Biomedical subjects

J Hofmann

Publications and source records attributed to J Hofmann.

At least 19 recordsLinked to original sources

PubMed2005

Significance of avidity and immunoblot analysis for rubella IgM-positive serum samples in pregnant women.

A total of 512 IgM-positive serum samples from 449 pregnant women referred by microbiologists and medical laboratories for additional testing and final interpretation were collected over a 3-year period. Employment of an IgM capture enzyme immunoassay (EIA) confirmed only 31% of the initial EIA-IgM-positive samples. In order to discriminate acute rubella virus infections, which are associated with increased risk of fetal infection and embryopathy, from persistent or non-specific IgM, IgG avidity index and the presence of IgG with specificity to rubella virus E2 glycoprotein was determined by Western immunoblot. In only six patients (1.3%), a primary infection with rubella virus was diagnosed on the basis of IgM positivity, low avidity IgG, absence of E2-specific IgG in immunoblot concordant with clinical findings as well as consistent changes in follow-up samples. The serological results were not compatible with rubella re-infection. The infection status in 14 patients (3.1%) remained inconclusive even when both avidity assay and immunoblot were used, while restriction to either test did not allow a conclusive interpretation in 11.6% of patients. The use of both assays is clearly better, and therefore, recommended in IgM-positive samples.

Adult↗

PubMed2004

Mitochondrial genotype and risk for Alzheimer's disease: cross-sectional data from the Vienna-Transdanube-Aging "VITA" study.

The Vienna Transdanube Aging (VITA) study searches for early markers of Alzheimer's disease (AD) by examining the mental status in a community-based cohort of 606, 75-years old volunteers that are then related to various clinical and genetic analyses. To determine whether mutations in mtDNA are involved in expression of AD, the mtDNA of 79 "control" participants is screened for alterations by sequencing of "hot-spot-regions". This study on mtDNA mutations has eliminated the influence of aging on the occurrence of mtDNA alterations by sequencing samples from persons at the age of exactly 75 years. Thus, our cohort reveals a snap-shot of mitochondrial sequences of elderly persons. So far, a high percentage (56%) of persons with known or unknown mutations in the fragments analyzed were found. These data will be compared in due time to a cohort of participants with proven late-onset AD.

Aged↗

PubMed2004

[Non-recurrent laryngeal nerve].

AIMS: The paper draws attention to the importance of rare, but important anatomical variety of nervus laryngeus recurrens, s.c. nervus laryngeus non-recurrens, for making thyroidectomy safely. Possible differences in the course of the nerve and the way of preparing the gland for minimizing the peroperation damage are presented. PATIENTS: Three cases out of 1,200 operations on thyroid gland (0.25%) had the anatomical deviation described. RESULTS: The nerve was saved from peroperation damage in two patients with nervus laryngeus recurrens. The third patient with this deviation ended up with permanent unilateral paralysis of the nerve, which indicated erroneous evaluation of nerve branches. CONCLUSIONS: Possible occurrence of rare varieties of nervus laryngeus recurrens point out necessary routine search and careful dissection during thyroidectomy. The diagnosis of nervus laryngeus non-recurrens is not possible in most cases. This contribution draws attention to basic operation procedures, which protect not only nervus laryngeus recurrens in its typical position, but also its varieties such as nervus laryngeus non-recurrens.

Humans↗

PubMed2003

Phylogenetic analysis of rubella virus including new genotype I isolates.

Infection during the first trimester of gestation with rubella virus (RV) is highly teratogenic. Embryopathy is a frequent outcome of the primary natural infection with wild type RV during pregnancy while accidental immunisation with life attenuated vaccine has apparently little or no adverse effect. Although the nucleic acid sequence of RV is exceptionally stable, differences between the vaccine and wild type viruses could play a role in the pathogenesis of intrauterine RV infection. Phylogenetic analysis of eight complete sequences (including two new isolates described in this paper, three vaccine strains, three cell culture adapted wild type viruses) confirms a striking low divergence of the RV genome. A variable region (amino acid residues 697-800) within the gene coding for the nonstructural protein NSP1 was defined. Phylogenetic analysis revealed a strong positive selection in this region. Multiple passages in vivo or in vitro did not account for this variability. As the function of the variable region has not yet been elucidated, reasons for and significance of positive selection are still speculative. It is conceivable that the variable region in NSP1 contributes to the molecular basis of RV embryopathy and other complications of postnatal RV infection.

