somatostatin decreases cyclic AMP levels in cyc- cells, inhibits the forskolin-stimulated adenylate cyclase and causes a concomitant increase in a high affinity GTPase activity in cyc- membranes. The data strongly suggest that both the hormone- and guanine nucleotide-induced adenylate cyclase inhibitions in cyc- cells are mediated by Ni and that the mechanisms of activation and inactivation of Ni are similar to those established for Ns.
Adenylyl Cyclase Inhibitors↗
The GTP-binding protein, Go, regulates neuronal calcium channels.
In neuronal cells, opioid peptides and opiates inhibit neurotransmitter release, which is a calcium-dependent process. They also inhibit adenylyl cyclase, presumably via the membrane signal-transducing component, Gi, a guanine nucleotide-binding protein (G-protein). No causal relationship between these two events has yet been demonstrated. Besides Gi, membranes of neuronal tissues contain large amounts of Go, a G-protein with unknown function. Both G-proteins are heterotrimers consisting of alpha-, beta- and gamma-subunits; the alpha-subunits can be ADP-ribosylated by an exotoxin from Bordetella pertussis (PT), which modification inhibits receptor-mediated activation of the G-protein. It was recently shown that noradrenaline, dopamine and gamma-aminobutyric acid (GABA) inhibit the voltage-dependent calcium channels in dorsal root and sympathetic ganglia; this inhibition is mimicked by intracellular application of guanine nucleotides and blocked by PT, suggesting the involvement of a G-protein. Here we report an inhibitory effect of the opioid D-Ala2, D-Leu5-enkephalin (DADLE) on the calcium current (ICa) in neuroblastoma X glioma hybrid cells (N X G cells). Pretreatment with PT almost completely abolishes the DADLE effect. The effect is restored by intracellular application of Gi and Go. As the alpha-subunit of Go (with or without beta-gamma complex) is 10 times more potent than Gi, we propose that Go is involved in the functional coupling of opiate receptors to neuronal voltage-dependent calcium channels.
Animals↗
Effect of epidermal growth factor on cell proliferation in normal and wounded connective tissue.
Epidermal growth factor has been previously shown to stimulate connective tissue repair in the perforated rat mesentery. The mechanism by which epidermal growth factor accelerates closure of mesenteric perforations has not been established, but epidermal growth factor may stimulate mitosis, contraction, migration, or angiogenesis. In the present investigation, the effect of epidermal growth factor on connective tissue cell proliferation was studied during the initial phase of repair of mesenteric perforations and in unwounded mesentery. Laparotomies were performed on Sprague-Dawley rats, and standardized perforations were made with a scalpel in the center of the mesenteric "windows," leaving every second window as an internal control. Twice daily for 4 consecutive days, beginning on the day of surgery, the animals received by intraperitoneal injection either 10 microg of epidermal growth factor dissolved in phosphate-buffered saline solution or phosphate-buffered saline solution alone. Cell proliferation was measured by either mitotic index of fibroblasts and mesothelial cells or DNA content of individual fibroblast cell nuclei in the wound area or in unperforated control windows. Laparotomy alone was found to enhance proliferation during the early postoperative period, as shown by increased numbers of S + G2 fibroblasts and a greater mitotic index. Epidermal growth factor treatment increased the mitotic index in perforated windows on the third postoperative day, compared with controls treated with phosphate-buffered saline solution, but did not significantly increase either the number of S + G2 fibroblasts or the mitotic index in unwounded tissue. Also, the proliferative response after epidermal growth factor treatment was significantly higher in wounded tissue. This study shows that epidermal growth factor stimulates proliferation of connective tissue cells in wounded but not unwounded tissue, and such enhancement of fibroblast proliferation might be of importance in epidermal growth factor-stimulated connective tissue repair.
Journal Article↗
Mechanisms of TGF-beta action in connective tissue repair of rat mesenteric wounds.
