Bald scalp in men with androgenetic alopecia retains hair fo

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Ambient nitric oxide levels control the rate of mitochondrial biogenesis - the producing of new mitochondria and replacement and removal of the older mitochondria in cells. Mitochondria in cells have a normal lifespan of a few months, and they get regularly replaced because they wear out pretty quickly.

When mitochondria wear out, they become leaky (leaking out protons, which then lead to more reactive oxygen species being produced in the cell) and much less efficient. So there needs to be a constant process of creating new mitochondrial, and replacement and removal of the older ones in the cell (otherwise cellular production is impaired, and the amount of damaging reactive oxygen species being created in the cell goes up).

This is why people suffer from male pattern baldness.. This is why finasteride works and people got brain fog and other side effects on it like a weak dick.



J Cell Sci. 2006 Jul 15;119(Pt 14):2855-62.
Nitric oxide and mitochondrial biogenesis.
Nisoli E, Carruba MO.
Source

Department of Pharmacology, Chemotherapy and Medical Toxicology, School of Medicine, Milan University, via Vanvitelli 32, 20129 Milan, Italy. [email protected]
Abstract

The characteristic structural organization of mitochondria is the product of synthesis of macromolecules within the mitochondria together with the import of proteins and lipids synthesized outside the organelle. Synthetic and import processes are required for mitochondrial proliferation and might also facilitate the growth of pre-existing mitochondria. Recent evidence indicates that these events are regulated in a complex way by several agonists and environmental conditions, through activation of specific signaling pathways and transcription factors. A newly discovered role of this organelle in retrograde intracellular signaling back to the nucleus has also emerged. This is likely to have far-reaching implications in development, aging, disease and environmental adaptation. Generation of nitric oxide (NO) appears to be an important player in these processes, possibly acting as a unifying molecular switch to trigger the whole mitochondrial biogenesis process. High levels of NO acutely inhibit cell respiration by binding to cytochrome c oxidase. Conversely, chronic, smaller increases in NO levels stimulate mitochondrial biogenesis in diverse cell types. NO-induced mitochondrial biogenesis seems to be linked to proliferation and differentiation of normal and tumor cells, as well as in aging.

PMID:
16825426
[PubMed - indexed for MEDLINE]

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Nitric oxide in the human hair follicle: constitutive and dihydrotestosterone-induced nitric oxide synthase expression and NO production in dermal papilla cells.
Wolf R, Schönfelder G, Paul M, Blume-Peytavi U.
Source

Department of Dermatology, University Medical Center Benjamin Franklin, Free University of Berlin, Berlin, Germany.
Abstract

The free radical nitric oxide, generated by different types of epidermal and dermal cells, has been identified as an important mediator in various physiological and pathophysiological processes of the skin, such as regulation of blood flow, melanogenesis, wound healing, and hyperproliferative skin diseases. However, little is known about the role of NO in the human hair follicle and in hair cycling processes. Here we demonstrate for the first time that dermal papilla cells derived from human hair follicles spontaneously produce NO by measuring nitrate and nitrite levels in culture supernatants. This biomolecule is apparently formed by the endothelial isoform of nitric oxide synthase, which was detected at the mRNA and protein levels. Remarkably, basal NO level was enhanced threefold by stimulating dermal papilla cells with 5alpha-dihydrotestosterone (DHT) but not with testosterone. Addition of N-[3-(aminomethyl)benzyl]acetamidine (1400W), a highly selective inhibitor of inducible nitric oxide synthase, restrained the elevation in NO level induced by DHT. Analyses of DHT-stimulated cells at the mRNA and protein levels confirmed the expression of inducible nitric oxide synthase. These findings suggest NO as a signaling molecule in human dermal papilla cells and implicate basal and androgen-mediated NO production to be involved in the regulation of hair follicle activity.

