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Lysosomal storage diseases form a category of genetic disord

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Lysosomal storage diseases form a category of genetic disord [#permalink] New post 18 Jul 2010, 03:48
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Lysosomal storage diseases form a category of genetic disorders resulting from defective enzymes that normally function to degrade unneeded molecules in cells. These enzymes do their work in the lysosome, a small compartment in a cell analogous to a garbage disposal. The lysosome contains between thirty and forty different degradative enzymes. When any one of the lysosomal enzymes is defective, the molecules requiring that specific enzyme for their degradation will accumulate and cause that individual's lysosomes to swell enormously. The physiological effects of such swelling on the individual include motor and mental deterioration, often to the point of premature death. But each disease resulting from one specific defective lysosomal enzyme has its own characteristic pathology. The age of onset, rate of progression, and severity of the clinical symptoms observed in patients with the same defective lysosomal enzyme are highly variable. For many years, this variability in patients with the same defective enzyme puzzled scientists. Only recently have researchers begun to answer the riddle, thanks to a genetic analysis of a lysosomal storage disorder known as Tay-Sachs disease.

As in most lysosomal storage diseases, patients suffering from Tay-Sachs disease show both mental and motor deterioration and variability in age of onset, progression, and severity. Physicians have categorized the patients into three groups: infantile, juvenile, and adult, based on onset of the disease. The infantile group begins to show neurodegeneration as early as six months of age. The disease advances rapidly and children rarely live beyond 3 years old. The first symptoms of the disease appear in juvenile cases between 2 and 5 years of age, with death usually occurring around age 15. Those with the adult form generally live out a normal lifespan, suffering from milder symptoms than do those with the infantile and juvenile forms. Researchers hoped that the categorization would yield insight into the cause of the variability of symptoms among Tay-Sachs patients, but this turned out not to be the case.

In Tay-Sachs disease, undegraded materials accumulate mainly in the lysosomes in the brains of patients, but the kinds of molecules left undegraded and the specific identity of the defective lysosomal enzyme responsible for the malfunction were not discovered until the 1950s and 60s, respectively. The main storage molecule was found to be a lipid-like material known as GM2 ganglioside. The defective enzyme was later identified as hexosaminidase. In 1985, the gene coding for the normal hexosaminidase enzyme was cloned and its DNA sequence determined. Shortly thereafter, the DNA sequences of genes encoding hexosaminidase from many Tay-Sachs patients were studied. It soon became apparent that not one or two but many different types of mutations in the hexosaminidase gene could result in Tay-Sachs disease. Some of the mutations prevented the synthesis of any hexosaminidase, preventing all such enzyme activity in the cell. Patients with this type of mutation all had the infantile form of Tay-Sachs disease. Other mutations were found in certain regions of the gene coding for areas of the enzyme known to be critical for its catalytic activity. Such mutations would allow for only extremely crippled hexosaminidase activity. Most of the patients with these mutations clustered in the juvenile category. Adult Tay-Sachs patients presented mutations in the regions of the hexosaminidase gene that were less important for the enzyme's activity than were those affected in juvenile patients. Scientists quickly hypothesized that the variation in age of onset and severity of Tay-Sachs disease correlated with the amount of residual enzymatic activity allowed by the genetic mutation. Though more research is needed to demonstrate similarity with other lysosomal storage diseases, the work done on Tay-Sachs disease has already offered a promising glimpse into the underlying mechanisms of these disorders.
Q1:
The passage suggests that which of the following lines of inquiry would be most useful in determining the relevance of the research done on Tay-Sachs disease to lysosomal storage diseases generally?
A. Do patients suffering from other lysosomal storage diseases have the same mortality rate as those suffering from Tay-Sachs?
B. Do other lysosomal storage diseases affect the hexosaminidase gene?
C. How many different mutations are present in the defective genes responsible for other lysosomal storage diseases?
D. Does the onset of other lysosomal storage diseases vary with the location of mutations in DNA sequences?
E. What purpose does GM2 ganglioside serve in the human body?
[Reveal] Spoiler:
D