We have recently reported that transforming growth factor-beta stimulates genuine connective tissue repair in the perforated rat mesentery and that this stimulation is not caused by increased macrophage chemotaxis. To further characterize the effect of transforming growth factor-beta(1) on the enhanced rate of wound closure, we performed a series of morphometric analyses with determination of mitotic index, fibroblast labeling index, cellular density, neovascularization, and scar tissue formation. Actin expression close to the wound margin was also evaluated morphologically. Fibroblast cell proliferation was not stimulated by transforming growth factor-beta(1) in either wounded or unwounded tissue. Transforming growth factor-beta(1) did, however, significantly increase the formation of healing tissue postoperative days 5 to 10 (p < 0.05) and angiogenesis was significantly stimulated by transforming growth factor-beta(1) postoperative days 7 and 10 (p < 0.005). The mean cellular density was significantly increased in unperforated, transforming growth factor-beta(1)-treated membranes from days 3 to 10, and increased expression of actin with time was observed close to the wound margin. Transforming growth factor-beta(1) was thus shown to be a potent stimulator of angiogenesis and healing tissue formation in connective tissue repair, but this stimulation mainly occurred after closure of perforations. The increased cellular density in the absence of stimulated proliferation and increased actin expression in wound cells indicate that contraction may be an important mechanism of connective tissue repair in the perforated rat mesentery.
Journal Article↗
Analysis of the acute and chronic wound environments: the role of proteases and their inhibitors.
To assess the differences in proteolytic activity of acute and chronic wound environments, wound fluids were collected from acute surgical wounds (22 samples) and chronic wounds (25 samples) of various etiologies, including mixed vessel disease ulcers, decubiti and diabetic foot ulcers. Matrix metalloproteinase (MMP) activity measured using the Azocoll assay was significantly elevated by 30 fold in chronic wounds (median 22.8 microg MMP Eq/ml) compared to acute wounds (median 0.76 microg MMP Eq/ml) (p < 0.001). The addition of the matrix metalloproteinase inhibitor Illomostat decreased the matrix metalloproteinase activity by approximately 90% in all samples, confirming that the majority of the activity measured was due to matrix metalloproteinases. Gelatin zymograms indicated predominantly elevated matrix metalloproteinase-9 with smaller elevations of matrix metalloproteinase-2. In addition tissue inhibitor of metalloproteinase-1 levels were analyzed in a small subset of acute and chronic wounds. When tissue inhibitor of metalloproteinase-1 levels were compared to protease levels there was an inverse correlation (p = 0.02, r = - 0.78). In vitro degradation of epidermal growth factor was measured by addition of 125I labelled epidermal growth factor to acute and chronic wound fluid samples. There was significantly higher degradation of epidermal growth factor in chronic wound fluid samples (mean 28.1%) compared to acute samples (mean 0.6%). This also correlated to the epidermal growth factor activity of these wound fluid samples (p < 0. 001, r = 0.64). Additionally, the levels of proteases were assayed in wound fluid collected from 15 venous leg ulcers during a nonhealing and healing phase using a unique model of chronic wound healing in humans. Patients with nonhealing venous leg ulcers were admitted to the hospital for bed rest and wound fluid samples were collected on admission (nonhealing phase) and after 2 weeks (healing phase) when the ulcers had begun to heal as evidenced by a reduction in size (median 12%). These data showed that the elevated levels of matrix metalloproteinase activity decreased significantly as healing occurs in chronic leg ulcers (p < 0.01). This parallels the processes observed in normally healing acute wounds. This data also supports the case for the addition of protease inhibitors in chronic wounds in conjunction with any treatments using growth factors.
Acute Disease↗
Imidazoline binding sites and signal transduction pathways.
1. Discrete, non-adrenergic binding sites for imidazolines have been characterized in the brain and periphery. The I1 clonidine-preferring site is mainly distributed in the brain and brain stem, while the I2 idazoxan-preferring site is more widely distributed. 2. The I1 site appears to be associated with modulation of blood pressure. Imidazolines act within the rostral ventrolateral medulla to produce hypotension. The underlying signal transduction mechanism is poorly understood. 3. The imidazolines clonidine and cirazoline inhibited nicotine-stimulated calcium entry into rat phaeochromocytoma (PC-12) cells by a non-adrenergic mechanism. This effect was not attributable to the stimulation of protein kinases. 4. Similarly, clonidine and cirazoline inhibited nicotine-stimulated inward currents into PC-12 cells. This inhibitory action was not altered by inhibitors of signal transducing G-proteins. 5. Clonidine and cirazoline displaced the ion channel ligand [3H]-phencyclidine from nicotinic acetylcholine receptors, suggesting that these drugs act by direct blockade of the intrinsic ion channel of the nicotinic acetylcholine receptor. 6. This ion channel-blocking activity represents a novel action of these imidazolines and may underlie some of the proposed physiological actions of I1 sites.
