psychobiological mechanisms, which trigger the hypothalamus-pituitary-adrenal axis (HPAA) can only indirectly be assessed by salivary cortisol measures. The different instances that control HPAA reactivity (hippocampus, hypothalamus, pituitary, adrenals) and their respective modulators, receptors, or binding proteins, may all affect salivary cortisol measures.
linear relationship with measures of plasma ACTH and cortisol in blood or urine does not necessarily exist
I am a kidney failure patient with only 25% of kidney function. Is it too late for me to take Micr-Chinese Medicine Osmotherapy ? In fact, as long as you still have urine, you can take this kind of medicine, it can help to improve your kidney function gradually.
urine alkalisation may induce calcium phosphate deposition
renal replacement therapy should be started on an emergency basis when hydration fails to produce a prompt metabolic improvement or when ARF develops
Up to 50% of patients with newly diagnosed multiple myeloma have renal failure and up to 10% require dialysis
renal ultrasonography remains the method of choice for investigating extra-renal obstruction
The relief of the obstruction, either by percutaneous nephrostomy or through a ureteral stent, is the cornerstone of treatment
TMA may be associated with the cancer itself, with cancer chemotherapy, or with allogeneic BMT
thrombotic microangiopathy (TMA)
it may be as high as 5%
Most of the cases occur in patients with solid tumours, the most common type being adenocarcinoma (stomach, breast and lung)
The pathophysiology of the TMA-malignancy association remains controversial, although many studies suggest an insult to the vascular endothelium
mitomycin C. Subsequently, TMA has been reported with many anti-cancer agents, including gemcita-bine, bleomycin, cisplatin, CCNU, cytosine arabinoside, daunorubicin, deoxycoformycin, 5-FU, azathioprine and interferon α
Plasma exchanges have been shown to improve prognosis in the general population of patients with TMA
Causative factors should be looked for and antihypertensive treatment given. Lastly, in the absence of guidelines, we believe that plasma exchange should be proposed in patients with severe cancer treatment-associated TMA
The most widely used protective measure is saline infusion to induce solute diuresis
During methotrexate infusion and elimination, fluids should be given to maintain a high urinary output and urinary alkalisation should be performed to keep the urinary pH above 7.5. Rescue with folinic acid (50 mg four times a day) should be started 24 hours after each high-dose metho-trexate infusion and serum methotrexate concentrations should be measured every day
The SOC for GBM was modified in this patient to initiate KMT prior to surgical resection, to eliminate steroid medication, and to include HBOT as part of the therapy
the greatest therapeutic benefit for patients (near 1.0)
The observed reduction in blood glucose in our patient would reduce lactic acid fermentation in the tumor cells, while the elevation of ketone bodies would fuel normal cells thus protecting them from hypoglycemia and oxidative stress
Previous studies showed that GBM survival and tumor growth was correlated with blood glucose levels
Evidence indicates that glioma cells cannot effectively use ketone bodies for energy due to defects in the number, structure, and function of their mitochondria
The accuracy of the GKI as a predictor for therapeutic efficacy, however, is better when ketone bodies are measured from the blood than when measured from the urine
A reduction of glucose-driven lactic acid fermentation would not only increase tumor cell apoptosis, but would also reduce inflammation and edema in the tumor microenvironment thus reducing tumor cell angiogenesis and invasion
Besides serving as a metabolic fuel for GBM, glutamine is also an essential metabolite for normal immune cells
therapies that inhibit glutamine availability and utilization must be strategically employed to avoid inadvertent impairment of immune cell functions
we used the non-toxic green tea extract, EGCG, and chloroquine in an attempt to limit glutamine availability to the tumor cells
EGCG is thought to target the glutamate dehydrogenase activity that facilitates glutamine metabolism in GBM cells
Chloroquine, on the other hand, will inhibit lysosomal digestion thus restricting fermentable amino acids and carbohydrates from phagocytosed materials in the tumor microenvironment
HBOT to increase oxidative stress in the tumor cells
As glucose and glutamine fermentation protect tumor cells from oxidative stress, reduced availability of these metabolites under ketosis could enhance the therapeutic action of HBOT, as we recently described
Prior to subtotal tumor resection and standard of care (SOC), the patient conducted a 72-h water-only fast
Following the fast, the patient initiated a vitamin/mineral-supplemented ketogenic diet (KD) for 21 days that delivered 900 kcal/day
KD (increased to 1,500 kcal/day at day 22
the patient received metformin (1,000 mg/day), methylfolate (1,000 mg/day), chloroquine phosphate (150 mg/day), epigallocatechin gallate (400 mg/day), and hyperbaric oxygen therapy (HBOT) (60 min/session, 5 sessions/week at 2.5 ATA)
Biomarkers showed reduced blood glucose and elevated levels of urinary ketones with evidence of reduced metabolic activity (choline/N-acetylaspartate ratio) and normalized levels of insulin, triglycerides, and vitamin D
This is the first report of confirmed GBM treated with a modified SOC together with KMT and HBOT, and other targeted metabolic therapies
Glioblastoma multiforme (GBM) is the most common and malignant of the primary adult brain cancers
less than 20% of younger adults generally survive beyond 24 months
glucose and glutamine are the primary fuels that drive the rapid growth of most tumors including GBM