Q2:
It can be inferred from the passage that which of the following statements is true of lysosomal storage diseases?
A. They are generally caused by mutations to the hexosaminidase gene.
B. They are undetectable until physical symptoms are present.
C. They can be fatal even when allowing some enzymatic activity.
D. They are most lethal when onset is in a patient's infancy.
E. Their causes were unknown before the 1950s.
[Reveal] Spoiler:
C


Q3:
The author of the passage is primarily concerned with
A. illuminating the physiological consequences of Tay-Sachs disease
B. explaining the importance of research on a specific disease to other diseases of that type
C. arguing for a more detailed examination of lysosomal storage diseases
D. challenging a traditional view of a class of diseases as incomplete
E. describing the implications of genetic mutations for mortality rates
[Reveal] Spoiler:
B


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Last edited by fameatop on 03 Aug 2013, 21:35, edited 2 times in total.
OA not Provided & improper formatting
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Re: Urgent help on Tough MGMAT RC [#permalink] New post 18 Jul 2010, 17:24
C,D,B
OA pls?

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Re: Urgent help on Tough MGMAT RC [#permalink] New post 20 Jul 2010, 00:39
Lots of information given. It took a whopping 9 minutes to answer the passage. Please provide the OA.

1) C. Read lines 3 to 5 in passage 3.
2) d. Answers to Inference q's will be in the passages. But the answers will use a different wording than in the passage. Read para2
3)b. The answer can be found in the last few lines of the final paragraph.
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Re: Urgent help on Tough MGMAT RC [#permalink] New post 20 Jul 2010, 06:35
me to took 9 mins......

1)D....just saw last few lines ...may be wrong ?

2)D...The infantile group begins to show neurodegeneration as early as six months of age and children rarely live beyond 3 years old. The first symptoms of the disease appear in juvenile cases between 2 and 5 years of age, with death usually occurring around age 15. Those with the adult form generally live out a normal lifespan, suffering from milder symptoms than those with the infantile and juvenile forms.

3)B...Intially starts with lysosomal storage diseases and becomes more specific...so i think this is the one ...
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Re: Urgent help on Tough MGMAT RC [#permalink] New post 26 Jul 2010, 02:13
The answer to question 2 is C

There is no information regarding the number of death proportional to onset. It does say infantile death does occur, but the information would be false if it were known that no of cases of infantile diseases is very very less as compared to adolescent

lets say perhaps out of 1000 2 infantile cases but 50 adolescent cases

without concrete info D cannot be true.
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Re: Urgent help on Tough MGMAT RC [#permalink] New post 01 Aug 2010, 17:38
OA?
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Re: Urgent help on Tough MGMAT RC [#permalink] New post 16 Aug 2010, 03:34
answer for the second question is 'C' i got it from other forums
Explanation is (C) CORRECT. This choice states that it can be inferred that lysosomal storage diseases "can be fatal even when allowing some enzymatic activity." This can be inferred from the fact that people suffering from juvenile Tay-Sachs have "extremely crippled hexosaminidase activity" (lines 91-93) and generally live to only 15 years of age (line 49).
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Re: Urgent help on Tough MGMAT RC [#permalink] New post 31 Aug 2010, 18:42
C D B
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Re: Urgent help on Tough MGMAT RC [#permalink] New post 09 Sep 2010, 12:33
D-found in the last 3 sentences of the paragraph. The puzzling question is what causes variability. Scientists are less concerned to figure out the number of possible genetic mutations of the deseases (even though it might be the next step of the research) , they would be happy enough to figure out the cause of variability before they go any futher.

D

B
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Re: Urgent help on Tough MGMAT RC [#permalink] New post 15 Oct 2010, 21:57
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Really tough passage. RC is one of my strengths, and it still took me 7 min to do this passage and the associated questions.

