Research
بروز بیماری قلبی و عروقی
سالانه 4000 مرگ و میر بر اثر آلودگی هوا در تهران رخ می‌دهد که علاوه بر این تعداد مشابهی نیز که به بیماری سرطان ریه مبتلا شده‌اند و در معرض اکسیدهای نیتروژن بوده‌اند گزارش شده اس
دکتر مسعود قاسمی رییس انجمن آترواسکلروز ایران در خصوص اثرات سوء استنشاق آلاینده های موجود در هوای تهران می گوید: تاثیر آلودگی هوا در بروز بیماری قلبی و عروقی نظیر افزایش فشار خون زیانبار است و تحقیقات نشان می دهد آلودگی هوا باعث غلیظ شدن خون و افزایش احتمال بروز التهاب می شود
وی سر درد، ضعف، سرگیجه، تهوع، اختلال در انتقال اکسیژن به بافت های بدن، ضربان شدید قلب، سکته قلبی و کاهش ظرفیت ششی را از آثار آلودگی هوا بر سلامت افراد برشمرد و خاطرنشان ساخت: افرادی که زمینه ناراحتی قلبی دارند، هنگام رفت و آمد در خیابان ها، بیش از افراد عادی در معرض خطر حملات قلبی هستند
وی با بیان اینکه مرگ زودرس ناشی از بیماری های قلبی در نواحی آلوده به اثبات رسیده است، می افزاید: آلودگی هوای ناشی از ترافیک اتومبیل ، دود کارخانه ها یا دود سیگار موجب نازک شدن سرخرگ گردن و در نهایت بیماری قلبی می شود
دکتر مسعود قاسمی رییس انجمن آترواسکلروز ایران
__________________________________________________________________
سرعت ترکیب اکسیدهای نیتروژن با هموگلوبین خون هزار مرتبه سریعتر از سرعت ترکیب مونواکسید کربن با هموگلوبین است که موجب تشکیل مواد سرطان زا در خون می‌شود و 200 برابر بیش از جذب اکسیژن است. تمایل جذب هموگلوبین خون با مونوکسید کربن و اثرات سوء آن بر سلامتی بصورت اختلال در بینایی، تار دیدن، خستگی، سردرد و خواب آلودگی بروز می کند و باعث ایجاد تغییر در عملکرد قلب و شش می‌شود
نتایج تحقیقات صورت گرفته در این زمینه حاکی است : آلودگی هوا در کاهش وزن نوزادان نیز بسیار موثر است و بر میزان مرگ و میر کودکان تأثیر می‌گذارد، زیرا حساسیت نوزادان به آلودگی هوا بیشتر است. ابتلای کودکان به سرطان خون اولین پیامد زندگی در خیابان‌های پر ترافیک است. منواکسید کربن ابتلا به بیماری‌های قفسه سینه در کودکان را افزایش داده و همچنین باعث عفونت‌های شدید تنفسی (ARI) در کودکان و اطفال، بیماری‌های مزمن تنفسی نظیر تنگی نفس و برونشیت، سرطان ریه و ابتلا به سرطان معده شده و اختلالات ژنتیکی و ابتلا به بیماری‌های موروثی و اختلال در حافظه را افزایش داده، حملات آسم را تشدید کرده و به DNA آسیب می‌رساند
مطالعات دانشمندان کانادایی نیز نشان می دهد، آلودگی هوا نـاشـی از خودروها جهش و آسیب ژنتـیکـی در حیوانات و انسان را سبب می شود و همچنین حاصلخیزی خاک را کاهش داده و آنرا از املاح تهی می‌کند
ابتلای کودکان به سرطان خون اولین پیامد زندگی در خیابان‌های پر ترافیک است
ایسکانیوز – محققان بر این باورند که عبور جریان خفیف الکتریکی از مغز افرادی که در خواب هستند می‌تواند سبب افزایش حافظه آنان شود
به گزارش سرویس علمی پژوهشی ایسکانیوز به نقل از ام.اس. ان طبق این گفته این جریان الکتریکی باید در فرکانس مشخصی باشد
این دانشمندان آزمایشات را بر روی عده ای دانش‌آموز امتحان کرده‌اند که نتایج آن پیشرفت حافظه‌ای آنان و سرعت به خاطر آوردن لغات بوده است. همچنین گفته می‌شود که می توان یک چنین درمانی را برای بیماران آلزایمری و یا کسانی که دچار اختلالات خواب هستند نیز انجام داد
یکی ازمحققان بر این باور است که نتایج حاصله می تواند ارتباط بین خواب و یادگیری را نشان دهد.
