Round Ring Pillow providing effective relief to pressure sores, the rendered round ring pillow is procured from reliable source. In additions to this, the round ring pillow provides effective cushioned seating and effectively enhances the healing process.
Round Ring Pillow Specifications
Provideds relief to pressure sores.
Provides orthopaedic cushioned seating and encourages healing.
Construction with soft PVC material.
Maximum weight of patient 75kgs.
Round Ring Pillow Features
Provides even weight bearing
Renders stability while seating
Easy to use
Lightweight Ergonomic Wheelchair is designed to cradle patients in comfort while reducing risk of pressure sores, relieving pressure, dispersing weight evenly and improving stability. The Ergo Lite Wheelchair is easy to lift and its small size makes it ideal for travel. Weighing only 19.8 lbs., the chair is easy to store and transport. The chair folds down the middle like a standard wheelchair and the backrest also folds down to make the wheelchair even more compact. Also features companion brakes located on handles for added safety and comfort. Ergonomic Wheelchairs are ultra lightweight and have a supportive seating system to provide pressure relief and anti-slippage giving the user excellent stability and posture support. .
Better Ergonomic wheelchair for Comfort: Sit for any length of time in a fixed position in a traditional transport chair and it will feel how painful bad ergonomics can be. It is fully reclined 25° angle, which minimizes slumping and sliding. And because of this can be easily adjusted with the push of a button, it can change positions frequently over time, reducing the chance of secondary conditions that may include pressure sores.
Designed to Fit Almost Everyone: It is one of the most extensively researched seat profiles specifically design to accommodate users ranging in size from small women to large men, with the greatest amount of comfort and proper posture/spinal support.
The Karman wheelchairs are exceptional in both their function and style. With comfort built right into the frame of a wheelchair eliminating the need for a "thick cushion" to add comfort, S-Shape seat allows the wheelchair to be "ergonomically correct" putting into a seating position and comfort conforming to natural body's curves. These chairs are built for comfort and quality to stand the test of time.
Ergonomic Wheelchair is Right: Ergonomic Wheelchair is designed for users who will spend a large amount of time in the chair. This wheelchair'
A high percentage of men that fail PDE5 therapy have low T and the addition of T therapy improves the effects of PDE5 therapy. T provides a positive impact on NO synthase which increased NO, which PDE5 therapies must have to work.
A transport wheelchair is designed to only be propelled by another individual and is sometimes referred to as a companion chair or rollabout chair. Transport chairs have four small wheels instead of two small and two large. They come in different widths and weight capacities and are usually the same basic frame as a standard manual wheelchair. Lightweight Transport wheelchair is one of the the lightest transport chairs on the market, weighing in at only 19 lbs! With four great colors to choose from, this can be transported in style. A seat belt and swing-away removable footrests are standard and make it easy to get in and out of this chair. A fold-down back allows for easier storage and transport and padded armrests add additional comfort.
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 sp
Transport wheelchairs are machines or equipment that facilitate for mobility and movement of wheelchair confined people at public places. While it is true that simple wheelchairs can do the trick, travel Wheelchair are specifically designed and manufactured to facilitate better roaming and mobility at malls, restaurants and parks where people usually converge to relax. A seat belt and swing-away removable footrests are standard and make it easy to get in and out of this chair. A fold-down back allows for easier storage and transport and padded armrests add additional comfort. The materials with which travel Wheelchair are made are of more superior quality and strength. That is because Travel Wheelchair are made very specifically to facilitate movement at public and outdoor places. Also, travel Wheelchair are made of materials that are highly durable to enable it to carry out its purpose. Thus, it is often that users complain about the limited usefulness and comfort of using the wheelchairs.
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
Disabled people not only have these challenges to face, but a number of other concerns. Disabled people who are blind, deaf and are wheelchair bound face additional challenges. Issues such as accessibility, being able to understand words that are spoken or written can make travel doubly difficult. Ultralight manual wheelchair are essential for ensuring a user's ability to use their wheelchair in the most functional, efficient, and healthy way possible. For individuals who have utilized an ultralight manual wheelchair for a number of years, it is common for them to know exactly how their wheelchair should be set-up from the precise seat to floor height measurement and vertical position of the rear wheel. On the other hand, a newer user may require adjustability to meet their changing needs over time as they continues to recover and/or adapt to using a wheelchair.
