Science topics: DipteraSepsis
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Sepsis - Science topic

Systemic inflammatory response syndrome with a proven or suspected infectious etiology. When sepsis is associated with organ dysfunction distant from the site of infection, it is called severe sepsis. When sepsis is accompanied by HYPOTENSION despite adequate fluid infusion, it is called SEPTIC SHOCK.
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Sepsis is a pervasive problem in hospital and other care facilities that causes an alarming amount of preventable deaths. Please review the attached document for more information on this problem to generate awareness and develop more scientific interest in eliminating the problem.
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Thank you, @ ,Beth Ann Fiedler ,Beth Ann Fiedler your information on this life-threatening emergency in developed and developing countries is apt. The threat of antimicrobial resistance in developing countries and upsurge of patients with pneumonia, UTI, malnutrition, immunodeficiency related diseases just to mention but a few coming down with sepsis is alarming. Sepsis is an important public health challenge, therefore creation of massive awareness Campaign on sepsis, and partnership with public health professionals, clinical experts, patient's advocacy groups and the public will cause more people to survive sepsis or avoid it entirely.
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I have read different protocolos both fast and slow instillation methods and using various volumes of bacterial suspension. I would need to know a standard protocol for intranasal instillation with good recovery of bacteria in lung.
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Hi,
I have been struggling to categorise two studies, which needs appraising. Both are 'before-and-after study', which implemented an intervention to the 'after' group and compared the results with 'before' group. Does this make it a cohort study? Which tool should I use?
The studies are:
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It sounds like a retrospective cohort study.
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UTI and maybe sepsis are occasionally encountered after URS and PCNL. From your daily practice What are the possible strategies to prevent infection after RIRS or PCNL?
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Hi, in our practise we routinely do Urine CS one week before PCNl if positive start antibiotics. If urgent need of surgery and patient is asymptomatic TLC is normal, even with urine CS positive we do PCNL with atheist few dose of preoperative antibiotics.
During surgery we do give antibiotics at the time of induction of surgery.
And at the time of stone breaking we guve one dose of amikacin along with lasix.
Post operative we do give antibiotics as required till discharge.
Of Pus during initial puncture we keep PC N for drainage and do surgery later
Thanx
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i tried performing a CLP procedure to induce sepsis in mice and i followed all the instructions in advertised protocols and videos.
after performing the procedure, even a successfull and clean one, with minimal injury the mice did not wake up and even died right after.
any one has an idea what could go wrong?
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Wrong anesthetic practice
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i tried performing a CLP procedure to induce sepsis in mice and i followed all the instructions in advertised protocols and videos.
after performing the procedure, even a successfull and clean one, with minimal injury the mice did not wake up and even died right after.
any one has an idea what could go wrong?
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I think you need to consider the surgical procedure especially the anaesthetic agent. Using ketamine with xylazine combination need to adjust carefully.
Personally, based on my experience with surgical procedures in mice, I prefer using an inhalation anaesthesia agent.
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What is the most common type of surgical site infection?
How do surgical site infections occur?
Can you get an infection 2 months after surgery?
What kind of infection can you get after surgery?
How common are surgical site infections?
What are the signs of sepsis after surgery?
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You can acquire SSI within 3 months of surgery.
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I work on UTI and sepsis. We find occasionally community-acquired UTI due to ESBL-producing E. coli which does not fulfill the MDR criteria (Magiorakos et al. 2013), because they are sensible to all other antibiotics. I have been searching for literature about this, but I have not been able to find studies that describe this fact.
Have you read studies that describes non-MDR ESBL-producing Enterobacteriaceae? Have you also found this?
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It's seems different,
Maybe this article help understanding of it and finding some facts direct you to the right answer
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Like three prevalance study design
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The general role in estimating prevalence is dividing the outcome of interest or an event (old or new) over the population group of interest at a specific period of time. Therefore, the sample size shoud be calculated out of the particular population of interest.
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PCT (Procalcitonin) is a biomarker of sepsis. There has been a link established between SARS-COV-2 and sepsis, but the understanding for how they interact in the body is not well understood. Would monitoring a patient's PCT levels be important in controlling COVID's impact in the body? Could a person's PCT levels be a biomarker for SARS-COV-2 severity?
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Elevated PCT (procalcitonin) levels are positively associated with the severity of COVID-19.
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any research relating to pre-hospital treatment for sepsis in the UK.
will early treatment of sepsis from the ambulance reduce the mortality rate?
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I think you might be looking for this sort of thing;
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Dear RG researchers, may I know how many of you found low lactate level associate with high sepsis mortality? I do encounter many of these cases in Malaysia. Theoretical, the low lactate is due to low pyruvate reserved in patients who had poor oral intake lead to starving.
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Lactate levels are good predictors of mortality in patients with sepsis
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I am going to study about cell population data generated by automated hematology analyzers related to Neutrophils in sepsis.Study will compare medians of several parameters between normal control group and sepsis patent group.So what would be the sample size determination formula? study is case unmached type and conventional formula needs "Percent of controls exposed"
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use the following equation
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  • late sepsis is a very important cause of mortality and morbidity in NICU , I wanted to know is there any body have experience about covid 19 in neonates who hospitalized due to late sepsis but the final diagnosis is covid 19.
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I am eager to know that, in my country, I haven't seen it
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what food and nutrient will recommend to sepsis patients after recovery? This is related with covid-19 to suggest to patients after discharging.
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i think need to follow fluid requirements
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Hi. I am looking for manual method for sepsis DNA extraction. No kit based method required. Can you please suggest some good protocols? I want DNA extraction of both, cfDNA and bacterial cell DNA.
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Did you ever find good resources? I'm looking for the exact same thing actually. Thank you in advance if you can send links for some materials!
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Sepsis is a life-threatening condition that arises when the body's defense reactions against infection damage its own tissues and organs. It is one of the most serious complications of infectious diseases caused by bacteria, viruses, fungi or parasites. There is no scientific literature that shows a connection between surviving sepsis and developing the new coronavirus. There are sayings tell that there are many of cases have developed sepsis. Do any one has Information
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Sepsis is a poorly understood condition with surge in cytokines. However there is functional immunosuppression. What's your view and experience?