 

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Nitric oxide (NO) is produced by many cells in the body; however, its production by vascular endothelium is particularly important in the regulation of blood flow. Because of its importance in vascular function, abnormal production of NO, as occurs in different disease states, can adversely affect blood flow and other vascular functions.

http://www.cvphysiology.com/Blood%20Flow/BF011.htm

Nitric oxide inhibits inflammation in blood vessels by blocking the inflammation that occurs in damaged endothelial cells. If these cells become damaged or dysfunctional, nitric oxide production becomes impaired, which leads to more inflammation and tissue damage.

 

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The expression of inducible nitric oxide synthase (iNOS) in the testis and epididymis of rats with a dihydrotestosterone (DHT) deficiency.
Kolasa A, Marchlewicz M, Kurzawa R, G?abowski W, Trybek G, Wenda-Rózewicka L, Wiszniewska B.
Source

Department of Histology and Embryology, Pomeranian Medical University, Powstanców Wlkp. 72, 70-111, Szczecin, Poland. [email protected]
Abstract

In our previous studies, we showed that a finasteride-induced DHT deficiency may cause changes in the morphology of the seminiferous epithelium without any morphological alteration of the epididymis. In this study, we demonstrated the constitutive immunoexpression of inducible nitric oxide synthase (iNOS) in the testis and epididymis of Wistar rats treated with finasteride for 28 days (the duration of two cycles of the seminiferous epithelium) and 56 days (the duration of one spermatogenesis). We noted that a 56-day finasteride treatment mainly caused a decrease in the level of circulating DHT, as well as a statistically insignificant decrease in the level of T. The hormone deficiency also led to a change in the iNOS immnoexpression in the testis and epididymis of the finasteride-treated rats. In vitro, DHT did not modify NO production by the epithelial cells of the caput epididymis even when stimulated with LPS and IFNgamma, but it did give rise to an increase in NO production by the epithelial cells of the cauda epididymis without the stimulation. DHT did not have a statistically significant influence on estradiol production by cultured, LPS- and IFNgamma-stimulated epithelial cells from the caput and cauda epididymis. In conclusion, our data clearly indicates that a finasterideinduced DHT deficiency intensifies the constitutive expression of iNOS in most rat testicular and epididymal cells, so it can be expected that the expression of inducible nitric oxide synthase (iNOS) could be regulated by DHT. On the other hand, the profile of the circulating DHT and T levels strongly suggests that the regulation of constitutive iNOS expression is complex and needs more detailed study.

 

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The eNOS cofactor tetrahydrobiopterin improves endothelial dysfunction in livers of rats with CCl4 cirrhosis.
Matei V, Rodríguez-Vilarrupla A, Deulofeu R, Colomer D, Fernández M, Bosch J, Garcia-Pagán JC.
Source

Hepatic Hemodynamic Laboratory, Liver Unit, Institut de Malalties Digestives i Metabòliques, Hospital Clínic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain.
Abstract

In cirrhosis, intrahepatic endothelial dysfunction is one of the mechanisms involved in the increased resistance to portal blood flow and therefore in the development of portal hypertension. Endothelial nitric oxide synthase (eNOS) uncoupling due to deficiency of tetrahydrobiopterin (BH4) results in decreased production of NO and plays a major role in endothelial dysfunction in other conditions. We examined whether eNOS uncoupling is involved in the pathogenesis of endothelial dysfunction of livers with cirrhosis. Basal levels of tetrahydrobiopterin and guanosine triphosphate (GTP)-cyclohydrolase (BH4 rate-limiting enzyme) expression and activity were determined in liver homogenates of control and rats with CCl4 cirrhosis. Thereafter, rats were treated with tetrahydrobiopterin, and eNOS activity, NO bioavailability, assessed with a functional assay, and the vasodilator response to acetylcholine (endothelial function) were evaluated. Livers with cirrhosis showed reduced BH4 levels and decreased GTP-cyclohydrolase activity and expression, which were associated with impaired vasorelaxation to acetylcholine. Tetrahydrobiopterin supplementation increased BH4 hepatic levels and eNOS activity and significantly improved the vasodilator response to acetylcholine in rats with cirrhosis. In conclusion, the impaired response to acetylcholine of livers with cirrhosis is modulated by a reduced availability of the eNOS cofactor, tetrahydrobiopterin. Tetrahydrobiopterin supplementation improved the endothelial dysfunction of cirrhotic livers.

