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Biomedical subjects

C Braun

Publications and source records attributed to C Braun.

At least 19 recordsLinked to original sources
PubMed1997

Extensive reorganization of primary somatosensory cortex in chronic back pain patients.

The hypothesis of reorganization of the primary somatosensory cortex in states of chronic pain was assessed in 10 low back pain patients and nine matched healthy controls. Intracutaneous electric stimuli were applied to the left back and index finger at a standard, a non-painful and a painful intensity. Magnetic fields were recorded by a 37-channel BTi biomagnetometer from the hemisphere contralateral to the site of stimulation. The power of the early evoked magnetic field (< 100 ms) elicited by painful stimulation of the painful back in very chronic patients was elevated relative to that elicited by painful back stimulation of healthy controls and showed a linear increase with chronicity (r = 0.74). The maximum activity elicited in primary somatosensory cortex was shifted more medially in the very chronic back pain subjects. These data suggest that chronic pain is accompanied by cortical reorganization and may serve an important function in the persistence of the pain experience.

Adult↗
PubMed1997

Microdomain Ca2+ activation during exocytosis in Paramecium cells. Superposition of local subplasmalemmal calcium store activation by local Ca2+ influx.

In Paramecium tetraurelia, polyamine-triggered exocytosis is accompanied by the activation of Ca2+-activated currents across the cell membrane (Erxleben. C., and H. Plattner. 1994. J. Cell Biol. 127:935-945). We now show by voltage clamp and extracellular recordings that the product of current x time (As) closely parallels the number of exocytotic events. We suggest that Ca2+ mobilization from subplasmalemmal storage compartments, covering almost the entire cell surface, is a key event. In fact, after local stimulation, Ca2+ imaging with high time resolution reveals rapid, transient, local signals even when extracellular Ca2+ is quenched to or below resting intracellular Ca2+ concentration ([Ca2+]e, < or = [Ca2+]i). Under these conditions, quenched-flow/freeze-fracture analysis shows that membrane fusion is only partially inhibited. Increasing [Ca2+], alone, i.e., without secretagogue, causes rapid, strong cortical increase of [Ca2+]i but no exocytosis. In various cells, the ratio of maximal vs. minimal currents registered during maximal stimulation or single exocytotic events, respectively, correlate nicely with the number of Ca stores available. Since no quantal current steps could be observed, this is again compatible with the combined occurrence of Ca2+ mobilization from stores (providing close to threshold Ca2+ levels) and Ca2+ influx from the medium (which per se does not cause exocytosis). This implies that only the combination of Ca2+ flushes, primarily from internal and secondarily from external sources, can produce a signal triggering rapid, local exocytotic responses, as requested for Paramecium defense.

Animals↗
PubMed1997

PMP-22 expression in the central nervous system of the embryonic mouse defines potential transverse segments and longitudinal columns.

PMP-22, a major constituent of peripheral nervous system (PNS) myelin, is also present in the central nervous system (CNS), in motoneurons of the cranial nerve motor nuclei and spinal cord (Parmantier et al. [1995] Eur. J. Neurosci. 7:1080-1088). The expression of PMP-22 in the CNS during embryonic and early postnatal development was investigated and showed a biphasic spatio-temporal pattern. The expression of PMP-22 started at embryonic day (E)11.5, in restricted longitudinal and transverse domains, in the ventricular zone of the spinal cord, rhombencephalon, mesencephalon and prosencephalon. In the mid- and forebrain, the PMP-22 signal was detectable in a longitudinal domain that followed ventrally the basal/alar boundary but could no longer be detected dorsally at some distance from the roof plate. Along the caudo-rostral axis, the territory in which PMP-22 was detected spanned the mesencephalon and the prosencephalon, extending caudally from the limit between the isthmus and the mesencephalon, and rostrally to the boundary between prosomeres 4 and 5 (p4/p5). In agreement with the prosomeric model of forebrain organization proposed by Puelles and Rubenstein ([1993] TINS 16:472-479), differences in the level of PMP-22 expression in p2, p3, and p4 clearly defined the p2/p3 and p3/p4 neuromeric boundaries. By E17.5, PMP-22 was no longer detected in the ventricular zone, but at E18.5 it began to be expressed in motoneurons of cranial nerve motor nuclei and, after birth, following a rostro-caudal gradient, in the ventral spinal cord.

Animals↗
PubMed1996

Bilateral vertebral artery lesion after dislocating cervical spine trauma. A case report.

