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Prevention - Science topic

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Questions related to Prevention
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I have been asking for the questioner (and only the person asking the question) to be able to downvote an answer and remove any points associated with the irrelevant answer. I do not suggest this is anonymous, and I do not suggest anyone but the questioner be given that ability. I know that previously, anyone could downvote for any reason and that this was done anonymously.
I don't ask many questions and when I do, they are very specific questions. I'm often dismayed that the person answering has obviously NOT read the whole question or worse, is plainly scamming the Research Gate score system.
The whole idea is to remove any points the scammer has obtained for answering the question so that they STOP giving, worse than useless answers. i.e. it removes any incentive to reply and game the system.
Better still would be the ability to delete such an answer from our questions but I doubt we could ever get that.
Be warned, I already report such answers to Admin. You are welcome to join the discussion but don't give a scam answer!
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The irony is that often the most worthless answers are those that get a good number of up-votes. For a community-based approach, I suspect that we don't have a robust enough group of active members to fight the tide of up-votes for worthless or misleading answers. And I suspect the people posting questions often don't have the expertise to know which to down-vote. A viable approach is to have communities and moderators (e.g. Reddit). Or to have enough active, knowledgeable members (like e.g. https://stats.stackexchange.com/ ) to dispense with unhelpful or ill-informed answers. I'm not sure any of these approaches would work here. But I really would like the opportunity to down-vote responses that show no effort towards reading the question, reading the other responses, or giving the least consideration as to what might actually be helpful for the questioner.
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Hello,
I am writing my BA thesis about the trend of "medical wellness" in the sector of health tourism.
Therefore, I am looking for literature in this field, specifically about health tourism and medical wellness tourism in general as well as the differentiation of target groups attracted to it.
I am very thankful for any literature recommendations.
Thank you in advance.
Noemi
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My searches have found these so far:
Zhong L, Deng B, Morrison AM, Coca-Stefaniak JA, Yang L. Medical, Health and Wellness Tourism Research-A Review of the Literature (1970-2020) and Research Agenda. Int J Environ Res Public Health. 2021 Oct 16;18(20):10875. doi: 10.3390/ijerph182010875.
Béland D, Zarzeczny A. Medical tourism and national health care systems: an institutionalist research agenda. Global Health. 2018 Jul 16;14(1):68. doi: 10.1186/s12992-018-0387-0.
Park J, Ahn J, Yoo WS. The Effects of Price and Health Consciousness and Satisfaction on the Medical Tourism Experience. J Healthc Manag. 2017 Nov/Dec;62(6):405-417. doi: 10.1097/JHM-D-16-00016.
Are the topics/articles the type you are looking for?
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Oil massage to newborn in India is practiced since Centuries and especially mentioned in Ayurveda. Which provides tactile stimulation to newborns and infants, also improves blood supply and reduces stress, results in better sleep (one of the importance factor for normal secretion og HGH). One of the theory established in pathogenesis of SIDS is chronic low grade hypoxia. Countries like USA are having more incidence of SIDS, where such practices are minimal. Can we hypothesized that Oil massage plays important role in preventing SIDS.
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Why don't we conduct an experiment on neonatal rabbits for instance to prove/disprove that claim?
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I first saw this in an online newspaper article:
but looked for any research into this and found:
Shmuel, K., Barbara, M., Dalia, M., Tair, L., & Yaakov, N. (2020). Low pH Hypromellose (Taffix™) nasal powder spray reduced SARS-CoV-2 infection rate post mass-gathering event at a highly endemic community: An observational prospective open label user survey.
If it is effective, I was wondering why it has not been publicised?
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I have also seen this preprint regarding another nasal spray:
Moakes, R. J., Davies, S. P., Stamataki, Z., & Grover, L. M. (2020). Formulation of a composite nasal spray enabling enhanced surface coverage and prophylaxis of SARS-COV-2. bioRxiv.
An effective nasal spray would be marvellous if it did give us more protection, especially before a vaccination program has been completed.
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Since more men and older women contract coronavirus, will it be useful to additionally use estrogen for its treatment or prevention?
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I wonder why the jump to hormonal reasons, there are so many other factors involved.
Could be that women tend to look after their health more, tend to be quicker to respond to indicators of poor health. behaviors over and above hormones.
Or there is more older women dying simply because they are a larger percentage of that population. Likewise more men may be dying simply because there is a larger percentage of males in the population, ok not that big a difference... to explain the higher death rate.
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If I count the number of risk factors at baseline and then after how many days of lifestyle modification (e.g. Physical Excercise with gamification, smoking stopping aid, etc) what type of instrument should be used because I might get biased data, however, I can check the body fat percentage to validate.
How to ensure adherence to a lifestyle modification program, or in other words how to reduce attrition rates?
I want to do an RCT, not a pre-and post-survey. So in this case how can I blind my outcome assessor?
For a lifestyle modification intervention done in at the LMIC setting, I need a good quality evidence-based program. The mobile reminder doesn't seem to work in LMIC as stated in a systematic review.
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You need to use standardised instruments like for physical activity use IPAQ or if you have budget use pedometer better and use BMI and other body composition analyser like tanita or any other brands. Regarding the intervention period should be 12 weeks and more to see any effects
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Mostly N95 masks have 0.1-0.3 um pore size range, while the SARS-COV-2 virus is less than 0.1 um. So, technically which type of masks are considered best to prevent coronavirus infiltration? Is there any solution available to the issue? And any advancement on behalf of scientific community to refine the available masks?
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Kindly go through the following RG link.
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Is the absence of decision by UK and NL to enforce social distanciation against Covid19 (unlike China, Italy, France, Spain, Germany, USA, etc) caused by memory loss of the positive effects of proactive enforcement of social distancing by US cities in the 1918 influenza pandemic? Death rates were reduced by 50%, source:
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Many thanks to all contributors. What emerges is that although the viruses of 1918 and 2019 are different, human behaviours in these two pandemics can be compared. Is it not notable that the portfolio of NPIs (non pharmaceutical interventions) is the same: handwash and reinforced hygiene, self-isolation, quarantine, lock-down, social distancing, gloves, face-masks?
100 years for not inventing better, and not learning from 1918 or from other countries (China/Wuhan) how to detect and implement early?
100 years to forget!
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Distinguished peers,
Although there is a plethora of international, multilingual scientific research and knowledge regarding COVID-19, there is also lot of discourse regarding the source of the virus. I would like some feed back from experts regarding their interpretation of the latest data so that future outbreaks may be prevented and focus can be directed towards solutions to existing problems.
Thank you and regards!
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The many referenced sources indicate the modulation of key cell-signaling pathways were effective in controlling the SARS-CoV infection. The same are as follows:
1- Targeting coronaviral replication and cellular JAK2 mediated dominant NF-κB activation for comprehensive and ultimate inhibition of coronaviral activity. Sci Rep 2017;7:1–13. doi:10.1038/s41598-017-04203-9.
