Annemarie Bourlind Executive Summary

Annemarie Bourlind Executive Summary
35% Introduction Deal
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The ESSENTIAL 5
Annemarie Börlind's Essential 5 skin care collection is an assortment of products crucial to
achieving great skin.
The Essential 5 collection includes:
1. Orange Blossom Energizer
2. Ceramide Vital Fluid
3. Eye Wrinkle Cream
4. Facial Firming Gel
5. Rose Blossom Revitalizer
This collection of skin care products is, by far, Börlind's most popular. Each product offers 5 distinct
skin care solutions:
1. Concentrated Vitamin C Serum, Free Radical Protection* | Orange Blossom Energizer *Perfect
for protecting Tattoo Ink from fading.
2. Collagen Boosting Serum, Free Radical Protection | Ceramide Vital Fluid
3. Intense hydrator, Guards Aging, Sensitive Skin | Eye Wrinkle Cream
4. Concentrated
... Get more on HelpWriting.net ...

Tamoxifen Research Paper
According to drugs.com, tamoxifen is a synthetic drug, that is used to treat some types of breast
cancer in men and women. It is also used to lower a woman's chance of developing breast cancer if
she has a high risk (such as a family history of breast cancer).
What is MRSA? Methicillin–resistant Staphylococcus aureus (MRSA) bacteria are resistant to all
beta–lactam antibiotics such as methicillin, penicillin, oxacillin, and amoxicillin. Sometimes called
a "super–bug" because of its ability to resist so many of our antibiotics. MRSA can be fatal and
according to the CDC, of the over 80,000 invasive MRSA infections every year, 11,285 related
deaths occur. Methicillin–resistant Staphylococcus aureus (MRSA) has become the bacteria of this
decade. ... Show more content on Helpwriting.net ...
NETS are a mesh of DNA, antimicrobial peptides, enzymes, and other protiens that neutrophils
spew out to kill pathogens. For the mice experiment they injected one set of mice with the
tamoxifen, and another with a control. After an hour once the tamoxifen had been fully absorbed
into their system, the researcher injected both sets of mice with MRSA (methicillin–resistant
Staphylococcus aureus). They treated the mice again with tamoxifen or the control one and eight
hours after infection and monitored them for five days. Tamoxifen significantly protected the mice –
none of the control mice survived longer than one day after infection, while about 35 percent of the
tamoxifen–treated mice survived five days. While 35% is not a large amount it is a step forward, it
is progress.
The Future While there is progress in tamoxifen becoming a treatment for MRSA, this isnt without
any drawbacks. While tamoxifen has been effetive against MRSA in the study
UC San Diego School of Medicine Department of Pharmacology had done, the outcome could be
vary with other pathogrens because there are several known bacterial species that have evolved
ways to escape NET

Lux Eyes Research Paper
Women go through a great deal of changes from the age of 18 to 38, including her skin, and even
more specifically, the skin around her eyes. The skin around the eyes is one of the first places that
aging shows up, it could be from fine lines or wrinkles, laugh lines or dark bags or it could be just a
lackluster tone to the skin, making your eyes look older than you really are. However, Luxx Eyes is
the perfect solution for combating the signs and appearance of aging to that delicate skin. It is
clinically proven and is all–natural.
What is It?
Luxx Eyes is a serum that has been carefully formulated to support and improve the health of the
skin under your eyes. Its specially chosen ingredients repairs damage, renews skin tone and evens
out ... Show more content on Helpwriting.net ...
As Luxx Eyes is completely natural, there are no associated side effects or risk of using the product
on a daily basis. As with trying anything new, if you have highly sensitive skin, it is recommended
to do a small spot test before using Luxx Eyes. It was formulated by dermatologists who know how
other eye creams can contain detrimental chemicals and even ingredients that can be cancer causing.
They carefully selected natural ingredients that you can feel good about using on your skin every
day.
How Do I Use It?
Luxx Eyes is a serum that can be applied every day, or once in the morning and once at night, in a
thin layer directly beneath your eyes in the bag region. Be careful not to apply it too close to your
eyes, and wash thoroughly with clean water if you do.
Why Do I Buy It?
Luxx Eyes is offering a free trial sample for a limited time. Visit their main website to access the
form to sign up for your sample, you only have to pay a small shipping charge and you can start
seeing what Luxx Eyes can do for your eyes

Skin Tightening Serum
Looking for the best skin tightening serums to contour your face without makeup? Well, you've
certainly to the right place. Read on to find out.
1. Caudalie Resveratrol Lift Firming Serum
This facial serum is formulated with Resveratrol, a powerful molecule extracted from the grapevine,
and which is very effective in tightening the skin. It contains micro hyaluronic acids that support the
skin's natural production of hyaluronic acid for better hydration and preservation. Also, this skin
tightening serum is infused with a unique peptide blend, which plays an essential role in stimulating
the production of more collagen and elastin to give you a firmer, smoother, as well as more toned
and reshaped complexion.
2. Clark's Botanical Cellular Lifting Serum ... Show more content on Helpwriting.net ...
The concentrated formula derived from this secret ingredient helps tighten the skin and improve the
youthful liveliness of your skin while providing long–term skin rejuvenation. Notably, the serum
can protect the skin cells against environmental aggressors (free radicals) and UV radiation.
3. Organic Pharmacy Gene Expression Serum
This skin tightening serum is scientifically proven to greatly improve the appearance of the seven
signs of aging. Gene Expression Serum basically contains a vegetable peptide gene cosmeceutical
that controls the release of the protein Progerin, which is associated with accelerating aging. Other
ingredients include grape stem cell for protecting the skin from UV radiation, hibiscus supports the
production of collagen, sea algae helps with hydration, retinol fights wrinkles, and sodium
hyaluronate algae cosmeceutical for plumping.
Gene Expression Serum diminishes the dark spots and makes the skin look plumper and smoother
just in 2

Looking After The Skin Around Your Eyes: 7 Tips
Looking After The Skin Around Your Eyes: 7 Tips
Unlike the skin on other areas of the face, the skin around the eye area is fine, delicate and sensitive.
Therefore special attention is necessary when looking after it in order to eliminate puffiness, dark
circles, wrinkles and fine lines. It is an important if you desire to look your best. Consider the
following tips for regular practice and achieve it!
1. Use products with particular components
Use a special product for your eye area as it is crucial to avoid certain components that generally
contain in other products such as oil as it will block the glands around the eyes. Go for the
moisturizers with haloxyl, peptides, nicotine acid, caffeine, ceramides, and retinol help to get rid of
bagginess, wrinkles, darkness, and fine lines.
2. Touch with care
The skin on the eye area is 6–10 times thinner than other parts ... Show more content on
Helpwriting.net ...
Opt out waxing
Waxing your eyebrows can be too harsh on the skin around your eyes. It can harm the top layer of
the skin although some people believe it is not true. However, it is wiser to tweeze eyebrows instead
of waxing them. Still if you find that waxing is the best option for you, stick with it but ensure your
beautician is very gentle with the procedure.
4. Use a product specially made for eye care.
As the skin around eyes is different compared to other areas, it requires special care. You should be
attentive to use a product specially made for eye care as other facial products contain components
which are harmful to the skin around the eyes, e.g.: abrasive particles in facial cleansers that are
added particularly to remove oil and dirt.
5. Wear sunscreen
It is unnecessary to mention that if the sun has a negative impact on the skin in general, the skin
around the eyes is, even more, susceptible as of its delicate structure. Sunscreen is a great solution to
stop sun damage and premature aging. Eye creams contain a broad spectrum of sun protection and
also keeps your skin smooth and

