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Biomedical subjects

U Schwarz

Publications and source records attributed to U Schwarz.

At least 55 records · Page 3Linked to original sources
PubMed1998

[Sedation and analgesia in childhood].

As a rule the indication for sedation should be broad. Any child who is, or could be, frightened by an intervention should have the benefit of sedation. Correspondingly, an analgesic should be chosen if the intervention is painful. The sedatives of choice are midazolam and chloral hydrate, and possibly a neuroleptic for interventions which require the child to be motionless. Any physician who sedates a child must be aware of the side effects of the sedation and be well versed in countermeasures, including resuscitation. The dangers of sedation arise from wrong selection of patients and also from postsedation and combination of sedatives and analgesics; both should be left to experienced physicians or specialists. If sedation or analgesia is planned with the rest of the intervention and the described guidelines are followed, the patient's safety is ensured. Despite all efforts a small proportion of patients show an inadequate response to the chosen medication. In young children and in sick children the specific physiological and anatomical features will overtax the therapist. In such cases the help and advice of a specialist trained in paediatric anaesthesia can and should be sought.

Analgesia↗
PubMed1998

MAGE-11 protein is highly conserved in higher organisms and located predominantly in the nucleus.

The MAGE-11 gene belongs to a family whose products were identified first in tumor tissue. The MAGE-11 gene product has not been characterized in detail. We have isolated MAGE-11 cDNA from HeLa cells and confirmed the presence of MAGE-11 protein and of at least 2 other MAGE proteins (MAGE-1 and MAGE-3) in this cell line. Monoclonal antibodies (MAbs), obtained by using a GST-MAGE-11 fusion protein, detect MAGE-11 protein in HeLa cells as a 48 kDa protein. In contrast to other known proteins of the MAGE family, MAGE-11 is found mainly in the nucleus. Immunoprecipitation out of whole-cell extracts from different species reveals that MAGE-11 protein is highly conserved among mammalian cells, suggesting a conserved and important function.

Animals↗
PubMed1998

Metabolism of aromatic aldehydes as cosubstrates by the acetogen Clostridium formicoaceticum.

When the acetogen Clostridium formicoaceticum was cultivated on mixtures of aromatic compounds (e.g., 4-hydroxybenzaldehyde plus vanillate), the oxidation of aromatic aldehyde groups occurred more rapidly than did O-demethylation. Likewise, when fructose and 4-hydroxybenzaldehyde were simultaneously provided as growth substrates, fructose was utilized only after the aromatic aldehyde group was oxidized to the carboxyl level. Aromatic aldehyde oxidoreductase activity was constitutive (activities approximated 0. 8 U mg-1), and when pulses of 4-hydroxybenzaldehyde were added during fructose-dependent growth, the rate at which fructose was utilized decreased until 4-hydroxybenzaldehyde was consumed. Although 4-hydroxybenzaldehyde inhibited the capacity of cells to metabolize fructose, lactate or gluconate were consumed simultaneously with 4-hydroxybenzaldehyde, and lactate or aromatic compounds lacking an aldehyde group were utilized concomitantly with fructose. These results demonstrate that (1) aromatic aldehydes can be utilized as cosubstrates and have negative effects on the homoacetogenic utilization of fructose by C. formicoaceticum, and (2) the consumption of certain substrates by this acetogen is not subject to catabolite repression by fructose.

Benzaldehydes↗
PubMed1998

Effect of 1,25 (OH)2 vitamin D3 on glomerulosclerosis in subtotally nephrectomized rats.

