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Biomedical subjects

M Ruppert

Publications and source records attributed to M Ruppert.

At least 19 recordsLinked to original sources
PubMed2001

Creatinine-kinase-MB determination in non-cardiac trauma: its difference with cardiac infarction and its restricted use in trauma situations.

Cardiac injuries can be life threatening. The possibility of late complications urges the practitioner to search for any evidence of cardiac trauma. But the diagnosis of cardiac injury remains difficult. Electrocardiography and cardiac enzyme determination are most widely used, because they are readily available. Many studies advocate creatine-kinase-MB (CK-MB) isoenzyme levels as a sensitive test for cardiac contusion. Others have discarded CK-MB testing as useless in trauma situations. An elevated CK-MB value in haemodynamically stable patients may confuse the individual practitioner. To better clarify its role we investigated the course of CK/CK-MB release after trauma, with no or only a very small chance of cardiac injury and compared it with patients with severe chest trauma having cardiac complications. A total of 25 trauma patients with only skeletal muscle injury were studied. Blood samples were taken during the first 4 days after trauma. These results were compared with those of a group of 91 consecutive patients with severe chest injury, including 10 with cardiac complications. Initial results in skeletal trauma patients were indicative of cardiac injury (CK > 5% of total CK and at least 20 U/l) in 10 patients. These findings were identical to those found in patients with severe chest injury having cardiac complications. CK/CK-MB tests are frequently positive after trauma without cardiac injury, even when selective criteria are used. The time each isoenzyme is released from muscle tissue after trauma greatly influences the outcome of the test. As this release does not occur at the same moment for each isoenzyme, the test result is very much time-dependent. As a result of these findings CK-MB testing tends to cause more confusion than clarification in trauma situations. We therefore eliminated CK-MB testing from our trauma protocol as a screening investigation for cardiac injury.

Adult↗
PubMed1999

Checking for breathing: evaluation of the diagnostic capability of emergency medical services personnel, physicians, medical students, and medical laypersons.

STUDY OBJECTIVE: International guidelines for cardiopulmonary resuscitation (CPR) recommend determination of unconsciousness, breathlessness, and absence of pulse to diagnose cardiorespiratory arrest. Thus far, there have been no scientifically proven data available regarding the quality of assessing breathlessness. The study objective was to evaluate the effectiveness of checking for breathing in an emergency situation, to determine the necessary amount of time until diagnosis, and to document used techniques. METHODS: Four different populations were tested for their ability to assess breathlessness: emergency medical services (EMS) personnel, physicians, medical students, and laypersons. Each participant was asked to perform the diagnostic procedure twice, first with a breathing or not-breathing unresponsive test person and then with a modified megacode manikin (with the possibility of simulated respiratory function). The order of testing and the respiratory status were strictly randomized. Diagnostic accuracy, time interval to diagnosis, and used techniques were documented. RESULTS: A total of 261 persons were tested in 522 trials, with a median time interval of 12 seconds for obtaining a diagnosis. Regarding all participants, the correct diagnosis was achieved in 81.0% (EMS personnel, 89.7%; physicians, 84.5%; medical students, 78.4%; laypersons, 71.5%). Only 55.6% of all participants showed correct diagnostic skills (EMS personnel, 91.3%; physicians, 51.5%; medical students, 61.9%; laypersons, 18.5%). CONCLUSION: Checking for breathing was shown to be mostly inaccurate and unreliable. This diagnostic procedure takes more time than recommended in international guidelines. Therefore CPR training should focus more on the determination of breathlessness. Also, the guidelines for CPR should be revised.

Apnea↗
PubMed1997

CD24, a mucin-type glycoprotein, is a ligand for P-selectin on human tumor cells.

