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Biomedical subjects

N Braun

Publications and source records attributed to N Braun.

10 recordsLinked to original sources
PubMed1995

Distribution of 5'-nucleotidase in the developing mouse retina.

The distribution of 5'-nucleotidase was investigated in the developing mouse retina and also in the retina of the adult mouse and rat using a monospecific antibody directed against 5'-nucleotidase isolated from bovine brain. Already at the stage of the formation of the eye cup strong immunofluorescence was found at the ventricular surface. Throughout development the enzyme remained associated with the outer surface of the retina that corresponds to the former inner surface of the eye vesicle. During embryonic development immunoreactivity was also associated with the proliferating cellular elements which at that stage cannot yet be attributed to a defined retinal cell type. In the adult stage the surface-located retinal immunoreactivity is assigned to Müller cells with strongest fluorescence at the apical and microvilli containing cell compartment. Also the cellular processes in the outer nuclear layer, the outer plexiform layer and to a minor extent the inner nuclear layer revealed immunoreactivity. 5'-Nucleotidase immunoreactivity was found at the ventricular surface also of the adult brain. There it was associated with the apical surface of ependymal cells. Our results suggest that 5'-nucleotidase is of general functional importance for the metabolism of nucleotides at the ventricular surface of the retina as well as the ventricles of the brain, a feature that is maintained throughout development. Müller cells thus share not only functional characteristics of astrocytes and oligodendrocytes, as previously revealed, but also of ependymal cells to which they are closely related.

5'-Nucleotidase↗
PubMed1995

Dyspnea in dystonia. A functional evaluation.

BACKGROUND: Dystonia consists of action-triggered sustained focal muscle contractions, worsened by effort, and resulting in voice changes, abnormal posturing, and dyspnea. The cause of dyspnea, previously unexplained, is the basis of this report. METHODS: Since the maximal efforts required to perform pulmonary function testing (PFT) could worsen the muscular contractions in dystonic patients, we used several tests to identify possible causes of dyspnea. These included spirometry with flow volume loops (FVL), tidal volume breathing, maximum voluntary ventilation (MVV), and inspiratory and expiratory muscle pressures (PImax, PEmax), sitting and supine. We used cycle ergometry with arterial blood gas (ABG) values to detect cardiac/pulmonary limitations and respiratory inductive plethysmography (RIP) to assess chest wall/abdominal movements for synchrony. Dynamic videofluoroscopy (VF) assessed and recorded the action-triggered muscle activity of the upper airways and the diaphragm during quiet breathing, speech, swallowing, and maximal respiratory maneuvers similar to the efforts required during PFT. RESULTS: Twenty-six dystonic patients, 12 women and 14 men, ages 14 to 70 years (mean age, 52.3 years) were evaluated. Their neurologic classification included 22 primary (idiopathic) and 4 secondary (2 postneuroleptic use, 2 posstraumatic). Four patients originally classified as having focal dystonia had dyspnea and were found to have diaphragmatic and/or upper airway dysfunction too. The PFTs showed abnormal FVL and/or tidal volume breathing patterns, with intermittent interruptions of air flow during inspiration or expiration in 20 of 24 patients. The VF was abnormal in 24 of 26 patients: 19 patients had combined upper airway (UA) and diaphragmatic dysfunction (DD); 1 patient had UA dysfunction alone, and 4 patients had DD alone. Except for poor effort and/or dystonic movements, cycle ergometry was normal in 18 of 21 patients. The ABG values and/or pulse oximetry were normal in 19 of 22 patients. CONCLUSION: Dyspnea in dystonia appears to be due to excessive and/or dysynchronized contractions of the upper airways and/or diaphragm, with usually normal gas exchange. These spasmodic and irregular muscular contractions during speech and daily activities are associated with the sensation of excessive effort to overcome the spasms. Excessive spasms can be triggered during PFT and are best detected on FVL patterns coupled with dynamic VF.

Adolescent↗
PubMed1995

Renal hemodynamics in essential hypertensives treated with losartan.

ACE-inhibitors are known to have special renal effects, i.e. they increase ERPF, decrease the filtration fraction and lower proteinuria. These effects can be due to a decrease in angiotensin II (AII) levels as well as an increase in bradykinin. New and more specific AII-receptor antagonists may help to distinguish between effects exerted by angiotensin II and those exerted by bradykinin. We investigated the effects of losartan in 9 patients with essential hypertension (sitting mean diastolic blood pressure 95-120 mmHg). Renal hemodynamics were measured by continuous inulin-and PAH-clearance (GFR and RPF) after stopping antihypertensive therapy for 1 week, followed by a 2-week placebo period and after a 4-week treatment phase with losartan (50 mg/die) followed by a therapy with an ACE-inhibitor (ramipril 5mg/die). Additionally, urine albumin excretion (UAE) was measured. Treatment of patients with essential hypertension with losartan resulted in a significant decrease of MAP after three weeks of treatment (121 +/- 8 mmHg under placebo and 114 +/- 10 mmHg under losartan; * = p < 0.05). MAP after four weeks of losartan treatment was 115 +/- 11 mmHg. Regarding changes in renal hemodynamics we could not demonstrate a significant change for neither losartan nor the ACE-inhibitor. Urine albumin excretion was reduced by both treatment regimens in correlation to the magnitude of blood pressure reduction. Our data indicate that losartan induced a significant reduction in MAP in patients with essential arterial hypertension with only moderate effects on renal hemodynamics.

