Procalcitonin (PCT), a member of the calcitonin (CT) superfamily, is a 116 amino acid, 13 kilodalton precursor protein produced in humans in the parafollicular cells of the thyroid as well as the neuroendocrine cells of the lungs and intestines of healthy individuals. PCT is coded for in the Calc‐I gene, located on chromosome 11. PCT is the precursor to the regulatory protein calcitonin but may have its own, separate role in the human body’s response to bacterial infection. There is a positive correlation between the concentration of PCT in the blood and the severity of a bacterial infection, making PCT an acute phase reactant. Under normal conditions, PCT undergoes proteolytic cleavage in the thyroid and is converted into CT, which then leaves the thyroid and enters the bloodstream; however, under inflammatory conditions, PCT is not cleaved and enters the bloodstream in a three‐section state comprising an amino terminus, immature calcitonin, and calcitonin carboxyl‐terminus peptide. Additionally, under inflammatory conditions, PCT is produced in other locations besides the parafollicular cells of the thyroid and the neuroendocrine cells of the lungs and intestines due to an increase in the expression of the Calc‐I gene. The reason for this increase may be related to potential anti‐inflammatory characteristics of PCT, including an ability to signal a reduction in the production of pro‐inflammatory proteins such as tumor necrosis factor‐alpha and interleukin 1‐beta. Furthermore, PCT in a specific concentration has been shown to reduce the reactivity of lipopolysaccharide (LPS) in gram‐negative bacteria. These properties of PCT have many potential applications in the medical field that are currently being studied or used. For example, detection of PCT in the blood can be used to determine if an infection is viral or bacterial or to evaluate the severity of infection in patients with sepsis. The determination of the pathogen allows for the correct course of appropriate treatment, potentially preventing the overprescription and overuse of antibiotics, a critical concern with the continued rise of bacterial antibiotic resistance. Additionally, as patients recover from a systemic bacterial infection, monitoring the level of PCT allows physicians to determine when the course of antibiotics may be stopped, once again minimizing antibiotic overuse. The Walton High School SMART Team has designed a 3D model of procalcitonin to investigate the relationship between procalcitonin’s structure and its function. Support or Funding Information MSOE Center for Biomolecular Modeling
Background The incidence of metastatic breast cancer is rising, but few studies have analyzed Asian American women with a focus on screening and obesity rates.Methods Data from the U.S. Cancer Statistics were examined for trends and incidence rates of breast cancer. Using the Center for Disease Control data mammogram compliance and obesity rates in Asian women were analyzed.Results Over our 18-year study period, the incidence of postmenopausal metastatic breast cancer increased by 2.19% annually in Asian women compared to only 1.03% in White women. Asians also had higher rates of mammogram non-compliance compared to other racial groups. Of Asians, the rates of obesity in postmenopausal women were highest in those aged 65–74 years.Conclusions Compared to other races, Asians have the highest increase in the incidence of metastatic breast cancer with lower rates of screening mammograms. Further research is needed to better understand these disparities.
While Parkinson's Disease is a multifactorial disease, influenced by both genetics and the environment, alpha‐synuclein was the first genetic factor to be linked to the disease. It has henceforth become a target in therapeutic research. A‐synuclein is a 140 amino acid neuronal protein that primarily regulates synaptic activity. It is considered to be intrinsically disordered as it does not have a defined structure in aqueous solutions. However, the protein forms α‐helical structures when it binds to negatively charged lipids, such as phospholipids in cell membranes. Α‐synuclein is a member of the synculein protein family, a group of three neuronal proteins with a highly conserved alpha‐helical lipid binding domain. Synucleins have been associated with a number of neurodegenerative disorders, including Parkinson's Disease (PD) and Alzheimer's Disease (AD), as well as some cancers. A‐synuclein is unique in the synuclein family for its non‐amyloid component (NAC) region, which has been linked to the formation of Lewy bodies. The wild type form of α‐synuclein is coded from the SNCA gene. This form has several functions, but it primarily functions as a presynaptic protein that controls neurotransmitter release by acting as a chaperone in the folding of Soluble NSF Attachment Protein Receptors (SNAREs). SNAREs mediate vesicle fusion with membranes, while α‐synuclein increases local Ca2+ release from microdomains to trigger ATP‐induced exocytosis. Certain mutations in SNCA cause α‐synuclein to polymerize into protofibrils that eventually coalesce into fibrils, a process called α‐synuclein aggregation. Aggregation of α‐synuclein leads to the creation of Lewy bodies, toxic clumps in the brains of patients with PD. PD is a progressive neurodegenerative disorder that affects movement. Common symptoms include bradykinesia, muscular rigidity, and tremor. Some studies have shown that deleting the NAC region prevented aggregation of α‐synuclein. Other α‐synuclein therapies have used receptor blocking strategies to inhibit the spread of the protein to other parts of the brain. There are also a variety of therapies that focus on preventing aggregation by decreasing the amount of α‐synuclein in the brain. While such therapies have shown positive results in fruit flies, mice, and rats, human trials have not been conducted. Medications to control symptoms are the main treatment for PD; these medications typically work by increasing or acting as a substitute for dopamine, as PD patients have low dopamine concentrations. In severe cases, surgeries like deep brain stimulations have helped to lessen tremors. Patients are encouraged to make lifestyle changes, such as uptaking aerobic exercise or physical therapy, which can improve symptoms. Further research on the relationship between α‐synuclein and Parkinson's Disease is required before human trials can begin. Nonetheless, the results of therapeutic studies have been promising.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.