The future is in the numbers: the power of predictive analysis in the biomedical educational environment.

Biomedical programs have a potential treasure trove of data they can mine to assist admissions committees in identification of students who are likely to do well and help educational committees in the identification of students who are likely to do poorly on standardized national exams and who may need remediation. In this article, we provide a step-by-step approach that schools can utilize to generate data that are useful when predicting the future performance of current students in any given program. We discuss the use of linear regression analysis as the means of generating that data and highlight some of the limitations.

Twelve tips for facilitating team-based learning.

Background: Team-based learning (TBL) has become a more commonly recognized and implemented pedagogical approach in curricula of numerous disciplines. The desire to place more autonomy on the student and spend less in-class time delivering content has resulted in complete or partial adoption of this style of learning in many educational settings.

Aim: Provide faculty with tools that foster a well facilitated and interactive TBL learning environment.

Tumor necrosis factor receptor 1 associates with CD137 ligand and mediates its reverse signaling.

Reverse signaling through CD137 ligand (CD137L) potently activates monocytes. However, the underlying mechanism is not well elucidated. This study provides evidence that tumor necrosis factor receptor 1 (TNFR1) acts as a coreceptor for CD137L and mediates CD137L signaling.

Inhibition of proliferation and induction of apoptosis in multiple myeloma cell lines by CD137 ligand signaling.

Background: Multiple myeloma (MM) is a malignancy of terminally-differentiated plasma cells, and the second most prevalent blood cancer. At present there is no cure for MM, and the average prognosis is only three to five years. Current treatments such as chemotherapy are able to prolong a patient's life but rarely prevent relapse of the disease.

Use of phage display to isolate specific human monoclonal antibody fragments against a potential target for multiple myeloma.

Introduction: Multiple myeloma (MM), a malignancy of plasma cells, accounts for 10% of all haematological malignancies and is currently incurable. Although it can be treated, the disease tends to relapse after several years and becomes increasingly resistant to conventional therapy. Investigations into using humoral therapy for MM are now underway with a view that novel therapeutic agents may provide a more targeted therapy for MM.

Association of Epstein-Barr virus with nasopharyngeal carcinoma and current status of development of cancer-derived cell lines.

It is well known that the Epstein-Barr virus (EBV) contributes directly to tumourigenesis in nasopharyngeal carcinoma (NPC), primarily in the undifferentiated form of NPC (WHO type III; UNPC or UC), which is commonly found in South East Asia. Unfortunately, research in NPC has been severely hampered by the lack of authentic EBV-positive (EBV+) human NPC cell lines for study. Since 1975, there have been more than 20 reported NPC cell lines.

Ku86 exists as both a full-length and a protease-sensitive natural variant in multiple myeloma cells.

Background: Truncated variants of Ku86 protein have previously been detected in 86% to 100% of freshly isolated patient multiple myeloma (MM) cells. Since, the Ku70/Ku86 heterodimer functions as the regulatory subunit of the DNA repair enzyme, DNA-dependent protein kinase, we have been interested in the altered expression and function of Ku86 variant (Ku86v) proteins in genome maintenance of MM.

Results: Although, a number of studies have suggested that truncated forms of Ku proteins could be artificially generated by proteolytic degradation in vitro in human lymphocytes, we now show using whole cell immunoblotting that the RPMI-8226 and SGH-MM5 human MM cell lines consistently express full-length Ku86 as well as a 69-kDa Ku86v; a C-terminus truncated 69-kDa variant Ku86 protein.

Use of ultraviolet-light irradiated multiple myeloma cells as immunogens to generate tumor-specific cytolytic T lymphocytes.

Background: As the eradication of tumor cells in vivo is most efficiently performed by cytolytic T lymphocytes (CTL), various methods for priming tumor-reactive lymphocytes have been developed. In this study, a method of priming CTLs with ultraviolet (UV)-irradiated tumor cells, which results in termination of tumor cell proliferation, apoptosis, as well as upregulation of heat shock proteins (HSP) expression is described.