Cryptococcus Neoformans is a Basidiomycetous Yeast Fungus
Introduction/Background
Cryptococcus neoformans is a basidiomycetous yeast fungus that is enclosed with a polysaccharide
capsule. C. neoformans can undergo sexual reproduction that is due to crossing α– and a–mating
types, resulting in the formation of sexual spores or basidiospores (Buchanan and Murphy, 1998). It
is an intracellular pathogen that affects more than one million individuals, resulting in over 700,000
deaths per year (Centers for Disease Control and Prevention, 2014). Individuals become infected
with this pathogen when they inhale fungal particles from the various sources that C. neoformans is
found in: bird guano, decaying vegetables and soil (Upadhya et al. 2013). These particles then enter
the alveoli within the lungs. In individuals with a healthy immune system, the infection is cleared or
stays dormant until an imbalance of the immune system occurs. However, in individuals with
compromised immune systems such as those with HIV, cancer or those taking corticosteroid
medications; the fungus can disseminate and enter the central nervous system. Symptoms include
coughing, chest pain, fever, weight loss, pneumonia and respiratory distress syndrome as well as
meningoencephalitis that is fatal if left untreated (Bose et al. 2003; Upadhya et al. 2013).
Cell mediated immunity in the infected host is very important to respond to fungal invaders.
Phagocytic cells like macrophages, and neutrophils produce reactive oxygen species (ROS) which
kill

Exosomes As A Whole Has Gained Momentum Through The Area...
The interest and research invested into the area of exosome biogenesis and the topic of exosomes as
a whole has gained momentum in the last decade (Urbanelli, L. et al. 2013). Their discovery in
1983, detailed in two papers published in JCB (Harding et al) and in Cell (Pan and Johnstone),
showed that the nomenclature had been prescribed wrongly to a broad range of membrane vesicles
that bud directly from the plasma membrane (Clifford V. Harding. et al. 2013). When in fact the
term 'exosome' more accurately describes small vesicles, ranging from 30–100nm in diameter
(Urbanelli, L. et al. 2013), that originate via a different mechanism of budding than apoptotic bodies
and microvesicles, (Yu, S. et al. 2015).
Exosome function was initially ... Show more content on Helpwriting.net ...
Whilst exosomes have been retrieved in many body fluids, for example; blood, urine, saliva and
cerebrospinal fluid (Urbanelli, L. et al. 2013). They are recently thought to be present in all
biological fluids.
Exosome Biogenesis
Exosomes are exceptional from other types of vesicles based on a number of factors; including their
size (relatively small in comparison), morphology, cargo composition and most distinctly, their
endosomal origin (Théry C. 2002). Familiar types of vesicles such as microvesicles are formed at
the cell surface, budding directly from the plasma membrane (Alenquer, M. et al. 2015). Exosome
biogenesis follows an alternative method that begins in the early endosome (Huotari, J and
Helemius, A. 2011), whereby the ultimate result is the formation of intraluminal vesicles (IVL's)
inside the lumen of the endosome, this aggregate body is known as the multivesicular body (MVB)
or the multivesicular endosome (MVE).
Initially the early endosomal membrane, tube–like in shape (Beach, A. et al, 2014), buds inwards via
intraluminal invagination (Lopez–Verrilli, M and Court, F. 2013), randomly engulfing sections of
the cytosol contents such as the peripheral and transmembrane proteins. This formation of the IVL's
noticeably augments as the endosomes mature (Huotari, J and Helemius, A. 2011) and after
transformation the late endosome is more spherical in shape (Beach, A. et al. 2014). It is known

Human Skin
1.1. Anatomy and Function of Skin:
The Human skin is the largest single organ of the body, with a surface area of one to two square
meters and accounts for approximately 16% of total body weight. It protects the body as an outer
barrier from external pathogenic factors and excessive water loss. The skin is composed of three
main layers: the epidermis, dermis, and hypodermis or subcutaneous layer1,2.
Epidermis:
The epidermis is the outermost layer of mammalian skin and contains four types of cells:
keratinocytes, which make up 90% of the cells found in this layer, Langerhans cells, melanocytes,
and Merkel cells. The epidermis is a stratified squamous epithelial layer, containing keratinocytes
organized in four main different strata (i.e. stratum ... Show more content on Helpwriting.net ...
Routes of skin penetration:
There are two diffusional routes to penetrate into human skin: the transappendageal and the
transepidermal routes.
The transappendageal route or so–called the skin shunts comprises transport via hair follicles, sweat
ducts and sebaceous glands. There is relatively small surface area (approximately less than 0.1% of
total surface) for this route and may be of some importance for ionic molecules or large polar
compounds. In addition, the relative surface area of the shunts in different areas of the body may be
various. For instance, in the scalp, the density and size of hair follicles are much greater than in
other location on the skin such as on the back12.
The transepidermal pathway is principally responsible for diffusion across the skin. This route can
be defined as the pathway where compounds permeate across the stratum corneum by using two
different passages: the transcellular and the intercellular13,14.
The intercellular pathway is generally regarded as the main route of permeation of most compounds
and provides a significant route by enhancing interaction with lipid remains in the corneocytes. The
transcellular (a polar pathway) pass through corneocytes and interleaving lipids15,16. Figure 1
presents routes of skin

Phosphocholine Lab Report
Ceramide is a lipid molecule comprised of sphigosine, an amino alcohol, and a free fatty acid. When
combined with phosphocholine a sphingomyelin is formed which is a member of the sphingolipid
family. These molecules are main components of the phospholipid bilayer that make up a cell's
membrane. Phosphoethanolamine can also be used in place of the phosphocholine to form a
sphingomyelin however *disadvantage*.
Ceramide is found in a high abundance in the cell membrane where it was thought that it only had
structural elements contributing to the bilayer. However it is now believed that ceramide contributes
in cell signalling. *REF*
There are a number of applications for the use of ceramide in clinical settings e.g. in the treatment of
some cancer via apoptosis. This process is vital to maintain a normal amount of cells in the body.
When combined ... Show more content on Helpwriting.net ...
The complete reaction involves four biological steps beginning with palmitate and serine and
resulting in a molecule of ceramide. The initial step is also the rate limiting step therefore the
slowest step. The enzyme serine palmitoyl transferase is used to catalyse the condensation reaction
between palmitate and serine which results in the molecule 3–keto–dihydrosphingosine. This
'molecule' is then reduced to dihydrosphingosine in the ........... Dihydroceramide synthase is used to
convert dihyrdosphingosine into dihydroceramide via acylation. The product has a similar chemical
structure, uptake and metabolism as ceramide and would have an effect on apoptosis except it lacks
the biological activity needed for this function. Finally, dihydroceramide desaturase catalyses the
final conversion to ceramide. Ceramide can be generated in the de novo synthesis via both the serine
palmitoyltranserase (SPT) and ceramide synthase which catalyse key steps in the pathway.
(Panjarian et al.,

