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Biomedical subjects

H Dietz

Publications and source records attributed to H Dietz.

At least 19 recordsLinked to original sources

Erich Fischer-brügge (28.12.1904-4.2.1951) -- founder of neurosurgery at the university of Münster.

In 1936, Erich Fischer-Brügge, who worked as a surgeon at the University Clinic of Münster, Westfalia, Germany, visited Wilhelm Tönnis in Würzburg, to receive neurosurgical training. He commenced his work in the field of neurosurgery in Münster from 1937. In 1938 he published a new classification of the anterior circulation of cerebral arteries in states of tumorous mass lesions. From 1939 through to the end of WW II, Tönnis and Fischer-Brügge worked closely together, mainly in the field of war surgery. After WW II, in 1949, Fischer-Brügge published another relevant clinical contribution on the "Clivuskantensyndom". He recognised the ipsilateral osseous compression of the oculomotor nerve at the sphenoidal ridge in raised intracranial pressure. Paul Sunder-Plassmann, successor of Hermann Coenen as chief of surgery at the University Clinic in 1946, inhibited Fischer-Brügge's neurosurgical work massively. After numerous unsuccessful applications for newly installed neurosurgical units, Fischer-Brügge died at the age of only 46 years.

Education, Medical↗

Growth rings in the roots of temperate forbs are robust annual markers.

There is increasing interest in the analysis of annual growth rings in the secondary root xylem of perennial forbs (herb-chronology). Therefore, we need to verify whether these growth rings are always formed annually. To investigate the formation of root rings we performed common garden experiments at two distinct sites in Switzerland. We grew nine unrelated forb species from seed and subjected them to competition and clipping treatments. Anatomical developments in the roots of the individuals were tracked during five growing seasons. Across all species and treatments at least 94 % of the expected growth rings associated with full growing seasons were identifiable and the development of the anatomical patterns was consistently seasonal. While the distinctness of annual rings varied somewhat between species and sites, the treatments had no effect on the presence of annual rings. In no case were false rings developed. The results of this study demonstrate that the growth rings in the roots of northern temperate forbs represent robust annual growth increments and, hence, can reliably be used in herb-chronological studies of age- and growth-related questions in plant ecology.

Ecosystem↗

Comparative analysis of growth rings in perennial forbs grown in an Alpine restoration experiment.

Recent studies have demonstrated that growth rings are widespread in the roots of forbs, and there is evidence that the rings are formed annually. However, the annual nature and development of the growth rings has not yet been examined in comparative experimental studies. In this study growth rings were analysed in the main roots of four alpine forbs (Lotus alpinus, Trifolium thalii, Silene willdenowii and Potentilla aurea) that were grown in an alpine restoration experiment for 6 years. All individuals of L. alpinus and T. thalii, and some individuals of S. willdenowii showed six clearly demarcated growth rings, demonstrating that the rings were formed annually. P. aurea did not show distinguishable growth rings. In L. alpinus and T. thalii there were fluctuations in growth ring width that were consistent between individuals and also between species, and matched variations in climatic growth conditions. Results of the present study indicate that conclusions drawn from previous studies suggesting that growth rings in the roots of forb species are most likely formed annually are also valid for alpine plants. In terms of annual ring width patterns, this study also provides the first strong evidence for consistent responses of different forb species and individuals to commonly experienced variations in habitat conditions.

Altitude↗

Biliary atresia: which factors predict the success of a Kasai operation? An analysis of 36 patients.

UNLABELLED: Biliary atresia (BA) is one of the most frequent causes of neonatal cholestasis. Portoenterostomy is one therapeutic option in these patients with a success rate of 30-40%. To answer the question of therapy liver transplantation or Kasai operation - we analyzed 36 consecutive patients being followed in our center during the past 7 years. Two groups were formed: group I : patients developing cirrhosis within the first 2 years of life with the need for liver transplantation (n = 21). Group II: patients without need for transplantation within the first 2 years of life (n = 15). The two groups were compared regarding birth weight, age at diagnosis, age at Kasai-procedure, liver histology. The following biochemical parameters were analyzed at the time of diagnosis, 1 week and 5 weeks after Kasai: AST, ALT, gammaGT, and bilirubin. - RESULTS: Clinical characteristics were similar in both groups. However BA was diagnosed in group I 8.2 weeks after birth compared to 5.6 wk in group II. gammaGT, ALT, AST, and bilirubin were similar in both groups at the time of diagnosis and 1 wk after Kasai. However 5 wk after Kasai gammaGT was 276 U/l in group I compared to 72 U/l in group II (p <0.001), bilirubin was 6.3mg/dl in group I compared to 2. 3mg/dl in group II (p <0.001). - CONCLUSION: Kasai operation before the 7th wk of life increases the success rate of this technique significantly. Children with cirrhosis at the time of diagnosis should be evaluated for primary liver transplantation. gammaGT and bilirubin 5 weeks after Kasai operation may be useful markers for the success of this procedure. Patients with a gammaGT > 100 U/l and a bilirubin level >5mg/dl should be followed closely and should be evaluated for liver transplantation early.

