Patients undergoing the best minimally invasive heart surgery in India often require heart procedures early in life to help improve blood flow to the lungs. After having any such methods, the patient may additionally or may not have an operating pulmonary valve that could lead to pulmonary regurgitation.
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The drug delivery technology market is segmented on the basis of route of administration into nine categories - oral, pulmonary, transdermal, injectable, ocular, nasal, topical, implantable, and transmucosal
There is just no reason to take SSRIs during pregnancy. SSRIs increase risk of miscarriage, birth defects, preterm birth, newborn behavior problems, pulmonary hypertension...All women considering pregnancy should removed, yet SSRIs are prescribed as if they are candy.
In early PET literature focusing on analysis of solitary pulmonary nodules, some researchers defined malignancy based on a SUVmax threshold of greater than 2.5
We contend that SUV analysis has virtually no role in this setting.
tumours grow as spheres, whereas inflammatory processes are typically linear
Far more important than the SUVmax is the pattern rather than intensity of metabolic abnormality and the correlative CT findings
Descriptively, we define SUV < 5 as “low intensity”, 5–10 as “moderate”, 10–15 as “intense” and >15 as “very intense”
Evolving literature suggests that intensity of uptake is an independent prognostic factor and in some tumour subtypes superior to histopathologic characterisation.
aerobic glycolysis
Our practice of thresholding the grey and colour scale to liver as detailed above results in similar image intensity to a fixed upper SUV threshold of 8 to 10
The advantage of using the liver as a reference tissue is also aided by this organ having rather low variability in metabolic activity
When the liver is abnormal and cannot be used as a reference organ, we use the default SUV setting of an upper SUV threshold of 8
One of the most challenging aspects of oncologic FDG PET/CT review, however, is to recognise all the patterns of metabolic activity that are not malignant and which consequently confound interpretation
Many benign and inflammatory processes are also associated with high glycolytic activity
Future articles in the “How I Read” series will address the specific details of reading PET/CT in various cancers
The intensity of uptake in metastases usually parallels that in the primary site of disease
For example, discordant low-grade activity in an enlarged lymph node in the setting of intense uptake in the primary tumour suggests it is unlikely malignant and more likely inflammatory or reactive
By CT criteria the enlarged node is ‘pathologic’ but the discordantly low metabolic signature further characterises this is as non-malignant since such a node is not subject to partial volume effects and therefore the intensity of uptake should be similar to the primary site
The exception is when the lymph node is centrally necrotic as a small rim of viable tumour is subject to partial volume effects with expectant lower intensity of uptake; integrating the CT morphology is therefore critical to reaching an accurate interpretation
Small nodes that are visualised on PET are conversely much more likely to be metastatic as such nodes are subject to partial volume effects.
The exception to this rule is tumours with a propensity for tumour heterogeneity at different sites
The combination of FDG and a more specific tracer, which visualises the well-differentiated disease can be very useful to characterise this phenomenon
“metabolic signature”
For the majority of malignant processes, the intensity of metabolic abnormality correlates with degree of aggressiveness or proliferative rate.
a negative PET/CT study in a patient with biopsy proven malignancy would be considered false-negative
Warburg effect
There, however, are a significant minority of tumours that utilise substrates other glucose such as glutamine or fatty acids as a source of the carbon atoms required for growth and proliferation
This includes a subset of diffuse gastric adenocarcinomas, signet cell colonic adenocarcinomas and some sarcomas, particularly liposarcoma
There may be a role for other radiotracers such as fluorothymidine (FLT) or amino acid substrates in this setting.
Some tumours harbour mutations that result in defective aerobic mitochondrial energy metabolism, effectively simulating the Warburg effect
patients with hereditary paraganglioma and pheochromocytoma highlight this phenomenon
These have intense uptake on FDG PET/CT despite often having low proliferative rate.
Uterine fibroids, hepatic adenomas, fibroadenomas of the breast and desmoid tumours are benign or relatively benign lesions that can have quite high FDG-avidity.