Galactocerebrosidase Enzyme
Galactocerebrosidase enzyme (GALC) is an enzyme with very low activity, it is a lysosomal acid
hydrolase or a lysosomal catabolism that stimulate the removal of a monosaccharide sugar which is
galactose that is found in galactosylceramide or galactocerebroside (GalCer) or anything descendant
from ceramide. Galactocerebroside is a marker for oligodendrocytes in the brain, regardless of
whether they shape myelin. It is encoded by a specific gene which is (GALC) which is is formed in
the endoplasmic reticulum (ER)–Golgi complex after which it is transferred via the mannose–6–
phosphate pathway to the lysosome. If a missense mutation happened in this gene, it will affect on
the Galactocerebrosidase enzyme. This mutation that happens exactly on chromosome 14 (14q31)
that encompasses 17 exons, will cause the gene to be unstable or misfolding which will ... Show
more content on Helpwriting.net ...
The best one was the twitcher mouse model which occurring human krabbe disease that is caused by
a mutation in galactocerebrosidase gene. Mutation analysis of the human GALC gene was
facilitated by the cloning and sequencing of GALC cDNA (5). Mutation analysis of the human
GALC gene was facilitated by the cloning and sequencing of GALC cDNA . This allowed DNA
obtained from Krabbe affected people to be sequenced and analysed against the normal GALC gene.
To date there have been over forty mutations identified that cause the galactosylceramidase
deficiency of Krabbe disease .The most common mutation in the European population is a 30kb
deletion which is associated with a C to T transversion at cDNA position 502. The large 30kb
deletion affects the production of galactosylceramidase since it removes a significant portion of the
enzyme coding region. This results in the cancellation of 5 amino acids and the insertion of 2 amino
acids which impacts on the quaternary structure of the

Atopic Dermatitis Essay
Immunological aspects and possible therapeutic targets in Sézary Syndrome and Atopic Dermatitis
Introduction:
Sézary syndrome (SS) is a rare erythrodermic and leukemic variant of cutaneous T cell lymphomas
(CTCL). SS belongs to the heterogeneous group of extranodal non–Hodgkin's lymphomas (NHL)
arising from the malignant proliferation of skin–homing T cells. SS together with mycosis fungoides
(MF) are the most common forms of CTCL accounting for around 65% of cases. SS and
erythrodermic MF (E–MF), an advanced form of MF has been referred as erythrodermic CTCL (E–
CTCL) and if blood involvement is present, the term leukemic CTCL (L–CTCL) has been used.
Atopic dermatitis (AD) is an important differential diagnosis of SS in adults with erythrodermic
dermatitis. Although in majority of cases there are characteristics such as typical predilection sites
for AD and palmoplantar hyperkeratosis for SS ... Show more content on Helpwriting.net ...
To confirm the definite diagnosis in E–CTCL, clinicopathological correlation often including
multiple skin biopsies with histopathological and immunohistochemical investigations and in most
cases staging examinations were needed.
Clinical Characteristics of AD
The most characteristic features of AD are intense itch and recurrent eczematous skin lesions, which
typically show an age–related morphology and distribution. The majority of patients display
generalized skin dryness and a personal or familial history of atopy. Other associated features are a
hyperlinearity of the palms and soles, Dennie–Morgan infraorbital folds, and Hertoghe's sign.
Distinct Features of Pathogenesis of SS (L–CTCL) and

Fabry Disease (ERT)
Fabry Disease Fabry disease is an inherited disorder which is caused from abnormal deposit of
globotriaosylceramide, a particular fatty substance, in blood vessel walls throughout the body. Some
symptoms that may be noticed are pain in the hands and feet, small red spots normally found
between belly and knees, cloudy vision, hearing loss, ringing in the ears, and a decreased ability to
sweat. The only FDA approved treatment for this disease is enzyme replacement therapy (ERT).
This replaces the enzyme that is not working correctly, which allows the body to break down fatty
substances the way it should. This disease is passed down through genes from parents. You either
were born without alpha–galactosidase A or it doesn't perform its duty.

24-Well Plate Lab
A 24–well plate was used to perform this experiment. For the start of the experiment, the 24–well
plate had 12 wells that contained our HepG2 cells. A cell suspension was created, that contained
0.5–1.0x10⁶ cells/ml containing 10% fetal bovine serum. 500µl of the cell suspension was then
added to each well in use. The well plate contained both the HepG2 cells, and cell suspension was
then incubated in a cell culture incubator for 24 hours; this allowed for a monolayer to be formed in
the wells. After the incubation period elapsed, the well plate was removed and placed inside a tissue
culture hood. We then carefully removed all the media from the wells with the use of a P1000
pipette; making sure not to touch the bottom of the well plate, and ... Show more content on
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Three wells where eliminated from the experiment, because a vehicle control was not needed for
this experiment. Images where then taken of the 9 wells, with the use of phase–contrast microscope,
these photos were labeled (T0). After the images where obtained, the well–plate was placed back
into the tissue culture hood, and the wells where treated with different treatments, so the effects
could be observed. In row "A" contained the HepG2 cells by themselves, no treatment was added.
Row "B" contained the HepG2 cells and 4.5µl of Ceramide, which was labeled as the positive
control, and finally in row "C" the wells contained our HepG2 cells and the compound
Epigallocatechin Gallate. The well was then placed back into the cell culture incubator for 24 hours.
Following the incubation, photos where taken using the same phase–contrast microscope and the
same area of each scratch, these photos are labeled (Tf). The before and after photos of the scratch
are then used to figure out the percent wound closure, which determines the cell migration. In order
to calculate the percent closure, the following equation was used; Percent closure=width of Tf
box/width of the T0

Hair Serums Research Paper
women shopping online
How hair serum can save your hair?
Description: Now you can get rid of your bad hair day with the help of hair serum. Here a few
things you should know about hair serum before buying it during women shopping online.
You may have heard term of hair serum in last few years but this term is common in trichology. You
can get hair serum in liquids and sprays while women shopping online. You can use these hair
serums on curly and frizzy hair. Hair serums include silicon, ceramide and amino acids, which
works as a mask on the scalp. You can get many types of hair serums but silicon based hair serums
are more popular. There are several benefits of the amazing product which you can get.
1) It provides protection against pollution,

Dennis Hill Cannabis Essay
Cannabis is better known by many people as just a recreational drug but studies show that the
chemical compounds in Cannabis to cause the death of cancer cells along with relieve chronic pain
and anxiety caused by other cancer treatments. Dennis Hill is a cancer survivor who treated and
cured himself using cannabis as a treatment he explains how THC works to kill cancer cells when he
states "Very simply, when THC connects to the CB1 or CB2 cannabinoid receptor site on the cancer
cell, it causes an increase in ceramide synthesis which drives cell death." THC when introduced to
the cancer cell causes a ceramide synthesis in which ceramide starts to build up causing the
Sphingolipid Rheostat to push Cytochrome c out of the mitochondria. Cytochrome

The Cause Of Alzheimer's Disease
Who would you be if you forgot everything and everyone you know? Does taking away someone's
memory mean taking away their identity? Living from day to day not knowing the people around
you or the home in which you live would be a terrible way to exist. Sadly such a disease as this
exists. It is called Alzheimer's, and it affects around five point three million Americans a year.
Alzheimer's is a progressive form of dementia that is characterized by the loss of memory and other
intellectual abilities such as thinking and behavior ("Stages of Alzheimer's & Symptoms"). Although
scientists have been unable to confirm a known cause or causes of Alzheimer's disease, there have
been many promising improvements to discover this. As this disease it becoming ... Show more
content on Helpwriting.net ...
The Alzheimer's Association lists ten items to watch for as follows: "1. Memory loss that disrupts
daily life, 2. Challenges in planning or solving problems, 3. Difficulty completing familiar tasks at
home, at work or at leisure, 4. Confusion with time or place, 5. Trouble understanding visual images
and spatial relationships, 6. New problems with words in speaking or writing, 7. Misplacing things
and losing the ability to retrace steps, 8. Decreased or poor judgment, 9. Withdrawal from work or
social activities, 10. Changes in mood and personality ("Memory Loss"). There are three main
stages of Alzheimer's that are characterized by specific signs that are generally similar at all ages.
The first stage, mild, "starts with mild impairments in memory, communication patterns and
executive ability, and depression," and in this stage the disease may be seen as only normal signs of
aging, not as Alzheimer's (Wattmo). In addition, in this stage there also may be a "marked reduction
in the capacity to conduct more advanced instrumental activities of daily living," and this may be
recognized more easily as Alzheimer's disease (Wattmo). In moving on to the moderate stages of
this disease, it has been shown that common symptoms are "disorientation of time and/or place,
dyspraxia, dysgnosia and decreased judgement and skills" (Wattmo). The