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Immunosuppression in sepsis is a real problem and very individual. Epigentic and metabolic reporgramming as well as the chronic release of DAMPS during the course of sepsis influence immunosuppression. The high prevalence of secondary viral infection (e.g. EBV, CMV) is one result of these processes. You might also find this articel informative.
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In my hospital practice, I have a lot of patients with various acute infections of different severity, and most of them with severe infections and sepsis have hypoalbuminemia of various degrees, as we all know, as a part of the acute-phase response. My question: Should we treat this hypoalbuminemia with albumin substitution or not, and if yes, what would be the albumin serum levels when we should start treatment, and what would be dose and percentage of albumin solution for substitution? I would like some references also.
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This question is debated for decades and you find plenty of literature for both standpoints. In my opinion you should treat a severe hypoalbuminemia (<20g/l) in fluid-resistant hypotension. You might also want to follow up the ongoing ARISS trial (NCT03869385).
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Dear researchers,
are any of u aware of any studies that have looked at obesity sepsis and metabolomics ? I am looking for studies that will look at obesity sepsis and metabolomics ?
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Hi, This is a very interesting and relevant question for the entire research community working in metabolomics. Please feel free to register (for free to create a login with your Email ID!) and join the International Metabolomics Society’s Forum: http://www.metabolomics-forum.com/index.php?action=forum;?action=forum#c12 to ask more specific questions any software, database, approach and platform (mass spectrometry, NMR) issues where you can get very specific responses from expert users and researchers! Thanks again, Biswa
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I have a 13 amino acids peptide and I want to inject it in mice to induce immunization. The injection will be in the tail vein. After 12 days I expect to have a peak in the production of antibodies, so in the 12th day after injection I will challenge these mice and matched controls with bacteria and perform a mortality curve. I believe this kind of immunization will be protective and prolong mice survival. How much peptide should I use to induce the immune response? One dose is enough? Do I need to inject it several times? When and how much?
If everything works well, I want to produce a monoclonal antibody against this peptide and inject it after the bacteria injections in non-immunized mice to see if this monoclonal antibody works as a new treatment for infections. How much antibody should I inject to try to treat wild-type mice with a monoclonal antibody? One dose is enough? Do I need to inject it several times? When and how much?
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many thanks, Markus and Aldo
I found that PEGylation prolongs the circulation time of proteins by decreasing the kidney filtration. PEGylation also increases the stability of proteins and decreases the immunogenicity of proteins, so I believe it is more appropriated for therapeutic than for immunization purposes.
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Currently working on a paper trying to capture Failure to Rescue by utilizing a clinical decision tool embedded into the EHR. I want to base this tool on SOFA scores and have the RNs utilize a qSOFA for patient's they have concerns about.
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We the non physician grs should nicely enjoying the discussion regarding SEPSIS-
A great cause of death . I specially thanks to Dr.Janeena Ieraci & Dr.Md Rabiul Alam
for technicalities of sepsis like EHR & qSOFA .
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While more than half of the ICU patients have either sepsis/infection or are on antimicrobial - How we practice infectious diseases differ significantly between an ICU and other even in the same country (sometimes even different ICUs in the same hospital).
Understanding such practice is fundamental to improve patients' outcome, antibiotic resistance, length of stay, morbidity as well as antimicrobial resistance.
Can you help by answering this survey:
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I have observed in recent years that critically ill patients in the ICU are sometimes maintained on mechanical hyperventilation with propofol sedation. ln my opinion, this is harmful and counterproductive. All hypnotics are inherently toxic, including anesthetic inhalation agents. The toxicity of propofol is notorious. George Washington Crile described how he cured sepsis and peritonitis 100 years ago when primitive needle technology made intravenous access impractical. He used massive doses of intramuscular morphine that caused his patients to become essentially comatose for up to a week, without the help of intravenous fluids or even antibiotics. This cured cases of sepsis and peritonitis. Crile had discovered the nervous component of what was then called "shock". He describes his discoveries and treatment strategies in his famous book called "Anoci-association" that can be accessed free of charge via the Internet. With our modern machines, medications and monitors we can do better. We can safely maintain deliberate high levels of "permissive hypercarbia" that offsets the respiratory depression caused by modern synthetic opioids; the combination works like love and marriage. Hypercarbia optimizes cardiopulmonary performance and enhances the release of oxygen from the hemoglobin molecule, and therefore optimizes tissue oxygenation. This is helpful in all forms of sepsis and especially helpful in stubborn cases of infestation with "facultative anaerobes" that proliferate in poorly perfused and oxygenated tissues where antibiotic "penetration" is limited, such as Lyme Disease, MRSA and so forth. Last, but not least, non-toxic opioid supplementation reduces reliance on toxic hypnotic agents. The best choice for a hypnotic agent is anesthetic inhalation agents, which can be maintained at precise levels, adjusted quickly, and rapidly rid from the body. These principles could revolutionize the care of critically ill patients if they were fully utilized.
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I am currently working with sepsis patients and I want to extend my research to cultures of monocytes from human blood. Does anyone have a reliable method to purify monocytes for culture?
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Yes. But you could ask to them to lend you a magnet if you don't have one already. They tend to do that.
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I want to run a meta-analysis on "corticosteroids in the treatment of severe sepsis and septic shock". Unfortunately it is already done. What do we do in such case? Can it be done again? Any suggestion would be appreciated. Thank you in advance.
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If you think your selected topic has already been done then why on earth would you want to pursue it? Meta-analysis is a design used to answer a gap in knowledge and if that gap does not exist then why do you still want to pursue a meta-analysis? A new meta-analysis should only be undertaken if a gap in knowledge exists and you believe you have the expertise to undertake a meta-analysis whose purpose is to conclusively answer a critical question.
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If you have devised any new parameters for sepsis
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Surviving Sepsis guidelines are clear on definitions in sepsis and septic shock. However, bundle in sepsis is the best strategy for our patients.
