Acute Inflammation (Induced by the derma roller)
Acute inflammation is a normal process that protects and heals the body following physical injury or infection.
Acute inflammation involves local dilation of blood vessels as well as increased vessel permeability to improve blood flow to the injured area. At the site of an infection or injury, mast cells, platelets, nerve endings, endothelial cells, and other resident cells release signaling molecules and chemoattractants that recruit leukocytes to the affected area. Neutrophils, a type of granulocyte, are the first leukocytes to appear at the injured site. These cells phagocytose (engulf) and kill invading microorganisms through the release of non-specific toxins, such as superoxide radicals, hypochlorite, and hydroxyl radicals; these reactive oxygen species (ROS) kill pathogens as well as adjacent cells, sick and healthy alike. Neutrophils also release cytokines, including interleukin (IL)-1, IL-6, tumor necrosis factor (TNF)-alpha, gamma interferon (INF-gamma), and others. Such pro-inflammatory cytokines in turn induce the liver to synthesize various acute phase reactant proteins and also induce systemic inflammatory responses (
e.g., fever and leukocytosis—a rise in the number of white blood cells). Neutrophils are short-lived and are thus primarily involved in the early stages of inflammation.
Chronic Inflammation (Male Pattern Baldness)
If the stimulus persists, inflammation can last days, months, and even years. Chronic inflammation is primarily mediated by monocytes and long-lived macrophages; monocytes mature into macrophages once they leave the bloodstream and enter tissues. Macrophages engulf and digest microorganisms, foreign invaders, and senescent cells.
Macrophages release several different chemical mediators, including IL-1, TNF-alpha, and prostaglandins, that perpetuate the pro-inflammatory response. At later stages, other cells, including lymphocytes, invade the affected tissues: T lymphocytes kill virus-infected cells and B lymphocytes produce antibodies that specifically target the invading microorganisms for destruction.
Macrophages and other leukocytes release ROS and proteases that destroy the source of inflammation; however, damage to the body's own tissues often results. In fact, tissue damage is a hallmark of chronic inflammation.
Another characteristic of chronic inflammation is repair of the damaged tissue by replacement with cells of the same type or with fibrous connective tissue. An important part of the inflammatory process involves local angiogenesis—the development of new blood vessels. In some instances, the body is unable to repair tissue damage, and the inflammatory cascade continues. Chronic inflammation is abnormal and does not benefit the body; in fact, chronic inflammation is involved in a number of disease states.
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Reduced blood flow and fibrosis are linked together...
Impaired Blood Vessel Function Found in Cystic Fibrosis Patients
Nov. 26, 2012 — The first evidence of blood vessel dysfunction has been found in a small cohort of generally healthy young people with cystic fibrosis, "Even though the lung function in these kids is fine at this point, there is evidence of vascular dysfunction and exercise intolerance," said Dr. Ryan A. Harris, clinical exercise physiologist at the Medical College of Georgia and Institute of Public and Preventive Health at Georgia Health Sciences University. "We think this blood vessel dysfunction could be contributing to their exercise intolerance, which is an independent predictor of mortality in these kids irrespective of their lung function."
The findings raise questions about whether dysfunctional arteries affect patients' ability to exercise, which is already recommended to help combat the disease's hallmark lung complications, and whether exercise can also improve blood vessel function and potentially help forestall cardiovascular disease.
Although their blood pressures tend to be normal and there is no established risk, cystic fibrosis patients have only recently lived long enough to acquire even an accelerated version of cardiovascular disease, said Dr. Katie T. McKie, Director of the Pediatric Cystic Fibrosis Center at the GHS Children's Medical Center. The median predicted age of survival is the mid-30s and nearly half the patients in the United States are over age 18, according to the Cystic Fibrosis Foundation. Fifteen years ago, survival rates for the genetic disease were about half that, McKie said.
The blood vessel or endothelial dysfunction Harris and McKie found in these patients is essentially the reduced ability of blood vessels to respond to important cues, such as dilating when exercise or stress increase the body's demand for blood and oxygen. The dysfunction may be linked to chronic inflammation and oxidative stress which, in turn, impair the body's ability to use nitric oxide, a major blood vessel dilator, said Harris, corresponding author of the study in
CHEST Journal.
Despite major advances in treatment and survival, cystic fibrosis patients tend to live with a chronic, low-grade inflammation resulting from a chronic state of infection. The genetic mutation that disrupts the body's balance of salt and fluid thickens lung mucus, which traps inhaled bacteria and viruses that are normally cleared.
"They are in a low-grade stage of inflammation all the time," Harris said. Patient participants in the study, for example, had a higher rate of inflammation than healthy controls and the higher their concentrations of inflammatory drivers such as C-reactive protein, the lower their pulmonary function.