C. Elegans
Take home quiz: 15 pts. Please use your own words. Any direct quote would result in an automatic
zero for the pertaining question. 1. 6 pts. Outline the main topic(s) of the article and briefly describe
the purpose of each This study looks into the effect of glucose diets and mutations in hyl–2
ceramide synthase on anoxia survival in C. elegans. This could have something to do with the
anoxia process in humans. This could help to understand why oxygen depletion is considered more
severe in patients with diabetes. C. elegans is used as a model organism for the studying of human
diseases. C. elegans is a good model for studying the effect of anoxia because it operates normally
under a broad range of oxygen concentrations Hyperglyciemia and obesity are ... Show more
6 pts. Reproduce (sketch or photocopy) 2 tables or figures or one of each and explain their
significance (what important information is relayed). What kinds of information were included in
the title and/or caption to describe/explain the table or figure and make it "self–contained"? Here the
effect of 2d anoxia is displayed along the life cycle of C. elegans. It displays that when the hyl–
2(tm2031) mutant is of adulthood, the effect of anoxia is much greater that its' N2 or control
counterpart. These effects are described in graphs B and C. B describes that the mutant is producing
fewer embryos than the N2 organism, where in graph C it shows that when fed a glucose–based diet,
the mutant shows a much lower survival rate than the N2 organism. All three graphs were color–
coded so that each bar was distinguished between the control and mutant genotype. These graphs
depict the various genes that were inhibited and the resulting effect on anoxia survival rates. The
color codes indicate a difference between those who received the gene knockout versus those that
did not. The table's figure states that these genes were selected earlier, and were predicted to
improve anoxia survival once knocked

Gaucher's Disease Research Paper
Gaucher's disease (GD) is the most common lysosome storage disease in the world. There are three
types of Gaucher's. All types except type 1 are neuropathic form. Type 2 specifically is the most
lethal and Type 3 neurological symptoms are need of the most support. Type 1 GD, can be observed
in an individual as early as infancy into adulthood. The disease causes symptoms in skeletal, lungs,
skin, eyes, lymphatic, blood and visceral organs. The drug Eliglustat is an agent that is used to treat
type I Gaucher disease and Fabry's disease. It is used with the method substrate replacement therapy
(SRT) and it is used when enzyme replacement therapy (ERT) is not an option. The drug itself treat's
milder cases of the disease and is used more as a method ... Show more content on Helpwriting.net
...
This causes glucosylceramide to accumulate in the body. Scientist have been trying to figure out a
way to combat this. Eliglustat is that answer. Glycosphingolipid synthesis and degradation relies on
glucosylceramide for its base cerebroside to make more complex glycosphingolipid. The
glycosphingolipid pathway starts with ceramide and UDP–glucose making glucosylceramide via
glucosylceramide synthase which will then be used to make Ceramide via β–glucocerebrosidase and
eventually Ganglioside GM2 and GM1. Now on a histology level glucosylceramide accumulate in
lysosomal compartment of macrophages which gives rise to foam cells or "Gaucher cells."
Eliglustat blocks glucosylceramide synthase cause a decrease in level of all glucosylaceramide
based glycospholipids (J. A. Shayman, 2010). Patients taking Eliglustat can experience fatigue, head
ache, back pain, nausea, diarrhea, pain in extremities and upper abdominal pain. These conditions
were said to be the most common for people taking the drug. Other symptoms that were reported
were dizziness, gastroesophageal reflux disease, palpitations, rash, cough, dyspepsia, constipation
and asthenia. Most adverse effects were said to occur within the first 6 months of treatment and of
those adverse effects only 19% were deemed relatable to the drug itself in a study (Poole,

Characteristics Of Prostate Cancer
There are some tumors found to be primarily relying on FAO for development and survival. Prostate
cancer suggested to has a characteristic of low a glycolysis rate and poor avidity to FDG 2–deoxy–
2–fluoro–d–glucose with positron emission tomography, that is using as diagnostic, staging, and a
monitoring therapy tool for several malignant tumors (9). Recent studies indicated that prostate
cancer cells have a low glucose consumption rate and exhibiting changes of fatty acid metabolism
for cancer cell proliferation and growth, also stated that glucose transporters (GLUT1) were found
with low expression levels in human prostate cancer cells (9,10). Another observation was proposed
by a study in which the inhibition of CPTI activity using safe ... Show more content on
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FAO produces a molecule of acetyl CoA in each oxidation cycle and two after full completed cycles.
The resulted acetyl CoA is the major requirement for producing the reduced NADP+ in which the
generated acetyl CoA enters the TCA cycle and with the availability of oxaloacetate provides citrate
that can be export to the cytoplasm. The citrate then enters two reactions to produce cytosolic
NADPH (1,3,12). These reactions include the conversion of malate to pyruvate that is catalyzed by
malic enzyme (ME1) and the oxidation of isocitrate to α–ketoglutarate by isocitrate dehydrogenase
(IDH1) (1,3,12). The produced cytosolic NADPH from FAO acts to sustain the antioxidant system
against oxidative stress and to promote cancer cell survival. For instance, during severe oxidative
stress the accumulation of oxygen reactive species (ROS) leads to cell death, cytosolic NADPH
counteracts ROS by maintaining the reduced form of glutathione (GSH) thereby promoting cancer
cell survival (12). In addition, the produced cytosolic NADPH from FAO targets ROS–induced
oxidative damage to prevent disrupting mitochondrial and glycolytic ATP production. For example,
in a study using SF188 glioblastoma cells the inhibition of FAO by CPTI inhibitor etomoxir
hindered NADPH production and resulted in significantly increased of superoxide level in etomoxir
treated cells, ATP depletion, and eventually cell death (12). A

Effect Of Hypoxia On Ceramide
As previously mentioned, the cellular adaptation to hypoxia is mainly mediated by hypoxia–
inducible factors (HIF). However, HIF–independent responses have been described upon hypoxia;
many of these responses have been attributable to sphingolipid metabolism and ceramide. Although
several studies were conducted in determining the effect of hypoxia on ceramide, ceramide
responses to hypoxia as well as their biological significance remain under debate [63, 78]. The
effect of hypoxia on Sphingolipid metabolism and Ceramide have been intensively studied in
cardiovascular diseases; in fact, studies performed on heart diseases have proven that the hypoxic
effects on cardiomyocytes are in favor of cell growth and proliferation. For instance,

Second Hand Smoke Research Paper
Approximately 20% of our youth today lives with a family member who smokes. It is estimated that
almost half of the U.S. population experiences secondhand smoke every day through the
environment they encounter. Many research studies support the notion that cigarette use and
secondhand exposure link to health side effects. Cigarette smoke has been especially found to be
detrimental to an individual's cardiovascular and metabolic health. New findings however, show that
exposure to cigarette smoke can correlate to weight gain, especially in children. In fact, exposure to
secondhand smoke alone has been linked to higher weight gain than the actual habit of smoking.
Benjamin Bikman, a professor of Physiology and Developmental Biology from Brigham Young
University and his team colleague Paul ... Show more content on Helpwriting.net ...
Because of this notion, Bikman and his team of researchers found a way to reverse the effects of
cigarette smoke. They found an inhibitor to inhibit ceramide, which inhibited the mitochondria from
performing its cellular role. This found inhibitor was called myriocin, a known ceramide blocker.
When this inhibitor was studied on a set of mice that were exposed to secondhand smoke, the mice
did not gain weight, as opposed to the previous set of mice that were exposed to secondhand smoke.
However, when an additional variable was introduced, a high–sugar diet, the inhibitor myriocin was
not found useful anymore. In relation to overweight children exposed to secondhand smoke,
scientists are searching for a nontoxic and safe type of ceramide inhibitor to reduce weight gain and
metabolism problems for humans. Children can possibly avoid excess weight gain if more studies
are found. However, with a diet rich in sugar, the myriocin would not be effective. Smokers would
need to simply, "just quit" to reduce the side effects secondhand smoke puts on their loved ones at