Animals↗

PubMed2002

Field trials with low power lasers concerning the blink reflex.

Laser belonging to class 2 emit in the visible part of the spectrum. The power is limited to 1 mW in the CW mode. Up to now the protection of the eyes has been supposed to be given by the blink reflex for incidentally intrabeam viewing in many regulations. In 3 field trials with 519 test persons we have shown that only 15.9% at 670 nm, 17.2% at 635 nm, and 20.3% at 532 nm had a blink reflex under laser irradiation. An analysis of the results showed neither significant differences concerning the age and the gender of the test persons nor whether they were wearer of glasses or right sighted. The frequent lack of the blink reflex demands organizational measures like instruction using laser class 2 in medical and other applications.

Accidents, Occupational↗

PubMed2002

[Measuring eyelid reflex with electroblepharography].

Safety regulations concerning the handling of low power lasers in the visible region (Class 2, according to DIN EN 60825-1) assume that the eye is protected by the eye-blink reflex, which should have completed within 250 ms during laser impact into the eye. A method has been developed to determine the temporal progression of the blink reflex by measuring the biosignal of the upper eyelid movement. In this procedure, which we call Electroblepharography (EBG), the electrical signal of the eyelid muscle is gained by means of self adherent electrode pads and is evaluated and charted after analog signal processing in the EBG-device. The graphical representation of the biopotential corresponds to the temporal position of the upper eyelid. Characteristic values as latency-time, position and velocity of the eyelid can be deduced.

Blinking↗

PubMed2001

Effect of site-directed asparagine to isoleucine substitutions at the N-linked E1 glycosylation sites on rubella virus viability.

The role of three N-linked glycosylation sites in rubella virus (RV) E1 protein on virion release was analyzed by transfecting Vero 76 cells with infectious RV RNA (Robo302WT) containing isoleucine substitutions at N76, N177, and N209 (individually and in combinations). RV RNAs were detected and found to retain substitutions in the transfected cells, but RV capsid indicative of infection was undetectable, except for in Robo302WT and Robo302-N177I transfected cells. Only culture supernatants of Robo302WT and Robo302-N177I RNA transfected cells were positive for RV, suggestive of the virion release into the culture medium. Further, detection of intracellular RV E1 and newly released virion-associated E1 was possible only from cells previously incubated with Robo302-N177I and Robo302WT culture supernatants, suggesting that N177I substituted virus retained infectivity. These results suggest that while glycosylation at N177 is not critical, N76I and N209I mutations are lethal to RV viability.

Amino Acid Substitution↗

PubMed2001

2-benzoxazolyl and 2-benzimidazolyl hydrazones derived from 2-acetylpyridine: a novel class of antitumor agents.

Here we describe the effects of novel benzoxazol-2-yl and benzimidazol-2-yl hydrazones derived from 2-pyridinecarbaldehyde and 2-acetylpyridine. The IC(50) values for inhibition of cell proliferation in KB-3-1, CCRF-CEM, Burkitt's lymphoma, HT-29, HeLa, ZR-75 and MEXF276L by most of the novel compounds are in the nanomolar range. In colony-forming assays with human tumor xenografts the compounds 2-actylpyridine benzoxazol-2-ylhydrazone (EPH52), 2-acetylpyridine benzoimidazol-2-ylhydrazone (EPH61) and 2-acetylpyridine 1-methylbenzoimidazol-2-ylhydrazone (EPH116) exhibited above-average inhibition of colon carcinoma (IC(50) = 1.3-4.56 nM); EPH52 and EPH116 also exhibited above-average inhibition of melanoma cells. As shown with human liver microsomes, EPH116 is only moderately metabolized. The compound inhibited the growth of human colon cancer xenografts in nude mice in a dose-dependent manner. Thiosemicarbazones derived from 2-formylpyridines have been shown to be inhibitors of ribonucleotide reductase (RR). The following results show that RR is not the target of the novel compounds: cells overexpressing the M2 subunit of RR and resistant to the RR inhibitor hydroxyurea are not cross-resistant to the novel compounds; inhibition of RR occurs at 6- to 73-fold higher drug concentrations than that of inhibition of cell proliferation; the pattern of cell cycle arrest in S phase induced by the RR inhibitor hydroxyurea is not observed after treatment with the novel compounds; and a COMPARE analysis with the related compounds 2-acetylpyrazine benzothiazol-2-ylhydrazone (EPH95) and 3-acetylisoquinoline benzoxazol-2-ylhydrazone (EPH136) showed that the pattern of these compounds is not related to any of the standard antitumor drugs. Therefore, these novel compounds show inhibition of colon cancers and exhibit a novel mechanism of action.