2- Severe acute respiratory syndrome Coronavirus ORF3a protein activates the NLRP3 inflammasome by promoting TRAF3‐dependent ubiquitination of ASC. FASEB J 2019;33(8):8865–8877. doi:10.1096/ fsb2.v33.810.1096/fj.201802418R.
3-Inhibition of NF- kB-mediated inflammation in severe acute respiratory syndrome coronavirus-infected mice increases survival. J Virol 2014;88:913–924. doi:10.1128/jvi.02576-13.
In reference to these published work, one may perform the experimental work using the strategies recently published in Medical Hypotheses Journal entitled " Serum albumin-mediated strategy for the effective targeting of SARS-CoV-2".
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Some articles have been reported pointing out that inhibiting the pro-inflammatory cytokine signalling pathways could be a very promising path. However, in my understanding, JAK or STAT3 inhibitors may not be as selective and interfere with the classic signalling of IL-6 (anti-inflammatory activity). However, antagonists of the trans-signalling of the soluble form of the interleukin sIL-6R, such as the monoclonal antibody Tocilizumab, have high selectivity in modulating only the trans-signalling. Currently, some isolated and non-randomized clinical tests have been published, indicating a great potential for the remission of symptoms of COVID-19.
Non-randomized clinical tests with Tocilizumab:
Mechanism of pharmacological action of Tocilizumab:
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Vagal activity has been shown to reduce inflammatory activity ( )and modulate immune responses. In COVID-19 infections young patients usually experience mild symptoms, whereas in some elder patients fatal interstitial pneumonias are observed.
Vagal activity, as seen from respiratory modulation of heart rate, is strong in childhood and dimishes with aging .
Is there any observation, that vagal activity might protect against too strong immune reaction as suspected in pneumonia?
Would it make sense to strengthen vagal activity as a preventive measure in the population before the big wave of infection arrives?
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In 8579 cases from 30 provinces out of Wuhan, “the median age of cases was 44 years (33-56)... “ though “schools in China were closed for most of the epidemic because of the 2020 Chinese New Year holidays” https://www.thelancet.com/pdfs/journals/laninf/PIIS1473-3099(20)30230-9.pdf
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From your point of view, what are the preventive measures to avoid COVID-19 infection and to reduce its severity ?
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The best ways to avoid the coronavirus (COVID-19) infection include stay at home, maintain social distance and practice good hygiene.
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I am currently doing a systematic review of health education programmes among music students in higher education (i.e. conservatoire students), but the way in which I define such a programme is essential to what papers I include.
Health education initiatives were eligible if they represented stand-alone interventions or were part of wider health promotion programmes. Health education programmes were defined according to WHO (1998) and had to be any planned activity or set of activities aimed at increasing health literacy and developing life skills conducing to health (e.g. decision making, problem solving, critical thinking, interpersonal skills, stress management, coping with emotions). The content of such programmes could comprise counseling, teaching, training or other educational processes such as guided group discussions or behavioural modification strategies (Zhu, Ho, & Wong, 2013). Such programmes could be part of or separate from the formal curriculum, yet taking place in a formal education music institution (college, high-school, conservatoire or university, not clinics) incorporating any relevant health-related content (focusing on psychological and/or physical issues), multi-component or formed of a single session, of any frequency and/or length and provided via any delivery method (i.e. face-to-face, via telephone or internet). Only studies focusing on universal preventative interventions were included (i.e. ‘a measure that is desirable for everybody in the eligible population’ [Mrazek & Haggerty, 1994]).
Now, according to this definition, health education (unlike health promotion) should be aimed primarily at outcomes such as increasing knowledge and/or awareness, changing attitudes, beliefs, perceived responsibility, self-efficacy, as well as training relevant skills/abilities such as critical thinking, decision-making or problem-solving. It should not necessarily or on its own be aimed, at changing actual health-related outcomes such as reducing risk of injury or lowering depression/anxiety - for such outcomes, we are talking about health promotion (which incorporates health education but goes beyond it, also encompassing changing the broader environment and ensuring relevant services are in place). However, many authors use health promotion when they only mean health education.
I have two questions:
1. Where should I draw the line given that using such a broad definition for health education programmes (aimed at developing health literacy and life skills) means I need to include both evaluations of formal health courses (that come in the traditional format of a series of lectures and seminars) and evaluations of interventions involving group discussions, more applied sessions and more focused training of specific skills, albeit with music students in a higher education institution? They both fit into the WHO definition!
2. Given that so many authors use health promotion and health education interchangeably and that only one evaluation of a health education programme looked at knowledge, attitudes and beliefs while all the others looked at health-related outcomes (although all were described as health courses), can I include all these outcomes as part of my systematic review? After all, I am looking at the effectiveness of health education programmes with regards to any outcomes! (health literacy and attitude change on one hand, and changes in actual health outcomes on the other hand)
Many thanks! I am really curious to read your views on the above!
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Health education is any combination of learning experiences designed to help individuals and communities improve their health, by increasing their knowledge or influencing their attitudes. WHO
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Our investigation group is currently working on a research about pornography consumption in adolescents and young people. We'd like to read your comments and any information you consider interesting regarding this topic. All contributions will be welcome.
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The Impact of Internet Pornography on Adolescents: A Review of the Research
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I m trying to do some research on oral cryotherapy as prevention of OM. Is there someone that would suggest few articles to study?
I appreciate topic on cancer patients, oral mucositis, prevention of OM, cryotherapy
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Robert John Wolff Yes! Please write this paper and send it to me when you're done. I'd appreciate reading more on this topic and seeing more articles and papers published on this topic.
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Hi everybody,
I'm treating my contaminated cell cultures by primocin. What experiences do you have? What is the optimal length of treatment to obtain healthy cell culture? Do you use primocin all the time as preventive step or only in the case of contamination? 
Thanks a lot
Pavla
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Routine use of antibiotics in cell culture is not recommended. since , antibiotic resistant strains may develop and may cause resistant cryptic infections such as mycoplasma. Moreover, some antibiotics may have effects in cellular functions. Otherwise, primocin is a good choice.
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Disabled people are considered under WHO recommandations for daily physical activity, but standard measures used for healthy people could them really be used at the same for disabled ?
In other way, for example, for a femoral amputee, walking at 4m/s speed is it under 3 MET (very low level activity) or over (low activity)?
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Emmanuelle Cugy Firstly, physical activity guidelines expressed using Metabolic Equivalent Tasks (METs) are not useful for the general public. The concept of METs is difficult to understand and few people are familiar with it. It is really challenging for the public to know the MET values for any/all the activities they do.
Secondly, The energy consumption in people with limb amputation would be certainly much higher for amputees. To my knowledge METs values and disability have not been worked on very much. See systematic review
Metabolic costs of activities of daily living in persons with a lower limb amputation: A systematic review and meta-analysis. https://www.ncbi.nlm.nih.gov/pubmed/30893346
Thirdly, there has been some work on METs and paraplegia which may help guide you.
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We are looking for prevention/intervention programs or good practices about child sexual abuse in early childhood institutions (kindergartens, pre-schools) worldwide. If you know any scientifically proven effective prevention/intervention program please share the relevant papers or pages in English.