Metabolic activity switches off rapidly following initiation of therapy
Common examples where patients have commenced active therapy but the referrer is requesting “staging” includes hormonal therapy (eg. tamoxifen) in breast cancer, oral capecitabine in colorectal cancer or high dose steroids in Hodgkin’s lymphoma
It is therefore critical to perform PET staging before commencement of anti-tumour therapy
The potential advantage of routine diagnostic CT is improved anatomic localisation and definition
Without intravenous contrast, additional identification of typical oncologic complications such as pulmonary embolism or venous thrombosis cannot be identified
If the study is performed as an “interim” restaging study after commencement of therapy but before completion, in order to reach a valid or clinically useful conclusion findings must be interpreted in the context of known changes that occur at a specific timing and type of therapy
The most well studied use of interim PET is in Hodgkin’s lymphoma where repeat PET after two cycles of ABVD-chemotherapy provides powerful prognostic information and may improve outcomes by enabling early change of management
good read on the PET/CT scan reading. They mention that tumors are spheres and inflammation is linear, yet inflammation coexists with cancer; hard to simply delineate these on simple terms. I do agree aon the metabolic signature of the PET/CT scan
Since its establishment in the year 2011, Krshna Physio Plus is aimed to provide patients with comprehensive, high quality and professional physiotherapy treatments and rehabilitation to people in need. The efficient team of three, Dr. Ravi Sahauta - A very well-known complex trauma surgeon and Orthopaedician, Dr. Dharm Pal Sharma - an ex-Air force Physio trainer and Dr. Parmila Sharma - an experienced and talented physio expert, Krshna Physio Plus is counted among the well-known Physiotherapy clinic in Gurgaon and Delhi/NCR regions.
This clinic is one of the oldest organizations which was started with a vision to help people suffering from diverse dysfunctionalities with proper guidance and treatment which encompasses mainly physical, psychological, emotional, and social well being. With 8 centers in Delhi/NCR and Bihar, we are aimed at setting over 300 centers across Asia by 2020 and become the Physiotherapy clinic in Gurgaon.
Moreover, KRSNA Physio Plus is well equipped with various advanced facilities and equipment used to treat people to assure patient satisfaction and fast recovery. We have with us Top Physiotherapist in Gurgaon and Delhi/NCR regions with us who are specialized in offering treatment in physiotherapy dealing with Orthopedic, Neurological, Pediatric, Cardio-pulmonary, and Sports Injury, etc. All the experts here put their best for providing the best results.
Our experienced team of doctors and physiotherapists in Gurgaon who would be better able to diagnose what might be making it impossible for you to crane your neck, or pick articles off the floor, or simply kneel before your deity.
Sports-Related Injuries Could Happen to Anyone
It could be just that badminton match on a winter evening, or an office football match. Before you realize what is happening you've pulled a back muscle or your hamstring. Playing tug-of-war in colleges and office parties is fraught with the risk of a rotator cuff injury. Cricketers diving to save
The lowest price for ICD implantation in India is also endorsed for heart attack survivors and sufferers who've currently had percutaneous coronary intervention or passed surgical procedures. ICD treatment centers in India to increase access to cardiac and pulmonary rehabilitation programs.
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Diamorphine 5mg and 10mg powder used for solution for injection ampoules will remain unavailable until February 2022, Department of Health and Social Care (DHSC) has said in an update.
These injection ampoules are used to treat severe pain associated with surgical procedures, pain in the terminally ill, and to provide relief in acute pulmonary oedema.
Diamorphine 30mg and 100mg ampoules are available, however, the stock is not enough to support an uplift in demand.
Separately, the DHSC has extended the Medicine Supply Notification for Kolanticon gel, which is expected to remain unavailable until October 2022.
The starting dose was 500 mg/day and if no toxicity was noted, the dose was then escalated to another level in the order of 1,000, 2,000, 4,000, 8,000, and 12,000 mg/day. There was no treatment-related toxicity up to 8 g/day but the bulky volume of the drug was unacceptable to the patients beyond 8 g/day.
