HKU Six Sigma & Lean Manufacturing FMEA Analysis Windows Standard Excel Worksheet

Molecular Mechanisms of Sepsis

Molecular Mechanisms of Sepsis. Title: Protein-protein interaction network and functional module analysis to reveal the mechanism of sepsis in polytrauma patients Highlights: We explored the molecular basis of sepsis induced by polytrauma using PPI network. A total of 342 DEGs including 110 up- and 232 down-regulated genes were obtained. TRAF3 was related with the innate immune responses in sepsis. ITGB3 was the key gene involved in coagulation dysregulation in sepsis. CASP6 and RASA1 played key roles in the cell apoptosis mechanism of sepsis. Abstract Objective Sepsis represents the systemic inflammatory response to microbial infection. The pathogenesis of sepsis remains unclear. In this study, we aimed to explore the molecular mechanism of sepsis inpolytrauma patients. Methods The differentially expressed genes (DEGs) between the polytrauma patients with and without sepsis were identified by analyzing the GSE12624 microarray data using the limma package of R. The protein-protein interaction (PPI) network was extracted from the human PPI datasets by using MATLAB. The functional modules in the PPI network were identified by the MCODE network clustering algorithm. The KEGG pathway analysis was performed in each module. The phylogenetic tree was constructed using phylogeny inference package (PHYLIP). Result Total of 342 DEGs including 110 up- and 232 down-regulated genes were obtained. The PPI network identified several hub genes which had more interactions with others, such as TRAF3, ITGB3, CASP6 and RASA1. Further phylogenetic analysis indicated the high conservation of these hub genes. In the module analysis, four significant modules were identified. All the genes (COL1A2, FN1, ITGA2B, ITGB3 and CD36) in module 2 were enriched in extracellular matrix (ECM)-receptor interaction pathway. In module 4, CASP6 and CASP3 were enriched in apoptosis pathway. Conclusion We predicted genes such as TRAF3, ITGB3, CASP6 and RASA1 which were closely associated with sepsis induced by polytrauma. Among them, ITGB3 may play key role in the coagulation dysregulation of polytrauma patients with sepsis, and CASP6 and RASA1 may be the key genes in the cell apoptosis mechanism of sepsis. Keywords Sepsis, DEGs, GO, PPI network, phylogenetic tree Introduction Polytrauma is a syndrome of multiple injuries exceeding a defined severity with sequential systemic reactions that can lead to dysfunction or failure of remote organs and vital systems, which have not themselves been directly injured [1]. Sepsis, as one of the complications of polytrauma [2], is the systemic inflammatory response to microbial infection that often leads to increasing susceptibility to secondary infections, multiorgan failure, and death [3]. A sixteen years clinical study indicated that 10.2% of polytrauma patients infected sepsis during their hospital course [4]. Polytrauma is a major cause of morbidity and mortality in global and sepsis (3.1-17%) is one of the predominant causes of late death in polytrauma patients [5]. The disease severity is increasing according to the order of sepsis, severe sepsis and septic shock in the systemic inflammatory response syndrome (SIRS) [6]. Mortality has been reported to be as high as 45.6% for patients with severe sepsis or septic shock [7]. Based on the pathogenesis of sepsis, many therapies have been applied in the clinical practice such as antimicrobial therapy [8, 9] and hemodynamic support and adjunctive therapy [10, 11]. Currently, the Surviving Sepsis Campaign (SSC) has attempted to increase the awareness and establish the practice guidelines to improve the recognition and treatment for the patients with sepsis [12, 13]. At present, there are four approved mechanisms in the pathogenesis of sepsis [14]. The first one is dysregulated coagulation. Sepsis patients frequently manifest disseminated intravascular coagulation (DIC) with consumption of platelets and prolongation of clotting times [15]. The second one is inflammatory response. The inflammatory response is an important and central component of sepsis because the elements of response drive the physiological alterations that manifest as the SIRS [16]. Third, many cellular aspects become dysfunctional in sepsis which behave either excessive activation or depressed function [17]. The last one is metabolic alterations. It was reported that endogenous glucose production was markedly increased in the patients [18]. However, the specific molecular mechanisms of them remain entirely unclear. In this study, the differentially expressed genes (DEGs) between the polytrauma patients with sepsis and without sepsis were identified. Gene ontology (GO) analysis, protein-protein interaction (PPI) network and phylogenetic tree construction were performed to explore the molecular basis of sepsis induced by polytrauma. Materials and methods Microarray data The gene expression profile of GSE12624 based on the CodeLink UniSet Human I Bioarray platform (GE Healthcare/Amersham Biosciences) was downloaded from National Center for Biotechnology Information (NCBI) Gene Expression Omnibus (GEO) database (http://www.ncbi.nlm.nih.gov/geo/). The dataset available in this analysis contained 70 samples including 34 polytrauma patients with sepsis and 36 polytrauma patients without sepsis. Data preprocessing and DEGs screening For the microarray data, Robust Multichip Average (RMA) in the Affy package of R was used to compute normalized expression measures from the raw expression values. Probe annotation was obtained by using the Bioconductor package. The limma package was used to identify the DEGs with p-value 1 [19]. GO enrichment analysis of DEGs GO analysis was performed using the DAVID online tool (http://david.abcc.ncifcrf.gov/) [20]. For GO enrichment of DEGs, we selected GOTERM_BP_FAT, GOTERM_CC_FAT and GOTERM_MF_FAT as the gene set categories. A p-value of less than 0.05 was set as the cut-off criterion. PPI network construction The human PPI datasets with 108477 interacting protein pairs were downloaded from PINA2 (http://cbg.garvan.unsw.edu.au/pina/interactome.stat.do) at December 26, 2013. The PPI networks of the DEGs in sepsis were extracted from the human PPI datasets by usingMATLAB [21]. The proteins in the network served as nodes and the degree of a node corresponded to the number of interactions with other proteins [22]. The protein with high degree was considered as the hub