Cell Membranes Of Proteins And Proteins Essay
CHAPTER ONE INTRODUCTION
Cell membranes of eukaryotes are complex structures, comprised of a highly regulated heterologous
distribution of lipids and proteins (Hanada, 2010). This distribution is determined to some extent by
the location and topology of lipid synthases, and results from the trafficking of proteins and lipids
(Hanada, 2010). Within the cell, transport vesicles and tubules mediate trafficking by loading
desired sets of proteins at one organelle and delivering them to the subsequent (Hanada, 2010;
Kumagai et al., 2005). Lipid influx routes such as the endocytosis of membrane lipids add further to
the diversity (Hanada, 2010). The result is an asymmetric distribution of protein and lipid types
across the membrane bilayer (Hanada, 2010).
Ceramides are an example of a family of cellular lipids (Yasuda et al., 2001). Ceramides are
synthesised at the endoplasmic reticulum from precursor compounds and are transported to the
Golgi apparatus for conversion into one of the several sphingolipids (Yasuda et al., 2001). The
transport of such compounds is highly selective if not specific (Kumagai et al., 2005; Yasuda et al.,
2001). Inhibiting transport is a useful tool in investigating the role of substrates (Yasuda et al., 2001)
and makes an attractive target for biochemical manipulation of the cell (Ueno et al., 2001).
Intracellular trafficking of ceramides is highly regulated. Two ceramide transport pathways have
been identified (Kumagai et al., 2005). The first is

Extracellular Vesimona Essay
EVs as Pathogenic Mediators in NASH Cells release diverse types of membrane–bound
extracellular vesicles into the extracellular milieu. These can be further classified into three main
subgroups based on their cellular biogenesis: exosomes, microvesicles, and apoptotic bodies.21
Exosomes (~50–100 nm diameter) originate from the multivesicular body (MVB); MVBs are well–
characterized endosomal precursors of the lysosomal degradation pathway. MVBs can also fuse
with the plasma membrane. In this case, their intraluminal vesicle contents are released into the
extracellular space; thus becoming "exosomes".22 Microvesicles (~50–1000 nm diameter) bud
directly from the plasma membrane. Apoptotic bodies (more than 500 nm in diameter) represent ...
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One of the early reports of their role in an animal model of NASH was the observation that adoptive
transfer of EVs isolated from the serum of high fat diet–fed mice into chow diet–fed mice results in
immature myeloid cells activation and homing to the liver, which was associated with increased
levels of hepatic proinflammatory markers and serum aminotransferases.32 Subsequent reports
demonstrated a significant increase in the release of EVs from hepatocytes upon treatment with
lipids such as palmitate and its active metabolite lysophosphatidylcholine (LPC),27 28 33 toxic
lipid–induced EV release by hepatocytes was observed across different species.28 EVs derived from
hepatocyte under lipotoxic stress are heterogeneous regarding their biogenesis, selected cargo,
release, and intended target cells. For example, LPC–induced EV release is mediated by the stress
kinase mixed lineage kinase 3 (MLK3).33 Furthermore, MLK3 regulates the chemotactic cargo of
the EVs. Genetic or pharmacological inhibition of MLK3 results in a reduced abundance of the
potent C–X–C motif chemokine ligand 10 (CXCL10) in vesicles derived from LPC–treated
hepatocytes.33 Likewise, MLK3–/– mice fed a NASH–inducing diet34 have reduced CXCL10
levels in their plasma EVs. This, in turn, is

Hepatic Fibrosis Case Study
FTY720 treatment reduces liver fibrosis. Hepatic fibrosis is a sequel of chronic liver injury and
inflammation; therefore, we asked if FTY720 treatment reversed fibrosis in addition to the observed
reduction in liver injury and inflammation. Fibrosis was assessed by picro–sirius red staining for
collagen accumulation in the liver. The control group (FFC–fed, saline treated) mice livers
demonstrated the typical peri–cellular (chicken wire) fibrosis observed in murine and human NASH
(Fig. 6A). This was reduced in the treated group (Fig. 6B). Consistent with the histologic data, there
was a reduction in fibrogenic gene expression in the liver. Alpha smooth muscle actin (αSMA), a
marker of activated hepatic stellate cells, and tissue inhibitor ... Show more content on
Helpwriting.net ...
Our previous data suggests that extracellular vesicles (EVs) released from stressed steatotic
hepatocytes are chemotactic toward macrophages (6), therefore, we next looked at circulating EVs
in all four groups of mice. As predicted there was an increase in circulating EVs in mice fed the FFC
diet in comparison to chow–fed mice (Fig. 7A). FFC–fed mice treated with FTY720 (treated group)
had lower circulating EVs than the FFC–fed saline injected (control group) mice, though the
circulating EVs in this group (FFC–FTY) remained higher than the chow–fed FTY treated group
(Fig. 7A). This reduction in EVs is likely due to a reduction in liver injury in the FFC–fed FTY
treated group, though we cannot exclude a direct effect of FTY720 on release of EVs by steatotic
hepatocytes. Furthermore, though EVs were lower in the treated group (FFC–FTY), the EV S1P
content and C16:0 ceramide content were not lower (Fig. 7B). This supports our hypothesis that EV
S1P acts as a chemoattractant to macrophages via S1P receptor activation on macrophages; and that
FTY720 administration to mice impairs the recruitment of proinflammatory monocyte–derived
macrophages to the

Cell Membranes Of Proteins And Proteins Essay
Chapter One – Introduction
Cell membranes of eukaryotes are complex in structure, comprised of a highly regulated
heterologous distribution of lipids and proteins (Hanada, 2010). This distribution is determined to
some extent by the location and topology of lipid synthases, and results from the trafficking of
proteins and lipids (Hanada, 2010). Within the cell, transport vesicles and tubules mediate
trafficking by loading desired sets of proteins at one organelle and delivering them to the next
(Hanada, 2010; Kumagai et al., 2005). Lipid influx routes such as the endocytosis of membrane
lipids add further to the diversity (Hanada, 2010). The result is an asymmetric distribution of protein
and lipid types across the membrane phospholipid bilayer (Hanada, 2010).
Ceramides are an example of a family of cellular lipids found in the cell membrane (Yasuda et al.,
2001). Ceramides are synthesised at the endoplasmic reticulum from precursor compounds and are
transported to the Golgi apparatus for conversion into one of several sphingolipids (Yasuda et al.,
2001). The transport of such compounds is highly selective if not specific (Kumagai et al., 2005;
Yasuda et al., 2001). Inhibiting transport is a useful tool in investigating the role of substrates
(Yasuda et al., 2001) and makes an attractive target for biochemical manipulation of the cell (Ueno
et al., 2001).
Intracellular trafficking of ceramides is highly regulated. Two ceramide transport pathways have
been identified