The serum concentration of curcumin usually peaked at 1 to 2 hours after oral intake of curcumin and gradually declined within 12 hours
Low endogenous bioavailable testosterone levels have been shown to be associated with higher rates
of all‐cause and cardiovascular‐related mortality.39,41,46–47 Patients suffering from CAD,13–18 CHF,137 T2DM,25–26 and obesity27–28
have all been shown to have lower levels of endogenous testosterone compared with those in healthy controls. In addition,
the severity of CAD15,17,29–30 and CHF137 correlates with the degree of testosterone deficiency
In patients with CHF, testosterone replacement therapy has been shown to significantly improve exercise tolerance while having
no effect on LVEF
testosterone therapy causes a shift in the skeletal muscle of CHF patients toward a higher concentration
of type I muscle fibers
Testosterone replacement therapy has also been shown to improve the homeostatic model of insulin resistance and hemoglobin
A1c in diabetics26,68–69 and to lower the BMI in obese patients.
Lower levels of endogenous testosterone have been associated with longer duration of the QTc
interval
testosterone replacement has been shown to shorten the QTc interval
negative correlation has been demonstrated between endogenous testosterone levels and IMT of the carotid arteries,
abdominal aorta, and thoracic aorta
These findings suggest that men with lower levels of endogenous testosterone may be at a higher risk of developing atherosclerosis.
Current guidelines from the Endocrine Society make no recommendations on whether patients with heart
disease should be screened for hypogonadism and do not recommend supplementing patients with heart disease to improve survival.
The Massachusetts Male Aging Study also projects ≈481 000 new cases of hypogonadism annually in US men within the same age
group
since 1993 prescriptions for testosterone, regardless of the formulation, have increased nearly 500%
Testosterone levels are lower in patients with chronic illnesses
such as end‐stage renal disease, human immunodeficiency virus, chronic obstructive pulmonary disease, type 2 diabetes mellitus
(T2DM), obesity, and several genetic conditions such as Klinefelter syndrome
A growing body of evidence suggests that men with lower levels of endogenous testosterone are more prone to develop CAD during
their lifetimes
There are 2 major potential confounding factors that the older studies generally failed to account for. These factors are
the subfraction of testosterone used to perform the analysis and the method used to account for subclinical CAD.
The biologically inactive form of testosterone is tightly bound to SHBG and is therefore unable to bind to androgen receptors
The biologically inactive fraction of testosterone comprises nearly 68% of the total testosterone in human serum
The biologically active subfraction of testosterone, also referred to as bioavailable testosterone, is either loosely bound
to albumin or circulates freely in the blood, the latter referred to as free testosterone
It is estimated that ≈30% of total serum testosterone is bound to albumin, whereas the remaining 1% to 3% circulates as free
testosterone
it can be argued that using the biologically active
form of testosterone to evaluate the association with CAD will produce the most reliable results
English et al14 found statistically significant lower levels of bioavailable testosterone, free testosterone, and free androgen index in
patients with catheterization‐proven CAD compared with controls with normal coronary arteries
patients with catheterization‐proven CAD had statistically significant lower levels of bioavailable
testosterone
In conclusion, existing evidence suggests that men with CAD have lower levels of endogenous testosterone,13–18 and more specifically lower levels of bioavailable testosterone
low testosterone levels are associated with risk factors for CAD such as T2DM25–26 and obesity
In a meta‐analysis of these 7 population‐based studies, Araujo et al41 showed a trend toward increased cardiovascular mortality associated with lower levels of total testosterone, but statistical
significance was not achieved (RR, 1.25
the authors showed that a decrease of 2.1 standard deviations in levels of total testosterone was associated
with a 25% increase in the risk of cardiovascular mortality
the relative risk of all‐cause mortality in men
with lower levels of total testosterone was calculated to be 1.35
higher risk of cardiovascular mortality is associated with lower levels of bioavailable testosterone
Existing evidence seems to suggest that lower levels of endogenous testosterone are associated with higher rates of all‐cause
mortality and cardiovascular mortality
studies have shown that lower levels of endogenous bioavailable testosterone are associated with higher rates
of all‐cause and cardiovascular mortality
It may be possible that using bioavailable testosterone to perform mortality analysis will yield more accurate results because
it prevents the biologically inactive subfraction of testosterone from playing a potential confounding role in the analysis
The earliest published material
on this matter dates to the late 1930s
the concept that testosterone replacement therapy improves angina has yet to be proven wrong
In more
recent studies, 3 randomized, placebo‐controlled trials demonstrated that administration of testosterone improves myocardial
ischemia in men with CAD
The improvement in myocardial ischemia was shown to occur in response to both acute and chronic
testosterone therapy and seemed to be independent of whether an intravenous or transdermal formulation of testosterone was
used.