In the past, there has been considerable concern that treatment with active vitamin D might accelerate progression independent of hypercalcemia and hypercalcuria. Nevertheless, 1,25(OH)2D3 has known antiproliferative properties and has also been shown to inhibit renal growth. Since glomerular growth is a permissive factor for the development of glomerulosclerosis, we reasoned that 1,25(OH)2D3 might even attenuate progression. To test this working hypothesis we performed two experiments of 8 and 16 weeks duration, respectively, to compare subtotally nephrectomized (SNX) rats treated with ethanol and SNX treated with 1,25(OH)2D3. Control animals were sham operated and pair-fed with SNX animals. 1,25(OH)2D3 (3 ng/100 g body wt/day) was administered by osmotic minipump. 1,25(OH)2D3 had no significant effect on systolic blood pressure and only a transient effect on weight gain. SNX reduced the number of glomeruli (left kidney) from an average of 3.3 x 10(4) to 1.2 x 10(4) per kidney. Mean glomerular volume was 3.87 +/- 0.71 x 10(6) microns 3 in sham operated animals and significantly (P < 0.05) higher (10.1 +/- 1.75 x 10(6) microns 3) in untreated animals 16 weeks after SNX. Glomerular volume was significantly (P < 0.05) less in 1,25(OH)2D3 treated SNX [10.1 +/- 1.75 in ethanol vs. 7.04 +/- 1.78 in 1,25(OH)2D3 treated SNX]. In parallel, there was significantly (P < 0.01) less glomerulosclerosis [glomerulosclerosis index 1.16 +/- 0.14 in the ethanol treated SNX vs. 0.80 +/- 0.16 in SNX treated with 1,25(OH)2D3] in the eight week experiment. Albuminuria was significantly (P < 0.01) lower in 1,25(OH)2D3 treated than in ethanol treated SNX (mean 0.785 mg/24 hr, range 0.43 to 1.80, vs. 3.75 mg/24 hr, 1.29 to 14.2). The morphological data were directionally analogous in a second 16 week experiment. Only slight changes of the vascular sclerosis index and tubulointerstitial index were seen in SNX and were not affected by 1,25(OH)2D3 further. To prove that the effect of 1,25(OH)2D3 was independent of PTH, parathyreoidectomized SNX rats without or with 1,25(OH)2D3 treatment were examined seven days post-SNX. PCNA staining showed suppression of cell proliferation. Furthermore, in situ hybridization for transforming growth factor-B (TGF-beta) showed less vascular and tubular expression in 1,25(OH)2D3 treated rats. We conclude that 1,25(OH)2D3 has antiproliferative actions during the compensatory growth of nephrons in response to subtotal nephrectomy. These effects are independent of PTH. The data document that 1,25(OH)2D3 reduces renal cell proliferation and glomerular growth as well as glomerulosclerosis and albuminuria as indicators of progressive glomerular damage.

Animals↗
PubMed1998

The renoprotective effect of angiotensin-converting enzyme inhibitors in experimental chronic renal failure is not dependent on enhanced kinin activity.

BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors have been shown to ameliorate the progression of glomerulosclerosis both in experimental models of uraemia and in patients with renal failure. It has not been documented, however, whether this is due to a decrease in angiotensin II generation or is a consequence of elevated local level of bradykinin. METHODS: Morphometric investigation of renal tissue was performed in 5/6 nephrectomized (SNx) rats, i.e. untreated or treated with the ACE inhibitor ramipril (SNx-RAM), the B2 kinin receptor antagonist HOE 140 (SNx-HOE), or a combination of both (SNx-RAM + HOE) over 8 weeks. A further group of SNx received delayed treatment with ramipril from week 5 onward (SNx-RAMD). In addition, a sham-operated (SHAM) control group was studied. RESULTS: Systolic blood pressure was significantly lower in both SNx-RAM and SNx-RAM + HOE groups compared to (untreated) SNx. The glomerulosclerosis index (GSI) was substantially higher in the (untreated) SNx group (0.24 +/- 0.04) vs SHAM (0.02 +/- 0.01). A significantly higher GSI was found in the SNx-HOE group (0.45 +/- 0.08) as compared to (untreated) SNx. However, in the SNx-RAM, SNx-RAM + HOE, and SNx-RAMD groups, the GSI was lowered to a similar extent (0.1 +/- 0.02, 0.09 +/- 0.02, and 0.07 +/- 0.01 respectively). In addition, a concomitant attenuation of tubulointerstitial damage was noted in all the above groups. CONCLUSION: Increased kinin activity does not appear to play a major role in the renoprotective effect of ACE inhibitors in the remnant kidney model.

Angiotensin Receptor Antagonists↗
PubMed1998

Nephroprotection of an ET(A)-receptor blocker (LU 135252) in salt-loaded uninephrectomized stroke-prone spontaneously hypertensive rats.

