For noradrenaline to be acted upon by PNMT in the cytosol, it must first be shipped out

of granules of the chromaffin cells. This may occur via the catecholamine-
H+ exchanger VMAT1. VMAT1 is also responsible for transporting newly synthesized
adrenaline from the cytosol back into chromaffin granules in preparation for release.[46]
In liver cells, adrenaline binds to the β adrenergic receptor, which changes conformation and
helps Gs, a G protein, exchange GDP to GTP. This trimeric G protein dissociates to Gs alpha
and Gs beta/gamma subunits. Gs alpha binds to adenyl cyclase, thus converting ATP into
cyclic AMP. Cyclic AMP binds to the regulatory subunit of protein kinase A: Protein kinase A
phosphorylates phosphorylase kinase. Meanwhile, Gs beta/gamma binds to the calcium
channel and allows calcium ions to enter the cytoplasm. Calcium ions bind to calmodulin
proteins, a protein present in all eukaryotic cells, which then binds to phosphorylase kinase
and finishes its activation. Phosphorylase kinase phosphorylates glycogen phosphorylase,
which then phosphorylates glycogen and converts it to glucose-6-phosphate.[citation needed]

Pathology[edit]
Increased epinephrine secretion is observed in pheochromocytoma, hypoglycemia,
myocardial infarction and to a lesser degree in benign essential familial tremor. A general
increase in sympathetic neural activity is usually accompanied by increased adrenaline
secretion, but there is selectivity during hypoxia and hypoglycaemia, when the ratio of
adrenaline to noradrenaline is considerably increased.[47][48][49] Therefore, there must be some
autonomy of the adrenal medulla from the rest of the sympathetic system.
Myocardial infarction is associated with high levels of circulating epinephrine and
norepinephrine, particularly in cardiogenic shock.[50][51]
Benign familial tremor (BFT) is responsive to peripheral β adrenergic blockers and β2-
stimulation is known to cause tremor. Patients with BFT were found to have increased
plasma epinephrine, but not norepinephrine.[52][53]
Low, or absent, concentrations of epinephrine can be seen in autonomic neuropathy or
following adrenalectomy. Failure of the adrenal cortex, as with Addisons disease, can
suppress epinephrine secretion as the activity of the synthesing
enzyme, phenylethanolamine-N-methyltransferase, depends on the high concentration of
cortisol that drains from the cortex to the medulla.[54][55][56]

Terminology[edit]
Epinephrine is the pharmaceutical's United States Adopted Name and International
Nonproprietary Name, though the name adrenaline is frequently used. The
term epinephrine was coined by the pharmacologist John Abel (from the Greek for "on top of
the kidneys"), who used the name to describe the extracts he prepared from the adrenal
glands as early as 1897.[57] In 1901, Jokichi Takamine patented a purified adrenal extract,
and called it "adrenalin" (from the Latin for "on top of the kidneys"), which
was trademarked by Parke, Davis & Co in the U.S.[57] In the belief that Abel's extract was the
same as Takamine's, a belief since disputed, epinephrine became[when?] the generic name in
the U.S.[57] The British Approved Name and European Pharmacopoeia term for this drug is
adrenaline and is indeed now one of the few differences between the INN and BAN systems
of names.[58]
Among American health professionals and scientists, the term epinephrine is used
over adrenaline. However, pharmaceuticals that mimic the effects of epinephrine are often
called adrenergics, and receptors for epinephrine are called adrenergic receptors or
adrenoceptors.
Emotional response[edit]
Every emotional response has a behavioral component, an autonomic component, and a
hormonal component. The hormonal component includes the release of epinephrine, an
adrenomedullary response that occurs in response to stress and that is controlled by
the sympathetic nervous system. The major emotion studied in relation to epinephrine is
fear. In an experiment, subjects who were injected with epinephrine expressed more
negative and fewer positive facial expressions to fear films compared to a control group.
These subjects also reported a more intense fear from the films and greater mean intensity
of negative memories than control subjects.[41] The findings from this study demonstrate that
there are learned associations between negative feelings and levels of epinephrine. Overall,
the greater amount of epinephrine is positively correlated with an arousal state of negative
feelings. These findings can be an effect in part that epinephrine elicits physiological
sympathetic responses including an increased heart rate and knee shaking, which can be
attributed to the feeling of fear regardless of the actual level of fear elicited from the video.
Although studies have found a definite relation between epinephrine and fear, other
emotions have not had such results. In the same study, subjects did not express a greater
amusement to an amusement film nor greater anger to an anger film.[41] Similar findings were
also supported in a study that involved rodent subjects that either were able or unable to
produce epinephrine. Findings support the idea that epinephrine does have a role in
facilitating the encoding of emotionally arousing events, contributing to higher levels of
arousal due to fear.[42]
Memory[edit]
It has been found that adrenergic hormones, such as epinephrine, can produce retrograde
enhancement of long-term memory in humans. The release of epinephrine due to
emotionally stressful events, which is endogenous epinephrine, can modulate memory
consolidation of the events, ensuring memory strength that is proportional to memory
importance. Post-learning epinephrine activity also interacts with the degree of arousal
associated with the initial coding.[43] There is evidence that suggests epinephrine does have a
role in long-term stress adaptation and emotional memory encoding specifically. Epinephrine
may also play a role in elevating arousal and fear memory under particular pathological
conditions including post-traumatic stress disorder.[42] Overall, "Extensive evidence indicates
that epinephrine (EPI) modulates memory consolidation for emotionally arousing tasks in
animals and human subjects.”[44] Studies have also found that recognition memory involving
epinephrine depends on a mechanism that depends on β adrenoceptors.[44]Epinephrine does
not readily cross the blood–brain barrier, so its effects on memory consolidation are at least
partly initiated by β adrenoceptors in the periphery. Studies have found that sotalol, a β
adrenoceptor antagonist that also does not readily enter the brain, blocks the enhancing
effects of peripherally administered epinephrine on memory.[45] These findings suggest that β
adrenoceptors are necessary for epinephrine to have an effect on memory consolidation.

