Experimental studies in animal models suggest that CoQ10 may protect against neuronal damage that is produced by ischemia, atherosclerosis and toxic injury.
Low Testosterone increased nonalcoholic fatty liver disease in men. The prevalence of NAFLD reached 85% with Total Testosterone was < 300 ng/dl. Free Testosterone required a greater drop to increase the NAFLD, but it to still was found to be associated.
This article focus' more on the liver and insulin effect of DHEA, but highlights the 2002 study of DHEA and decreased aberrant crypt foci in potential cancer prevention.
Reduced SOD activity might be responsible for excessive accumulation of superoxide anions leading to increased free radical mediated injury. Increased free radical production has been shown to be responsible for chromosomal damage leading to mutagenecity, cell proliferation and carcinogenesis. SOD activity showed marked improvement after mastectomy indicating the lowering of oxidative stress.
The increased production of reactive oxygen species causes oxidative stress leading to cell proliferation and hence increased inflammatory conditions
Superoxide dismutase is an important antioxidant enzyme which decomposes the harmful superoxide anions into hydrogen peroxide thus protects the body from the action of free radicals
Females suffering from breast cancer had significantly decreased Superoxide dismutase (SOD) and reduced glutathione (GSH) levels in comparison to normal females
ADA seems to be a promising marker of inflammation in breast cancer thereby suggesting that it can be used as a diagnostic tool to detect the stage of breast cancer along with cytopathological studies
In conclusion, our study confirmed the role of oxidative stress in the pathogenesis of breast cancer.
Another potent antioxidant molecule is reduced glutathione. It acts as reductant which converts hydrogen peroxide into water and reduces lipid peroxidation products into their corresponding alcohols and thus mediates protective action.
In the present study, significantly low SOD activity has been observed in female patients suffering from carcinoma breast both pre as well as post operative in comparison to healthy females.
We observed significantly decreased SOD activity and GSH levels in patients belonging to clinical stage 4 as compared to those having stages 1, 2 or 3 of breast cancer.
Increased ADA activity in breast cancer patients has also been reported
The compromised antioxidant defence system produces the oxidative stress which in turn creates the inflammatory response shown by concomitant increased adenosine deaminase (ADA) activity in female patients.
Experimental and epidemiological evidences implicate the involvement of oxygen derived free radical in the pathogenesis of breast cancer.
Antioxidant status was highly depressed in advanced stages of breast cancer as compared to initial stage.
In the present study, significantly low GSH levels were observed in female patients of carcinoma breast as compared to normal females
Walia et al. (1995) reported increased ADA activity in breast cancer patients as compared to age matched normal subjects.
These free radicals are able to cause damage to membrane, mitochondria and macromolecules including proteins, lipids and DNA and actively take part in cell proliferation. This cascade in turn generates the inflammatory response and causes the progression of the disease.
increased oxidative stress gives rise to inflammation which could further aggravates the disease
Breast carcinoma involves a cascade of events that are highly inflammatory.
Marked oxidative stress in stage 4 of breast cancer indicated advancement of the disease, hence checking oxidative stress at initial stage could be helpful for controlling the progression of the disease.
They concluded that ADA is a better probable parameter for detection of breast cancer
Adenosine deaminase enzyme (ADA) catalyzes the conversion of adenosine to inosine which finally gets converted to uric acid
serum ADA activity tends to increase with advancing age,
Prevalence of oxidative stress gives rise to inflammation.
Study finds a reduction in SuperOxide Dismutase and Glutathione Perioxidase in advancing breast cancer. Cancer is a high oxidative stress disease that results in inflammation, mitochondrial dysfunction and proliferation. Adenosine Deaminase (ADA) is proposed to be another biomarker to assess tumor stage.
Karma KM 2500 Small Wheel Wheelchair:
Karma KM 2500 Small Wheel Wheelchair Specifications:
Width 18"
Front/Rear Wheels 6" to 14"
Seat Width 47cm
Seat Depth 40cm
Overall Width 66cm
Overall Collapsed Width 36cm
Armrest Height 21cm
Overall Length 90cm
Seat Height 47cm
Backrest Height 38cm
Overall Height 86cm
Weight 9.2 k.g.
