Search PubMed⌕ Search

Biomedical subjects

H Arnold

Publications and source records attributed to H Arnold.

At least 19 recordsLinked to original sources
PubMed1992

Cyclic alternating chemotherapy of high-grade malignant non-Hodgkin lymphomas with VIM-Bleo and CHOP.

Between 1986 and 1988, 81 patients with high grade malignant non-Hodgkin lymphoma according to the Kiel classification were treated with the VIM-Bleo/CHOP-regimen: etoposide 100 mg/m2 intravenously on days 1-3, ifosfamide 1.5 g/m2 intravenously days 1-5 with mesna for prophylaxis of cystitis, methotrexate 30 mg/m2 intravenously on days 3, bleomycin 10 mg intravenously on days 8 and 15, cyclophosphamide 750 mg/m2 day 22, doxorubicin 50 mg/m2 day 22, vincristine 1.4 mg/m2 on day 22, and prednisolone 100 mg postoperatively on days 1-5 and 22-26. Cycles were repeated four times beginning on day 43. Regions with bulky disease were irradiated after chemotherapy. 36 patients (44%) had stage II, 12 (15%) stage III and 33 (41%) stage IV disease. B-symptoms were present in 49% of patients. Serum lactate dehydrogenase activity was elevated in 53%. Overall, 59 patients (73%) achieved a complete and 14 (17%) a partial remission. 8 (9%) had stable or progressive disease. After a median follow up of 30 months thus far, probability of long-term relapse free survival is 66% for patients in complete remission. Overall survival is 72% at 24 months. Toxicity from treatment was very low with leukopenia being the main side effect. Major infections were observed in only 2% of cycles with one treatment related death. VIM-Bleo/CHOP is a well tolerated regimen with remission rates in the range of other, more toxic regimens. However, cyclic alternating treatment did not improve results as compared with repeated treatment with a single standard protocol.

Adult↗
PubMed1992

Two years serial lymphocytapheresis of progressive hyperleukocytosis in a patient with a non-Hodgkin's lymphoma.

A patient with non-Hodgkin's lymphoma was treated by ambulant lymphocytapheresis once a month over a period of 2 years and 8 months. The cytoreductive effect resulted in a decrease of white blood cells from 410/nl to 130/nl. The patient tolerated the procedure, which lasted 3-4 h, without any side effects. He could be kept in good condition by monthly apheresis. So lymphocytapheresis is a means to reduce hyperleukocytosis in patients with non-Hodgkin's lymphoma.

Ambulatory Care↗
PubMed1991

Delivery of very premature infants: does the caesarean section rate relate to mortality, morbidity, or long-term outcome?

A retrospective analysis of obstetric factors influencing mortality and morbidity of very premature infants (1500 g, less than or equal to 32 weeks' gestation) was undertaken. The study included 275 such infants born in the Department of Obstetrics of the University of Tübingen during the period January 1977 to June 1987. The caesarean section rate of very preterm infants increased from 28% during the period 1977-1982 to 87% during the period 1982-1987 (P less than 0.005), accompanied by an increase in survival rate from 63% to 70%. The improvement in survival rate was statistically significant for the group with birth weight 751-1000 g (P less than 0.01). The overall mortality rate was 31% after caesarean section and 36% after vaginal delivery. Amongst the causes of death of the non-survivors, acidosis was more frequent and amniotic infection syndrome less frequent in the infants delivered vaginally than in those delivered abdominally. The proportion of children with normal development at two years of age was significantly (P less than 0.02) greater amongst those born in 1982-1987 than in those born in 1977-1981. The interpretation of these findings is by no means clear but must include the hypothesis that the increased caesarean section rate may be incidental and in no way related to the improved outcome.

Acidosis↗
PubMed1991

[Abscess of the pyramidal apex].