Titre du document / Document title
"Health effects and time course of particulate matter on the cardiopulmonary system in rats with lung inflammation."
Auteur(s) / Author(s)
ULRICH Magda M. W. (1) ; ALINK Gerrit M. (1) ; KUMARATHASAN Premkumari (2) ; VINCENT Renaud (2) ; BOERE A. John F. (3) ; CASSEE Flemming R. (3)
Recent epidemiological studies associate health effects and particulate matter in ambient air Exacerbation of the particle-induced inflammation can be a mechanism responsible for increased hospitalization and death due to cardiopulmonary events in high-risk groups of the population. Systems regulating blood pressure that depend on lung integrity can be involved in progression of cardiovascular diseases. This study focused on the expression levels of various genes involved in cardiovascular and pulmonary diseases to assess their role in the onset of cardiovascular problems due to ambient particulate matter and compared these with the corresponding products. Rats with ozone-induced (1600 μg/ m[3]; 8 h) pulmonary inflammation were exposed to 0.5 mg, 1.5 mg, or 5 mg of particulate matter (PM) from Ottawa Canada (EHC-93) by intratracheal instillation. mRNA levels of various genes and their products were measured 2, 4, and 7 d after instillation. At 2 d after exposures to PM, tumor necrosis factor (TNF)-α levels in bronchoalveolar lavage fluid (BALF) were elevated approximately 4 times for the highest EHC-93 dose. MIP-2 protein levels in BALE were elevated approximately three times during the entire time period studied, whereas IL-6 levels were not affected compared to control groups. The MIP-2 mRNA levels revealed a similar pattern of induction. A twofold increase in endo-thelin (ET)-1 levels at d 2 and a 20% decrease in angiotensin-converting enzyme (ACE) activity at d 7 were measured in plasma. A 60% decrease of ACE and ET-1 mRNA levels suggested a possible endothelial damage in the lung blood vessels. Inducible nitric oxide synthase (iNOS) mRNA was found to be increased 3.5 times 2 d after instillation of the particles. Therefore, the endothelial damage could have been caused by large amounts of the free radical NO. Also, plasma levels of fibrinogen were elevated (20%), which could presumably increase blood viscosity, leading to decreased tissue blood flow. These changes in hematological and hemodynamic parameters observed in our study are in line with heart failure in high-risk groups of the population after high air pollution episodes
برنامه پیشگیری از دیابت
افرادی که خطر ابتلا به دیابت را دارند ، باید پیش از موقع مورد مشاوره قرار گرفته و عوامل مهم شیوه زندگانی که سبب تأخیر یا حتی مانع پیشرفت این بیماری می شوند را مورد توجه قرار دهند
برنامه پیشگیری از دیابت
The devastating consequences of the environmental destruction on the occurance of the cardiovascular diseases may be a little controversial, but gradually , it appears to some scientists that these deterioration of the health of environment and increasing of risk factors will have the severe impacts for develping of the blood vessel diseases; they see this issue as a " black box" within these impacts, which need to be studied and analayzed more carefully.
Depspite of capabilty of humans for rationalization and focusing on these impacts and to know whether these environmental factors are targeting and harming our strategic parts of body such as the endothelial cells, unfortunately they are failing in right decsions and in right focusing.
As a strategic barrier between the intravascular compartment and underlying tissues, endothelial cells are exposed to low ambient oxygen tension, i.e. hypoxia, during their development.As a strategic barrier between the intravascular compartment and underlying tissues, endothelial cells are exposed to low ambient oxygen tension, i.e. hypoxia, during their development.
