San夫
說
減少卡路里的攝取可以延年益壽
San夫
說
不會特化的細胞會自滅! 其餘的會經由telomere的簡短而慢慢邁向死亡
San夫
說
apoptosis -> proteolysis, lipid modification, nucleolysis
yao280
說
?
San夫
說
YAO開始老化了!
San夫
說
survival + reproduction = reproductive success of GENES! WE ARE CONTROLLED BY GENES
San夫
說
我們只是受基因操控的軀殼
San夫
說
A 好基因傳給下一代, B 壞基因繁殖前死亡 被天擇篩選掉, C到晚年才生病，不好的基因已傳下去
San夫
說
antagonistic pleiotropic 基因互抗多效性 = 年輕時expression = good, 老時就不好
San夫
說
mutation accumulation - 環境因子破壞細胞到無法修補的狀態
San夫
說
Life span and Reproduction - 有限的資源導致競爭->生育causes somtatic damage
San夫
說
long life span = low fecundity, vice versa. Where fecundity = 生出來的小孩可長到成年繼續繁殖下一代(通常只算女性)
San夫
說
shorter lifespan = faster evolution
San夫
說
Interphase = G1 (mRNA+protein produced), S (DNA copy)+ G2 (chromosome > 2 chromatids)
San夫
說
Hayflick limit - normal cell can only divide a limited number of times, after that it senesces
San夫
說
cancer = accumulation of aneuploid cells + mutations
San夫
說
truly immortal cells = germ line cells
Shelly魚乾
說
快點筆記~~~~!!!
San夫
說
MC (Mutation accumulation) - free radicals (usually H,N,O,)= lonely electron, 好可憐 causing deletorius effect on the cells
San夫
說
ROS (Reactive oxygen species) - itself a free radical or causes new radical, such as *OH O2-* *NO
San夫
說
ROS causes mutaiton in G and T, causes lipid peroxidation
San夫
說
free radical is countered by antioxidant (lets ROS strip electron off of itself, 
)
)
San夫
說
antioxidant such as SOD (oxidize O2-* --> H2O2 and catalase H2O2 --> water )
San夫
說
vitamin c and E + glutathion are also antioxidant, so EAT YOUR VEGETABLE + FRUIT
San夫
說
G normally pairs with C with 3 hydrogen bonds, ROS changes binding of G with A, in next transcription A binds with T.
San夫
說
ROS is produced from other free radicals, also by mitochondria
San夫
說
DNA replicates 5' --> 3'
San夫
說
DNA polymerase requires RNA primer to initiate DNA synthesis
San夫
說
lagging strand - Primase synthesis RNA primer -> DNA polymerase GO! -> cuts, and ligase comes in
San夫
說
2009 Nobel prize (medicine) how chromosomes are protected by telomeres
San夫
說
telomere = TTAGGTTAGGTTAGGTTTAGGGTTAGG at 3' end
San夫
說
Telomere length = cell age marker
San夫
說
Dyskeratosis congenita = premature aging, 16~50 
San夫
說
mortal <---> crisis <--> immortal
San夫
說
regarding cancer cells, mutation in cells cause cancer, natural apoptosis causes aging
San夫
說
on the cellular level, cancer cells may be immortal, but the organism as a whole dies.
San夫
說
INK4a de-repression causes aging
San夫
說
quantity Erythrocyte > platelet > leukocytes
San夫
說
life span leuko > erythro > platelet
San夫
說
hematopoesis = formation of blood cell components
San夫
說
fetus in liver and spleen
San夫
說
bone marrow: red + yellow marrow
San夫
說
adipogenesis in bone marrow, birth till 30, then again at 70 drastically. starting with long bone such as femur
San夫
說
erythrocyte - biconcave, 7.5x2 um. 120 days life span, more in male > female. testosterone stimulates production, and also no periods
San夫
說
essential RBC formation nutrients : folic acid (DNA), VitB12 (DNA) + Fe2+ (Hemoglobin
San夫
說
with aging, RBC membrane fluidity decreases
San夫
說
higher oxidative stress and decrease in antioxidant defense
San夫
說
function of spleen is blood filter --> bile and into stool. contains many platelet, important in immune system
San夫
說
reserves half monocyte in red pulp, antibodies in white pulp (rich in B and T cells)
San夫
說
monocyte = type of white blood cell. pulp = part of spleen
San夫
說
declining p53 function lead to senescence. apoptosis of cancer cells higher at young age.
San夫
說
erythropoetic aging --> environment is a major contributing factor
San夫
說
aging --> lose of immune function. PNAS downregulates lyphoid genes and up regulates myeloid genes.
San夫
說
lymphoid system: neutrophil, first line of defense by diapedeis. baso release histamine and heparin. eosinophil atks parasite...