Evaluation Of Glucosylceramide Synthase ( Gcs )
Abstract
Glucosylceramide synthase (GCS) is an enzyme that catalyzes the first step in the biosynthesis of
glucosylceramide (GlcCer)–related glycosphingolipids (GSLs). In the present report we have used
atom–based 3D–QSAR method to analyze the structural aspect on a series of iminosugar derivatives
as potent inhibitors of glycosylceramide synthase. In this approach the experimental dataset was
divided into training and test sets and the model was chosen based on randomized trial distribution
which has high correlation factors. A ligand–based pharmacophore and atom–based 3D–QSAR
studies were carried out on a set of 65 inhibitors of GCS. After the QSAR studies, a five–point
pharmacophore with two hydrogen bond acceptors (A), two hydrophobic group (H) and one ring
aromaticity (R) was obtained. The pharmacophore hypothesis yielded a 3D–QSAR model with good
partial least square statistics results. The training set correlation has these partial least square factors
(R2=0.92, SD = 0.178, F = 843.9, P = 1.12e–15). The test set correlation has these partial least
square factors (Q2 = 0.25, RMSE = 0.665, Pearson–R =0.54).
After the QSAR studies, docking study is being carried out. The docking study will reveal the
binding orientation of the active ligands on the protein which will be completed in BTP–phase II.
The result for QSAR and docking studies will provide structural characteristics of the active ligands
and also give detailed information about binding features which can useful

Sphingolipid Synthesis Essay
GENERAL DESCRIPTION OF THE PROPOSED RESEARCH
The overall goal of this research is to explore the role of sphingolipids as eventual pathogenic
factors and molecular markers for disease state/severity in adults with Attention–
deficit/Hyperactivity disorder (ADHD). Our specific aims are organized in 2 major areas I)
Clinical/basic research–aims targeting to explore the eventual etiologic role of sphingolipids in adult
ADHD and to provide the first evidence towards pathogenic mechanisms in humans; and II)
Applied/translational aims directed to the characterization of the components of the serum
sphingolipid profile as potential molecular markers for disease state/severity. Using a case–control
observational design nested within the ongoing protocol for the Maule Cohort of Chronic Diseases
(MAUCO), which is actively following 10,000 adults in the range 38–74y in the Maule region of
Chile1, we expect to provide the first evidence regarding:
1) ... Show more content on Helpwriting.net ...
2) The eventual correlation between serum levels of targeted sphingolipids and the microstructural
characteristics of the brain white matter, assessed by DTI–NMR and, finally,
3) Whether specific serum sphingolipids and/or distinctive characteristics of the serum sphingolipid
profile may be clinically useful as eventual biomarkers for ADHD, including the ability of the
components of the serum sphingolipid profile to discriminate between ADHD affected and non–
affected subjects, their specificity in relation to other common neuropsychiatric disorders and the
correlation of eventual alterations in the sphingolipid profile and symptom

What Is Myelin Gene Regulatory Factor ( MRF )?
Recently, it has been demonstrated by DNA microarray analysis that myelin gene regulatory factor
(MRF) expression is specific to terminally differentiated oligodendrocytes (Cahoy et al., 2008;
Heiman et al., 2008). Importantly, knockdown of MRF in oligodendrocytes by RNA interference
downregulates expression of the majority CNS myelin genes (Emery et al., 2009). In contrast,
overexpression of MRF in in vitro cultured OPCs can promote myelin gene expression.
Oligodendrocyte lineage–specific MRF knockout mice show normal premyelinating
oligodendrocytes but they display severe myelin gene expression deficits and subsequently fail to
myelinate axons. In addition, these knockout mice die early due to severe seizures.
Oligodendrocyte ... Show more content on Helpwriting.net ...
Ye et al., 2009).
In addition to transcriptional regulation and epigenetic mechanisms, posttranscriptional regulation
by microRNAs is also critically involved in the intracellular signaling of oligodendrocyte
differentiation. Studies using transgenic mice in which microRNA processing is specifically
disrupted in the oligodendrocyte lineage by way of Dicer enzyme knockout have shown that
microRNA processing is indispensible for normal CNS myelination (Dugas et al., 2010), and that in
vitro OPCs also fail to differentiate in the absence of mature microRNAs. Specifically, three
microRNAs including miR–219, miR–138, and miR–338 are found to be elevated by 1–2 orders of
magnitude during OPC differentiation into oligodendrocytes, and that miR–219 when induced
alone, is sufficient to promote the differentiation (Dugas et al., 2010). The downstream target of
miR–219, ELOVL7, is also identified as a main molecular component involved in the development
of the Dicer mutant phenotype (Shin, Shin, McManus, Ptacek, & Fu, 2009), and that overexpression
of ELOVL7 results in lipid accumulation, which is in turn suppressed by co–overexpression of
miR–219. Other important target genes of the above mentioned microRNAs include PDGFRa,
Sox6, and Hes5 (Dugas et al., 2010; X. Zhao et al., 2010), all of which serve to

Essay On Eczema Flarees
Managing eczema flares can be difficult, and when living with eczema, you primary goal should be
to prevent eczema flares instead of only treating it when it occurs. You may not be able to prevent
all eczema flares, as some triggers are out of your control, but you can minimize flares by following
these tips.
1. Use a Gentle, Ph–balanced Skin Cleanser
There are several elements that contribute to a good cleanser for eczema–prone skin, but the two
most important factors are that the cleanser is made of only gentle sufactants and that it is the same
pH level as healthy skin.
As a general rule, avoid bar soaps. Typical bar soaps are highly alkaline, and they disrupt your skin's
natural lipid layer greatly. Some foaming cleansers also have high pHs and should be avoided. Look
for a cleanser with a pH level between 4.5 and 5.5, as this will prevent disturbance of ... Show more
Also, look for added skin–soothing ingredients, such as colloidal oatmeal and soothing natural oils.
2. Optimize Your Post–shower Routine
After taking a cool to warm shower (never hot) with a gentle cleanser, it is the perfect time to feed
moisture back into your skin that even the most gentle cleanser can remove. Apply a moisturizer to
moist skin that is full of skin–soothing ingredients, such as colloidal oatmeal and ceramides.
Ceramides are natural components of healthy skin that are often lacking in eczema–prone and other
disordered skin types.
Your moisturizer should also include an occlusive, such as petroleum jelly, that forms a protective
barrier between your skin and the environment. Occlusives also help prevent TEWL, or trans–
epidermal water loss, that contributes to dry skin. It can be a great idea to slather a layer of pure
petroleum jelly over your moisturizer to get the added benefit of this extra layer of occlusive.
3. Know the First Signs of an Eczema

Sphingosine-1 Lab Report
The high–dose I+ exposure significantly induced the expression of sphingosine–1–phosphate
phosphatase 1 (SGPP1), a gene encodes a key enzyme that catalyzes the degradation of S1P to
long–chain ceramides [21], at three time points (6h: FC=1.62; 12h FC=1.58 and 24h: FC=2.00, p–
value and FDR< 0.01 at three time points). Without the cytokine mix, the high–dose I the elevated
expression of SGPP1 started after 12h of incubation (12h FC=1.42 and 24h: FC=1.5, p–value and
FDR< 0.01 at both time points). After exposure to the high–dose I+, the expression of the ceramide
synthase 6 (CERS6), encoding the enzyme that catalyzes the synthesis of ceramide [40], was first
decreased at 12 h (FC=–1.28, p–value=0.02 and FDR=0.054) and followed by a considerable ...
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The high–dose I– administration only significantly decreased the expression of NAAA at 12h (FC=–
1.38, p–value and FDR< 0.01). However, the ASAH2 encoding the neutral ceramidase was
upregulated 24h after the high–dose I+ treatment (FC= 1.48, p–value and FDR< 0.05; 12h: FC=1.50
p–value < 0.05 and 24h: FC=1.29, p–value and FDR < 0.01). After the high–dose I+ exposure, the
expression of sphingosine Kinase 1 (SPHK1), a gene encoding the enzyme that further catalyzes the
formation of ceramide–derived S1P [43], was first downregulated at 6 h (FC=–1.37, p–value and
FDR < 0.01), but its expression was progressively recovered after 12 h. The SPHK2 expression,
which was significantly upregulated at 6 h (FC=1.39, p–value=0.011 and FDR= 0.043), was
dropped gradually from 12 h (FC=1.01) and markedly suppressed 24 h after the high–dose I+
treatments (FC= –1.48, p–value=0.006 and