 

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Skip Navigation LinksHome > January 2006 - Volume 24 - Issue 1 > Quercetin downregulates NADPH oxidase, increases eNOS activi...
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Journal of Hypertension:
January 2006 - Volume 24 - Issue 1 - p 75-84
Original papers: Endothelium
Quercetin downregulates NADPH oxidase, increases eNOS activity and prevents endothelial dysfunction in spontaneously hypertensive rats
Sánchez, Manuela; Galisteo, Milagrosa; Vera, Rocíoa; Villar, Inmaculada Ca; Zarzuelo, Antonioa; Tamargo, Juanb; Pérez-Vizcaíno, Franciscob; Duarte, Juana
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Abstract

Background and objective: Several studies have found that chronic treatment with the dietary flavonoid quercetin lowers blood pressure and restores endothelial dysfunction in hypertensive animal models. We hypothesized that increased endothelial nitric oxide synthase (eNOS) and/or decreased nicotinamide adenine dinucleotide phosphate (NADPH) oxidase protein expression and activity, and reduced reactive oxygen species might be involved in the improvement of endothelial function induced by quercetin in sponataneously hypertensive rats (SHR).

Design and methods: Male SHR and Wistar-Kyoto (WKY) rats (5 weeks old) were treated with quercetin (10 mg/kg) or vehicle for 13 weeks. Changes in vascular expression of eNOS, caveolin-1 and p47phox were analysed by Western blot, eNOS activity by conversion of [3H]arginine to L-[3H]citrulline, and NADPH oxidase activity by NADPH-enhanced chemoluminescence of lucigenin.

Results: In SHR, quercetin reduced the increase in blood pressure and heart rate and enhanced the endothelium-dependent aortic vasodilation induced by acetylcholine, but had no effect on the endothelium-independent response induced by nitroprusside. However, quercetin had no effect on endothelium-dependent vasoconstriction and aortic thromboxane B2 production. Compared to WKY, SHR showed upregulated eNOS and p47phox protein expression, downregulated caveolin-1 expression, increased NADPH-induced superoxide production but, paradoxically, eNOS activity was reduced. Chronic quercetin treatment prevented all these changes in SHR. In WKY, quercetin had no effect on blood pressure, endothelial function or the expression or activity of the proteins analysed.

Conclusions: Enhanced eNOS activity and decreased NADPH oxidase-mediated superoxide anion (O2-) generation associated with reduced p47phox expression appear to be essential mechanisms for the improvement of endothelial function and the antihypertensive effects of chronic quercetin.

 

[John979]

Dr. George Cotsarelis and Follica's approach is to regenerate follicles via skin trauma:

http://www.follicabio.com/content/scien ... echnology/

 

[diffuse propecia]

Endocrinology. 2003 Dec 18

Dihydrotestosterone Promotes VCAM-1 Expression in Male Human Endothelial
Cells via a NF-{kappa}B Dependent Pathway.

Death AK, McGrath KC, Sader MA, Nakhla S, Jessup W, Handelsman DJ,
Celermajer DS.