The authors report on one case of an abscess at the pyramidal apex. The 52-year old male patient presented with pareses of the fifth and seventh cranial nerves and hypacusis on the right side. After diagnostic procedures (CT-scan, carotid angiography), a tumor at the apex of the right pyramid was expected. During surgery a large encapsulated mass was found containing pus. A bacterial agent could not be isolated. The abscess bordered on the mucosal lining of the sphenoid sinus and on the cells of mastoid bone. The starting point of an abscess at the pyramidal apex is most commonly an otitis media, most frequently caused by staphylococcus. Sterile abscesses are seen in almost 20%. Of differential diagnosis on has to keep in mind other space-occupying lesions especially epidermoid or dermoid cysts.

Brain Abscess↗
PubMed1991

Early expression of the myogenic regulatory gene, myf-5, in precursor cells of skeletal muscle in the mouse embryo.

We have analysed by in situ hybridization the expression of myf-5, the murine homologue of the human myogenic regulatory sequence myf5, during embryogenesis in the mouse. myf-5 sequences were first detected in the earliest somites (from about 8 days p.c.) in the dermomyotome, before formation of the dermatome, myotome and sclerotome. The dermomyotome is classically considered to give rise to the precursor muscle cells of body and limb skeletal muscle. myf-5-positive cells were also detected early in the visceral arches and limb buds. In this case, as in somites, myf-5 expression precedes that of the two related myogenic regulatory sequences, myogenin and MyoD1, and indeed any other skeletal muscle marker examined to date. myf-5 is not detected at any stage in developing cardiac muscle. From 11.5 days p.c., the level of myf-5 transcripts begins to decrease to become undetectable (by in situ hybridization) from 14 days p.c. Both the appearance and disappearance of myf-5 follow the anteroposterior gradient of somite formation and maturation in the embryo. The time and place of myf-5 expression are consistent with a role in the early events of myogenic differentiation, possibly during determination of the myogenic lineage.

Animals↗
PubMed1991

Developmental patterns in the expression of Myf5, MyoD, myogenin, and MRF4 during myogenesis.

By using the polymerase chain reaction to amplify specific regions of the respective cDNAs, we have studied the expression of genes encoding the myogenic regulatory factors Myf5, MyoD, Myogenin, and MRF4 (Myf6, herculin) in cultured mouse muscle cells (inducible and permissive C2 cells and Sol8 cells). These cell lines may represent distinct stages in the progression of determined, or committed, muscle cells toward terminal differentiation. Transcripts for Myf5 were detected at the myoblast stage in all the committed muscle cells tested. Expression of the gene for MyoD appeared to be optional at the myoblast stage (MyoD is present in permissive myoblasts and absent from inducible myoblasts) but, like Myogenin, was found to accompany terminal differentiation. Furthermore, forced expression of MyoD converted inducible C2 cells into permissive cells. Expression of MRF4 was found to follow expression of the three other factors and to occur after the onset of terminal differentiation. Of particular interest was the finding that expression of MRF4 was temporally correlated with expression of the gene for the acetylcholine receptor epsilon-subunit that is characteristic of the adult receptor. In vivo, the only transcripts for myogenic regulatory factors to be detected in 8-day mouse embryos were those for Myf5, while expression of MRF4 followed expression of Myf5, MyoD, and Myogenin in developing limbs. Temporal and phenotypic differences related to the expression of Myf5, MyoD, Myogenin, and MRF4 suggest that these factors fulfil distinct roles in the control of myogenesis.

Animals↗
PubMed1979

[A prospective multi-centre study of the response of metastatic gastrointestinal tumours (author's transl)].