Karma KM 2500 Small Wheel Wheelchair Seat and Back:
AEGIS Microbe Shield Approved by the FDA, EPA, EU, etc., bonded anti-microbial barrier upholstery protects from odor, staining and deterioration from bacteria, fungus and other microorganisms. It is a shield for your health.
Karma KM 2500 Small Wheel Wheelchair Extended Armrest:
By simulating the natural position of arms, the extended armrest design is ergonomic and creates bigger seating space.
An Ultra lightweight wheelchair (9.2 kg) with a compact design for either attendant assisted or self propelling users.
The use of aircraft-grade aluminium alloy and double cross brace provide this model with outstanding strength and durability.
Karma Healthcare KM-2500 Premium Wheelchair is amazingly light and compact transit wheelchair which is ideal for outings and travelers. It folds down to take up virtually no space in the boot of a car and weighs just over 9.2 kg making it easy for anyone to lift into a vehicle.
Backrest folds-down for easy transportation.
Maximum user weight: 100 K.g.
Aluminium frame.
Fixed armrest/fixed footrest.
Foldable frame via double cross bars.
Comfortable & durable upholstery.
Swing-away foot plates.
Puncture proof tyres.
Attendant cable brake.
14" flat-free rear wheels.
Detachable and washable cushion.
One Year Warranty.
It folds down to take up virtually no space in the boot of a car.
This amazingly light and compact transit wheelchair is ideal for outings and travelling.
It comes with detachable and washable cushion.
The wheel chair has attendant cable brake.
It is made from aircraft-grade aluminium alloy fra
Laser toning is simply using of laser light to penetrate the dermal layers of skin and break the pigment that results in ageing, dark spots even acne.
Laser toning is performed using non ablative lasers thus depending on thermolysis and not causing any damage to the surface skin. This thermal injury causes triggering of collagen production in the dermis and rejuvenates the skin as a result.
GCs induce increased cellular expression of receptors for several pro-inflammatory cytokines including interleukin (IL)-1 (Spriggs et al. 1990), IL-2 (Wiegers et al. 1995), IL-4 (Paterson et al. 1994), IL-6 (Snyers et al. 1990), and IFN-g (Strickland et al. 1986), as well as GM-CSF
GCs have also been shown to stimulate effector cell functions including phagocytosis by monocytes (van der Goes et al. 2000), effector cell proliferative responses (Spriggs et al. 1990), macrophage activation (Sorrells and Sapolsky 2010), and a delay of neutrophil apoptosis
a concentration- and time-dependent range of GC effects that are both pro- and anti-inflammatory
basal (diurnal) concentrations of cortisol do not exert an anti-inflammatory effect on several pro-and anti-inflammatory mediators of the human immune inflammatory response
withdrawal of cortisol activity in vivo did not lead to increased inflammatory responsiveness of immune effector cells
maximal suppression of inflammation was achieved by a stress-associated, but still physiologic, cortisol concentration. There was no greater anti-inflammatory effect at higher cortisol concentrations (Yeager et al. 2005) although IL-10 concentrations continued to increase with increasing cortisol concentrations as we and others have shown
acutely, physiological cortisol concentrations are anti-inflammatory and, as proposed, act to limit over expression of an inflammatory response that could lead to tissue damage
Acutely, cortisol has anti-inflammatory effects following a systemic inflammatory stimulus (Figure 4). However, a cortisol concentration that acts acutely to suppress systemic inflammation also has a delayed effect of augmenting the inflammatory response to subsequent, delayed stimulu
1) GCs can exert pro-inflammatory effects on key inflammatory processes and, 2) GC regulation of inflammation can vary from anti- to a pro-inflammatory in a time-dependent manner
The immediate in vivo effect of both stress-induced and pharmacological GC concentrations is to suppress concurrent inflammation and protect the organism from an excessive or prolonged inflammatory response
GCs alone, in the absence of an inflammatory stimulus, up-regulate monocyte mRNA and/or receptors for several molecules that participate in pro-inflammatory signaling, as noted above and in the studies presented here.