P-selectin (CD62P) is a Ca2+-dependent endogenous lectin that can be expressed by vascular endothelium and platelets. The major ligand for P-selectin on leukocytes is P-selectin glycoprotein ligand-1 (PSGL-1). P-selectin can also bind to carcinoma cells, but the nature of the ligand(s) on these cells is unknown. Here we investigated the P-selectin binding to a breast and a small cell lung carcinoma cell line that are negative for PSGL-1. We report that CD24, a mucin-type glycosylphosphatidylinositol-linked cell surface molecule on human neutrophils, pre B lymphocytes, and many tumors can promote binding to P-selectin. Latex beads coated with purified CD24 from the two carcinoma cell lines but also neutrophils could bind specifically to P-selectin-IgG. The binding was dependent on divalent cations and was abolished by treatment with O-sialoglycoprotein endopeptidase but not endoglycosidase F or sialidase. The beads were stained with a monoclonal antibody (MoAb) to CD57 (HNK-1 carbohydrate epitope) but did not react with MoAbs against the sialylLe(x/a) epitope. The carcinoma cells and CD24-beads derived from these cells could bind to activated platelets or P-selectin transfected Chinese hamster ovary cells (P-CHO) in a P-selectin-dependent manner and this binding was blocked by soluble CD24. Transfection of human adenocarcinoma cells with CD24 enhanced the P-selectin-dependent binding to activated platelets. Treatment of the carcinoma cells or the CD24 transfectant with phosphatidylinositol-specific phospholipase C reduced CD24 expression and P-selectin-IgG binding concomitantly. These results establish a role of CD24 as a novel ligand for P-selectin on tumor cells. The CD24/P-selectin binding pathway could be important in the dissimination of tumor cells by facilitating the interaction with platelets or endothelial cells.

Amino Acid Sequence↗
PubMed1996

Role of epinephrine-induced hypokalemia in the regulation of renin and aldosterone in humans.

Circulating epinephrine induces both stimulation of plasma renin activity (PRA) and a decrease in serum potassium concentration. This study was designed to determine the dose-response effects of systemic epinephrine infusion on the relationship of PRA and plasma aldosterone concentration. Twenty-one men with normal blood pressure received either an intravenous infusion of epinephrine at 12.5, 25, and 50 ng/(kg x min) by stepwise increments for 1 hour each or isotonic saline solution. Infusion of epinephrine led to a dose-dependent increase in plasma epinephrine concentration, systolic blood pressure, and heart rate, whereas diastolic blood pressure was decreased. PRA was elevated in a dose-dependent manner, whereas the plasma aldosterone concentration was reduced. During infusion of epinephrine, the serum potassium concentration and renal potassium excretion were significantly decreased. We conclude that despite marked stimulation of PRA, the plasma aldosterone concentration was further decreased because of a dose-dependent decrease in serum potassium concentration induced by epinephrine. Thus hypokalemia appears to be the predominant regulator of plasma aldosterone during incremental epinephrine infusion.

Adult↗
PubMed1996

A parastomal hernia causing small-bowel obstruction.

A parastomal hernia is an incisional hernia that occurs at the site of an intestinal stoma on the abdominal wall. We report the case of a 52-year-old woman who had had ulcerative colitis and a total colectomy and ileostomy 9 years before being evaluated for a 2-year history of intermittent small-bowel obstruction thought initially to be due to Crohn's disease. On examination, a clear parastomal hernia was detected and confirmed by a small-bowel series. At surgery the hernia was corrected, and her intermittent episodes of small-bowel obstruction resolved. A parastomal hernia should be considered as a cause of intermittent small-bowel obstruction in anyone who has a stoma. Careful history and physical examination should suffice in establishing a diagnosis.

Colitis, Ulcerative↗
PubMed1995

The alpha 4 integrin chain is a ligand for alpha 4 beta 7 and alpha 4 beta 1.