Biliary Atresia↗

Reversion of human glioblastoma malignancy by U1 small nuclear RNA/ribozyme targeting of scatter factor/hepatocyte growth factor and c-met expression.

BACKGROUND: Expression of scatter factor (SF), also known as hepatocyte growth factor (HGF), and its receptor, c-met, is often associated with malignant progression of human tumors, including gliomas. Overexpression of SF/HGF in experimental gliomas enhances tumorigenicity and tumor-associated angiogenesis (i.e., growth of new blood vessels). However, the role of endogenous SF/HGF or c-met expression in the malignant progression of gliomas has not been examined directly. In this study, we tested the hypothesis that human glioblastomas can be SF/HGF-c-met dependent and that a reduction in endogenous SF/HGF or c-met expression can lead to inhibition of tumor growth and tumorigenicity. METHODS: Expression of the SF/HGF and c-met genes was inhibited by transfecting glioblastoma cells with chimeric transgenes consisting of U1 small nuclear RNA, a hammerhead ribozyme, and antisense sequences. The effects of reduced SF/HGF and c-met expression on 1) SF/HGF-dependent induction of immediate early genes (c-fos and c-jun), indicative of signal transduction; 2) anchorage-independent colony formation (clonogenicity), an in vitro correlate of solid tumor malignancy; and 3) intracranial tumor formation in immunodeficient mice were quantified. Statistical tests were two-sided. RESULTS: Introduction of the transgenes into glioblastoma cells reduced expression of the SF/HGF and c-met genes to as little as 2% of control cell levels. Reduction in c-met expression specifically inhibited SF/HGF-dependent signal transduction (P<.01). Inhibition of SF/HGF or c-met expression in glioblastoma cells possessing an SF/HGF-c-met autocrine loop reduced tumor cell clonogenicity (P =.005 for SF/HGF and P=.009 for c-met) and substantially inhibited tumorigenicity (P<.0001) and tumor growth in vivo (P<.0001). CONCLUSIONS: To our knowledge, this is the first successful inhibition of SF/HGF and c-met expression in a tumor model directly demonstrating a role for endogenous SF/HGF and c-met in human glioblastoma. Our results suggest that targeting the SF/HGF-c-met signaling pathway may be an important approach in controlling tumor progression.

Animals↗

Surgical decompression for traumatic brain swelling: indications and results.

OBJECT: Decompressive craniectomy has been performed since 1977 in patients with traumatic brain injury. The authors assess the efficacy of this treatment and the indications for its use. METHODS: The clinical status of the 57 patients, their computerized tomography (CT) scans, and intracranial pressure (ICP) levels were documented prospectively in a standard protocol. At the beginning of the study, all patients older than 30 years were excluded. As of 1989 patients older than 40 years were excluded until 1991; since that time patients older than 50 years have been excluded. Primary brain or brainstem injury with fully developed bulbar brain syndrome, loss of auditory evoked potentials (AEPs), and/or oscillation flow in a transcranial Doppler ultrasound examination were contraindications to decompressive craniectomy. A positive indication for decompression was given in the case of progressive therapy-resistant intracranial hypertension in correlation with clinical (Glasgow Coma Scale [GCS] score, decerebrate posturing, dilating of pupils) and electrophysiological (electroencephalography, somatosensory evoked potentials, and AEPs) parameters and with findings on CT scans. Unilateral decompressive craniectomy was performed in 31 patients and bilateral craniectomy in 26 patients. In all cases, a wide frontotemporoparietal craniectomy was followed by a dura enlargement covered with temporal muscle fascia. The outcomes of the treatment were surprisingly good. Only 11 patients (19%) died, three of whom died of acute respiratory disease syndrome. Five patients (9%) survived, but remained in a persistent vegetative state; six patients (11%) survived with a severe permanent neurological deficit, and 33 patients (58%) attained social rehabilitation. Two patients (3.5%) did not have a follow-up examination. The GCS score on the 1st day posttrauma and the mean ICP turned out to be the best predictors for a good prognosis. The results demonstrate the importance of decompressive craniectomy in the treatment of traumatic brain swelling. CONCLUSIONS: Surgical decompression should be routinely performed when indicated before irreversible ischemic brain damage occurs.