testosterone had no effect on endothelial nitric oxide activity
There is growing evidence from in
vivo animal models and in vitro models that testosterone induces coronary vasodilation by modulating the activity of ion channels,
such as potassium and calcium channels, on the surface of vascular smooth muscle cells
Experimental studies suggest that
the most likely mechanism of action for testosterone on vascular smooth muscle cells is via modulation of action of non‐ATP‐sensitive
potassium ion channels, calcium‐activated potassium ion channels, voltage‐sensitive potassium ion channels, and finally L‐type
calcium ion channels
Corona et al confirmed those results by demonstrating that not only total testosterone levels are lower among diabetics,
but also the levels of free testosterone and SHBG are lower in diabetic patients
Laaksonen et al65 followed 702 Finnish men for 11 years and demonstrated that men in the lowest quartile of total testosterone, free testosterone,
and SHBG were more likely to develop T2DM and metabolic syndrome.
Vikan et al followed 1454 Swedish men for 11
years and discovered that men in the highest quartile of total testosterone were significantly less likely to develop T2DM
authors demonstrated a statistically significant increase in the incidence of T2DM in subjects receiving gonadotropin‐releasing
hormone antagonist therapy. In addition, a significant increase in the rate of myocardial infarction, stroke, sudden cardiac
death, and development of cardiovascular disease was noted in patients receiving antiandrogen therapy.67
Several authors have demonstrated
that the administration of testosterone in diabetic men improves the homeostatic model of insulin resistance, hemoglobin A1c,
and fasting plasma glucose
Existing evidence strongly suggests that the levels of total and free testosterone are lower among diabetic patients compared
with those in nondiabetics
insulin seems to be acting as a stimulant for the hypothalamus to secret gonadotropin‐releasing
hormone, which consequently results in increased testosterone production. It can be argued that decreased stimulation of the
hypothalamus in diabetics secondary to insulin deficiency could result in hypogonadotropic hypogonadism
BMI has been shown to be inversely associated with testosterone levels
This interaction may be a result
of the promotion of lipolysis in abdominal adipose tissue by testosterone, which may in turn cause reduced abdominal adiposity.
On the other hand, given that adipose tissue has a higher concentration of the enzyme aromatase, it could be that increased
adipose tissue results in more testosterone being converted to estrogen, thereby causing hypogonadism. Third, increased abdominal
obesity may cause reduced testosterone secretion by negatively affecting the hypothalamus‐pituitary‐testicular axis. Finally,
testosterone may be the key factor in activating the enzyme 11‐hydroxysteroid dehydrogenase in adipose tissue, which transforms
glucocorticoids into their inactive form.
increasing age may alter the association between testosterone and CRP. Another possible explanation
for the association between testosterone level and CRP is central obesity and waist circumference
Bai et al
have provided convincing evidence that testosterone might be able to shorten the QTc interval by augmenting the activity of
slowly activating delayed rectifier potassium channels while simultaneously slowing the activity of L‐type calcium channels
consistent evidence
that supplemental testosterone shortens the QTc interval.
