Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pedicled skin flaps in the pig have been used to investigate the effects of 3-h ischemia and reperfusion on the epidermal metabolism of glycogen and glucose. Epidermal glycogen content fell steadily at a rate of about 1.2 mumol of glucose-equivalents per g wet weight per h whereas the rate of glucose consumption declined from 1.8 mumol per g wet weight during the first hour to about 0.25 mumol per g wet weight in the third hour. During ischemia the proportion of glycogen synthase in the I form increased progressively from an initial value of about 8% to about 70%, but the proportion of phosphorylase in the a form decreased only in the third hour of ischemia. The concentration of ATP decreased and ADP and AMP increased but the total pool of epidermal adenine nucleotides was not depleted. On reperfusion, these changes were reversed and normal epidermal concentrations of glucose and adenine nucleotides were restored within 30 min and remained stable thereafter. The resynthesis of glycogen proceeded at a steady rate of about 1 mumol per h per g wet weight and the phosphorylation state of both glycogen synthase and phosphorylase approached normal values after 3 h. It is concluded that epidermal glycogenolysis in ischemia is, at least in part, a consequence of activation of phosphorylase b by AMP, and that glycogen resynthesis on reperfusion is promoted by the ischemic activation of glycogen synthase.
J Invest Dermatol 1986 Jan
PMID:Effect of ischemia and reperfusion of pig skin flaps on epidermal glycogen metabolism. 309 2

Venous thrombosis in an extremity, when extensive, can cause reversible tissue ischemia or frank gangrene even without arterial or capillary occlusion. Patients gradually or abruptly develop severe pain, extensive edema, and cyanosis of the extremity, nearly always in the legs. Gangrene can occur unless the venous obstruction is relieved. Such ischemic venous thrombosis can complicate surgery, trauma, childbirth, or prolonged immobility, but malignant neoplasms, either obvious or occult, are a major predisposing factor. The optimal therapy is anticoagulation and thrombectomy. Patients with venous gangrene may require amputation if extensive, deep-tissue destruction occurs. The mortality rate for ischemic venous thrombosis is about 40%, the cause of death usually being the underlying disease or pulmonary emboli.
Arch Dermatol 1987 Jul
PMID:Ischemic forms of acute venous thrombosis. 330 May 67

Acral ischemia with lividity is a well-described dermatologic sign in the myeloproliferative diseases polycythemia vera and essential thrombocythemia. It has not previously been reported as a sign of chronic myelogenous leukemia (CML). We suggest the term acral lividosis to describe this clinical entity in patients with any myeloproliferative disease. We propose that the pathophysiology of acral lividosis in CML involves occlusion of small blood vessels of the skin by large, nondeformable myeloblasts, a process that has been shown histologically to occur in other organs in patients with CML. This process, called leukostasis, occurs in patients with CML who have over 50.0 X 10(9)/L (50,000/mm3) circulating myeloblasts. Patients manifest cardiorespiratory and central nervous system compromise, a clinical constellation known as the hyperleukocytosis syndrome. Acral lividosis occurred in a patient with CML in whom nearly every organ demonstrated leukostasis on autopsy.
Arch Dermatol 1987 Jul
PMID:Acral lividosis--a sign of myeloproliferative diseases. Hyperleukocytosis syndrome in chronic myelogenous leukemia. 347 43

Postoperative localized alopecia has been reported most commonly after certain gynecologic and open heart surgery procedures, the likelihood of hair loss and the chance of permanence correlating with the length of the anesthesia and the intubation. Some cases of pressure-induced alopecia have been described after prolonged coma from other causes. Coma blisters have been reported after drug overdoses, but clinically similar blisters (not tested by biopsy) have been seen in other cases of coma. We present three cases of postoperative (pressure) alopecia and propose that both coma blisters and postoperative alopecia arise from the same phenomenon--probably pressure-induced ischemia.
J Am Acad Dermatol 1985 Jan
PMID:Postoperative (pressure) alopecia. 397 18

The cyclic AMP level in epidermis of psoriatic patients was reappraised with a highly sensitive radioimmunoassay method in conjunction with an improved skin biopsy technique to avoid any artificial rise of cyclic AMP due to ischemia. Local intradermal injection before biopsy was avoided, since even saline injection caused a clear-cut ischemia effect. The results concur with our previous study: i.e., on a tissue dry weight or protein basis, the cyclic AMP level in the involved epidermis is 20% higher than that in the uninvolved spidermis of psoriatic patients, and on a DNA basis, there was no significant difference. The cyclic AMP level in normal epidermis from non-psoriatic subjects is the same as that in the uninvolved epidermis of psoriatic patients. Such characteristics in psoriatic lesions as the increased mitosis, incomplete, differentiation and increased glycogen content cannot be simply related to a cyclic AMP deficiency.
J Invest Dermatol 1980 Feb
PMID:Epidermal cyclic AMP is not decreased in psoriasis lesions. 624 35