Endothelial cells lie in a strategic anatomical position between the circulating blood and vascular smooth muscle. They are thus most exposed to physical forces such as shear stress,1 hydrostatic pressure,2 and pulsatile stretch, particularly in the arterial circulation. Changes in local flow acutely increase nitric oxide (NO) release in vitro1 and cause flow-dependent vasodilation in vivo.3 On the other hand, increases in hydrostatic pressure cause vasoconstriction,1 reduce NO production,4 and increase endothelin release.5 This may explain the greater endothelium-dependent relaxation in arteries than veins.6
circulation
The response of blood vessels to low oxygen levels may be the Achilles’ heel of a developing tumor, according to a study led by University of California, San Diego biologists.
The study, published in the November 15 issue of the journal Cancer Cell, is the first to examine how blood vessels respond to the low oxygen conditions that result from the presence of a growing tumor. Previous work by the UCSD group and others has shown that tumors, which need a blood supply to provide oxygen and nutrients, release chemical signals that summon the blood vessels to grow toward them.
chemical signals
Vascular endothelium, a monolayer of cells lining the intima of the blood vessels, is involved in a variety of functions, including coagulation, vascular permeability, vascular tonus, and remodeling.1 Endothelial cells, which are in direct contact with plasma and cellular components of blood, are the target of many cytokines and growth factors,2 3 and they alter the metabolic status of their own cells.4 Abnormalities of endothelial function may contribute to certain diseases of blood vessel walls, such as thrombosis, atherosclerosis, and vasculitis.5 6 Endothelial cell survival under pathological conditions, such as hypertension, atherosclerosis, vascular prosthesis,7 endoarterectomies,8 and angioplasties,9 is assumed to be a consequence of the proliferative and apoptotic status of cells, which may be particularly important in preventing the development of vascular diseases.6
http://hyper.ahajournals.org/cgi/content/full/30/5/1198
The endothelial cells that line its intimal surface throughout the circulatory tree, a surface area equivalent to a half dozen tennis courts in an average-sized man (1), occupy a continuous and strategic interface between blood and body. Among the myriad of regulatory roles vascular endothelium subserves, it is the pivotal modulator of blood fluidity and hemostasis.
regulatory roles vascular endothelium
Endothelial cells (EC) occupy a strategic location in the vasculature as a barrier between the intravascular compartment and underlying tissues; as such, they are often exposed to stresses, such as decreases in ambient oxygen, diminished metabolic substrate, or changes in temperature, that could affect their ability to divide and proliferate. The present study characterizes cell counts, cell cycle distribution, and bromodeoxyuridine incorporation in pulmonary artery and aortic EC exposed to acute and/or chronic hypoxia and other cellular stresses. During hypoxia, EC division slows but does not arrest; progression through the G[1]-to-S transition point and/or progression from S to G[2]/M is altered with an increased percent of EC in S phase. These changes in EC cell cycle distribution with hypoxia are dependent on the origin of the EC as well as the ambient oxygen concentration; moreover, they are distinct from changes observed with elevated temperature or glucose deprivation and differ from the quiescent pattern induced by serum deprivation or high-density confluence. These findings demonstrate that hypoxia exerts a distinct effect on the cell cycle distribution and proliferation of EC.
vasculature
The increased studies of scientists on the endothelial dysfunction in the absence or presence of any additional substance or whether such effects from these agents can be prevented by supplementation with some new strategies, are reflecting the increased interests for finding some new results.
Accodring to the results of some researchers, any exposure to some risk-related environmental factors can be associated with an increase in coronary artery disease events and mortality. Coronary heart diseaes(CHD) is the most common, serious, chronic, life-threatening illness in many countries.
Of paramount importance for the environmental risk factors for CHD, are those environmental exposures, which may also contribute to the risk of development of many diseases, which related to the atherosclerosis.
Also some scientists, previously, have demonstrated that these risk-related environmental factors like tobacco smoke causes endothelial dysfunction and atherosclerosis in rabbits with diet-induced hypercholesterolemia and atherosclerosis and that chronic dietary L-arginine supplementation prevents this.
Some sicnetists claim that endothelial dysfunction secondary to risk-related environmental factosr such as tobacco smoke may occur in the absence of diet-induced hypercholesterolemia and atherosclerosis.
They suggest that chronic dietary supplementation with a nitric oxide donor such as L-arginine offsets the endothelial dysfunction associated with environmental tobacco smoke in normocholesterolemic rabbits, possibly through substrate loading of the nitric oxide pathway.
