Antimicrobial resistance in bacterial pathogens is a challenge that is associated with high morbidity and mortality. Multidrug resistance patterns in Gram-positive and -negative bacteria are difficult to treat and may even be untreatable with conventional antibiotics. There is currently a shortage of effective therapies, lack of successful prevention measures, and only a few new antibiotics, which require development of novel treatment options and alternative antimicrobial therapies. Biofilms are involved in multidrug resistance and can present challenges for infection control. Virulence, Staphylococcus aureus, Clostridium difficile infection, vancomycin-resistant enterococci, and control in the Emergency Department are also discussed.

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The purpose of this review article is to highlight articles and new research regarding the link between NF-ĸB and several cancers. This review presents the most up-to-date NF-ĸB research and how it links this important transcription factor with hematology and oncology. It was written by conducting a thorough search of Pubmed as well as several journals such as Cancer, Nature, Science, Cell and those of one of the authors. The articles relating to the link between NF-ĸB and cancer were used to write this review. The results of this study clarified that there is a critical link between NF-ĸB and cancer. NF-ĸB has often been implicated in a variety of different diseases and it plays a variety of roles in cell survival, differentiation, and proliferation of cells. In cancer, NF-ĸB plays a pivotal role by facilitating oncogenesis as well as metastasis. A thorough understanding of NF-ĸB and its role in cancer can lead to future studies and drug development which could provide a novel option in the treatment of this disease.

Nanomaterials, substances below 100 nm, are increasingly used in medical diagnosis and treatment every day. The use of such materials has helped deliver drugs across the blood-brain barrier, alleviate allergy symptoms, specifically target cancer or HIV cells, and more. However, the tunable characteristics of such materials have not been perfected. The different materials, sizes, shapes, and structures have different responses on the body. This paper will investigate the successful treatments made with nanoparticles and some general health effects. A review of the literature revealed an inflammatory response and an increased production of reactive oxidative species (ROS) to be common immune responses to nanomaterial use. The mechanisms by which the inflammatory response and ROS production occur will also be discussed.

Mastocytosis has a bimodal distribution often presenting in children from birth to 2 years of age and in those over the age of 15. Pediatric mastocytosis is due to the effects of mast-cell degranulation enzymes such as histamine and tryptase causing the presentation of pruritis, flushing, vesicles, abdominal and bone pain, or headache. Three different forms of mastocytosis can occur: urticaria pigmentosa, diffuse cutaneous, and solitary mastocytoma. Systemic symptoms are typically a result of mast-cell mediator release but do not prove systemic mast-cell hyperplasia. In this review, we present several research studies related to pediatric mast-cell disorders, and discuss several cases of pediatric mastocytosis, acute myeloid leukemia, pathophysiology, genetic studies, and treatment. Introduction and Research Studies

The T-cell immunoglobulin and mucin domain (Tim) gene family is a relatively newly discovered group of molecules with a conserved structure and important immunologic functions. Tim molecules express on many types of immune cells including T cells, B cells, dendritic cells, macrophages, and mast cells that have been shown to be involved in asthma, allergic rhinitis, food allergy, and autoimmunity. Tim-1-Tim-4 interaction promotes Th2 cytokine responses, and blocking this interaction can decrease airway inflammation in asthma and in allergic rhinitis. Tim-3 stimulates mast cells to produce Th2 cytokines, and anti-Tim-3 is able to dampen asthmatic inflammation. The Tim-3 ligand was shown to be greatly enhanced on intestinal epithelial cells in patients with food allergy and Tim-4 may play a role in maintaining oral tolerance and prevention of food allergy. Tim-3 deregulation plays a role in the pathogenesis of multiple sclerosis. Increased Tim-1 expression has been shown in mononuclear cells from systemic lupus erythematosus patients and Tim-3 may be involved in a protective role in rheumatoid arthritis.

Nitric oxide is a free radical molecule that can have both homeostatic and proinflammatory roles in the nasal mucosa, sinuses and airway. We have demonstrated elevated levels of nitric oxide in either nasal fluid, serum and spontaneous, or antigen-stimulated mononuclear cells from patients with allergic rhinitis, sinusitis, and asthma. We also showed that various therapeutic agents such as glucocorticoids, theophylline and macrolides can decrease nitric oxide levels in these patients. Thus determination of nasal, serum, mononuclear cell or airway production of nitric oxide may be an important biomarker of inflammation for monitoring newer anti-inflammatory therapy.

Mast cell activation syndrome (MCAS) is a condition with signs and symptoms involving the skin, gastrointestinal, cardiovascular, respiratory, and neurologic systems. It can be classified into primary, secondary, and idiopathic. Earlier proposed criteria for the diagnosis of MCAS included episodic symptoms consistent with mast cell mediator release affecting two or more organ systems with urticaria, angioedema, flushing, nausea, vomiting, diarrhea, abdominal cramping, hypotensive syncope or near syncope, tachycardia, wheezing, conjunctival injection, pruritus, and nasal stuffiness. Other criteria included a decrease in the frequency, severity, or resolution of symptoms with anti-mediator therapy including H(1) and H(2)histamine receptor antagonists, anti-leukotrienes, or mast cell stabilizers. Laboratory data that support the diagnosis include an increase of a validated urinary or serum marker of mast cell activation (MCA), namely the documentation of an increase of the marker above the patient's baseline value during symptomatic periods on more than two occasions, or baseline serum tryptase levels that are persistently above 15 ng/ml, or documentation of an increase of the tryptase level above baseline value on one occasion. Less specific assays are 24-h urine histamine metabolites, PGD(2) (Prostaglandin D(2)) or its metabolite, 11-β-prostaglandin F(2) alpha. A recent global definition, criteria, and classification include typical clinical symptoms, a substantial transient increase in serum total tryptase level or an increase in other mast cell derived mediators, such as histamine or PGD2 or their urinary metabolites, and a response of clinical symptoms to agents that attenuate the production or activities of mast cell mediators.