node. Identification of functional modules in PPI network PPI network visualization and network parameters evaluation were performed by using Cytoscape software. The modules were identified by the MCODE (a cytoscape plug-in) network clustering algorithm with the default parameters [23]. The module with score larger than 2 was considered as significant. KEGG pathway analysis of each module was performed by applying the DAVID annotation tool. Phylogenetic tree construction In this study, we constructed the phylogenetic tree based on the nucleotide sequences to investigate the sequence conservation of the DEGs whosedegree were large than 30. The BLAST program is used to search for homologous sequences of these DEGs. The DNA sequence of these DEGs and their homologous genes in FASTA format were obtained from the nucleic acid database in NCBI (http://www.ncbi.nlm.nih.gov/nuccore). The phylogenetic tree was constructed by using phylogeny inference package (PHYLIP) with the default parameters [24]. The gene conservation was estimated by the distance from gene to the phylogenetic tree root. Result DEGs between the patients with and without sepsis After statistical analysis of the microarray data, a total of 342 DEGs were screened out. Among them, 110 were down-regulated and 232 were up-regulated in sepsis. The top 20 significantly up- and down-regulated DEGs are shown in Table 1. GO enrichment analysis The 342 DEGs were significantly enriched into 95GOterms including 81 biological processes terms, 10 cellular component terms and 4 molecular function terms. The top 10 GO biological processes termswere mainly related to the purine base (purine base biosynthetic process, purine base metabolic process, purine nucleoside monophosphate biosynthetic process and purine ribonucleoside monophosphate biosynthetic process), nucleobase (nucleobase metabolic process and nucleobase biosynthetic process) and regulation of protein modification (regulation of protein modification process and positive regulation of protein modification process). The 10 significantly enriched GO terms of cellular component included four lumen related terms (organelle lumen, membrane-enclosed lumen, intracellular organelle lumen and nuclear lumen), two membrane related terms (extrinsic to membrane and plasma membrane part) and four other cellular component terms (peroxisome, microbody, nuclear body and Golgi apparatus). For molecular function, four significant GO terms were enriched finally. They were acyl-CoA binding, sons of mothers against decapentaplegic homologue (SMAD) binding, aryl hydrocarbon receptor binding and potassium channel inhibitor activity (Table 2). PPI network of DEGs A PPI network consisting of 225 DEGs and 1048 non-DEGs is shown in Fig. 1. This network included 1145 gene nodes and 1273 interactions. The connectivity degree of each node in this PPI network was calculated and the results of top 20 nodes are listed in Table 3. Among them, the genes CRK (encoding CDC2 related protein kina), RASA1 (encoding RAS p21 protein activator 1), TRAF3 (encoding tumour-necrosis-factor receptor associated factor 3), ZHX1 (encode zinc-fingers and homeoboxes), ITGB3 (encoding integrin β3), RPA1 (encoding replication protein A1), JAK3 (encoding Janus kinases 3), and CASP6 (encoding caspase-6) with the degree over 30 were selected as the hub genes. Module analysis of PPI network A total of 7 modules were constructed by using MCODE plug-in. After excluding the modules with the score less than 2, 4 significant modules were considered as functional ones associated with sepsis (Table 4). According to the Fig. 2, the numbers of nodes and edges were similar in each model. The detailed results of KEGG pathway analysis for each module are provided in Table 5. For module 1, no pathway was enriched in the KEGG pathway analysis. For module 2, a total of 14 significant enriched pathways were identified. Among them, all the genes in this module were enriched in the pathway of extracellular matrix (ECM)-receptor interaction. In addition, except CD36 (encoding glycoprotein IV), the other four genes (ITGB3 and ITGA2B encoding integrin αIIbβ3, COL1A2 encoding the α 2 chain of type 1 collagen and FN1 encoding fibrinogen 1) were enriched in the focal adhesion and phosphatidylinositol 3-kinase (PI3K)-Akt signaling pathway. There were three significant enriched pathways in module 3. HIF1A (encoding hypoxia inducible factor-1), ARNT (encoding arylhydrocarbon receptor nuclear translocator) and ARNT2 (encoding arylhydrocarbon receptor nuclear translocator 2) were enriched in the pathway of renal cell carcinoma and pathways in cancer. HIF1A and ARNT were enriched in the pathway of Hypoxia-inducible factor 1 (HIF-1) signaling. For the module 4, five significant pathways were found. Among them, CASP3 (encoding caspase 3) and BIRC5 (encoding baculoviral IAP repeat–containing 5 and also called survivin) were enriched in the pathway of colorectal cancer, hepatitis B and pathways in cancer. CASP6 and CASP3 were enriched in apoptosis pathway. CASP3 and RASA1 were enriched in the mitogen-activated protein kinase (MAPK) signaling pathway (Table 5). Phylogenetic tree analysis Based on the result of PPI network analysis, the selected hub genes were chosen to construct the phylogenetic tree. The phylogenetic tree of ZHX1 was unable to be constructed, as only three homologous sequences were searched out. The phylogenetic trees of the other seven hub genes were constructed by the DEGs and their top nine significant homologous genes. The results showed that CRK, RASA1, TRAF3, ITGB3, RPA1 and CASP6 were the genes that were closer to tree roots indicating that the conservation of these genes was high during evolution. However, the conservation of JAK3 was low because of appearing in the late period of evolution (Fig. 3). Discussion Currently, sepsis remains a serious clinical problem. The four approved mechanisms of sepsis were dysregulated coagulation, inflammatory response, and cellular dysfunctional and metabolic alterations. However, the specific molecular mechanisms are still incompletely understood. For better understanding the pathogenesis, we identified and analyzed the DEGs between the patients with and without sepsis. As a result, a total of 342 DEGs including 110 up-regulated genes and 232 down-regulated genes were found. These genes were significantly enriched in GO terms including purine base biosynthetic process, regulation of protein modification process and peroxisome. Among them, the process