Animals↗
Immunolocalization and quantitation of transforming growth factor alpha in hydatidiform mole.
Complete hydatidiform mole (CHM), a condition related to abnormal gestation, occurs predominantly in the young reproductive age group and has a high prevalence rate in the Trivandrum region, occurring in 1.2% of deliveries. Transforming growth factor alpha (TGF-alpha) is an important growth regulatory molecule, the location and function of which at the human fetomaternal interface in CHM remains to be determined. The present study examined the presence of TGF-alpha in the normal and complete molar placenta and decidua throughout gestation. A total of 149 complete molar placental tissue samples and 96 normal placental tissue samples were evaluated for TGF-alpha expression by immunohistochemistry and 50 each of CHM and normal placental tissue for TGF-alpha concentration by radioimmunoassay. The peptide was localized immunocytochemically with a monoclonal anti-TGF-alpha antibody on paraffin-embedded tissue using the avidin-biotin complex peroxidase technique with aminoethyl carbazole as the chromogen. In molar placenta, villous trophoblast cells (syncytiotrophoblasts and cytotrophoblasts) showed intense cytoplasmic staining at all gestational ages compared to normal placenta of the same gestational age. The tissue concentration of TGF-alpha was highly overexpressed in the molar placenta (10-1000 fold) compared to that in the normal placenta. The results indicate that TGF-alpha is present in trophoblasts throughout human gestation and may provide additional growth advantage to maintenance of the hyperproliferative condition in trophoblastic tumors.
Adult↗
Development of lower leg strength and flexibility with the strength shoe.
The Strength Shoe is a modified athletic shoe with a 4-cm thick rubber platform attached to the front half of the sole. It is promoted as an effective method of increasing "speed, quickness, and explosive power," as well as ankle flexibility and calf circumference, when used in a plyometrics-based training regimen. This study evaluates, in a prospective, randomized trial, the efficacy and safety of the Strength Shoe training regimen for increasing lower leg flexibility and strength in intercollegiate track and field participants. No enhancement of flexibility, strength, or performance was observed for participants wearing the Strength Shoe at the end of an 8-week training program, following the suggested regimen of the manufacturer. The use of the Strength Shoe cannot be recommended as a safe, effective training method for development of lower leg strength and flexibility. However, the use of plyometrics in a properly supervised setting may improve athletic performance and merits further investigation.
Evaluation Studies as Topic↗
Moyamoya-like vasculopathy from cocaine dependency.
We herein describe two cases of moyamoya vasculopathy occurring in two men who used alkaloidal cocaine for years. One patient presented with aneurysmal subarachnoid hemorrhage and one with infarction in both lobes. Particularly impressive was a significant degree of collateral development with lenticulostriate networks.
Adult↗
Reduction of adenylate cyclase activity in lysates of human platelets by the alpha-adrenergic component of epinephrine.
The effects of the alpha- and beta-adrenergic components of epinephrine on adenylate cyclase activity were studied in lyastes of human platelets. The beta-adrenergic component increased enzyme activity between 20 and 50%, whereas the alpha-adrenergic component caused a concentration-dependent reduction of adenylate cyclase activity. The maximal inhibition of adenylate cyclase was 50 to 60% with about 100 muM epinephrine; about 1 muM epinephrine caused half-maximal inhibition. The alpha-adrenergic reduction of adenylate cyclase activity appeared to be immediate and was specific for platelets from species in which alpha-adrenergic stimulation caused aggregation. Adenylate cyclase activity measured in the presence of prostaglandins of fluoride was also reduced by the alpha-adrenergic component of epinephrine, but the inhibitory effect was less than on basal activity. In contrast, the 5'-guanylylimidodiphosphate-stimulated enzyme was not affected by stimulation of alpha-adrenergic receptors.
Adenosine Triphosphate↗
[Morphological and functional changes of the gastric mucosa in chronic hepatitis and liver cirrhosis].
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Biopsy↗