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Biomedical subjects

J Hermann

Publications and source records attributed to J Hermann.

At least 55 records · Page 3Linked to original sources
PubMed1997

Allogeneic bone marrow transplantation for chronic myelomonocytic leukemia in childhood: a report from the European Working Group on Myelodysplastic Syndrome in Childhood.

PURPOSE: To evaluate the role of allogeneic bone marrow transplantation (BMT) in children with chronic myelomonocytic leukemia (CMML). PATIENTS AND METHODS: Forty-three children with CMML given BMT and reported to the European Working Group on Myelodysplastic Syndrome in Childhood (EWOG-MDS) data base were evaluated. In 25 cases, the donor was a human leukocyte antigen (HLA)-identical or a one-antigen-disparate relative, in four cases a mismatched family donor, and in 14 a matched unrelated donor (MUD). Conditioning regimens consisted of total-body irradiation (TBI) and chemotherapy in 22 patients, whereas busulfan (Bu) with other cytotoxic drugs was used in the remaining patients. RESULTS: Six of 43 patients (14%), five of whom received transplants from alternative donors, failed to engraft. There was a significant difference in the incidences of chronic graft-versus-host disease (GVHD) between children transplanted from compatible/one-antigen-mismatched relatives and from alternative donors (23% and 87%, respectively; P < .005). Probabilities of transplant-related mortality for children given BMT from HLA-identical/one-antigen-disparate relatives or from MUD/ mismatched relatives were 9% and 46%, respectively. The probability of relapse for the entire group was 58%, whereas the 5-year event-free survival (EFS) rate was 31%. The EFS rate for children given BMT from an HLA-identical sibling or one-antigen-disparate relative was 38%. In this latter group, patients who received Bu had a better EFS compared with those given TBI (62% v 11%, P < .01). CONCLUSION: Children with CMML and an HLA-compatible relative should be transplanted as early as possible. Improvement of donor selection, GVHD prophylaxis, and supportive care are needed to ameliorate results of BMT from alternative donors.

Bone Marrow Transplantation↗
PubMed1996

A cysteine proteinase, which cleaves human C3, the third component of complement, is involved in tumorigenicity and metastasis of human melanoma.

The DM-4 human melanoma cell line, which is highly metastatic in nude mice, expresses a C3-cleaving activity that proteolyzes labeled as well as unlabeled human C3. This C3-cleaving activity is a cysteine proteinase characterized by a M(r) 41,000. The p41 proteinase shares antigenic determinants with murine p39 procathepsin-L and human procathepsin-L. Preincubation of DM-4 cells with anti-p39 F(ab')2 induced up to 45% decrease in their complement resistance. Pretreatment of DM-4 cells with anti-p39 Ab strongly inhibited their tumorigenicity and significantly decreased their metastatic potential in nude mice. Thus, the p41 C3-cleaving proteinase contributes to tumorigenicity and metastasis of human melanoma DM-4 cells.

Animals↗
PubMed1996

[Possible diagnostic error of "Bechterew disease"].

A 41-year old caucasian male presented with limited range of motion of the entire spine and myogenous intermittent claudication. He was referred with the diagnosis "ankylosing spondylitis". The clinical picture mimicked ankylosing spondylitis, but there were no corresponding radiological abnormalities despite a 13-year history of his disease. Laboratory values showed markedly elevated levels of muscle enzymes. The diagnosis of rigid spine syndrome, a subtype of muscular dystrophy, was made from the clinical picture a normal EMG and degenerative changes on a biopsy from the muscle trapezius. We would like to draw attention to this rare cause of back pain.

Adult↗
PubMed1995

Identification on melanoma cells of p39, a cysteine proteinase that cleaves C3, the third component of complement: amino-acid-sequence identities with procathepsin L.

We previously identified, on normal or tumour cells, two membrane proteinases, p57 and p65, that cleave human C3, the third component of complement, thus regulating C3's biological properties. Whereas p57 was purified from human erythrocytes, p65 was identified using polyclonal anti-p57 antibodies on a human melanoma cell line resistant to complement lysis. Analysis of cell distribution of C3-cleaving proteinases established that DSm, a murine melanoma cell line, expressed a C3-cleaving proteinase distinct from p57 and p65 proteinases. Thus we purified the C3-cleaving proteinase solubilized from membranes of DSm cells. The purified proteinase, termed 'p39' on the basis of its molecular mass of 39 kDa, was identified, using specific proteinase inhibitors, as a cysteine proteinase. Anti-p39 antibodies, prepared against highly purified p39, localized the p39 C3-cleaving proteinase mainly at the cell surface and demonstrated that p39 is also secreted. Anti-p39 antibodies inhibited solubilized C3-cleaving activity. Preincubation of DSm cells with anti-p39 F(ab')2 fragments increased up to 60% complement cell susceptibility. Amino acid analysis of N-terminal and three other regions of p39 demonstrated that this C3-cleaving proteinase carries 100% identity within four regions of procathepsin L. This is the first demonstration that a melanoma cell line expresses on its surface and secretes a p39 C3-cleaving cysteine proteinase that shares sequence identities with procathepsin L. Thus the p39 cysteine proteinase represents a new member of the C3-cleaving proteinase family associated with, and/or expressed on, the cell surface.

