Hello,
Here are two examples of OCR. They are both done from the same scanned image.
The first was scanned By VueScan which then did the OCR. The second used the
same scan, but it was processed by ABBYY FineReader.
Notice that VueScan has treated the double page as just one page thereby
producing utter rubbish.
Cheers,
Anne
VueScan
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ity (0 diSCz\S¢. llfltlt nrc' directed at Llmlclïlitmlllig how μvnvtlc vawlutlon
'llicsc nutrient signals ln turn induce robust hormonal responses that
explains differences in the dietary responses of lndlvldtmls. l*`«›r example,
further impact regulatory control over a broad range of physiologic pro-
suppose that you and your co-worker agree to eat the exact saine diet for
cesses, and these responses can differ greatly depending on both the mac-
one month. Results of laboratory work indicate your eo-workers cho- ronutrient
and micronutrient compositions of the diet. Moreover, there
lesterol increased while yours decreased. A nutrigenetic approach would are
important interactive effects that change the way the body processes
look at just a few gene candidates (“suspects') and aim to determine the ge-
nutrients. For example, iron is handled very differently by the body when
netic differences between you and your co-worker and how those genetic consumed
with vitamin C, and saturated fat intake has a variable effect in
variations (alleles) relate to your distinct cholesterol responses. the body
depending on how much carbohydrate is consumed along with
it. And finally, when you add other variables like dosage and timing of
Nutrigenomics, on the other hand is concerned with discovery. _. it looks
ingestion that Can also change the Signal dynamics) the Vast permutations
at many genes at Once' A nutrigen0miCS approach might involve extract' of
nutrient signals impacting physiologic outcomes become an extraordi-
ing a small piece of adipose tissue from you and your co-worker before narny
Complex system t 0 Study
and after your 1-month diet to measure the activity of an array of hun-
dreds of genes to see which ones were responsive to the diet. Sometimes
the gene products (proteins, metabolites) are measured, so nutrigenom-
C°mPleXitY °f the Genome
ics is tighdy linked With lproteomicsl and cmetabolomicsl' In Short nu' The
genome consists of over 3 billion base pairs made up of long chains of
trigenetics analyzes how genetic variation among people allows them to adenine
guanine Cytosine and thymine on the 23 Chmmosûmest Humans
respond diñerently to the Same diet Or the Same Supplement' whereas have about
21 000 genes, each encoding a protein, scattered around the
nutrigenomics refers to how nutrients alter gene expression. Sometimes enome
Theltength of DNA that contains a t ical ene extends about
distinguishing between the two is not clear-cut and some experts prefer îo 000
Éase pairs of Which only a fraction Sšpl 00š__a~CtuanY encode
to use a catch all term like nutritional genomics to describe any effort that
the protein Sequence. This means the majority of the genome (~98%)
probes the relationships between genes and diet' consists of expanses of DNA
whose function(s) remain unknown. This
is sometimes called 'junk' DNA. Interestingly, functions are being found
Complexity of Nutritional Signals for some of this junk. Por example some
noncoding DNA sequences
are genetic “switches” that regulate when and where genes are expressed.
Nutrients are broadly classified into 4 macronutrient categories (carbo- One
expert estimates that 5% of the nOn_COding DNA has a function S0
hydrate, fat, protein, alcohol) that provide energy. We also need a regular
Whether a DNA Variant is found in a gene Or in a nOn_C0ding expanse of
source of several essential micronutrients (vitamins, minerals) that our
DNA, it may have meaning for some yet unknown dietary response.
body cannot make and we therefore must obtain from food. There are
also a host of other nonessential chemicals in food broadly referred to as Any
one person's DNA is about 99-99.5% identical to any other person°s
phytonutrients that can elicit important effects on metabolism and health. DNA.
There are two major causes of person-to-person genetic differenc-
Therefore when we eat typical meals consisting of multiple foods, the body l
es. The major cause is named copy number variants. These are many
must process potentially a hundred or more different chemical signals.
different places in the DNA where the number of copies of a gene can
vary from one to many hundreds. For instance, on average, people from
cultures that historically have high starch diets (such as Japanese and Eu-
l
136 137
i
ABBYY FineReader
Th$ Art aM ScJtnctof
ity to disease. Both are directed at understanding how genetic variation
explains differences in the dietary responses of individuals. l;or example,
suppose that you and your co-worker agree to eat the exact same diet for
one month. Results of laboratory work indicate your co-worker's cho-
lesterol increased while yours decreased. A nutrigenetic approach would
look at just a few gene candidates ('suspects') and aim to determine the ge-
netic differences between you and your co-worker and how those genetic
variations (alleles) relate to your distinct cholesterol responses.
Nutrigenomics, on the other hand is concerned with discovery... it looks
at many genes at once. A nutrigenomics approach might involve extract-
ing a small piece of adipose tissue from you and your co-worker before
and after your 1-month diet to measure the activity of an array of hun-
dreds of genes to see which ones were responsive to the diet. Sometimes
the gene products (proteins, metabolites) are measured, so nutrigenom-
ics is tightly linked with 'proteomics' and 'metabolomics'. In short nu-
trigenetics analyzes how genetic variation among people allows them to
respond differently to the same diet or the same supplement, whereas
nutrigenomics refers to how nutrients alter gene expression. Sometimes
distinguishing between the two is not clear-cut and some experts prefer
to use a catch all term like nutritional genomics to describe any effort that
probes the relationships between genes and diet.
Complexity of Nutritional Signals
Nutrients are broadly classified into 4 macronutrient categories (carbo-
hydrate, fat, protein, alcohol) that provide energy. We also need a regular
source of several essential micronutrients (vitamins, minerals) that our
body cannot make and we therefore must obtain from food. There are
also a host of other nonessential chemicals in food broadly referred to as
phytonutrients that can elicit important effects on metabolism and health.