STUDY DESIGN: This case report illustrates the problems associated with diagnosis and management of vertebral artery injuries resulting from dislocating cervical spine trauma. OBJECTIVES: Treatment involved the principles of anterior stabilization of dislocating cervical spine fracture as well as the diagnostic procedures and therapeutic modalities appropriate for vertebral artery lesions. SUMMARY OF BACKGROUND DATA: Because vertebral artery injuries with cervical spine trauma are rarely symptomatic, they can easily be overlooked. Bilateral or dominant vertebral artery occlusion, however, may cause fatal ischemic damage to the brain stem and cerebellum. METHODS: Cervical spine dislocation was stabilized immediately after admission using internal fixation by ventral plate and corticocancellous bone graft. Immediate angiography was performed when brain stem neurologic dysfunction manifested 36 hours after surgery. The patient was treated with anticoagulation, osmotherapy, and controlled hypertension. RESULTS: A fatal outcome resulted in this case of dominant left vertebral artery occlusion. Necropsy even revealed bilateral vertebral artery damage at the level of the osseous lesion. CONCLUSIONS: The possibility of the complication of a vertebral artery lesion should be kept in mind when examining patients with cervical spine trauma, especially in patients with fracture-dislocation. Immediate identification by vertebral angiography, magnetic resonance imaging, or thin-slice computed tomography scan is necessary for optimal management of this injury.

Adult↗
PubMed1996

[Chronic recurrent subileus due to Strongyloides stercoralis infection under immunosuppressive therapy].

HISTORY AND CLINICAL FINDINGS: A 33-year-old woman from Laos was admitted due to recurrent vomiting and weight loss. Since one year, she was receiving immunosuppressive therapy (azathioprine 50 mg/d and methylprednisolone 18 mg/d) for a mixed connective tissue disease. Because of a drug induced Stevens-Johnson-Syndrome one month earlier high doses of methylprednisolone (100 mg/d intravenously) had been administered. The patient's general condition was reduced. Examination elicited a mild pain in the middle abdomen on palpation but no resistance or tumour. The differential diagnosis included obstructive and (or) inflammatory disease of the gastrointestinal tract. INVESTIGATIONS: Elevated IgE-levels (1111 IU/ml; normal up to 100 IU/ml) and eosinophilia (8%) lead to the suspicion of a helminthiasis. Oesophagogastroduodenoscopy showed a significant duodenal stenosis. Duodenal biopsy revealed a severe infestation with Strongyloides stercoralis. Stool examinations were negative though. TREATMENT AND COURSE: With administration of thiabendazole (2 g/d) a rapid recovery was noted. A second oesophagogastroduodenoscopy one week after the onset of therapy revealed no further stenosis. Since there was no activity of the mixed connective tissue disease the methylprednisolone dosage was reduced and the administration of azathioprine was ceased. 3 weeks after beginning of treatment the patient was discharged in improved condition. CONCLUSION: In immunocompromised patients suffering from gastrointestinal complaints who have been in endemic areas an infection with Strongyloides stercoralis should be excluded. Without treatment, this helminthiasis may be fatal.

Adult↗
PubMed1996

Identification of Asp 549 as the catalytic nucleophile of glycogen-debranching enzyme via trapping of the glycosyl-enzyme intermediate.

Glycogen-debranching enzyme catalyzes the removal of branching from glycogen via a two-step process involving first the transfer of a maltotriosyl unit from the branch to the main chain and second the hydrolysis of the residual alpha-(1,6)-linked glucose moiety. Since the transfer occurs with retention of anomeric configuration, a mechanism involving a maltotriosyl-enzyme species is presumed. 4-Deoxy-alpha-maltotriosyl fluoride functions as an incompetent substrate for this transferase activity since a glycosyl-enzyme species in formed, as witnessed by a "burst" of fluoride release, but turned over only very slowly unless a suitable acceptor such as maltotriose is added, at which point 4-deoxymaltohexaose is released. Peptic proteolysis of this trapped enzyme generated a mixture of peptides which was separated by reverse phase high-performance liquid chromatography, and the glycosylated peptide was located by use of tandem mass spectrometry in the neutral loss mode. Subsequent tandem mass spectrometric experiments on this peptide identified it as one surrounding Asp 549. This amino acid is completely conserved in all alpha-glucanotransferases and alpha-glucosidases belonging to this sequence -related family and is hereby identified as the catalytic nucleophile.