In humans, as shown here, if in vivo GC concentrations are elevated concurrent with an inflammatory stimulus, anti-inflammatory effects are observed
In sharp contrast, with a time delay of 12 or more hours between an increased GC concentration and the onset of an inflammatory stimulus, enhancing effects on inflammation are observed. These effects have been shown to persist in humans for up to 6 days
GC-induced enhancement of inflammatory responses is maximal at an intermediate concentration, in our studies at a concentration that approximates that observed in vivo following a major systemic inflammatory stimulus
In addition to enhanced responses to LPS, recently identified pro-inflammatory effects of GCs also show enhanced localization of effector cells at inflammatory sites
we hypothesize that pre-exposure to stress-associated cortisol concentrations “prime” effector cells of the monocyte/macrophage lineage for an augmented pro-inflammatory response by; a) inducing preparative changes in key regulators of LPS signal transduction, and b) enhancing localization of inflammatory effector cells at potential sites of injury
The ‘Glucose Ketone Index’ (GKI) was created to track the zone of metabolic management for brain tumor management
The GKI is a biomarker that refers to the molar ratio of circulating glucose over β-OHB, which is the major circulating ketone body.
We present evidence showing that the GKI can predict success for brain cancer management in humans and mice using metabolic therapies that lower blood glucose and elevate blood ketone levels
The zone of metabolic management is likely entered with GKI values between 1 and 2 for humans
Optimal management is predicted for values approaching 1.0, and blood glucose and ketone values should be measured 2–3 hours postprandial, twice a day if possible
Preclinical studies have demonstrated a clear linkage between GKI and therapeutic efficacy
the Warburg effect (aerobic fermentation of glucose) is a common metabolic malady expressed in nearly all neoplastic cells of these and other malignant tumors
Aerobic fermentation (Warburg effect) is necessary to compensate for the insufficiency of mitochondrial oxidative phosphorylation in the cells of most tumors
Normal brain cells gradually transition from the metabolism of glucose to the metabolism of ketone bodies (primarily β-hydroxybutyrate and acetoacetate) for energy when circulating glucose levels become limiting
Ketone bodies bypass the glycolytic pathway in the cytoplasm and are metabolized directly to acetyl CoA in the mitochondria
Tumor cells are less capable than normal cells in metabolizing ketone bodies for energy due to their mitochondrial defects
daily activities and emotional stress can cause blood glucose levels to vary making it difficult for some people to enter the predicted zone of metabolic management
a clear association of the GKI to the therapeutic action of calorie restriction against distal invasion, proliferation, and angiogenesis in the VM-M3 model of glioblastoma
The results suggest that GKI levels that approach 1.0 are therapeutic for managing brain tumor growth
Therapeutic efficacy of the KD or calorie restriction is greater with lower GKI values than with higher values
The glucose ketone index shown to predict dietary metabolic success. In humans with brain cancer-- the target is 1. The glucose and ketone (betahydroxybutyrate) should be measured 2-3 hours postprandial twice daily.
The serum level of LDH correlated with tumor burden and was thought to reflect the tumor’s growth and invasive potential
the majority of patients with advanced or metastatic disease could be detected to have extremely high serum level of LDH
strong evidence to support effective chemotherapy of full dose even in patients with high LDH level
LDH is a key enzyme in the process of energy production in cancer cells, it catalyzes the conversion of pyruvate to lactate in hypoxic conditions
its function in anaerobic metabolism, cancer cells grow even after their rapid proliferation that leads to low-oxygen conditions in the tumor microenvironment
LDH plays an important role in tumor progression and maintenance
inhibition of LDH inhibits tumor progression and has been considered for the therapeutic target of cancer energy metabolism
LDH levels are increased in response to tissue injury or during disease states
LDH could be a marker of tumor burden for advanced cancer patients
Are you living your life in depression? If yes then there is a chance you can lose your memory. There are types, symptoms & causes of Amnesia / Memory loss
Amnesia is commonly known as memory loss. The reason of memory loss can be an emotional or physiological disorder, drugs abusement or Brian injuries. The memory loss can be temporary or permanent but mostly refers to temporary memory loss.
Serum ferritin levels correlate with total body iron storage and systemic inflammation
The level of serum ferritin, an acute phase protein, is increased in an inflammatory environment
Previous studies have reported that elevated serum ferritin levels are associated with insulin resistance syndrome, hypertension, dyslipidemia, obesity, and metabolic syndrome as risk factors of CKD
elevated serum ferritin levels in hemodialysis patients predict higher mortality