When the 15 patients, age 8-18, peddled a stationary bike as long and hard as they could, it was leg fatigue rather than lung limitations, which stopped them. "It's not their lungs that are limiting their exercise capacity," Harris said. "But what about non-pulmonary factors that we had no idea existed in these kids?"
"At this stage, their lungs are as healthy as those of their healthy counterparts," McKie added.
They found that even though the patients could take in oxygen well they were not as good as their 15 healthy counterparts at using it. At rest, oxygen saturation in the patients' blood was lower. During peak exercise, the amount of oxygen they consumed was 14 percent lower while expelled air had higher oxygen levels, indicating that their muscles were not as efficient at using it.
Another telltale sign was the fact that their blood vessels simply didn't dilate as well. The researchers put a cuff on the lower arm to increase blood flow through the brachial artery, a major vessel in the bicep. How much the artery dilates in response to the increased flow when the cuff is released depends on how much nitric oxide is available and it was significantly less in patients versus controls.
Future studies are needed to determine exactly why cystic fibrosis patients appear to have less nitric oxide available and whether improving lung function and exercise capacity can improve the vascular health of patients of all ages.
MCG researchers already are doing a small pilot study giving over-the-counter antioxidants to combat oxidative stress, enhance nitric oxide availability and improve blood-vessel dilation. "If we can help improve vascular function, we can hopefully improve their ability to deliver oxygen and increase their exercise capacity," Harris said.
Maintaininggood lung function typically requires multiple medications and several hours of daily therapy to break up the mucus, said McKie, a study co-author. She also encourages patients to live full, active lives. "We tell them they are going to live a full life, get married, be president, play baseball, whatever they want to do, it just takes a little extra work." Patient study participants included a swimmer, basketball, baseball and softball players. Guidelines for routine exercise testing of cystic fibrosis should be published early next year.
Abstract
Background
Although myocardial interstitial fibrosis has been considered to play a pathogenic role in chronic heart failure (HF), the role of perivascular fibrosis, another form of fibrosis, remains to be elucidated.
Methods
We examined 64 consecutive patients with non-ischemic HF caused by hypertrophic cardiomyopathy (HCM,
n
=
16), hypertensive heart disease (HHD,
n=
11), or dilated cardiomyopathy (DCM,
n=
37), diagnosed by both cardiac catheterization and endomyocardial biopsy (right ventricular side of the interventricular septum) in the Tohoku University Hospital between January 2001 and April 2009. We calculated the collagen volume fraction (CVF) and perivascular fibrosis ratio (PFR) in biopsy samples and also examined Thrombolysis in Myocardial Infarction (TIMI) frame count to evaluate coronary blood flow.
Results
There was no significant correlation between CVF and PFR (
r[SUP]2[/SUP]
=
0.0007). Although CVF was comparable among HCM, HHD, and DCM (1.11
±
1.04, 1.89
±
1.61, and 1.41
±
1.48, respectively), PFR was significantly higher in HCM than in DCM (1.78
±
1.09 vs. 1.23
±
0.44,
p<
0.05). PFR was not correlated with cardiac function parameters, such as left ventricular (LV) ejection fraction, cardiac output, LV end-diastolic pressure, LV end-diastolic volume, aortic pressure, or pulmonary artery pressure. However, PFR was significantly correlated with coronary flow in the left anterior descending coronary artery (as evaluated by TIMI frame count) (
r[SUP]2[/SUP]
=
0.3351,
p<
0.0001, in all-cases combined population), but not with that in the left circumflex or right coronary artery. This correlation remained significant in a logistic regression model tested in 7 variables (body mass index, PVR, CVF, presence of hypertension, dyslipidemia, diabetes mellitus, and atrial fibrillation).
Conclusions
These results indicate that coronary perivascular fibrosis is associated with the impairment of coronary blood flow although not associated with interstitial fibrosis or cardiac function, suggesting that it can be a new therapeutic target to improve coronary microcirculation.
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Marry Christmas hellouser, I will pray for you my friend ( If you remember me: lol ) , I wish you're hairline will be like the good pics which I have seen before from you.:santa:
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Hey Guys, I know maybe you answered this question before but because I surprised to see many post here and read some and didn't find it , I will ask !
When you Doing Hard Derma how long does it take that scar or blood on you're scalp remove completely? Because I saw the pictures and I said OMG ! How they
are going to public with this ****tt!! Anyway , Is it necessary to use cream after that? and which one do you have better experience? ( EMU OIL or..? )
---
I hope with the success with this method we will change the history of hair loss !! Since it hurts us a lot!!!
First and foremost, derma roller don't scar.. even hard rolling. It looks terrible in the pics but you just need to wipe out the blood and pretty much nothing is visible.. just some redness (like a sunburn) for few days which is fine and normal. No cream are used, this can alters or retard the healing process. Just buy a good Numbcream to reduces the pain.