The present study was designed to assess whether the orally active and highly specific endothelin A (ET(A)) receptor antagonist LU 135252 affects progressive renal dysfunction in a hypertensive rat model of renal damage, ie, the uninephrectomized (UNX) stroke-prone spontaneously hypertensive rat (SHRsp). The animals were examined on a normal salt (0.25%) diet and, to sensitize the kidney to hypertensive injury, also on a high salt (3%) diet. Stereological methods were used to quantify indices of glomerulosclerosis, vascular damage, and tubulointerstitial damage. Treatment with LU 135252 (100 mg/kg body wt) did not affect systolic blood pressure (BP) in animals on a normal salt diet during the whole period of the experiment (18 weeks) or in salt-loaded animals until week 10; subsequently, BP was slightly but significantly lower in salt-loaded UNX-SHRsp given LU 135252. Between weeks 6 and 12, 40% of the untreated UNX-SHRsp on a high salt diet, but none on a standard salt diet, died; such mortality was completely prevented by LU 135252. Indices of renal damage were more abnormal in salt-loaded UNX-SHRsp compared with UNX-SHRsp on a normal salt diet. Development of glomerulosclerosis and tubulointerstitial and vascular damage in UNX-SHRsp on high salt was completely prevented by LU 135252. The respective indices were no longer significantly different from those of salt-loaded sham-operated SHRsp controls. In the less severely damaged kidneys of UNX-SHRsp on normal salt, treatment with LU 135252 tended to ameliorate the indices, but the difference was not statistically significant. The results document a role of the ET system, specifically of ET(A) receptors, in the development of progressive renal injury in salt-loaded UNX-SHRsp. LU 135252 completely prevented death and renal damage resulting from salt loading.

Animals↗
PubMed1997

The role of posterior parietal cortex in visually guided reaching movements in humans.

Positron emission tomography (PET) was used to identify the brain areas involved in visually guided reaching by measuring regional cerebral blood flow (rCBF) in six normal volunteers while they were fixating centrally and reaching with the left or right arm to targets presented in either the right or the left visual field. The PET images were registered with magnetic resonance images from each subject so that increases in rCBF could be localized with anatomical precision in individual subjects. Increased neural activity was examined in relation to the hand used to reach, irrespective of field of reach (hand effect), and the effects of target field of reach, irrespective of hand used (field effect). A separate analysis on intersubject, averaged PET data was also performed. A comparison of the results of the two analyses showed close correspondence in the areas of activation that were identified. We did not find a strict segregation of regions associated exclusively with either hand or field. Overall, significant rCBF increases in the hand and field conditions occurred bilaterally in the supplementary motor area, premotor cortex, cuneus, lingual gyrus, superior temporal cortex, insular cortex, thalamus, and putamen. Primary motor cortex, postcentral gyrus, and the superior parietal lobule (intraparietal sulcus) showed predominantly a contralateral hand effect, whereas the inferior parietal lobule showed this effect for the left hand only. Greater contralateral responses for the right hand were observed in the secondary motor areas. Only the anterior and posterior cingulate cortices exhibited strong ipsilateral hand effects. Field of reach was more commonly associated with bilateral patterns of activation in the areas with contralateral or ipsilateral hand effects. These results suggest that the visual and motor components of reaching may have a different functional organization and that many brain regions represent both limb of reach and field of reach. However, since posterior parietal cortex is connected with all of these regions, we suggest that it plays a crucial role in the integration of limb and field coordinates.

Adult↗
PubMed1997

UNICEF/WHO baby-friendly hospital initiative: does the use of bottles and pacifiers in the neonatal nursery prevent successful breastfeeding? Neonatal Study Group.

UNLABELLED: To promote breastfeeding, UNICEF/WHO have launched the "baby-friendly hospital initiative" focusing on hospital care routines during delivery and the first days of life. In industrialised countries, two aspects of the initiative have raised controversy: how do restriction of supplemental feedings and ban of bottles and pacifiers affect long-term breastfeeding performance? From ten centres 602 healthy newborns were randomly assigned either to a UNICEF group with restrictive fluid supplements and avoidance of bottles and pacifiers during the first 5 days of life, or to a standard group with conventional feeding practice. Breastfeeding was encouraged in both groups. The main study endpoints were the prevalences of breast-feeding on day 5, and after 2, 4 and 6 months. Of the newborns 46% violated the UNICEF protocol, mostly because of maternal requests to give a pacifier or supplements by bottle. In the standard group, the drop-out rate was 9.7%. No significant differences in breastfeeding frequency and duration could be found: (UNICEF vs standard) day 5: 100% vs 99%; 2 months: 88% vs 88%; 4 months: 75% vs 71%; 6 months: 57% vs 55%. Inclusion of drop-outs due to pacifier use did not alter the results. CONCLUSION: In our study population fluid supplements offered by bottle with or without the use of pacifiers during the first 5 days of life were not associated with a lower frequency or shorter duration of breastfeeding during the first 6 months of life.