Methods: Peripheral blood mononuclear cells (PBMC) were primed weekly with UV-irradiated or mitomycin-treated RPMI 8226 multiple myeloma cells.

Detection and quantification of the abelson tyrosine kinase domains of the BCR-ABL gene translocation in chronic myeloid leukaemia using genomic quantitative real-time polymerase chain reaction.

Introduction: Since undetectable BCR-ABL mRNA transcription does not always indicate eradication of the Ph+ CML clone and since transcriptionally silent Ph+ CML cells exist, quantitation by genomic PCR of bcr-abl genes can be clinically useful. Furthermore, hotspot mutations in the Abelson tyrosine kinase (ABLK) domain of the bcr-abl gene translocation in Philadelphia chromosome-positive (Ph+) chronic myeloid leukaemia (CML) cells confer resistance on the specific kinase blocking agent, STI571.

Materials And Methods: Genomic DNA from K562, CESS and patient CML cells were amplified using rapid cycle quantitative real-time polymerase chain reaction for the gene regions spanning the mutation hotspots.

The biology of Ku and its potential oncogenic role in cancer.

Ku is a heterodimeric protein made up of two subunits, Ku70 and Ku80. It was originally identified as an autoantigen recognized by the sera of patients with autoimmune diseases. It is a highly versatile regulatory protein that has been implicated in multiple nuclear processes, e.

Defective B cell responses in the absence of SH2D1A.

More than half of patients with X-linked lympho-proliferative disease, which is caused by a defect in the intracellular adapter protein SH2D1A, suffer from an extreme susceptibility to Epstein-Barr virus. One-third of these patients, however, develop dysgammaglobulenemia without an episode of severe mononucleosis. Here we show that in SH2D1A(-/-) mice, both primary and secondary responses of all Ig subclasses are severely impaired in response to specific antigens.

Expression of the SH2D1A gene is regulated by a combination of transcriptional and post-transcriptional mechanisms.

The SH2D1A gene, which is altered or deleted in patients with X-linked lymphoproliferative disease, encodes the small protein SAP (for SLAM-associated protein) that is expressed in T and NK cells. A 22-bp fragment in close proximity to an initiator-like site was defined as the basal promoter of mouse SH2D1A, and a highly homologous 33-bp segment was defined as the human basal promoter. When an Ets consensus site was mutated, no reporter activity was detectable.

Heat shock proteins: to present or not, that is the question.

The contribution of major histocompatibility complex (MHC) I and II to the adaptive immune response has been well documented. In 1996, Peter Doherty and Rolf Zinkernagel were awarded the Nobel Prize, for their fundamental observations concerning the genetic elements involved in specific antigen (Ag) recognition. These elements encode molecules that present self and non-self peptide fragments to both CD4+ and CD8+ cytolytic T lymphocytes (CTL).

The cell surface receptor SLAM controls T cell and macrophage functions.

Signaling lymphocyte activation molecule (SLAM), a glycoprotein expressed on activated lymphocytes and antigen-presenting cells, has been shown to be a coregulator of antigen-driven T cell responses and is one of the two receptors for measles virus. Here we show that T cell receptor-induced interleukin (IL)-4 secretion by SLAM(-/-) CD4(+) cells is down-regulated, whereas interferon gamma production by CD4(+) T cells is only slightly up-regulated. Although SLAM controls production of IL-12, tumor necrosis factor, and nitric oxide in response to lipopolysaccharide (LPS) by macrophages, SLAM does not regulate phagocytosis and responses to peptidoglycan or CpG.

The role of SAP in murine CD150 (SLAM)-mediated T-cell proliferation and interferon gamma production.

CD150 (signaling lymphocyte activation molecule [SLAM]) is a self-ligand cell surface glycoprotein expressed on T cells, B cells, macrophages, and dendritic cells. To further explore the role of CD150 signaling in costimulation and T(H)1 priming we have generated a panel of rat antimouse CD150 monoclonal antibodies. CD150 cell surface expression is up-regulated with rapid kinetics in activated T cells and lipopolysaccharide/interferon gamma (IFN-gamma)-activated macrophages.