of purine base biosynthesis is the most significantly enriched process. It was reported that de novo purine biosynthesis was essential for infectivity, growth and virulence of many bacteria in mammals [25]. The pathogenesis of sepsis was related with the bacterial infection [26]. Therefore, the purine base biosynthesis process may associate with sepsis based on the tissue response to bacterial infection. For the regulation of protein modification, Wu et al. reported that the alterations in the phosphorylation of myofibrillar proteins and the Ca2 sensitivity of myofibrillar ATPase might contribute to alter cardiac function during the progression of sepsis [27]. The cardiac dysfunction was the clinical characteristic in severe sepsis and septic shock [28]. Thus, the phosphorylation of myofibrillar proteins may be related with the sepsis-induced cardiac dysfunction. Furthermore, we mapped the DEGs to the PPI network and identified high conserved hub genes. Among them, the high conservation of CRK, RASA1, TRAF3, ITGB3, RPA1 and CASP6 were proved by the phylogenetic tree analysis. They may be the crucial genes in the pathogenesis of sepsis. For TRAF3, it is a member of the TNF receptor (TNFR) associated factor (TRAF) protein family [29]. This protein participates in the activation of the innate immune response [30]. In the PPI network, TBK1 (encoding TANK-binding kinase 1) was a non-DEG interacted with TRAF3. It was reported that TIR domain-containing adaptor-inducing IFN-β (TRIF) could interact with noncanonical IKKs (IKKϵ and TBK-1) and IKKι (also called IKKϵ) through TRAF3 in the Toll-like receptors (TLR) signaling pathway [31]. The innate immune system constitutes the first line of defense by rapidly detecting invading pathogens through the TLR [32] and is a danger signal in systemic inflammatory response syndrome and sepsis [33]. Thus, TRAF3 may be the mediator of innate immune responses in sepsis induced by polytrauma. We also performed the modular analysis of the PPI network and four functional modules were identified. Based on the result of the KEGG pathway analysis of each module, we found that the pathways in module 2 and 4 were more related with sepsis. The ECM-receptor interaction pathway was the most significant pathway in module 2 and all the genes of this module were enriched in this pathway. Fibronectin and collagen are the components of ECM [34]. Integrin family are the receptors transducing signals from the ECM [35]. Among them, integrin αIIbβ3 is the platelet integrin promoting theaggregation of platelets [36-38]. Moreover, it was reported that collagen type I could induce the aggregation of platelet [39]. Integrin αIIbβ3 is one of the platelet collagen receptors in platelets [40]. It was reported that platelet-specific elements initiated at the cytoplasmic domains of integrin αIIbβ3, which was a signal that leaded to conformational changes within the extracellular domains of integrin and expression of the fibrinogen receptor, then the simultaneous occupancy on adjacent platelets of receptors with dimeric fibrinogen molecules leaded to platelet aggregation [41]. In addition, CD36 is spatially associated with the αIIbβ3 integrin on the surface of platelets [42]. Thus, we speculated that the binding of collagen type I and αIIbβ3 might need the participation of CD36, and then conformational changes within the extracellular domains of integrin and the binding between fibrinogen and fibrinogen receptor could lead to platelet aggregation. Disseminated platelet aggregation is one of the characteristics of the DIC in sepsis [43, 44]. The up-regulated expression of ITGB3 in sepsis may lead to the disseminated platelet aggregation. Hence, we concluded that the coagulation dysregulation in the polytrauma patients with sepsis may be associated with the increase of disseminated platelet aggregation caused by the up-regulated expression of ITGB3. Thus, ITGB3 may play key roles in the coagulation dysregulation of the polytrauma patients with sepsis. Hub nodes CASP6 and RASA1 were predicted to be closely interacted with each other in module 4. Besides, CASP3, TOP1, BIRC5 and AURKB (Aurora B kinase) were also included in module 4. Among them, CASP6 and CASP3 were enriched in apoptosis pathway. It was reported that CASP6 may be associated with the cell apoptosis in sepsis [45] and blocking caspases might have some beneficial effects in decreasing cell apoptosis in sepsis [46]. Thus, we further confirmed that the up-regulated expression of CASP6 may promote cell apoptosis in sepsis. Besides, TOP1 is cleaved late during cell apoptosis by CASP6 and CASP3 [47]. The TOP1 cleavage complexes contribute to cell apoptosis [48]. Therefore, the increase of these complexes induced by the up-regulated CASP6 can promote the cell apoptosis in sepsis. Moreover, full-length TOP1 could induce DNA cleavage by single-strand breaks which is the signal of cell apoptosis [49, 50]. Therefore, the exaggerated gene expression of TOP1 in our study might contribute to cell apoptosis in sepsis. In addition, it was reported that CASP3 could modulate a given set of proteins to generate, depending on the intensity of the input signals, opposite outcomes (survival vs death) through differential processing of RASA1 [51]. Some articles reported that low CASP3 activity leaded to the cleavage of the RASA1 protein into an amino-terminal fragment [52, 53]. RASA1 bound BIRC5 is a bifunctional protein complex that can suppress cell apoptosis and regulated cell division, so as to generate anti-apoptotic signals [54]. AURKB exists in a complex with BIRC5 [55]. Considering the up-regulated expression of RASA1 and AURKB, we speculated that there may be a switch mechanism of CASP3-RASA1 in cell apoptosis and BIRC5 and AURKB might play roles in the anti-apoptosis mechanism of RASA1. In summary, CASP6 and RASA1 are the key genes in the pathogenesis of sepsis induced by polytrauma. Conclusion In this study, we obtained four key genes related with pathogenesis of sepsisinduced by polytrauma. Among them, TRAF3 was related with the innate immune responses in sepsis,ITGB3 may play key role in the coagulation dysregulation of the polytrauma patients with sepsis and CASP6 and RASA1 were associated with the mechanism of cell apoptosisin sepsis. For further investigating the association of these hub nodes with sepsis and verifying the role of the interactions among the genes in the pathogenesis of sepsis, more studies are required in the future. Molecular Mechanisms of Sepsis