Karma KM 2500 L Big Wheel Wheelchair:
Karma KM 2500 L Wheelchair Specifications:
Width 18"
Front/Rear Wheels 6" to 22"
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 11.kg
Karma KM 2500 L 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 L 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 (11 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 L Premium Wheelchair is amazingly light and compact transit wheelcha
Transport wheelchairs are machines or equipment that facilitate for mobility and movement of wheelchair confined people at public places. While it is true that simple wheelchairs can do the trick, travel Wheelchair are specifically designed and manufactured to facilitate better roaming and mobility at malls, restaurants and parks where people usually converge to relax. A seat belt and swing-away removable footrests are standard and make it easy to get in and out of this chair. A fold-down back allows for easier storage and transport and padded armrests add additional comfort. The materials with which travel Wheelchair are made are of more superior quality and strength. That is because Travel Wheelchair are made very specifically to facilitate movement at public and outdoor places. Also, travel Wheelchair are made of materials that are highly durable to enable it to carry out its purpose. Thus, it is often that users complain about the limited usefulness and comfort of using the wheelchairs.
Karma Travel Wheelchair KM TV 20.2:
Karma Travel Wheelchair KM TV 20.2 - 606 T-6 aircraft-grade aluminum-alloy frame provides incredible strength. Easy-to-fold in three seconds.
Karma Travel Wheelchair KM TV 20.2 Features:
Type: Travel Wheelchair
T-6 aircraft-grade aluminum
Secure brake improve safety
Padded flip back armrest
PU front caster & rear wheel
Karma Travel Wheelchair KM TV 20.2 Measurements:
Weight: 8.9kg
Seat width: 39.5cm
Tyre: PU front casters and rear wheels
Capacity: 100kg
Folded size: (L/W/H): 610mm x 350mm x710mm.
Ultra Lightweight Wheelchair:
Its compact design and feather light weight makes it suitable for people on the go.
Ultra Lightweight Wheelchair Specifications:
Frame Style : Foldable
Frame Material : Aluminium (Light weight)
Rear wheel to wheel width in open position (inches) : 20"
Handle to Handle : 16"
Seat Width (inches): 13"
Rear Wheel Size: 7"
Front Wheel Size: 5"
Seat to floor height (inches): 19"
Seat Dep
Travel Wheelchairs are usually designed for being as lightweight as is possible for the health of performance or maybe portability. People exactly who travel frequently because of their wheelchairs by means of car or maybe airplane roommates wish a wheelchair is not just lightweight but takes the least number of space doable. Travel information wheelchairs are classified as the most sleek and stylish, lightweight collapsible wheelchairs. The lightest wheelchairs do not need some on the accessories a usual manual wheelchair often have, but almost all models is usually customized to add in items like fold-away footrests in addition to adjustable buttocks.
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
Mouse study finds THC and CBD agonist reduce tumor growth, inhibit angiogenesis, induce apoptosis, and reduce metastasis. In addition, 91% of breast cancers in animal study expressed CB2 receptors.
Only abstract available here. Study finds association between high tumor burden, more aggressive disease, and lower NK cell numbers. In addition, inverse assocation with CD16/56 and LDH found. Most likely direct tumor suppression as cause.
Calorie restriction and protein restriction inhibit IGF-1, insulin, AkT, PI3K, and mTOR. In addition, those with protein intake >20%, compared to 10%, was associated with a 4 fold increase in cancer death risk and a 75% increase in overall mortality. Protein restriction inhibits tumor growth, associated with a 30-70% reduction in IGF-1, reduced the accumulation of oxidized proteins. The restriction of tryptophan alone reduced inflammation.
Quercetin sensitized both chemo and radiation and it reduces side effects. That is in addition to its inhibition of NF-kappaB and inhibition of aromatase.
2017 meta-analysis finds no increase relative risk (RR) of cancer with coffee consumption. First, this must consider all the "other" junk put in coffee these days. Second, and most important, this study looked at RR which tells us nothing about risk. Studies like this don't do much more than confuse the general public, doctors, and judges--recent judge ruling in California that coffee needs a carcinogenic lable. Third, epigenetis will tell us about individual risk. I am growing more concerned that the majority of studies published today are merely statistical dances to ensure publication. Is it good that no RR was found? yes, does that give any indication of absolute risk? No. Take home: enjoy your morning cup of joe as nature prescribed--no additives.