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Dear friends,
Recently, we use LPS to induce 24h-mouse spesis model to explore the effect of some drugs to splenic Treg expansion. However, sometimes we failed to induce sepsis and splenic Treg expansion after LPS i. p. injection. I asked some friends and they told me that the mice in USA and mice in China have different lethal dose of LPS injection. In addition, they encourage me to use LPS produced in China, which may be a misture instead of ultrapure LPS from sigma. I wonder why sometimes LPS failed to expand Tregs in mice? In addition, may I know the different between LPS from Sigma and beyotimes? May I know some details about LPS subtype and application in experiments.
Yours
Shuoyang Liu
LPS from sigma is:
L9764 Sigma-Aldrich Lipopolysaccharides (rough strains) from Salmonella enterica serotype minnesota Re 595 (Re mutant).
LPS from beyotime(China) is : lipopolysaccharide purified from E. coli O111:B4, which is specific for TLR4 activation or TLR2.
The mice are bought from other labs. The body weight is from 17g-19g. The mice from other labs and from our breeding sometimes are different in response to LPS induction.
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Why are you using LPS isolated from different bacteria?
Even LPS isolated from different stains of E.coli will have differences in activation/stimulation of immunity.
You can buy LPS from E.coli O111;B4 from Sigma too.
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How is it possible these threads are now appearing? Can there be a correlation?
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If silk was used while closing the fascia, it may cause a local and sometimes systemic reaction. A granulation tissue may adsorb the silk threads and within time the granulation tissue drains to skin and this is how you see threads many times after the surgery
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I want general information about sepsis and related mechanisms. If you provide me general informatin and details I will thankfull.
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This is the fundamental. All other details you can find from the literature at the end of manuscript.
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Dear researchers,
Have any of you come across specifically publications looking at Right ventricular diastolic dysfunction and sepsis ? I dont there are any studies out there ? if there are any could you forward me the citation please
cheers,
Rakesh
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kindly inform what dose is suitable to get sick. I hope not to lose them so quickly. I don't need a sepsis and septic shock model.
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take a look at Mc Allen RM, AJP, last paper in AJP
THE ANTI-INFLAMMATORY REFLEX ACTION OF THE SPLANCHNIC SYMPATHETIC NERVES IS DISTRIBUTED ACROSS ABDOMINAL ORGANS.
Martelli D, Farmer DG, McKinley MJ, Yao ST, McAllen RM.
Am J Physiol Regul Integr Comp Physiol. 2018 Dec 21. doi: 10.1152/ajpregu.00298.2018. [Epub ahead of print]
PMID: 30576218
Similar articles
This may help. Best. LQ.
@
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I want to conduct a parallel trial study in which 3 care bundles will be implemented aimed to decrease neonatal sepsis.How is sample size calculated?
Data to be collected from patients will be clinical signs of sepsis and blood samples for culture to determine the presence of infection. The outcome variable will be incidence of neonatal sepsis among participants.The study aims to evaluate the impact of the intervention on incidence of sepsis. What will be the best method to analyze this data
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Hi
For sample size calculation you will need what is the current incidence of sepsis and what amount of changes you are expecting from the intervention. You can go for both randomized and non-randomized design. In the sample size calculation, you have decide how much absolute precision (1-alfa) and power (1-beta) you want. Usually, absolute precision of 5% and power of 80% is acceptable lower limit. If your trial is non-randomized, it is better to put a design effect. You can use online free statistical site www.openepi.com for this.
For analysis, it depends on the data. but from your objective, it appears that you will require unpaired t-test, Fisher's exact/Chi-square test. You can also calculate the sensitivity and specificity if the intervention is diagnostic and calculate the area under the curve for all interventions. For this you have to have one gold standard (these tests will be required if intervention is diagnostic only). At present statistical software also prompts what tests are appropriate provided you enter the data type correctly.
Hope this helps you
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i think the methods used to detect the septicemia and bacteriemia is critical and need a professional Technic . isn't it?
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The yield of the cultures with blood or plasma is better than with serum. The same applies to molecular diagnostics with better yield from plasma as compared to serum. The yield is poor with serum.
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Imagine you have sepsis whole human blood (heparin), if you centrifuge, where the bacteria/fungi will be at? Are the bugs in plasma or with human cell?
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I agree with Dr.Evers .
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Dear Researchers, I am trying to induce Motile Aeromonas Septicemia in Loach (15 gram)fish by injecting fish pathogenic strain of Aeromonas, injecting intra- muscular,at different doses 10^6 ,10^7. But there are no sign of disease (7 days)
The water temperature is 26c .Fish were kept without any feed, 3 days prior to experiment to induce the stress.
Please provide your kind suggestions.
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Good proposal, I hope you find answer, you can check the following
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Dear researchers, I share with you this important and interesting article, I hope it is of your interest and that you recommend it and share it because it is of interest
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Nice read, I agree with some previous comments, I liked that reference #13- year 2014 artcile with comprehensive review - Catia Cillóniz Ian Ewart
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Vitamin C is an important anti-oxidant and an enzyme cofactor for many important biological reactions . Sepsis is associated with an acute deficiency of vitamin C , recently vitamin C-containing regimens as adjunctive therapy in sepsis have received much attention.
What do you think, some experience?
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Linus Pauling who won the Nobel Prize twice wrote a book on Vitamin C and suggested that we take at least 4,000 mg a day. I have been taking 3,000 a day for the past 20 years and seldom do I get sick! Amir
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Mouse models of endotoxemia (such as an LPS injection) are associated with increased cell death. Such as increases in cell death seen in the spleen.
In human patients with endotoxemia I think cell death is also observed. However, I am unsure where it occurs, to what degree, what cells? What similarities are there to the mouse model?
I would assume there is. However, I don't know any critical-care clinical pathologists to whom I can pose this puzzler.
I can mention that this 12 year old article by L. Moldawer makes reference to cell death in humans; http://www.fasebj.org/content/15/6/879.long Back then it was of course referred to as apoptosis. Which, IMO is a just a general term used by many people for cell death.
