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Biomedical subjects

H Haller

Publications and source records attributed to H Haller.

At least 199 records · Page 11Linked to original sources
PubMed1994

Decidual-trophoblast interactions: decidual lymphoid cell function in normal, anembryonic, missed abortion and ectopic human pregnancy.

This study was designed to investigate the consequences of decidua-trophoblast interactions on the phenotype, spontaneous and induced proliferation and immunoregulatory potential of decidual leukocytes in normal pregnancies (NP), anembryonic pregnancies (AP), missed abortions (MA) and ectopic pregnancies (EP). Spontaneous proliferation of decidual non-adherent cells (NAD) from pregnancies with viable trophoblast inside the uterus is significantly higher than proliferation of peripheral blood lymphocytes (PBL) from the same groups (P < 0.001 for NP; P < 0.05 for AP). Spontaneous proliferation of decidual NAD cells from NP was higher (P < 0.001) when compared with AP and EP. The induced (PHA and Con A) responses of PBL from women with normal and pathological pregnancies were significantly higher than that of decidual NAD cells (P < 0.001). Higher proliferation of NAD decidual cells was obtained when Con A-stimulated NP were compared with MA and EP (P < 0.01). The interaction of viable trophoblast with intrauterine decidua appears to be a prerequisite for the activation of NAD suppressor cells, since NAD cells from MA produced stimulation instead of suppression, and NAD cells from EP had no suppressive effect. On the contrary, both NAD and adherent (AD) decidual leukocytes from NP and AP produced very strong suppression of PHA or alloantigen-induced PBL proliferation. The contact between trophoblast and AD decidual leukocytes is not necessary for their suppressive function, since even higher suppression is obtained with the cells from ectopic pregnancies.

Abortion, Missed↗
PubMed1994

Nuclear calcium signaling is initiated by cytosolic calcium surges in vascular smooth muscle cells.

Calcium is not only a second messenger in the cytoplasm but also may be involved in signaling within the nucleus itself. The regulation of the nuclear calcium signal is imperfectly defined. The purpose of our study was to further elucidate the relationship between cytosolic [Ca++]c and nuclear calcium concentration [Ca++]n in vascular smooth muscle cells and to test the hypothesis that components of the phospholipase C-induced signaling system are responsible for the hormone-induced increase in [Ca++]n. Cytosolic [Ca++]c and nuclear calcium concentration [Ca++]n were measured by confocal microscopy in primarily cultured vascular smooth muscle cells from rat aorta. Basal [Ca++]n was lower than the cytosolic calcium [Ca++]c concentration. Angiotensin II (10(-7) M) induced a rapid increase in [Ca++]c which was immediately followed by a surge in [Ca++]n. The high [Ca++]n was maintained for 20 to 30 seconds and returned to basal values thereafter. Increased transmembraneous calcium influx by KCl (80 mM) led to a rapid rise in [Ca++]n. Treatment of vascular smooth muscle cells with ionomycin (10(-4) M) also induced an increase in [Ca++]c accompanied by an increase in [Ca++]n. The calcium channel agonist A 2386 led to a slower increase in both [Ca++]c and [Ca++]n. An increase in extracellular calcium to 6 mM under these conditions enhanced the surge of [Ca++]c but not [Ca++]n. Removal of extracellular calcium by EGTA decreased both the angiotensin II-induced increase in [Ca++]c and the increase in [Ca++]n. Nitrendipine (10(-7) M) had the same effect as EGTA. Inhibition of the intracellular release by preincubating vascular smooth muscle cells with thapsigargin (10(-5) M) also partially inhibited the effect of angiotensin II (Ang II) on [Ca++]n. However, combined EGTA and thapsigargin abolished both the rise in [Ca++]c and the surge in [Ca++]n. The protein kinase C inhibitors staurosporine (5 x 10(-8) M) and H7 (10(-7) M) had no effect on the Ang II-mediated increases in [Ca++]c and [Ca++]n. Our results demonstrate that the angiotensin II-induced increase in [Ca++]c is rapidly followed by a rise in [Ca++]n. This effect on [Ca++]n is not mediated by an angiotensin II-induced generation of IP3 or activation of protein kinases, but rather seems to depend on an increase in [Ca++]c.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1994

Platelet-derived growth factor and angiotensin II induce different spatial distribution of protein kinase C-alpha and -beta in vascular smooth muscle cells.