Proof of conept finds IV vitamin C is synergistic with chemotherapy in ovarian cancer. In addition, a reduction in toxic side effects were also seen. Why is vitamin C not used??? The results were found in in vivo and in vitro study.
An extensive panel of 43 tumor and 5 normal cell lines were exposed to ascorbate in vitro for ≤2 h to mimic clinical pharmacokinetics
effective concentration that decreased survival 50% (EC50) was determined. EC50 was <10 mM for 75% of tumor cells tested, whereas cytotoxicity was not evident in normal cells with >20 mM ascorbate
The addition of catalase to the medium ameliorated death of ovarian carcinoma (Ovcar5), pancreatic carcinoma (Pan02), and glioblastoma (9L) cells exposed to 10 mM ascorbate (1 h), indicating cytotoxicity was mediated by H2O2
A treatment dose of 4 g ascorbate/kg body weight either once or twice daily did not produce any discernible adverse effects
Xenograft experiments showed that parenteral ascorbate as the only treatment significantly decreased both tumor growth and weight by 41–53%
Peak plasma concentrations of ascorbate approached 30 mM
Pharmacologic concentrations of ascorbate decreased tumor volumes 41–53% in diverse cancer types known for both their aggressive growth and limited treatment options.
Our findings showed that pharmacologic ascorbic acid concentrations were cytotoxic to many types of cancer cells in vitro (Fig. 1A) and significantly impeded tumor progression in vivo without toxicity to normal tissues
The amelioration of ascorbate cytotoxicity in vitro by the addition of catalase was consistent among sensitive cancer cells (Fig. 1B) and points unambiguously to H2O2 generation in the extracellular medium
the current in vivo data support that pharmacologic ascorbate concentrations, which can readily be achieved in humans (Fig. 3E), diminished growth of several aggressive cancer types in mice (Fig. 2) without causing apparent adverse effects.
These intratumoral H2O2 concentrations of >125 μM persisted for >3 h after ascorbate administration
Data from the American Cancer Society show that the rate of increase in cancer deaths/year (3.4%) was two-fold greater than the rate of increase in new cases/year (1.7%) from 2013 to 2017
cancer is predicted to overtake heart disease as the leading cause of death in Western societies
cancer can also be recognized as a metabolic disease.
glucose is first split into two molecules of pyruvate through the Embden–Meyerhof–Parnas glycolytic pathway in the cytosol
Aerobic fermentation, on the other hand, involves the production of lactic acid under normoxic conditions
persistent lactic acid production in the presence of adequate oxygen is indicative of abnormal respiration
Otto Warburg first proposed that all cancers arise from damage to cellular respiration
The Crabtree effect is an artifact of the in vitro environment and involves the glucose-induced suppression of respiration with a corresponding elevation of lactic acid production even under hyperoxic (pO2 = 120–160 mmHg) conditions associated with cell culture
the Warburg theory of insufficient aerobic respiration remains as the most credible explanation for the origin of tumor cells [2, 37, 51, 52, 53, 54, 55, 56, 57].
The main points of Warburg’s theory are; 1) insufficient respiration is the predisposing initiator of tumorigenesis and ultimately cancer, 2) energy through glycolysis gradually compensates for insufficient energy through respiration, 3) cancer cells continue to produce lactic acid in the presence of oxygen, and 4) respiratory insufficiency eventually becomes irreversible
Efraim Racker coined the term “Warburg effect”, which refers to the aerobic glycolysis that occurs in cancer cells
Warburg clearly demonstrated that aerobic fermentation (aerobic glycolysis) is an effect, and not the cause, of insufficient respiration
all tumor cells that have been examined to date contain abnormalities in the content or composition of cardiolipin
The evidence supporting Warburg’s original theory comes from a broad range of cancers and is now overwhelming
respiratory insufficiency, arising from any number mitochondrial defects, can contribute to the fermentation metabolism seen in tumor cells.