San夫
說
...mono convert to macrophage, consists peroxidase. lymphocytes provides immunity.
San夫
說
cord blood has highest count in all cell types
San夫
說
cell count decrease as one ages, most apparent decrease in lymphocyte, eosinophil and basophils
San夫
說
T cell --> cellular immunity, B cell --> plasma cell --> humoral immunity
San夫
說
lymphocytes are formed in lymph nodes, bone marrow, thumus and spleen
San夫
說
thymic atrophy = functional cells replaced by adipose tissues
San夫
說
thymic output decrease as a person gets older
San夫
說
thymic stimulatory cytokines --> robust thymus..and thymic repressive cytokines --> atrophied thymus. IL7 and IL6 respectively
San夫
說
Platelets (Thrombocytes) lacks nucleus. do not change shape in age. count either normal or decrease. function varies
San夫
說
primary thrombocytosis aka essential thrombothemia
San夫
說
risk factor of venous thromboembolism -- > 40 years old. heart faulure, immobolization for 3 days. trauma. hypercoagulate state
San夫
說
(to be continued)
Shelly魚乾
說
拜託!!! 我在記了!!!!!!
Shelly魚乾
說
謝謝SAN!!! 你拯救我了
San夫
說
是時候繼續了 (continues)
San夫
說
again in cardiovascular system
San夫
說
every patient (no matter young or old) is unique. HETEROGENEITY
San夫
說
the heart, is a pump. provides the drive for blood to circulate throughout the entire organism
San夫
說
artery - resistance system, low volume, high pressure
San夫
說
vein - capacitance system, high volume, low pressure
San夫
說
capillaries - exchange system
San夫
說
coronary artery provides blood to the heart itself
San夫
說
heart beats as SA node provides a signal
San夫
說
SA- internodal pathway - AV node - bundle of his -(branches)-> left and right bundle --> purkinje fibres
San夫
說
e signal -> signals heart -> contraction and expansion --> pressure in vessels --> blood circulates
San夫
說
SA node decrease in cell # starting 20 years old. 10% left when 75
San夫
說
conduction system start to calsify + 纖維化
San夫
說
artery length increase and distorted. thickness increases, more friction and breakage of fibr-protein increase
San夫
說
hardening artery --> more CV disease
San夫
說
as with spleen, more fat and lesss specialized cells in an aged heart
San夫
說
aortic and mitral valves become thickened. but appears more skimpy
San夫
說
endothelial cells in artery are mislined. onset of high blood pressure and atherosclerosis
San夫
說
右心房-->右心室-->肺動脈
San夫
說
左心房-->左心室-->主動脈
San夫
說
systole - contradtion, diastole - expansion
San夫
說
1. atrial systole, pushes blood into ventricles --> 2. isovolumetric contraction -->push blood (open PSV+ASV) into aorta and pulmonary trunk
San夫
說
4. isovolumetric relaxation, -->5 late diastole
San夫
說
requires 80 mmHg to opens aortic valve, but merely 8mmHg to open pulmonary valve
San夫
說
25% blood refills atrium at late diastole
San夫
說
end-diastolic volume - total volume of blood at the end of late diastole (phase 2)
San夫
說
stroke volume - amount of blood ejected from ventricles during systole
San夫
說
correction : 25% blood refills ventricles at late diastole
San夫
說
end- systolic volume - total volume of blood in ventricles at the end of systole
San夫
說
miral valvle (valve between left atrium and ventricle) seems to close slower in older people
San夫
說
when blood refills blood (phase 5), heart mucles/myocardium is stretched. then it contracts more forcefull. stretched elastic band hurt more
San夫
說
frank-starling law --> more EDV, greater volume pumped later into the aorta (Stroke Volume)
San夫
說
cardiac output = stroke volume x heart rate
San夫
說
CO is about 5L/ min !
San夫
說
stroke volume (SV) is regulated by four things -- 1. EDV (preload), 2. total peripheral resistance (TPR)affects after load, 3. contractility
San夫
說
4. ventricular size (larger heart) more EDV
San夫
說
afterload *unclear - wiki: afterload is used to measure the tension produced by a chamber of the heart in order to contract
San夫
說
Nervouse regulation: autonomic nervous system
San夫
說
sympathetic nervous sysmte - increase heart beat, SA node signal frequency upup, AV node transduction upup. myocardium contracts harder
San夫
說
parasympathetic nervous system - decrease everything above
San夫
說
sympathetic nervious system stimulation - norepinephrine (stress hormome, such as dopamine. binds to B1(beta-1) receptor
San夫
說
ATP ->cAMP activates Protein kinase (PKA), which opens the Ca2+ channel -->stimulates actin/myosin, which makes muscle contract harder
San夫
說
propanolol blocks B1 receptor --> thus heart beat slower. For some reason, older hearts have more blocked B1 receptors
San夫
說
一塊蛋糕
楊涵中
說
一塊蛋糕?