If you're like me, you probably have an "oh crap" meter that kicks in pretty quickly after starting a passage. If you're not a science person, that meter probably kicked in *really* quickly here. When/if that happens, you have two options (1) panic or (2) focus even more. And although it may not seem to be the case, the path you take *is* a choice. What are the concrete things that you DO understand? What are the structural elements of the passage that will allow you to map out what is important and what is microscopic detail you may not need to pay attention to?

My mental process reading and taking notes on this passage went something like what is below. My thoughts are in parentheses, and the structural words I paid attention to are highlighted. In general, when I read--ESPECIALLY if it's a topic I don't understand--my mental highlighter pops out for structure words.

Lysosomal storage diseases (looks like it's going to be a science psg) form a category of genetic disorders resulting from defective enzymes that normally function to break down unneeded molecules in cells. (part of a category...ok) These enzymes do their work in the lysosome, a small compartment in a cell analogous to a garbage disposal. (lysowhatever =cellular garbage disposal) When any one of the lysosomal enzymes is defective, the molecules that would have been broken down by that enzyme instead accumulate and cause that individual's lysosomes to swell enormously, resulting in motor and mental deterioration, often to the point of premature death. (broken garbage disposal...overflow...bad outcome) The age of onset, rate of progression, and severity of the clinical symptoms observed in patients with the same defective lysosomal enzyme are highly variable. For many years, this variability in patients with the same defective enzyme puzzled scientists. Only recently have researchers begun to answer the riddle, thanks to a genetic analysis of a particular lysosomal storage disorder known as Tay-Sachs disease. (BINGO-- contender for main thought...looks like this is going to be a problem-solution type passage)

NOTES FOR PARAGRAPH 1:
LSD-genetic disorder (defective enzymes in lyso. --cell garbage disp.)
broken disp->swelling/death?
symptoms VAR.
RECENTLY begun to answer WHY VAR. thanks to TSD (type of LSD)


As in most lysosomal storage diseases, patients suffering from Tay-Sachs disease show both mental and motor deterioration and variability in age of onset, progression, and severity. (ok still focus on VAR...paragraph will be about this) Physicians have categorized the patients into three groups based on onset of the disease: infantile, juvenile, and adult. (3 types, ok) The infantile group begins to show neurodegeneration as early as six months of age and children rarely live beyond 3 years old. The first symptoms of the disease appear in juvenile cases between 2 and 5 years of age, with death usually occurring around age 15. Those with the adult form generally live out a normal lifespan, suffering from milder symptoms than those with the infantile and juvenile forms.

NOTES FOR PARAGRAPH 2:
VAR in onset, progress, severity
Inf-show @ 6 mo, die @ 3 yr
Juv-show@ 2-5, die @ 15
Adult-normal die, mild


In Tay-Sachs disease, scientists were aware that molecules accumulated mainly in the brains of patients, but they did not discover the specific identity of the defective lysosomal enzyme responsible for the malfunction, hexosaminidase,(culprit=hexoblahblah) until the 1960s. (id specific enzyme....first specific date in psg! chronology starting...a lot of science-y words focus on DATES and subject-verbs to get gists of sentences) In 1985, the DNA sequence for the normal enzyme was determined. Shortly thereafter, the DNA sequences of genes encoding hexosaminidase from many Tay-Sachs patients were studied. It soon became apparent that not one or two but many different types of mutations in the hexosaminidase gene could result in Tay-Sachs disease. (many diff causes) These different mutations resulted in various levels of impaired enzymatic activity; those in the infantile category had little to no normal activity, while those in the adult category suffered only moderate impairment. (infant/adult diff...) Scientists quickly hypothesized that the variation in age of onset and severity of Tay-Sachs disease correlated with the amount of residual enzymatic activity allowed by the particular genetic mutation a patient had. Though more research is needed to demonstrate similarity with other lysosomal storage diseases, the work done on Tay-Sachs disease has already offered a promising glimpse into the underlying mechanisms of these disorders.