data from the nuclear and mitochondrial transfer experiments suggest that oncogene changes are effects, rather than causes, of tumorigenesis
Normal mitochondria can suppress tumorigenesis, whereas abnormal mitochondria can enhance tumorigenesis
In addition to glucose, cancer cells also rely heavily on glutamine for growth and survival
Glutamine is anapleurotic and can be rapidly metabolized to glutamate and then to α-ketoglutarate for entry into the TCA cycle
Glucose and glutamine act synergistically for driving rapid tumor cell growth
Glutamine metabolism can produce ATP from the TCA cycle under aerobic conditions
Amino acid fermentation can generate energy through TCA cycle substrate level phosphorylation under hypoxic conditions
targeting glucose and glutamine will deprive the microenvironment of fermentable fuels
Although Warburg’s hypothesis on the origin of cancer has created confusion and controversy [37, 38, 39, 40], his hypothesis has never been disproved
Warburg referred to the phenomenon of enhanced glycolysis in cancer cells as “aerobic fermentation” to highlight the abnormal production of lactic acid in the presence of oxygen
Emerging evidence indicates that macrophages, or their fusion hybridization with neoplastic stem cells, are the origin of metastatic cancer cells
Radiation therapy can enhance fusion hybridization that could increase risk for invasive and metastatic tumor cells
Kamphorst et al. in showing that pancreatic ductal adenocarcinoma cells could obtain glutamine under nutrient poor conditions through lysosomal digestion of extracellular proteins
It will therefore become necessary to also target lysosomal digestion, under reduced glucose and glutamine conditions, to effectively manage those invasive and metastatic cancers that express cannibalism and phagocytosis.
Previous studies in yeast and mammalian cells show that disruption of aerobic respiration can cause mutations (loss of heterozygosity, chromosome instability, and epigenetic modifications etc.) in the nuclear genome
The somatic mutations and genomic instability seen in tumor cells thus arise from a protracted reliance on fermentation energy metabolism and a disruption of redox balance through excess oxidative stress.
According to the mitochondrial metabolic theory of cancer, the large genomic heterogeneity seen in tumor cells arises as a consequence, rather than as a cause, of mitochondrial dysfunction
A therapeutic strategy targeting the metabolic abnormality common to most tumor cells should therefore be more effective in managing cancer than would a strategy targeting genetic mutations that vary widely between tumors of the same histological grade and even within the same tumor
Tumor cells are more fit than normal cells to survive in the hypoxic niche of the tumor microenvironment
Hypoxic adaptation of tumor cells allows for them to avoid apoptosis due to their metabolic reprograming following a gradual loss of respiratory function
The high rates of tumor cell glycolysis and glutaminolysis will also make them resistant to apoptosis, ROS, and chemotherapy drugs
Despite having high levels of ROS, glutamate-derived from glutamine contributes to glutathione production that can protect tumor cells from ROS
reason to eliminate glutamine in cancer patients and even GSH with cancer patients
It is clear that adaptability to environmental stress is greater in normal cells than in tumor cells, as normal cells can transition from the metabolism of glucose to the metabolism of ketone bodies when glucose becomes limiting
Mitochondrial respiratory chain defects will prevent tumor cells from using ketone bodies for energy
glycolysis-dependent tumor cells are less adaptable to metabolic stress than are the normal cells. This vulnerability can be exploited for targeting tumor cell energy metabolism
In contrast to dietary energy reduction, radiation and toxic drugs can damage the microenvironment and transform normal cells into tumor cells while also creating tumor cells that become highly resistant to drugs and radiation
Drug-resistant tumor cells arise in large part from the damage to respiration in bystander pre-cancerous cells
Because energy generated through substrate level phosphorylation is greater in tumor cells than in normal cells, tumor cells are more dependent than normal cells on the availability of fermentable fuels (glucose and glutamine)
Ketone bodies and fats are non-fermentable fuels
Although some tumor cells might appear to oxidize ketone bodies by the presence of ketolytic enzymes [181], it is not clear if ketone bodies and fats can provide sufficient energy for cell viability in the absence of glucose and glutamine
Apoptosis under energy stress is greater in tumor cells than in normal cells
A calorie restricted ketogenic diet or dietary energy reduction creates chronic metabolic stress in the body
. This energy stress acts as a press disturbance
Drugs that target availability of glucose and glutamine would act as pulse disturbances
Hyperbaric oxygen therapy can also be considered another pulse disturbance
The KD can more effectively reduce glucose and elevate blood ketone bodies than can CR alone making the KD potentially more therapeutic against tumors than CR
Campbell showed that tumor growth in rats is greater under high protein (>20%) than under low protein content (<10%) in the diet
Protein amino acids can be metabolized to glucose through the Cori cycle
The fats in KDs used clinically also contain more medium chain triglycerides
Calorie restriction, fasting, and restricted KDs are anti-angiogenic, anti-inflammatory, and pro-apoptotic and thus can target and eliminate tumor cells through multiple mechanisms
Ketogenic diets can also spare muscle protein, enhance immunity, and delay cancer cachexia, which is a major problem in managing metastatic cancer
GKI values of 1.0 or below are considered therapeutic
The GKI can therefore serve as a biomarker to assess the therapeutic efficacy of various diets in a broad range of cancers.