In a prospective, multi-centre, randomized study of 109 patients with metastatic gastro-intestinal adenocarcinomas the response rate, survival time and side-effects of two drug combinations, carmustin +5-fluorouracil and carmustin + ftorafur, were compared (same carmustin dosage in both groups). Response to the treatment was 32.7% in those receiving carmustin +5-fluorouracil, 26.3% in those on carmustin + ftorafur. This difference occurred among the 42 patients with gastric adenocarcinoma (33.3% compared with 25%), as well as in 11 with pancreatic adenocarcinoma, and in 56 with colorectal adenocarcinoma (32.1% and 28.6%). Median survival time for 5-fluorouracil + carmustin was 330 days, double that for ftorafur + carmustin (163 days). Bone-marrow toxicity (leukopenia, thrombopenia) was below 10% for both drug combinations. Alopecia occurred in only a few patients. Gastro-intestinal toxicity was common (20% and 18.5%, respectively), but there was no difference between the two groups. The somewhat lower effectiveness of ftorafur compared with 5-fluorouracil was probably due to the deliberately smaller dosage of the former.

Adenocarcinoma↗
PubMed1979

Inherited glucosephosphate isomerase deficiency. A review of known variants and some aspects of the pathomechanism of the deficiency.

Since the first report of GPI deficiency in 1967 many patients from all over the world have been described. The patients suffer from a typical nonspherocytic hemolytic anemia with hemolytic crises during acute infections. The disease is inherited as an autosomal recessive, half of the patients are homozygotic, the others are double heterozygotes. The biochemical properties of the deficient enzymes vary widely. Thus, many well characterized enzymes have been designated as different variants. The modification of physicochemical properties surpasses kinetic aberrations. All defective variants are more or less unstable. The activity diminishes progressively, leading to a rise in G6P concentration and in red cells after aging in vitro to a dramatic impairment of glycolysis and concomittant hemolysis. The cause of the metabolic block is the diminished GPI activity itself and not an inhibition of hexokinase by the high G6P.

Anemia, Hemolytic, Congenital Nonspherocytic↗
PubMed1978

Creatine kinase in human erythrocytes: a newly detected genetic anomaly.

In a family of Italian origin, we found four members with a considerable activity of creatine kinase inside their erythrocytes. All other clinical and hematological findings were normal. The enzyme anomaly seems to be inherited in the autosomal mode. The creatine kinase CK) activity in freshly drawn blood was about 12 U/g Hb. The activity was higher in young red cells than in older ones. Studies with specific antibodies against human CK isoenzymes revealed the CK activity in the probands' red cells to be due to about 90% to the BB-isoenzyme normally found in brain and nerve tissue. The presence of CK in the erythrocytes does not seem to have any consequences for the energy metabolism of the cells. Creatine concentration was slightly elevated, but creatine phosphate could not be detected.

Adult↗
PubMed1978

[Controlled desferrioxamine treatment of congenital anaemia and transfusion siderosis (author's transl)].

A 19-year-old patient with congenital Blackfan-Diamond anaemia has been maintained on a regular red cell transfusion schedule since he was two months old. From the age of four he has received desferrioxamine injections at regular intervals with different dose levels. In spite of the treatment with the chelating agent secondary siderosis developed with typical endocrinological abnormalities and cardiac arrhythmias. Increasing the dose of desferrioxamine to 16 g/24 h resulted in an iron excretion of 184 mg/24 h. Such an intensification of treatment finally produced a negative iron balance and the cardiac arrhythmias disappeared. Desferrioxamine therapy should be done under controlled circumstances only, an iron balance is mandatory, and the dose should be adjusted to the results of the balance.

Adolescent↗
PubMed1978

Findings in computerized axial tomography after intrathecal methotrexate and radiation.

Medulloblastoma and acute lymphocytic leukemia patients treated by intrathecal methotrexate and radiation were investigated by means of computerized axial tomography. More than 50% of them turned out to have acquired encephalopathy. Only gross morphologic brain defects, as visualized by computerized tomography, caused manifest clinical signs of brain dysfunction, such as epilepsy, mental retardation, paresis, and apallic syndrome. Mild morphologic changes were found even in asymptomatic children. The preferred site of defects in brain substance was the paraventricular white matter.

Brain↗