Biomedical subjects

F Marti

Publications and source records attributed to F Marti.

17 recordsLinked to original sources

PubMed2004

[Smoking cessation with ear acupuncture. Descriptive study on patients after a smoking cessation treatment with ear acupuncture].

BACKGROUND: In complementary medicine literature studies on long-term observation of one of its methods are rare. OBJECTIVE: The present study is an evaluation of the smoking behavior of patients treated with ear acupuncture for smoking cessation. Additionally we investigated factors that favor or impede smoking cessation. PATIENTS AND METHODS: 249 patients who had undergone ear acupuncture for smoking cessation between 1985 and 1998 in a practice in Aarau (Switzerland) were asked before the first treatment to fill in a form regarding their smoking behavior and retrospectively in autumn 1998 a questionnaire regarding the success of therapy. Ear acupuncture treatment consisted of 2 consultations at an interval of 10 days. The responder rate was 53.8% (134 questionnaires were returned). Finally the data of 126 persons could be evaluated. RESULTS: The Kaplan Meier analysis of the abstinence time yielded a one-year success rate of 41.1%. Men gave up smoking more easily than women. Start of smoking as well as start of treatment between the age of 20 and 40 years were favorable conditions for smoking cessation. People who had smoked 20 cigarettes or more per day before treatment profited the best. For people who smoked as a way of passing the time or because of tediousness it was easier to stop smoking than for people smoking because of nervousness. People living in a non-smoker household were able to stop smoking significantly easier than persons living in a smoker household. CONCLUSIONS: With a one-year success rate of 41.1% ear acupuncture is a competitive alternative to orthodox medicine withdrawal methods. Acupuncture treatment can be applied and adapted individually, furthermore it is economical and without side effects.

Acupuncture, Ear↗

PubMed2001

A transcription function for the T cell-specific adapter (TSAd) protein in T cells: critical role of the TSAd Src homology 2 domain.

T cell-specific adapter (TSAd) protein is an Src homology 2 (SH2) domain-containing adapter molecule implicated in T cell receptor for antigen (TCR)-mediated interleukin 2 (IL-2) secretion in T cells. Here, we demonstrate that a substantial fraction of TSAd is found in the T cell nucleus. Nuclear import of TSAd is an active process that depends on TSAd SH2 domain recognition of a phosphotyrosine-containing ligand. Importantly, we show that TSAd can act as a potent transcriptional activator in T cells. Furthermore, the TSAd SH2 domain appears to be essential for this transcription-activating function independent of its role in nuclear import. Biochemical analyses suggest that a single TSAd SH2 domain ligand of 95-100 kD may be involved in these processes. Consistent with a role as a transcription activator, cotransfection of TSAd with an IL-2 promoter-reporter gene construct results in a considerable upregulation of IL-2 promoter activity. Further, we show that this augmentation requires a functional TSAd SH2 domain. However, TSAd does not appear to modulate the activity of the major recognized IL-2 gene transcription factors, nuclear factor kappaB (NF-kappaB), nuclear factor of activated T cells (NFAT), or activator protein 1 (AP-1). These findings point to the function of TSAd as a novel transcription-regulatory protein in T cells and illustrate the importance of the TSAd SH2 domain in this role.

Active Transport, Cell Nucleus↗

PubMed2001

Negative-feedback regulation of CD28 costimulation by a novel mitogen-activated protein kinase phosphatase, MKP6.

TCR and CD28 costimulatory receptor-cooperative induction of T cell IL-2 secretion is dependent upon activation of mitogen-activated protein (MAP) kinases. Using yeast-hybrid technology, we cloned a novel CD28 cytoplasmic tail (CD28 CYT) interacting protein, MAP kinase phosphatase-6 (MKP6), which we demonstrate inactivates MAP kinases. Several lines of evidence indicate that MKP6 plays an important functional role in CD28 costimulatory signaling. First, in human peripheral blood T cells (PBT), expression of MKP6 is strongly up-regulated by CD28 costimulation. Second, transfer of dominant-negative MKP6 to PBT with the use of retroviruses primes PBT for the secretion of substantially larger quantities of IL-2, specifically in response to CD28 costimulation. A similar enhancement of IL-2 secretion is observed neither in response to TCR plus CD2 costimulatory receptor engagement nor in response to other mitogenic stimuli such as phorbol ester and ionomycin. Furthermore, this hypersensitivity to CD28 costimulation is associated with CD28-mediated hyperactivation of MAP kinases. Third, a retroviral transduced chimeric receptor with a CD28 CYT that is specifically unable to bind MKP6 costimulates considerably larger quantities of IL-2 from PBT than a similar transduced chimeric receptor that contains a wild-type CD28 CYT. Taken together, these results suggest that MKP6 functions as a novel negative-feedback regulator of CD28 costimulatory signaling that controls the activation of MAP kinases.

Adult↗

PubMed2000

T cell-specific adapter protein inhibits T cell activation by modulating Lck activity.