Animals↗

PubMed2001

Regulation of phospholipase D isoenzymes by transforming Ras and atypical protein kinase C-iota.

The activation of phospholipase D (PLD) by transforming Ras is well documented. Although two distinct PLD isoforms, PLD1 and PLD2, have been cloned from mammalian cells, it has remained unclear whether both isoenzymes are activated by Ras and, if this is the case, whether they are stimulated by a common mechanism. In the present study we show that expression of transforming Ras in HC11 mouse mammary epithelial cells enhanced the activity of endogenous PLD. Co-expression of Ras with either PLD1b or PLD2 resulted in elevated activities of both PLD isoenzymes in HC11 cells, indicating that transforming Ras was capable of activating both PLD isoforms in vivo. Ras-induced activation of PLD was resistant to the protein kinase C (PKC) inhibitor GF109203X, which preferentially affects conventional- and novel-type PKCs, but sensitive to Ro-31-8220, which inhibits atypical PKCs more effectively. Co-transfection of atypical PKC-iota with either PLD1b or PLD2 led to a selective activation of PLD2 by PKC-iota, whereas PLD1b was not affected. PLD1b, however, was found to be a potent activator of PKC-iota, whereas PLD2 was less effective in this respect. The data suggest that PKC-iota acts upstream of PLD2 and that PLD1b is implicated in the activation of PKC-iota. The data are discussed as indicating a putative signalling cascade comprising Ras-->PLD1b-->PKC-iota-->PLD2. Evidence for the implication of this pathway in the transcriptional regulation of cyclin D1 is also presented.

Animals↗

PubMed2001

Effects of miltefosine on various biochemical parameters in a panel of tumor cell lines with different sensitivities.

We investigated endocytosis activity, uptake of miltefosine (hexadecylphosphocholine), phospholipid and cholesterol content, the cell cycle, and apoptosis in 13 tumor cell lines (MCF7, MCF7/ADR, KB-3-1, KB-8-5, KB-C1, HeLa, HeLa-MDR1-G185, HeLa-MDR1-V185, CCRF/CEM, CCRF/VCR1000, CCRF/ADR5000, HL-60, HL-60/AR) with different sensitivities to treatment with the antitumor phospholipid analogues miltefosine and D-21266 (octadecyl-(N,N-dimethyl-piperidino-4-yl)-phosphate). In this panel of cell lines, MDR1 (multidrug resistance gene 1)- and MRP1 (multidrug resistance-associated protein)-expressing cells were found to be slightly more resistant to both compounds than sensitive parental cells. No correlation was found between resistance to miltefosine and endocytosis, intracellular concentration of miltefosine, the phospholipid and cholesterol content, induction of apoptosis, or cell cycle alterations in all the cell lines tested. Wild-type p53 containing WMN Burkitt's lymphoma cells and wild type p53-deficient CA46 exhibited similar sensitivities to miltefosine. The low percentage of apoptosis induced in MCF7 cells lacking caspase 3 indicated that caspase 3 seems to play an essential role in miltefosine-induced apoptosis.

Antineoplastic Agents↗

PubMed2001

Synthesis, cytotoxicity, and antitumor activity of copper(II) and iron(II) complexes of (4)N-azabicyclo[3.2.2]nonane thiosemicarbazones derived from acyl diazines.