Protein kinase C is an important second-messenger system that is translocated from the cytosol to the cell membrane on cell stimulation. We used confocal microscopy to study the spatial distribution of protein kinase C isoforms after stimulation of cultured vascular smooth muscle cells with platelet-derived growth factor and angiotensin II (Ang II). Monoclonal antibodies for the isoforms alpha and beta were used. Translocation was also assessed by Western blot. Isoform alpha was evenly distributed in the cytosol, whereas the beta isoform formed coarse granules in the perinuclear region. Both isoforms shifted from the cytosolic to the membrane fraction after exposure to Ang II (10(-7) mol/L) and platelet-derived growth factor (100 ng/mL at 6, 12, and 20 minutes). Confocal microscopy showed a rapid assembly of isoform alpha along cytosolic fibers at 6 minutes followed by a translocation toward the nucleus at 12 minutes with Ang II. Platelet-derived growth factor engendered a similar response; however, a cytoskeletal distribution was not observed. The beta isoform was rapidly translocated by both inducers to the perinuclear region and the nucleus. Our results show that inducers cause a translocation of protein kinase C isoforms not only into the cell membrane but also into the cell nucleus. We suggest that protein kinase C may also be important for nuclear signaling.

Angiotensin II↗
PubMed1994

LDL increases (CA++)i in human endothelial cells and augments thrombin-induced cell signalling.

Low-density lipoproteins (LDLs) stimulate cytosolic calcium ([Ca++]i) in endothelial cells. To elucidate the mechanisms of this response, we compared the effects of low-density lipoprotein (LDL) with those of thrombin, a known endothelial cell agonist. [Ca++]i was measured in cultured endothelial cells from human umbilical veins. Both spectrofluorometry of single cells with fura-2 and confocal microscopy were used. LDL (100 micrograms/ml) led to a rapid increase in [Ca++]i (143 +/- 46 nmol/L to 426 +/- 69 nmd/L; p < 0.05) followed by a sustained plateau phase. Higher concentrations did not increase this response further. Removal of extracellular calcium resulted in a significant decrease of the plateau phase, which remained significantly elevated as compared with baseline values. On the other hand, the initial peak was only slightly altered. Incubation of endothelial cells with thapsigargin (10(-6) mol/L) reduced the initial calcium peak, while the incubation of the cells with pertussis toxin (10(-6) mol/L) for 24 hours abolished the LDL-induced [Ca++]i response together. Down-regulation of LDL receptors by exposing the endothelial cells to high LDL concentrations (500 micrograms/ml) for 24 hours abolished the LDL-induced calcium signal, while preincubation of the cells with acetylated LDL (500 micrograms/ml) did not alter the cellular response to LDL. Visualization of the calcium signal showed a rapid increase in [Ca++]i followed by an increase in the nuclear calcium concentration. The LDL calcium signalling was shorter than that observed with thrombin (0.1 U/ml). Administration of thrombin and LDL together resulted in an increased [Ca++]i response as compared with either substance alone. Our results show that (1) LDL leads to both a release of calcium from intracellular stores and a transmembranous calcium influx, (2) the effect of LDL is dependent on binding to a specific G-protein-coupled receptor, and (3) LDL enhances the activation induced by other agonists.

Calcium↗
PubMed1994

Angiotensin II infusions elevated blood pressure independently of platelet cytosolic calcium concentrations in humans.