Therefore when we eat typical meals consisting of multiple foods, the body
must process potentially a hundred or more different chemical signals.
136
Ihese nutrient signals in turn Induce robust hormonal responses that
further impact regulatory control over a broad range of physiologic pro-
cesses, and these responses can differ greatly depending on both the mac-
ronutrient and micronutrient compositions of the diet. Moreover, there
are important interactive effects that change the way the body processes
nutrients. For example, iron is handled very differently by the body when
consumed with vitamin C, and saturated fat intake has a variable effect in
the body depending on how much carbohydrate is consumed along with
it. And finally, when you add other variables like dosage and timing of
ingestion that can also change the signal dynamics, the vast permutations
of nutrient signals impacting physiologic outcomes become an extraordi-
narily complex system to study.
Complexity of the Genome
The genome consists of over 3 billion base pairs made up of long chains of
adenine, guanine, cytosine and thymine on the 23 chromosomes. Humans
have about 21,000 genes, each encoding a protein, scattered around the
genome. The length of DNA that contains a typical gene extends about
50,000 base pairs, of which only a fraction, say 1,000—actually encode
the protein sequence. This means the majority of the genome (-98%)
consists of expanses of DNA whose function(s) remain unknown. This
is sometimes called 'junk' DNA. Interestingly, functions are being found
for some of this junk. For example some noncoding DNA sequences
are genetic "switches" that regulate when and where genes are expressed.
One expert estimates that 5% of the non-coding DNA has a function. So
whether a DNA variant is found in a gene or in a non-coding expanse of
DNA, it may have meaning for some yet unknown dietary response.
Any one person's DNA is about 99-99.5% identical to any other persons
DNA. There are two major causes of person-to-person genetic differenc-
es. The major cause is named copy number variants. These are many
different places in the DNA where the number of copies of a gene can
vary from one to many hundreds. For instance, on average, people from
cultures that historically have high starch diets (such as Japanese and Eu-
137
Iht Art emaScTincio} low UArMfiywm UVMf
ity to disease. Noth arc directed at understanding how genetic variation
explains differences in the dietary responses of individuals. I-'or example,
suppose that you and your co-worker agree to eat the exact same diet for
one month. Results of laboratory work indicate your co-worker's cho-
lesterol increased while yours decreased. A nutrigenetic approach would
look at just a few gene candidates ('suspects') and aim to determine the ge-
netic differences between you and your co-worker and how those genetic
variations (alleles) relate to your distinct cholesterol responses.
Nutrigenomics, on the other hand is concerned with discovery... it looks
at many genes at once. A nutrigenomics approach might involve extract-
ing a small piece of adipose tissue from you and your co-worker before
and after your 1-month diet to measure the activity of an array of hun-
dreds of genes to see which ones were responsive to the diet. Sometimes
the gene products (proteins, metabolites) are measured, so nutrigenom-
ics is tightly linked with 'proteomics' and 'metabolomics'. In short nu-
trigenetics analyzes how genetic variation among people allows them to
respond differently to the same diet or the same supplement, whereas
nutrigenomics refers to how nutrients alter gene expression. Sometimes
distinguishing between the two is not clear-cut and some experts prefer
to use a catch all term like nutritional genomics to describe any effort that
probes the relationships between genes and diet.
Complexity of Nutritional Signals
Nutrients are broadly classified into 4 macronutrient categories (carbo-
hydrate, fat, protein, alcohol) that provide energy. We also need a regular
source of several essential micronutrients (vitamins, minerals) that our
body cannot make and we therefore must obtain from food. There are
also a host of other nonessential chemicals in food broadly referred to as
phytonutrients that can elicit important effects on metabolism and health.
Therefore when we eat typical meals consisting of multiple foods, the body
must process potentially a hundred or more different chemical signals.
136
i r»nmm/n
'Ihesc nutrient signals In turn Induce robust hormonal responses that
further impact regulatory control over a broad range of physiologic pro-
cesses, and these responses can differ greatly depending on both the mac-
ronutrient and micronutrient compositions of the diet. Moreover, there
are important interactive effects that change the way the body processes
nutrients. For example, iron is handled very differently by the body when
consumed with vitamin C, and saturated fat intake has a variable effect in
the body depending on how much carbohydrate is consumed along with
it. And finally, when you add other variables like dosage and timing of
ingestion that can also change the signal dynamics, the vast permutations
of nutrient signals impacting physiologic outcomes become an extraordi-
narily complex system to study.
Complexity of the Genome
The genome consists of over 3 billion base pairs made up of long chains of
adenine, guanine, cytosine and thymine on the 23 chromosomes. Humans
have about 21,000 genes, each encoding a protein, scattered around the
genome. The length of DNA that contains a typical gene extends about
50,000 base pairs, of which only a fraction, say 1,000—actually encode
the protein sequence. This means the majority of the genome (-98%)
consists of expanses of DNA whose function(s) remain unknown. This
is sometimes called 'junk' DNA. Interestingly, functions are being found
for some of this junk. For example some noncoding DNA sequences
are genetic "switches" that regulate when and where genes are expressed.
One expert estimates that 5% of the non-coding DNA has a function. So
whether a DNA variant is found in a gene or in a non-coding expanse of
DNA, it may have meaning for some yet unknown dietary response.
Any one person's DNA is about 99-99.5% identical to any other person's
DNA. There are two major causes of person-to-person genetic differenc-
es. The major cause is named copy number variants. These are many
different places in the DNA where the number of copies of a gene can
vary from one to many hundreds. For instance, on average, people from
cultures that historically have high starch diets (such as Japanese and Eu-
137
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