0000000000053786

AUTHOR

T Kindler

showing 3 related works from this author

Fatal sepsis due to mycobacterium tuberculosis after allogeneic bone marrow transplantation.

2001

Mycobacterium tuberculosis is a serious, but rare infectious complication after allogeneic bone marrow transplantation. We describe a case of fatal sepsis due to Mycobacterium tuberculosis after allogeneic bone marrow transplantation for Philadelphia chromosome-positive ALL. The diagnosis was made after BAL. Although broad-spectrum antituberculous therapy was started immediately after diagnosis, blood cultures became positive for Mycobacterium tuberculosis. The patient developed severe pyrexias and finally died of multi-organ failure. Rapid progression of mycobacterial infection should be considered in patients post BMT with unexplained fever, particularly in patients from endemic areas.

AdultMaleMycobacterium tuberculosisSepsisFatal OutcomeAcute lymphocytic leukemiamedicineHumansTransplantation HomologousTuberculosisIn patientAutogenous boneBone Marrow TransplantationTransplantationbiologybusiness.industryMarrow transplantationHematologyMycobacterium tuberculosisPrecursor Cell Lymphoblastic Leukemia-Lymphomamedicine.diseasebiology.organism_classificationmedicine.anatomical_structureImmunologyBone marrowbusinessComplicationBone marrow transplantation
researchProduct

BCR-ABL as a target for novel therapeutic interventions.

2002

The BCR-ABL oncogene is the result of a reciprocal translocation between the long arms of chromosome 9 and 22 t(9; 22). There is good experimental evidence demonstrating that BCR-ABL is the single causative abnormality in chronic myeloid leukaemia (CML), making it a unique model for the development of molecular targets. In addition to CML, BCR-ABL transcripts can be found in a minority of acute lymphoblastic leukaemias and very rarely in acute myeloid leukaemia (AML). Elucidating the molecular mechanisms and downstream pathways of BCR-ABL has led to the design of several novel therapeutic approaches. In this review, molecular targeting of BCR-ABL will be discussed based on the inhibition of…

medicine.drug_classmedicine.medical_treatmentT-LymphocytesClinical BiochemistryFusion Proteins bcr-ablChromosomal translocationChromosome 9Antineoplastic AgentsBiologyGenes ablTyrosine-kinase inhibitorhemic and lymphatic diseasesNeoplasmsDrug DiscoverymedicineAnimalsHumansneoplasmsGenePharmacologyOncogeneImmunotherapyProtein-Tyrosine KinasesFusion proteinCell Transformation NeoplasticImmunologyMolecular MedicineSignal transductionSignal TransductionExpert opinion on therapeutic targets
researchProduct

BAX inhibitor-1 is a Ca(2+) channel critically important for immune cell function and survival.

2015

The endoplasmic reticulum (ER) serves as the major intracellular Ca(2+) store and has a role in the synthesis and folding of proteins. BAX (BCL2-associated X protein) inhibitor-1 (BI-1) is a Ca(2+) leak channel also implicated in the response against protein misfolding, thereby connecting the Ca(2+) store and protein-folding functions of the ER. We found that BI-1-deficient mice suffer from leukopenia and erythrocytosis, have an increased number of splenic marginal zone B cells and higher abundance and nuclear translocation of NF-κB (nuclear factor-κ light-chain enhancer of activated B cells) proteins, correlating with increased cytosolic and ER Ca(2+) levels. When put into culture, purifie…

0301 basic medicineProgrammed cell deathCytoplasmEncephalomyelitis Autoimmune ExperimentalCell SurvivalT-LymphocytesActive Transport Cell NucleusApoptosisBiologyEndoplasmic Reticulum03 medical and health sciencesAnimalsCalcium SignalingObesityMolecular BiologyCalcium signalingMice KnockoutOriginal PaperB-LymphocytesBAX inhibitor 1Endoplasmic reticulumNF-kappa BMembrane ProteinsCell BiologyLeukopeniaNFKB1Acquired immune systemCell biologyEnzyme ActivationMice Inbred C57BLCytosol030104 developmental biologyApoptosisCaspasesCalciumFemaleSpleen
researchProduct