Thank you for your help, Zsuzsa F. Lassú (Hungary)
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hi am passionate about child protection issues, however what work in a given environment may not work elsewhere, therefore consensus building discussions and brainstorming is key to answering this partinet question of what is the most viable intervention
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Can Metformin use as a medicine for breast cancer?
What are the advantages and disadvantages of using Metformin in patients with breast cancer?
Is it possible to use Metformin for both diabetes mellitus and breast cancer?
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There is no known medication or therapeutic technique that is able to completely prevent malignancies, oral or otherwise. Anyone who claims that metformin completely prevents Breast cancer is either a misinformed medical lay person, or a quack practitioner.
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I'm looking for people with an interest in developing interventions aimed at increasing health literacy that would be part of the higher education curriculum.
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All MD colleges of medicine (not sure about DO schools) are required to address in their curriculum mental and physical health, managing stress, and changing behavior. The competencies required for graduation require critical thinking skills, which are a strong focus of the various schools' curricula, no matter how differently they are structured. You might want to check with the education or pre-clinical curricular dean of a medical school in your area to discuss.
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I combined  QCM  with loop-mediated isothermal amplification (LAMP) for the detection of specific DNA. But the false positive result is big problem. Can anyone help solving this problem?
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I am curious whether there are any studies that have analysed the question whether there is a relationship between the average number of coffee consumption per person per day and the average number of hours of sleep per person per day. Is there a relationship?
Published studies in all languages would be relevant, as coffee is consumed in many parts of the world.
If you came across something, please feel free to reply.
Thanks so much and best regards,
Rainer
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Rainer:
You've already received some excellent feedback from Dennis Mazur, so I'll restrict my comments to a brief summary of an internal review on this issue I recently was commissioned to undertake by a European regulatory authority, and hope it adds to the conversation.
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Coffee Consumption and Sleep
It is known that coffee consumption, driven by underlying caffeine (and to a lesser extent, theobromine, theophylline and xanthine metabolites) has been consistently shown to reduce both the quality of sleep and the duration of sleep during the night [Richards 2016] [Gomez-Ruiz 2007] [Distelberg 2017], typically prolonging sleep latency, reducing total sleep time and sleep efficiency, and worsening perceived sleep quality, and incereasing stage-1, wakefulness, and arousals while reducing slow-wave sleep and activity  [Clark 2017]. The recent Loma Linda University randomized, double-blind, longitudinal study [Distelberg 2017] found consistent decreases in the quality (~40% reduction), and quantity of sleep (~10% reduction) during the treatment phase in the intervention group, sustained for as long as 3 days after treatment termination as priorly confirmed [Ohayon  2010].
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Coffee Consumption and the Sleep Regulatory Process
And given that the caffeine consumed affects circadian and homeostatic sleep regulatory processes, negative impact on other outcomes of mood and HRQL are observed, with the strongest adverse effect on anxiety, and with some of the anxiety measures' negative impacts maintained into the post-treatment phase, again indicating durable negative sequelae. And it has been demonstrated that high-caffeine consumption blocks cerebral adenosine A1 and A2A receptors,increases intracellular cAMP signaling, attenuates the buildup of homeostatic sleep propensity during waking, and delays the circadian clock via its effects on the timing of melatonin production in people, and when taken 3 hours before habitual bedtime in the evening, strongly and consistently delayed melatonin rhythm by ~40 min. [Burke 2015], and even at 6 hours prior to bedtime, caffeine reduced sleep by more than 1 hour, strongly suggesting that the rather common practice of afternoon caffeine consumption should at a minimum be restricted to before 5:00 PM, especially given moderate-large doses of caffeine (~400+ mg) commonly found in popular premium coffees [Drake 2013]. 
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Variability and Genetics
It is also important to appreciate that the adverse impact is not restricted to adults, so that caffeine impact in pre-teens, primarily from coffee/tea and sodas, was significantly associated with sleep disruption, morning fatigue/impaired attention, restless sleep, as well as with internalizing behavioral problems [Watson 2017], found to be true also of adolescents [Aepli 2015].
We know further that there is some considerable inter-individual variation in impact, and through genetic studies we have learned that several functional polymorphisms of genes have been isolated, all closely implicated in adenosine neurotransmission and metabolism which contribute to individual sensitivity and variation to such observed sleep disruption: it appears that the hepatic CYP1A enzymes (CYP1A1, 1A2) are the loci for genetic variance in caffeine, accounting for up to 40% variance in caffeine pharmacokinetics, with several genes implicated specifically in the  association with habitual coffee consumption (principally, ABCG2, AHR, POR, CYP1A2, BDNF and SLC6A4) [Coffee 2015] [Cornelis 2016] and the ADORA2A gene, as per the EPISONO study [Nunes 2017]. Age plays a role also, with caffeine-associated increases in sleep latency, shortened total sleep duration and reduced sleep efficiency, being more pronounced in middle-aged than in young adults [Robillard 2015].
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BOTTOM LINE: Coffee consumption consistently negatively impacts the length (~10% reduction) and quality of sleep (~40% reduction), sleep latency and efficiency (as to degree of restless sleep), morning fatigue/impaired attention; the architecture of sleep and the circadian regulatory process and associated melatonin metabolism, with negative effects on mood, HRQL, and anxiety, all with non-trivial individual, age, and genetic variability.
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REFERENCES
[Aepli 2015] Aepli A, Kurth S, Tesler N, Jenni OG, Huber R. Caffeine Consuming Children and Adolescents Show Altered Sleep Behavior and Deep Sleep. Brain Sci. 2015 Oct 15; 5(4):441-55.
[Burke 2015] Burke T, Markwald RR, McHill AW, et al. Effects of caffeine on the human circadian clock in vivo and in vitro.  Sci Transl Med. 2015 Sep 16; 7(305):305ra146.
[Clark 2017] Clark I, Landolt HP. Coffee, caffeine, and sleep: A systematic review of epidemiological studies and randomized controlled trials. Sleep Med Rev 2017; 31:70–78.
[Coffee 2015] Coffee and Caffeine Genetics Consortium, Cornelis MC, Byrne EM, Esko T, et al. Genome-wide meta-analysis identifies six novel loci associated with habitual coffee consumption. Mol Psychiatry 2015; 20(5):647-56.
[Cornelis 2016] Cornelis MC, Kacprowski T, Menni C, et al, Swiss Kidney Project on Genes in Hypertension (SKIPOGH) team. Genome-wide association study of caffeine metabolites provides new insights to caffeine metabolism and dietary caffeine-consumption behavior. Hum Mol Genet. 2016 Dec 15; 25(24):5472-5482.]
[Distelberg 2017] Distelberg BJ, Staack A, Elsen K'dee D, Sabaté J. The Effect of Coffee and Caffeine on Mood, Sleep, and Health-Related Quality of Life. J Caffeine Res June 2017; 7(2): 59-70.