Intima‐media thickness (IMT) of the carotid artery is considered a marker for preclinical atherosclerosis
Studies have shown that levels of endogenous testosterone are inversely
associated with IMT of the carotid artery,126–128,32,129–130 as well as both the thoracic134 and the abdominal aorta
1 study has demonstrated that lower levels of free testosterone are associated with accelerated progression
of carotid artery IMT
another study has reported that decreased levels of total and bioavailable testosterone are associated with progression
of atherosclerosis in the abdominal aorta
These findings suggest that normal physiologic testosterone levels may help to protect men from the development of atherosclerosis
Czesla et al successfully demonstrated that the muscle specimens that were exposed to metenolone had a significant shift
in their composition toward type I muscle fibers
Type I muscle fibers, also known as slow‐twitch or oxidative fibers, are
associated with enhanced strength and physical capability
It has been shown
that those with advanced CHF have a higher percentage of type II muscle fibers, based on muscle biopsy
Studies have
shown that men with CHF suffer from reduced levels of total and free testosterone.137 It has also been shown that reduced testosterone levels in men with CHF portends a poor prognosis and is associated with
increased CHF mortality.138 Reduced testosterone has also been shown to correlate negatively with exercise capacity in CHF patients.
Testosterone replacement therapy has been shown to significantly improve exercise capacity, without affecting LVEF
the results of the 3 meta‐analyses seem to indicate that testosterone replacement therapy does not cause an increase
in the rate of adverse cardiovascular events
Data from 3 meta‐analyses seem to contradict the commonly
held belief that testosterone administration may increase the risk of developing prostate cancer
One meta‐analysis reported
an increase in all prostate‐related adverse events with testosterone administration.146 However, when each prostate‐related event, including prostate cancer and a rise in PSA, was analyzed separately, no differences
were observed between the testosterone group and the placebo group
the existing data from the 3 meta‐analyses seem to indicate that testosterone replacement therapy does not increase
the risk of adverse cardiovascular events
the authors correctly
point out the weaknesses of their study which include retrospective study design and lack of randomization, small sample size
at extremes of follow‐up, lack of outcome validation by chart review and poor generalizability of the results given that only
male veterans with CAD were included in this study
the studies that failed to find an association
between testosterone and CRP used an older population group
low testosterone may influence the severity of CAD by adversely affecting
the mediators of the inflammatory response such as high‐sensitivity C‐reactive protein, interleukin‐6, and tumor necrosis
factor–α
Good review of Testosterone and CHD. Low T is associated with increased all cause mortality and cardiovascular mortality, CAD, CHF, type II diabetes, obesity, increased IMT, increased severity of CAD and CHF. Testosterone replacement in men with low T has been shown to improve exercise tolerance in CHF, improve insulin resistance, improve HgbA1c and lower BMI in the obese.
Honey plus coffee found to be better in resolving post-infectious cough than prednisolone. This study was a head to head study. The honey consisted of 500 grams and the coffee was a instant coffee of 70 grams. The dosing frequency was 3 x daily.
Golden Technologies takes all the worry out of purchasing a power wheelchair. Designers blend the most technologically advanced components with superior designs to provide with the almost in quality, comfort and style. Motorized wheelchairs to enter bike lanes if a sidewalk isn't available or passable by wheelchair. Wheelchair users would be required to yield the right-of-way to bikers. The proposal also adds motorized wheelchairs to current law affecting vehicles and bicycles on the road, including the required three foot law between bikers and drivers. Supporters bill would help wheelchair users get around quickly and that areas without sidewalks are often difficult to navigate. It's the standard chair, with the main frame attaches to the front. This isn't a futuristic design as such, but a very good way of maintaining or building strength in those who are bound to a wheelchair, and may hope to walk again in their future. Personally, this bike is pretty cool. It's got a front frame similar to a chopper, with the added comfort of a chair appose to a saddle.
