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L H Block

Publications and source records attributed to L H Block.

At least 73 records · Page 4Linked to original sources
PubMed1986

Ubiquinone-8 stimulates phagocytosis in macrophages by modulation of the kinetics of the Fc receptor.

The effect of exogenous ubiquinone-8 (Q8) on IgG- and C3b-mediated phagocytosis of sensitized sheep red blood cells and of opsonized Staphylococcus aureus by macrophages was studied by morphological and quantitative methods. Q8 stimulated the initial events of phagocytosis, that is, attachment and ingestion, in which occupancy of the Fc receptor by IgG was shown to be of critical significance. The kinetics of competitive inhibition of phagocytosis of opsonized bacteria by macrophages by using Fc fragments suggested the intimate role of the kinetics of the Fc receptor in the initial events of phagocytosis and, further, the modulation of the kinetics of the Fc receptor by Q8 as the basis of enhanced phagocytosis by Q8.

Animals↗
PubMed1985

Isolation and characterization of an RNA-proteolipid complex associated with the malignant state in humans.

An RNA-proteolipid complex was isolated from sera of patients with a variety of malignant disorders as well as from culture media of malignant cell lines. The complex, characterized by a relatively constant composition, contains 27S poly(A)+ RNA and Mr 1250 oligopeptide(s) and is rich in phospholipids and glycosphingolipids. Serum lipoproteins (low and high density) differ from this complex in density, chemical composition, and immunological reactivity. The complex was detected in 94 of 96 cases of malignancy tested but not in any of 58 patients with nonmalignant disorders or in 46 healthy individuals.

Apolipoproteins↗
PubMed1985

(-)-Adrenaline-induced, calcium-dependent phosphorylation of proteins in human platelets.

In human platelets, adrenaline stimulated, approximately four-fold, as compared with controls, the phosphorylation of primarily two proteins of apparent molecular weights of 20,000 and 40,000, respectively. Maximum phosphorylation occurred after incubation for 1 min and was inhibited by the addition of either yohimbine, prostaglandin E1, or EGTA. Phosphorylation of the two proteins was accompanied by diacylglycerol formation. The (-)-adrenaline-induced phosphorylation of proteins corresponds to the activation of a calcium-dependent protein kinase partially purified by DEAE-cellulose and Sephadex G150 column chromatography. The enzymatic activity was modulated by addition of (-)-adrenaline and CaCl2, by diolein, and in the presence of membranes or phosphatidylinositol but not phosphatidylethanolamine and phosphatidylcholine. A phospholipid-dependent reaction appears to be involved in the molecular mechanism of action of adrenaline.

Adrenergic alpha-Antagonists↗
PubMed1984

Dissociation of human interferon-gamma-like activity from migration-inhibition factor.

Supernatants harvested from concanavalin A-stimulated human peripheral mononuclear cells after 24 hr of incubation contain one interferon species similar to human interferon-gamma (IFN-gamma) with a pI of 4.6-5.3 (first day pH 5 IFN-gamm). In contrast, during the subsequent 24 hr of incubation two species with properties of IFN-gamma are produced with pI of 3.6-4.0 (second day pH 4 IFN-gamma) and 4.6-5.6 (second day pH 5 IFN-gamma), respectively. First day pH 5 IFN-gamma and second day pH 5 IFN-gamma have been found to differ on the basis of trypsin sensitivity. This pattern of polymorphism is similar to the pattern previously described for human migration-inhibitory factor (MIF) which can be separated into first day pH 5 MIF, second day pH 3 MIF, and second day pH 5 MIF. However, IFN-gamma-like species can be differentiated from MIF biochemically and antigenically. Fractions with second day pH 4 IFN-gamma have no MIF activity and fractions with second day pH 3 MIF contain no IFN activity. In addition, first and second day pH 5 MIF, which also contain IFN-gamma activity, can be separated from the latter by precipitation as well as neutralization with polyclonal and monoclonal anti-human MIF antibodies.

Antibodies↗
PubMed1984

Renin profiling to select antihypertensive baseline drugs. Renin inhibitors for high-renin and calcium entry blockers for low-renin patients.

Renin profiling stimulated research into the pathophysiology of essential hypertension and influenced the development of antihypertensive treatment strategies. Patients with a high renin value and usually younger age respond better to drugs that interfere with the renin-angiotensin system, that is, beta blockers or converting enzyme inhibitors. Patients with a low renin value and often older age respond better to calcium entry blockers or diuretics. Patients with normal renin levels exhibit mixed but, on average, equal responses to these types of drugs. A pathophysiology-oriented antihypertensive treatment strategy is proposed in which beta blockers or converting enzyme inhibitors are used as one and calcium entry blockers--in the place of diuretics when possible--as the other baseline drug, and this approach may provide a cardiac-protective effect.