he adrenal medulla is a minor contributor to total circulating catecholamines(L-DOPA is at a

higher concentration in the plasma),[11] though it contributes over 90% of circulating
epinephrine. Little epinephrine is found in other tissues, mostly in scattered chromaffin cells.
Following adrenalectomy, epinephrine disappears below the detection limit in the blood
stream.[12]
 The adrenal glands contribute about 7% of circulating norepinephrine, most of which is a spill
over from neurotransmission with little activity as a hormone.[13][14][15] Pharmacological doses of
epinephrine stimulate α1, α2, β1, β2, and β3 adrenoceptors of the sympathetic nervous system.
Sympathetic nerve receptors are classified as adrenergic, based on their responsiveness to
adrenaline.[16]
The term "adrenergic" is often misinterpreted in that the main sympathetic neurotransmitter is
norepinephrine (noradrenaline), rather than epinephrine, as discovered by Ulf von Euler in
1946.[17][18]
Epinephrine does have a β2 adrenoceptor-mediated effect on metabolism and the airway,
there being no direct neural connection from the sympathetic ganglia to the airway.[19][20][21]
The concept of the adrenal medulla and the sympathetic nervous system being involved in
the flight, fight and fright response was originally proposed by Cannon.[22] But the adrenal
medulla, in contrast to the adrenal cortex, is not required for survival. In adrenalectomized
patients hemodynamic and metabolic responses to stimuli such as hypoglycemia and
exercise remain normal.[23][24]
Exercise[edit]
One physiological stimulus to epinephrine secretion is exercise. This was first demonstrated
using the denervated pupil of a cat as an assay,[25] later confirmed using a biological assay
on urine samples.[26] Biochemical methods for measuring catecholamines in plasma were
published from 1950 onwards.[27] Although much valuable work has been published using
fluorimetric assays to measure total catecholamine concentrations, the method is too non-
specific and insensitive to accurately determine the very small quantities of epinephrine in
plasma.

FDA Orange Book

1. Prescription Drug Products
<="" div="" style="box-sizing: border-box; padding: 1em 1px 0.2em; width:
598.59375px; overflow-x: auto; max-width: 100%;">
Prescription Drug Products: 1 of 12 (RX Drug Ingredient)

Drug Ingredient EPINEPHRINE

Proprietary Name EPIPEN

MYLAN SPECIALITY LP (Application Number: N019430.