There exists a striking gender difference in atherosclerotic vascular
disease. For decades, estrogen was considered atheroprotective, however
an alternative is that androgen exposure in early life may predispose
men to earlier atherosclerosis. We recently demonstrated that the potent
androgen, dihydrotestosterone (DHT), enhanced the binding of monocytes
to the endothelium, a key early event in atherosclerosis, via increased
expression of vascular cell adhesion molecule-1 (VCAM-1). We now show
that DHT mediates its effects on VCAM-1 expression at the promoter
level, through a novel androgen receptor (AR)/nuclear factor-kappaB
(NF-kappaB) mechanism. Human umbilical vein endothelial cells (HUVECs)
were exposed to 4-400 nM DHT. DHT increased VCAM-1 mRNA in a dose- and
time-dependent manner. The DHT effect could be blocked by the androgen
receptor (AR) antagonist, hydroxyflutamide. DHT increased VCAM-1
promoter activity via NF-kappaB activation without affecting VCAM-1 mRNA
stability. Using 5' deletion analysis, it was determined that the
NF-kappaB sites within the VCAM-1 promoter region were responsible for
the DHT-mediated increase in VCAM-1 expression, however
coimmunoprecipitation studies suggested there is no direct interaction
between AR and NF-kappaB. Instead, DHT treatment decreased the level of
the NF-kappaB inhibitory protein, IkappaB. DHT did not affect VCAM-1
protein expression and monocyte adhesion when female endothelial cells
were tested. AR expression was higher in male- relative to female-
endothelial cells, associated with increased VCAM-1 levels. These
findings highlight a novel AR/NF-kappaB mediated mechanism for VCAM-1
expression and monocyte adhesion operating in male endothelial cells
that may represent an important unrecognized mechanism for the male
predisposition to atherosclerosis.


I MAKE SCIENCE

 

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Endocrinology. 2003 Dec 18

Dihydrotestosterone Promotes VCAM-1 Expression in Male Human Endothelial
Cells via a NF-{kappa}B Dependent Pathway.

Death AK, McGrath KC, Sader MA, Nakhla S, Jessup W, Handelsman DJ,
Celermajer DS.

There exists a striking gender difference in atherosclerotic vascular
disease. For decades, estrogen was considered atheroprotective, however
an alternative is that androgen exposure in early life may predispose
men to earlier atherosclerosis. We recently demonstrated that the potent
androgen, dihydrotestosterone (DHT), enhanced the binding of monocytes
to the endothelium, a key early event in atherosclerosis, via increased
expression of vascular cell adhesion molecule-1 (VCAM-1). We now show
that DHT mediates its effects on VCAM-1 expression at the promoter
level, through a novel androgen receptor (AR)/nuclear factor-kappaB
(NF-kappaB) mechanism. Human umbilical vein endothelial cells (HUVECs)
were exposed to 4-400 nM DHT. DHT increased VCAM-1 mRNA in a dose- and
time-dependent manner. The DHT effect could be blocked by the androgen
receptor (AR) antagonist, hydroxyflutamide. DHT increased VCAM-1
promoter activity via NF-kappaB activation without affecting VCAM-1 mRNA
stability. Using 5' deletion analysis, it was determined that the
NF-kappaB sites within the VCAM-1 promoter region were responsible for
the DHT-mediated increase in VCAM-1 expression, however
coimmunoprecipitation studies suggested there is no direct interaction
between AR and NF-kappaB. Instead, DHT treatment decreased the level of
the NF-kappaB inhibitory protein, IkappaB. DHT did not affect VCAM-1
protein expression and monocyte adhesion when female endothelial cells
were tested. AR expression was higher in male- relative to female-
endothelial cells, associated with increased VCAM-1 levels. These
findings highlight a novel AR/NF-kappaB mediated mechanism for VCAM-1
expression and monocyte adhesion operating in male endothelial cells
that may represent an important unrecognized mechanism for the male
predisposition to atherosclerosis.


I MAKE SCIENCE

Bad ***! Welcome to the forum elequent!

 

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C-reactive protein attenuates endothelial progenitor cell survival, differentiation, and function: further evidence of a mechanistic link between C-reactive protein and cardiovascular disease.
Verma S, Kuliszewski MA, Li SH, Szmitko PE, Zucco L, Wang CH, Badiwala MV, Mickle DA, Weisel RD, Fedak PW, Stewart DJ, Kutryk MJ.
Source

Division of Cardiac Surgery, Toronto General Hospital, 14EN-215, 200 Elizabeth St, Toronto, Ontario, Canada M5G 2C4. [email protected]
Abstract
BACKGROUND:

Myocardial ischemia provides a potent stimulus to angiogenesis, and the mobilization and differentiation of endothelial progenitor cells (EPCs) has been shown to be important in this process. An elevated level of C-reactive protein (CRP) has emerged as one of the most powerful predictors of cardiovascular disease. However, the impact of CRP on EPC biology is unknown.
METHODS AND RESULTS:

EPCs were isolated from the peripheral venous blood of healthy male volunteers. Cells were cultured in endothelial cell basal medium-2 in the absence and presence of CRP (5 to 20 microg/mL), rosiglitazone (1 micromol/L), and/or vascular endothelial growth factor. EPC differentiation, survival, and function were assayed. CRP at concentrations > or =15 microg/mL significantly reduced EPC cell number, inhibited the expression of the endothelial cell-specific markers Tie-2, EC-lectin, and VE-cadherin, significantly increased EPC apoptosis, and impaired EPC-induced angiogenesis. EPC-induced angiogenesis was dependent on the presence of nitric oxide, and CRP treatment caused a decrease in endothelial nitric oxide synthase mRNA expression by EPCs. However, all of these detrimental CRP-mediated effects on EPCs were attenuated by pretreatment with rosiglitazone, a peroxisome proliferator-activated receptor-gamma (PPARgamma) agonist.
CONCLUSIONS:

Human recombinant CRP, at concentrations known to predict adverse vascular outcomes, directly inhibits EPC differentiation, survival, and function, key components of angiogenesis and the response to chronic ischemia. This occurs in part via an effect of CRP to reduce EPC eNOS expression. The PPARgamma agonist rosiglitazone inhibits the negative effects of CRP on EPC biology. The ability of CRP to inhibit EPC differentiation and survival may represent an important mechanism that further links inflammation to cardiovascular disease.

 

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http://www.rbclife.com/stem-kine/story.html

 

[ukmale24]

Isn't that stuff similar to ActiStem?

 

[ukmale24]

Btw, I didn't read much of this as all that science stuff is like Chinese to me. But is the jist of it that we should concentrate our efforts on regenerating follicle cells rather than what most of us are doing?

 

[BitchBoy]

Interesting.

 

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What are the benefits of elevated stem cells?
E-mail
Print

Over the last 30 years, with reduced cholesterol and an emphasis on increased physical activity, cardiovascular health has improved. There is still work to be done however, as the World Health Organization predicts almost 400,000 Americans will die of coronary disease in 2010. Fortunately, Research scientists have discovered that the number of circulating adult stem cells in the blood stream is beneficial for good health. Even better are the recent studies that have shown the more adult stem cells circulating in the blood, the better cardiovascular health will be.

Some of these studies were reviewed in order for you to understand the health benefits of naturally increasing the release of adult stem cells into the blood stream.

Clinical interest in bone marrow-derived circulating endothelial progenitor cells as a novel vascular risk factor has increased due to their importance in vascular repair and noted inverse relation with endothelial dysfunction as well as cardiovascular and cerebrovascular disease (1-3).

Vasa, et, al (2001) discovered that people with poor cardiovascular health have less endothelial progenitor stem cells (EPC's) in the blood stream than those with good cardiovascular health (4). EPC's are certain type of stem cell that can create new blood vessels. They are considered to be subgroup of the 'CD34+ stem cells'. The study showed that EPC's taken from people with poor cardiovascular health had less ability to migrate into tissues. The Vasa study also found that people who smoked had fewer EPC's in the blood stream.

Schmidt-Lucke et al (2005) conducted an experiment where 120 individuals (43 control and 77 at risk of cardiovascular health problems) had the number of EPC's in their blood stream measured. The subjects were observed for a period of 10 months and the Schmidt-Lucke study concluded that cardiovascular health problems were linked to a reduced number of EPC's in the blood stream (5).