What new information is out there regarding cell death observed in humans? Are there any existing treatments which attempt to address/prevent cell death in human clinical endotoxemia (assuming it is looked for)?
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Agree with Hans-Dieter Volk. In contrast to murine endotoxaemia, in human no standardization may be achieved. We had several studies of LPS, EndoCAb, cytokines, and apoptosis markers as well, etc. in both humans and rats. Comparing is difficult as humans have disease status when raised LPS is only a part of condition, while in rodents we use industry made LPS with standardized source, activity, etc. PCT, lactate, total cholesterol or other markers are useless when trying to achieve direct effect of LPS. Furthermore, LPS-binding protein influences the pro-apoptotic effect of LPS multiple times. Same levels of serum LPS under different conditions (for example, sepsis, IBD or fatty liver disease in our studies) cause different levels of apoptosis.
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I am interested both in positive outcomes and the implications of policy including: impact on practice, the amount of antibiotic use (maternal and neonatal) both where sepsis is proven and not proven, length of hospital stay, psychological effects on the mother. How many mothers and neonates are we treating to reduce the risk of negative sepsis outcomes? Does the use of broad spectrum antibiotics in the initial response provide us with a false re-assurance and delay recognition of the underlying infection that requires a different response?
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the link is mainly related to effect of the microbiome, but some clues
check the ORACLES studies on maternal antibiotics to delay preterm birth in mothers with or without ruptured membranes.
on neonates, some recent meta-analyses:
Reviewing the WHO guidelines for antibiotic use for sepsis in neonates and children.
Fuchs A, Bielicki J, Mathur S, Sharland M, Van Den Anker JN.
Paediatr Int Child Health. 2018 Nov;38(sup1):S3-S15
Antibiotic exposure in neonates and early adverse outcomes: a systematic review and meta-analysis.
Esaiassen E, Fjalstad JW, Juvet LK, van den Anker JN, Klingenberg C.
J Antimicrob Chemother. 2017 Jul 1;72(7):1858-1870.
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We are addressing sepsis and how the family can be part of the alert process. We are partnering with our Patient and Family Engagement department and were just wondering if this will be part of your research ? thanks
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What you're proposing isn't a part of any research here formally,but has been highlighted yet again in the UK news recently where the family of a child with sepsis were not only the first to realise,but tried on several occasions to get appropriate care.
Family involvement could clearly play an increasing role in early diagnosis and management of sepsis.
Good luck.
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Working in a medical college in India as the head of department of obstetrics I get to see a lot of cases of sepsis in obstetrics . My interest is both in enhancing my own knowledge and contributing our experiences to studies or analysis dealing with this issue
My email ID amitarays@gmail.com
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yes you can join our research .but what is the type of patrticipation you can share us?
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I was wondering if any of you are aware of any sepsis pertinent severity score, not APCHE or SOFA?
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Thanks.
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Inflammatory mediators promote insulin resistance, suggesting perhaps that critical care patients may exhibit hyperinsulinemia. However, I have great difficulty finding an article referring to serum insulin levels (there is an overabundance of publications on hyperglycaemia and insulin resistance but not insulin).
I would very much appreciate it if anyone can refer me to a manuscript making reference on insulin levels in any severe inflammatory setting (burns, sepsis, trauma, and surgery… any context where a strong inflammatory response is solicited).
Note: hyperglycaemia is often treated with intensive insulin therapy –it would be super if the study refer to untreated patients.
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Hi Ian, many thanks!
Honestly, I was absolutely smitten as why I could not find any reference to serum insulin levels. However, that there is in fact not many publications on this topic is even stranger though...
In any case, articles definitely seem relevant. Will most certainly have a closer look -thanks!
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I am currently writing an assignment on use of IVC Point Of Care Ultrasound to assess Dehydration in Elderly Patient, more talking about sepsis induced dehydration in Emergency Department. If you have personal experience or aware of a relevant publication please let me know
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this study was conducted with patients of aged median (5th and 95th percentiles) of 63 (6 -70) years found that in spontaneously breathing patients with ACF, high cIVC values (>40%) are usually associated with fluid responsiveness while low values (< 40%) do not exclude fluid responsiveness
IVC collapsibilty index measured by ultrasound is useful for the detection of early intravascular volume change induced by 2 min passive leg raising. However, its ability to detect the increased Intravascular volume value is influenced by age, BMI, and baseline CI. Moreover, they found poor sensitivity.
As vascular calcification is common in elderly, it may affect the collapsibility and therefore a hypothesis that elderly population may respond differently is possible and will require further direct research.
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For example Patient came with Post trauma sepsis and doctor ordered Inj. Meropenem . Now If in this case doctors need emergency Craniotomy. now how would you suggest surgical prophylaxis in terms of Drug, dose and duration??
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The aim of perioperative antibiotics is prophylaxis of infection caused by surgical trauma. If you are performing craniotomy, you need antibiotics against skin pathogens (e.g staphyloccocus), by urogenital surgery against typical uro bacteria, (e.g for E.coli Ciprofloxacine).
If you have other source of infection and antibiotic therapy you need to check, if your antibiotic therapy is effective for the bacteria on your surgical site.
Secondly, the timing of antibiotics before surgery is crucial. Before your incision, you need effective dosis of antbiotics in your surgical site. 30-60 Minutes before incision is the recommendation.
In Your case I would suggest:
mostly the therapy plan of meropenem doesn´t match with time of surgery, you do not have guarantee for the peak level of antibioticasin your surgical site. I would suggest the additional dose of cephalosporine (eg. Cephazoline) 2g (in 10ml Saline). You give 1 ml testdosis the check allegic reaction, than the rest. The timing 30-60 before incision.
If the surgery takes longer than 4 hours, you give the second dose.
at the day of surgery you give one dosis cephalosporins at night after surgery and the last one the next day. You have very good effectivness of cephalosporines against staphylococcus.
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For exemple in sepsis model some researchers use intravenous inoculation and others intraperitoneal.