Adolescent↗

Induction of beta-lactamase in Enterobacter cloacae.

beta-lactamase induction in Enterobacter cloacae, which is linked to peptidoglycan recycling, was investigated with use of high-performance liquid chromatography of cell wall fragments in genetically defined cells of Escherichia coli. After treatment of cells with beta-lactams, we detected in the periplasm an increase of D-tripeptide (N-acetylglucosaminyl-1,6 anhydro N-acetylmuramyl-L-alanyl-D-glutamyl-meso-diaminopimelic acid), D-tetrapeptide (N-acetylglucosaminyl-1, 6 anhydro N-acetylmuramyl-L-alanyl-D-glutamyl-meso-diaminopimelic acid -D-alanine), and a yet-unknown anhydromuropeptide. We identified this anhydromuramylpeptide by fast atom bombardment-mass spectrometry as anhydromuramyl-pentapeptide. The amount of these molecules did not alter after treatment with cell wall-active non beta-lactams. The transmembrane protein AmpG transports not only D-tripeptide but also D-pentapeptide into the cell. In the cytoplasm these molecules are degraded into the corresponding monosaccharide peptides M-tripeptide (N-acetylmuramyl-L-alanyl-D-glutamyl-meso-diaminopimelic acid) and M-pentapeptide (N-acetylmuramyl-L-alanyl-D-glutamyl-meso-diaminopimelic acid-alanine-D-alanine). These findings indicate that besides M-tripeptide and D-tripeptide, probably M-tetrapeptide, D-tetrapeptide, M-pentapeptide, and D-pentapeptide are also signal muropeptides for beta-lactamase induction.

Bacterial Proteins↗

On the effect of calcium antagonists on cerebral blood flow in rats. A comparison of nimodipine and flunarizine.

To assess the influence of nimodipine treatment in brain tissue at different levels of blood pressure, we estimated the cerebral blood flow using hydrogen clearance. Rats were treated with nimodipine (n = 8), its placebo (n = 10), flunarizine (n = 11) and its placebo (n = 10), and a group of controls (n = 10). Cerebral blood flow was estimated during arterial normo-, hyper- and hypotension. The lowest cerebral blood flow estimates calculated for nimodipine were 43.8 +/- 7.8, 90.9 +/- 13.3, and 33.6 +/- 6.1 ml/min/100 g for normo-, hyper- and hypotension, respectively. Cerebral blood flow in the nimodipine placebo group was 84.1 +/- 10.3, 139.9 +/- 19.9, and 55.2 +/- 10.5 ml/min/100 g. In the flunarizine group, the blood flow was 77.3 +/- 15.2, 144.7 +/- 15.0, and 43.8 +/- 5.9 ml/min/100 g. In the control group, cerebral blood flow was 90.0 +/- 29.1, 143.0 +/- 42.1, and 75.5 +/- 29.8 ml/min/100 g. The low blood flow in the nimodipine group might have been a consequence of brain edema caused by extravasates. Thus impaired blood flow reduces the usefulness of nimodipine in the prevention of vasospasm. Flunarizine is a potential alternative treatment of vasospasm treatment as well as for cerebral blood flow improvement, as shown in our experimental study.

Animals↗

Clinical predictors of the psychosocial long-term outcome after brain injury.