A remarkably close correlation between platelet cytosolic calcium ([Ca2+i]) and arterial blood pressure has been identified in patients with essential hypertension. We tested the notion that a pharmacologically relevant infusion of angiotensin (Ang) II is associated with an increase in cytosolic calcium [Ca+2i]. Five normal volunteers received Ang II (5 ng/kg/min) for three hours or vehicle intravenously in random sequence respectively. The investigations were conducted at least 14 days apart. Plasma renin activity and blood pressure were measured every 20 minutes. [Ca+2i] was measured with the fluorescent indicator fura-2 before and at the end of the last hour of Ang II infusion. Mean arterial blood pressure increased by 10 mmHg during Ang II infusion (P < 0.05). Plasma renin activity decreased from 2.21 +/- 0.28 to 1.31 +/- 0.22 ng/ml/hour during the Ang II infusion (P < 0.05). On the other hand, [Ca+2i] was 131 +/- 13 nmol/l before and 129 +/- 13 nmol/l after the infusion (P = NS). The data suggest that agonists may increase blood pressure without an increase in platelet [Ca+2i]. Furthermore, Ang II may increase blood pressure independently of [Ca+2i].

Adolescent↗
PubMed1993

Different effects of eicosapentaenoic acid and olive oil on blood pressure, intracellular free platelet calcium, and plasma lipids in patients with essential hypertension.

In a randomized, double-blind, crossover study our specific aim was to examine the effects of a dietary fish oil or olive oil supplementation on blood pressure, intracellular free platelet calcium, plasma lipoproteins, and circulating vasoactive substances such as norepinephrine, epinephrine, and renin in patients with essential hypertension. Ten hypertensive patients (WHO classes I, II) were randomly assigned to receive 9 g fish oil or 9 g olive oil daily for 6 weeks after a 4-week baseline period. The 6-week treatment periods were separated by a 4-week wash-out. During treatment with fish oil diastolic blood pressure decreased from 103 +/- 1 to 98 +/- 2 mmHg (P < 0.05) but did not change significantly during olive oil intake. Systolic blood pressure was not affected by either treatment. Intracellular free platelet calcium decreased in patients receiving fish oil (from 102 +/- 8 nM to 86 +/- 6 nM, P < 0.05) but was not significantly altered by olive oil treatment. In contrast, the dose-response curve for thrombin-induced intracellular free platelet calcium was not altered by the fish oil enriched diet. Plasma triglycerides decreased by approximately 40% in the fish oil group while low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and total cholesterol were not altered. Renin activity, norepinephrine, and epinephrine in plasma were not influenced by fish oil supplementation. We conclude that a moderate increase in dietary fish oil reduces diastolic blood pressure, intracellular free platelet calcium, and plasma triglycerides in patients with essential hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Polytrauma and predicting fatality. Comparative evaluation of the value of the Kirkpatrick-Youmans Trauma Index (TI), Schreinlechner-Eber modified TI (TI mod.), and the Baker Injury Severity Score].

The Trauma Index (TI) of Kirkpatrick and Youmans modified by Schreinlechner and Eber performed better than the Injury Severity Score (ISS) in predicting case fatality of 234 patients with major trauma treated during the years 1985 through 1987. Logistic regression was used for determining the cut-points: Death was considered as predicted by ISS if it was greater than 53 or by TI if it was greater then 3.74. Specificity was 95% for ISS and 94% for TI. Sensitivity was 49% for ISS and 73% for TI.

Adult↗
PubMed1993

Management and complications of urolithiasis during pregnancy.

OBJECTIVE: To identify all pregnant women with urolithiasis, and to determine the mode of diagnosis and treatment with reference to obstetric outcome. METHOD: From January 1, 1986 to December 31, 1991, relevant medical records were retrospectively analyzed. RESULTS: Among 21,597 deliveries 10 pregnant women were diagnosed as having urolithiasis. They constituted 0.04% of all women who delivered at the Department of Obstetrics and Gynecology in Rijeka during this period. Conservative treatment was successful in 5 patients. Ureteral stents were inserted in 3 patients, nephrostomy was performed in 1 patient and a nephrectomy was necessary in 1 patient because of a nonfunctional kidney and chronic pyelonephritis. CONCLUSION: In our series all applied procedures in diagnosis and treatment of urolithiasis resulted in favorable maternal and perinatal outcome.