Adrenergic beta-Antagonists↗
PubMed1984

[Biology and clinical aspects of intracellular resistance to infection].

Normal functioning of phagocytic cells depends upon the integration of chemotaxis, phagocytosis, degranulation and oxidative metabolism. The availability of in vitro assays for the separate quantitative evaluation of each function has permitted the definition of specific congenital and acquired abnormalities of phagocytic cells which are associated with defective mechanisms of host resistance. The appreciation of complex and often adverse effects of certain systemic diseases and pharmacological agents on the phagocytes, as well as the use of new approaches to therapy underline the importance of assessing the role of phagocytic cells in states of impaired host defence. In addition, cellular immune mechanisms involving the interaction of T-cells and macrophages contribute essentially to the proper functioning of intracellular host defence, as indicated by the delayed type hypersensitivity reaction.

Antigens, Bacterial↗
PubMed1984

High salt intake blunts plasma catecholamine and renin responses to exercise: less suppressive epinephrine in borderline essential hypertension.

Graded physical exercise was associated with a parallel increase in plasma epinephrine and norepinephrine concentrations, and increments in the latter correlated directly with concurrent increases in plasma renin activity, heart rate, and blood pressure as studied in four normal subjects. With a high salt intake, plasma catecholamine levels were lower at each grade of exercise; the norepinephrine-renin response curve was shifted to the right and the norepinephrine-heart rate response curve to the left. In five patients with borderline essential hypertension, after salt loading epinephrine concentrations were higher and their responses during exercise greater than in normal subjects. A high salt intake suppresses the activity of the sympathetic nervous system as well as the renin system but increases cardiovascular responsiveness to pressor hormones. A high dietary salt intake may contribute to elevated concentrations of plasma epinephrine and to its cardiovascular effects in borderline essential hypertension.

Adult↗
PubMed1984

Antihypertensive therapy with the long-acting calcium antagonist nitrendipine.

The antihypertensive efficacy of the calcium entry blocker nitrendipine administered as monotherapy (20-80 mg; mean, 36/day) on the average for 144 days to 46 patients with essential hypertension (WHO I and II) was investigated in relation to age, pretreatment blood pressure, and plasma renin activity. In addition, we compared the blood pressure responses to verapamil (n = 11) and nifedipine (n = 15) with those to nitrendipine. Nitrendipine monotherapy reduced blood pressure from 168 +/- 16/107 +/- 7 mm Hg to 145 +/- 13/91 +/- 6 (both p less than 0.001); in 33 of 46 patients a diastolic pressure less than or equal to 95 mm Hg was achieved. During long-term treatment, heart rate and body weight remained unchanged. Thirteen of 16 patients in whom blood pressure was measured 24 h after a single oral dose (20 to 40 mg) reached a diastolic pressure less than or equal to 95 mm Hg. Treatment with nitrendipine had to be discontinued because of severe headache in two and ankle oedema in one patient. The fall in mean blood pressure after nitrendipine was directly related to age (r = 0.553; p less than 0.001) and pretreatment mean blood pressure (r = 0.470; p less than 0.01) and inversely related to plasma renin activity (r = 0.558; p less than 0.001). These correlations were also significant for systolic and diastolic blood pressure. There was comparable antihypertensive efficacy, as expressed by changes in mean blood pressure, between nitrendipine and verapamil (r = 0.869; p less than 0.01), and nitrendipine and nifedipine (r = 0.953; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Adrenaline induces vasoconstriction through post-junctional alpha 2 adrenoceptors and this response is enhanced in patients with essential hypertension.

The role of adrenaline-induced postjunctional alpha 2 adrenoceptor-mediated vasoconstriction was studied in seven patients with essential hypertension (EHT) and eight normotensive subjects (NT) using forearm venous occlusion plethysmography. Adrenaline (0.01 to 0.08 micrograms/min/100 ml of tissue) infused into the forearm circulation via the brachial artery during alpha l adrenoceptor blockade with prazosin (0.05 micrograms/min/100 ml of tissue) and beta adrenoceptor blockade with propranolol (2 micrograms/min/100 ml of tissue) decreased forearm blood flow (FAF) dose-dependently below basal FAF (P less than 0.001). The adrenaline-induced decrease in FAF was greater in EHT than in NT (P less than 0.01) and was blocked in both groups by alpha 2 adrenoceptor blockade with yohimbine (30 micrograms/min/100 ml of tissue). The increase in FAF following postjunctional alpha-2 blockade as well as following postjunctional alpha-1 blockade was greater in EHT than in NT (P less than 0.01) but was similar in both groups following 'non-specific' vasodilation with sodium nitroprusside. Postjunctional alpha 1 and alpha 2 adrenoceptor-mediated vasoconstriction is enhanced in patients with essential hypertension. Adrenaline induced postjunctional alpha 2 adrenoceptor-mediated vasoconstriction could contribute to elevated vascular resistance in patients with EHT and elevated plasma adrenaline concentrations particularly in the presence of blunted beta adrenoceptor-mediated functions.