The heterodimeric alpha 4 integrins alpha 4 beta 7 lymphocyte Peyer's patch adhesion molecule ([LPAM]-1) and alpha 4 beta 1 (very late antigen-4) are cell surface adhesion molecules involved in lymphocyte trafficking and lymphocyte-cell and matrix interactions. Known cellular ligands include vascular cell adhesion molecule (VCAM)-1, which binds to alpha 4 beta 1 and alpha 4 beta 7, and the mucosal addressin cell adhesion molecule (MAdCAM)-1, which binds to alpha 4 beta 7. Here we show that the alpha 4 chain of these integrins can itself serve as a ligand. The alpha 4 chain, immunoaffinity purified and immobilized on glass slides, binds thymocytes and T lymphocytes. Binding exhibits divalent cation requirements and temperature sensitivity which are characteristic of integrin-mediated interactions, and is specifically inhibited by anti-alpha 4 integrin antibodies, which exert their effect at the cell surface. Cells expressing exclusively alpha 4 beta 7 (TK-1) or alpha 4 beta 1 (L1-2) both bound avidly, whereas alpha 4-negative cells did not. A soluble 34-kD alpha 4 chain fragment retained binding activity, and it inhibited lymphocyte adhesion to alpha 4 ligands. It has been shown that alpha 4 integrin binding to fibronectin involves an leucine-aspartic acid-valine (LDV) motif in the HepII/IIICS region of fibronectin (CS-1 peptide), and homologous sequences are important in binding to VCAM-1 and MAdCAM-1. Three conserved LDV motifs occur in the extracellular sequence of alpha 4. A synthetic LDV-containing alpha 4-derived oligopeptide supports alpha 4-integrin-dependent lymphocyte adhesion and blocks binding to the 34-kD alpha 4 chain fragment. Our results suggest that alpha 4 beta 7 and alpha 4 beta 1 integrins may be able to bind to the alpha 4 subunit on adjacent cells, providing a novel mechanism for alpha 4 integrin-mediated and activation-regulated lymphocyte interactions during immune responses.

Amino Acid Sequence↗
PubMed1995

[Potassium citrate versus potassium chloride in essential hypertension. Effects on hemodynamic, hormonal and metabolic parameters].

A study was conducted on 25 patients (18 men, seven women; mean age 48 [24-70] years) with essential hypertension (EH) to see whether an increase in potassium supply influences blood pressure as well as metabolic and hormonal parameters, and whether the anion administered together with potassium affects the results. In a randomized, cross-over trial sequence the patients daily received 120 mmol potassium chloride, 120 mmol potassium citrate or a placebo, each for 8 weeks. Between each of the three periods there was a "wash-out" phase of 4 weeks each. After 8 weeks of potassium citrate intake the systolic and diastolic pressures were reduced significantly, by a mean of 6.2/3.8 mm Hg (P < 0.05). But after potassium chloride there was only a small, not significant, reduction. Metabolic and hormonal parameters (fasting glucose concentration, glucose tolerance test, lipid electrophoresis; plasma renin activity, plasma concentration of aldosterone, noradrenaline and insulin) were not significantly changed.--These findings suggest that an increased supply of potassium has a favourable haemodynamic effect, but this varies markedly between different potassium salts. An increase in potassium supply should thus be considered as an additional measure in the treatment of EH. As long as renal function is normal no unfavourable metabolic effect need be feared.

Adult↗
PubMed1995

Age is a major determinant of the divergent blood pressure responses to varying salt intake in essential hypertension.

Blood pressure responses to 1 week of low (20 mmol sodium/day) and high (300 mmol sodium/day) salt intake were investigated in a double-blind, randomized study in 46 white, nonobese subjects with essential hypertension (13 women, 33 men; mean age 45.3 +/- 2.2 years, age range 25 to 80 years). The individuals were classified as salt-sensitive when mean arterial blood pressure rose by at least 5 mm Hg during high salt intake, as salt-resistant when mean arterial blood pressure changed by less than 5 mm Hg, and as "counter-regulators" when mean arterial blood pressure fell by at least 5 mm Hg during the high salt diet. Mean arterial blood pressure of all subjects taken together increased from 101.9 +/- 1.4 mm Hg during salt restriction to 103.7 +/- 1.5 mm Hg (P < .05) during salt loading. Eleven subjects (23.9%) were classified as salt-sensitive, 27 (58.7%) as salt-resistant, and 8 (17.4%) as counter-regulators. Multiple regression analysis revealed that age, but not baseline blood pressure, sex, body mass index, or family history of hypertension contributed significantly to the change in blood pressure following the diets. Ten of the 11 salt-sensitive subjects were older than the median age of 45 years. In salt-sensitive, as compared to salt-resistant, hypertensive subjects, creatinine clearance was lower and plasma renin activity was suppressed at baseline as well as during low and high salt intake. In contrast, plasma concentrations of norepinephrine and atrial natriuretic peptide were elevated in salt-sensitive subjects. These differences between the groups appeared, at least partially, to be age-related.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