Cyclic GMP levels in epidermis of normal subjects and of psoriatic patients were measured with a highly sensitive radioimmunoassay method. Technical improvements for the assay are 2-fold: (1) skin samples were frozen in vivo before biopsy and local injection of any anesthetic was avoided to overcome ischemia effect which could lower cyclic GMP artificially; (2) epidermis was microdissected to avoid contamination of dermis and keratin layers. The results show that on a per mg tissue dry weight basis the cyclic GMP levels are about 200 fmol in the involved lesional epidermis and 70 fmol in the uninvolved or normal epidermis. Similarly increases in the cyclic GMP levels in the lesional epidermis are observed when the data are expressed either on a DNA or protein basis. The cyclic GMP level in normal epidermis from nonpsoriatic subjects is the same as that in the uninvolved epidermis of psoriasis patients.
J Invest Dermatol 1981 Jan
PMID:Epidermal cyclic GMP is increased in psoriasis lesions. 625 90

The incubation of adult mouse skin pieces in a buffered salts medium at 37 degrees C led to a rapid accumulation of cyclic adenosine 3'5-monophosphate (cyclic AMP) in the tissue. In mouse skin maximum accumulation occurred after 2 min incubation; levels reverted to near control levels after a further 7 min incubation. the increase in cyclic AMP contents of the skin pieces was probably not due to the release of materials which activate adenylate cyclase after binding to cellular receptors. Thus, cyclic AMP accumulation was unaffected by the inclusion of alpha- or beta-adrenergic antagonists, or by the pretreatment of adult mouse skin with indomethacin (an inhibitor of prostaglandin synthetase). Furthermore, adenosine, a known activator of epidermal adenylate cyclase, could not be detected in the incubation medium. The functional integrity of epidermal adenylate cyclase was maintained during the cyclic AMP accumulation in response to ischemia. Thus, adenosine, histamine, isoproterenol and prostaglandin E2 (PGE2) augmented the cyclic AMP response. Cyclic AMP accumulation at 37 degrees C was not observed in newborn mouse skin; this lack of cyclic AMP accumulation was probably not due to increased activity of low affinity cyclic AMP phosphodiesterase in newborn mouse skin.
J Invest Dermatol 1982 Jan
PMID:The effect of ischemia on cyclic adenosine 3',5'monophosphate accumulation in mouse skin. 627 64

The effect of 12-0-tetradecanoyl-phorbol-13-acetate (TPA) on cyclic adenosine 3',5'-monophosphate (cyclic AMP) level in adult mouse skin in response to ischemia was examined. The incubation of skin pieces in a buffered salts medium at 37 degrees C resulted in a rapid accumulation of cyclic AMP. In mouse skin pieces maximum accumulation (about 6 times the basal level) occurred after 2 min incubation and was followed by a rapid decline in the cyclic AMP level. This "ischemic" rise in epidermal cyclic AMP was greatly reduced if skin was used 16 hr after a single application of 17 nmoles of TPA. The effect of TPA on cyclic AMP accumulation in response to ischemia was first observed at 1 hr after TPA treatment and was maximal at 4 hr. The lack of "ischemic" response in TPA-treated skin was not related to an increase in the activity of cyclic AMP phosphodiesterase after TPA application. In addition, the accumulation of cyclic AMP in skin in response to both ischemia and exposure to isoproterenol, adenosine, histamine, or prostaglandin E2 (PGE2) was not observed in skin treated with the tumor promoter TPA.
J Invest Dermatol 1982 Apr
PMID:Decreased accumulation of cyclic adenosine 3',5'-monophosphate in "ischemic" skin after 12-0-tetradecanoyl-phorbol-13-acetate treatment. 627 33

Cyclic AMP-dependent protein kinase isozymes of pig and human skin (epidermis) were separated by DEAE-cellulose column chromatography after micromodification for small biopsy samples. Clear-cut separations of type I and type II isozymes, which were of about equal amounts, could be obtained only when the ischemia effect was avoided by in vivo freezing of skin and homogenization for less than 10 s. Intradermal injections of epinephrine caused dose-dependent activation of type I isozyme, but not of type II. Injections of other skin adenylate cyclase stimulators such as histamine, adenosine, and prostaglandin E2 elevated the local cyclic AMP levels to not more than 5 pmol/mg protein and also stimulated only the type I isozyme. Incubation of keratome-sliced pig skin under various conditions caused both activation by dissociation and inactivation by reassociation of the subunits, which appeared to be dependent on the cyclic AMP content. Epinephrine added to the incubation medium led to complete activation of both type I and type II isozymes (the intraepidermal cyclic AMP contents ranged from 20-50 pmol/mg protein). The isozymes of normal skin and involved skin of psoriatics showed identical peaks of type I and type II isozymes of equal amounts. The data indicate that protein kinase in the involved skin is not in an activated (by cyclic AMP) state.
J Invest Dermatol 1983 Feb
PMID:Cyclic AMP-dependent protein kinase isozymes of pig skin and human skin from normal and psoriatic subjects. 629 36

In 12 healthy, adult males, the epidermal content of both cAMP and cGMP was determined radioimmunologically every 6 h over a period of 30 h, avoiding any ischemia, which can alter unphysiologically the in vivo levels of epidermal cyclic nucleotides. For cAMP a diurnal fluctuation with maximal level at midnight could be proved (p less than 0.05), whereas cGMP, in contrast to experiments in mice, revealed no significant variation during the test period. The presented results describe for the first time the diurnal course of human epidermal cGMP.
J Invest Dermatol 1984 Feb
PMID:Cyclic nucleotides in human epidermis--diurnal variations. 631


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