It is important to remember that insulin drives glycolysis through stimulation of the pyruvate dehydrogenase complex
The water-soluble ketone bodies (D-β-hydroxybutyrate and acetoacetate) are produced largely in the liver from adipocyte-derived fatty acids and ketogenic dietary fat. Ketone bodies bypass glycolysis and directly enter the mitochondria for metabolism to acetyl-CoA
Due to mitochondrial defects, tumor cells cannot exploit the therapeutic benefits of burning ketone bodies as normal cells would
Therapeutic ketosis with racemic ketone esters can also make it feasible to safely sustain hypoglycemia for inducing metabolic stress on cancer cells
Ketones are much more than energy adaptabilit, but actually are therapeutic.
ketone bodies can inhibit histone deacetylases (HDAC) [229]. HDAC inhibitors play a role in targeting the cancer epigenome
Therapeutic ketosis reduces circulating inflammatory markers, and ketones directly inhibit the NLRP3 inflammasome, an important pro-inflammatory pathway linked to carcinogenesis and an important target for cancer treatment response
Chronic psychological stress is known to promote tumorigenesis through elevations of blood glucose, glucocorticoids, catecholamines, and insulin-like growth factor (IGF-1)
In addition to calorie-restricted ketogenic diets, psychological stress management involving exercise, yoga, music etc. also act as press disturbances that can help reduce fatigue, depression, and anxiety in cancer patients and in animal models
Ketone supplementation has also been shown to reduce anxiety behavior in animal models
This physiological state also enhances the efficacy of chemotherapy and radiation therapy, while reducing the side effects
lower dosages of chemotherapeutic drugs can be used when administered together with calorie restriction or restricted ketogenic diets (KD-R)
Besides 2-DG, a range of other glycolysis inhibitors might also produce similar therapeutic effects when combined with the KD-R including 3-bromopyruvate, oxaloacetate, and lonidamine
oxaloacetate is a glycolytic inhibitor, as is doxycycline, and IVC.
A synergistic interaction of the KD diet plus radiation was seen
It is important to recognize, however, that the radiotherapy used in glioma patients can damage the respiration of normal cells and increase availability of glutamine in the microenvironment, which can increase risk of tumor recurrence especially when used together with the steroid drug dexamethasone
Poff and colleagues demonstrated that hyperbaric oxygen therapy (HBOT) enhanced the ability of the KD to reduce tumor growth and metastasis
HBOT also increases oxidative stress and membrane lipid peroxidation of GBM cells in vitro
The effects of the KD and HBOT can be enhanced with administration of exogenous ketones, which further suppressed tumor growth and metastasis
Besides HBOT, intravenous vitamin C and dichloroacetate (DCA) can also be used with the KD to selectively increase oxidative stress in tumor cells
Recent evidence also shows that ketone supplementation may enhance or preserve overall physical and mental health
Some tumors use glucose as a prime fuel for growth, whereas other tumors use glutamine as a prime fuel [102, 186, 262, 263, 264]. Glutamine-dependent tumors are generally less detectable than glucose-dependent under FDG-PET imaging, but could be detected under glutamine-based PET imaging
GBM and use glutamine as a major fuel
Many of the current treatments used for cancer management are based on the view that cancer is a genetic disease
Emerging evidence indicates that cancer is a mitochondrial metabolic disease that depends on availability of fermentable fuels for tumor cell growth and survival
Glucose and glutamine are the most abundant fermentable fuels present in the circulation and in the tumor microenvironment
Low-carbohydrate, high fat-ketogenic diets coupled with glycolysis inhibitors will reduce metabolic flux through the glycolytic and pentose phosphate pathways needed for synthesis of ATP, lipids, glutathione, and nucleotides
Studies have shown that the production of nagalase has a mutual relationship with Gc-MAF level and immunosuppression
It has been demonstrated that serum levels of nagalase are good prognosticators of some types of cancer
The nagalase level in serum correlates with tumor burden and it has been shown that Gc-MAF therapy progresses, nagalase activity decreases
It has been shown that Gc-MAF can inhibit the angiogenesis induced by pro-inflammatory prostaglandin E1
The effect of Gc-MAF on chemotaxis or activation of tumoricidal macrophages is likely the main mechanism against angiogenesis.