EDU 146 Pitt Community College Personal Bias in Children Behavior Discussion

online homework help EDU 146 Pitt Community College Personal Bias in Children Behavior Discussion.

How can Does personal bias affect an adult’s reaction to a child’s challenging behavior?
How can you become more aware of your own personal bias?
In what ways can appropriate and thorough observation and recording help you to develop a better behavior plan?

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Textbook
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You will be responsible for creating your own discussion thread (think of this as your response or statement regarding the discussion board topic/question) and for responding to at least two other student’s posts.  
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Responses to other classmates’ posts should be a minimum of three sentences in length and address the information contained in the student’s original post while also expanding on the concepts within the text and course material. When you respond to classmates, please be respectful of other viewpoints and make sure that your response is thoughtful, insightful and extends the content of the initial discussion question.  Responses such as “good job,” “I agree,” “I never thought of that,” etc., will not be counted as a productive response and will not receive any credit.
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Post your opening response to the question early in the assignment period so that others have time to respond to you.First person to respond to:
by Elin ShearinNumber of replies: 3
Personal bias affects an adult’s reaction to a child’s challenging behavior differently for everyone. Some things that affect personal bias are gender, culture, age, experiences, and temperament. For example, our textbook discusses a child named Ava. Her former teacher enjoyed having her in his class while her new teacher does not. This is because Ava’s old teacher likes her creativity because it reminds him of himself when he was younger. Her new teacher was brought up in a strict home so she does not feel the same.
You can become more aware of your own personal bias by separating facts from opinions. You can do this with objective observations instead of subjective interpretations. With objective observations, you are describing what happens without making judgments. These observations can be seen, heard, smelled, tasted, or touched. With subjective interpretations, you are using objective observations to think about and express ideas, explanations, and perceptions of what happened. According to our textbook, when one’s opinions are stated separately from observable facts and those opinions are clearly labeled “subjective,” it is easier to recognize and deal with personal bias.
Appropriate and thorough observations and recordings can help to develop a better behavior plan by helping teachers be more effective when working with children. Observations help determine learning and developmental goals. This helps make concrete plans, make changes in the curriculum and environment, and improve the quality of care and education provided. Watching and recording behavior helps select appropriate methods to prevent or respond to various problems, and to evaluate how effective the chosen guidance technique has been in solving the problem.