Applicant
Patents: 7449012, 7794432, 8048035, 8870827, 9586010)

from FDA Orange Book

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598.59375px; overflow-x: auto; max-width: 100%;">
Prescription Drug Products: 2 of 12 (RX Drug Ingredient)

Drug Ingredient EPINEPHRINE; LIDOCAINE HYDROCHLORIDE

 Prescription Drug Products: 2 of 12 (RX Drug Ingredient)

LIDOCAINE
Proprietary Name
HYDROCHLORIDE AND EPINEPHRINE

1. EASTMAN KODAK (Application

Number: A040057)
2. HOSPIRA (Application Number: A078772)
3. HOSPIRA (Application Number: A088571)
Applicant 4. HOSPIRA (Application Number: A089635)
5. HOSPIRA (Application Number: A089644)
6. HOSPIRA (Application Number: A089645)
7. HOSPIRA (Application Number: A089646)
8. HOSPIRA (Application Number: A089651)
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598.59375px; overflow-x: auto; max-width: 100%;">
Prescription Drug Products: 3 of 12 (RX Drug Ingredient)

Drug Ingredient EPINEPHRINE; LIDOCAINE HYDROCHLORIDE

Proprietary Name XYLOCAINE W/ EPINEPHRINE

FRESENIUS KABI USA (Application

Applicant
Number: N006488)

from FDA Orange Book

View All 12 Prescription Drug Products
2. Discontinued Drug Products
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Discontinued Drug Products: 1 of 21 (DISCN Drug Ingredient)

EPINEPHRINE BITARTRATE; PRILOCAINE

Drug Ingredient
HYDROCHLORIDE

Proprietary Name CITANEST FORTE

Applicant ASTRAZENECA (Application Number: N014763)

from FDA Orange Book

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598.59375px; overflow-x: auto; max-width: 100%;">
Discontinued Drug Products: 2 of 21 (DISCN Drug Ingredient)

Drug Ingredient EPINEPHRINE; LIDOCAINE HYDROCHLORIDE

Proprietary Name LIDOCAINE HYDROCHLORIDE W/ EPINEPHRINE

1. ABBOTT (Application Number: A083154)

2. BEL MAR (Application Number: A080757)
3. BEL MAR (Application Number: A080820)
4. DELL LABS (Application Number: A083389)
Applicant 5. DELL LABS (Application Number: A083390)
6. INTL MEDICATION (Application
Number: A086402)
7. WATSON LABS (Application Number: A080377)
8. WATSON LABS (Application Number: A085463

Epinephrine is the active sympathomimetic hormone from the ADRENAL MEDULLA.

It stimulates both the alpha- and beta- adrenergic systems, causes systemic
VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and
dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC
FAILURE and to delay absorption of local ANESTHETICS.
from MeSH
Epinephrine is an alpha-Adrenergic Agonist, and beta-Adrenergic Agonist, and
Catecholamine. The mechanism of action of epinephrine is as an Adrenergic alpha-
Agonist, and Adrenergic beta-Agonist. The chemical classification of epinephrine is
Catecholamines.
FDA Pharmacology Summary from FDA Pharm Classes
Epinephrine Hydrochloride is the hydrochloride salt of the naturally occurring
sympathomimetic amine with vasoconstricting, intraocular pressure-reducing, and
bronchodilating activities. By stimulating vascular alpha-adrenergic
receptors, epinephrinecauses vasoconstriction, thereby increasing vascular resistance and
blood pressure. When administered in the conjunctiva, this agent binds to alpha-
adrenergic receptors in the iris sphincter muscle, resulting in vasoconstriction, a decrease
in the production of aqueous humor, and a lowering of intraocular pressure. Through its
beta1 receptor-stimulating actions, epinephrine increases the force and rate of myocardial
contraction and relaxes bronchial smooth muscle, resulting i