NOTES FOR PARAGRAPH 3:
ID enz. (hex.) in '60s
'85 seq. normal enz., LATER-> TS hex. seq.
MANY mutations -> diff in inf/adult TS
sci: VAR effects bc of var mutations ....promising glimpse of LSD mech !



Took me a little longer than I would have liked (close to 4 min) but I can forgive myself bc (1) it was a really tough passage (2) I tend to skew more twds quickly moving through questions after taking slightly longer to read and (3) not forgiving myself wouldn't do me any good---I just spent 4 min so what I need to spend my time on is focusing on the next task, *not* beating myself up for spending 1 more min than the "ideal" test taker.

Q.1
Q is about relevance of TSD research to general LSD...
Thought process...was this vaguely alluded to in P1? Quick look at my notes says no--oh wait, it's that last underlined part in my P3 notes.
(A) mortality rate? not relevant--research was about mutation (mortality rate was in P2, and more about categorization than research) Out.
(B) hexoblahblah gene was specifid TSD culprit, but promise was about underlying MECHANISM of "VAR mutations-> VAR effects" not the enzyme itself. Out.
(C) Hmmm...something related to number of diff mutations...I don't exactly understand what this says on a first quick read so I'll leave it for now and keep going.
(D) Pretty much what the last sentences said about TSD...var mutation->var effects. Keep it.
(E) Purpose of hexoblahblah...don't care (for same reason as choice B). Out.

I'm down to C and D, and D looked pretty good. I take one more (careful) read of C to be sure. Would the answer to the question in choice C, a *number*, provide useful information about how the mechanisms are analogous? Beyond knowing that the number is greater than 1, probably not. Whereas with D, knowing the link between different ages of onset/severities and different mutations is exactly the kind of mechanism explored with TSD. Vote for D.

Q.2
(A) Sneaky GMAC, I see your trap-- no, hexoblahblah was the culprit for TSD, not LSD in general. Out.
(B) Can't remember from passage, leave it for now.
(C) Can't remember from passage, leave it for now.
(D) Same trap as A. Out.
(E) Dates only mentioned in reference to ID-ing enzymes for TSD. Out.

Now I search through the passage to choose between B and C. LSD in general are talked about a lot in P1. The third sentence of P1 says when ANY ONE of the enzymes is defective, bad things happen (up to and including death).
I'll go with C. (B makes a strong black-and-white claim--"undetectable" that I can't find concrete evidence for, and since C lines up with what the passage says there isn't a reason for me to waste more time looking.)

Q.3
A general question--phew. I've done a lot of hard work already so this one should come quickly. The passage mainly seemed to focus on recent research findings for TSD (var mutations=var manifestations of disease) and how this could illuminate the larger category of LSDs.

(A) Does not mention link between TSD and LSDs. Out.
(B) Pretty much what I said above. Keep it.
(C) Arguing against who? It seems like scientists are looking into this stuff in detail already. Out.
(D) What is the "traditional view"? Out.
(E) The first part of this sounds good, but the second ("mortality rates") is too narrow-- there are all kinds of implications (age of onset, severity, etc). Out.

Wow, this is a LONG post. RC is really hard to cover in detail without, well, a lot of details. And RC approaches/note-taking will vary tremendously among students. But as you're working on a really challenging passage, the most important thing is to pay attention to the specifics in structure (NOT of content details...that part comes later, when you're answering questions) --don't let passage itself overwhelm you by becoming a general wash of verbiage. And if you didn't understand the passage entirely (and I'm not even sure I did...there's a lot of technical stuff in there that I didn't both trying to grasp fully), there are still some answer choices that you can eliminate based on what you specifically DID understand. After you've eliminated what you can eliminate, just guess and move on, no hard feelings. Hope this helps.
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Re: Urgent help on Tough MGMAT RC [#permalink] New post 20 Oct 2010, 09:33
Parker,

Thanks for such nice explanation +1. I have read it over and over again to get it all clear in my mind.
However, few doubts:
1. Do u advice to write notes? I guess, It will take somewhere around a minute to put it down.
2. In case, If I fail to understand something in passage. In my case, while dealing with 700 level RC, many a times I do fail to understand some bit in the passage. What would you suggest?