Amino Acid Sequence↗
PubMed1996

No attenuation of ischaemic preconditioning by the calcium antagonist nisoldipine.

In anaesthetized dogs, intracoronary infusion of calcium prior to a prolonged ischaemic period reduced infarct size, thereby mimicking the protective effects of ischaemic preconditioning and suggesting that an increase in the intracellular calcium concentration might be an important mechanism underlying this phenomenon. The aim was to determine whether pretreatment with the calcium antagonist nisoldipine attenuates the reduction in infarct size achieved by ischaemic preconditioning. In 10 enflurane-anaesthetized pigs serving as controls (group 1), the inflow into the cannulated left anterior descending coronary artery was reduced (low-flow ischaemia) to achieve a 90% reduction in an anterior myocardial work index (sonomicrometry) for 90 min. In 11 pigs (group 2), a cycle of 10 min of low-flow ischaemia and 15 min of reperfusion (preconditioning) preceded the prolonged ischaemia. In groups 3 (n = 9) and 4 (n = 7), nisoldipine was administered by intravenous infusion (500 ng/kg/min) starting 40 min prior to and then throughout a protocol identical to that of groups 1 and 2, respectively. Subendocardial blood flow was measured with radiolabelled microspheres. Infarct size (% area at risk) was determined by triphenyltetrazolium staining in all pigs after 120 min of reperfusion. Subendocardial blood flow in the area at risk was similar in all four groups (group 1: 0.09 +/- 0.04 ml/min/g; group 2: 0.05 +/- 0.03; group 3: 0.09 +/- 0.03; group 4: 0.07 +/- 0.03). Group 2 had reduced infarct size when compared with group 1 (2.6 +/- 3.0% v 12.4 +/- 8.7%, P = 0.004), and there was a trend for a reduction in infarct size following nisoldipine treatment (group 3: 10.2 +/- 7.1%, group 4: 1.6 +/- 2.8%, P = 0.01). Thus administration of nisoldipine in pigs tended to decrease infarct size, and did not abolish the cardioprotection afforded by ischaemic preconditioning.

Analysis of Variance↗
PubMed1996

[Defect fractures of the tibia--various forms of bone replacement].

Different bone substitutes exist for reconstruction of segmental tibial bone defects. The choice of bone substitute is limited by the quality of the surrounding tissue and the size of the bone defect. Especially in large bone defects, the freely or microvascularly transferred autogenic graft should be preferred. Allogenic transplants or artificial bone substitutes, such as spongy calcium phosphate materials, are suitable only for implantation in smaller, well-vascularized bone defects or as an additional procedure in large bone defects. In infected cases, allogenic and artificial, especially slowly resorbable implants, have to be avoided. The prerequisite for defect reconstruction is stable internal fixation.

Bone Substitutes↗
PubMed1996

Left and right visual field advantages are a function of scotopic and photopic retinal adaptation, respectively, in simple reaction time to near-threshold targets.

Modulation of stimulus luminance in a tachistoscopic face discrimination task has been found to significantly invert visual hemifield advantage in reaction time (RT) (Sergent, 1982a, Sergent, 1982b). However, there is no more physiological rationale for that than for a similar effect, say, of retinal adaptation, and it is even conceivable that the latter may have confounded the former in past experiments. The experiments reported here were therefore designed to tease out the relative contributions of stimulus luminance and of background illumination (i.e., retinal adaptation) in a simple RT task. Two equally difficult conditions of dim targets were set up, one with light-adapted subjects and one with dark-adapted subjects. Similarly, two equally difficult conditions of bright targets were set up with light and dark-adapted subjects. It was found that dim targets (near detection threshold) yielded a significant right visual field RT advantage in light-adapted subjects and that dim targets (equally near detection threshold) yielded a significant left visual field RT advantage in dark-adapted subjects. Future experiments will determine whether cone-mediated RT to detection is left hemisphere dominant and whether rod-mediated RT to detection is right hemisphere dominant.

Adaptation, Ocular↗
PubMed1996

Autoregulation of renal blood flow and pressure-dependent renin release in autosomal dominant polycystic kidney disease of rats.

