The Presence Of Dna Damage

According to information published by the Mayo Clinic, sepsis has three stages: sepsis, severe sepsis and septic shock. The mortality rate for septic shock is nearly 50 per cent, and an episode of severe sepsis increases the risk of future infections. Severe sepsis causes blood flow to the vital organs, such as the brain, heart and kidneys, to become impaired. Sepsis can also cause blood clots to form in organs and extremities such as arms, legs, fingers and toes, which can lead to organ failure and tissue death (gangrene).

When a patient has sepsis early symptoms will include those that define SIRS; abnormal body temperature, increased heart rate, increased respiratory rate, and/or abnormal white blood cell count. If these symptoms are left untreated, organ failure will start to occur. Signs of organ failure can include decreased urine output, sudden changes in mental status, difficulty breathing, decrease in platelets and abnormal heart rhythms. Decreased cardiac output and hypotension may also start to occur, which indicates septic

The fundamental principle of the phenomenon known as sepsis is an amplified immune response to a pathogen. It is important to note that the insult originates from the excessive host response to, rather than the pathogenicity of, the infective agent1. The upregulation of pro-inflammatory (TNF-α, IL-1α/β, IL-6, IL-12, IFN-γ, and MIF) and anti-inflammatory (IL-10, TGF-β, and IL-4) mediators have been found in various sepsis states2. The exact function, value, and limits of this peculiar, and extravagant, immune response is not fully understood3. Historically, sepsis and processes within the sepsis spectrum have been difficult to truly identify and diagnose1. In 2012, the Surviving Sepsis Campaign identified three major categories of the phenomenon: sepsis, severe sepsis, and septic

Pediatric sepsis can present itself in a number of ways, it is manifested by: rashes, changes in skin color, decreased amount of urine, lethargy, fever above 1004 F, and disinterest or difficulty feeding, among others (Rory Staunton Foundation for Sepsis Prevention, n.d.) When sepsis takes place, the circulatory system is often the first system to become compromised. Tachycardia, tachypnea, peripheral vasodilation, fever, or worst case scenario, circulatory collapse can happen (Santhanam, 2016). If continued, sepsis can eventually affect multiple organs, also known as multiple organ dysfunction syndrome (MOBS), or worse lead to death. The signs and symptoms of sepsis reflect the systemic inflammatory response syndrome (SIRS). As medical doctor Shankar Santhanam (2016) states in the “Pediatric Sepsis,” SIRS can be caused by infectious or

LBP is an acute-phase reactant that forms a complex with LPS. The LPS-LBP complex binds to CD14 and to the Toll-like receptor 4/MD2-complex resulting in transcription of cytokines and other pro-inflammatory mediators [5, 6]. In human serum, LBP is constitutively present at a concentration of 5 to 10 μg/ml [17]. During sepsis, LBP levels increase to median peak levels of 30-40 μg/ml within 24 h [7, 8, 17 These properties made LBP promising for the diagnosis of sepsis. Indeed, a good discrimination between SIRS and sepsis was reported].

Sepsis is a life-threatening response to an infection and is the leading cause of death for hospitalized patients. It is estimated that 1.6 million hospitalized patients are treated for sepsis annually, with the approximate health care cost of $16.7 billion dollars. The mortality rate for sepsis is estimated to be as high as fifty percent. However, research evidence shows that early detection of sepsis can improve survival rates by twenty percent (Winterbottom, 2012, p. 247). In 2010, the Surviving Sepsis Campaign created evidence-based guidelines to improve outcomes for patients with early sepsis, and to create awareness and education for health care professionals regarding the impact of early detection (Levy et al., 2010). Recommendations for the early detection of sepsis include specific monitoring of lab work and vital signs, goal-directed therapy such as fluid replacement, and the early administration of the appropriate board-spectrum antibiotic’s.

Sepsis is a condition of growing concern for nursing professionals, as the mortality rate has increased each year since its initial documentation in the early 1990s (Levy et al., 2012). Sepsis was first defined in 1991 as a systemic inflammatory response syndrome (SIRS). Since this time, improvements have been made in developing a worldwide definition of sepsis (Levy et al., 2012). Specifically, sepsis is considered to be a life-threatening dysfunction of the organs that results from the dysregulation of a host response to an infectious agent (American Association of Critical-Care Nurses, AACN, 2018).

Sepsis and Septic Shock have been my personal topic after the life of young Kamil Williams and a 31-year-old Texas man who both contacted a bacterial infection later turn into sepsis. Although I have not formally studied it during my school or university years, I still find the human body, how it can break down and react to certain ailments interesting. The next question would be why does this happen? Well when there is infection or insult upon the body’s immune system normal reacts and causing an inflammatory response. This normally a good thing and it promotes healing and the resolution of the insult, however in Septic Shock the inflammatory response comes explosive and uncontrollable. According to Allison Hotujec, the author of “Severe Sepsis and Septic Shock Protocols,” Sepsis has been called a “malignant intravascular inflammation.” The term malignant is because it is uncontrolled unregulated and self-perpetuating, in the usual immune response here is release of both pro-inflammatory and anti-inflammatory mediators, these balance to promote tissue

Since people with a GBS infection are typically asymptomatic, this type of bacteria doesn’t typically harm them. However, during pregnancy, mothers with group b strep may develop other infections such as a urinary tract infection, an infection of the amniotic fluid or an infection of the lining of the uterus. If the infant swallows the infected amniotic fluid during labor, they are at risk for developing a more life-threatening disease. Common complications for newborns include meningitis, pneumonia and sepsis. Meningitis is an infection of the brain and spinal cord. Pneumonia is an infection of the lungs causing respiratory distress. Sepsis is an infection of the blood that spreads throughout the body. The Center for disease control classifies Group B Streptococcus as the, “leading cause of meningitis, and sepsis, in a newborn’s first week of life” (Center for disease control, 2016). An infant who tests positive for any of these infections will be closely monitored in the intensive care unit for neonates. Since these complications are life-threatening, early detection can be the best defense in saving an infant’s life.