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سالانه 4000 مرگ و میر بر اثر آلودگی هوا در تهران رخ می‌دهد که علاوه بر این تعداد مشابهی نیز که به بیماری سرطان ریه مبتلا شده‌اند و در معرض اکسیدهای نیتروژن بوده‌اند گزارش شده اس
دکتر مسعود قاسمی رییس انجمن آترواسکلروز ایران در خصوص اثرات سوء استنشاق آلاینده های موجود در هوای تهران می گوید: تاثیر آلودگی هوا در بروز بیماری قلبی و عروقی نظیر افزایش فشار خون زیانبار است و تحقیقات نشان می دهد آلودگی هوا باعث غلیظ شدن خون و افزایش احتمال بروز التهاب می شود
وی سر درد، ضعف، سرگیجه، تهوع، اختلال در انتقال اکسیژن به بافت های بدن، ضربان شدید قلب، سکته قلبی و کاهش ظرفیت ششی را از آثار آلودگی هوا بر سلامت افراد برشمرد و خاطرنشان ساخت: افرادی که زمینه ناراحتی قلبی دارند، هنگام رفت و آمد در خیابان ها، بیش از افراد عادی در معرض خطر حملات قلبی هستند
وی با بیان اینکه مرگ زودرس ناشی از بیماری های قلبی در نواحی آلوده به اثبات رسیده است، می افزاید: آلودگی هوای ناشی از ترافیک اتومبیل ، دود کارخانه ها یا دود سیگار موجب نازک شدن سرخرگ گردن و در نهایت بیماری قلبی می شود
دکتر مسعود قاسمی رییس انجمن آترواسکلروز ایران
__________________________________________________________________
سرعت ترکیب اکسیدهای نیتروژن با هموگلوبین خون هزار مرتبه سریعتر از سرعت ترکیب مونواکسید کربن با هموگلوبین است که موجب تشکیل مواد سرطان زا در خون می‌شود و 200 برابر بیش از جذب اکسیژن است. تمایل جذب هموگلوبین خون با مونوکسید کربن و اثرات سوء آن بر سلامتی بصورت اختلال در بینایی، تار دیدن، خستگی، سردرد و خواب آلودگی بروز می کند و باعث ایجاد تغییر در عملکرد قلب و شش می‌شود
نتایج تحقیقات صورت گرفته در این زمینه حاکی است : آلودگی هوا در کاهش وزن نوزادان نیز بسیار موثر است و بر میزان مرگ و میر کودکان تأثیر می‌گذارد، زیرا حساسیت نوزادان به آلودگی هوا بیشتر است. ابتلای کودکان به سرطان خون اولین پیامد زندگی در خیابان‌های پر ترافیک است. منواکسید کربن ابتلا به بیماری‌های قفسه سینه در کودکان را افزایش داده و همچنین باعث عفونت‌های شدید تنفسی (ARI) در کودکان و اطفال، بیماری‌های مزمن تنفسی نظیر تنگی نفس و برونشیت، سرطان ریه و ابتلا به سرطان معده شده و اختلالات ژنتیکی و ابتلا به بیماری‌های موروثی و اختلال در حافظه را افزایش داده، حملات آسم را تشدید کرده و به DNA آسیب می‌رساند
مطالعات دانشمندان کانادایی نیز نشان می دهد، آلودگی هوا نـاشـی از خودروها جهش و آسیب ژنتـیکـی در حیوانات و انسان را سبب می شود و همچنین حاصلخیزی خاک را کاهش داده و آنرا از املاح تهی می‌کند
ابتلای کودکان به سرطان خون اولین پیامد زندگی در خیابان‌های پر ترافیک است
ایسکانیوز – محققان بر این باورند که عبور جریان خفیف الکتریکی از مغز افرادی که در خواب هستند می‌تواند سبب افزایش حافظه آنان شود
به گزارش سرویس علمی پژوهشی ایسکانیوز به نقل از ام.اس. ان طبق این گفته این جریان الکتریکی باید در فرکانس مشخصی باشد
این دانشمندان آزمایشات را بر روی عده ای دانش‌آموز امتحان کرده‌اند که نتایج آن پیشرفت حافظه‌ای آنان و سرعت به خاطر آوردن لغات بوده است. همچنین گفته می‌شود که می توان یک چنین درمانی را برای بیماران آلزایمری و یا کسانی که دچار اختلالات خواب هستند نیز انجام داد
یکی ازمحققان بر این باور است که نتایج حاصله می تواند ارتباط بین خواب و یادگیری را نشان دهد.
