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Fig. 4

Phylodynamic analyses. Figure shows the sampling rate and birth rate derived from the BEAST analysis for the 36 US genomes. Solid white lines with square boxes indicate the posterior median, with the shaded region indicating the 95 % highest posterior density. Darker colors are associated with regions of higher posterior density, with the shape representing the actual posterior density. Despite the birth rate remaining higher after the switch to aP, the sampling rate declines. This pattern would be expected with an increasing rate of asymptomatic transmission

Fig. 5

Comparing disease-free weeks in pre- and post-vaccination scenarios. Panel a shows the proportion of disease-free weeks (fade-outs) per year for the 50 US states in the pre-vaccine (1920–1945, black points and line) and post-vaccine (2006–2013, blue points and line) eras. Lines indicate best-fit exponential curves. Panel b shows the mean duration of consecutive disease-free weeks in both eras

Fig. 6

Changes in transmission in pre- and post-vaccination scenarios? Figure shows the proportion of disease-free weeks (fade-outs) for various population sizes from the stochastic formulation of the model. Panel a compares the symptomatic cases in the aP vaccination era with those in the pre-vaccine era; panel b compares the symptomatic to asymptomatic cases in the vaccine era; panel c compares the asymptomatic cases in the post-vaccine era with those in the pre-vaccine era. These results demonstrate no changes in transmission due to vaccination. Parameters: birth rate () = death rate () = 1/75 years ; recovery rates for symptomatic () and asymptomatic () = 14 days ; probability of symptomatic infection () = 0.25; transmissibility () is calculated per value of

Fig. 7

How does an inefficient vaccine affect situational awareness? Figure shows the percent difference in observed infections (symptomatic) from true infections (symptomatic + asymptomatic) at steady state as aP vaccination rate increases and the probability of symptomatic infection increases. Shaded area indicates a range of reasonable aP vaccination rates. At current aP vaccination coverage levels, the majority of cases are asymptomatic and therefore undetected. See Additional file Sky Blue High Waisted Herringbone Linen Trousers Anderson amp; Sheppard Sneakernews Cheap Online Drop Shipping Free Shipping Low Price Fee Shipping lZbTSu
for model details. Parameters: birth rate () = death rate () = 1/75 years ; recovery rates for symptomatic () and asymptomatic () = 14 days ; baseline vaccination rate = 0.9; transmissibility () is calculated such that =18. Note that previously published values of for pertussis range from 16–20 [ 71 ] to closer to 5 in some populations [ 72 ]

Fig. 8

Can an inefficient vaccine lead to increased transmission? Figure demonstrates the fold increase in observed symptomatic and unobserved asymptomatic infections after transitioning from a wP to an aP vaccine. This is calculated by dividing the number of symptomatic or asymptomatic cases with various levels of aP coverage (reported on the x-axis) and 0 % wP coverage by the number of cases with 90 % wP coverage and 0 % aP coverage. This was designed to simulate the switch from wP to aP in the US and UK (going from high wP coverage to coverage with aP). We see an increase in symptomatic cases across a large range of aP vaccination coverage levels. See Additional file 1 for model details. The gray band indicates the empirical 5.4-fold (95 % bootstrap confidence interval: 0.4–13.3) increase in cases in the US comparing 2012 to the years 1985 through 1995. The model recreates the observed increase in cases. Parameters: birth rate () = death rate () = 1/75 years ; recovery rates for symptomatic () and asymptomatic () = 14 days ; probability of symptomatic infection () = 0.25; baseline vaccination rate = 0.9; transmissibility () is calculated such that =18

As aP vaccination coverage increases, asymptomatic infections increase up to nearly 30-fold. We see a substantial increase in the observed numbers of symptomatic cases after wP vaccination is replaced by aP vaccination. At low to moderate levels of aP vaccination, there is a 5- to 15-fold increase in symptomatic cases. Only at extremely high levels of aP vaccination (>99 % ) is there no change in symptomatic infections. This is in line with the observed rise in B. pertussis incidence: cases in 2012 were 5.4-fold (95 % bootstrap confidence interval: 0.4–13.3) higher than cases in years 1985 through 1995 ([ 46 ]). This result is similar to previous findings by van Boven et al. (2005) [ 47 ], who found that as wP vaccination coverage increased, primary infections (symptomatic) decreased, while secondary infections (subclinical, or asymptomatic) increased.