Sepsis-3 focuses specifically on the role of organ dysfunction as its pathological feature of host response. Identification of organ dysfunction requires identification of specific diagnostic criteria. The current diagnostic tests (SOFA and qSOFA) establishes or excludes the diagnosis through nonspecific discoveries of acute illness during its early stage. The problem with this is that sepsis varies in severity from patient to patient. Practitioners want a set of clinical criteria that can reliably be used to make clinical decisions (Angus, 2016, p. 14). They want a test guide as well as a therapeutic guide, with the ability to modulate host response (Marshall, 2016, p. 1459). They seek something Sepsis-3 does not offer - a further refinement

In early 1990’s the Early goal-directed therapy Rivers and colleagues challenged the standard sepsis care as an ICU disease by using early goal-directed therapy , with similar urgent diagnostic and therapeutic principles that were used for acute myocardial infarction, stroke, and trauma in the emergency department. There was no protocol to follow to identify early signs and symptoms of sepsis and its management. The high mortality and care that did not have any guidelines and most of the time was unorganized, triggered a series of investigations to identify the reasons for delay in identification and subsequently management of sepsis patients. In 2001, study by Rivers and colleagues, showed a significant reduction in mortality rate in sepsis patients. The reduction in mortality rate was 16% in patients treated with this

Sepsis is a clinical syndrome defined as a potentially fatal systemic response to an infection. It can affect patients across their life span. And it is usually caused by both gram positive and gram negative bacterial infections. Sepsis can develop from a systemic inflammatory response syndrome (SIRS) which is used to describe the early response to injury, which might be infective or non-infective, to a severe sepsis and septic shock if it was not recognized early and promptly, and effectively managed (2). Abnormalities in the inflammation, immune, coagulation, oxygen delivery, and utilization pathways play a role in organ dysfunction and death. Sepsis is a cause of considerable mortality, morbidity, health care utilizations and cost

UV rays damages the DNA in skin cells. Skin cancer starts when the skin cell growth DNA is damaged. UVA and UVB both have effects from lighting that are common in skin cancer. Time of day to reflections off of surfaces UV rays are a higher risk or damage. For example, 10am-4pm UV rays are stronger and UV rays can bounce off of water, sand,snow etc. Amount of exposure depends on the amount of of strength the rays are sending off, length of time the skin is exposed, and if the skin is protected or not. I would recommend seeking shade, avoiding tanning, and use a spectrum (UVA/UVB) sunscreen.

When mammalian DNA is injected into the body, dendritic cells are not stimulated. Moreover, it also failed to elicit appreciable antibody response even when it coupled with a protein carrier and presented in adjuvant (Madaio et al., 1984). This failed action is quite the opposite of animal disease models that are stimulated by immunization with protein auto-antigens such as experimental allergic encephalomyelitis or collagen-induced arthritis, inferring that DNA is different from other biomolecules in its immunological properties. Various studies, including from our lab (Dixit et al., 2005; Tripathi et al., 2014) as well as from others (Al Arfaj et al., 2007) propose that the DNA molecule undertake structural changes leading to the formation of new epitopes or neo-epitopes that are recognized as foreign by the immune system and are able to bring out antibody responses. However, when single stranded DNA is used for immunization, it can bring a restricted antibody response, and other helical nucleic acid species including double stranded RNA, RNA-DNA hybrids, carcinogen or drug modified DNA or complexes of DNA with proteins that can bind DNA are considered to be effective immunogens (Stollar, 1975; Anderson et al., 1988; Desai et al., 1993; Moinuddin and Ali, 1994; Dixit et al., 2005; Khan et al., 2006; Tripathi et al., 2013). Due to the presence of distinctive sequence motifs, bacterial DNA can induce the immune system to generate antibodies to sequential rather that backbone

Modification of damaged DNA seems to be an understudied subject, there is much to understand on the restoration of DNA damage, repair and DNA methylation. Genomic DNA can be modified by methylation but much of it is affected on a gene when silenced. When epigenetic modification has been implicated with cancer and aging it causes DNA methylation to also have an impact on the double strand of DNA analysis. Modification as such provoke deteriorating changes like aging found in multicellular organisms and DNA damage may magnify biochemical pathways that regulate a cells growth or control DNA replication with DNA repair. In the article “DNA Damage, Homology-Directed Repair, and DNA Methylation” written by Concetta Cuozzo, Antonio Porcellini, Tiziana Angrisano, et al. they hypothesize how DNA damage and gene silencing may induce a DNA double-strand break within a genome as well as when DNA methylation is induced by homologous recombination that it may somewhat mark its reparation through a DNA segment and protect its cells against any unregulated gene expression that may be followed by DNA damage. The experiments used to demonstration how gene conversion can modify methylation pattern of repaired DNA and when that occurs methylation is able to silence the recombined gene. When exploring the molecular mechanisms that link DNA damage and the silencing gene then there is an induced double strand break that can be found at a specific location or DNA sequence in where the