Amino Acid Sequence↗
PubMed1995

Stressed rats fail to expand the CD45RC+CD4+ (Th1-like) T cell subset in response to KLH: possible involvement of IFN-gamma.

Exposure to stressors effects various aspects of immune function, including the in vivo antibody response. We have previously reported that rats exposed to an acute session of inescapable tail shock (IS) show long-term reductions in anti-KLH (keyhole limpet hemocyanin) IgM and IgG. The mechanisms responsible for this suppression are currently unknown. Previous work has suggested changes in CD4+ T cells could be important. We report here that exposure to IS results in a reduction in Con A-stimulated IFN-gamma levels in mesenteric lymphocytes and splenocytes taken immediately after IS termination. In addition, IS exposure prevents the KLH-induced increase in the number of CD45RC+CD4+ T cells (Th1-like) in both the mesenteric lymph nodes and the spleen 4 days after immunization. The failure of KLH to expand the CD45RC+CD4+ subset could be due to the stress-induced reduction in IFN-gamma levels reported in cells taken at the time of immunization. Implications of these findings as a mechanism for the decrease in the in vivo antibody response previously reported is discussed.

Animals↗
PubMed1995

Interleukin-1 beta induced corticosterone elevation and hypothalamic NE depletion is vagally mediated.

Processes occurring within the immune system can alter neural function. Cytokines released by cells of the immune system during illness are key messengers in immune-to-brain communication. Interleukin-1 beta (IL-1 beta) is particularly important in this regard and is known to stimulate a myriad of illness-related outcomes such as fever, sickness behavior, aphagia, adipsia, hypothalamic-pituitary-adrenal activation, and changes in pain reactivity. Thus peripherally released IL-1 beta has potent neural effects and is a critical mediator of the impact of immune processes on brain. There is, however, uncertainty concerning the communication pathways involved. We provide evidence that a primary route of peripheral cytokine signalling is through stimulation of peripheral vagal afferents rather than or in addition to direct cytokine access to brain. Subdiaphragmatic, but not hepatic vagotomy, blocked rhIL-1 beta-induced hypothalamic norepinephrine depletion and attenuated rhIL-1 beta-induced increases in serum corticosterone. These data suggest that rhIL-1 beta activates the hypothalamic-pituitary-adrenal axis via stimulation of peripheral vagal afferents and further support the hypothesis that peripheral cytokine signalling to the CNS is mediated primarily by stimulation of peripheral afferents.

Animals↗
PubMed1995

[Coronary aneurysm in a 69-year-old patient. Transthoracic echocardiography].

This case report is on a 69-year old male patient treated with cephalosporins because of suspected myocarditis due to borreliosis. Using transthoracic echocardiography a big aneurysm of the proximal part of the left coronary artery was detected. Coronary angiography revealed an aneurysm 1.2 cm in diameter at the origin of the left anterior descending branch and confirmed the initial diagnosis. In addition, coronary three-vessel disease with reduced left ventricular function was found. Coronaritis due to Lyme borreliosis could not be ruled out with certainty. The patient was relatively asymptomatic, and hence conservative therapy was recommended. The case described here serves as a basis for a discussion on the aetiology, clinical manifestation, diagnosis and therapeutic management of coronary aneurysms.

Aged↗
PubMed1994

Human erythrocyte ankyrin, a cytoskeleton component, generates the p57 membrane proteinase which cleaves C3, the third component of complement.

Human erythrocytes express a p57 membrane serine proteinase which cleaves C3, the third component of complement. Amino acid analysis of the first 20 N-terminal residues of the purified p57 proteinase demonstrated 100% homology with residues 910-929 of erythrocyte ankyrin, a sequence localized in its Mr = 62 kDa fragment. Thus, we analyzed whether ankyrin could generate the p57 C3-cleaving activity. We demonstrate herein that: 1) anti-ankyrin antibodies react with purified p57 proteinase; 2) anti-p57 proteinase antibodies react with purified ankyrin but not with spectrin, another cytoskeleton component; 3) while purified ankyrin did not carry any detectable proteinase activity, limited proteolysis of ankyrin by immobilized chymotrypsin generated this C3-cleaving serine proteinase. Spectrin did not generate any C3-cleaving activity. This is the first demonstration that erythrocyte ankyrin could generate a proteinase activity, which in addition, cleaves specifically human C3.

Amino Acid Sequence↗
PubMed1994

Cell-type specific response of peripheral blood lymphocytes to methotrexate in the treatment of rheumatoid arthritis.