[Drake 2013] Drake C, Roehrs T, Shambroom J, Roth T. Caffeine effects on sleep taken 0, 3, or 6 hours before going to bed. J Clin Sleep Med. 2013 Nov 15; 9(11):1195-200.
[Gomez-Ruiz 2007] Gomez-Ruiz JA, Leake DS, Ames JM. In vitro antioxidant activity of coffee compounds and their metabolites. J Agric Food Chem. 2007; 55:6962–6969.
[Nunes 2017] Nunes RA, Mazzotti DR, Hirotsu C, Andersen ML, Tufik S, Bittencourt L. The association between caffeine consumption and objective sleep variables is dependent on ADORA2A c.1083T>C genotypes. Sleep Med. 2017 Feb; 30:210-215.
[Ohayon 2010] Ohayon MM. Nocturnal awakenings and difficult resuming sleep: Their burden in the European general population. J Psychosom Res. 2010;69:565–571.
[Richards 2016] Richards G, Smith AP. A review of energy drinks and mental health, with a focus on stress anxiety and depression. J Caffeine Res 2016; 6:49–63.
[Robillard 2015] Robillard R, Bouchard M, Cartier A, Nicolau L, Carrier J. Sleep is more sensitive to high doses of caffeine in the middle years of life. J Psychopharmacol. 2015 Jun; 29(6):688-97.
[Watson 2017] Watson EJ, Banks S, Coates AM, Kohler MJ. The relationship between caffeine, sleep and behavior in children. J Clin Sleep Med. 2017; 13(4):533–543.
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I am looking for collaboration in data collection and processing to perform a supply chain resilience study. During the emergency situation, we won't bother anyone, but we can start to collect data from online sources.
Let me know if you have the capacity to help me in that.
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You would first have to specify the industry/ market of the chain referred and even so you may be only able to generalise until after the actual event. It is impossible to accurately forecast precisely the type and degree,likely series of impacts a hurricane can have and its immediate and longer term disruptive effects. Kudan Sagar's comments above are relevant. Notwithstanding and in light of the unpredictability of this type of event,increased focus must continue to be be placed on building robust and resilient supply chains in the first place and on risks and business continuity planning.
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As my test always incubation at water bath in EP. But i really do not know how to keep the Cu(l) in the reaction. I an afraid it will be oxidated to Cu(ll)? is there other thing added to prevent it ??
Reaction:  ATP, Cu(l), protein in tris buffer, 37degree
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Reaction can be carried out in an appropriate pH.
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What I want to know, is what ar the recommended Benzalkonium Chloride final concentrations for cleaning surfaces and to add to the water tray of a CO2 incubator. Looking forward for your answers!
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0.02% benzalkonium chloride works well for the water tray. 
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I am currently looking for any applications of restorative practices and RJ that have already been put into use in relation to radicalisation and extremism, particularly in the prison and probation context but also for its prevention. Of much interest would be to know how circles, conferencing and other restorative practices are put into use and with what results.
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Hi Ruari-Santiago, thank you for the reading suggestions, very interesting. I had been looking at some articles from Northern Ireland but had not come accross these, yet. All the best, Claudia
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How caffeine is associated with Cancers
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Dear Ishor,
an interesting question, indeed. Did you read already the following papers?
Monteiro J, Alves M, Oliveira P, Silva B. Structure-Bioactivity Relationships of Methylxanthines: Trying to Make Sense of All the Promises and the Drawbacks. Molecules. 2016 Jul 27;21(8). pii: E974. doi: 10.3390/molecules21080974
Amigo-Benavent M, Wang S, Mateos R, et al. Antiproliferative and cytotoxic effects of green coffee and yerba mate extracts, their main hydroxycinnamic acids, methylxanthine and metabolites in different human cell lines.Food Chem Toxicol. 2017 May 12;106(Pt A):125-138. doi: 10.1016/j.fct.2017.05.019.
Kalthoff S, Ehmer U, Freiberg N, et al. Coffee induces expression of glucuro-nosyltransferases by the aryl hydrocarbon receptor and Nrf2 in liver and stomach. Gastroenterology. 2010;139:1699-710, 1710.e1-2. doi: 10.1053/j.gastro.2010.06.048
Merighi S, Benini A, Mirandola P et al. Caffeine inhibits adenosine-induced accumulation of hypoxia-inducible factor-1alpha, vascular endothelial growth factor… human colon cancer cells.Mol Pharmacol. 2007 Aug;72(2):395-406.
 Lentini et al. Protein-polyamine conjugates by transglutaminase 2 as potential markers for antineoplastic screening of natural compounds. Amino Acids 2009, 36:708-9. Doi: 10.1007/s00726-008-0157-z
 good luck with your rResearch!
Sibylle
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Distinct histologic sub-types of breast carcinomas (ie, ductal, medullary, and lobular) suggest distinct etiology and risk factors which in turn call for different preventive and curative strategies.This is a  fact suggests that different preventive and curative strategies are needed for different types of Breast cancer. Should we care about it ?!!
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The scientific basis for treatment and prevention of breast cancer is one treatment protocol can be adopted to be Suitable or fit of the needs of patient,in addition to what previously mentioned , Perhaps unproved methods are still under testing for fighting breast cancer
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Giving iv cannula to children is a difficult task. In clinical practice we r seeing frequent thrombophlebitis, Is there any work somebody is doing regarding this.
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Thats fine and interesting.
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as you know in dam operation we should prevent from reduce of water volume until a critical value because of water quality and structural problems. my question is that how this critical value is determined?
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no. as I mentioned before my mean is volume in dam that water should not be extracted more.
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How to prevent macro segregation in medium carbon steel..
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Dear Ankur,
I am not an expert in this field;  I have come accross a few papers but on high carbon steel. Please see whether these papers give references to medium carbon steel. Please see the links if you have access:-
Best wishes
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I have a crystallization problem in %20 mannitol solutions (parenteral solution), Only known excipient is water for injection.Can anyone give me some advice to retard, prevent or decrease the rate of mannitol crystallization in solutions?
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Try adding a crystallization inhibitor like PVP.
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I observe that the  interaction effect of A ~B, and the effect of B are significant (P <.001), but the effect of A is not significant. However when I use  Anova One way  to analyze the effect  of A alone, I observe that the effect of  A is significant(p < 0.05). Does the factor B prevents factor A from expressing? if it is yes, how to  know it
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The easy example. I have a chemical reaction. I find that as the concentration of chemical 1 increases in the reactor, I get increased yields. I now add some powdered platinum. No matter how much platinum I add, nothing changes. However, platinum is a catalyst. It does not consumed, it only facilitates the reaction of interest. Thus I expect that there is a significant effect of chemical 1, and that platinum is not significant. However, there is a huge interaction effect. Biological examples are more messy.
One problem is interpreting a non-significant statistical outcome as support for the null-hypothesis. It isn't. Please do not do this. Failing to find a statistically significant relationship may only mean that your sample size was too small.