Lorenzen et al (2010) followed 265 patients with chronic kidney disease stage V receiving hemodialysis therapy. During a median follow-up period of 36 months 109 (41%) patients experienced a cardiovascular event and 70 patients died. They found a significant association between the number of functionally active EPCs and cardiovascular events in patients with chronic kidney disease. Thus, defective vascular repair and regeneration may be responsible, at least in part, for the enormous cardiovascular morbidity in this population. High level of EPCs was associated with lower level of cardiovascular events and longer survival (6).
Cardiovascular disease is the most frequent cause of death in both men and women. However, between the ages of 45 and 65 years, the prevalence of coronary heart disease and the incidence of myocardial infarction and stroke is ?50% higher in men compared with women. The mechanisms responsible for this sex-related disparity was unclear, until Greta L. et al (2007) demonstrated that EPC colony forming capacity was ?150% higher in women than in men. Furthermore, migratory activity was ?40% greater in middle-aged women compared with men. This study is noteworthy since there are no apparent sex differences in the incidence and prevalence of traditional cardiovascular disease risk factors such as hypertension, obesity, tobacco use, hyperlipidemia, diabetes, or sedentary lifestyle in middle-aged adults (7).

Tomás Sobrino et al (2007) have demonstrated that circulating EPC increase in response to cerebral ischemia in patients after acute ischemic stroke, and that the magnitude of this increase is directly related to a better functional outcome. These findings are in line with experimental and human studies which indicate that EPC might mediate endothelial cell regeneration and neovascularization. A higher increase in circulating EPC during the first week is independently associated with a better clinical outcome in acute ischemic stroke patients. However, whether circulating EPC are able to incorporate into brain ischemic areas and to promote regenerative vasculogenesis in humans remains to be clarified. Finally, the role of EPC as a new therapeutic tool able to promote chronic neurorepair of brain tissue damaged by ischemia needs to be further explored, wrote the researchers in 2007. (8)

Because of these recent studies, scientists understand the link between a greater number of circulating adult stem cells and better cardiovascular health. Essentially, poor circulation is a lack of oxygen. When oxygen is lacking, the tissue releases compounds for two tasks. One, to attract EPC's to the tissue and two, to convert EPC's into new capillary cells. We can conclude then, that a tissue lacking oxygen triggers a process where circulating adult stem cells travel to the tissue and become new capillary cells. New capillaries allow for more efficient delivery of oxygen and nutrients and thus better health.

In summary, we are well aware that the efficient delivery of oxygen and nutrients to the organs and tissues is vital to optimal health. Thanks to scientists, we are now also aware that the best way to maintain our bodies intricate network of delivery -- the capillaries -- and ultimately our good health, is by increasing the number of circulating adult stem cells in the blood steam.

 

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Diabetes mellitus type-2 (DM-2) contributes to atherogenesis by inducing endothelial cell injury and dysfunction. Endothelial progenitor cells (EPCs) are essential to blood vessel formation, can differentiate into mature endothelial cells, and promote the repair of damaged endothelium. In DM-2, the circulating EPC count is low and their functionality is impaired. The mechanisms that underlie this reduced count and impaired functionality are poorly understood. Nitric oxide (NO) is a short-lived signalling molecule that is produced by vascular endothelial cells and participates in the maintenance of vascular tone. NO is also known to participate in other physiological processes, such as cell survival, proliferation, and migration. The bioavailability of NO is reduced in EPCs from DM-2 patients. Interestingly, an inverse relationship exists between the reduction in NO bioavailability in EPCs and the patient's plasma glucose and glycated haemoglobin levels. In addition, NO bioavailability in EPCs correlates with plasma oxidized low-density lipoprotein levels in DM-2. Although this reduction in NO bioavailability could be attributed to oxidative stress in DM-2 patients, it also may be due to impairment of one or more members of the protein signalling cascades that are responsible for NO production. The stimulation of NO production or its signalling cascades in EPCs may increase their numbers and improve their function, thus attenuating endothelium damage, independent of the vasodilatory effects of NO. This review summarizes the metabolic alterations that underlie the molecular mechanisms that may be responsible for EPC decrease and dysfunction in DM-2 with emphasis on the involvement of the NO system.

 

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How Hypothyroidism Induces Atherosclerosis

Hypothyroidism contributes to atherosclerosis by increasing low-density (LDL) lipoprotein cholesterol levels, causing diastolic hypertension (blood pressure elevation of bottom measurement), and negatively affecting vascular smooth muscle function. The effects of hypothyroidism on atherosclerosis are most pronounced in females, particularly women older than 50 years.