The correlation of clinical with psychological and social data is an attempt to find predictors of the definite long-term outcome after brain injury. 34 patients were reexamined 3 to 8 years after the accident using a number of psychological tests. Additionally, life quality was defined and evaluated. Only patients with an initial Glasgow Coma Scale-Score of 3-12, an intracranial traumatic lesion on computertomography and age 16-65 years at the time of accident were included in this study. Patients exhibited a uniform pattern of disturbances in psychosocial long-term outcome. These disturbances were compared with initial clinical data: memory, attention and learning were significantly correlated with the duration of coma and the presence of additional extracerebral injuries. From the initial computerized tomography, the findings 'compression of basal cisterns' and 'intracerebral contusion' showed to be predictors of the cerebral function. Late social status and behavior, defined as quality of life, were clearly related with initial clinical findings. In conclusion, there are early clinical predictors of the long term social and psychological outcome after brain injury.

Adolescent↗

The signal molecule for beta-lactamase induction in Enterobacter cloacae is the anhydromuramyl-pentapeptide.

Beta-lactamase induction in Enterobacter cloacae, which is linked to peptidoglycan recycling, was investigated by high-performance liquid chromatographic analysis of cell wall fragments in genetically defined cells of Escherichia coli. After treatment of cells with beta-lactams, we detected an increase in a D-tripeptide (disaccharide-tripeptide, N-acetylglucosaminyl-1,6-anhydro-N-acetylmuramyl-L-alanyl-D-glutamyl-mes o-diaminopimelic acid), aD-tetrapeptide (disaccharide-tetrapeptide, N-acetylglucosaminyl-1,6-anhydro-N-acetylmuramyl-L-alanyl-D-glutamyl-mes o-diaminopimelic acid-D-alanine), and aD-pentapeptide (disaccharide-pentapeptide, N-acetylglucosaminyl-1,6-anhydro-N-acetylmuramyl-L-alanyl-D-glutamyl-mes o-diaminopimelic acid-D-alanyl-D-alanine)levels in the periplasms of bacterial cells. Furthermore, only the accumulation of aD-pentapeptide correlates with the beta-lactamase-inducing capacity of the beta-lactam antibiotic. The transmembrane protein AmpG transports all three aD-peptides into the cytoplasm, where they are degraded into the corresponding monosaccharide peptides. In the absence of AmpD the constitutive overproduction of beta-lactamase is accompanied by an accumulation of aM-tripeptide (monosaccharide-tripeptide, anhydro-N-acetylmuramyl-L-alanyl-D-glutamyl-meso-diaminopimelic acid) and aM-pentapeptide (L1,6-anhydro-N-acetylmuramyl-L-alanyl-D-glutamyl-meso-diaminopimelic acid-D-alanyl-D-alanine), but not aM-tetrapeptide (anhydro-N-acetylmuramyl-L-alanyl-D-glutamyl-meso-diaminopimelic acid-D-alanine), in the cytoplasm. Only the amount of aM-pentapeptide is increased upon treatment with imipenem. These findings indicate that aD-pentapeptide is the main periplasmic muropeptide, which is converted into the cytoplasmic signal molecule for beta-lactamase induction, the aM-pentapeptide.

Acetylmuramyl-Alanyl-Isoglutamine↗

Linkage of the locus for cerebral cavernous hemangiomas to human chromosome 7q in four families of Mexican-American descent.

OBJECTIVE: To determine with greater precision the map location of the locus associated with familial cavernous hemangiomas. BACKGROUND: Cavernous malformations of the brain are a significant cause of seizures, progressive or apoplectic neurologic deficit, and headache. Prevalence estimates from autopsy series vary from 0.39 to 0.9%. This disorder (OMIM #116860) can be inherited as an autosomal dominant trait with variable penetrance. Linkage to markers on the long arm of chromosome 7 was recently reported in separate reports in three apparently unrelated Hispanic kindreds as well as in two kindreds of non-Hispanic descent. DESIGN/METHODS: We examined clinically, by MRI scanning, and by pathologic examination of surgical specimens, members of four large Mexican-American families segregating cavernous hemangiomas of the brain. Linkage analysis was performed with use of blood specimens from morphologically proven cases. Two-point linkage analysis was performed with the MLINK program of the LINKAGE package. Multipoint analysis was performed between two markers and the disease locus with LINKMAP in the FASTLINKAGE package. Allele frequencies were set as described by the Genome Database (GDB). Maximum penetrance for the disease allele was set to 0.75. RESULTS: The highest lod score was observed for marker D7S652 with Zmax = 6.66 at theta(max) = 0.00. Multipoint LOD score analysis placed the disease locus in the 11 cM interval between markers D7S630 and D7S527 with Zmax = 9.19. Haplotype analysis is in agreement with the placement of the disease gene between D7S630 and D7S527 and further shows a minimal shared region within this interval, indicating a founder effect in the establishment of the mutation in these families. CONCLUSIONS: We confirmed the linkage of cavernous hemangioma to markers on the long arm of chromosome 7q, and the estimate of the map location has been refined to a region of shared haplotype between markers D7S630 and D7S527 in four Mexican-American families who may be descended from a common ancestor in Sonora County, Mexico.

