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T Hahn

Publications and source records attributed to T Hahn.

153 records · Page 9Linked to original sources
PubMedDate not supplied

Sustained hypoglycemia affects glucose transporter expression of human blood leukocytes.

The scarce data available on leukocyte glucose transporter expression are contradictory and nothing is known about its regulation by glycemic state. Therefore, cytospin preparations of blood leukocytes were searched immunocytochemically for the high-affinity glucose transporters GLUT1, 3, and 4. Hypoglycemia-associated quantitative changes in transporter expression were assessed by flow cytometry. Granulocytes and monocytes stained for GLUT1, 3, and 4. Granulocyte GLUT4 levels were increased by 73% (P < 0.05) under hypoglycemic conditions, which was paralleled by a reduction in GLUT1 and a rise in GLUT3. In monocytes, GLUT3 was elevated by 134% (P < 0.05), whereas GLUT1 and GLUT4 remained unaffected upon hypoglycemia. Apart from a minor subpopulation, lymphocytes were negative for these carriers. In conclusion, GLUT1, 3, and 4 are abundantly expressed in granulocytes and monocytes. The differential response of individual isoforms to hypoglycemia may represent a mechanism to protect the cells from the stress of glucose deprivation.

Adaptation, Biological↗
PubMedDate not supplied

The effect of different nutritional states on cell-mediated cytotoxicity.

We have studied the effect of acute short-term starvation (in 9 patients) and of prolonged caloric deprivation (in 10 patients with anorexia nervosa), on cell-mediated cytotoxicity (CMC). CMC became severely depressed after six days on a very low caloric diet (1.2 +/- 1.4 vs. 7.0 +/- 2.9 lytic units/10(6) cells; P less than 0.01). CMC was also low in our patients with anorexia nervosa compared to a matched control group (3.3 +/- 1.7 vs. 10.0 +/- 3.0 lytic units/10(6) cells; P less than 0.01) and increased in most of the patients studied (five cases) after the first 3-4 weeks of refeeding in correlation with weight gain. Dietary deprivation may lead to a significant impairment in cell-mediated cytotoxicity, which appears to be reversible after refeeding.

Adolescent↗
PubMedDate not supplied

Endothelin A and B receptors change their expression levels during development of human placental villi.

Endothelin receptors have recently been found in non-vascular tissues including the human placenta. The present study investigated developmental changes in location and expression levels of endothelin A and B receptors (ETA-R, ETB-R) in human placentae and isolated trophoblast by comparing first and third trimester tissues. In the first trimester all cells and tissues were immunolabelled for ETA-R and ETB-R, whereas in third trimester placentae the syncytiotrophoblast (ETA-R, ETB-R) and macrophages (ETA-R) were unstained. Immunoblotting for both receptors revealed up to three bands at 33-35, 50 and 75 kDa, respectively, which were differentially present in the first and third trimester. Pre-adsorption of antibodies with oligopeptides used for antigen-generation weakened the immunoreactions. ETA-R protein levels decreased (P< 0.05) in total villous tissue and isolated trophoblast, whereas ETB-R was unchanged. ETB-R transcripts (RT-PCR) prevailed in both stages and tissues, but in contrast to the protein levels its preponderance decreased from first trimester to term in villous tissue (P< 0.01), because of a four to five-fold increase in ETA-R and only a two-fold (P< 0.05) increase in ETB-R mRNA levels (P< 0.01). We conclude that ET receptor location, intracellular processing and expression levels in human villous tissue change between the first and third trimester. This may reflect changing functions of ET-1 during placental development.

Abortion, Legal↗
PubMedDate not supplied

Triple anti-TNF-alpha therapy in early sepsis: a preliminary report.

Ten of 26 patients with sepsis were given a combination of dexamethasone (0.15 mg/kg, intravenously, once on admission), colchicine (0.5 mg, orally, daily, for 3 days) and pentoxifylline (DCP) (400 mg, orally, daily, for 3 days), together with best medical therapy. Serum tumour necrosis factor-alpha (TNF-alpha) levels were undetectable at 24 h compared with about 4 IU/ml (mean) in 16 similar control patients who were not given DCP (P < 0.06). Although the clinical course in the two groups was not significantly different, this simple, well-tolerated and inexpensive regimen should be further evaluated as a possible means of preventing the deleterious effects of TNF-alpha in sepsis.

Acute Disease↗
PubMedDate not supplied

The effect of growth hormone and IGF-I on clonogenic growth of hematopoietic cells in leukemic patients during active disease and during remission--a preliminary report.

The number of survivors of childhood leukemia treated with growth hormone for growth retardation is increasing. The debate about the direct or indirect relationship of GH and insulin-like growth factor I (IGF-I) to the occurrence or recurrence of malignancy, especially in the case of GH therapy in patients with leukemia, is still unresolved. We, therefore, studied the effect of GH and IGF-I on bone marrow of patients with acute leukemia (ALL and AML) in diagnosis and recurrence and in chronic leukemia patients (CML) in remission. GH increased blast colony numbers by a mean of 68% and 77% at GH concentrations of 250 and 300 ng/ml, respectively. IGF-I increased blast colony numbers in ALL patients by 50, 93 and 105%, and in AML patients by 33, 58 and 65%, at IGF-I concentrations of 0.05, 0.25 and 0.5 ng/ml, respectively. In 3 CML patients in remission a granulocyte-macrophage colony forming assay did not reveal stimulation of peripheral blood blast colony formation by GH or IGF-I. Our in vitro data (as previously reported) suggest that GH and IGF-I may promote blast cell proliferation, and the supplemental administration of these peptides in leukemia patients in remission must be carefully monitored for early relapse. Additional studies on bone marrow cells of leukemic patients in remission are needed in order to examine the effects of GH and IGF-I on these cells.

Bone Marrow↗
PubMedDate not supplied

Interferon anti-viral system in Bell's palsy.

Thirty-two consecutive Bell's palsy patients were examined clinically and virologically. All the patients were assayed for serum interferon (IFN) levels at onset of the disease and most of them had repeated IFN assays during the course of the disease. In 15 patients the peripheral blood mononuclear cells (PBMC) were also evaluated for the presence of an anti-viral state (AVS). In viral infections, blood IFN levels are invariably increased, and the PBMC are usually in an AVS. Twenty-three patients (72%) had increased serum IFN values or were in an AVS. The mean serum IFN level was 95 U/ml (normal less than or equal to 16 U/ml) during the first 3 days following onset of the disease, declining later to normal values from the seventh day onwards. No patient had increased antibody titers to herpes simplex and varicella-zoster viruses. The increased blood IFN levels and the AVS of blood cells are compatible with an acute viral infection. It is concluded that the etiology of Bell's palsy is most likely an acute viral infection, possibly due to an unidentified or unusual virus, or to reactivation of a latent virus.

Facial Paralysis↗