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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.

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There was a time when it was commonly thought that the best way to help an individual with a drug problem was to wait until he hits “rock bottom.” When that person’s life was adversely affected enough by addiction and destructive behaviors, he would enter rehab or seek help.

However, over the past few years, this thought process has evolved. The medical community has concluded that addiction is a disease and not a series of bad life choices. As a result, more attention has been given toward helping those afflicted with addiction, rather than punishing them.

An intervention is the process by which the family, friends, counselors or professional intervention specialists can show a person struggling with drug addiction the negative impact of the disease in his life and on those who care for him.

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While family members perform interventions, anyone with a sincere and loving relationship with the individual can participate.

This might include:

It is also a good idea to use the services of a person trained in the process of drug and alcohol intervention. That person can provide the family and friends with the information they need to conduct a thorough and safe intervention.

The purpose of an intervention is to help the person struggling with addiction to enter a rehabilitation program, usually in an inpatient facility.

Including friends, family and concerned relations in the intervention is not to “gang up” on the person needing help, but to show him how widespread his addiction truly is. When the individual sees how his drug problem affects others’ lives, he may be motivated to seek treatment. An intervention may serve as a final warning, of sorts, that these people will no longer support the destructive addiction in his life.

The first step to setting up an intervention for a loved one is to determine what help the individual may have already sought for himself. Does he have a counselor he speaks with regularly?

According to the American Psychological Association, a counselor or psychologist is prohibited from discussing confidential interactions with their clients or patients; however, they can help you to determine whether it is time for an intervention to take place and the probable success of the intervention. 1 They may choose to be a part of the intervention process.

The intervention takes place in a safe environment with the participation of every family member, friend or professional who has a stake in the outcome.

Going to a zoo gives you a great chance to learn about some really cool organisms found in different parts of the world. One of the most fascinating creatures that you may find is the common ostrich, a large bird from Africa. Ostriches do not fly but instead use their large, powerful legs to run fast. You may notice that these birds, like humans, run on two legs instead of four. Both ostriches and humans also engage in dancing as a courtship ritual. What other things do humans and ostriches have in common? Look at the table to see how the two compare when classified according to the Linnaean system.

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Despite their dance moves in common, as well as being multi-celled animals with a spinal column, humans and ostriches are categorized very differently. The Linnaean system was designed to describe organisms via structural differences alone, a major feat since the field of genetics had not been discovered yet, so evolutionary relationships were not known. Both humans and ostriches were classified and described by Linnaeus himself; it is amazing to think that many of the organisms on the planet are still classified according to Linnaeus' original descriptions!

Naming Organisms

If you look back up at the table again, you may notice that the Genus and Species names for both humans and ostriches have been italicized. As previously mentioned, the Linnaean system allows for scientists to universally use one name for a specific organism. Referring to an organism using its genus and species names is known as . A few rules have been made regarding how to name an organism using this system. A few important ones are:

So the binomial name for a human is a and for an ostrich is . There may be many different common names for an organism, like how a mountain lion can also be called a cougar or a puma, but an organism will only have one binomial name (). Following these rules makes it easy to refer to a specific organism in both written and spoken word, no matter what language you speak.

Lesson Summary

An is simply defined as any living thing, ranging from microscopic bacteria to the large African bush elephant and everything in-between. Scientists estimate about 8.7 million different species of organisms, not including microorganisms like bacteria, are on planet Earth right now. There is an entire science dedicated to organizing and describing all the organisms that previously existed, currently exist, or have yet to be discovered. That science is called .

In 1758, Karl von Linne, a Swedish biologist more commonly known as Carolus Linnaeus, came up with a logical system that separates groups based on similarities and differences in body structure, and allows scientists everywhere to refer to a particular organism in the same way. Originally, all life was divided in the to the kingdoms -- Animalia (multi-celled organisms that eat organic matter) and Plantae (multi-celled, usually non-mobile organisms that make their own food). With the invention of the microscope, life was further divided into three more Kingdoms -- Protista (most single-celled organisms), Fungi, and Monera (blue-green algae and bacteria). Following Kingdom, organisms are further divided into Phylum, Class, Order, Family, Genus, and Species, getting more specific and closely related going down the list.

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To determine if ingestion of the dietary supplement creatine ethyl ester results in statistically and clinically relevant elevation in serum and urine creatinine levels, a crossover trial in which participants will receive creatine ethyl ester or creatine monohydrate will be employed.

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In this IRB-approved, blinded, crossover trial, 25 healthy subjects ingested 10 grams of either creatine ethyl ester or creatine monohydrate. Each subject served as his or her own control and ingested the other sample greater than two weeks later. Serum and urine creatinine were assayed at 0,1,2,3,4,6, and 24 hours after acute ingestion. Statistical analysis was performed by Wilcoxon Matched Pair Signed-Ranks test. All subjects completed informed consent documentation prior to participation.

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All subjects had significant increases in serum creatinine. For the creatine monohydrate group; baseline mean serum creatinine (Crn) was 0.97 +/- 0.13 mg/dL, peak mean serum Crn was 2.49 +/- 0.81mg/dL, and 24 hour post-ingestion Crn was 0.97 +/- 0.14 mg/ dL. For the creatine ethyl ester group: baseline mean serum Crn was 0.94 +/- 0.14mg/d; peak mean serum Crn was 6.71 +/- 1.59 mg/dL; 24hr post ingestion serum Crn was 1.13 +/- 0.23 mg/dL.

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Serum creatinine was elevated to levels mimicking acute kidney injury (AKI) in both creatine monohydrate and Creatine Ethyl Ester groups. Urine creatinine after ingestion of single-dose creatine ethyl ester demonstrated an excretion pattern, whereas urine creatinine after ingestion of single-dose Creatine Monohydrate demonstrated an absorption pattern. These findings support other research suggesting Creatine Ethyl Ester may actually break down and excrete it before it is active as an ergogenic substance. Additionally, these findings provide important context for interpreting serum creatinine values that would otherwise indicate an AKI in patients who use creatine supplements.

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Creatine is an organic acid that is synthesized from arginine, glycine, and methionine in a two-step reaction involving the kidney (1st step) and the liver (2nd step) (13). It can also be ingested from various meat sources, with the highest concentrations being found in some cuts of beef (21). Creatine acts as an energy buffer by directly rephosphorylating ADP to create ATP during short duration exercise; specifically, creatine acts when endogenous ATP sources are depleted during the first 10 seconds of exercise and glycolysis has not yet taken over as the primary means of generating ATP within the muscle cell (21). Creatine also seems to localize within muscle cells, further demonstrating its efficiency as a buffer system (36).

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