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Of the epidemiological literature available on SBI, the most credible and generalizable data come from representative community samples, from which the general population prevalence of SBI has been estimated as 10% to 20%, with longitudinal studies suggesting a yearly incidence of 3% to 4%. 2 However, this climbs as high as 55% in clinical-based studies of otherwise healthy patients 3 and is higher than 90% in certain disease-specific populations. 4

Despite such a high prevalence, mounting evidence suggests that SBI is not a silent event at all but is associated with subtle neurological deficits, neurocognitive dysfunction, psychiatric disorders, an increased incidence of overt stroke, and early mortality. In light of these associations, it has been proposed that the designation silent be replaced with the term covert. 5

The principle objective of this article is to review the current body of published medical research critically to (1) define SBI and highlight problems inherent in that definition; (2) examine the risk factors, incidence and prevalence of SBI; (3) assess theories on the underlying pathogenesis of SBI; and (4) discuss the clinical consequences of these lesions.

What Constitutes a SBI?

There is no universally accepted definition of SBI, which hampers attempts to characterize and investigate these lesions fully. In general, SBI has been described as cerebral infarcts that are observed on either computed tomographic or MRI scans in the absence of any corresponding, clinically apparent cerebrovascular ischemic event.

Problems in the Detection and Diagnosis of SBIs

The rigor with which corresponding clinical events are identified dramatically affects the reported incidence of SBI, and investigators have deviated widely in their means of clinical detection. In many studies, such events have been determined by self-report only or through retrospective medical record review. These methodologies are clearly subject to bias, given variability in the recall, presentation, and investigation of possible cerebrovascular events.

Similarly, variations in diagnostic imaging strategies have important implications for estimates of SBI incidence and prevalence. MRI is now regarded as the imaging modality of choice for diagnosing SBI; however, significant interstudy differences exist in the application of this technology. Major sources of heterogeneity in the literature include varying MRI acquisition protocols, the imaging definition of infarcts applied, and the strategies for excluding entities with overlapping imaging appearances.

MRI Acquisition Protocols

Lower strength magnets, thicker slices, and larger gap intervals all reduce MRI sensitivity for SBI detection. In the past, slice thickness and slice gap intervals were greater than the size of the SBI structures now being observed, with subsequent inaccuracies in reporting. Until 2009, magnet strengths were ranged from 0.2 Tesla (T) to 1.5T, but interim technological advances have led to widespread use of superconducting magnets with 1.5T now the minimum for brain imaging. Furthermore, improved receiver coils and signal processing allow for faster acquisitions with higher resolution. Thus, an advanced MRI system is no longer required to perform imaging at a sufficient resolution to delineate SBI structures properly. Therefore, practical standardization is attainable with the recently suggested neuroimaging research standards by the STandards for ReportIng Vascular changes on nEuroimaging working group.

Imaging Definitions of Infarction and Differential Diagnoses

Although the greatest heterogeneity in the SBI literature exists in defining the imaging characteristics of infarcts, the majority of studies have concentrated on chronic subcortical cavitatory infarcts. These lesions are relatively distinctive and with cavitatory neuronal and glial loss specific for the pathophysiological end point of chronic infarction. However, SBI is not restricted to chronic lesions. Imaging may capture an infarct in an earlier phase, before it has cavitated and indeed not all SBI cavitate. Furthermore, SBI is not restricted to subcortical regions and can occur in noneloquent areas of the cerebral cortex, the cerebellum, and brain stem.

Below we delineate the SBI imaging spectrum and describe imaging progression from an acute to chronic and cavitated infarct. It is important to recognize that there is no current evidence to show that all chronic SBI lesions necessarily begin as infarcts with acute imaging features. In fact, multiple variances from the continuum exist. Therefore, distinction is made between acute and nonacute infarcts on imaging, recognizing that while a subset of lesions will follow the continuum, these may also represent different pathophysiological entities of SBI.

In recent years, diffusion-weighted MRI (DWI) has been increasingly used for determining the incidence of SBI after various high-risk procedures. Indeed, the main clinical application of this technology has been for the diagnosis of acute stroke because it is more sensitive and specific to the associated early changes than traditional MRI measures and thus allows more accurate diagnoses.

If any other Wings player was on the ice without Jensen, they had a tougher time against the opposition. Usually allowing many more shots and not generating enough to balance it out. It’s obviously not the most impressive group of players, but an established player like Henrik Zetterberg goes from being demolished on both axis, to being turn around completely when he on the ice with Jensen. This can be said of most Wings forwards or defensemen this year.

Jensen obviously does not belong to be on the Red Wings team. The most common defensive partner he had last year was Danny DeKeyser – an offensive blackhole that has one skill, to stand at their own blueline and not allow zone entries.

While Jensen and DeKeyser were paired together, they had a top-15 Expected Goals For Percentage (56.76) among all defensive pairs in the whole league (min. 400 minutes). Among all the pairings that are ranked higher than Jensen and DeKeyser, they had the fewest amount of offensive zone starts. Meaning they most likely had the least amount of chances to actually get some scoring chances for their team. If Jensen can tilt the ice the Wings’ way when he is paired with DeKeyser, he should be able to do wonders with any of the left-handed defensemen the Leafs have.