The L1 adhesion molecule is a cellular ligand for VLA-5.

The L1 adhesion molecule is a member of the immunoglobulin superfamily shared by neural and immune cells. In the nervous system L1 can mediate cell binding by a homophilic mechanism. To analyze its function on leukocytes we studied whether L1 could interact with integrins. Here we demonstrate that VLA-5, an RGD-specific fibronectin receptor on a wide variety of cell types, can bind to murine L1. Mouse ESb-MP cells expressing VLA-5 and L1 could be induced to aggregate in the presence of specific mAbs to CD24 (heat-stable antigen), a highly and heterogeneously glycosylated glycophosphatidylinositol-linked differentiation antigen of hematopoietic and neural cells. The aggregation was blocked by both mAbs to L1 and VLA-5, respectively. Aggregation was blocked also by a synthetic RGD-containing peptide derived from the Ig-domain VI of the L1 protein. ESb-MP subclones with low L1 expression could not aggregate. In heterotypic binding assays mouse bone marrow cells could adhere in an L1-dependent fashion to platelets that expressed VLA-5. Also purified L1 coated to polystyrene beads could bind to platelets. The binding of L1-beads was again inhibited by mAbs to L1 and VLA-5, by soluble L1 and the L1-RGD peptide in a dose-dependent manner. Thymocytes or human Nalm-6 tumor cells expressing VLA-5 could adhere to affinity-purified L1 and to the L1-derived RGD-containing peptide coated to glass slides. The adhesion was strongly enhanced in the presence of Mn(2+)-ions and blocked by mAbs to VLA-5. We also demonstrate a direct L1-VLA-5 protein interaction. Our results suggest a novel binding pathway, in which the VLA-5 integrin binds to L1 on adjacent cells. Given its rapid downregulation on lymphocytes after induction of cell proliferation, L1 may be important in integrin-mediated and activation-regulated cell-cell interactions.

Amino Acid Sequence↗
PubMed1995

Heat stable antigen (mouse CD24) supports myeloid cell binding to endothelial and platelet P-selectin.

P-selectin is a Ca(2+)-dependent lectin that participates in leukocyte adhesion to vascular endothelium and platelets. Myeloid cells and a subset of T lymphocytes express carbohydrate ligands at the cell surface. Previously, we suggested that heat stable antigen (HSA/mouse CD24), an extensively glycosylated cell surface molecule on many mouse cells, is a ligand for P-selectin. Here we show that HSA mediates the binding of monocytic cells and neutrophils to P-selectin. The monocytic cell lines ESb-MP and J774, peritoneal exudate cells, and bone marrow neutrophils could bind to lipopolysaccharide-activated bend3 endothelioma cells under rotation-induced shear forces and this binding was inhibited by mAb to P-selectin and HSA. Blocking was weak at room temperature but more efficient at 4 degrees C when integrin-mediated binding was decreased. Also the adhesion of neutrophils to stimulated platelets expressing P-selectin was blocked by HSA- and P-selectin-specific mAb. Latex beads coated with purified HSA from myeloid cells bound to activated endothelioma cells or platelets, and the binding was similarly blocked by mAb to P-selectin and HSA respectively. The HSA-coated beads were stained with P-selectin-IgG, very weakly with L-selectin-IgG but not with E-selectin-IgG. The staining was dependent on divalent cations and treatment with endoglycosidase F or neuraminidase indicated that sialylated N-linked glycans were recognized. The presence of these glycans was confirmed by biosynthetic labeling studies. Our data suggest that HSA, in addition to the recently identified 160 kDa glycoprotein ligand on mouse neutrophils, belongs to a group of monospecific P-selectin ligands on myeloid cells.