by Alexus HandsNumber of replies: 2
1. How can personal bias affect an adult’s reaction to a child’s challenging behavior?
Biases are one’s own set of beliefs, values, perceptions, and assumptions (Miller, 2016). The concept of bias comes from the development of a person’s upbringing and past experiences with others. We perceive our points of view through a filtered version of bias. All aspects of an individual shape and affect our perceptions and biases. It is usual for a person to find others more appealing than others because of an opinion that has been formed about certain people. However, adults must remain respectful towards children no matter what.
Personal bias affects an adult’s reaction to a child’s challenging behavior by causing a rift between the child and the adult. For example, the adult may behave more harshly with that child than a child behaving more appropriately. “To respond more effectively to children’s behaviors, we must discover our areas of bias (Miller, 2016, p. 82).” Acknowledging our biases enables us to learn and research about the cultural differences of individuals. Also, we can dissuade any prejudice or preconceived notions we may have about certain groups of people.
2. How can you become more aware of your own personal bias?
One can become aware of their personal bias by being honest, remaining respectful, learning more about individuals, and consciously separate facts from opinions. Adults must be honest with their feelings about genders, cultures, ages, experiences, and temperaments. Each child will be unique when it comes to all these concepts, and that will cause teachers to feel a certain way towards certain children. Therefore, we should not be quick to label anyone before taking the time to understand better a child’s behavior and temperament, which could influence their learning and overall development.
One can also dismiss any stereotypes they may have about specific ethnic or gender groups. It will be beneficial to learn about an individuals’ character so that adults can form a more cooperative relationship with the children they work closely with. “One way to increase objectivity is to consciously separate facts from opinions (Miller, 2016, p. 82).” Adults can make both objective and subjective observations; being objective would include describing what is happening without making judgments. In contrast, subjective observations use thinking and expressing ideas and perceptions of what happened.
3. How can appropriate and thorough observation and recording help you develop a better behavior plan?
Through objective and subjective observation, an adult should determine learning and developmental goals, which improve the quality of education, allow concrete plans to be formed and change curriculums and the environment if need be. Recording behavior helps teachers choose appropriate teaching methods and evaluate which guidance techniques are being applied in the classroom (Miller, 2016). Thorough observation serves many purposes to help develop a better behavior plan: communication with families, evaluating a child’s overall development, and identifying children’s needs or interests. A teacher can use various observation strategies to make a classroom a developmentally appropriate place for young children. For example, a teacher may use a recording to have a physical indication of how a child is progressing within the classroom.Anecdotal records are detailed and describe a child’s event that is of particular interest or concern. This specific kind of record is clear, concise, and, most importantly, factual. Another type of recording would be a running record, a detailed commentary describing an event as it is happening (Miller, 2016). Typically, it describes a child’s behavior and any specific patterns occurring within the classroom. There is no one correct approach to observing or recording; however, using both, an adult can make the proper changes to ensure a child is thriving.
References
Miller. (2016). Positive Child Guidance. Cengage Learning. 
EDU 146 Pitt Community College Personal Bias in Children Behavior Discussion

