A5062429208- Tryptophan and brain disorders
- Stress Responses and Cortisol
- Malaria Research and Control
- Bipolar Disorder and Treatment
- Mosquito-borne diseases and control
- Neuroinflammation and Neurodegeneration Mechanisms
- Retinoids in leukemia and cellular processes
- Gut microbiota and health
- Pneumonia and Respiratory Infections
- Bacterial Infections and Vaccines
- Receptor Mechanisms and Signaling
- Neuropeptides and Animal Physiology
- Acute Myeloid Leukemia Research
- Complement system in diseases
- Advanced Radiotherapy Techniques
- Prostate Cancer Diagnosis and Treatment
- Neuroendocrine regulation and behavior
- Prostate Cancer Treatment and Research
- Immune Response and Inflammation
- Nuclear Structure and Function
- Chemokine receptors and signaling
- interferon and immune responses
- Heme Oxygenase-1 and Carbon Monoxide
- RNA Interference and Gene Delivery
- Ion channel regulation and function
The University of Sydney
2013-2024
Cooperative Trials Group for Neuro-Oncology
2017
Robert Bosch (Australia)
2007-2017
Oregon Health & Science University
1999
Icahn School of Medicine at Mount Sinai
1997-1999
Institute of Cancer Research
1999
Leukemia Research Foundation
1999
Brookdale University Hospital and Medical Center
1999
Garvan Institute of Medical Research
1992-1997
St Vincent's Hospital
1992-1995
Neuropeptide Y (NPY) is one of the most abundant neuropeptides in mammalian nervous system and exhibits a diverse range important physiological activities, including effects on psychomotor activity, food intake, regulation central endocrine secretion, potent vasoactive cardiovascular system. Two major subtypes NPY receptor (Y1 Y2) have been defined by pharmacological criteria. We report here molecular cloning cDNA sequence encoding human corrected for rat homologue. Analysis this confirms...
Abstract Cerebral malaria (CM) can be a fatal manifestation of Plasmodium falciparum infection. Using murine models malaria, we found much greater up-regulation number chemokine mRNAs, including those for CXCR3 and its ligands, in the brain during CM (FMCM) than model non-CM. Expression CXCL9 CXCL10 RNA was localized predominantly to cerebral microvessels adjacent glial cells, while expression CCL5 restricted mainly infiltrating lymphocytes. The majority mice deficient were protected from...
Summary Reduced neurogenesis in the aging mammalian hippocampus has been linked to cognitive deficits and increased risk of dementia. We utilized postmortem human hippocampal tissue from 26 subjects aged 18–88 years investigate changes expression six genes representing different stages across healthy adult lifespan. Progressive significant decreases mRNA levels proliferation marker Ki67 ( MKI 67 ) immature neuronal doublecortin DCX were found over In contrast, for stem cell glial fibrillary...
Altered iron and copper levels in the Parkinson's disease substantia nigra are confined to cytosolic compartment of cell.
AbstractThe promyelocytic leukemia zinc finger (PLZF) protein is a transcription factor disrupted in patients with t(11;17)(q23;q21)-associated acute leukemia. PLZF contains an N-terminal BTB/POZ domain which required for dimerization, transcriptional repression, formation of high-molecular-weight DNA-protein complexes, nuclear sublocalization, and growth suppression. X-ray crystallographic data show that the forms obligate homodimer via extensive interface. In addition, dimer possesses...
Chromosomal translocation t(11;17)(q23;21) is associated with a retinoic acid-resistant form of acute promyelocytic leukemia. The fuses the <i>RARα</i> gene to the<i>PLZF</i> gene, resulting in formation reciprocal fusion proteins, hypothesized play prominent roles leukemogenesis. Promyelocytic leukemia zinc finger (PLZF) encodes transcription factor nine Krüppel-like fingers, seven which are retained t(11;17) protein RARα-PLZF. We identified specific DNA-binding site for PLZF and showed...
The ETO protein was originally identified by its fusion to the AML-1 transcription factor in translocation (8;21) associated with M2 form of acute myeloid leukemia (AML). resulting AML-1–ETO is an aberrant transcriptional regulator due ability ETO, which does not bind DNA itself, recruit corepressors N-CoR, SMRT, and Sin3A histone deacetylases. promyelocytic zinc finger (PLZF) a sequence-specific DNA-binding fused retinoic acid receptor α (11;17)(q23;q21) translocation. PLZF also mediates...
The mechanisms involved in the anabolic effect of interferon gamma (IFNγ) on bone have not been carefully examined. Using microarray expression analysis, we found that IFNγ upregulates a set genes associated with tryptophan degradation pathway, known as kynurenine osteogenic differentiating human mesenchymal stem cells (hMSC). We, therefore, hypothesized activation pathway plays role osteoblastogenesis even absence IFNγ. Initially, observed strong increase during and without media. We next...
To quantify the clinical practice of respiratory motion management in radiation oncology.A survey was designed and conducted based on clinician guidelines. The administered to American Association Physicists Medicine (AAPM) members 17 August 2020 closed 13 September 2020.A total 527 respondents completed entire 651 part survey, with partially surveys included analysis. Overall, 84% used deep inspiration breath hold for left-sided breast cancer. 83% perceived thoracic abdominal cancer...
ABSTRACT Cerebral malaria (CM) is an infrequent but serious complication of Plasmodium falciparum infection in humans. Animal and human studies suggest that the pathogenesis CM immune mediated, precise mechanisms leading to cerebral pathology are unclear. In mice, with berghei ANKA results on day 6 postinoculation (p.i.), while closely related strain P. K173 does not result CM. Infection was associated increased plasma gamma interferon (IFN-γ) at 24 h p.i. splenic hepatic mRNAs for a range...
Abstract The pathology associated with Streptococcus pneumoniae meningitis results largely from activation of immune-associated pathways. We systematically investigated the production IFN subtypes, as well their influence on pathology, in a mouse model S. meningitis. Despite occurrence mixed type I/II gene signature, no evidence for or involvement I IFNs disease progression was found. In contrast, II (IFN-γ) strongly induced, and IFN-γ−/− mice were significantly protected severe disease....