The Han:SPRD (PKD) rat is a new animal model of autosomal dominant polycystic kidney disease (ADPKD) which resembles many clinical and pathoanatomical features of human ADPKD. The aim of the present study was to analyse age-dependent changes in renal haemodynamics and renal renin secretion which could be of pathophysiological importance in the course of the disease. We investigated glomerular filtration rate (GFR), renal blood flow (RBF), renal vascular resistance (RVR), plasma renin activity (PRA), the autoregulatory behaviour of RBF and the pressure-dependent plasma renin activity in conscious PKD rats compared with age-matched controls. Experiments were performed in conscious chronically instrumented PKD rats (age: 3 and 9 months) and their age-matched genetic controls. GFR in 3-(0.52 +/- 0.07 ml/min/100 g; n = 9) and 9-month-old (0.42 +/- 0.03 ml/min/100 g; n = 21) PKD rats were significantly lower (P < 0.05) than 3- (0.92 +/- 0.07 ml/min/100 g; n = 17) and 9-month-old (0.67 +/- 0.05 ml/min/100 g; n = 17) controls. Nine-month-old PKD revealed a significant (P < 0.005) resetting of the breakpoint of RBF autoregulation towards lower pressures (85.5 +/- 4.4 mmHg; n = 10) than either age-matched controls (102.8 +/- 2.5 mmHg; n = 11) or young PKD (107.5 +/- 4.4 mmHg; n = 6). The basal plasma renin activity was significantly (P < 0.05) lower in 3-month-old PKD than in old PKD and age-matched controls. A significant shift of threshold pressure for pressure-dependent renin release to lower pressures was observed in PKD rats. The observed improvement of autoregulatory reserve, at least in the low pressure range, could be of pathophysiological importance in delaying the progression of chronic renal failure in ADPKD. The suppression of the renin angiotensin system in young PKD could explain the fact that we did not observe hypertension in PKD rats, which is a major difference between this animal model and human ADPKD.

Aging↗
PubMed1995

Mechanism-based inhibition of yeast alpha-glucosidase and human pancreatic alpha-amylase by a new class of inhibitors. 2-Deoxy-2,2-difluoro-alpha-glycosides.

2-Deoxy-2,2-difluoroglycosides are a new class of mechanism-based inhibitors of alpha-glycosidases, which function via the accumulation of a stable difluoroglycosyl-enzyme intermediate. Two members of this new class of inhibitor have been synthesized and kinetic studies performed with their target glycosidases. Thus 2,4,6-trinitrophenyl 2-deoxy-2,2-difluoro-alpha-glucoside is shown to inactivate yeast alpha-glucosidase with a second order rate constant of ki/Ki = 0.25 min-1 mM-1. The equivalent difluoromaltoside inactivates human pancreatic alpha-amylase with ki/Ki = 0.0073 min-1 mM-1. Competitive inhibitors protect the enzyme against inactivation in each case, showing reaction to occur at the active site. A burst of release of one equivalent of trinitrophenolate observed upon inactivation of human pancreatic alpha-amylase proves the required 1:1 stoichiometry. These are the first mechanism-based inhibitors of this class to be described, and the first mechanism-based inhibitors of any sort for the medically important alpha-amylase. In addition to having potential as therapeutics, compounds of this class should prove useful in subsequent structural and mechanistic studies of these enzymes.

Carbohydrate Sequence↗
PubMed1995

Pain-related cerebral potentials in patients with frontal or parietal lobe lesions.

The present study investigated the processing of painful electrical stimuli in patients with unilateral frontal or parietal lobe damage and matched control subjects. Patients with frontal lesions showed increased pain thresholds when the stimuli were administered contralateral to the lesion. While the peak-to-peak amplitudes of the N150/P250 components of the somatosensory potentials increased linearly with stimulus intensity in the control subjects, the responses in the frontal group did not change significantly between stimulation at pain and tolerance threshold. There was no evidence for altered pain processing in patients with parietal lobe lesions. The findings of the present study support the hypothesis of an involvement of the frontal cortex in pain perception in humans.

Adult↗
PubMed1995

Peripheral myelin protein-22 is expressed in rat and mouse brain and spinal cord motoneurons.