Igniting Flammable Liquids with Cigarettes

Cigarettes seem like a probable ignition source for flammable liquids. Cigarettes have been blamed for the cause of many fires, far more than they should. But Cigarettes are more than tobacco wrapped in paper. They are in fact carefully engineered to burn in a certain way Cigarettes vary considerably from brand to brand in their burning characteristics. Modern cigarettes contain an engineered chemistry of additives to control the burning rates and moisture content of the tobacco and paper and anyone who has been a smoker knows the fact that manufactured Cigarettes go on burning when not being puffed. This spares smokers the trouble of lighting up again unlike with rolled up cigarettes and Cigars where the smoker has to keep smoking for the combustion of the tobacco to remain lit. This is good for the cigarette companies and pays off in higher sales from cigarettes. So yes this does mean that a cigarette rolling off onto a mattress or into the crack of a sofa can smoulder undetected for 30 to 40 minutes before bursting into flames. Smouldering is a form of flameless combustion which can occur in materials capable of charring. Smouldering can occur at very low oxygen concentrations then proceeds at a very slow rate before flaming occurs. This makes people understand the real hazard of manufactured cigarettes. But that is found out through the visual fact of witnessing a cigarette stay lit and burn. So people will believe most of what they see as fact, but when many people sit down in their local theatre to watch the latest Hollywood movie they usual see the spectacular visual effects of a character throwing a lit cigarette on to a puddle of fuel and watching a large fire ball appear before their eyes which causes an amazing explosion. Igniting puddles of petrol for example with cigarettes in movies is a common device. The character takes a few puffs and tosses the glowing cigarette in the puddle. Immediately the petrol ignites. But Experiments with flammable gases and vapours have shown that many of the most commonly-encountered substances, including methane and petrol vapour, were not ignited by a lighted cigarette[1] So Petrol vapour cannot normally be ignited by glowing cigarettes, a fact which has been verified by many experiments. Cigarettes are rather uncommon as the source of ignition for a successful structure fire. If they are set to ignite liquid flammables, they will almost certainly fail[2] This paper looks to answer why a lighted cigarette when tested against the ignition of common flammable vapours such as petrol fail but other more volatile liquids tested are capable of ignition. Previous work carried out on cigarette ignition, related research in this field of combustion and ignition of flammable gases and liquids will be studied and researched to give the author a better understanding of the fallacy that a lit cigarette can be a danger that can readily ignite flammable liquids or gases. But not to underestimate the potential danger of such an ignition source in circumstances where many factors can come together to form self sustained combustion. Flammable substances and liquids are used for a wide variety of purposes and are commonly found in the home. Petrol is the most common, but there are other flammable and combustible liquids and gases used Table shows other flammable liquids commonly found around the home Lighter fluid Oil Propane Butane Aerosol Cans Diesel fuel Wood preservatives Kerosene White spirits Flammable materials found in the gaseous form will burn whenever mixed with the proper amount of air and properly ignited. A flammable liquid in its liquid state will not burn. It will only ignite when the vapours from the liquid evaporate in air. All flammable liquids give off vapours that can ignite and burn when an ignition source is introduced. Flammable liquids require an initial energy input to produce an air/vapour mixture within the limits of flammability (niamh mc daid) Ignition is the transition from a nonreactive to a reactive state in which external actions lead to thermo chemical runaway followed by rapid transition to self sustained combustion The usual conditions for ignition are given by a 3t rule of thumb. The three T’s stand for: Temperature. Must be high enough to cause significant chemical reactions and/or pyrolysis Time. Must be long enough to allow the heat input to be absorbed by the reactants so that a runaway thermo chemical process can occur Turbulence. Must be high enough so that there is good mixing between fuel and oxidizer and heat can be transferred from the reacted media to the unreacted media (cite the book) Ignition will occur when the process of a rapid exothermic reaction is started, which then gains momentum and causes the fuel to undergo change. When a flammable liquid is poured or spilled on a surface it is the vapours that are actually ignited. Vapours from liquids are what directly support the flame. To understand how volatile certain flammable liquids are it is useful to be familiar with the terms used to describe their chemical properties. Vapour density This is a property of a vapour that predicts its behaviour when released in air. when calculating the vapour density of a liquid fuel the molecular weight of gas of the vapour by that of air in normal conditions. (approx 29) (niamh mc daid) Flash point The flash point is the lowest temperature at which a liquid fuel will produce a flammable vapour. A liquid fuel must be able to generate a vapour in sufficient quantity to reach that lower limit in air before it can burn. This flash point is measured in two different ways, first being a closed cup measurement and the latter being an open cup. Flammable ranges Petrol has a narrow flammable range. Thus petrol vapour mixed with air has a lower flammability limit of just over 1% and an upper limit of 6% by volume petrol vapour in air, at normally encountered temperatures. (hollyhead) Flammable range refers to the percentage of a flammable liquid in its gaseous state to air to create an explosive mixture. Mixtures of flammable vapours with air will combust only when they are within particular ranges of vapour/air concentration. Outside of these limits the fuel-air mixture is either too lean or too rich to ignite (niamh mc daid) This varies with different flammable liquids. Gasoline has a flammability range of 1.4 to 7.6 percent. This means it will ignite when there is 1.4 parts of gasoline mixed with 100 parts air Ignition temperatures This is the temperature at which a particular flammable liquid gives off vapours and evaporates in air and therefore can ignite. Gasoline will ignite when a heat source or electrical spark of at least 853 degrees comes in contact with it. Natural gas (methane) needs an ignition temperature of around 1000 degrees Auto-ignition temperature (AIT) This is the temperature at which a fuel will ignite on its own without any additional source of ignition. (Niamh mcdaid) Fires will occur because there is high temperature introduced to an area in which there is a fuel-air mixture within its flammability range. There are so atmospheric factors that affect the Auto-ignition temperature e.g. Oxygen levels in the area of the mixture. But so long as the heat energy can be transferred from the source to the fuel ignition fire may result Flammability In Hollyhead’s paper he mentions the flammability of certain liquids e.g., kerosene, white spirit and diesel oil, which are flammable liquids with flash point temperatures above normal ambient. So therefore, an ignition source has to ignite not only the flammable mixture of fuel vapour but to generate this mixture in the first place by heating the bulk liquid. (hollyhead) Cigarette Components Modern manufactured cigarette comprise of different components. The components combined can affect the performance of the cigarette including the emissions of toxicants. In British manufactured cigarettes the tobacco used is Virginia. There are two other main types used in commercial cigarettes which are Burley and Oriental. Each has different characteristics. These tobacco types will also vary depending on their variety, in what environment they are cultivated and how that cultivation is carried out. The paper around the tobacco of commercial cigarettes in modified in different brands. It can be more porous in some brands so that the amount of air passing through the paper affects the yield of a puff. The more air that can pass through the paper the more the smoke constituents passing through the cigarette are weakened which then