MIZENÍ HERCE BENDY

Druhého září zmizel herec Benda, mistr Jan Benda, jak se mu říkalo od té doby, co jediným
rozběhem vystoupil na jednu z nejvyšších příčlí herecké slávy. Totiž druhého září se nestalo
docela nic; posluhovačka, která v devět hodin ráno přišla poklidit Bendův byt, našla zválenou
postel a celý ten kančí nepořádek, který obyčejně Bendu obklopoval, jenom pan mistr nebyl
doma; ale jelikož na tom nebylo nic neobvyklého, dala byt svým sumárním způsobem do
pořádku a šla zase po svém. Dobrá. Ale od té doby nebylo po herci Bendovi ani památky.
Paní Marešová (totiž ta posluhovačka) se nepodivila příliš ani tomu; prosím vás, tihle herci, to
vám je jako cikáni; kdopak ví, kam zas jel hrát nebo flámovat. Ale desátého září se strhla po
herci Bendovi sháňka; měl přijít do divadla, kde se začínaly zkoušky na Krále Leara; když
Benda nepřišel ani na třetí zkoušku, vzbudilo to přece jen nepokoj a z divadla telefonovali
doktoru Goldbergovi, Bendovu příteli, neví-li, co se děje s Bendou.
Ten doktor Goldberg byl chirurg a vydělával ukrutné peníze na slepých střevech; to už je
taková židovská specialita. Jinak to byl tlustý člověk s tlustými zlatými brýlemi a tlustým
zlatým srdcem; hořel pro umění, měl byt od podlahy po strop ověšený samými obrazy a
oddaně miloval herce Bendu, který k němu choval přátelské opovržení a s jistou
blahosklonností mu dovoloval, aby za něj platil; což, mezi námi, nebyla zrovna maličkost.
Tragická maska Bendova a zářící obličej doktora Goldberga (který pil jenom vodu), to už
patřilo k sobě při všech těch sardanapalských flámech a divokých výtržnostech, které byly
druhou stránkou proslulosti velkého mima.
Tedy tomu doktoru Goldbergovi telefonovali z divadla, co prý se děje s Bendou. Odpověděl, že
nemá ponětí, ale že se po něm podívá; co neřekl, bylo, že už ho sám po celý týden shání po
všech nočních lokálech a výletních hotelech s rostoucím znepokojením; měl tísnivou
předtuchu, že se něco Bendovi stalo. To bylo totiž tak: Doktor Goldberg byl, pokud mohl
zjistit, poslední, kdo Jana Bendu viděl. Někdy koncem srpna s ním ještě podnikl triumfální
tažení noční Prahou; ale pak už Benda nepřišel na žádnou obvyklou schůzku. Snad stůně, řekl
si konečně doktor Goldberg a zajel si jednou večer do Bendova bytu; bylo to právě prvního
září. Zvonil u dveří; nikdo nešel otevřít, ale uvnitř bylo slyšet nějaký šramot. Tu drnčel doktor
dobrých pět minut na zvonek; najednou zazněly kroky a dveře se otevřely; stál v nich Benda
zahalený v županu, a doktor Goldberg se ho zděsil: tak zdivočele vypadal slavný herec s
rozcuchanými a slepenými vlasy a vousy dobrý týden neholenými; zdál se přepadlý a špinavý.
“A, to jste vy,” řekl nevlídně, “co chcete?”
“Proboha, copak se s vámi stalo?” vyhrkl doktor užasle.

Diabetologie, endokrinologie, metabolismus

1. Mezi typické příznaky hypotyreózy nepatří:
hmostnostní přírůstek
zácpa
bradykardie
snížení TSH

2. Bílkovinný komplex s klíčovým významem pro endocytózu se nazývá

Klarithin
Karnitin
Klathrin
Keratin

3. Co nepatří pod diagnózu prediabetes?

hraniční glykemie nalačno (HGL, angl. IFG) jako důsledek inzulinové rezistence
postihující játra
úzký vztah k metabolickému syndromu
nenápadný diabetes v mládí, který hrozí zhoršením ve vyšším věku
porušená glukózová tolerance (PGT, angl. IGT) jako důsledek inzulinové
rezistence postihující kosterní svalstvo
4. Pro energetický metabolismus kosterního svalstva má význam
keratin (ve formě difosfátu)
kreatinin
karnitin
kreatin (ve formě fosfátu)

5. Metabolický syndrom je charakterizován především

zvýšenou činností štítné žlázy
patologickou aktivací mikrozomálních enzymů P450 v důsledku dlouhodobého
metabolizování léků nebo toxinů
inzulinovou rezistencí
sníženou činnosti štítné žlázy

6. Metabolická paměť
je jiný termín pro dlouhodobou paměť (její podstatou je metabolismus bílkovin)
je přetrvávání poškození buněk u diabetu i po normalizaci glykemie
je pojem z evoluční biologie označující funkci starých proteinových domén v
enzymech spojených s evolučně mladými metabolickými cestami
je souhrnný pojem pro imunologickou paměť a další podobné formy v protikladu
k paměti v běžném slova smyslu