A series of thiosemicarbazones (TSCs) (bearing a (4)N-azabicyclo[3.2.2]nonane moiety) derived from 3-acylpyridazines, 4-acetylpyrimidines, and 2-acetylpyrazines (1-8) were synthesized as potential antitumor agents. TSCs 1-8 exhibited potent cytotoxic activity against human acute lymphoblastic leukemia CCRF-CEM cells (IC(50) = 0.05-0.77 microM) and colon adenocarcinoma HT-29 cells (IC(50) = 0.011-2.22 microM). Copper II complexes of TSCs 1-8 showed significant improvement in cytotoxic activity against HT-29 cells (IC(50) = 0.004-1.51 microM) by a factor of 3. However, complexation of ligands 1, 2, 4, and 6 with Fe(II) results in lowering of cytotoxic activity by a factor of approximately 7. In clonogenic assays involving human tumor cells of different tumor origins, compounds 5, 7, 8, and their copper complexes 5Cu(II), 7Cu(II), and 8Cu(II) exhibited remarkable cytotoxic activities with mean IC(50) values of 6, 0.18, 1, 1, 0.37, and 0.37 nM, respectively. In particular, the compounds were highly effective against human colon carcinoma and large and small cell lung carcinoma cells. The TSC derivative 5 was evaluated in vivo in nude mice bearing LXFL 529 human large cell lung carcinoma cells. With respect to antitumor activity, application of 30 mg/kg/d resulted in moderate inhibition (42%) of tumor growth. No effect on tumor growth was observed at a dose of 10 mg/kg/d. However, a dose of 40 or 60 mg/kg/d resulted in 50 and 75% death, respectively, in the treated mice, indicating the high toxicity of these compounds. Using human liver microsomes, compound 5 was found to be rapidly and highly metabolized in vitro. In actual fact, only 2% of the unmetabolized compound could be detected in the incubation medium after 5 min. The IC(50) for cell proliferation (0.006-0.022 microM) elicited by these compounds is much lower than that of the inhibition of [(14)C]cytidine incorporation into DNA (0.18-3.32 microM). These compounds are also noncell cycle specific agents. Interestingly, compounds 5, 5Cu(II), and 8 were found to be potent inducers of apoptosis in Burkitt's lymphoma cells.

Antineoplastic Agents↗

PubMed2001

MDR1 causes resistance to the antitumour drug miltefosine.

Miltefosine (hexadecylphosphocholine) is used for topical treatment of breast cancers. It has been shown previously that a high percentage of breast carcinomas express MDR1 or MRP. We investigated the sensitivity of MDR1 -expressing cells to treatment with miltefosine. We show that cells overexpressing MDR1 (NCI/ADR-RES, KB-8-5, KB-C1, CCRF/VCR1000, CCRF/ADR5000) were less sensitive to miltefosine treatment when compared to the sensitive parental cell lines. HeLa cells transfected with MDR1 exhibited resistance to the compound, indicating that expression of this gene is sufficient to reduce the sensitivity to miltefosine. The resistance of MDR1-expressing cells to miltefosine was less pronounced than that to adriamycin or vinblastine. Expression of MDR2 did not correlate with the resistance to miltefosine. As shown by a fluorescence quenching assay using MIANS-labelled P-glycoprotein (PGP), miltefosine bound to PGP with a K(d)of approximately 7 microM and inhibited PGP-ATPase activity with an IC(50)of approximately 35 microM. Verapamil was not able to reverse the resistance to miltefosine. Concentrations of miltefosine up to approximately 60 microM stimulated, whereas higher concentrations inhibited the transport of [3H]-colchicine with an IC(50)of approximately 297 microM. Binding studies indicated that miltefosine seems to interact with the transmembrane domain and not the cytosolic nucleotide-binding domain of PGP. These data indicate that expression of MDR1 may reduce the response to miltefosine in patients and that this compound interacts with PGP in a manner different from a number of other substrates.

ATP Binding Cassette Transporter, Subfamily B↗

PubMed2001

Protein kinase C effectors bind to multidrug ABC transporters and inhibit their activity.

P-Glycoprotein and homologous multidrug transporters contain a phosphorylatable linker sequence that was proposed to control drug efflux on the basis that it was indeed phosphorylated in vitro and in vivo, and that inhibitors of protein kinase C (PKC) inhibited both P-glycoprotein phosphorylation and activity. However, site-directed mutagenesis of all phosphorylatable residues did not alter the drug resistance. The present work shows that PKC effectors are able to bind directly to multidrug transporters, from either cancer cells (mouse P-glycoprotein), yeast (Saccharomyces cerevisiae Pdr5p), or protozoan parasite (Leishmania tropica ltmdr1), and to inhibit their energy-dependent drug-efflux activity. The binding of staurosporine and derivatives such as CGP 41251 is prevented by preincubation with ATP, suggesting at least partial interaction at the ATP-binding site. In contrast, more hydrophobic compounds such as calphostin C and CGP 42700 bind outside the ATP-binding site and strongly interfere with drug interaction. A direct correlation is obtained between the efficiencies of PKC effectors to inhibit energy-dependent interaction of rhodamine 6G with yeast Pdr5p, to promote intracellular drug accumulation in various multidrug resistant cells, and to chemosensitize growth of resistant cells. The noncompetitive inhibition by PKC effectors of rhodamine 6G interaction with Pdr5p suggests that the binding might interfere with signal transduction between nucleotide hydrolysis and drug interaction. The overall results indicate that the multidrug transporters from different species display common features for interaction with PKC inhibitors. The hydrophobic derivative of staurosporine, CGP 42700, constitutes a potentially powerful modulator of P-glycoprotein-mediated multidrug resistance.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed2001