San夫
說
studies also show, in addition to more blocked beta1 receptors, the quantity of betal receptors also decrease
San夫
說
in resting phase - CO and SV are not affected in an old heart
San夫
說
max heart beat : 220 - current age. this equation is applicable to 15+ years old
San夫
說
so max SAN heart beat = 200
Shelly魚乾
說
WOW! SAN is so young 
San夫
說
shhhhhhhhhhh secret
San夫
說
atrial fibrillation (心房纖維顫動) - can cause 腦中風.
San夫
說
baroreflex (壓力反射) - declines when you are 80 years old, often contribute to 姿勢性低血壓
San夫
說
adding notes to atrial fibrillation (心房纖維顫動) - can cause 腦中風. This means heart muscles do not beat together. corrected by burning SA node
San夫
說
refer to 醫龍3 - episode 2. 黑木 
San夫
說
so how does 姿勢性低血壓 affect an elderly? not enough blood pressure. valves not opened. poor blood circulation --> hypoxia. anemia
San夫
說
Baroreceptor has carotid sinus and aortic arch. carotid body are chemoreceptors.
San夫
說
forgot to takes notes. dont know their importance
San夫
說
baroreceptor sense blood pressure --> accordingly affects 交感 and 副交感神經纖維的活性.
San夫
說
so if blood pressure too high --> parasympathetic activated ->lowers blood pressure. vice versa
San夫
說
MAP = HR x SV x TPR, where MAP is mean artery pressure. HR is heart beat rate. SV is stroke volume. TPR is resistance in blood vessels
San夫
說
modification of which one of HR, SV and TPR can lead to most noticeable MAP change?
San夫
說
baroceptor can affect HR fastest.
San夫
說
lying position to standing position lead to decrease in venous return due to gravity --> EDV decrease --> stroke volume decrease
San夫
說
circulation of blood to brain decreased --> anemia. you feel dizzy when you 蹲太久 then stand up
San夫
說
stroke volume decrease --> blood pressure decrease -- > baroreceptor sense low pressure --> activates sympathetic --> heart beat faster
San夫
說
as a person ages, systolic pressure and pulmonary pressure (脈壓) increase
San夫
說
diastolic pressure does not increase with over 60+ instead it declines
San夫
說
gene and environment affects blood pressure. city vs wilderness
San夫
說
healthy diet + lots of exercise = better health in 部落
San夫
說
artery (low volume, high pressure) function as a pressure reservoir, maintaining blood flow to tissues.
San夫
說
during ventricular relaxtion (phase 5)
San夫
說
arterial pulse = sys/dis = 120/80 during a cardiac cycle. I like simple math
San夫
說
pulse pressure : sys - diastolic = 120 - 80 = 40 mmHg
San夫
說
mean arterial pressure : dias pressure (80) + 1/3 pulse (1/3*40) = ~93
San夫
說
or 1/3 syst (1/3*120=40)+ 2/3 dias (2/3*80 =~50) = ~90
San夫
說
pulse presure too high not good for the blood vessels, eventually blood vessels thickens = more TPR = less CO
San夫
說
why do arteries need pressure. presure helps keep blood vessels intact (maintains shape)
San夫
說
systolic pressure and pulse pressure will increase with age. diastolic pressure will decline after 60 years old
San夫
說
blood lipips - triglycerol, phospholipid and cholesterol
San夫
說
creatinekinase: CK declines with age. LDH-5 also declines with age. these 2 lipid enzymes are good lab indicators of aging
San夫
說
total cholesterol increase, Low density lipoprotein about same, high-densit lipoprotein decrease with age
San夫
說
triglyceride increase with age
San夫
說
above changes not observed in tribal villages due to more healthy lifestyle
San夫
說
total cholesterol >240mg/dl very dangerous. avg asian = 200 OK
San夫
說
High density lipoprotein (HDL) good protein. LDL bad keep low
San夫
說
more 三高 = more heart problem -->arterial stiffness
San夫
說
高血壓,動脈粥狀硬化, 冠狀動脈硬化
San夫
說
blood cholesterol --> accumulation of platelets = thickenened blood vessle --> hypertention --> congestive heart failure --> stroke
San夫
說
atherosclerosis begins as a result of damage of endothelial cell wall. caused by hypertention, high cholesterol and diabetes
San夫
說
corononary artery disease (CAD) angina or chest pain. myocardial infarction MI. also 心律不整
San夫
說
age related changes in cardiovascular physiology - CO decrease, heart beat slower, stroke volume decrease, LV stiffness increase. EDV dcreas
San夫
說
endothelium progenitor cells 內皮先驅細胞 may be used to repair damaged endothelial cells
San夫
說
THATS ALL FOLKS