7. Karnitin
je bílkovina s klíčovým významem pro endocytózu
je látka, která se ve formě fosfátu podílí na energetickém metabolismu svalových
buněk
je látka, která ve formě acylkarnitinu usnadňuje transport mastných kyselin přes
vnitřní mitochondrální membránu
odpadní dusíkatá látka využívaná pro měření glomerulární filtrace, její zvýšená
hladina v plasmě však sama upozorňuje na renální insuficienci (i bez měření
GFR)

Všeobecně používaným kritériem nadváhy a obezity je index tělesné hmotnosti - BMI. Jeho
výhody a nevýhody jsou všeobecně známé, výhodou je snadný výpočet (stačí obyčejná
kalkulačka) a zejména fakt, že vztah mezi BMI a zdravotními důsledky obezity je
ověřen mnoha velmi dobře provedenými vědeckými studiem. Nevýhodou pak je například
skutečnost, že BMI nedokáže odlišit, do jaké míry se na tělesné hmotnosti podílí tuk a do jaké
třeba svaly - stokilový kulturista s výškou 180 cm má stejné BMI jako stejně vysoký a stejně
těžký tlouštík.
Rozdíl mezi oběma přitom poznáme bez velkého měření a vážení. Je to tím, že intuitivně
sledujeme objem břicha a objem horní poloviny těla. Medicína proto paralelně s BMI používá
jako další kritérium nadváhy také obvod pasu, který se navíc ukázal jako mimořádně vhodné
kritérium tzv. metabolického syndromu (podrobněji zde). Je totiž známo, nejen celkové
množství tělesného tuku, ale také jeho rozložení v těle, ovlivňuje zdravotní rizika.
Nejnebezpečnější je přitom tuk v krajině břciha (a spolu s ním tzv. viscerální tuk - podrobněji
zde), jehož zvýšené množství se označuje jako centrální obezita, která je právě spojena s
metabolickým syndromem.
Kritéria pro obvod tuku se přitom značně liší mezi Evropou a Severní Amerikou. Zatímco
European Group for the Study of Insulin Resistance považuje za hranici centrální
obezity obvod pasu 94 cm u mužů a 80 cm u žen, americké instituce v čele s American
Heart Association uvádějí jak hraniční hodnoty 102 cm u mužů a 88 cm u žen.
Již dlouho bylo zřejmé, že by bylo vhodné vytvořit kritérium, které by dokázalo kombinovat
výhody BMI i obvodu pasu, dlouho šlo však jen o formální hru se zlomky a mocninami bez
experimentálního ověření. V červenci letošního roku vyšla v internetovém lékařském
časopise PLoS ONE práce týmu vedeného Dr. Nirem Krakauerem ze City College of New York,
ve které autoři analyzovali data získaná od více než 14 000 dospělých osob (součást National
Health and Nutrition Examination Survey). Na základě této analýzy navrhli nový index, který
nazvali nazvali ABSI - A Body Shape Index, tedy Index tvaru těla.

Evrim Mekanizmaları Ne Demektir?