Adverse reactions associated with mobile therapeutic apheresis: analysis of 17,940 procedures.

In order to evaluate the nature and frequency of adverse reactions associated with Therapeutic Apheresis (TA), database information from two large mobile apheresis services was analyzed. A total of 17,940 procedures performed on 3,583 patients were studied using an Access Database. Seventy percent (12,558) of the procedures were performed on a Fresenius AS104 blood cell separator and 30% (5,382) were performed on a COBE Spectra. The five most commonly treated diseases were Guillain-Barre Syndrome (25%), thrombotic thrombocytopenic purpura (20%), myasthenia gravis (18%), the hyperviscosity syndrome (12%), and chronic inflammatory demyelinating polyneuropathy (9%). All patients received calcium gluconate supplement during the procedures. Cardiac monitoring was used during 80% of the procedures and blood pressure monitoring was used during all procedures. All procedures were supervised by a physician. Both apheresis services fully comply with the ASFA Guidelines for Therapeutic Apheresis Providers. Adverse reactions occurred in 3.9% of all procedures. The following adverse reactions were documented: reactions related to ACD toxicity (3%), vasovagal reactions (0.5%), vascular access related complications (0.15%), reactions related to FFP (0.12%), hepatitis B from FFP (0.06%), arrhythmias (0.01%), hemolysis due to inappropriate dilution of 25% albumin (0.01%), and one death (from underlying disease) during a TA procedure (0.006%). These data demonstrate that therapeutic apheresis is associated with a low rate of side effects when performed by well-trained and certified nurses under the direction of experienced physicians, even in the diverse setting of large mobile therapeutic apheresis programs.

Blood Component Removal↗

PubMed2001

Modulation of protein kinase C in antitumor treatment.

PKC isoenzymes were found to be involved in proliferation, antitumor drug resistance and apoptosis. Therefore, it has been tried to exploit PKC as a target for antitumor treatment. PKC alpha activity was found to be elevated, for example, in breast cancers and malignant gliomas, whereas it seems to be underexpressed in many colon cancers. So it can be expected that inhibition of PKC activity will not show similar antitumor activity in all tumors. In some tumors it seems to be essential to inhibit PKC to reduce growth. However, for inhibition of tumor proliferation it may be an advantage to induce apoptosis. In this case an activation of PKC delta should be achieved. The situation is complicated by the facts that bryostatin leads to the activation of PKC and later to a downmodulation and that the PKC inhibitors available to date are not specific for one PKC isoenzyme. For these reasons, PKC modulation led to many contradicting results. Despite these problems, PKC modulators such as miltefosine, bryostatin, safingol, CGP41251 and UCN-01 are used in the clinic or are in clinical evaluation. The question is whether PKC is the major or the only target of these compounds, because they also interfere with other targets. PKC may also be involved in apoptosis. Oncogenes and growth factors can induce cell proliferation and cell survival, however, they can also induce apoptosis, depending on the cell type or conditions in which the cells or grown. PKC participates in these signalling pathways and cross-talks. Induction of apoptosis is also dependent on many additional factors, such as p53, bcl-2, mdm2, etc. Therefore, there are also many contradicting results on PKC modulation of apoptosis. Similar controversial data have been reported about MDR1-mediated multidrug resistance. At present it seems that PKC inhibition alone without direct interaction with PGP will not lead to successful reversal of PGP-mediated drug efflux. One possibility to improve chemotherapy would be to combine established antitumor drugs with modulators of PKC. However, here also very contrasting results were obtained. Many indicate that inhibition, others, that activation of PKC enhances the antiproliferative activity of anticancer drugs. The problem is that the exact functions of the different PKC isoenzymes are not clear at present. So further investigations into the role of PKC isoenzymes in the complex and interacting signalling pathways are essential. It is a major challenge in the future to reveal whether modulation of PKC can be used for the improvement of cancer therapy.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed2001

Determination of vibration-related spinal loads by numerical simulation.