result in lower yields of various smoke products. Just as Baker describes when a cigarette burns, thousands of products are formed. They are distributed between the gas phase and aerosol particles which make up smoke. (baker) Modern commercial cigarettes are made with a filter. The filter is different on most brands. The way the filter is designed can affect the amount of filtration. Different cigarette brands can regulate the taste and smoking experience. Introducing vents in the paper surrounding the filter end can allow for dilution of smoke in lighter branding cigarettes. The bigger the length results in longer fibres and also the materials used for the fibres all play a part in making a certain cigarette different from other brands in the market. Figure shows the different components of a manufactured cigarette, how smoke moves through the tobacco and filter and how air moves through the paper (bat) Cigarette Combustion Many of the components identified in tobacco have also been identified in its smoke because they transfer in part from tobacco to its smoke during the smoking process. Many other identified tobacco components are not found in smoke because they decompose during the smoking process. (cite tobacco book) There has been work carried out to measure the burning temperature of a cigarette particularly those by Dr Richard R Baker have provided fundamental knowledge about the combustion/pyrolysis processes during smouldering and puffing of a cigarette. Dr Richard R. Baker has established the distributions of combustion temperature, gas velocity and key smoke constituents inside a burning cigarette. These experiments have become the foundation for the study of cigarette combustion. Dr Barker’s paper studied the process of thermo physical concurrencies inside and around a burning cigarette (barker) Figure 2 shows combustion of a cigarette when being smoked (bat) The formation of smoke from a burning cigarette depends on a series of mechanisms, including generation of products by pyrolysis and combustion, aerosol formation, and physical mass transfer and filtration processes. Each mechanism, and their interactions, has a profound effect on the levels of chemical constituents in tobacco smoke. An enormous amount of research has been done on these subjects over the last 50 years. (barker) Figure 2 describes the two types of burning that take place when the cigarette is puffed. There is also a natural smoulder occurring between the puffs by the smoker. There are two main regions at the tip on the ‘coal’, namely the combustion zone A and the pyrolysis and distillation zone B. Combustible vapours are produced in zone B prior to ignition in zone A. During puffing, air is drawn into the cigarette through the paper and at the paper bum line. When a smoker draws on a lit cigarette, the temperature of the cigarette coal rises rapidly from its resting smouldering temperature of around 600 °C. Peak puff temperatures at the periphery of the coal can exceed 900 °C during a 35 mL, 2-sec puff. The high temperature inside the coal causes an increase in the viscosity of the air flowing through and a concomitant increase in the resistance to the draw of air through the coal. This effect forces air to be drawn primarily into the periphery of the coal around the paper burn line, which causes more complete combustion in this peripheral region. The depletion of oxygen due to combustion results in the formation of a region immediately behind the coal where the temperatures remain high enough for thermal decomposition of tobacco (the pyrolysis/distillation zone). Large amounts of volatile and semi-volatile smoke constituents are produced in this region. A small amount of air is drawn in along the tobacco rod through permeable cigarette paper and smoke temperature decreases rapidly to produce a supersaturated aerosol. The smoke thus formed during a puff is subjected to filtration by the remaining tobacco rod and cigarette filter, as well as dilution by any filter ventilation holes. Some proportion of the light gases (such as CO) will diffuse out of the highly permeable cigarette paper. The smoke that leaves the mouth end of the cigarette is called mainstream smoke. Between puffs, hot smoke escapes from the top of the cigarette and forms the sidestream smoke. In the author’s research for this paper the general opinion that cigarettes are the cause of fires is truthful, as there is no question that many fires are started by cigarettes and the careless smoker is usually the reason for the high number of fires originating from smoking cigarettes. Despite advances in the fire retardant foams in furnishings and mattresses, smoking in bed remains a threat to the safety of people. But it is a common occurrence to hear theories about how smoking caused a fire when the alleged ignition would not have been successful under certain circumstances. No one combustion parameter alone can be used to explain why gasoline (petrol) vapour and methane are not ignited by cigarettes whereas hydrogen and carbon disulphide are. In fact, the parameters themselves are inter-related and taken as a whole can express the propensity of a substance to react with oxygen to form combustion products. This is directly related to the ease with which chemical bonds are broken to lead to the formation of the more stable products of carbon dioxide and water, which result from the combustion of most of these fuels. hollyhead Recent tests by the ATF Fire research Laboratory involved contact of burning tobacco cigarettes of different brands with petrol vapour from a pool at room temperature. A total of 137 attempts were made using both smouldering and actively drawn puffs with no ignitions observed. De haan Tests have shown the oxygen levels in cigarettes in the vicinity of combustion to be very low and carbon dioxide levels to be very high, both factors reducing the chances of vapour ignition The conditions in the combustion zone of a cigarette, which is deficient in oxygen and rich in hydrogen and carbon dioxide, together with the rapid and efficient tobacco-oxy- preparation of the oxygen reaction conspire to allow only the most reactive of substances to be ignited, and result in flame propagation to the vapour air mixtures outside the cigarette coal. Repeated attempts to cause explosions by inserting a lit cigarette into an explosive fuel vapour-air mixture have resulted in failure over many experiments. Hollyhead The residence time of airborne vapours in the cigarette being puffed is so short that there is not enough time for any but the most reactive species to ignite. The fuel elements in a commercially manufactured cigarette is such that quenching distance of all but most reactive gases is not exceeded, suppressing any sustained ignition. Experimental evidence and consideration of the cigarette combustion process, alongside ignition parameters of substances, show that mixtures in air of petrol and methane are not ignited by a lighted cigarette. It is very likely, therefore, that many fires have been wrongly attributed to a lighted cigarette; such a cause fire can often be the refuge of the uninitiated ‘No Smoking’ regimes at chemical plants, oil gas installations and indeed petrol filling stations is, therefore, not in vain. Although a cigarette may not be an immediate problem, the lighted match or cigarette lighter flame used to light it, certainly could Occasionally contaminates or faults from the manufacture of the cigarettes, may it be in the tobacco filling or paper can cause some brief tiny flames. Given the right conditions and such an atmosphere where there is a fault and a perfect fuel-air mixture. Such flames would be a suitable ignition source. So even though many tests have proved that it is virtually impossible for a lit cigarette or cigar to ignite most flammable vapours, this could ensure the ignition of a fire, explosion or both. In study for this paper the author came across a message board where a guy was irate at the fact he seen another person smoke a cigarette on the fore court of a filling station. To his dismay when confronting the person in question about the stupidity of his action he promptly got the reply that cigarettes don’t lit petrol, I seen it on myth busters. Goes to show that what some people see on Television is believed as fact, just like in the Movies. Some things will never change[1] 1. www.wikilaw3k.org/forum. Cars-Transportation-Safety/Smoking-at-the-gas-pump. [cited 2010 4/11]; Available from: http://www.wikilaw3k.org/forum/Cars-Transportation-Safety/Smoking-at-the-gas-pump-345109.htm.