Peripheral myelin protein PMP-22 is expressed by Schwann cells and is a constituent of peripheral nervous system (PNS) myelin. Two PMP-22 transcripts, SR13 and CD25, differing in their 5' non-coding sequences have been described. SR13 is present both in the PNS and in non-neural tissue, whereas CD25 mRNA is almost exclusively expressed in Schwann cells. PMP-22 mRNA is also present in the central nervous system (CNS), but at much lower levels than in the PNS. We have investigated the regional distribution of PMP-22 mRNA in the rat and mouse CNS by the reverse transcriptase-polymerase chain reaction method, using oligonucleotide primers specific for the SR13 or CD25 transcripts. SR13 mRNA was detected in all the CNS regions analysed, whereas the CD25 message was present only in the brainstem and the spinal cord. Localization of the PMP-22 transcripts, determined by in situ hybridization in 21 day-old animals, showed selective expression in the motor nuclei. The PMP-22 signal was very weak in the nuclei of the oculomotor and trochlear nerves and absent in the nucleus of the abducens nerve. A strong PMP-22 signal was observed in the motor nuclei of the trigeminal, facial, ambigus, vagus, hypoglossal and accessory spinal nerves and in the ventral horn of the spinal cord. The PMP-22-positive cells were identified as motoneurons on the basis of topographic and morphological criteria, as well as immunolabelling with neuron-specific antibodies.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Nitric oxide reductase from Pseudomonas stutzeri. Primary structure and gene organization of a novel bacterial cytochrome bc complex.

Nitric oxide (NO) reductase is an integral membrane component of the anaerobic respiratory chain of Pseudomonas stutzeri that transforms nitrate to dinitrogen (denitrification). The enzyme catalyzes the reduction of NO to nitrous oxide. The structural genes for the NO reductase complex, norC and norB, were sequenced and their organization established by primer extension and Northern blot analysis. The norCB genes encoding the cytochrome c and cytochrome b subunits of the enzyme are contiguous and transcribed as a single 2.0-kb transcript. The promoter region has a canonical recognition motif for the transcriptional activator protein Fnr, centered at -40.5 nucleotides from the initiation site of transcription. No similarity of the derived gene products to known cytochromes of b- or c-type was found in a data bank search. Post-translational processing of the two subunits was limited to the removal of the terminal methionine to leave an N-terminal serine in either subunit. The mature cytochrome c subunit (16508Da, 145 residues) is predicted to be a bitopic protein with a single membrane anchor. The mature cytochrome b subunit (53006Da, 473 residues) is a putatively polytopic, strongly hydrophobic membrane-bound protein with 12 potential transmembrane segments. Several histidine and proline residues were identified with potentially structural and/or functional importance. Mutational inactivation of NO reductase by deletion of norB or the norCB genes affected strongly the in vivo activity of respiratory nitrite reductase (cytochrome cd1), but to a much lesser extent the expression level of this enzyme. In turn, mutational inactivation of the structural gene for cytochrome cd1, nirS, or loss of in vivo nitrite reduction by mutation of the nirT gene, encoding a presumed tetraheme cytochrome, lowered the expression level of NO reductase to 5-20%, but hardly its catalytic activity. The cellular concentration of NO reductase increased again on restoration of nitrite reduction in the nirS::Tn5 mutant MK202 by complementation with nirS or with the heterologous nirK gene, encoding the Cu-containing nitrite reductase from Pseudomonas aureofaciens. Thus, NO may be required as an inducer for its own reductase. Our results show that the nitrite-reducing system and the NO-reducing system are not operating independently from each other but are interlaced by activity modulation and regulation of enzyme synthesis.

Amino Acid Sequence↗
PubMed1994

Veratridine triggers exocytosis in Paramecium cells by activating somatic Ca channels.

Paramecium tetraurelia wild-type (7S) cells respond to 2.5 mM veratridine by immediate trichocyst exocytosis, provided [Ca2+]o (extracellular Ca2+ concentration) is between about 10(-4) to 10(-3) M as in the culture medium. Exocytosis was analyzed by light scattering, light and electron microscopy following quenched-flow/freeze-fracture analysis. Defined time-dependent stages occurred, i.e., from focal (10 nm) membrane fusion to resealing, all within 1 sec. Veratridine triggers exocytosis also with deciliated 7S cells and with pawn mutants (without functional ciliary Ca channels). Both chelation of Ca2+o or increasing [Ca2+]o to 10(-2) M inhibit exocytotic membrane fusion. Veratridine does not release Ca2+ from isolated storage compartments and it is inefficient when microinjected. Substitution of Na+o for N-methylglucamine does not inhibit the trigger effect of veratridine which also cannot be mimicked by aconitine or batrachotoxin. We conclude that, in Paramecium cells, veratridine activates Ca channels (sensitive to high [Ca2+]o) in the somatic, i.e., nonciliary cell membrane and that a Ca2+ influx triggers exocytotic membrane fusion. The type of Ca channels involved remains to be established.

Aconitine↗