Another scenario: Treatment A and treatment B are applied to improve crop growth. The effect of treatment A is similar to treatment B, but they also act synergistically. Thus, either treatment A or treatment B will be significant, and the one that is significant depends on which one enters the model first (Type I sums of squares). If you want to use Type III SS, then suppose that A and B are correlated, and that your sample size of 20 replicates results in a power of 0.9 for treatment A, while it is only 0.3 for treatment B. If treatment B enters the model alone, then it is just barely significant. Once treatment A is included, the correlation between the two knocks B out of the model. However, the interaction term is still significant. The solution is to keep models hierarchical: If the AB interaction term is significant, then B is kept in the model regardless.
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Hi All, I am seeking liaise with colleagues that have an interest in examining the performance of the standard risk assessment scales (e.g., Waterlow, Norton, Braden scales) for the prevention of pressure ulcers in the UK, N. America and so forth. I would appreciate your response. Many thanks, Panos.
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Could Islamic Banking have prevented the financial crisis if only it had been further established in the western world?
May it help prevent future crisis due to its Shari'a based approach?
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Dear Sarah
What you call 'Islamic banking' is what we call 'non-interest banking' in the Western part of the world.
Non-interest banking or Islamic banking is banking without charging interest on loan. I assume that you are referring to the 2007-2009 financial crisis. Your question subtly assumes that interest rates (or high interest rates) charged on loan played a significant role in the recent financial crisis.
If you feel you are very sure about this, then you will first need to prove that the 2007-2009 global financial crisis was caused by the presence of interest on loan, or caused by high interest on loans (or securitised loans).
While the literature boasts that Islamic banking rules improves the performance of individual banks that adopt those rules, 'Islamic banking' or 'non-interest banking' itself is not an explanation for a systemic financial crisis, or a global financial crisis.
Why? Because...
In an interconnected banking/financial system where banks are interconnected by financial claims and obligations, a financial crisis will most likely occur when defaults/failure of one bank leads to successive defaults/failure of other banks connected to it. As you can now see, Islamic banking does not have a systemic property that can have widespread implications for all banks in the global financial system purely because only few banks in the world today adopt Islamic banking rules, compared to conventional banks.
Two, the absence of Islamic banking is not a cause for the financial crisis because the crisis was not caused by high interest rates rather the crisis began as a result of falling house prices when debtors could not even repay the principal on the mortgage loan repayment. The demand for houses fell short of supply, and as a result banks made losses on the mortgage-backed securities they held which had now become worthless. Many banks that made losses were too-big-to-fail and too-interconnected-to-fail, therefore the crisis became widespread. As you can see, the crisis has little (or nothing) to do with charging interest or high interest on loans (which is opposed to Islamic banking). Charging interest on loan is normal because it is a reward to the lender and it reflects the riskiness of the borrower. The cause of the crisis was not interest rates rather it was caused by (i) greed by Wall street bank CEOs (ii) lack of regulatory oversight (iii) excessive bank leverage and capital shortage, among other factors, liquidity withdrawal from the inter-bank market, among other factors.
As you can see from the points above, interest rates (or high interest rates) was not a significant cause of the crisis, therefore, the argument that 'Islamic' banking could prevent the financial crisis is not a valid argument. Except your question is referring to a different financial crisis which you did not make clear in your question.
Hope this helps!
Best Wishes
Peterson.
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In the US, we must document a face-to-face assessment within one hour of restraint application when the restraints are used to prevent patient from self-harm or harming others. I've not been able to locate a  validated tool to do this reassessment. Many folks reference an article by Nadler-Moodie from 2009 but the standards have changed since then. Any help would be appreciated.
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Laske and Stephens discuss the assessment tools for delirium and restraints in this article. While not exactly restraints, perhaps this will get you started on your research.
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Does Nance appliance prevent maxilla growth? Does it need to be reconstructed while the child grows?
Does Nance appliance prevent maxilla growth? Does it need to be reconstructed while the child grows?
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Thanks Sir for opening a window about the anterior esthetic fixed appliance. I am performing such an appliance for children for whom & their parents the esthetic is of big concern. But what do you think about the effect of Nance on maxilla growth? 
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Hello,
One of the outcomes of my cost-effectiveness analysis is admission to a nursing home prevented (at patient level 0=no, 1=yes, prevented), calculated as a proportion per group. Differences between groups are quite small, for example 0.2 with +€250 differences in cost, resulting in an ICER of €1250 for 1....?? It should be one nursing home admission prevented...but what, 1 proportion, 1 person?? 1 proportion is odd, as that equals 100%,right?  
Kind regards, Ronald
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Hello Susanne
For now I settled with an additional percent, as I am still not sure how this works for dichotomous outcomes. This means I multiplied the proportions (0.95 became 95%) etc.)
What I found on wiki regarding efficacy:
When talking in terms of efficacy vs. effectiveness, effectiveness relates to how well a treatment works in the practice of medicine, as opposed to efficacy, which measures how well treatment works in clinical trials or laboratory studies  
I am not sure if and how an equivalence trial and cost-effectiveness relate, but my guess is that the cost-effectiveness analysis are actually the same, but should be framed/interpreted differently? 
KR Ronald
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Is there a connection between the increasing existence of autism and the use of oxytocin receptor antagonists (OTRa)?
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I would not rule out such a possible causal connection.  But.....
Firstly I have already done extensive study concluding that the increase of autism has been entirely due to the introduction of non-gamma-2 dental amalgams 40 years ago.  (But this has been blocked from publication by the pseudic "peer review" system.) 
Secondly, some "leading experts" are asserting that no increase has happened anyway.   As for instance my discussion of this recent paper: https://www.researchgate.net/publication/283543620_Identifying_the_lost_generation_of_adults_with_autism_spectrum_conditions
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I am planning to spray a solution composed of hazardous chemicals for thin film growth. Is there any product or method for an enclosure to be used in a fume hood to prevent aerosols from spreading around the fume hood and contamination. Thanks.
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Hi Muhammed,
I have the sealed box because I use highly toxic hydrazine solution. We also have a spray system for metal oxides, which is open to ambient. The aqueous precursor solution for FTO that you are going to use is relatively benign and does not need a sealed chamber. However, I think your lab manager's worry is reasonable. It is probably not a good idea to leave it open in the fume hood. Your approach is OK. You can buy some plastic sheets and use epoxy to glue them into a box  like a storage chamber with a door.Then you can set up your atomizer/lab stand/heater inside the box, and keep it in the fume hood. 
When you start to spray, clean the box routinely, because you will find it gets dirty really quick. Even though your atomizers is very directional, aerosols go everywhere. 
Zhaoning
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I apply ar(1) as my regressor to prevent autocorrelation using Eviews.
How do I predict future output using this model (I have a quadratic regressor) ? 
After I added ar(1), 1 regressor changed from a significant regressor to be an insignificant one. What does it mean ?
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Dear Muhamad: X[t-1] and (X[t])^2 have no problems, they can be treated as exogenous regressors. The problem is Y[t-1]: The OLS estimators are biased and not consistent if you include Y[t-1] as an explanatory variable. Are you using E-views? If you are using E-views, and you estimate directly the model you have writen (Yt=Yt-1*rho+a*Xt+rho*Xt-1+bXt^2-rho*Xt-1), you are going to get a biased result. But if you type AR(1) instead of Y(t-1), E-views automatically switches to an iterative estimation method and you get consistent estimates.
