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the SAT contains a Math No Calculator subsection for which you may not use a calculator.

As a result, if you struggle with solving math quickly or without a calculator, you'd probably fare better on ACT Math than you would on SAT Math. On the other hand, if you’re confident in your math skills and can work fast without a calculator, the SAT is a solid option.

Know this, though: on both the ACT and SAT, you can technically solve all math questions without a calculator. So, really, the No Calculator questions aren't all that different from Calculator questions. That said, the No Calculator questions are meant to be easier to solve without a calculator and are thus generally more reasoning based than arithmetic heavy .

on both the ACT and SAT, you can technically solve all math questions without a calculator.

In regard to math content, the ACT and SAT both have a big emphasis on algebra. But the ACT also tests a couple of concepts that the SAT doesn’t focus on as much.

algebra.

To start, the ACT has a much larger focus on geometry, which makes up about 35-45 percent of ACT Math. By contrast, geometry accounts for less than 10 percent of SAT Math questions. In addition, Petunia floralprint asymmetric dress Preen Discount Aaa DXrHB2jOUf
but less than 5 percent of the SAT , so there's a slightly larger emphasis of trig on the ACT than there is on the SAT.

geometry,

The ACT also tests a few concepts that the SAT doesn’t test at all. These include things such as matrices, graphs of trig functions, and logarithms.

The ACT also tests a few concepts that the SAT doesn’t test at all.

So what does all of this mean for you? If you’re good at algebra and data analysis, you’ll likely do well on the SAT. But if you’re a fan of trig functions and geometry, the ACT is a better choice.

Here's another math-related difference: the SAT provides you with a diagram of math formulas, whereas the ACT does not.

the SAT provides you with a diagram of math formulas, whereas the ACT does not.

Before the two SAT Math subsections, you'll be given a diagram containing 12 geometry formulas and three laws:

Although all of these formulas and laws pertain to geometry — which, as you now know, doesn’t make up a huge part of the SAT —having this diagram handy means you won’t need to spend a ton of time memorizing formulas beforehand (though you should take care to memorize some important formulas not included in the diagram ).

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Published online before print November 2011 , doi: 10.2215/​CJN.01970211

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Author Affiliations

Correspondence:

J.A.M. and C.M.-C. contributed equally to this work.

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Summary

Hematuria is a common finding in various glomerular diseases. This article reviews the clinical data on glomerular hematuria and kidney injury, as well as the pathophysiology of hematuria-associated renal damage. Although glomerular hematuria has been considered a clinical manifestation of glomerular diseases without real consequences on renal function and long-term prognosis, many studies performed have shown a relationship between macroscopic glomerular hematuria and AKI and have suggested that macroscopic hematuria-associated AKI is related to adverse long-term outcomes. Thus, up to 25% of patients with macroscopic hematuria–associated AKI do not recover baseline renal function. Oral anticoagulation has been associated with glomerular macrohematuria–related kidney injury. Several pathophysiologic mechanisms may account for the tubular injury found on renal biopsy specimens. Mechanical obstruction by red blood cell casts was thought to play a role. More recent evidence points to cytotoxic effects of oxidative stress induced by hemoglobin, heme, or iron released from red blood cells. These mechanisms of injury may be shared with hemoglobinuria or myoglobinuria-induced AKI. Heme oxygenase catalyzes the conversion of heme to biliverdin and is protective in animal models of heme toxicity. CD163, the recently identified scavenger receptor for extracellular hemoglobin, promotes the activation of anti-inflammatory pathways, opening the gates for novel therapeutic approaches.

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Glomerular hematuria, when not accompanied by mild to severe proteinuria, has been considered a benign manifestation of glomerular diseases that does not influence long-term prognosis. Nevertheless, macroscopic hematuria can induce AKI through a direct harmful effect on renal tubules. Information on pathogenesis and long-term consequences of such macrohematuria-induced AKI is remarkably scarce. The aim of this article is to review the clinical data on hematuria and glomerular disease, as well as the pathophysiology of hematuria-associated AKI.