Breast Feeding↗
PubMed1997

Rats with moderate renal failure show capillary deficit in heart but not skeletal muscle.

In previous studies on experimental renal failure, hypertrophy of cardiomyocytes, diminished capillarization, and increased intercapillary distances had been observed, abnormalities that will expose the heart to reduced ischemia tolerance. It has not been established, however, whether such structural alterations are unique for the heart (eg, as a consequence of left ventricular hypertrophy) or are demonstrable in other tissues as well. Clarification of this point is important to test hypotheses on some potential mechanisms for cardiac undercapillarization. To address this issue further, we compared capillary length density (by stereologic techniques) in perfusion-fixed skeletal muscle (m. psoas) and hearts of subtotally nephrectomized (SNX) rats with moderate renal failure to those in sham-operated pair-fed controls. The duration of renal failure was 8 weeks. SNX rats had significantly higher mean systolic blood pressure (128 mm Hg v 109 mm Hg), serum creatinine, and urea levels. Despite pair feeding, the mean body weight was significantly lower in the SNX rats (409 g v 471 g), but the left ventricular weight to body weight ratio tended to be higher than in the sham-operated controls (2.39 mg/g v 2.13 mg/g). In the heart, myocyte mean cross-sectional area (675 +/- 112 microm2 v 545 +/- 111 microm2) and volume density of nonvascular interstitial tissue (3.47 +/- 1.04 v 1.33 +/- 0.22) were significantly higher in the SNX rats than in the controls. In parallel, myocardial capillary length density was significantly reduced after subtotal nephrectomy (3,036 +/- 535 mm/mm3 v 3,916 +/- 615 mm/mm3). In contrast, in skeletal muscle, myocyte cross-sectional area (3,109 +/- 783 microm2 v 3,042 +/- 639 microm2), capillary length density (718 +/- 248 mm/mm3 v 717 +/- 184 mm/mm3), and three-dimensional capillary fiber ratio (2.10 +/- 0.26 v 2.13 +/- 0.4) were similar in SNX and control rats. These data document a selective defect of capillarization in the heart of animals with moderate renal failure, pointing to tissue-specific abnormalities of cardiac capillarogenesis.

Animals↗
PubMed1997

Responses of MT and MST neurons to one and two moving objects in the receptive field.

To test the effects of complex visual motion stimuli on the responses of single neurons in the middle temporal visual area (MT) and the medial superior temporal area (MST) of the macaque monkey, we compared the response elicited by one object in motion through the receptive field with the response of two simultaneously presented objects moving in different directions through the receptive field. There was an increased response to a stimulus moving in a direction other than the best direction when it was paired with a stimulus moving in the best direction. This increase was significant for all directions of motion of the non-best stimulus and the magnitude of the difference increased as the difference in the directions of the two stimuli increased. Similarly, there was a decreased response to a stimulus moving in a non-null direction when it was paired with a stimulus moving in the null direction. This decreased response in MT did not reach significance unless the second stimulus added to the null direction moved in the best direction, whereas in MST the decrease was significant when the second stimulus direction differed from the null by 90 degrees or more. Further analysis showed that the two-object responses were better predicted by taking the averaged response of the neuron to the two single-object stimuli than by summation, multiplication, or vector addition of the responses to each of the two single-object stimuli. Neurons in MST showed larger modulations than did neurons in MT with stimuli moving in both the best direction and in the null direction and the average better predicted the two-object response in area MST than in area MT. This indicates that areas MT and MST probably use a similar integrative mechanisms to create their responses to complex moving visual stimuli, but that this mechanism is further refined in MST. These experiments show that neurons in both MT and MST integrate the motion of all directions in their responses to complex moving stimuli. These results with the motion of objects were in sound agreement with those previously reported with the use of random dot patterns for the study of transparent motion in MT and suggest that these neurons use similar computational mechanisms in the processing of object and global motion stimuli.

Algorithms↗
PubMed1997

Aortic changes in experimental renal failure: hyperplasia or hypertrophy of smooth muscle cells?