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I think intraperitoneal administration is easier to achieve from the perspective of compound solubility and injection volume. IV administration requires that the compound be dissolved, and limits the injection volume. For a compound with poor solubility, IV may be not allow a sufficient quantity of the compound to be administered in a single dose. Another option, is IV infusion, in which the dose is delivered by an infusion pump over several hours, allowing a larger volume/more dilute solution, and therefore greater exposure to the compound.
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Any strong evidence for c-reactive protein and albumin ratio in sepsis as predictor of mortality ?
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I am going to send you several studies from Manu Malbrain and colleagues, from which I first heard for CRP/Alb ratio or CLI (capillary leak index). They have an idea of resuscitation and deresuscitation in septic shock. I think this will help you a little bit. Anyway, good idea which should be investigated and spread.
PS. I tried....it works if the time is correct.
Wish you all the best.
Natalija
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Always we use low dose (max 75mg/die) of diclofenac intravenous infusion during septic shock or sepsis when physically or with others therapies it's not possible to reduce temperature to avoid its emodinamic and metabolic effects. Many times, without renal adverse effects, it seems a good choice and often it changes the global clinical set of the patient.
Have you any study regarding this aspect?
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It is controversial if controlling fever can affect patients' outcome. Apart from specific subgroups (Neuro, IHD where tachycardia can induce ischemia). Moreover, in sepsis, we monitor response to antimicrobials by monitoring the temperatur. So, and in order to avoid the undesirable NSAIDs, I think paracetamol in general is more than enough.
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Hi, does anyone have an information regarding further treatment options for a 61 year old male with mCRC with secondaries to the left lung and mediastinal nodes who has DPG deficiency confirmed after two doses of Avastin and Folfox when he presented with neutropenic sepsis/typhilitis and local perforation. Any options other than single dose irinotecan?
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Hi, try with mitomycin C plus irinotecan, or with regorafenib or pemetrexed. You can find several phase II trials suporting this therapies. 
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Presently I am using the following steps:
1.    I'm using freshly collected blood in EDTA- vacutainer tube.
2.    Then, the blood was dilution at 1:3 ratio (blood: Media) in a cell culture plate at 37oC,  5%CO2 for 2h.  Then cells were stimulated with or without LPS (1-10 µg/ml)  for 6 to 24 h.
3.    Surface staining with CD14, HLA-DR, CD80, and CD86 was performed for flow cytometry.
I am trying to quantify the expression of above mentioned surface markers in monocytes gating. So far I have obtained poor results.
The problem is that I am not getting proper results and non-reproducible results.
Any hints or tips would be well highly appreciated.
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Dear Sagar,
Your problem is likely EDTA, try Heparin as the anticoagulant instead, this usually works fine. No need to place the cells in culture media, the blood is a rich source of everything they need. Best regards Christoph
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While using antibiotic Ceftriaxone in mice for  CLP model of sepsis, it is always used with some other antibiotics like metronidazole or clindamycin and not alone. Can't we use ceftriaxone alone at higher dose.
Thank you
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Komal, 
Ceftriaxone is inactive against most strains of Pseudomonas aeruginosa, many strains of Enterobactor cloacae and methicillin resistant strains of staphylococci. This is the primary reason to utilize dual therapy. 
Regards,
Christopher
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sepsis among diabetic elderly- impact on their survival - is this too narrow or too wide?
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One way to approach the topic is as folllows:
1.  define sepsis rigorously
2.  separate sepsis from other types of infections in diabetic elderly patients
3.  you may want to separate sepsis into 2 groups:
3.1  septic elderly diabetic patients "who require intensive unit care vs.
3.2  septic elderly diabetes patients" "who are treat on a hospital ward."
Please let me know if the following references/sites are helpful to you:
1.  Severe sepsis and septic shock in the elderly: An overview
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3956061/Feb 4, 2012 ... The elderly are predisposed to sepsis due to co-existing ... as cancer, diabetes, obesity, and human immunodeficiency virus, among others[6].
2.  Sepsis Linked to Dementia in Elderly - WebMD
http://www.webmd.com/healthy-aging/news/20101026/sepsis-linked-to-dementia-in-elderlyOct 26, 2010 ... Oct. 26, 2010 -- Sepsis is a leading cause of death in hospital ICUs, and the elderly are particularly vulnerable to the life-threatening blood ...
3.  Sepsis Requires Urgent Attention - Today's Geriatric Medicine
http://www.todaysgeriatricmedicine.com/archive/050613p26.shtmlThey know about heart attack, stroke, diabetes but not sepsis.” ... nearly normal in an elderly patient, preventing the connection to sepsis from being obvious.
4.  Sepsis in Elderly Patients - Nursing Home Abuse Guide
http://www.nursinghomeabuseguide.org/injuries/sepsis-in-elderly-patients/Anyone who has an elderly loved one as well as anyone who works in a nursing home must know the signs of sepsis so that it can be recognized as quickly as ...
5.  Sepsis Symptoms, Treatment, Causes - What are sepsis (blood
...
http://www.medicinenet.com/sepsis/page5.htmMar 8, 2017 ... What are sepsis (blood poisoning) symptoms and signs? ... The very young and the elderly are at greatest risk; People who are very ill due to an ... Diabetes: Tips for Managing Glucose Levels and Blood Sugar Swings.
Dennis
Dennis; Mazur
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Dear All!
I am going to start thesis work on identifying better methods of preprocessing including normalization and imputation of missing values of microRNA in microarray data . It is request if anyone can share with me regarding microRNA data preprocessing methods of sepsis and normal patients.
best regards, Awais
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Hello Folks,
I am searching for mathematical models for Trauma induced patients with Hypovolemic shock, Spesis etc based on Non-Linear Adaptive Closed Loop Control Systems.
I would appreciate any articles or journals or thesis written that could help me develop the model various models.
Also how would you bench test these types of systems?
Thanks
Tim
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George C. Kramer of UTMB is working on similar projects. Try to contact him at https://www.researchgate.net/profile/George_Kramer3 in Research Gate. If he is not answering (your message can get lost in the multitude of the RG communications), I can ask him for permission to give you his direct email.
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We need to get the bacteria from the blood of patients with sepsis for diagnosis, is there any commercial device or prototype capable of efficiently purifying bacteria from blood sample (5-7ml)?