Adult↗
PubMed1993

An immunohistochemical study of leucocytes in human endometrium, first and third trimester basal decidua.

An immunohistochemical quantitative study of leucocyte subpopulations on fresh human endometrium and on biopsy specimens of first and third trimester basal decidua in normal (uncomplicated) pregnancies was performed. The most prominent population in endometrial and decidual stroma of basal decidua are macrophages. B cells as well as gamma/delta T cell receptor positive cells were found occasionally, scattered throughout the endometrial/decidual stroma. CD3+ cells were present in a relatively small number in the endometrium as well as in the first trimester basal decidua, but their number was elevated (doubled) in the third trimester of pregnancy. CD2+ cells showed a slight increase in first trimester basal decidua when compared with both endometrium and third trimester basal decidua. Cells with positive NKH-1 marker (CD56+) showed a significant increase in the first trimester, while in the third trimester their number diminished drastically. CD56:CD3 cell ratio increased to more than five times in first trimester basal decidua, while in the third trimester basal decidua decreased drastically. The mentioned increase of CD56+ cells in the first trimester and that of CD3+ cells at term suggests that these cells could have some specific function(s). However, it still has to be established whether the described quantitative changes of decidual leucocytes in basal decidua during pregnancy are of any importance for the mechanism(s) for the fetal allograft protection.

Antigens, CD↗
PubMed1993

Calcium channel blockers in current medical practice: an update for 1993.

Calcium channel blocking drugs (CCB) have been used to lower blood pressure since 1970. Three classes are currently available, the phenylalkylamines, the benzothiazepines, and the dihydropyridines. The structure of the L-type, voltage dependent calcium channel has been elucidated with molecular techniques and the different binding sites of the various CCB described. CCB have specific effects at the site of target organs. In the kidney, all classes produce natriuresis. Their action appears independent of the level of salt intake. CCB may favorably influence the course of chronic renal disease; the results of a trial comparing nifedipine to the converting enzyme inhibitor captopril showed no difference between the two drugs. CCB may impede the progression of atherosclerosis in the coronary arteries; a prospective study of nifedipine on coronary artery morphology supports this view. In the brain, nimodipine improves the outcome of patients with stroke from subarachnoid hemorrhage. Positive effects on patients with ischemic stroke have not been corroborated. CCB are approved primary treatment for patients with hypertension and are readily combined with other antihypertensive agents. They are well tolerated and have no adverse metabolic side effects. The advent of molecular pharmacology will advance current efforts to develop new CCB, which are highly selective in their site and mode of action.

Brain↗
PubMed1993

Calcium antagonists and cellular mechanisms of glomerulosclerosis and atherosclerosis.

Glomerulosclerosis is the final common glomerular lesions in many renal diseases. The histological features of focal glomerulosclerosis resemble the lesion of atherosclerosis and may indicate a parallel pathogenesis. Central to the pathogenesis of atherosclerosis is the interaction of blood cells and endothelial cells with subsequent proliferation of smooth muscle cells and enhanced production of collagen. The mechanisms that appear to be responsible for this increased proliferative response are growth factors, cytokines, and local alterations in the extracellular matrix. The corresponding counterparts in glomerulosclerosis include mesangial expansion with mesangial cell proliferation, mesangial foam cell accumulation, tissue necrosis, and eventual sclerosis. Substances that interfere with the interaction between the different cell types, such as endothelial cells, macrophages, and platelets, and with the proliferative responses of both vascular and mesangial cells may be of therapeutic value in both diseases. Calcium antagonists interfere with the cellular activation induced by growth factors and vasoactive hormones and, in platelets, they decrease aggregation and the secretion of thromboxane from these cells. In addition to their relaxant effect, calcium antagonists diminish the proliferative response of vascular smooth muscle and mesangial cells to growth factors while, in macrophages, production of superoxides is decreased after incubation with calcium antagonists. In mesangial cells it has been demonstrated that calcium antagonists decrease the expression and secretion of matrix proteins. That these cellular mechanisms result in an anti-atherosclerotic effect in vivo has been shown by various animal studies, and a beneficial effect of calcium antagonists on the progression of glomerulosclerosis has also been observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Properties of protein kinase C associated with nuclear membranes.