Cardiovascular complications are a well-known feature of chronic renal failure. Increased wall thickness of intramyocardial arterioles and elastic (aorta) and peripheral (mesenteric) arteries is seen even after normalization of blood pressure. It is currently unknown whether such increases result from hyperplasia of vascular smooth muscle cells, hypertrophy, or a combination of both or from an increase in aortic extracellular matrix. Using a recently developed unbiased stereological technique (the dissector), we investigated the aortas of subtotally nephrectomized rats and sham-operated controls after perfusion fixation. We determined aortic wall thickness, cross-sectional area of aortic media, total number of vascular smooth muscle cells per unit aortic length (1 mm), mean cell and nuclear volumes, volume density of elastic fibers, extracellular matrix, vascular smooth muscle cells, and total volumes of these structures per unit of aortic length (1 mm). Blood pressure was not significantly increased in subtotally nephrectomized rats. In contrast, wall thickness, cross-sectional media, total number of aortic vascular smooth muscle cells, and volume of extracellular matrix including collagen were significantly increased after subtotal nephrectomy, whereas cellular hypertrophy was only modest and an increase in elastic fibers did not occur. In conclusion, increased aortic wall thickness in experimental renal failure results primarily from an increase in aortic extracellular matrix. In addition, however, proliferation of aortic vascular smooth muscle cells resulting in cell hyperplasia also contributed to aortic wall thickening to a minor degree. It appears that aortic wall thickening is caused by secretory stimulation of the proliferating vascular smooth muscle cells, resulting in increased matrix production. The nature of the underlying stimulus requires further investigation.

Animals↗
PubMed1996

[Permissive effect of PTH on vascular wall hypertrophy of intramyocardial arteries in experimental renal failure].

BACKGROUND: Abnormalities in cardiovascular structure e.g. LV hypertrophy and thickening of vessels (elastic and peripheral arteries, veins) are hallmarks of renal failure. Among other hormones parathyroid hormone (PTH) has been shown to affect cardiac function and has also been identified at a permissive factor for the activation of the cardiac interstitium leading to myocardial fibrosis. The present study was designed to examine whether PTH was also permissive for intramyocardial arteriolar wall thickening in an experimental model of renal failure. MATERIAL AND METHODS: Sham operated or subtotally nephrectomized rats (SNX) were parathyroidectomized (PTX) and received either saline or rat 1,34 PTH by osmotic minipump. After perfusion fixation, intramyocardial arterioles were assessed using stereological techniques (wall thickness, wall/lumen ratio, minimal lumen diameter, length density). RESULTS: Wall thickness of intramyocardial arterioles was significantly higher in SNX than in sham-op controls. SNX-PTX animals receiving solvent did not differ from sham-op controls while SNX-PTX animals receiving PTH had increased values which were comparable with those of SNX. In addition, PTH treated animals showed signs of marked vascular smooth-muscle cell and endothelial cell activation. CONCLUSIONS: The data suggest that intramyocardial arteriolar wall thickening in experimental renal failure and probable changes of vessel architecture in renal insufficiency in general are dependent upon the permissive effect of PTH.

Animals↗
PubMed1996

Characterization of the single-strand-specific BPV-1 origin binding protein, SPSF I, as the HeLa Pur alpha factor.

SPSF I and II are two cellular proteins which bind specifically to single-stranded DNA. SPSF I and II binding sites are found in the minimal origin of replication of BPV-1 DNA and near the P2 promoter of the cellular c-myc gene. DNA-binding properties of the two proteins to single-stranded oligonucleotides of different lengths and sequences were quantified by determination of DNA-binding constants. The binding constant of SPSF proteins to the lower strand of the BPV-1 origin was determined to be 1.5 x 10(-10) M-1. Peptide sequences derived from purified SPSF I and II revealed the identity of at least one of the SPSF proteins with the so-called HeLa Pur alpha factor. The HeLa Pur alpha factor was identified previously by virtue of its capacity to bind to purine-rich strands of the PUR element found in initiation zones of DNA replication [Bergemann, A.D., Ma,Z.-W. and Johnson, E.M. (1992) Mol. Cell. Biol. 12, 5673-5682]. Expression of the Pur cDNA confirmed the identity of the Pur alpha protein with the 42 kDa SPSF I protein. Analysis of several Pur alpha cDNA clones revealed the existence of an extended 3'-untranslated region in all Pur mRNAs.

Animals↗