Evrim Mekanizmaları, temel olarak, evrimin gerçekleşmesini tetikleyen ve/veya sağlayan
doğal olgular ve süreçler olarak tanımlanabilir. Tıpkı cisimlerin yere doğru hareket
etmesi olayını sağlayan/tetikleyen olgunun cisimler arası kütleçekimi (veya daha isabetli
tabiriyle, uzay-zamanın bükülmesi) olması gibi, canlı popülasyonlarının nesiller içinde
değişmesini sağlayan bazı mekanizmalar bulunmaktadır. Evrim Mekanizmaları, genel
olarak, canlılar üzerinde sürekli veya aralıklarla etkiyen doğa yasalarıdır. Bu olgu ve
süreçlerin etkisi altında, canlı popülasyonları zaman içerisinde değişir ve hatta, daha
önce Türleşme yazı dizimizde açıkladığımız yöntemlerle, birden fazla yeni türe
ayrılabilir.
Bu mekanizmaları iki ana başlık altında toplamak mümkündür: Seçilim
Mekanizmaları ile Çeşitlilik Mekanizmaları.Yani bu yazı dizimizde
öğreneceğiniz mekanizmalardan bir kısmı canlıları "seçer" (Richard Dawkins'in
deyimiyle "kayırır") ya da "eler"ken, bir takım mekanizmanın etkisi altında seçilim
gerçekleşmez; ancak popülasyon içerisindeki çeşitlilik miktarında değişim (artış veya
azalış) olur. Örneğin mutasyonlar ikinci kategorideki mekanizmalardandır. Dolayısıyla
daha bu temel ayrımdan bile görebileceğiniz üzere, mutasyonlar gibi çeşitlilik
mekanizmaları, evrimin kendisi değillerdir ve asla olamazlar. Çeşitlilik ve seçilim
mekanizmaları bir arada çalışarak evrimi yaratırlar.
Bu yazı dizimiz içinde işleyeceğimiz Seçilim Mekanizmaları şunlardır: Doğal Seçilim,
Yapay Seçilim, Cinsel Seçilim, Akraba Seçilimi.
Ele alacağımız Çeşitlilik Mekanizmaları ise şunlardır: Gen Akışı (Göç), Genetik
Sürüklenme, Mutasyonlar, Crossing-Over, Transpozonlar, Plazmidler, Yatay Gen
Transferi ve Virüsler.
Bunların haricinde ikincil (minör) mekanizmalardan da bahsetmek mümkündür.
Bunlara ikincil mekanizmalar dememizin nedeni, türlerin genel evrimsel değişimi
sürecinde, az önce saydığımız mekanizmalara göre kısmen daha kesintili veya zayıf
etkiye sahip olmalarıdır. Bunlar arasında sayısız doğa yasası ve olgu bulunsa da, en
yaygın olanları Gen Düzenlemeleri, Alternatif Birleşme (Alternative Splicing),
Epigenetik, Endosimbiyotik Gen Transferi ve Rekombinasyon'dur. Biz, bu yazı
dizimizde temel mekanizmalara ağırlık verecek olsak da, olmak üzere, ikincil
mekanizmalardan da yer yer bahseceğiz.
Şimdi, bu temel mekanizmalara genel bir bakış atacağız ve genel hatlarıyla ne olduklarını
anlatacağız. Bu, genel bir özet olacak. Böylece kavramsal aşinalığa erişebilmenizi
umuyoruz. Yazı dizimizin ilerleyen yazılarındaysa, her birinin detaylarına daha da fazla
girerek, bu mekanizmaları tek tek irdeleyeceğiz.

Seçilim Mekanizmaları

1) Doğal Seçilim
Doğal Seçilim, bir popülasyon dahilindeki genetik ve fenotipik varyasyon (çeşitlilik)
içerisinde, yaşanılan ortama (habitata) en çok uyum sağlayabilme potansiyeline sahip
canlıların potansiyel olarak var olması ve bunların, değişen ortam koşulları dahilinde aktif
olarak bu ortamlara uyum sağlamaları sonucunda, fenotipik yapısından dolayı habitata uyum
sağlayamayanlara göre yaşam mücadelesinde daha başarılı olabilmeleri ve bunun sonucunda
daha fazla ve kolay üreyerek kendilerindeki göreceli "avantaj" sağlayan genleri yavrularına
aktarma şanslarını arttırmalarına bağlı olarak popülasyonların sürekli olarak daha uyum
sağlayan bireylerin bulunduğu bir yapıya doğru evrimleşmesini sağlayan mekanizmadır.

Evrimle ilgili halk arasında yazılan, çizilen, söylenen şeylerin ezici çoğunluğu herhangi
bir bilimsel temele dayanmıyor. Daha önemlisi, evrimin mekanizmalarının
sistematiğinden bihaber kimseler, evrimle ilgili "eleştiri" ve "yanlışlamalarını" medya
organları aracılığıyla halka ulaştırıyorlar. Buna karşılık, bilim camiası halka gerçekleri
yeterince hızlı ve etkili bir şekilde taşıyamıyor. Bu durumda, evrimin temellerine dair
bilgisizlik, bu bilgisizlikten nemalanmak isteyen gerici ve bilim düşmanlarının etkili
araçlarıyla birleştiğinde, giderek artan bir cehalet ortaya çıkıyor. İşte bu yazı dizisi, tüm
insanlarımızın evrimin temelleri konusundaki bilgi ve donanım düzeyini arttırmaları ve
internette görebilecekleri hatalı bilgileri kendi başlarına tespit edebilmeleri için yazıldı.
Evrimin temel mekanizmalarını bilen birinin, evrim karşıtı propagandalara
kanmayacağını düşünüyoruz. Bu nedenle bu yazı dizimizin okunması ve anlaşılmasının
çok önemli olduğu kanısındayız.