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We would like to know if there is anything known about the safety en efficacy of Omega-3 fatty acid administration in patients with sepsis or SIRS. 
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Start with a September 2010 nature reviews paper by Martin et.al. omega-3 fatty acids in critical illness 
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Which antibiotic is used in the latest protocol?
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I think Medscape is so helpful (link below)
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My group is trying to validate a real time PCR detection method for contaminated Total Parenteral Nutritional samples, using 16s rRNA as a target. For this, we need a method of isolating bacterial DNA from this lipid, glucose and amino acids rich sample. Our objective is to create a faster way of diagnosing sepsis in intensive care patients, as the traditional method of culturing takes up to 4 days.
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Hi Diego. What a good idea!  I have not done DNA extraction from such material, in fact in my google scholar search I could find no reference to it. However, I suggest good starting point for this work would be to test kits that are suitable for blood, serum, stool and/or food.  In particular, there are several papers concerning extraction of bacterial DNA from milk. Some of the methods/kits for food will have more mechanical and enyzmatic digestion required for your samples.
Almost certainly a column based method will be appropriate.  If you have the money, it's worth checking out Qiagen kits - whenever I have used them I got good results.  If you have a chat with the technical help people at the companies that make the DNA extraction kits I am sure they will be very helpful, and possibly even supply you with free samples.  
Here are a few articles to give you some ideas:
Best regards
Roger Latham
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Sepsis, Nephrology, Internal Medicine.
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Based on meta-analyses (eg, Vasu, J Intens Care Med 2012) and the SOAP II trial (De Backer, NEJM, 2010), we prefer norepinephrine over dopamine in shock.
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Any clinical experience in using ursodeoxycholic acid in sepsis induced cholestatic jaundice?
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ursodeoxycholic acid is a  chelator of bile acids, has cytoprotective and immunomodulatory effects, it has been used to treat cholestatic diseases .it could be considered for sepsis-induced cholestasis , but no data currently support such an assertion.
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According to analyses the strain is also able to adapt very quick.
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What happened to piperacillin/tazobactam sensitivity?
The use of carbapenems agains these urinary pathogens is risky, as you can see with the most recent antibiogram.
The first step when we face against multiresistant urinary gram negative bacteria is to separate infection from colonization. In case of infection, we must define if it's confined to lower urinary tract (aka cystitis) or if we have bacteriemia. In cystitis, due to an extraordinary multiplication of urinary concentrations, even in vitro resistant antibiotics may work in vivo. It happens for TMP-SMX, nitrofurantoine and norfloxacin.
For urinary sepsis our last weapon in Portugal is IV colistin. Off label, in my hospital, we use sometimes intravesical colistin: no systemic side effects and good results in eradicating MR Klebsiella, providing no sepsis is suspected.
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I read in an article written by Daniel Rittirsch published in 2008 (Harmful molecular mechanisms in sepsis) that a sepsis can trigger thrombosis and large-scale haemorrhage simultaneously. I just wondering why patients with a sepsis triggered stroke are treated with thrombolytic substances. These substances are already hazardous for patients without sepsis in concern of brain haemorrhage. The combination of the enhanced bleeding risk due to the sepsis and the thrombolytic substance most likely result in a considerable higher probability of the occurrence of a brain haemorrhage compared to the treatment of a “normal” stroke.
Does anyone have an explanation for this doubtful therapeutic approach?
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Dear Martin,
The following recent review article entitled " Absolute and Relative Contraindications to IV rt-PA for Acute Ischemic Stroke" published in Neurohospitalist. 2015 Jul; 5(3): 110–121 may shed light on the use of IV rt-PA for Acute Ischemic Stroke:
Abstract
Most of the contraindications to the administration of intravenous (IV) recombinant tissue plasminogen activator (rtPA) originated as exclusion criteria in major stroke trials. These were derived from expert consensus for the National Institute of Neurological Disorders and Stroke (NINDS) trial. Despite the fact that the safety and efficacy of IV rtPA has been repeatedly confirmed in large international observational studies over the past 20 years, most patients with acute ischemic stroke disappointingly still do not receive thrombolytic treatment. Some of the original exclusion criteria have proven to be unnecessarily restrictive in real-world clinical practice. It has been suggested that application of relaxed exclusion criteria might increase the IV thrombolysis rate up to 20% with comparable outcomes to thrombolysis with more conventional criteria. We review the absolute and relative contraindications to IV rtPA for acute ischemic stroke, discussing the underlying rationale and evidence supporting these exclusion criteria.
Hoping this will contribute to the discussion on this very important issue.
Rafik
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Our NICU wants to send heel prick blood for sepsis for work up. Query any experience in this? Any helpful suggestions to reduce contamination rate?
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Hello Omar,
It's an interesting thought. One could use Hydrex - 0.5% Chlorhexydine with 70% alcohol - to prepare the skin although I suspect one would need to prep the entire foot to be sure. I don't see why not but as an exception as opposed to as standard, as the risk of false-positive would be higher - one can test that in a study of course. However, it would be hard to maintain the same rigour of antiseptic cleansing in "real life" compared to study conditions. Let me know how you get on with it, cheers, Art
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metabolic demands of fever vs the natural response to infection.
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Fever should be treated only when it is higher than 41 celcius, or when it is causing symptomatic disturbance to the patient like diaphoresis, anxiety, tachypnea, tachycardia and/or hypotension. However we use antipyretics only as needed, not in a long term basis as fever is an important sign to follow the response to treatment or to identify the presence of a new infection or resistance to treatment. 
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While reading different books ,I found many confusing things about the indication of anticoagulants in sepsis. Is there any particular guidelines for the indication of anticoagulants in sepsis?
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The HETRASE trial randomly assigned 319 patients with sepsis to receive low dose intravenous heparin (500 units per hour) or placebo for seven days. The trial found no improvement in any clinical outcome. It has been suggested that the conflicting results were due to the randomized trial using a low dose of heparin; as a result, a randomized trial comparing various doses of heparin in patients with septic shock is being conducted:  http://www.clinicaltrials.gov/ct2/show/NCT01234285
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Pre-transplant splenectomy enhances allograft survival in adults, but that possibilty is unknown in children, whereas splenectomy in children is associated with overwhelming sepsis. 