Module 5 – SLP Scholars vs. Practitioners SLP

Module 5 – SLP Scholars vs. Practitioners SLP. I’m trying to study for my Business course and I need some help to understand this question.

Module 5 – SLP
Scholars vs. Practitioners
For this assignment, choose an article from one of the practitioner journals that includes some use of data from the stock market or company financials. No need to find an article with a lot of fancy statistics, but the article should involve some type of numbers and data that you can find online from Yahoo Finance or other Web pages with financial data on publicly-traded corporations. If one of the papers from your Module 5 Case meets this description, you can use it for this assignment as well.
Once you have found an article that meets this description, try your hand at repeating some of the calculations or analysis in the article. Again, no need to do any fancy statistics. Just take a stab at using financial data either from the Internet or even financial data from your workplace if it is available, and apply the techniques from this article to the data you find.
For example, if the article proposes a new way to look at financial ratios for a given company, then look up the financial ratios for a major corporation on Yahoo Finance. Or if the article discusses new ways to pick stocks to invest in, try picking some stocks based both on the methods proposed in the article as well as information that you find online about different companies. Again, no need to do any fancy statistics but at least find some data and do some simple analysis of the data based on the article you found.
Your paper should be 3–5 pages and should include:

An overview of the analysis technique that you found in the article.
Your calculations and data presented in an organized and easy to understand manner.
Discussion about the results and implications of your analysis.

SLP Assignment Expectations

Answer the assignment questions directly.
Stay focused on the precise assignment questions. Do not go off on tangents or devote a lot of space to summarizing general background materials.
For computational problems, make sure to show your work and explain your steps.
For short answer/short essay questions, make sure to reference your sources of information with both a bibliography and in-text citations. See the Student Guide to Writing a High-Quality Academic Paper, including pages 11-14 on in-text citations. Another resource is the “Writing Style Guide,” which is found under “My Resources” in the TLC Portal.

Module 5 – Background
Scholars vs. Practitioners
To start off this module, take a look at the following practitioner-oriented finance journals. These journals have a mix of opinion articles, statistical studies, and guidance and suggestions for financial practitioners. Below is a link to each of the journals’ home pages. To access the journals you will need to go Business Source Complete in the Trident Online Library (click “Additional Library Resources” at the bottom of the Online Classroom and Library section of the main TLC portal page). Note that articles from the past year are not always available in the library, but previous issues of these journals are. Take a look at both the general description of the journal as well as a few recent articles in each journal:
Journal of Applied Corporate Finance was originally started by the investment bank Morgan Stanley and covers a range of issues from the perspective of corporate financial strategies.
Journal of Portfolio Management covers financial issues from the point of view of the investor.
Financial Analysts Journal is the official journal of the CFA Institute, the organization that gives out the Certified Financial Analyst Certificate. Articles in this journal tend to be a bit more technical than articles in other practitioner journals.
Journal of Wealth Management presents research from a financial planning perspective.
Now that you’ve reviewed the practitioner-oriented journals, take a look at some of the academic finance journals that specialize in more scholarly and theory-oriented research.
Here are a couple of scholarly finance journals that are highly ranked and are available in Business Source Complete:
The Review of Financial Studies is one of the toughest finance journals in the world to get published in and has highly technical articles.
Journal of Financial and Quantitative Analysis: As you can probably tell its name, this journal also publishes highly technical papers.
For a list of additional prestigious scholarly finance journals, check out Google Scholar’s Top Publications in Finance list. Google Scholar is also a good way to find scholarly finance studies, as many of the papers are available online.
Check out at least a few articles from top-ranked scholarly journals in finance. You don’t have too read too much in depth, as these articles are often extremely complex. But try to get an idea of the kind of technical or theoretical articles they publish and see if you can find any articles that interest you.

Module 5 – SLP Scholars vs. Practitioners SLP