Cannabis Oil Works
How Cannabis Oil Works to Kill Cancer Cells
________________________________________
First lets look at what keeps cancer cells alive, then we will come back and examine how the
cannabinoids CBD (cannabidiol) and THC (tetrahydrocannabinol) unravels cancers aliveness.
In every cell there is a family of interconvertible sphingolipids that specifically manage the life and
death of that cell. This profile of factors is called the Sphingolipid Rheostat. If endogenous
ceramide(a signaling metabolite of sphingosine–1–phosphate) is high, then cell death (apoptosis) is
imminent. If ceramide is low, the cell is strong in its vitality.
Very simply, when THC connects to the CB1 or CB2 cannabinoid receptor site on the cancer cell, it
causes an ... Show more content on Helpwriting.net ...
How did this pathway come to be? Why is it that the body can take a simple plant enzyme and use it
for profound healing in many different physiological systems? This endocannabinoid system exists
in all animal life, just waiting for its matched exocannabinoid activator. This is interesting. Our own
endocannabinoid system covers all cells and nerves; it is the messenger of information flowing
between our immune system and the central nervous system (CNS). It is responsible for
neuroprotection, and micro–manages the immune system. This is the primary control system that
maintains homeostasis; our well being.
Just out of curiosity, how does the work get done at the cellular level, and where does the body
make the endocannabinoids? Here we see that endocannabinoids have their origin in nerve cells
right at the synapse. When the body is compromised through illness or injury it calls insistently to
the endocannabinoid system and directs the immune system to bring healing. If these homeostatic
systems are weakened, it should be no surprise that exocannabinoids are therapeutic. It helps the
body in the most natural way possible.
To see how this works we visualize the cannabinoid as a three dimensional molecule, where one part
of the molecule is configured to fit the nerve or immune cell receptor site just like a key in a lock.
There are at least two

Coma Membrane: Lipid Rafts
Lipid rafts are defined as the subdomains of the plasma membrane that exist as distinct liquid–
ordered regions of the membrane [1]. These membrane domains preferentially arise due to the
interaction of specific lipids. They are mobile, dynamic and insoluble in non–ionic detergents such
as Triton X–100 [2]. Lipid rafts are enriched in cholesterol, sphingolipids and phospholipids within
cell membranes (Figure 1).
Figure 1. Organization of lipid rafts (Note the higher concentration of cholesterol and sphingolipids)
within the raft region. (Image: WikiBooks Structural Biochemistry/Lipids/Lipid Rafts).
Sphingomyelin (SM) (also called ceramide phosphocholine), a type of sphingolipid, is a ubiquitous
component of the animal membrane [3].The major sources of sphingomyelin are the bovine brain,
egg yolk and milk [4]. It is, being analogous of phosphatidylcholine, typically consists of a ceramide
unit with a phosphocholine moiety attached to position 1. A typical example of sphingomyelin is a
d18:1/16:0 molecular species: ... Show more content on Helpwriting.net ...
These lipid rafts have been proposed to serve many functions in cell signalling, membrane
trafficking and signal transduction [7]. There are some special types of proteins (e.g.,
transmembrane proteins and GPI–anchored proteins) that can anchor on the nanodomains to play an
important role in transporting chemicals through the membrane [8]. Sphingomyelin rich rafts act as
hotspots or platforms to enable transmembrane proteins to aggregate so that they can promote cell
signalling events

Sphingolipid Synthesis
Sphingolipids are crucial for myelination and neurite outgrowth and maturation, but their role as
pathogenic factors in ADHD is still underexplored. Here, we present the first direct evidence
supporting the association between variants in genes from the sphingolipid pathway and ADHD.
Figure 1 shows a schematic representation of the sphingolipid metabolic pathway along with the
genes encoding for the principal enzymes in sphingolipid biosynthesis. Genes identified by this
study as significantly associated with ADHD susceptibility are highlithed. Briefly, ceramide is
central in sphingolipid metabolism and is produced by de novo and recycling pathways 23. In de
novo synthesis, serine and palmitoyl–CoA are substrates of serine palmitoyl–transferase (SPT), the
rate limiting ... Show more content on Helpwriting.net ...
Ketosphinganine is reduced to form sphinganine, which is posteriorly N–acylated with fatty acids of
different chain lengths by ceramide synthases (CerS), producing dihydroceramides. Six types of
CerS exist in mammals, each one encoded by a different gene (CERS1 to CERS6). Because each
CerS is specific to different lengths of fatty–acyl CoAs, they determine the acyl chain length of
sphingolipids, including ceramides, sphingomyelin and glycosphingolipids. Several studies suggest
that sphingolipids with defined acyl chain lengths play distinct pathophysiological roles in disease
models24,25. Under this new evidence, alterations in the relative balance of molecular species with
different acyl–chain lengths might be of pathogenic relevance for complex disorders like ADHD.
We found variants in 3 out of the 6 genes encoding for CerS significantly associated with ADHD
(CERS6 rs4668077, p–value=0.006; CERS4 rs17160349, p–value=0.039; CERS3 rs1023783, p–
value=0.015), with 2 of these variants representing missense mutation encoding for significant
changes in the protein amino–acid sequence (rs17160349 and rs1023783). An interesting –although
non–significant– trend was also observed for a

Gaucher Disease
Gaucher disease (GD) is an inherited gene that stops glucocerebroside (type of lipid) to be broken
down correctly. When this lipid cannot be broken down, buildups appear in the liver, spleen, and
bone marrow which affects normal functioning. These organs begin to grow to an irregular size,
amenia becomes present within the patient, and easy bruising appears due to the decrease in blood
platelets. Gaucher disease is created during an autosomal recessive pattern, which means that two
genes have a mutation, which causes the disorder. Normally, if a child is born with this disease, both
parents carry one copy of the mutated gene. The gene that the mutation appears in is the GBA gene.
GBA is located in chromosome one. The GBA gene is in charge of creating the instructions for
producing an enzyme called beta–glucocerebrosidase. This enzyme breaks down the
glucocerebroside into glucose and ceramide (a simpler fat molecule). When mutations appear in the
GBA gene, the activity of the beta–glucocerebrosidase is reduced abundantly. Without this
important breaking down of the ... Show more content on Helpwriting.net ...
They are working to uncover the spectrum of symptoms related to Gaucher disease. They have
studied into the history of GD, where they found most of their answers. They have found a link
between glucocerebrosidase and parkinsonism. They have discovered that the mutation in the GBA
gene is the most common genetic risk factor for developing the other disorder, parkinsonism. This
led them to believe that if they can stop the mutation in the gene, or find a way to silence it, that
both these disorders can be cured. Scientists that have researched this disease believe that restricting
people from getting married that carry the gene is unnecessary and everyone can risk the chance if
they want to. Therefore, the bioethical implications of eugenics is not needed for this