Titre du document / Document title
"Health effects and time course of particulate matter on the cardiopulmonary system in rats with lung inflammation."
Auteur(s) / Author(s)
ULRICH Magda M. W. (1) ; ALINK Gerrit M. (1) ; KUMARATHASAN Premkumari (2) ; VINCENT Renaud (2) ; BOERE A. John F. (3) ; CASSEE Flemming R. (3)
Recent epidemiological studies associate health effects and particulate matter in ambient air Exacerbation of the particle-induced inflammation can be a mechanism responsible for increased hospitalization and death due to cardiopulmonary events in high-risk groups of the population. Systems regulating blood pressure that depend on lung integrity can be involved in progression of cardiovascular diseases. This study focused on the expression levels of various genes involved in cardiovascular and pulmonary diseases to assess their role in the onset of cardiovascular problems due to ambient particulate matter and compared these with the corresponding products. Rats with ozone-induced (1600 μg/ m[3]; 8 h) pulmonary inflammation were exposed to 0.5 mg, 1.5 mg, or 5 mg of particulate matter (PM) from Ottawa Canada (EHC-93) by intratracheal instillation. mRNA levels of various genes and their products were measured 2, 4, and 7 d after instillation. At 2 d after exposures to PM, tumor necrosis factor (TNF)-α levels in bronchoalveolar lavage fluid (BALF) were elevated approximately 4 times for the highest EHC-93 dose. MIP-2 protein levels in BALE were elevated approximately three times during the entire time period studied, whereas IL-6 levels were not affected compared to control groups. The MIP-2 mRNA levels revealed a similar pattern of induction. A twofold increase in endo-thelin (ET)-1 levels at d 2 and a 20% decrease in angiotensin-converting enzyme (ACE) activity at d 7 were measured in plasma. A 60% decrease of ACE and ET-1 mRNA levels suggested a possible endothelial damage in the lung blood vessels. Inducible nitric oxide synthase (iNOS) mRNA was found to be increased 3.5 times 2 d after instillation of the particles. Therefore, the endothelial damage could have been caused by large amounts of the free radical NO. Also, plasma levels of fibrinogen were elevated (20%), which could presumably increase blood viscosity, leading to decreased tissue blood flow. These changes in hematological and hemodynamic parameters observed in our study are in line with heart failure in high-risk groups of the population after high air pollution episodes
برنامه پیشگیری از دیابت
افرادی که خطر ابتلا به دیابت را دارند ، باید پیش از موقع مورد مشاوره قرار گرفته و عوامل مهم شیوه زندگانی که سبب تأخیر یا حتی مانع پیشرفت این بیماری می شوند را مورد توجه قرار دهند
برنامه پیشگیری از دیابت
The devastating consequences of the environmental destruction on the occurance of the cardiovascular diseases may be a little controversial, but gradually , it appears to some scientists that these deterioration of the health of environment and increasing of risk factors will have the severe impacts for develping of the blood vessel diseases; they see this issue as a " black box" within these impacts, which need to be studied and analayzed more carefully.
Depspite of capabilty of humans for rationalization and focusing on these impacts and to know whether these environmental factors are targeting and harming our strategic parts of body such as the endothelial cells, unfortunately they are failing in right decsions and in right focusing.
As a strategic barrier between the intravascular compartment and underlying tissues, endothelial cells are exposed to low ambient oxygen tension, i.e. hypoxia, during their development.As a strategic barrier between the intravascular compartment and underlying tissues, endothelial cells are exposed to low ambient oxygen tension, i.e. hypoxia, during their development.