If he can contribute more than any other Red Wings defenseman, with that group of players that earned them a 26th-overall spot in the league, imagine what he could do with the Leafs. It’s not like he’s absolutely inept at distributing the puck either.

Provided by Ryan Stimson and Corey Sznajder , here is how Jensen was able to pass his way through that Red Wings lineup, compared to Ron Hainsey.

Jensen doesn’t blow anyone out of the water in most pass types, but he is an extremely solid depth defender to have on your roster. He won’t be able to make the most difficult of passes or set up forwards from various parts of the ice, but he can defend well and that might be an understatement.

Nick Jensen was by far the best defenseman on the Red Wings last year, not that it was hard to do but still impressive. Demonstrated by CMHockey66’s Goals Above Replacement metric, he was able to outshine any of his peers on the roster at even-strength.

It was only at even-strength that Jensen’s GAR shows because Jeff Blashill never put Jensen on the powerplay, at all. He is not the most offensive-heavy defender, but he can certainly move his feet well enough to control the blueline on the man advantage.

But the best part of this is that Jensen did kill penalties.

In fact, he had the lowest Goals Against/60 among all regular Red Wings penalty killers, with Mens Saucony Fastwitch 8 outlet cheap quality free shipping huge surprise TMOb3R
. The Wings had a terrible penalty kill, but that 6.5 GA/60 was the exact same that Ron Hainsey had with the Leafs’ PK this year.

Jensen can provide that balance that fans want to see. Never the most flashiest player on the ice, but can always be that solid force on the backend. The modern stay-at-home defenseman, if you will.

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32:06

I am grateful to be here with my wife, Debi, and my two youngest children—who are currently attending BYU—and several other family members who have come to be with us.

It is an honor to be invited to speak to you today. Several years ago I received an invitation to speak at Women’s Conference. When I told my wife, she asked, “What have they asked you to speak on?”

I was so excited that I got my words mixed up and said, “They want me to speak about changing strengths into weaknesses.”

She thought for a minute and said, “Well, they’ve got the right man for the job!”

RELATED SPEECH

She’s correct about that. I could give a whale of a talk on that subject, but I think today I had better go back to the original topic and speak about changing weaknesses into strengths and about how the grace of Jesus Christ is sufficient (see Ether 12:27 , DC 17:8 , 2 Corinthians 12:9 )—sufficient to cover us, sufficient to transform us, and sufficient to help us as long as that transformation process takes.

A BYU student once came to me and asked if we could talk. I said, “Of course. How can I help you?”

She said, “I just don’t get grace.”

I responded, “What is it that you don’t understand?”

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RELATED TOPICS

She said, “I know I need to do my best and then Jesus does the rest, but I can’t even do my best.”

She then went on to tell me all the things she should be doing because she’s a Mormon that she wasn’t doing.

She continued, “I know that I have to do my part and then Jesus makes up the difference and fills the gap that stands between my part and perfection. But who fills the gap that stands between where I am now and my part?”

She then went on to tell me all the things that she shouldn’t be doing because she’s a Mormon, but she was doing them anyway.

Finally I said, “Jesus doesn’t make up the difference. Jesus makes all the difference. Grace is not about filling gaps. It is about filling us.”

Seeing that she was still confused, I took a piece of paper and drew two dots—one at the top representing God and one at the bottom representing us. I then said, “Go ahead. Draw the line. How much is our part? How much is Christ’s part?”

She went right to the center of the page and began to draw a line. Then, considering what we had been speaking about, she went to the bottom of the page and drew a line just above the bottom dot.

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Perspective Development
How does temperature determine sex?

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11 May 2018: Vol. 360, Issue 6389, pp. 601-602 DOI: 10.1126/science.aat5993
Arthur Georges
University of Canberra, ACT 2601, Australia.
Clare E. Holleley
Commonwealth Scientific and Industrial Research Organisation, GPO Box 1700, Canberra, ACT 2601, Australia.

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Summary

Sex determination in reptiles is a complex affair, because incubation temperature and genes interact in many species to regulate sexual development and decide sexual fate, male or female (–). A central question that has remained unanswered is, what molecular mechanism allows temperature to so profoundly influence the developmental pathways that determine sex? The means to identify a master sex-determining gene in species with genetic sex determination is well established—identify genes on the sex chromosomes, demonstrate which of these are differentially expressed in male and female embryos early in development, and manipulate their expression to demonstrate reversal of sex (–). Not so with identifying the mechanisms of temperature-dependent sex determination (TSD). Temperature could exert its effect on any of the many autosomal genes involved in sexual differentiation, even those peripherally involved, provided their altered expression is capable of reversing sex. Little wonder that, in the 50 years since TSD was discovered in reptiles (), we have not advanced far in our understanding of the mechanisms of TSD. This is about to change. On page 645 of this issue, Ge () report that transcription of the chromatin modifier gene (lysine-specific demethylase 6B) responds to temperature in the red-eared slider turtle , and confers temperature sensitivity to a key sex-determining gene, (doublesex- and mab-3–related transcription factor 1).

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Vol 360, Issue 638911 May 2018

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How does temperature determine sex?

By Arthur Georges , Clare E. Holleley

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