A new module is set to transform electric powered wheelchairs into communication hubs. An powerchair is more compact and has a better turning radius than an electric scooter; making it is easier to navigate narrow doorways and tight turns. Another advantage of the powerwheelchair is that its armchair joystick does not require an upright posture like an electric scooter's handlebars. Most power wheelchairs can also be taken apart and stowed, while scooters usually can't. Powerwheelchairs are also usually less expensive than scooters. For many disabled people, the only way to move around is by using a wheelchair. Those who cannot powered wheelchairs propel themselves with their arms, which often leads to fatigue, pain, and even permanent damage to arms and shoulders.
BENEFITS:
Activates circulation system and improves cardio-pulmonary function.
Helps prevent decubitus sores.
Improves bowel regu
reducing oxidative stress with powerful antioxidants, is an important strategy for cancer prevention, as it would suppress one of the key early initiating steps where DNA damage and tumor-stroma metabolic-coupling begins. This would prevent cancer cells from acting as metabolic “parasites
Oxidative stress in cancer-associated fibroblasts triggers autophagy and mitophagy, resulting in compartmentalized cellular catabolism, loss of mitochondrial function, and the onset of aerobic glycolysis, in the tumor stroma. As such, cancer-associated fibroblasts produce high-energy nutrients (such as lactate and ketones) that fuel mitochondrial biogenesis and oxidative metabolism in cancer cells. We have termed this new energy-transfer mechanism the “reverse Warburg effect.
Then, oxidative stress, in cancer-associated fibroblasts, triggers the activation of two main transcription factors, NFκB and HIF-1α, leading to the onset of inflammation, autophagy, mitophagy and aerobic glycolysis in the tumor microenvironment
oxidative stress and ROS, produced in cancer-associated fibroblasts, has a “bystander effect” on adjacent cancer cells, leading to DNA damage, genomic instability and aneuploidy, which appears to be driving tumor-stroma co-evolution
tumor cells produce and secrete hydrogen peroxide, thereby “fertilizing” the tumor microenvironment and driving the “reverse Warburg effect.”
This type of stromal metabolism then produces high-energy nutrients (lactate, ketones and glutamine), as well as recycled chemical building blocks (nucleotides, amino acids, fatty acids), to literally “feed” cancer cells
loss of stromal caveolin (Cav-1) is sufficient to drive mitochondrial dysfunction with increased glucose uptake in fibroblasts, mimicking the glycolytic phenotype of cancer-associated fibroblasts.
oxidative stress initiated in tumor cells is transferred to cancer-associated fibroblasts.
Then, cancer-associated fibroblasts show quantitative reductions in mitochondrial activity and compensatory increases in glucose uptake, as well as high ROS production
These findings may explain the prognostic value of a loss of stromal Cav-1 as a marker of a “lethal” tumor microenvironment
aerobic glycolysis takes place in cancer-associated fibroblasts, rather than in tumor cells, as previously suspected.
our results may also explain the “field effect” in cancer biology,5 as hydrogen peroxide secreted by cancer cells, and the propagation of ROS production, from cancer cells to fibroblasts, would create an increasing “mutagenic field” of ROS production, due to the resulting DNA damage
Interruption of this process, by addition of catalase (an enzyme that detoxifies hydrogen peroxide) to the tissue culture media, blocks ROS activity in cancer cells and leads to apoptotic cell death in cancer cells
In this new paradigm, cancer cells induce oxidative stress in neighboring cancer-associated fibroblasts
cancer-associated fibroblasts have the largest increases in glucose uptake
cancer cells secrete hydrogen peroxide, which induces ROS production in cancer-associated fibroblasts
Then, oxidative stress in cancer-associated fibroblast leads to decreases in functional mitochondrial activity, and a corresponding increase in glucose uptake, to fuel aerobic glycolysis
cancer cells show significant increases in mitochondrial activity, and decreases in glucose uptake
fibroblasts and cancer cells in co-culture become metabolically coupled, resulting in the development of a “symbiotic” or “parasitic” relationship.
cancer-associated fibroblasts undergo aerobic glycolysis (producing lactate), while cancer cells use oxidative mitochondrial metabolism.