Antihypertensive Agents↗
PubMed1994

Pharmacokinetics of torasemide and its metabolites in end-stage renal disease.

The pharmacokinetics of torasemide, a new loop diuretic, as well as its active metabolites M1 and M3, and its inactive main metabolite, M5, were studied in 12 patients with end-stage renal failure during single i.v. (n = 6) or single oral (n = 6) dosing of 200 mg torasemide, and during chronic oral treatment for 9 days (n = 12). The elimination half-life (t1/2) of torasemide was unchanged in renal failure, whereas t1/2 of the torasemide metabolites M1, M3, and M5 were markedly prolonged. However t1/2 as well as the area under the plasma level time curve of torasemide and its metabolites were unchanged during chronic compared to acute administration. The results of this study suggest that despite the increased half-life of torasemide metabolites M1, M3 and M5 in end-stage renal failure patients, no accumulation of the parent drug torasemide and its metabolites during chronic dosing is demonstrable.

Diuretics↗
PubMed1994

Do different dialysis-membranes affect beta 2-microglobulin kinetics during chronic hemodialysis?

Hemodialysis is not an absolute prerequisite for the formation of beta 2-microglobulin amyloidosis, but it enhances the progression of this complication related to long-standing renal failure. Thus the clearance and turnover of beta 2-microglobulin seems to play a major role in this disease. In a prospective multicenter study the beta 2-microglobulin clearance was studied in 87 patients starting hemodialysis. Serum samples were taken prior to and after the first dialysis session and also before and after dialysis at 4, 6, 12, 16, 26 and 52 weeks. Patients were either treated by cuprophane or a polyacrylonitril membrane. At the start, the mean serum beta 2-microglobulin level was about 18 mg/L in patients treated with a cuprophane membrane, but the levels increased after hemodialysis and reached a plateau, which was always higher than in those treated with polyacrylonitril, which cleared beta 2-microglobulin from the serum. However, after 12 months the difference was no longer significant. Thus beta 2-microglobulin excretion during dialysis differs between the two membranes, but seems to lose its significance for the beta 2-microglobulin serum level in chronic hemodialysis treatment.

Acrylic Resins↗
PubMed1994

[Therapy of primary chronic glomerulonephritis].

Primary chronic glomerulonephritis may emerge clinically as acute nephritis, the nephrotic syndrome as well as asymptomatic hematuria and proteinuria. Therapeutic consequences still depend on the morphological diagnosis. In cases of minor proteinuria [< 3,5 g/24 h] immunosuppressive therapy is not superior to symptomatic therapy. In patients with nephrotic syndrome immunosuppressive therapy depends on the morphological diagnosis. Glucocorticoids are the therapy of choice in minimal changes glomerulopathy and should be tried in focal segmental sclerosing glomerulonephritis. Steroids may be tried in pure mesangial as well as in IgA and IgM nephropathy. Especially Ponticelli claims significant therapeutic success in patients with membranous glomerulonephritis treated with Prednisolone and Chlorambucil. Failures and relapses may be treated with Cyclophosphamide, Chlorambucil or Cyclosporin A. Anticoagulants may be advantageous in the therapy of membranoproliferative glomerulonephritis.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1988

Cell cycle dependent distribution of the proliferation-associated Ki-67 antigen in human embryonic lung cells.

The cell cycle-dependent distribution of the proliferation-associated Ki-67 antigen has been evaluated immunocytochemically in L-132 human fetal lung cells. The cells were synchronized and cell cycle phases were determined: G1 = 6.7 h, S = 5.4 h, G2 = 8.5 h and mitosis = 1.3 h. The Ki-67 patterns were strictly correlated with the cell cycle phases. In late G1-phase, Ki-67 antigen was present only in the perinucleolar region. In the S-phase, Ki-67 staining was found homogeneously in the karyoplasm and in the perinucleolar region. G2-phase cells contained a finely granular Ki-67 staining in the karyoplasm with Ki-67-positive specks and perinucleolar staining. In early mitotic cells (pro- and metaphase) an intense perichromosomal Ki-67 staining was observed in addition to a homogeneously stained karyoplasm in prophase, and cytoplasm in metaphase. During ana- and telophase the Ki-67 antigen disappeared rapidly. In resting cells there was no Ki-67 staining.

Antigens↗