Animals↗
PubMed1994

The lymphocyte Na+/H+ antiport: activation in primary hypertension and during chronic NaCl-loading.

Increased activity of the Na+/H+ antiport may be a major abnormality in essential hypertension. The activity of this transport system was investigated in lymphocytes from 13 patients with untreated essential hypertension (Ht) and 13 normotensive control subjects (Nt) on an ad libitum (130-170 mmol d-1) NaCl intake. Furthermore, the effects of different states of NaCl balance on lymphocyte Na+/H+ antiport were evaluated in two groups of Nt volunteers receiving 20 vs. 300 mmol d-1 (n = 8) and 85 vs. 200 mmol d-1 (n = 14) of NaCl for 1 week each and in seven Ht patients (20 vs. 300 mmol NaCl d-1 for 1 week each). Additionally, during the 20 and 300 mmol/d NaCl intake red blood cell membrane transport was studied in eight subjects. For the determination of lymphocyte antiport activity, cells were loaded with the cytosolic pH (pHi) indicator bis-carboxyethyl carboxyfluorescein (BCECF-AM) and acidified by addition of different amounts of Na(+)-propionate (5-40 mM). Initial pHi-recovery was taken as the activity of the antiport system and plotted against pHi-values after acidification. Non-linear regression analysis yielded higher 'apparent' maximal transport rates in Ht than Nt (Nt: 2.00 +/- 0.22; Ht: (3.81 +/- 0.59) x 10(-3) s-1; P < 0.025). In contrast, baseline pHi-values and pHi-values at half-maximal activity (pK) were identical in Nt and Ht. In normotensive control subjects on an NaCl intake of 20, 85, 200 and 300 mmol d-1 for 7 d, 'apparent' maximal transport rates averaged 2.75 +/- 0.20, 2.89 +/- 0.17, 2.81 +/- 0.18 and (3.62 +/- 0.25) x 10(-3) s-1, respectively. Thus, antiport activity was significantly (P < 0.05) stimulated on the 300 mmol d-1 intake as compared to the three other NaCl intakes. The extreme intakes of NaCl (20 vs. 300 mmol d-1) in normotensive volunteers did not affect the erythrocyte Na+/K+ pump, Na+/K+ cotransport and Na+/Li+ countertransport. Our study supports the concept that a group of patients with primary hypertension exhibit an activated Na+/H+ antiport. Furthermore, our data demonstrate that a chronic high intake of NaCl is associated with an increase in lymphocyte antiport activity towards the high values observed in primary hypertension.

Adult↗
PubMed1994

Effects of severe and moderate salt restriction on serum lipids in nonobese normotensive adults.

The effects of severe and moderate sodium restriction on blood pressure and serum lipids were studied in nonobese normotensive adults. Subjects (n = 163) were given a low (20 mmol Na/d) and high (300 mmol Na/d) salt diet for 1 week each in random order. Of these subjects, 25 were selected to participate in a second study with moderate salt restriction (85 mmol na/d) or "normal" sodium diet (200 mmol Na/d) given for 4 weeks each in random order. After severe salt restriction, 19% of the 163 subjects had a significant decrease in blood pressure (salt-sensitive), 15% showed a significant rise (counter-regulator), and 66% exhibited no change (salt-resistant). Severe sodium restriction increased serum total and low density lipoprotein (LDL) cholesterol and triglycerides. After correction for hematocrit, the changes in blood lipids remained significant in the counter regulators only. After moderate salt restriction, serum lipid concentrations and blood pressure did not change.

Adult↗