To study signal transduction directed towards the cell nucleus and at the nuclear membranes, we investigated the association of protein kinase C (PKC) with nuclear membranes obtained from nuclei isolated from bovine brain. By use of phorbol-ester-binding assays, significant amounts of PKC could be demonstrated in nuclei and nuclear membranes. Nuclear membranes are shown to be able to activate purified PKC. The PKC endogenously present in nuclear membranes appears to be a so-called 'membrane-inserted' form: it is permanently active, still binds phorbol ester, but its activity is no longer dependent on Ca2+ and cannot be activated by phorbol ester. On the other hand, this form of PKC can be inhibited by specific PKC inhibitors. By using histone HIIIS and a specific peptide substrate, it could be shown that after extraction with Triton X-100 the PKC can be stimulated by phospholipid again. Immunoblot analysis with isoenzyme-specific antibodies revealed that the alpha- and gamma-isoenzymes, but not the beta-isoenzyme, are associated with membranes derived from brain nuclei.

Amino Acid Sequence↗
PubMed1992

Ectopic pregnancy among past IUD users.

The relationship between return to fertility and pregnancy outcome in women with IUD removal for planned pregnancy as well as the frequency of ectopic pregnancy among all former IUD users in comparison with the general population was studied. The cumulative conception rate in the group of women with IUD removal for planned pregnancy (n = 748) was 93.7% after 5 years, 93.4% being intrauterine and 0.3% ectopic. Rates of ectopic pregnancy in women with IUD removed for planned pregnancy were 2.7/1000 women, 3.6/1000 deliveries and 2.9/1000 pregnancies vs. 3.9, 13.4 and 5.6 in the general population. Only when the number of deliveries is used as denominator, have these differences reached statistical significance (P less than 0.05). Except for bleeding/pain and PID removals (6.0 vs. 3.9), in all other groups of former IUD users the incidence of ectopic pregnancy was also lower than in the control group. From the results of this study it was concluded that former IUD users are not at an increased risk for ectopic pregnancy.

Adolescent↗
PubMed1992

Protein phosphorylation and intracellular free calcium in platelets of patients with essential hypertension.

Platelet intracellular free calcium concentration [Ca2+]i from patients with essential hypertension has been found to be elevated, but the intracellular effects of this increase are still unclear. As protein phosphorylation is an important regulatory step in cell activation and increased protein phosphorylation has been demonstrated in platelets from hypertensive animals, we investigated protein phosphorylation and [Ca2+]i in platelets from patients with essential hypertension and age-matched normotensives. We measured the 32P incorporation into a 20 kDa protein and a 47 kDa protein in 17 hypertensive patients and 20 normotensive, age-matched subjects. The [Ca2+]i was measured with the fluorescent dye fura-2. Protein phosphorylation and [Ca2+]i were assessed in unstimulated platelets and after exposure of the cells to 0.1 and 0.25 U/mL thrombin at 20, 60, and 300 sec. In addition we assessed the activity of protein kinase C by incubating the platelets with phorbol-ester TPA at 20, 60, and 300 sec. Basal phosphorylation of the two proteins was not different between the two groups. After exposure of the platelets to thrombin 32P, incorporation into the 20 kDa protein and the 47 kDa protein was significantly increased in platelets from hypertensive patients at all times. Furthermore, the specific stimulation of protein kinase C with TPA resulted in a significantly higher phosphorylation of the 47 kDa protein, whereas the 20 kDa protein was not phosphorylated after incubation with TPA for 1 min. Basal [Ca2+]i was higher in platelets from hypertensive patients (124 +/- 7 nmol/L v 104 +/- 5 nmol/L, P less than .05), although there was a wide overlap between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Platelets↗
PubMed1992