The problem for long-term forecasting with this model is that you need to know the value of the X variable for the periods you want to predict. This is: let's suppose you have monthly data until October of 2015 and you want to predict November and December of 2015. To do it, you need to know the value of the X variable for November and December of 2015. If you have these values or a good prediction of them, you can predict these two observations (simply, when estimating the model, set the sample until October of 2015, and when you select the "Forecast" option, change the sample to "First observation - December of 2015" and you'll get the predictions you need. The problem is obtaining the values of the X variable for two months that are still in the future!
If your model is a "pure" autorregressive model (this is: Y[t] = a*Y[t-1] + u[t] ), then this problem does not arise, as you can feed the model with the previously predicted values of Y (this is, first, you predict Y[t+1] using Y[t]; then, you predict Y[t+2] using the predicted value of Y[t+1] and so on -remember the variance of the predictions increases as you go further into the future-),  but in the model you have, there is no way of knowing or estimating the future values of X, so you cannot use it for prediction.
You might try to specify an auxiliary model for X, which should be a "pure" ARIMA model (this is, X[t] = f( X[t-1], X[t-2], X[t-3], ...) to predict future values of X. Then, for future observations, you can "feed" the model with the predicted values of X and get predicted values for Y. I'm afraid the variance of this predictions would be quite large, though.
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When I am using Pva electrolyte, after some time it's turning to solid, there by performance degrades is there is any way to prevent that?
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I,m sorry
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the patient transferred to Gynae ward on empirical I.V ampicillin-sulbactam. The patient remains febrile with only a slightly clinical improvement. On day two, the laboratory reports in urine hematuria, 500 leucocytes per µL and an Escherichia coli isolate [105 CFU/mL] with the phenotype presented below. The MIC values were obtained with an automated system (only fosfomycin and colistin were tested with the Etest) and interpreted according to the current CLSI and EUCAST criteria. Furthermore,. phenotypic tests (i.e., synergy with clavulanate) also indicate that the E. coli isolate is not an extended-spectrum β-lactamase (ESBL) producer. ANTIMICROBIALS TESTED CLSI 2012 EUCAST 2012
Ampicillin (≥32 mg/L) R R
Amoxicillin-clavulanate (≥32 mg/L) R R
Piperacillin (64 mg/L) I R
Piperacillin-tazobactam (16 mg/L) S I
Ampicillin-sulbactam (16 mg/L) I R
Cephalotin (≥32 mg/L) R Not available
Cefoxitin (≥64 mg/L) R Not available
Cefuroxime p.o. (≥64 mg/L) R R
Cefuroxime i.v. (≥64 mg/L) R R
Ceftriaxone (2 mg/L) I I
Cefotaxime (2 mg/L) I I
Ceftazidime (8 mg/L) I R
Cefepime (≤1 mg/L) S S
Imipenem (0.25 mg/L) S S
Meropenem (≤0.25 mg/L) S S
Ertapenem (0.5 mg/L) S S
Aztreonam (8 mg/L) I R
Gentamicin (8 mg/L) I R
Amikacin (4 mg/L) S S
Trimethoprim/sulfamethoxazole (≥320 mg/L) R R
Ciprofloxacin (1 mg/L) R I
Nitrofurantoin (8 mg/L) S S
Fosfomycin (64 mg/L) S R
Colistin (0.5 mg/L) Not available S
The patient does not have renal or hepatic impairments, and her BMI is within normal values. What would you use for the directed treatment of the above case
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i,m sorry. i haven't a clinician. 
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Does it play any role in preventing early restenosis?
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i,m sorry .i haven't a clinician. 
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Pregnancy intendedness not only predicts birth outcomes, but is a vital indicator of economic, eduational and health potential across the lifespan. The state of MI collects PRAMS (Pregnancy Risk Assessment Monitoring System) data, but this is not generalizable to the county level. MIHP (Maternal Infant Health Program) collects this data on the clients they serve, but the data is unavailable at this time and does not represent the entire population. The CDC and state epidemiologists will not come out in support of including pregnancy intendedness as a vital statistic on the birth certificate worksheet because they believe the timing is wrong (i.e. after giving birth, as opposed to in the course of prenatal care). ACOG won't include it on the "Antepartum Record" because they feel the research isn't there to support it. In the meantime, those of us in the trenches are stuck with little data to show whether our initiatives to reduce unintended pregnancies are working or not - what's a local public health worker to do?
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Because PRAMS is oversampled in some areas, it is not possible to use the data at the county level.  However, I did finally reach someone on the ACOG committee responsible for reviewing the form and they were supposed to consider adding a question on pregnancy intendedness, but I am not aware of the outcome, as I no longer work in public health.
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Recent studies on the role of nutrition in healthcare systems and best practices in nutrition promotion
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Nutrition is the backbone of proper cell growth and metabolism. Without it the body will not be able to sustain good health for long.
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Periodic testing for HDV infection by anti-HDV antibody in HBsAg positive carriers on chronic hemodialysis treatment is recommendable. Reduction of HBV infection in HD patients would be the best solution to control the HDV infection in HD patients. The transmission of HDV infection between HBV infected in HBs Ag positive carriers on chronic hemodialysis is very critical. Is dedication of HDV/HBV machines and infected patients in HD centers a standard strategy or not? It is obvious that the HDV infection in HD patients has been forgotten! There is an apparent lack of attempts to conduct more investigations and create definite protocols to reduce the incidence of HDV infection in HD patients. The global attempt should start soon. Tomorrow is too late!
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No,There is not nessesary
thanks a lot
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Are pre-diabetics included in primary prevention?
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What sort of prevention (if any) do you apply?
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Staph Epidermidis.
1. give cefazolin 2 g 15' before skin inicision
2. adequate skin asepsis
3. double glove for all surgeons and scrub nurse
4. open the package of the device just before implantation
5. Always cover the device with vancocin impregnated sponge before implantation
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Any One working On MET In specific for LBA
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with the involvement of hamstrings tightness, MET works brilliant to ease the muscle. however with added soft tissue releases on the antagonists will have a good beneficial effect. 
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the reaction is in between 4-chlorophenol and benzoyl chloride in the presence of catalyst(AlCl3 and nitrobenzene). is there any option for this reaction?
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I assume you wish to avoid deprotonation because you want substitution at the 2-position of the phenol rather than reaction at oxygen (which forms the ester)?  The reaction at oxygen remains the kinetically preferred pathway, but that doesn't have to be the end of the reaction; look up the Fries Rearrangement and you should obtain the desired 2-acyl phenol.
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work risk factors and preventive measures among dentists and nurses
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many thanks for all
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I'm doing an immunoprecipiatation of UGT2B15 (mw 61). My WB showed bands at 61kDa as well as 150kDa. I'm assumming that the second band is from immunoglobulin binding. How do I prevent that? I am thinking of adding more beads to the preclearing step. I used 20uL in 500uL. I'm using protein A/G agarose beads. 