The mode of action of methotrexate in the treatment of rheumatoid arthritis is still questionable. Although in vitro results suggest an immunosuppressive effect of methotrexate, several clinical studies have failed to confirm these effects in patients treated with oral low-dose methotrexate. With respect to the highly variable bioavailability of methotrexate, we investigated the effects of an intravenous administration of 15 mg methotrexate per week on peripheral blood lymphocyte subsets in eight patients with rheumatoid arthritis. Methotrexate after 12 weeks significantly (P < 0.01) reduced total peripheral blood lymphocytes and led to a pronounced redistribution of lymphocyte subsets with a preferred reductive effect on B-lymphocytes (P < 0.005) and T-lymphocytes (P < 0.05). Natural killer cells and killer cell-like T cells, on the other hand, were unaffected by the treatment. Our results suggest a cell-type specific effect of intravenously administered low-dose methotrexate on peripheral blood lymphocytes. This effect, in our opinion, may contribute to the mode of action of methotrexate as an immunosuppressive drug in the treatment of rheumatoid arthritis.

Adult↗
PubMed1994

Serum levels of interleukin-6 and tumour-necrosis-factor-alpha are not correlated to disease activity in patients with rheumatoid arthritis after treatment with low-dose methotrexate.

Cytokines are major mediators of inflammatory responses in rheumatoid arthritis. Some of them have been shown to correlate with the disease activity and thus are proposed to be used for monitoring patients. Therefore the effects of a low-dose therapy with methotrexate on serum concentrations of interleukin-6 (IL-6) and tumour-necrosis-factor-alpha (TNF-alpha) were examined in eight patients with seropositive rheumatoid arthritis. Serum levels of IL-6 and TNF-alpha were significantly elevated in patients compared to healthy controls. Before the onset of MTX treatment IL-6 concentrations were correlated to the c-reactive protein (P < 0.05) but the correlation was abolished after treatment. For TNF-alpha no correlations neither before nor after treatment were observed. Both cytokines remained substantially elevated after MTX treatment despite a clear reduction in disease activity. Thus we suggest that one of the effects of MTX might be the inhibition of some of the actions of IL-6 and TNF-alpha.

Arthritis, Rheumatoid↗
PubMed1993

Relationships between dietary minerals and plasma lipids and glucose among older adults.

This study evaluated the relationships between dietary minerals and plasma lipids and glucose of forty-three adults, age 60 and above. Subjects self-selected diets averaged 33% of calories from fat, and 205 mg of cholesterol per day. Plasma total cholesterol, HDL-cholesterol, triglycerides and glucose were determined enzymatically, and LDL-cholesterol was calculated. Plasma lipid values for subjects with dietary mineral intakes less than 2/3 of the RDA were compared to those with intakes greater than 2/3 of RDA. With lower copper intakes plasma triglycerides were elevated (p < or = 0.05). Both plasma total cholesterol and LDL-cholesterol were elevated with lower zinc intakes (p < or = 0.05). LDL-cholesterol was elevated with lower calcium intakes (p < or = 0.05) and with lower magnesium intakes fasting glucose was elevated (p < or = 0.05). No significant differences were observed in plasma lipids due to dietary fat, saturated fat or cholesterol intakes. In these older adults, dietary mineral intakes showed more relationships to plasma lipid parameters than did amount or composition of dietary fat or cholesterol.

Age Factors↗
PubMed1992

EBV/C3d receptor (CR2) interacts by its intracytoplasmic carboxy-terminal domain and two distinct binding sites with the p53 anti-oncoprotein and the p68 calcium-binding protein.

EBV/C3d receptor (CR2) interacts with the p53 anti-oncoprotein expressed in the human B lymphoma cells, Raji but not in normal B cells, and with the p68 calcium-binding protein, expressed in normal B lymphocytes but not in transformed B lymphocytes. To characterize the CR2 domain interacting with these two intracellular proteins, we synthesized a 34-amino acid peptide, pep34, corresponding to its intracytoplasmic carboxy-terminal domain and analyzed its binding and antigenic properties. Binding of 125I-labeled p53 or 125I-labeled p68 on immobilized pep34 was specific, additive, and totally inhibited by unlabeled p53 or p68, respectively, but not by unlabeled p68 or p53, respectively. Antigenic properties of pep34 were analyzed by immunizing rabbits with particle-bound pep34. Polyclonal anti-pep34 Ab carried anti-CR2 specificities that recognized only the intracellular domain of CR2. In addition, anti-pep34 Ab also carried anti-p53 or anti-p68 specificities. Anti-p53 or anti-p68 specificities were not due to putative common structural or conformational antigenic determinants between the pep34 synthetic peptide and the p68 or p53 proteins. These anti-p53 and anti-p68 specificities were identified as anti-idiotypic anti-CR2 Ab mimicking either p53 or p68 binding sites of CR2. These data clearly establish that despite its short length, the intracytoplasmic C-terminal tail of CR2 is involved in direct protein-protein interactions with the two intracellular regulatory proteins, p53 and p68. An additional feature of these data is the demonstration that particle-bound pep34 triggered "in vivo" anti-Id Ab restricted to either p53 or p68 specificities.

Amino Acid Sequence↗