Fat Burner scientific update |
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Gan To Kagaku Ryoho. 2007 May;34(5):789-92.
Nakane T, Yamane T, Nakamae H, Ichihara H, Koh H, Takeoka Y, Kanashima H, Sakamoto E, Koh KR, Hino M.
Dept. of Clinical Hematology and Clinical Diagnostics, Graduate School of Medicine, Osaka City University.
[Improved outcome in brain abscess during induction in acute myelocytic leukemia.][Article in Japanese]
A 31-year-old female with acute myelocytic leukemia was admitted to our hospital in June 2004. She had complications of brain abscess at the WBC nadir after
the second course of induction therapy. However,because the platelet count was low, neurosurgical procedures, including craniotomy/abscess resection, or
abscess drainage, were not performed, and we could not detect bacteria or fungus as the cause of brain abscess. Combination therapy with meropenem trihydrate
and fosfluconazole was effective. Thereafter, she underwent related peripheral blood stem cell transplantation, and has had no recurrence of brain abscess.
Brain abscess during chemotherapy for patients with acute leukemia is commonly due to fungus,particularly Aspergillus,which has a very high fatality rate.
Therefore,the treatment of brain abscess without the detection of bacteria and fungus requires combination therapy with antifungal agents and antibiotics. In
this case, methionine-positron emission tomography was useful for the evaluation of therapeutic effectiveness for brain abscess.
Cell Calcium. 2007 May 11;
Devogelaere B, Verbert L, Parys JB, Missiaen L, De Smedt H.
Laboratory of Molecular and Cellular Signalling, Division of Physiology, Department of Molecular Cell Biology, Katholieke Universiteit Leuven, Campus Gasthuisberg O/N1, bus 802, B-3000 Leuven, Belgium.
The complex regulatory function of the ligand-binding domain of the inositol 1,4,5-trisphosphate receptor.
The inositol 1,4,5-trisphosphate (IP(3)) receptor (IP(3)R) can be divided in three functionally distinct regions: a ligand-binding domain, a modulatory
domain and a channel domain. Numerous regulatory mechanisms including inter- and intra-molecular protein-protein interactions and phosphorylation events act
via these domains to regulate the function of the IP(3)R. Regulation at the level of the ligand-binding domain primarily affects the affinity for IP(3). The
extent of IP(3)-induced Ca(2+) release (IICR) is, however, not only determined by the affinity for IP(3) but also by the effectiveness of the coupling
between ligand binding and channel opening. As a result, regulation as well as malfunction of IICR may be affected by both steps in the activation mechanism.
The 3D structures of the two subdomains of the ligand-binding domain have recently been determined by X-ray diffraction analysis. This allows a more detailed
molecular explanation of the regulatory events situated at the ligand-binding domain of the IP(3)R. In this review, we will focus on recent structural and
functional data on the ligand-binding domain that have extended and clarified the view on the molecular mechanisms of IP(3)R regulation.
J Reprod Immunol. 2007 May 8;
Scioscia M, Gumaa K, Whitten M, Selvaggi LE, Rodeck CH, Rademacher TW.
Department of Immunology and Molecular Pathology, Molecular Medicine Unit, Royal Free and University College London Medical School, London, UK; Department of Gynaecology, Obstetrics and Neonatology, University of Medical Science of Bari, Bari, Italy.
Inositol phosphoglycan P-type in healthy and preeclamptic pregnancies.
An association between inositol phosphoglycan P-type (P-IPG) and preeclampsia has been demonstrated over recent years. This molecule can mediate many of the
metabolic and growth promoting effects of insulin. Dysregulation of the mediator family is associated with insulin resistance. An increased concentration of
P-IPG has been reported in preeclamptic placenta, although its precursor (GPI) was undetectable in those placental samples. Insulin administration, that
induces P-IPG release in normal human placenta, was shown not to cause production/release of the mediator from preeclamptic placental tissue as a consequence
of a disturbed insulin signalling. Amniotic fluid is enriched of this mediator, with further increase during preeclampsia. We have found that the fetus
released increasing amounts of P-IPG in the urine between 13 and 18 weeks of gestation, reaching a plateau beyond 20 weeks. Cord blood of infants of
preeclamptic mothers showed an increased content of soluble P-IPG compared to controls and to the mother.
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 Fat Burner scientific update
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