Thank you!
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As others have mentioned, in WB of IPs there should not be 150kDa band in reducing SDS-PAGE. Using primary and secondary antibodies of different species minimises the detection of heavy and light chains of IgG. In some IP, I use a secondary antibody against the light chain of the primary antibody, which also helps remove background bands. Detection of 61kDa band in IP from 293T cells may suggest that these cells express low levels of the target protein. In our experience, some endogenous proteins in 293T cells are undetectable by WB of cytosolic lysates, but weak bands can be observed following IP or co-IP procedures, suggesting low cellular expression. Furthermore, an antibody may preferentially recognize a protein in its native form as we have experienced in our work.
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We know that suicide has a low base rate and that most individuals with suicidal ideation will never make an attempt, much less, complete a suicide. Given this very low rate of individuals who are at great risk for suicide, how can we best identify and prevent the act of suicide?
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I believe the best way to prevent completed suicide is to treat all suicidality instead of only treating other psychiatric disorders.  If every person experiencing any level of suicidality (even those only experiencing passive suicidal ideation) had access to proper anti-suicidality treatments (not just anti-depressants) then the likelihood that a patient's suicidality would progress to the stage of a completed suicide would be reduced.  Unfortunately, this will take researchers shifting their perspective from suicidality being the result of depression or some other psychiatric disorder to suicidality being a disorder or even a set of disorders.  Once researchers make this shift they may find that treatments have specific anti-suicidality effects.  At which point, those treatments could be given to patients that experience suicidality in order to reduce their suicidality and lessen the likelihood they will actually take their own life.
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We are about to do so for our SALSA study in prevention of obesity and would welcome any suggestion on the process of administering a web questionnaire for Year 8 students.
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thank you we developed a web based questionnaire which has really easy to use in high schools
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Obesity, hypertension, dyslipidemia, etc.?
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The best recipe: Avoidance of smoking/drug use.  A minimum of  30 min of aerobic exercise five days per week and the Mediterranean diet-avoidance of processed foods and absolute avoidance of ingestion of liquid calories. "If a cave man couldn't get it, think twice about eating it" would be good general advice. This stance would exclude chips, sweets, soft drinks, and baked goods. Goal: flat belly, adequate fuel, lots of movement!
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Multiple studies have shown that inhibition of the renin-angiotensin-aldosterone (RAAS) system have been effective in reducing microalbuminuria among patients with diabetic nephropathy. Despite their usage, prevalence of CKD/ESRD persists (even becoming more prevalent). I have 2 questions: (1) How much renoprotection do ACEIs and/or ARBs provide to this population group? (or how much is the prevalence of CKD/ESRD related to ACEIs and/or ARBs usage?) (2) Are there any studies that predict the occurrence of CKD and/or ESRD among patients being treated with ACEIs and/or ARBs for the purpose of renoprotection, especially among paints with diabetic nephropathy?
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ACEI & ARB'S are excellent reno-protective drugs , as they delay progression of CKD & also protect from cardiovascular complications . But , there are situations , when caution should be exercised in initiating ACEI / ARB , such as in 1) DN with hyperkalemia ( K.> 5 Meq /l ) due to type 4 RTA . 2) In DN without proteinuria due to macrovascular bilateral renovascular disease ( Ischemic nephropathy  ) . If ACEI / ARB's are initiated , a rapid rise of creatinine of > 0.5 mg / dl due to AKI & should lead to rapid discontinuation of these drugs .
  In addition , ACEI / ARB's should not be combined with NSAID'S , should be discontinued before contrast studies ,  pre-operatively before surgery  & in volume depleted states caused by diuretics , diarrhea & sepsis . In all these conditions , the development of AKI can lead to progression of renal disease & also increase mortality .
 These factors should be considered in evaluating the side effects of ACEI /ARB's , as in addition ,multiple drugs such as Beta - blockers & spironolctone may cause hyperkalemia , with increase in mortality . 
 Therefore , the development of AKI & Hyperkalemia due to various factors should be considered , in assessing the prognosis of CKD in DN . The primary care doctors should be aware of these side effects & should monitor their patients by checking serum creatinine & K levels frequently in such situations . The syndrome of Rapid Onset ESRD ( SORO-ESRD ) due to AKI on CKD should be kept in mind .
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Biofouling is caused by the adhesion of microbial slimes on the membrane.This needs expensive periodic cleaning.
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The challenge is to have a biofouling management strategy that works in all cases. The presence of a biofilm does not mean that there is biofouling. Biofouling causes operational problems. One plant owner may accept a strong pressure drop increase while another plant owner may consider a lower pressure drop increase unacceptable. Also for cleanings, some plants accept to chemically clean the membranes twice/one a week while other plants do not accept an annual chemical cleaning frequency. So, it can be difficult to interpret literature.   
Another important aspect is that studies should be done with representative tools under representative conditions for practice. The results of those studies may be more effective than applying results obtained with a non representative tool operated under non representative conditions. In general no information is provided about the representativeness of research tools for practice.     
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Instead of vitamin K.
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We do have over 500 VTE patients treated with rivaroxaban in the RIETE Registry.
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It is said that pioglitazone and statins are useful in preventing endothelial dysfunction and are drugs of choice for erectile dysfunction in males.
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At present there is no hardcore data to support  that  Pioglitazone  helps in combating  endothelial  dysfunction  but they are good drug to start with in  young diabetics in early state
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In particular lipid testing, moving machines around (transport) etc.
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Thanks Clayton.  We have been using them for almost two years with satisfactory results.  However our new manager is worried because we transport them.  I am trying to find research to back up my claim that transport does not affect results.  It is really good to hear others have similar success.
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Can a detox therapy be monitored by means of sound medicine?
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What about weight loss?
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I have certain inclusion criteria for my exercise study and am now doing telephone screening to check eligibility of potential participants. When I have someone who has to be excluded because of let's say age or location I am offering to give the treatment (exercise programme) after study completion. This is what I read in most papers and what people recommended me to do. Now, I am asking myself why can't I give them the programme while the study is running? Do you know of any literature I can read to be able to answer this competently?
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In cases where exclusion criteria identify individuals who would be harmed, not benefit, or not be able to do the intervention, you would not offer it. In cases where exclusion criteria are used to screen out people as a means of control (e.g., limit to certain age ranges), it is probably not necessary. If you are going to give them the intervention anyway, you could include them in the study and see if the exclusion variables relate to outcomes, e.g., age effects. Often when individuals are randomly assigned to intervention or a control group, the control group is given the intervention at the end of the study, assuming the intervention worked, or at least was not harmful. There can be advantages in doing so as one can see if the control group benefits from the intervention in order to replicate findings from the initial intervention group.
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I am at a stage of my research where I will start recruiting participants soon. My sample is reasonably healthy older adults (55-70 years). I have given a number of health talks in community centres where people could sign up for the study. However, relatively strict inclusion criteria will be applied. Hence, I will need to exclude people. Now, I would like to get some idea on how to best do it. People should still feel valued but I also need to make sure I conduct valid research. What are your experiences and suggestions?