Adult↗
PubMed1983

Cyclosporin A: pharmacologic activity on the immune system and effects in clinical organ transplantation.

The recently discovered fungal metabolite cyclosporin A (CsA) is a potent immunosuppressant that is effective in preventing transplantation rejection due to allografts and even xenografts. Due to its influence on the biological activity of T-helper lymphocytes CsA's mechanism of action includes inhibition of cell-mediated cytolysis and delayed-type hypersensitivity (DTH) reaction. In addition to studies of the molecular mechanism of action, data on the pharmacokinetics of CsA are given. CsA does not cause anti-mitotic and/or cytotoxic effects. The side effects of the agent are relatively mild and appear to be reversible. CsA has been successfully used clinically in renal, bone-marrow, heart, heart-lung, liver, and pancreas transplantation. The application of the compound in organ transplantation appears to be superior to conventional immunosuppressive therapy.

Biological Availability↗
PubMed1983

[Fever].

Explore the source record for details and available documents.

Antibody Formation↗
PubMed1983

Beta 2-adrenoceptor density on membranes and on intact mononuclear cells in essential hypertension.

Alterations in the status or in the regulation of adrenoceptors may contribute to essential hypertension. This could be studied using the recently introduced radio-ligand binding techniques to characterize the adrenoceptors on human peripheral blood cells. The present study shows that patients with essential hypertension have a twofold increase of beta 2-adrenoceptor density on intact mononuclear cells as compared to normotensive controls: 859 +/- 260 (n = 10) vs. 420 +/- 119 (n = 10) maximal binding sites for (+/-) 125-Iodocyanopindolol expressed as molecules per cell (P less than 0.001). Furthermore, there is a highly significant correlation (r = 0.86) between the calculated mean arterial blood pressure and the beta 2-adrenoceptor density over a wide range of normal and increased blood pressure. These findings could only be demonstrated with intact mononuclear cells but not with membrane fractions. No difference was found in receptor affinity between patients with essential hypertension and normotensive controls. Thus, essential hypertension is combined with a higher beta 2-adrenoceptor density on intact mononuclear cells which might represent, for example, an increased density of prejunctional beta 2-adrenoceptors. Mean arterial blood pressure is positively correlated with beta 2-adrenoceptor density over a wide range of blood pressure in normotensives and hypertensives. The expression of beta 2-binding sites on the cell surface is possibly altered in essential hypertension resulting in a disparity between intracellular and extracellular binding sites as compared with normotensives.

Adult↗
PubMed1983

Interactions between 8-L-arginine vasopressin and prostaglandin E2 in human mononuclear phagocytes.

The effect of 8-L-arginine vasopressin (AVP) on biosynthesis of prostaglandins in human mononuclear phagocytes was examined. AVP, oxytocin, and deamino-(8-D-arginine) vasopressin (dDAVP) affected prostaglandin biosynthesis in a rank order that parallels their pressor but not antidiuretic activity (AVP greater than oxytocin greater than dDAVP). Radioimmunoassay, incorporation studies using [14C]arachidonic acid and radiometric thin-layer chromatography, revealed prostaglandin E2 (PGE2) to be the only prostaglandin synthesized by the mononuclear phagocytes. While high concentrations of PGE2 elevated cytoplasmic levels of cyclic AMP by five- to sevenfold above basal values, low concentrations of PGE2 that are released by the cells in the presence of AVP failed to increase cyclic AMP content in the cells. However, PGE2 at concentrations that do not alter cyclic AMP levels markedly interferes with the activity of AVP. This effect is, however, very time dependent. Addition of PGE2 to the cells 30 min before AVP, was followed by a period of unresponsiveness to the hormone that lasts at least 30 min. Pretreatment of the cells with indomethacin enhanced the AVP-mediated accumulation of intracellular cyclic AMP level. PGE2 did not modify [3H]AVP binding, indicating that its inhibitory effect on the activity of the peptide is not due to downregulation of vasopressin receptors.

Arginine Vasopressin↗