We previously reported the isolation of a cDNA encoding a T cell-specific adapter protein (TSAd). Its amino acid sequence contains an SH2 domain, tyrosines in protein binding motifs, and proline-rich regions. In this report we show that expression of TSAd is induced in normal peripheral blood T cells stimulated with anti-CD3 mAbs or anti-CD3 plus anti-CD28 mAbs. Overexpression of TSAd in Jurkat T cells interfered with TCR-mediated signaling by down-modulating anti-CD3/PMA-induced IL-2 promoter activity and anti-CD3 induced Ca2+ mobilization. The TCR-induced tyrosine phosphorylation of phospholipase C-gamma1, SH2-domain-containing leukocyte-specific phosphoprotein of 76kDa, and linker for activation of T cells was also reduced. Furthermore, TSAd inhibited Zap-70 recruitment to the CD3zeta-chains in a dose-dependent manner. Consistent with this, Lck kinase activity was reduced 3- to 4-fold in COS-7 cells transfected with both TSAd and Lck, indicating a regulatory effect of TSAd on Lck. In conclusion, our data strongly suggest an inhibitory role for TSAd in proximal T cell activation.

Adaptor Proteins, Signal Transducing↗

PubMed1998

LCK-phosphorylated human killer cell-inhibitory receptors recruit and activate phosphatidylinositol 3-kinase.

HLA-specific killer cell inhibitory receptors (KIR) are thought to impede natural killer (NK) and T cell activation programs through recruitment of the SH2 domain-containing tyrosine phosphatases, SHP-1 and SHP-2, to their cytoplasmic tails (CYT). To identify other SH2 domain-containing proteins that bind KIR CYT, we used the recently described yeast two-bait interaction trap and a modified version of this system, both of which permit tyrosine phosphorylation of bait proteins. Using these systems, we show that KIR CYT, once phosphorylated by the src-family tyrosine kinase LCK, additionally bind the p85alpha regulatory subunit of phosphatidylinositol (PI) 3-kinase. Furthermore, we show that in an NK cell line, NK3.3, cross-linking of KIR results in recruitment of p85alpha to KIR and activation of PI 3-kinase lipid kinase activity. One consequence of KIR coupling to PI 3-kinase is downstream activation of the antiapoptotic protein kinase AKT. Therefore, in addition to providing negative signals, KIR may also contribute positive signals for NK and T cell growth and/or survival.

Cell Line↗

PubMed1991

Abnormal levels of platelet-specific proteins and mitogenic activity in myeloproliferative disease.

It has been postulated that platelet-derived growth factor and platelet factor 4 (PF4) are involved in the imbalance of the mechanism of medullar stroma maintenance which triggers off the bone marrow myelofibrotic process. In this work we compare the PF4 and the beta-thromboglobulin (beta-TG) and mitogenic activity in platelet-poor plasma (PPP) and platelet extracts (PE) from patients with myeloproliferative disorders (MPD) with those of secondary thrombocytosis (ST) and normal volunteers. Statistically significant differences were found between MPD and ST patients or controls, but none between ST and controls in all the parameters studied. Maximal differences in platelet-derived factors (PDFs) between MPD and control groups were found in polycythemia vera patients. However, the relationship between the presence of myelofibrosis and abnormal levels of beta-TG, PF4 and mitogenic activity in PPP and PE was only observed in patients with agnogenic myeloid metaplasia (AMM). These results show that PDFs are specifically decreased in MPD platelets. Furthermore, no statistical correlation was found between PDFs and the number of platelets. However, other unknown factors or conditions would be necessary to develop myelofibrosis in MPD, which is present in AMM.

Adult↗

PubMed1989

Artefactual low lymphocyte activity caused by platelet contamination in the mononuclear cell preparations.

Platelet (PLT) contamination in preparations of mononuclear cells (MNC) produces a significant decrease (P less than 0.02) in lymphoproliferative activity and interleukin 2 (IL2) production. This effect was observed in MNC preparations from either healthy blood donors or polyglobulic patients. In a dose-response curve carried out with increasing PLT number per MNC, progressive inhibition was found, reaching to 62.6% and 49.5%, respectively, to phytohemagglutinin and IL2 lymphoproliferative response and 87.8% in IL2 production, at 80 PLTs/MNC.

Blood Platelets↗

PubMed1985

[Granulomatous hepatitis caused by nomifensine].

Four patients are described who developed granulomatous hepatitis 4-6 weeks after treatment with nomifensin. The granulomas were located both in the portal tract and the liver parenchyma, and contained eosinophils and a few polynuclear giant cells. Serum alkaline phosphatase, alanine aminotransferase and bilirubin were raised in three, two and one patient respectively. After medication was discontinued all abnormalities disappeared within 6-10 weeks. After oral intake of 25-50 mg nomifensin all patients experienced paroxysms of high body temperature for several hours. Reexposure in one patient resulted in another fever spike 6 hours after ingestion. No other cause of the fever or the granulomatous hepatitis was identifiable. The clinical data, especially the simultanous occurrence of drug fever and the histologic pattern, are compatible with an allergic mechanism of the liver granulomas. In the presence of high fever and abnormal liver tests in relation to nomifensin treatment, an allergic drug reaction should be considered.

Aged↗

PubMed1985