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Re: Urgent help on Tough MGMAT RC [#permalink] New post 11 Dec 2010, 13:19
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Oh my goodness, I'm so sorry I just saw that I hadn't replied to this! You may have already taken your test but just in case--

Your Questions:
1. Yes, I absolutely write notes. There's way too much information to hold in my brain, so I make a structural map of the passage as I go along-- we teach something called the "skeletal sketch" in classes; this method focuses on comprehending much of the first paragraph and only the gist of the second. Within that technique there is a still a spectrum of how much/little people write for their own comfort levels--I tend to read pretty quickly but need to stay active to not have my attention wander, so I may write a little more than others. The important thing is to avoid getting bogged down in details during the entire passage-- comprehending every single thing is not your goal (it would take waaay to long and probably not yield you many points. The heavy detail work is for (1) when you're reading the beginning of the passage to get the gist and (2) when you go back to the passage while answering specific questions).

2. The answer to your second question is related to the answer to your first-- do NOT try to comprehend everything-- there's not enough time, so don't stress out if you don't grasp every little detail. Structure and main point are your goals for the first read. The little details can be dealt with if (and only if!) you're asked about them in the questions--you get points for correct answers, not for total comprehension :)
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Re: Urgent help on Tough MGMAT RC [#permalink] New post 15 Dec 2010, 06:52
+1 to Parker for coming back though the qstn is age old
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Lysosomal storage diseases form a category of genetic [#permalink] New post 23 Dec 2012, 06:15
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Lysosomal storage diseases form a category of genetic
disorders resulting from defective enzymes that normally
function to degrade unneeded molecules in cells. These
enzymes do their work in the lysosome, a small
compartment in a cell analogous to a garbage disposal.
The lysosome contains between thirty and forty different
degradative enzymes. When any one of the lysosomal
enzymes is defective, the molecules requiring that specific
enzyme for their degradation will accumulate and cause
that individual’s lysosomes to swell enormously. The
physiological effects of such swelling on the individual
include motor and mental deterioration, often to the point
of premature death. But each disease resulting from one
specific defective lysosomal enzyme has its own
characteristic pathology. The age of onset, rate of
progression, and severity of the clinical symptoms
observed in patients with the same defective lysosomal
enzyme are highly variable. For many years, this variability
in patients with the same defective enzyme puzzled
scientists. Only recently have researchers begun to answer
the riddle, thanks to a genetic analysis of a lysosomal
storage disorder known as Tay-Sachs disease.

As in most lysosomal storage diseases, patients suffering
from Tay-Sachs disease show both mental and motor
deterioration and variability in age of onset, progression,
and severity. Physicians have categorized the patients into
three groups: infantile, juvenile, and adult, based on onset
of the disease. The infantile group begins to show
neurodegeneration as early as six months of age. The
disease advances rapidly and children rarely live beyond
3 years old. The first symptoms of the disease appear in
juvenile cases between 2 and 5 years of age, with death
usually occurring around age 15. Those with the adult
form generally live out a normal lifespan, suffering from
milder symptoms than do those with the infantile and
juvenile forms. Researchers hoped that the categorization
would yield insight into the cause of the variability of
symptoms among Tay-Sachs patients, but this turned out
not to be the case.