Studies of patients treated for hypothyroidism indicate that patients whose hypothyroidism is under-treated (TSH level greater than 4.0) have a higher prevalence of coronary artery disease than age-matched subjects. In one study of patients undergoing coronary angiography imaging studies, patients on inadequate therapy for hypothyroidism were more likely to have angiographic progression of coronary artery disease than those with adequate replacement.

Studies show that hypothyroidism causes oxidative changes in circulating lipoproteins (blood lipids) that make these substances more likely to adhere to artery wall. Hypothyroidism also causes a decrease in high-density-lipoprotein (HDL) cholesterol that prevents its protective effects. Other risk factors for atherosclerosis associated with hypothyroidism include increased inflammation as demonstrated by an increased level of C-reactive protein (CRP), coagulation abnormalities, insulin resistance, and endothelial dysfunction.

Read more at Suite101: Hypothyroidism and Atherosclerosis: Increased Risk of Atherosclerosis in Autoimmune Hypothyroidism | Suite101.com http://www.suite101.com/content/hypothy ... z1UGYFJSDn

 

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he Thyroid Gland

It is the thyroid gland, lying in front of the throat below the Adam's apple and just above the breastbone, which regulates the rate at which the body utilizes oxygen and controls the rate at which various organs function and the speed with which the body utilizes food. Thyroid secretion is essential for the operation of the cells and, in effect, determines how hot the fire gets in the cell and the speed of activity in the cell. The influence of thyroid secretion on body processes and other organs is incredibly widespread and important. When the thyroid gland is removed from an otherwise normal animal, all metabolic activity is reduced. After removal of the thyroid gland, excess amounts of water, salts, and protein are retained within the body. Blood cholesterol also goes up.

The thyroid, the body's thermostat, secretes two hormones that regulate body temperature, energy usage, and calorie burning. The thyroid has many effects on all the cells in the body, including the synthesis of RNA protein and consumption of oxygen by cells, affecting overall bodily metabolism. Thyroid function influences and is influenced by the pituitary, adrenals, parathyroid, and sex glands, all of which work together. The pituitary produces TSH (thyroid-stimulating hormone), which helps regulate thyroid hormone production. Thyroid malfunctioning is also influenced by abnormal immune responses and the adrenals. People with type-O blood are said to be genetically prone to hypothyroidism and low levels of iodine. Approximately 46% of people are blood Type-O.

The thyroid plays an important role in growth processes. In the human, growth and maturation fail to take place normally when the thyroid is absent or functioning far below normal. Children lacking normal thyroid function may remain small; their stature can be improved considerably by thyroid supplementation and detoxification started at an early age. Growth of the skin, hair, and nails may be retarded in thyroid deficiency and accelerated again by thyroid treatment. Healing of bone is delayed in thyroid deficiency. A rather severe anemia may develop in severe hypothyroidism. Thyroid hormone is essential for normal nervous system functioning and reaction time, and hypothyroidism may produce slow reactions and mental sluggishness. Muscle health too is dependent on thyroid secretion and with marked thyroid deficiency the muscles may become sluggish and infiltrated with fat. There are interrelationships between the thyroid and the other endocrine glands. When, for example, thyroid deficiency is marked, the effect on the sex glands is shown by subnormal sexual development and function and impairment of libido. In hypothyroid women, menstrual disturbances are present frequently.