Breast Cancer - Moose and Doc

A breast cancer explanations website

By Steven Halls

The term ‘‘ is basically just another term for flat epithelial atypia (FEA) and columnar cell hyperplasia . Essentially it describes neoplastic cell growth in the breast ducts, primarily of epithelial cells and not mixed cells types, and with some odd features but without the characteristic cellular mutations and odd formations associated with malignancy. There is considerable difference in opinion as to whether these kinds of proliferations are fully benign or not , as in some instances they do develop alongside ductal carcinoma in situ . It is also not uncommon for flat epithelial proliferations to develop at the site of breast cancer surgical treatments. So,when this term, ‘‘ () is used () it is likely an attempt to describe a kind of ‘‘ diagnosis between flat epithelial hyperplasia (), and Cheap Original Cheap Get To Buy Printed Racerback Top Amazonite Waves Tank by VIDA VIDA Buy Cheap New Styles Free Shipping Genuine Discount 100% Original jacl04NEC
, which is considered suspicious for malignancy.

Background on proliferative breast neoplasia

Breast cancer screening often reveals potential or developing lesions composed of unexpected new cell growth . In general, new cell growth is often called a ‘‘, and where it seems to be very rapid and extensive , it might be called ‘.’ Any time new cells are growing, the finding can be called a ‘‘ lesion, as opposed to a non-proliferative lesion caused by a ‘‘ blockage of some kind (). An ‘‘ means that epithelial cells () appear to be growing and accumulating more than normal. An ‘‘ epithelial proliferation indicates that the new growth is occurring around the breast ducts , and may even compromise their function to a degree.

Most proliferative neoplasms, including a generic () epithelial proliferation are considered benign and of zero-to-very low risk of breast cancer development. But, when certain ‘‘ features () are highly ‘‘, this raises additional concern that the lesion might possibly indicate a very, very early presentation of breast carcinoma.

Atypical epithelial proliferation will likely emerge as a distinct category of breast lesion

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tend to grow in a ‘‘ pattern, or form into columns. But, it is a very consistent and regular formation that is not considered ‘‘ enough to constitute atypical ductal hyperplasia. Cancer researchers and pathologists who use this term ‘‘ are trying to make a point that even very subtle non-typical features may be significant enough to diagnose a specific, potentially malignant or pre-DCIS situation.

Some of these mildly atypical features might include and complex or odd ‘‘ formations involving and ‘‘ fenestrations. However, there is a danger that creating a new ‘‘ for these subtle differences, which have not yet been convincingly proven to have any direct link to DCIS or definitive increased risk of breast cancer, may cause needless anxiety and over-treatment . However, a body of new data is emerging which seems to suggest that usual ductal hyperplasia and atypical ductal hyperplasia are not related, but should be considered as distinct breast lesions , at least from a genetic point of view. Once this is established, then risk factors

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Methods.

Results. Informants developed a unique definition, attribution, theory, and theodicy about suffering based on the particularity of the experience as well as how they “fit” suffering into their lives as a whole. Brief case studies illustrate how themes emerged in elders' stories of suffering.

Results.

Discussion. On the basis of this research, it appears that, although they have some similarities, elders' experiences of suffering are unique and incomparable. Similarities concern informants' connection of suffering with finitude. The incomparability of suffering experiences relate to informants' unique personal histories, perceptions, and “cause” of suffering. Through the process of the interview, elders connect the suffering experience to the entirety of the life lived and the story of suffering to the life story.

Discussion.
Issue Section:

SUFFERING is a ubiquitous human experience but is not specifically the same as depression, grief, illness, pain, or similar events that occur in later life. Some elders explain that negative events, such as depression or suffering, differ from each other in their causes, outcomes, and quality. Although suffering can be defined from an etic perspective (as we do in the paragraphs that follow), this article focuses on how a sample of community-dwelling elders narrated their own suffering and what events precipitated it. We describe how individual experiences of suffering in later life can be organized thematically.

Factors that differentiate suffering from some of the events just named are that suffering affects the individual on many fronts, may reach the core of the self, and may consume the self. A trigger may be an event such as grief or illness, or a state of being such as poverty. Elders note that the enduring nature of suffering might overwhelm their aging minds and bodies; they worry that they will die before suffering ends.

Our goal in this article is to describe a significant aspect of the aging experience that is infrequently discussed. On the basis of our research, most individuals have experienced suffering. One of our informants noted that “suffering is a normal part of life.” We also take up the theme of the deviancy of suffering, that is, that suffering is strange and “wrong” to the one who suffers. The fact that suffering is both familiar and alien touches on a component of suffering that waxed significant in our study—the paradox of suffering.

For purposes of discussion, we define the terms that are integral to and related in this article, such as culture, self, and suffering. Culture is our native starting point; it is the shared blueprint of both the local and larger world into which we are born and take part in shaping. Culture cannot be abstracted from a society's historical reality; interaction among members is central to inheriting and bequeathing a culture ( Hall, 1959 ; Turner, 1996 ). The self may be defined as two complementary faculties: a process that is unfolding and an object that is observed ( Charmaz, 1995 ). In this definition the self includes an abiding identity that is both actor and acted upon, watcher and watched, and subject and object of life experiences.

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