Administration of Gc-MAF stimulates immune-cell progenitors for extensive mitogenesis, activates macrophages and produces antibodies. “This indicates that Gc-MAF is a powerful adjuvant for immunization.”
Cancer cell lines do not develop into tumor genes in mouse models after Gc-MAF-primed immunization (29-31) and the effect of Gc-MAF has been approved for macrophage stimulation for angiogenesis, proliferation, migration and metastatic inhibition on tumors induced by MCF-7 human breast cancer cell line
The protocol included: "a high dose of second-generation Gc-MAF (0.5 ml) administered twice a week intramuscularly for a total of 21 injections.”
Yamamoto et al. showed that the administration of Gc-MAF to 16 patients with prostate cancer led to improvements in all patients without recurrence
Inui et al. reported that a 74-year-old man diagnosed with prostate cancer with multiple bone metastases was in complete remission nine months after initiation of GcMAF therapy simultaneously with hyper T/NK cell, high-dose vitamin C and alpha lipoic acid therapy
It has also been approved for non-neoplastic diseases such as autism (41), multiple sclerosis (42, 43), chronic fatigue syndrome (CFS) (40), juvenile osteoporosis (44) and systemic lupus erythematous (45).
Gc-MAF has been verified for use in colon, thyroid (38), lung (39), liver, thymus (36), pancreatic (40), bladder and ovarian cancer and tongue squamous carcinoma
Prostate, breast, colon, liver, stomach, lung (including mesothelioma), kidney, bladder, uterus, ovarian, head/neck and brain cancers, fibrosarcomas and melanomas are the types of cancer tested thus far
weekly administration of 100 ng Gc-MAF to cancer at different stages and types showed curative effects at different follow-up times
this treatment has been suggested for non-anemic patients
Studies have shown that weekly administration of 100 ng Gc-MAF to cancer patients had curative effects on a variety of cancers
Because the half-life of the activated macrophages is approximately one week, it must be administered weekly
In vivo weekly intramuscular administration of Gc-MAF (100 ng) for 16-22 weeks was used to treat patients with breast cancer
individuals harboring different VDR genotypes had different responses to Gc-MAF and that some genotypes were more responsive than others
Administration of Gc-MAF for cancer patients exclusively activates macrophages as an important cell in adaptive immunity
Gc-MAF supports humoral immunity by producing, developing and releasing large quantities of antibodies against cancer. Clinical evidence from a human model of breast cancer patients supports this hypothesis
There is also evidence that confirms the tumoricidal role of Gc-MAF via Fc-receptor mediation
It is likely that the best therapeutic responses will be observed when the nutritional and inflammatory aspects are taken together with stimulation of the immune system
it should be noted that no harmful side effects of Gc-MAF treatment have been reported, even when it was successfully administered to autistic children
The natural activation mechanism of macrophages by Gc-MAF is so natural and it should not have any side effects on humans or animal models even in cell culture
Besides the Gc-MAF efficacy on macrophage activity, it can be a potential anti-angiogenic agent (28) and an inhibitor of the migration of cancerous cells in the absence of macrophages (47).
Activating or modifying natural killer cells, dendritic cells, DC, CTL, INF and IL-2 have all been recommended for cancer immunotherapy
It has been reported that nagalase cannot deglycosylate Gc-MAF as it has specificity for Gc globulin alone
inflammation-derived macrophage activation with the participation of B and T lymphocytes is the main mechanism
macrophages highly-activated by the addition of Gc-MAF can show tumoricidal activity
Previous clinical investigations have confirmed the efficacy of Gc-MAF. In addition to activating existing macrophages, Gc-MAF is a potent mitogenic factor that can stimulate the myeloid progenitor cells to increase systemic macrophage cell counts by 40-fold in four days