No abstract

It is well established that central tolerance of B cells involves the deletion of large numbers of B cell clones. However, the mechanism of this deletion remains unclear. Chickens are one of the classic models of vertebrate immunity and bursa of Fabricius presents model system to study this process. Our lab has been interested in the role of the chB6 alloantigen (formerly called Bu1) in the developing of B cells within the bursa. We have shown that chB6 can trigger apoptosis when stimulated by anti-chB6 antibody and this apoptosis uses intermediates commonly found in death receptor signaling pathways. Recently, chB6 has been found in close proximity to the BCR on DT40 cells. Others have noted that BCR signals in DT40 lead to apoptosis. Homology analysis places chB6 within the larger CD2/SLAM family of proteins based on the presence of two extracellular Ig domains. CD2/SLAM family members serve to modulate signals in immune cells. How chB6 initiates signals, and how those signals might be coordinated with other components of the BCR complex, remains unclear. Previous work indicated a 15 amino acid stretch in the cytoplasmic domain and critical in initiating apoptosis. Within this region is the PXXP motif indicating a binding site for SH3 domain containing proteins. We have mutated the proline codons within this region and transfected these mutated chB6 cDNAs into BK3a cells to test the hypothesis that this SH3 binding site is important in death signaling via chB6. Preliminary evidence suggests that this region is in fact critical in transducing a death signal. This project furthers our efforts to understand the biology of chB6. This work supported by a grant from the DePaul University Research Council.

The aim of this study was to develop biotinylated chitosan (Bio–Chi) decorated multi-walled carbon nanotubes (MWCNTs) for breast cancer therapy with the tyrosine kinase inhibitor, neratinib (NT).

: Diabetes mellitus is found to be among the most suffered and lethal diseases for mankind. Diabetes mellitus type-1 is caused by the demolition of pancreatic islets responsible for the secretion of insulin. Insulin is the peptide hormone (anabolic] that regulates the metabolism of carbohydrates, fats, and proteins. Upon the breakdown of the natural process of metabolism, the condition leads to hyperglycemia (increased blood glucose levels]. Hyperglycemia demands outsourcing of insulin. The subcutaneous route was found to be the most stable route of insulin administration but faces patient compliance problems. Oral Insulin delivery systems are the patient-centered and innovative novel drug delivery system, eliminating the pain caused by the subcutaneous route of administration. Insulin comes in contact across various barriers in the gastrointestinal tract, which has been discussed in detail in this review. The review describes about the different bioengineered formulations, including microcarriers, nanocarriers, Self-Microemulsifying drug delivery systems (SMEDDs), Self-Nanoemulsifying drug delivery systems (SNEDDs), polymeric micelles, cochleates, etc. Surface modification of the carriers is also possible by developing ligand anchored bioconjugates. A study on evaluation has shown that the carrier systems facilitate drug encapsulation without tampering the properties of insulin. Carrier-mediated transport by the use of natural, semi-synthetic, and synthetic polymers have shown efficient results in drug delivery by protecting insulin from harmful environment. This makes the formulation readily acceptable for a variety of populations. The present review focuses on the properties, barriers present in the GI tract, overcome the barriers, strategies to formulate oral insulin formulation by enhancing the stability and bioavailability of insulin.