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Inflammation has been recognized as a medical condition dating back to the ancient Egyptian and Greek cultures. In the 5th century B.C.E. Hippocrates described inflammation as an early component of the healing process after tissue injury. Since then the definition of inflammation has changed but the foundation remains the same—inflammation is the body’s defense in response to environmental insult. In recent years, a deeper understanding of inflammation underlying Systemic Inflammatory Response Syndrome (SIRS) has come from the intersection of molecular biology and immunological discoveries. Advancements in genomics and proteomics have proven instrumental in the dissection of molecular mechanisms of inflammation; recognition of the signaling pathway crossroads has become a guiding light to the development of novel immune therapies in many inflammation-induced diseases. An in-depth look at one potential therapeutic agent, lactoferrin (LTF), demonstrates how an immune modulator may hold potential to control the inflammatory response. The clinical impact of this knowledge is enormous and holds promise on further development of new technologies for multiple clinical applications.

The pathomechanism of Alzheimer's disease (AD) is multifactorial although the most popular hypotheses are centered on the effects of the misfolded, aggregated protein, amyloid beta (Abeta) and on Tau hyperphosphorylation.Double blinded clinical trials were planned to demonstrate the effect of Colostrinin (CLN) on instrumental daily activities of AD patients. The potential molecular mechanisms by which CLN mediates its effects were investigated by gene expression profiling.RNAs isolated from CLN-treated cells were analyzed by high-density oligonucleotide arrays. Network and pathway analyses were performed using the Ingenuity Pathway Analysis software.The Full Sample Analysis at week 15 showed a stabilizing effect of CLN on cognitive function in ADAS-cog (p = 0.02) and on daily function in IADL (p = 0.02). The overall patient response was also in favor of CLN (p = 0.03). Patients graded as mild on entry also showed a superior response of ADAS-cog compared to more advanced cases (p = 0.01). Data derived from microarray network analysis show that CLN elicits highly complex and multiphasic changes in the cells' transcriptome. Importantly, transcriptomal analysis showed that CLN alters gene expression of molecular networks implicated in Abeta precursor protein synthesis, Tau phosphorylation and increased levels of enzymes that proteolitically eliminate Abeta. In addition, CLN enhanced the defense against oxidative stress and decreased expression of inflammatory chemokines and cytokines, thereby attenuating inflammatory processes that precede Alzheimer's and other neurological diseases.Together these data suggest that CLN has promising potential for clinical use in prevention and therapy of Alzheimer's and other age-associated central nervous system diseases.

Vancomycin and daptomycin MICs from 161 isolates of methicillin-resistant Staphylococcus aureus (MRSA) were compared using commercial and in-house broth microdilution, Etest, and common automated methods. Vancomycin Etest MICs were higher than those of other methods, whereas the MICs for daptomycin testing were comparable. Vancomycin MICs vary depending on the testing methodology.