Increased number of alveolar macrophages expressing adhesion molecules of the leukocyte adhesion molecule family in smoking subjects. Association with cell-binding ability and superoxide anion production.

This study was designed to investigate whether the expression and functional properties of leukocyte adhesion molecules (LeuCAM; CD11/CD18) are altered in human alveolar macrophages (AM) from smokers. Cells were obtained from 38 smokers (S) and 27 nonsmokers (NS) by bronchoalveolar lavage (BAL). Expression of LeuCAM on freshly isolated cells was studied using a sensitive peroxidase-antiperoxidase method with monoclonal antibodies (mAB) against CD11a, CD11b, CD11c, and CD18. The functional properties of the adhesion molecules were studied by measuring in vitro the binding of AM to the intracellular adhesion molecule-1 (ICAM-1) on human umbilical-vein endothelial cells (HUVEC). The influence of LeuCAM on the increased superoxide anion production (O2-) of smoker AM was quantified after blocking the CD18 molecule by a mAB. Compared with nonsmoker AM, significantly more AM from smokers expressed CD11b (p < 0.001), CD11c (p < 0.001), CD18 (p < 0.001), and CD11a (p < 0.004), whereas there was no difference in the expression of other common epitopes of human macrophages such as CD68, CD71, CD45, HLA-DQ, and HLA-DR. The number of AM expressing CD11a, CD11c, and CD18 showed a correlation to the total number of AM obtained by BAL (p < 0.001). Adherence of AM to HUVEC was higher for smoker than for nonsmoker AM (p < 0.05). The increased binding of smoker AM to endothelial cells could be inhibited by treating the HUVEC with a mAB against ICAM-1. The mAB anti-CD18 reduced O2- release from smoker AM by 42 +/- 5% after 120 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Amelioration of ischemic acute renal failure by dietary fish oil administration in conscious dogs.

The hypothesis that dietary fish oil would protect dogs from ischemic acute renal failure was tested. Fish oil (eicosapentaenoic acid, 55 mg/kg per day, and docosahexaenoic acid, 40 mg/kg per day was given to eight instrumented, female, beagle dogs for 6 wk, while seven control dogs received vehicle. After 3 wk, unilateral nephrectomy was performed and a pneumatic cuff with flow probe was placed around the remaining renal artery of each dog. Three weeks thereafter, the cuff was inflated for 120 min. Renal function, RBF, and prostanoid excretion were measured 24 and 72 h after ischemia. In dogs receiving fish oil, blood pressure, GFR, RBF, renal vascular resistance (RVR), cholesterol, triglycerides, and prostanoid excretion were measured weekly for 6 wk. Further, cytosolic calcium was measured before and five times after fish oil. Blood pressure decreased, serum cholesterol and triglycerides decreased, and the cytosolic calcium within platelets decreased. The urinary excretion (expressed as picograms per milligram of creatinine) of the thromboxane (TX) metabolite TXB2 and the excretion of prostaglandin (PG)E2, as well as the excretion of the PGI2 metabolite 6-keto PGF1 alpha were decreased. GFR, RBF (Cl inulin and Cl para-aminohippuric acid), and RVR were not influenced by fish oil. Unilateral nephrectomy decreased GFR and RBF and increased RVR as expected, whereas it further decreased prostanoid excretion. Acute renal ischemia caused a significant, reversible decrease in GFR and urine volume in vehicle-treated animals, whereas no significant effect on renal function or urine volume was observed in animals pretreated with fish oil.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