We have previously shown that oxidative stress in cancer-associated fibroblasts drives a loss of stromal Cav-1, due to its destruction via autophagy/lysosomal degradation
a loss of stromal Cav-1 is sufficient to induce further oxidative stress, DNA damage and autophagy, essentially mimicking pseudo-hypoxia and driving mitochondrial dysfunction
loss of stromal Cav-1 is a powerful biomarker for identifying breast cancer patients with early tumor recurrence, lymph-node metastasis, drug-resistance and poor clinical outcome
this type of metabolism (aerobic glycolysis and autophagy in the tumor stroma) is characteristic of a lethal tumor micro-environment, as it fuels anabolic growth in cancer cells, via the production of high-energy nutrients (such as lactate, ketones and glutamine) and other chemical building blocks
the upstream tumor-initiating event appears to be the secretion of hydrogen peroxide
one such enzymatically-active protein anti-oxidant that may be of therapeutic use is catalase, as it detoxifies hydrogen peroxide to water
numerous studies show that “catalase therapy” in pre-clinical animal models is indeed sufficient to almost completely block tumor recurrence and metastasis
by eliminating oxidative stress in cancer cells and the tumor microenvironment,55 we may be able to effectively cut off the tumor's fuel supply, by blocking stromal autophagy and aerobic glycolysis
breast cancer patients show systemic evidence of increased oxidative stress and a decreased anti-oxidant defense, which increases with aging and tumor progression.68–70 Chemotherapy and radiation therapy then promote further oxidative stress.69 Unfortunately, “sub-lethal” doses of oxidative stress during cancer therapy may contribute to tumor recurrence and metastasis, via the activation of myofibroblasts.
a loss of stromal Cav-1 is associated with the increased expression of gene profiles associated with normal aging, oxidative stress, DNA damage, HIF1/hypoxia, NFκB/inflammation, glycolysis and mitochondrial dysfunction
cancer-associated fibroblasts show the largest increases in glucose uptake, while cancer cells show corresponding decreases in glucose uptake, under identical co-culture conditions
Thus, increased PET glucose avidity may actually be a surrogate marker for a loss of stromal Cav-1 in human tumors, allowing the rapid detection of a lethal tumor microenvironment.
it appears that astrocytes are actually the cell type responsible for the glucose avidity.
In the brain, astrocytes are glycolytic and undergo aerobic glycolysis. Thus, astrocytes take up and metabolically process glucose to lactate.7
Then, lactate is secreted via a mono-carboxylate transporter, namely MCT4. As a consequence, neurons use lactate as their preferred energy substrate
both astrocytes and cancer-associated fibroblasts express MCT4 (which extrudes lactate) and MCT4 is upregulated by oxidative stress in stromal fibroblasts.34
In accordance with the idea that cancer-associated fibroblasts take up the bulk of glucose, PET glucose avidity is also now routinely used to measure the extent of fibrosis in a number of human diseases, including interstitial pulmonary fibrosis, postsurgical scars, keloids, arthritis and a variety of collagen-vascular diseases.
PET glucose avidity and elevated serum inflammatory markers both correlate with poor prognosis in breast cancers.
PET signal over-estimates the actual anatomical size of the tumor, consistent with the idea that PET glucose avidity is really measuring fibrosis and inflammation in the tumor microenvironment.
human breast and lung cancer patients can be positively identified by examining their exhaled breath for the presence of hydrogen peroxide.
tumor cell production of hydrogen peroxide drives NFκB-activation in adjacent normal cells in culture6 and during metastasis,103 directly implicating the use of antioxidants, NFκB-inhibitors and anti-inflammatory agents, in the treatment of aggressive human cancers.
Higher Testosterone and DHT levels in men was found to be positively associated with FEV1 and FVC; Estradiol was not. The question here is cause or effect.
Also interesting is the fact that smokers had higher Testosterone levels compared to non-smokers.