OBJECTIVE: Dynamic spinal loads due to human whole body vibrations are extremely difficult to determine experimentally. However, they can be predicted by numerical simulation. This paper presents an approach for the prediction of dynamic spinal loads caused by whole body vibrations, as well as some basic considerations concerning the process of numerical simulation. BACKGROUND: Long-term whole body vibrations have been found to cause health risks for the lumbar spine. As an increasing percentage of the population is exposed to whole body vibrations at work, more and more people have to face the risk of whole body vibrations-related injury. Knowledge about the actual loads in the lumbar spine is essential when spinal loads are to be compared with spinal strength in order to assess the possible health risks caused by whole body vibrations. METHODS: Since an extrapolation of results to unknown data such as spinal loads can only be done using anatomical models of the human body, a simplified finite-element model is presented which is adaptable to body height, body mass, and posture of any specific subject under investigation. The model has been built by reducing a very detailed, nonlinear finite-element model of seated man in its complexity (number of degrees of freedom). Furthermore, the simplified model has been linearised to avoid nonlinear solution procedures. RESULTS: The model has been verified for vertical and horizontal excitation at the seat. Model results have been compared to measurements on subjects. Individual exposure-effect relationships may be predicted by this model, due to the adaptability to a specific subject. Additionally, a new phenomenological method of eliminating the influence of local skin-accelerometer vibrations on vibration measurements on the skin surface is discussed. This method may provide data about bone acceleration that can be used in the process of model verification. CONCLUSIONS: Integral loading measures, such as spinal loads, may be predicted with simplified finite-element models. Quantitative judgements of these loads may be performed for individual conditions. Linearised models may be used for limited ranges of excitation intensities. Energy dissipation should be modeled by discrete dashpot elements instead of proportional damping. RELEVANCE: In order to assess the risk of an injury to the lumbar spine due to whole body vibrations, spinal loads have to be compared with spinal strength. This paper presents the development and verification of a simplified finite-element model of the human body which is based on human anatomy and therefore well-suited to occupational/clinical biomechanics for the prediction of spinal loads.

Acceleration↗

PubMed2001

[Aneurysm of the popliteal vein].

Venous aneurysms are a rare pathology. The possible complications are rupture, thrombosis and subsequently pulmonary embolism. The case of a 54-year-old male is reported, who was admitted on the suspicion of pulmonary embolism to our department. This suspicion was confirmed by scintigraphy and computed tomography. Further examination by colour coded duplex sonography showed an aneurysm of the popliteal vein in clinically asymptomatic legs, as a possible cause of the pulmonary embolism. The finding was confirmed phlebographically. After successful surgical treatment of the aneurysm the patient got an anticoagulation therapy for 6 months. In the case of thromboembolism the entire venous system can be affected. Therefore an examination of the peripheral veins should be carried out whenever there is an occurrence of pulmonary embolism.

Aneurysm↗

PubMed2001

Choriocarcinoma cells modulate the cytokine production of decidual large granular lymphocytes in coculture.

PROBLEM: How do major histocompatibility complex (MHC) I positive/negative choriocarcinoma (CC) cells affect the production of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin-10 (IL-10), interleukin-4 (IL-4), and granulocyte-macrophage colony-stimulating factor (GM-CSF) by decidual CD56++ cells (large granular lymphocytes [LGL]), LGL-depleted decidual cells (WASH) and unseparated decidual cells (DEC) in cocultures? METHOD OF STUDY: Decidual tissue was obtained by legal abortions. CD 56++ LGL were isolated in a magnetic cell separator. Cytokines were measured by ELISA. Differences were analyzed for significance by Wilcoxons test. RESULTS: We found a significant increase of IL-10 in LGL/JEG-3 and of TNF-alpha in LGL/JAR cocultures compared to noncocultured decidual cells. There was a significant increase of IL-10 and TNF-alpha and a significant decrease of GM-CSF in WASH and DEC cocultures with both JEG-3 and JAR. IFN-gamma was only found in 3/11 cases of LGL/JAR cocultures. No IL-4 was found in any experiment. CONCLUSION: MHC class I positive/negative CC modulate the cytokine production of decidual LGL in different ways.

Cell Fractionation↗