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Friday, 10 November 2017
Philadelphia woman tries passing fake scripts at Palmer pharmacy
PALMER TWP., Pa. – A Philadelphia woman is facing fraud charges after
she allegedly arrived at a Northampton County pharmacy Wednesday night
with fake prescriptions for more than 200 pills.
Police arrested Samantha M. Brown at a Palmer Township Rite Aid with
fraudulent prescriptions for Oxycodone, Alprazolam and Flexiril. The
25-year-old now faces three felony counts of trying to acquire a
controlled substance. District Judge James Narlesky arraigned Brown late
Wednesday night, setting bail at $7,500.
Palmer Township police were dispatched to the Rite Aid at 601 S. 25th
St. about 8:30 p.m. The pharmacist told officers that a woman later
identified as Brown was sitting in the waiting area, according to court
records.
The pharmacist said she tried filling prescriptions for 120 30
mg tablets of Oxycodone, 60 1 mg tablets of Alprazolam and 30 10
mg tablets of Flexiril. Alprazolam is an anxiety medication, and
Flexiril is a muscle relaxant.
The prescription was in another person’s name, and the pharmacist
told police that she confirmed with the doctor listed on the script that
it was a fake. A search of the doctor’s name listed in the criminal
complaint shows a physician in Williamsport, Lycoming County.
The doctor notified the pharmacist that the prescription was not
filled out in the manner he usually writes scripts and that the person
listed on the prescription was not a patient.
The science of Sad: understanding the causes of ‘winter depression’
For
many of us in the UK, the annual ritual of putting the clocks back for
daylight saving time can be accompanied by a distinct feeling of winter
blues as autumn well and truly beds in. This might be felt as a lack of
energy, reduced enjoyment in activities and a need for more sleep than
normal. But for around 6% of the UK population and between 2-8% of people in other higher latitude countries
such as Canada, Denmark and Sweden, these symptoms are so severe that
these people are unable to work or function normally. They suffer from a
particular form of major depression, triggered by changes in the
seasons, called seasonal affective disorder or Sad.
In addition to depressive episodes, Sad is characterised by various
symptoms including chronic oversleeping and extreme carbohydrate
cravings that lead to weight gain. As this is the opposite to major
depressive disorder where patients suffer from disrupted sleep and loss
of appetite, Sad has sometimes been mistakenly thought of as a “lighter”
version of depression, but in reality it is simply a different version
of the same illness. “People who truly have Sad are just as ill as
people with major depressive disorder,” says Brenda McMahon,
a psychiatry researcher at the University of Copenhagen. “They will
have non-seasonal depressive episodes, but the seasonal trigger is the
most common. However it’s important to remember that this condition is a
spectrum and there are a lot more people who have what we call sub-syndromal Sad.”
Around 10-15% of the population has sub-syndromal Sad. These
individuals struggle through autumn and winter and suffer from many of
the same symptoms but they do not have clinical depression. And in the
northern hemisphere, as many as one in three of us may suffer from
“winter blues” where we feel flat or disinterested in things and
regularly fatigued.
One theory for why this condition exists is related to evolution. Around 80% of Sad sufferers are women,
particularly those in early adulthood. In older women, the prevalence
of Sad goes down and some researchers believe that this pattern is
linked to the behavioural cycles of our ancient ancestors. “Because it
affects such a large proportion of the population in a mild to moderate
form, a lot of people in the field do feel that Sad is a remnant from
our past, relating to energy conservation,” says Robert Levitan,
a professor at the University of Toronto. “Ten thousand years ago,
during the ice age, this biological tendency to slow down during the
wintertime was useful, especially for women of reproductive age because
pregnancy is very energy-intensive. But now we have a 24-hour society,
we’re expected to be active all the time and it’s a nuisance. However,
as to why a small proportion of people experience it so severely that
it’s completely disabling, we don’t know.”
There are a variety of biological systems thought to be involved,
including some of the major neurotransmitter systems in the brain that
are associated with motivation, energy and the organisation of our
24-hour circadian rhythms.
“We know that dopamine and norepinephrine play critical roles in terms
of how we wake up in the morning and how we energise the brain,” Levitan
says. One particular hormone, melatonin,
which controls our sleep and wake cycles, is thought to be “phase
delayed” in people with severe Sad, meaning it is secreted at the wrong
times of the day.
Another system of particular interest relates to serotonin,
a neurotransmitter that regulates anxiety, happiness and mood.
Increasing evidence from various imaging and rodent studies suggests
that the serotonin system may be directly modulated by light. Natural
sunlight comes in a variety of wavelengths, and it is particularly rich
in light at the blue end of the spectrum. When cells in the retina, at
the back of our eye, are hit by this blue light, they transmit a signal
to a little hub in the brain called the suprachiasmatic nucleus that integrates different sensory inputs, controls our circadian rhythms, and is connected to another hub called the raphe nuclei
in the brain stem, which is the origin of all serotonin neurons
throughout the brain. When there is less light in the wintertime, this
network is not activated enough. In especially susceptible individuals,
levels of serotonin in the brain are reduced to such an extent that it
increases the likelihood of a depressive episode.
Read More: http://snip.ly/25gi4#https://www.theguardian.com/lifeandstyle/2017/oct/30/sad-winter-depression-seasonal-affective-disorder Click here To join us for more information, get in touch
Precision medicine: From ‘one-size-fits-all’ to personalized healthcare
Imagine a future in which, rather than using symptoms to
identify a disease, your genes, metabolism, and gut microbiome inform
how your individual health is managed. This is the vision of precision
medicine.
Traditional medicine uses symptoms to diagnose diseases, and drugs to
treat these symptoms. But precision medicine aims to turn this concept
on its head. By identifying the factors that predispose a person to a
particular disease and the molecular mechanisms that cause the
condition, treatment and prevention strategies can be tailored to each
individual.
So, how do we get from traditional to precision medicine? Advances in
genetics and molecular analysis techniques have been a deciding factor,
as has getting patients involved with managing their own health.
However, is precision medicine going to revolutionize how we treat
all medical conditions, or will it be the privilege of a select few?
Innovation drives precision medicine
To the National Institutes of Health
(NIH), “[P]recision medicine is a revolutionary approach for disease
prevention and treatment that takes into account individual differences
in lifestyle, environment, and biology.”
Launched by President Barack Obama in 2015, the Precision Medicine Initiative “will
pioneer a new model of patient-powered research that promises to
accelerate biomedical discoveries and provide clinicians with new tools,
knowledge, and therapies to select which treatments will work best for
which patients.”
Breakthroughs in molecular biology have been key to getting precision medicine off the ground.
Next-generation DNA sequencing is now routinely used to identify genetic mutations that drive specific cancers,
and biomarkers that predict disease risk or how well a person will
respond to a particular treatment are increasingly becoming reality in
medical practice. Cancer is the one area wherein precision medicine seems to be
making significant headway. New therapies seek to target the specific
cellular pathway that is being exploited by a cancer, with the view to
making short the life of the tumor.
This approach is already being employed in clinical trials to treat patients with melanoma who have a mutation in the BRAF gene, as Medical News Todayreported recently. Are you ready to join us to Keep Growing Up
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