Single domain antibody

Title: Targeted Therapy in Ovarian Cancer Authors: Hui Jun, Lim1 and William, Ledger2 Affiliations: University of New South Wales, Australia1, School of Women and Children’s Health, Prince of Wales Hospital, Sydney, Australia2   Abstract Among female-specific cancers worldwide, ovarian cancer is the leading cause of death from gynaecologic malignancy in the Western world. Despite radical surgery and initial high response rates to first-line chemotherapy, up to 70% of patients experience relapses

microvascular permeability and neovascularization in response to vascular endothelial growth factor (VEGF) binding to it. Inactivation of the receptor serves as a viable treatment for angiogenesis-related illnesses. Current treatment plans include VEGF antibodies and/or VEGFR2

Ebola Hemorrhagic Fever is caused by a virus found in the family of filoviridae, in genus known as ebolavirus. There are currently four known Ebola virus strands that are deadly to humans. The virus is transmitted through bodily fluids so it can be transferred via mucosal surfaces or abrasions on the skin when being in direct contact to an infected person. It is highly pathogenic and causes death in approx. 50 -90% of all known cases. This laboratory and numerous experiments has shown that antigen

HIV Genome Organization and Structure: The HIV-1 virion is approximately 120 nm in diameter, roughly spherical, and is composed of two copies of a single stranded positive sense RNA enclosed by a capsid (24). The HIV-1 genome is less than 10 kb and encodes for more than nine different gene products. It encodes for 3 major structural protein genes: gag (group-specific antigen), pol (DNA polymerase), and env (Envelope), which code for major structural proteins and essential enzymes. Gag generates the

complete extracellular α subunit and a large β subunit, presenting the following extracellular domains: sema (semaphoring domain), PSI (also called MET-Related Sequence - MRS), four IPT domains (immunoglobulin – plexin - transcription domains), and 3 intracellular regions: juxtamembrane (containing tyrosine 1003, which negatively regulates c-MET by inducing its ubiquitination), a tyrosine kinase domain (with tyrosines Y1234 and Y1235, which positively modulate the receptor function) and a carboxy-terminal

HIV The human immunodeficiency virus (HIV) is a lentivirus (a subgroup of retrovirus) that causes HIV infection and acquired immunodeficiency syndrome (AIDS). AIDS is a condition in humans in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive. Without treatment, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype. Infection with HIV occurs by the transfer of blood, semen,

the fact that the immune system is dynamic, diverse, distributed and error tolerant. It is dynamic, which means that individual components are continually created, destroyed, and circulated the body. It is error tolerant because the effect of any single immune

Campylobacter jejuni   Campylobacter jejuni Biological Classification Domain: Bacteria Phylum: Proteobacteria Class: Epsilonproteobacteria Order: Campylobacterales Family: Campylobacteraceae Genus: Campylobacter Species: Campylobacter jejuni Figure 1: Scanning electron microscope image of Campylobacter iejuni, demonstrating its helical structure and polar flagellum. Source: Virginia-Maryland Regional College of Veterinary Medicine, Blacksburg, Virginia. Campylobacter jejuni is a species of

Introduction RNA interference (RNAi) is a biological process where a double stranded RNA (dsRNA) activates the degradation of the sequence-dependent RNA target cell, causing a posttranscrip-tional gene-silencing mechanism or inhibition of cellular gene expression. 1 This mechanism was first discovered in Caenorhabditis elegans in 1998 by Andrew Z. Fire and Craig C. Mello, where they observed that the introduction of the dsRNA in the animal cell resulted in an inhibition expression of the homologous

complement. If influenza viruses escape from these early defense mechanisms, they are captured and destroyed by adaptive immune mechanisms, where T and B cells and their antigen-specific effectors (cytotoxic T lymphocytes, cytokines such as IFNc and antibodies) target the virus. subsequent viral infection is prevented by Antigen-specific memory cells (T and B cells) (Capelozzi et al.,