Endothelial cells lie in a strategic anatomical position between the circulating blood and vascular smooth muscle. They are thus most exposed to physical forces such as shear stress,1 hydrostatic pressure,2 and pulsatile stretch, particularly in the arterial circulation. Changes in local flow acutely increase nitric oxide (NO) release in vitro1 and cause flow-dependent vasodilation in vivo.3 On the other hand, increases in hydrostatic pressure cause vasoconstriction,1 reduce NO production,4 and increase endothelin release.5 This may explain the greater endothelium-dependent relaxation in arteries than veins.6
circulation
The response of blood vessels to low oxygen levels may be the Achilles’ heel of a developing tumor, according to a study led by University of California, San Diego biologists.
The study, published in the November 15 issue of the journal Cancer Cell, is the first to examine how blood vessels respond to the low oxygen conditions that result from the presence of a growing tumor. Previous work by the UCSD group and others has shown that tumors, which need a blood supply to provide oxygen and nutrients, release chemical signals that summon the blood vessels to grow toward them.
chemical signals
Vascular endothelium, a monolayer of cells lining the intima of the blood vessels, is involved in a variety of functions, including coagulation, vascular permeability, vascular tonus, and remodeling.1 Endothelial cells, which are in direct contact with plasma and cellular components of blood, are the target of many cytokines and growth factors,2 3 and they alter the metabolic status of their own cells.4 Abnormalities of endothelial function may contribute to certain diseases of blood vessel walls, such as thrombosis, atherosclerosis, and vasculitis.5 6 Endothelial cell survival under pathological conditions, such as hypertension, atherosclerosis, vascular prosthesis,7 endoarterectomies,8 and angioplasties,9 is assumed to be a consequence of the proliferative and apoptotic status of cells, which may be particularly important in preventing the development of vascular diseases.6
http://hyper.ahajournals.org/cgi/content/full/30/5/1198
The endothelial cells that line its intimal surface throughout the circulatory tree, a surface area equivalent to a half dozen tennis courts in an average-sized man (1), occupy a continuous and strategic interface between blood and body. Among the myriad of regulatory roles vascular endothelium subserves, it is the pivotal modulator of blood fluidity and hemostasis.
regulatory roles vascular endothelium
Endothelial cells (EC) occupy a strategic location in the vasculature as a barrier between the intravascular compartment and underlying tissues; as such, they are often exposed to stresses, such as decreases in ambient oxygen, diminished metabolic substrate, or changes in temperature, that could affect their ability to divide and proliferate. The present study characterizes cell counts, cell cycle distribution, and bromodeoxyuridine incorporation in pulmonary artery and aortic EC exposed to acute and/or chronic hypoxia and other cellular stresses. During hypoxia, EC division slows but does not arrest; progression through the G[1]-to-S transition point and/or progression from S to G[2]/M is altered with an increased percent of EC in S phase. These changes in EC cell cycle distribution with hypoxia are dependent on the origin of the EC as well as the ambient oxygen concentration; moreover, they are distinct from changes observed with elevated temperature or glucose deprivation and differ from the quiescent pattern induced by serum deprivation or high-density confluence. These findings demonstrate that hypoxia exerts a distinct effect on the cell cycle distribution and proliferation of EC.
vasculature
The increased studies of scientists on the endothelial dysfunction in the absence or presence of any additional substance or whether such effects from these agents can be prevented by supplementation with some new strategies, are reflecting the increased interests for finding some new results.
Accodring to the results of some researchers, any exposure to some risk-related environmental factors can be associated with an increase in coronary artery disease events and mortality. Coronary heart diseaes(CHD) is the most common, serious, chronic, life-threatening illness in many countries.
Of paramount importance for the environmental risk factors for CHD, are those environmental exposures, which may also contribute to the risk of development of many diseases, which related to the atherosclerosis.
Also some scientists, previously, have demonstrated that these risk-related environmental factors like tobacco smoke causes endothelial dysfunction and atherosclerosis in rabbits with diet-induced hypercholesterolemia and atherosclerosis and that chronic dietary L-arginine supplementation prevents this.
Some sicnetists claim that endothelial dysfunction secondary to risk-related environmental factosr such as tobacco smoke may occur in the absence of diet-induced hypercholesterolemia and atherosclerosis.
They suggest that chronic dietary supplementation with a nitric oxide donor such as L-arginine offsets the endothelial dysfunction associated with environmental tobacco smoke in normocholesterolemic rabbits, possibly through substrate loading of the nitric oxide pathway.
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