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Hematuria is defined as the presence of red blood cells (RBCs) in urine ( 1 ). Macroscopic hematuria is always pathologic and is characterized by massive presence of RBCs in urine. Microscopic hematuria is defined by the presence of more than 2 RBCs per high-power field in urine sediment in the absence of colored urine. Macroscopic hematuria may be differentiated from hemoglobinuria and myoglobinuria: a heme-positive red supernatant may contain hemoglobin or myoglobin, whereas RBCs are observed in the sediment in hematuria. Smoky gray–colored urine, the presence of RBC casts, and dysmorphic RBCs favor a glomerular origin of hematuria, and blood clots and bright red urine support a urinary tract origin.

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Figure 4
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W-derived transcripts, expression profiles and genomic PCR amplification. (A) Hierarchical cluster analysis of W-derived transcripts. Expression profiles of transcripts in mixed embryos (0–24 hpo) were clustered and visualized in a heatmap. (B) PCR amplification of W-derived transcripts in cDNA (Left panel) and gDNA (Right panel). RT-PCR (cDNA) showed expression as cluster A (female embryos specific) or cluster B (in both female and male embryos). However, a PCR test of genomic DNA showed both transcript RNAs were female-specific, indicating that they are W-derived, but cluster A RNAs are zygotically expressed in female embryos whereas cluster B RNAs are probably maternal RNAs deposited into eggs. (C) qPCR of a cluster B RNA (DN42314_c0) from 0 to 36 hpo exhibited its sex-biased expression in embyos.

Figure 4
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W-derived transcripts, expression profiles and genomic PCR amplification. (A) Hierarchical cluster analysis of W-derived transcripts. Expression profiles of transcripts in mixed embryos (0–24 hpo) were clustered and visualized in a heatmap. (B) PCR amplification of W-derived transcripts in cDNA (Left panel) and gDNA (Right panel). RT-PCR (cDNA) showed expression as cluster A (female embryos specific) or cluster B (in both female and male embryos). However, a PCR test of genomic DNA showed both transcript RNAs were female-specific, indicating that they are W-derived, but cluster A RNAs are zygotically expressed in female embryos whereas cluster B RNAs are probably maternal RNAs deposited into eggs. (C) qPCR of a cluster B RNA (DN42314_c0) from 0 to 36 hpo exhibited its sex-biased expression in embyos.

To confirm that these RNAs were indeed W-derived, five candidates were selected for examining their expression in individual embryos. We designed primers using their W- k -mers ( Supplementary Table S3 ) in the same way as for W-BAC ends. We isolated both DNA and RNA from single embryos aged 16 hpo, and used DNA to detect the presence of the W chromosome by PCR ( Supplementary Fig. S3 ), while we followed RNA by RT-PCR to examine expression ( Fig.4B ). The RT-PCR results showed cluster A RNAs were expressed only in female embryos, whereas cluster B RNAs were expressed in both female and male embryos. For further verification, we performed a separate PCR test of both cluster A and B RNAs with female and male genomic DNA. For these five RNAs, PCR bands appeared only in female genomic DNA ( Fig.4B ), indicating both cluster RNAs were transcribed on the W chromosome. These results suggested that cluster B RNAs are very likely to be maternal RNAs deposited in the embryos as they are present throughout early embryos of both females and males. An interesting phenomenon in RT-PCR of cluster B RNAs is that bands were brighter in female than in male, which indicated the expressions of cluster B RNAs are different in female and male embryos. Thus, we did the qPCR of a cluster B RNAs (DN42314_c0) in female and male embryos from 0 to 36 hpo, and found sex-biased expression starting from 8 hpo ( Fig.4C ). The expression levels were almost same in both sex embryos before 8 hpo, but after that, it seemed to fade away in male embryos and de novo expressed in female embryos.

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