Selling Body Shame
Selling Body Shame
Body–shaming perpetuates the degradation of women and is a recurring theme in advertising.
Women have always been measured by cultural ideas of beauty; and advertising exploits and
reinforces stereotypes of women as sex objects. The iPant Long Leg Shaper, "shapes and sculpts as
it releases ingredients into your skin while you move throughout the day" as stated at the bottom of
the advertisement. This product claims to correct the appearance of cellulite and construct a bulge–
free silhouette. The advertisement flaunts a beautiful, flawless, slender, Hispanic woman wearing
her shapewear. It implies that her super–model appearance is within reach of any woman wearing
this product. These pervasive images prey on the insecurities of teens and young women regarding
their body image and forces them to scrutinize each body part separately to achieve an unattainable
goal of perfection.
The iPant Anti–Cellulite Shapewear is a mid–end product selling for $60.00 that is geared towards
teens and young women to their mid–to–late 30s who desire to be shaped and sculpted like the
model in this advertisement. It is recommended that the iPant be worn 8 hours a day, for 7 days a
week for 28 days for optimal results and the active ingredients released are still present up to 100
washes. As stated at the bottom of the advertisement, the iPant uses "caffeine to promote fat
destruction; Vitamin E to prevent the effects of aging; ceramides to restore and maintain skin's

Azone Research Paper
2.1.7.3.3. Azone and derivatives: Azone (laurocapram, Figure 5) is a highly lipophilic liquid with an
octanol/water partition coefficient of 6.21. It is a chemically stable compound and an excellent
solvent for many drugs. Azone has a low irritating potential, a very low toxicity and nearly no
pharmacological activity (56, 58). It can be used as penetration enhancers for hydrophilic and
lipophilic substances such as steroids, antibiotics and antiviral agents and for peptide molecules as
well, such as insulin and vasopressin (58). The efficacy of Azone is concentration dependent and is
influenced by the choice of vehicle from which it is applied. Azone is most effective at low
concentrations, being employed typically between 0.1% and 5%, often between 1% and 3% (56).
Addition ... Show more content on Helpwriting.net ...
To overcome this issue, many Azone–like compounds have been synthesized (55). Modification in
the structure of Azone includes change in: a) The optimal hydrocarbon chain length The
enhancement activities increased as the length of the hydrophobic chains increased, but when the
length of the chain was longer than a certain limit, the activities rather decreased. The optimal
hydrocarbon chain length was between 8 and 14 carbons, which would vary according to their
different polar heads. The action of an enhancer was dependent on the balance between its
hydrophilic and lipophilic nature, and therefore different length of alkyl chain was required for best
incorporation of the enhancer with different polar heads into the skin lipid bilayers (60). b)
Heterocyclic ring size The presence of five–member cycle increased the activity, while six and
seven member cycle exhibited lower activity. Azone analogs with a small polar head might be
expected to be situated well into the polar lipid domain, thus disrupting the ordered organization of
the lipid layers (61). c) The heteroatoms in the polar

Niemann: Pick's Disease Essay
Niemann: Pick's Disease
Niemann Pick disease consists of a group of genetic disorders in which the common feature is a
varying degree of sphingomyelin storage in certain tissues of the body. According to the current
classification based on the enzymatic defect underlying these disorders, two main groups are
distinguished. The first group, which comprises type A, which is characterized by a severe
deficiency in acid sphingomyelinase activity, includes infantile neuronopathic form; and type B, an
adult chronic form without neurologic symptoms. In the second heterogeneous group called type C,
neuro–visceral involvement is massive and lipid metabolism is affected.
The sphingomyelin that accumulates in the lysosomes of the ... Show more content on
Helpwriting.net ...
The reason for this significant difference in neurological involvement is not clear, but it may be
consistent with the level of residual sphingomyelinase activity. Fibroblasts from normal individuals
and patients with Niemann– Picks disease types A and B, synthesize the sphingomyelinase
polypeptide having the same molecular mass 110 Kilo Daltons (KDa) and in the same degree of
abundance, during further processing the 110 KDa polypeptide is processed to a lower molecular
weight 84 KDa. Deficiency of sphingomyelinase is due to intragenic defects. Experiments done so
far, suggest that specific defects could be small inframe deletions or additions or point mutations.
The differences in clinical course of types A and B suggest that mutations are different.
Sphingomyelinase follows the same intracellular targeting and post–translational processes as the
majority of the lysosomal hydrolases. However, unlike any other enzyme there are two differently
sized polypeptides which are differentially distributed in tissues. In tissues like brain the smaller
polypeptide (molecular weight = 80 KDa) is found, whereas kidney contains both the polypeptides
(110 and 80 KDa). There is no precise explanation for the occurrence of single differently sized
polypeptides in some tissues, and the presence of both forms in tissues

Tay Sachs Disease Case Study
Tay–Sachs disease is an autosomal recessive disease. Tay Sachs disease can be attributed to the
inhibited activity of the hydrolase enzyme b–Hexosaminidase–A (HEX A). The Hex A gene is on
the q arm of chromosome 15. When mutated the breakdown of ganglioside from
disialotetrahexosylganglioside (GM2) to monosialodihexosylganglioside (GM3) is defective. This
results in a buildup of GM2 in the lysosomes in nerve cell. These lysosomes swell in size and can
rupture resulting in many neurological defects and hepatosplenomegaly. The accumulation and burst
of the lysosome manifest itself in three different, but categorically similar ways depending on the
type of mutation in Hex A. While many therapies are in clinical trials most of the treatment options
are done just to treat the symptoms of Tay Sachs because no cure exists.
Introduction ... Show more content on Helpwriting.net ...
Tay Sachs has a significant higher incidence in the Ashkenazi Jewish population. In the general
population, Tay–Sachs is rare disease, with a prevalence of 1/201,000 live births and incidence of
1/220,000 live births (1). The Tay Sachs mutation has a carrier frequency that, as expected is much
higher in the Ashkenazi Jewish. With a frequency of 1/30 in the Ashkenazi population. This high
rate of prevalence, incidence, and carrier percentage can be attributed to a history of consanguineous
relationships. In addition, eastern Quebec French Canadians also experience similar problems with
high mutation carrier frequency of 1/14 compared with that in the general population with a carrier
mutation rate of just 1/300 (1). Tay Sachs disease is a disease that claims the life of most people in
the first few years of life due to the metabolic nature of the disease. The metabolism of ganglioside
lipids is rendered ineffective in patient with Tay Sachs disease.

Macromolecules And Structure Of A Cell
A cell is a dynamic and complex structure surrounded by a very thin membrane known as a plasma
membrane or a cytoplasmic membrane. This membrane acts as a barrier between the inside of the
cell and the outside, which results in different chemical environments on either side. The plasma
membrane is selectively permeable to ions and organic molecules, so it can regulate substances
coming in and out of the cell. These membranes have played a crucial role in the evolution of
prokaryotes to multicellular eukaryotes. (Figure 1) In prokaryotes, there is only one type of
membrane i.e. plasma membrane but in eukaryotes, they have intracellular membranes
compartmentalizing its contents into chambers called organelles. These organelles have their own
specific functions; they interact with each other and the membrane to work as a unit.
The membrane therefore has several functions, which can be attributed by its molecular composition
and structure.
Figure 1. Diagram showing the evolution of prokaryotes.
The lipid bilayer [figure 4] is organised in distinct regions primarily because of the hydrophobic
effect caused by the amphipathic nature of these molecules. In order to reduce the contact of the
nonpolar regions with the aqueous environment, lipid molecules arrange themselves in a manner so
that the hydrophobic tails point towards each other and the hydrophilic polar head groups are
exposed on the outside facing the aqueous environment. These lipids also form structures called

Annemarie Bourlind Executive Summary

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