In Tay-Sachs disease, undegraded materials accumulate
mainly in the lysosomes in the brains of patients, but the
kinds of molecules left undegraded and the specific identity
of the defective lysosomal enzyme responsible for the
malfunction were not discovered until the 1950s and 60s,
respectively. The main storage molecule was found to be
a lipid-like material known as GM2 ganglioside. The
defective enzyme was later identified as hexosaminidase.
In 1985, the gene coding for the normal hexosaminidase
enzyme was cloned and its DNA sequence determined.
Shortly thereafter, the DNA sequences of genes encoding
hexosaminidase from many Tay-Sachs patients were
studied. It soon became apparent that not one or two but
many different types of mutations in the hexosaminidase
gene could result in Tay-Sachs disease. Some of the
mutations prevented the synthesis of any hexosaminidase,
preventing all such enzyme activity in the cell. Patients
with this type of mutation all had the infantile form of
Tay-Sachs disease. Other mutations were found in certain
regions of the gene coding for areas of the enzyme known
to be critical for its catalytic activity. Such mutations would
allow for only extremely crippled hexosaminidase activity.
Most of the patients with these mutations clustered in the
juvenile category. Adult Tay-Sachs patients presented
mutations in the regions of the hexosaminidase gene that
were less important for the enzyme’s activity than were
those affected in juvenile patients. Scientists quickly
hypothesized that the variation in age of onset and severity
of Tay-Sachs disease correlated with the amount of
residual enzymatic activity allowed by the genetic mutation.
Though more research is needed to demonstrate similarity
with other lysosomal storage diseases, the work done on
Tay-Sachs disease has already offered a promising
glimpse into the underlying mechanisms of these
disorders.

1) The passage suggests that which of the following lines of inquiry would be most useful in determining the relevance of the research done on Tay-Sachs disease to lysosomal storage diseases generally?

. Do patients suffering from other lysosomal storage
diseases have the same mortality rate as those
suffering from Tay-Sachs?
. Do other lysosomal storage diseases affect the
hexosaminidase gene?
· How many different mutations are present in the
defective genes responsible for other lysosomal
storage diseases?
· Does the onset of other lysosomal storage diseases
vary with the location of mutations in DNA sequences?
· What purpose does GM2 ganglioside serve in the
human body?

2. It can be inferred from the passage that which of the following statements is true of lysosomal storage diseases?

· They are generally caused by mutations to the
hexosaminidase gene.
· They are undetectable until physical symptoms are
present.
· They can be fatal even when allowing some
enzymatic activity.
· They are most lethal when onset is in a patient’s
infancy.
· Their causes were unknown before the 1950s.

3. The author of the passage is primarily concerned with
· illuminating the physiological consequences of Tay-
Sachs disease
· explaining the importance of research on a specific
disease to other diseases of that type
· arguing for a more detailed examination of lysosomal
storage diseases
· challenging a traditional view of a class of diseases
as incomplete
· describing the implications of genetic mutations for
mortality rates
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Re: Lysosomal storage diseases form a category of genetic [#permalink] New post 26 Dec 2012, 12:21
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Re: Lysosomal storage diseases form a category of genetic disord [#permalink] New post 15 Oct 2013, 23:38
It took me exactly 10 mins for this RC

1.C
2.D
3.B

Still I am not sure, i got the answers correct.
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Re: Lysosomal storage diseases form a category of genetic disord [#permalink] New post 16 Oct 2013, 03:47
My answers are- 1) C 2) D 3) B
It took me nearly 9- 10 mins to solve this question, certainly more than double the time ideal time. This passage is 600 words. Can we expect such long passages with only 3 question on the GMAT. If yes, I probably need to improve my timings.. :D

I have one more doubt- how to effectively tackle and let go of few sentences that I could not understand properly. Why I spend extra time in sentences I dont understand is beacuse I have mostly seen questions coming from that specific part of the passage. (I am sorry I cant provide any example in this passage though)..
Re: Lysosomal storage diseases form a category of genetic disord   [#permalink] 16 Oct 2013, 03:47
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Lysosomal storage diseases form a category of genetic disord

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