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Dear Michaela Yakubovich-Dirks ,
Sorry for delay to see your question or doubt, I´m reffering to any transplantation with prognosis risk of rejection experienced.
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Found many articles that there is always a pre-treatment before injecting the LPS (in mouse), but how can this data be interpreted considering the real status of a patient, who can't have a pre-treatment like this. 
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I think the question refers to treatment with glucosamine or another agent to make the mouse more sensitive to LPS (endotoxin). Mice can tolerate mg of LPS, while humans become ill (fever, etc) with doses in ng/kg.
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Is SIRS really not needed anymore? How does this new definition help physicians in a earlier recognition of sepsis if it is focus on organ damage (SOFA score/qSOFA)? Opinion question of course
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I agree to Roop Kishan. Close clinical monitoring of patient with impending sepsis teaches you a lot than following the algorithms and score.Of course scores and algorithms have their own place for follow up management of sepsis.
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my drug doesn't last long (~1hr at best) in the blood stream, so need know how long the lps actually remains there to cause sepsis. 
I found that treating my drug (20mg/kg bw; i.p.) after 1hr of LPS (E. coli: O55:B5, 15mg/kg bw; i.p.) made the survival rate 100% up to 33hr and then all the mice in the group died wihtin 60hrs. If LPS lasts long in blood stream then I have to inject my drug at least 3 times at every 1hr after LPS administration. 
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.....Endotoxin release is episodic and circulating LPS has a short half-life (minutes), obscuring the value of a single determination. In the bloodstream, LPS is distributed in varying proportions bound by LBP, micelles, chylomicrons, and various other lipid fractions; some of these bound moieties are biologically inactive, but most assays measure all LPS whether biologically active or not—again, making the relevance of the results uncertain.
.....The susceptibility of different animal species to the toxicity of lipopolysaccharide (LPS) is highly variable.
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Best mouse strain for sepsis model. Is there any background for selecting the appropriate strain?
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Most strains are OK to use, but you should avoid using the C3H/HeJ mouse strain as it has a mutation in TLR4 making it non-responsive to LPS treatment.
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Hello!
I believe most of you must have read the new definitions of sepsis and septic shock published in the "JAMA" latest issue. A new definition in which the SOFA score becomes a diagnostic tool and not just a prognosis-assesment one.
The score in itself is quite easy to use but when it comes to the GCS, what should one do? Most of ICU patients or those with septic shock are sedated. How can we evaluate the GCS then, should we always use the last GCS measured before sedation, or should we assign a random medium number in such cases??
Many thanks for your insight.
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Measuring GCS in the sedated population can lead to incorrect SOFA scoring, even in those patients receiving a daily drug "holiday". The lingering effects of sedatives can decrease perceived/measured mentation. So, my answer is, that there is no easy way to address this precisely. We try to assess prior to sedation, when able, then continue with this score until off sedation for an adequate period of time to clear sedative effects.
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Assay: Cytokine profile and Survival rate determination
Animal Model: C57BL/6 mouse (6weeks)
LPS: E. coli: O111:B4, O55:85, O127:B8, Salmonella enterica ser. enteritidis/typhimurium
Dose: 15mg/kg bw in 0.9% NaCl
Which one should I use?
Are there any rules/criteria for selecting LPS? 
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The E. coli: O111:B4 is the best characterized   
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LPS mediated sepsis in mice for cytokine profile to test a drug's anti-inflammatory activity. 
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LPS is well tolerated by rodents, dogs and cats (Warren et al., 2010), but it is very dangerous for humans, causing septic shock (Yamamoto et al., 2011). Rodents are 1000-10000 less sensitive than humans due to special LPS binding proteins, but I do not know, if everything is clarified. 
Warren TS, Fitting C, Hoff E, Adib-Conquy M, Beasley-Topliffe L, Tesini B, et al. Resilience to bacterial infection: difference between species could be due to proteins in serum. J Infect Dis. 2010;201:223-32.   
Yamamoto Y, Harashima A, Saito H, Tsuneyama K, Munesue S, Motoyoshi S, et al. Septic shock is associated with receptor for advanced glycation end products ligation of LPS. J Immunol. 2011;186(5):3248-57.  
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Need to know the concentration, dosage and preparation of LPS, I am going to test my drug whether it has any anti-sepsis action. 
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Dear Khan,
Please read the followings:
1-A single injection of endotoxin, or LPS, is the most commonly used toxemia model. Compared with humans, laboratory animals appear relatively insensitive to LPS and, therefore, require higher doses of LPS to produce a shock-like state. In a study directly comparing the effects of LPS, the dose required to produce similar cytokine responses was 250 times higher in mice than in humans.16 A single dose of LPS (approximately 2 ng/kg) could produce profound physiologic effects in humans (for example, increases in body temperature, systolic blood pressure, and heart rate), whereas similar signs were not seen in mice despite a much higher dose of LPS (500 ng/kg).16 The amount of LPS used to produce systemic signs in murine models varies widely, depending on the origin of LPS and mouse strain, but doses of approximately 10 mg/kg or higher are not atypical. Alternatively, doses may be reduced by sensitizing animals to LPS by coinjection of D-galactosamine.11
for more details, please use the following link:
2-Compared with humans, mice, even “normally responsive” strains, are remarkably less sensitive to the toxic or lethal effects of LPS. Thus, the dose of LPS, which leads to death in approximately half of mice (i.e., the LD50 dose) is about 1–25 mg/kg.37-39 This dose is about 1 000 000 times greater than the typical dose of LPS (2–4 ng/kg), which has been used in studies with human volunteer to induce symptoms (e.g., fever or myalgia) and the release of proinflammtory cytokines, such as TNF, into the circulation.40,41 The LD50 dose of LPS in mice is about 1000-fold to 10 000-fold greater than the dose of LPS that is required to induce severe illness and hypotension in humans.42 In other words, the roughly 40-fold difference in the dose of LPS that is required to produce toxicity or death in “normally responsive” vs. “hyporesponsive” strains of mice is orders of magnitude smaller than is the difference in LPS dose that is required to produce death or serious illness in “normally responsive” mice as compared with human beings. The biological mechanism(s) that are responsible for the enormous difference between mice and humans with respect to responsiveness to LPS remain to be fully elucidated, but recent evidence obtained by Warren and colleagues suggests that one or more factors, which are present in murine sera, but are absent (or present in much lower concentrations) in human sera, are capable of suppressing the production of pro-inflammatory cytokines by murine (or human) mononuclear cells following stimulation with LPS or other TLR agonists, such as peptidoglycan (major component of the cell wall of gram-positive bacteria), zymosan (a glucan present in the cell wall of yeast) or bacterial DNA.43 One of these factors may be the iron-binding acute phase protein, hemopexin.44 Other factors, which have yet to be identified, may be important as well. In any event, the marked discrepancy in LPS sensitivity between mice and people suggests that data obtained using murine models of sepsis may be inapplicable to the human illness.