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It can be really hard to turn folks away. Hence compassion and still "hearing" their story is of great value. Especially with an older adult population. I think everyone appreciates a thank you and recognition for their willingness to support research. You can certainly post the criteria and indicate that the current research focus won't allow inclusion of a huge number of people without this specific criteria. You can do this up front and limit the volunteers. And many people simply send out a letter indicating their thanks and appreciation with the information about not being included. Offering to share your results with folks at the appropriate time - whether they were within the study or not- can also be a way of recognizing their value. Clearly any steps need to honor the ethics of the study and research. Good luck with your study!
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The prevention agenda was at the heart of health and social care policy under new Labour and there was a proliferation of research in this field. However, although the coalition government seemed to support this in principle, in an age of 'austerity', funding appears to have been directed more towards those with substantial and critical needs and away from preventive services. Also there appears to be a lack of recent academic work on prevention - or is it being described in different terms? Does anyone know of any recent work in this field, i.e. looking at what has happened to low level preventive services under the coalition government? If you could help it would be appreciated!
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The Public Health Agency of Barcelona is actually developing a study on caregiving. The austerity measures had also affected the research fundings and these kind of studies does not have an immediate effect in economies. That's why research groups have troubles to fund these kind of projects, consequently papers are not being published.
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Cellphone radiation accelerates mesenchymal stem cell growth, impairs DNA repair, and interferes with apoptosis. Cancerous cells are inherently more rapidly growing with defects in DNA repair and apoptosis. Given the determination of the World Health Organization that cellphone and other wireless radiation should be regarded as a class IIB ("possible carcinogen--the same category as DDT and engine exhausts), why not inquire about past uses of this device, and also recommend prudent precautions such as those that are currently embedded within all smart phones--to keep the phone some distance from the body?
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Dear colleague,
I’ve just posted a paper on the subject - “Estimations of local thermal impact on living organisms irradiated by non-thermal microwaves” that gives clear physically based answer to the question: What does RF power first of all (before it “accelerates mesenchymal stem cell growth, impairs DNA repair, and interferes with apoptosis”… et cetra)? Let us try to look at the problem from a physical point of view. I believe that the physics of alive is the common physics. If it is true then RF power first of all affects the electric charges, currents and magnetic momentums. All abovementioned bioeffects are just long chain past sequences. We must print this fact in our minds to make true conclusions.
Best regards
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Do we need to learn more from looking into the minutia of everyday interactions between people and their social and physical environments? What are the implications?
Recent years has seen an escalation and variation in the application and scope of social ecological frameworks with the common intent of wishing to effectively interpret factors that influence human behaviour (Holt, Spence, Sehn, & Cutumisu, 2008; O’Connor, Alfrey, & Payne, 2011; Sallis, Owen, & Fisher, 2008; Stokols, Misra, Runnerstrom, & Hipp, 2009). To date the dominant discourse for social ecological research in the scholarly community has been heavily located in conducting large scale studies, the employment of gross markers and distant analysis with a key outcome of finding the big macro levers that aim to achieve a population shift in human behaviour.
References
Holt, N., Spence, J., Sehn, Z., & Cutumisu, N. (2008). Neighborhood and developmental differences in children’s perceptions of opportunities for play and physical activity. Health & Place, 14, 2-14.
Krieger, N. (1994). Epidemiology and the web of causation: Has anyone seen the spider? Social Science & Medicine, 39(7), 887-903.
O’Connor, J., Alfrey, L., & Payne, P. (2011). Beyond games and sports: A socio-ecological approach to physical education. Sport Education and Society, 17(3), 365-380.
Sallis, J., Owen, N., & Fisher, E. (2008). Ecological models of health behavior. In K. Glanz, B. Rimer & K. Viswanath (Eds.), Health behavior and health education: Theory, research, and practice (pp. 465-482). San Francisco, California: Jossey-Bass.
Stokols, D., Misra, S., Runnerstrom, M., & Hipp, A. (2009). Psychology in an age of ecological crisis: From personal angst to collective action. American Psychologist, 64(3), 181-193.
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Dear Alice
Thanks for your question about the type of research we are doing at St Andrews. We spend a lot of effort on trying to understand the links between the expression of emotion in conversations between health providers and patients. As I think
I mentioned previously the way in which health providers respond to open, frank or hidden emotive content in a patient's speech is of importance to outcome. I have been impressed by the late Peter Maguire from Univ of Manchester UK and his work with staff at Christie's Hospital with cancer patients. If emotional concerns in diagnostic interviews expressed by patients were 'blocked' by clinicians then lowered mood in patients was detected at follow up.
Do look at examples of my work with the talented Research Fellow - Yuefang Zhou in a couple of recent papers we have published (the PLoS-One article and the paper in Annals of Behavioral Medicine). The former is about medical students' responses to simulated patient emotional expression and the later about reassurance producing counter-intuitive effects in young children receiving a preventive intervention). Both papers show the importance of timing and investigating contextual factors. The later article has been captured nicely in a piece now on Reuter's Health web-site page.
Hope this is of interest and adds to the discussion.
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You can review the full text and after that responds to my question.
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The newbornS vaccination has long time ago been started in Iran, even before European countries! AND as a great achievement the rate of HBV related HCC has dramatically been decreased. Also, due to this program the rate of HBV chronicity has considerably been decreased.
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I'm reviewing the literature on adolescent subclinical depression, and am hoping to spot anything I may have overlooked. Thanks!
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Dear Christine, I am not sure which type of Depression specifically, or in which field, but I am aware of one that has looked at physiological markers and has identified specific ones. It is the first study of its kind and could be used to predict and identify those with depression. If this is of interest and you do not have it, I will send you the information. Keep well.
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Do you think productively to conduct a survey among patients during treatment, immediately after treatment, or the public?
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Undoubtedly, the quality of health care can be measured by measuring the quality of life of patients before and after care with the help of the questionnaire SF-36. Our experience shows, however, that it is appropriate to use a special questionnaire for patients before discharge to identify the subjective assessment of parameters such as the ratio of doctors, nurses to patients as individuals, abstracting from direct patient care.
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Wich kind of Alzheimer's Disease they are talking about?
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Look at the paper by Deschaintre and others (Neurology 2009;73:674-680), where a group of 301 consecutive AD patients without CVD was followed over 6 years. Baseline MMSE scores were similar in all three groups. Those who had vascular risk factors (VRF) managed carefully had a slower cognitive decline than those who had some VRF treated or no VRF treated (BP, HLD, DM, smoking, etc).
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Social capital improvement takes a long time and some times it might be like learning from history and changing the future, but can we really improve social capital in a short duration (e.g. months)?
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If you want an answer to this question, please read the story of Japan and South Korea's socioeconomic progress and policies adopted by them. These two East Asian tigers are classic examples for rapid socioeconomic progress in a short period of time. Though, policies are very important to such progress, but along with good policies, good governance and corruption free system also plays important role.