Adolescent↗

[Treatment outcome in patients with chronic subdural hematoma with reference to age and concurrent internal diseases].

The chronic subdural hematoma (CSH) is a disease in elderly patients beyond the 5th decade. Treatment of CSH is normally a burr hole trephination and subdural drainage. Although this technique is simple, lethality is reported to be up to 20% in literature. The records of 314 patients with CSH were analyzed. Attention was focussed on complicating diseases and distribution of age. Patients were categorized neurologically before and after trephination using the Bender scale. The portion of patients suffering from cardiological diseases was 14.3%, 6.7% were treated by anticoagulants because of cardiac valve implant. Alcoholics were found in 15.9% of patients and hypertension in 12.8%. Complicating diseases were found in 51.3% of patients. Multiple internal diseases are likely to affect prognosis more than hematoma thickness. These patients also brought about a higher rate of infection (4.8%), secondary hemorrhages (2.5%), pneumonia (3%) and seizures (5%) after trephination. Lethality was highest in patients with diabetes mellitus, cardiogenic diseases and hypertension as well as in elderly patients. The latter have also a poor post-operative outcome: 22 patients died. In contrast to hematoma thickness and midline shift, which do not have any influence on outcome, prognosis is mainly determined by age, complicating diseases, hypertension and diabetes mellitus. The chronic subdural hematoma is often found in multi-morbid patients.

Adult↗

[Hemangioblastoma: description of a disease picture and report of 41 cases].

Hemangioblastomas are benign tumors of the central nervous system (CNS) with a predominance of the cerebellar hemispheres. They are one of the most frequent tumors of the posterior fossa in adults. In this retrospective study the data of 41 operated patients (23 men and 18 women) with a hemangioblastoma of the CNS are demonstrated. The mean age of the patients was 42.2 years (Range 4-70 years). 76% of the hemangioblastomas were located in the cerebellum, 9% in the cerebral hemispheres, 7% in the spinal canal and 5% in the brain stem. Signs of increased intracranial pressure and cerebellar dysfunction were the most frequent symptoms. Complete tumor removal was achieved in 90% of all operated cases. 82% of the hemangioblastomas were cystic and 18% solid. The mean diameter of the tumor cysts was 36 mm (Range 20-60 mm) and 18 mm (Range 2-40 mm) of the solid tumors. In 7% of the cases tumor recurrence was seen with a mean time interval of 5.7 years.

Adolescent↗

Primary structure of cyclohydrolase (Mch) from Methanobacterium thermoautotrophicum (strain Marburg) and functional expression of the mch gene in Escherichia coli.

The gene mch encoding N5,N10-methenyltetrahydromethanopterin cyclohydrolase (Mch) in Methano-bacterium thermoautotrophicum (strain Marburg) was cloned and sequenced. The gene, 963 bp, was found to be located at the 3' end of a 3.5-kbp BamHI fragment. Upstream of the mch gene two open reading frames were recognized, one encoding for a 25-kDa protein with sequence similarity to deoxyuridylate hydroxymethylase and the other encoding for a 34.6-kDa protein with sequence similarity to cobalamin-independent methionine synthase (MetE). The N-terminal amino acid sequence deduced for the deoxyuridylate hydroxymethylase was identical to that previously published for thymidylate synthase (TysY) from M. thermoautotrophicum. The 3' end of the tysY gene overlapped by 8 bp with the 5' end of the mch gene. Despite this fact, the mch gene appeared to be transcribed monocistronically as evidenced by Northern blot analysis and primer-extension experiments. The mch gene was overexpressed in Escherichia coli yielding an active enzyme of 37 kDa with a specific activity of 30 U/mg cell extract protein.

Amino Acid Sequence↗