For more details, please use the following link:
Hoping this will be helpful,
Rafik
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I want to check infection in the blood for identification of SEPSIS patients. 
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How do I diagnose sepsis (being an infection with systemic features and evidence of organ impairment)? - this is a clinical/laboratory diagnosis which combines clinical features of inflammation (fever, tachycardia, diaphoresis, apparent focus of infection) with laboratory parameters (white cell count, neutrophil count, C-reactive protein, pro-calcitonin), and where appropriate radiological evidence of a focus (CXR -pneumonia, CT abdomen -intra-abdominal collection etc...).  Ideally one also takes appropriate samples for microbiological testing, either by culture, molecular testing or serology.  The firmest diagnosis is based on a combination of clinical, laboratory, radiological and microbiological results, where all point in the same direction.  If you are specifically interested in blood stream infections, then detection of the organism of interest in the blood is the key, as blood stream infections do not generally have focal signs  (that being said a pure 'bacteraemia' without primary source is pretty rare - most bacteraemias arise from a reservoir of infection such as the lung, abdomen/renal tract, intravascular line or heart valve).
The problem is that no single one of these tests and clinical features is either very sensitive nor very specific for sepsis - they may be absent in the presence of sepsis and equally may be present when there is no sepsis.  This is why it requires an integration of multiple data sources to make the diagnosis.  PCT has been touted as a specific and sensitive test for bacterial infection, however it is not sensitive to all bacterial infections and fails to account for non-bacterial infections - its best use is probably in helping limit antibiotic therapy duration.
There are novel diagnostics either close to or on the market - the wider range of molecular diagnostics will make it easier to detect organisms which are hard to culture (due to either innate difficulty of culturing, or pre-test use of antibiotics which inhibit growth).  Markers of immune status, either soluble cytokines or cell surface markers are also touted, although the stereotyped response to bacterial and sterile insults suggests to me that these will suffer from the same problems as existing laboratory measures of infection/inflammation.
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sepsis spinal regional
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It is a very controversial topic. Infectious complications of the central nervous system (e.g., meningitis, epidural abscess, or others) following regional anesthesia on febrile / septic patients . In 2006, a well written paper by Dr. Horlocker from Mayo Clinic summarized the conflicting results of the studies that examined neurological complications in septic patients undergoing regional anesthesia (Link). Recently and to my best knowledge, my research group have a developed the first meta-analysis of individual participant data (in Peer review yet) on this topic. A total of 234 meningitis cases were found following regional anesthesia, 199 of them were related to spinal anesthesia, of which only 2 cases had previous bacteremia / septicemia. However, it is important to say that in 110 of the 199 cases had not a clear cause of infection (not reported).
In conclusion, actually, there is not a general consensus. As for the actual clinical practice on this topic, sepsis or bacteremia is not still a contraindicated condition for spinal neither epidural anesthesia. 
Of course, it is advised to follow an aseptic technique during the procedure and, from my perspective, wearing surgical masks because the droplets may be a potential source of infection according to our recent work.
Hope this help to answer your interesting question.
Regards
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My name is Jeremy, I am a senior staff nurse working in a general medical and surgical ICU in the UK.
With recently reading some work on Immunomodulatory Effect of Continuous Venovenous Hemofiltration during Sepsis: Preliminary Data.
As such I would like to ask for the readers help and advice.
With some of our septic patients experiencing acute renal failure needing CVVHDF, I have posed the question, that as yet I can find no answer to.
With 'normal' patients in ARF on CVVHDF, they would become hypothermic to a temperature of 35 Degrees or below. Hence needing active warming through a Bear Hugger and filter heater aids.
With septic patients on CVVHDF, I have seen temperatures of 36-37 Degrees with no heater elements to aid this.
If this is the case, should we not then be complementing them with heater elements to achieve an active temperature of 38-38.5 Degrees? As you may see in the normal immune response to increase an individuals temperature.
Patients are not actively given antipyretic's due to the researched based evidence of increased mortality.
If we are placing septic patients on CVVHDF, then we are actively cooling them! As such, are we not increasing the patients chances of mortality and morbidity?
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Fabulous question. I thought one of the reasons we avoid administering pharmocological antipyretics was their anti-inflammatory effects not necessarily the effect of reducing core temperature. CVVHDF cools by convection so the effect of cooling is confined to the reduction in temperature rather than the effect on of reduced cytokine release on the inflammatory response. 
I will continue to follow this question with interest. 
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A patient with paraneoplastic hypercalcemia from metastatic neuroendocrine pancreatic neoplasia shows very high levels of both procalcitonin and calcitonin, in the absence of clinical and lab findings of sepsis. Does anyone have an explanation for this situation?
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PCT is a relatively specific marker of bacterial disease and may be produced by various organs including the thyroid, liver, testis, lung, prostate, kidney, and small intestine, but the secretion of PCT by a tumour has mainly been reported in small-cell
lung carcinoma and medullary thyroid carcinoma or neuroendocrine neoplasia.