 

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Oxygen affects human endothelial cell proliferation by inactivation of fibroblast growth factors


Abstract

The fibroblast growth factors (FGF), including endothelial cell growth factor (ECGF)/acidic FGF and basic FGF, are important modulators of endothelial cell replication in vitro and in vivo. Premature infants and adults with lung injuries are often treated with high levels of inspired O2, which can be necessary for survival but potentially injurious to developing lungs and in tissue repair following injury. Human umbilical artery and vein endothelial cells were grown in ECGF- or FGF-supplemented Medium 199 and exposed to ambient levels of O2 from 10 to 95%. Endothelial cell growth, measured by [3H]thymidine incorporation, was inhibited by increasing levels of O2 and ceased above 50% O2. Vein endothelial cells could recover from up to 24 h of hyperoxic exposure when given fresh medium, but not after 48 h. Artery-derived cells were more sensitive to O2 than were vein-derived cells. Complete medium without endothelial cells, preincubated 24 h in 95% O2, lost its ability to support cell growth under normoxic conditions. Exposing individual medium components to high O2 demonstrated that purified natural ECGF and recombinant acidic or basic FGF were all inactivated by O2. Human recombinant superoxide dismutase prevented FGF inactivation. O2 inactivation of essential growth factors could thus have major consequences for lung development or repair of injured capillaries in infants or adults inspiring high levels of O2

 

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The endothelium is a thin layer of epithelial cells lining the inside of the blood vessels. It lines the entire circulatory system, including the heart and all the veins, arteries, and capillaries. The endothelium lining the heart is also called the endocardium, though it is similar to the tissue the lining blood vessels. The endothelium forms a barrier between the blood and the other structures of the circulatory system, allowing the blood to flow more smoothly, and therefore to circulate more quickly throughout the body.

The endothelium is simple squamous epithelium, meaning that it consists of a single layer of flat, or squamous, epithelial cells, making it the thinnest possible type of membrane. This single layer of cells may also be referred to as a monolayer. An epithelium in general is any type of tissue that serves to line the surface or cavity of any structure in the body. Epithelium is one of the four primary tissue types in the human body, the others being connective tissue, nervous tissue, and muscle tissue.

The endothelium is involved in a number of important functions. It helps control blood pressure through vasodilation and vasoconstriction, the widening and constricting of the blood vessels respectively. It also aids in blood clotting, minimizing damage and blood loss in the case of wounds.

Other endothelial functions include angiogenesis, or the growth of new blood vessels, and serving as a barrier by selectively allowing certain materials to exit or enter the bloodstream. In addition to the above functions, the endocardium also controls the development of the heart muscle in the embryo and into adulthood. It is also responsible for regulating the function of the myocardium, or the heart muscle.

The endothelium can also be involved in a variety of disorders. Both inflammation, an immune response characterized by redness and swelling, and atherosclerosis, in which the blood vessels become clogged with a fatty buildup that impedes blood flow, involve the endothelium. Endothelial dysfunction, in which the endothelium ceases to work properly, is an early sign of atherosclerosis, in addition to other circulatory system disorders. Loss of healthy endothelial function is also associated with smoking, coronary artery disease, diabetes mellitus, hypercholesterolemia, and hypertension or high blood pressure. Endothelial disfunction is typically an indicator of future cardiovascular problems.

 

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http://www.fightaging.org/archives/2006 ... e-an-1.php


The problem is rooted in the body's response to vascular injury. The bone marrow churns out cells crucial to repairing the damaged lining of blood vessels. But sometimes they fail to report for duty.

"Part of the defect we think is occurring in diabetic patients is these cells do not carry out appropriate repair, and therefore these patients are at higher risk for cardiovascular disease and other complications," Segal said.

...

UF researchers isolated these repair cells from blood samples drawn from patients with diabetes and chronic kidney disease and studied them in the laboratory. The cells were unable to move about normally. But when nitric oxide gas was added, Segal said, the cells lost their rigidity, becoming suppler, and their ability to move dramatically improved.

In the body, nitric oxide occurs naturally. It helps the repair cells move out of the bone marrow where they are made, and it opens blood vessels and improves the uptake of oxygen. Patients with diabetes, however, commonly have low levels of nitric oxide.

"We went on to show that actually what's happening is nitric oxide is affecting the skeleton, or scaffold of the cell, and by adding nitric oxide we're able to rearrange the scaffold," Segal said. "When we rearrange the scaffold, the cells are able to migrate. The benefit of this is that when cells have improved movement they are able to repair the endothelium (the lining of the blood vessels) better and perhaps prevent atherosclerosis."