Glucose drives tumor growth through aerobic fermentation (Warburg effect), while glutamine drives tumor growth through glutaminolysis
The fermentation waste products of these molecules, i.e., lactic acid and succinic acid, respectively, acidify the tumor microenvironment thus contributing further to tumor progression
Glucose and glutamine metabolism is also responsible for the high antioxidant capacity of the tumor cells thus making them resistant to chemo- and radiotherapies
The reliance on glucose and glutamine for tumor cell malignancy comes largely from the documented defects in the number, structure, and function of mitochondria and mitochondrial-associated membranes
These abnormalities cause the neoplastic GBM cells to rely more heavily on substrate level phosphorylation than on oxidative phosphorylation for energy
dexamethasone not only increases blood glucose levels but also increases glutamine levels through its induction of glutamine synthetase activity
Calorie restriction and restricted KD are anti-angiogenic, anti-inflammatory, anti-invasive, and also kill tumor cells through a proapoptotic mechanism
Evidence also shows that therapeutic ketosis can act synergistically with several drugs and procedures to enhance cancer management improving both progression free and overall survival
hyperbaric oxygen therapy (HBOT) increases oxidative stress on tumor cells especially when used alongside therapies that reduce blood glucose and raise blood ketones
The glutamine dehydrogenase inhibitor, epigallocatechin gallate (EGCG) is also proposed to target glutamine metabolism
In this article we covered Flu Symptoms And Home Remedies. Influenza is a common respiratory illness that affects people from all age groups. Flu symptoms include a runny nose, sore throat, catarrh, and headache. Home remedies for flu are being used for centuries and have proven to be effective.
Influenza is a highly contagious, respiratory illness that affects people from all age groups and geographic backgrounds. In temperate regions, it occurs mostly in the winter months. There is no clear seasonal pattern in tropical climates. It varies in its severity from person to person. Sometimes, it presents as a mild, temporary infection. Other times, it can cause complications like red urine and ultimately lead to death. Influenza causes approximately 375,000 deaths worldwide each year.
diet enriched in fruits and vegetables (and consequently phytochemicals) was able to reverse the process and maintain and even elevate insulin sensitivity and glucose tolerance
LPS-mediated effects are related to an increase in TLR4 levels that triggers the activation of nuclear factor-kB (NF-kB), a transcription factor that activates a cascade of inflammatory mediators [41]. These factors control the transcription of inflammatory mediators, such as IL-1β, IL-6, TNF-α, TNF-β, INF-α, INFβ, INF-γ
Inflammation can alter insulin action and give rise to diabetes and obesity by blocking insulin receptor downstream events, impairing insulin receptor substrate 1 (IRS-1) activation and phosphatidylinositol 3-kinase-dependent (PI3K) pathways, therefore compromising insulin signaling
systemic inflammation (generated by LPS) also increased neopterin levels in the urine and resulted in altered neuronal activity by decreasing dopamine (DA) metabolism
an increase in neopterin levels has been recognized a sensitive biomarker for immune system activation
Our experiments denoted that these diets were able to diminish inflammatory mediators and oxidative damage
The data show that pharmacologic ascorbate concentrations produced Asc•− selectively in extracellular fluid compared with blood and that H2O2 formation occurred when Asc•− concentrations were >100 nM in extracellular fluid.
These data validate the hypothesis that ascorbate is a prodrug for selective delivery of reactive species to the extravascular space
pharmacologic ascorbate as a prooxidant drug for therapeutic use.
Recently we reported that pharmacologic ascorbic acid concentrations produced H2O2 concentrations of ≥25 μM, causing cancer cell death in vitro
We found that H2O2 concentrations generated in vivo were those that caused cancer cell death in vitro
When ascorbate was given parenterally, Asc•−, the product of a loss of one electron from ascorbate, was detected preferentially in extracellular fluid compared with blood
Asc•− generation in extracellular fluid depended on the ascorbate dose and the resulting concentrations
With i.v. administration of ascorbate, Asc•− concentrations were as much as 12-fold greater in extracellular fluid compared to blood and approached 250 nM
In blood, such Asc•− concentrations were never produced and were always <50 nM
These data are all consistent with the hypothesis that pharmacologic ascorbate concentrations in vivo serve as a prodrug for selective delivery of H2O2 to the extracellular space
After oral ingestion, control of intracellular and extracellular ascorbate concentrations is mediated by three mechanisms: intestinal absorption, tissue transport, and renal reabsorption
intestinal absorption, or bioavailability, declines at doses >200 mg
also at ≈60 μM, renal reabsorption approaches saturation, and excess ascorbate is excreted in urine
Parenteral administration bypasses tight control
When tight control is bypassed, H2O2 forms in the extracellular space
in vivo validation of ascorbate as a prodrug for selective H2O2 formation
Temporarily bypassing tight control with parenteral administration of ascorbate allows H2O2 to form in discrete time periods only, decreasing likelihood of harm, and provides a pharmacologic basis for therapeutic use of i.v. ascorbate
H2O2 formation results in selective cytotoxicity
Tumor cells are killed with exposure to H2O2 for ≤30 min
In vitro, killing is mediated by H2O2 rather than Asc•−
In addition to cancer treatment, another potential therapeutic use is for treatment of infections. H2O2 concentrations of 25–50 μM are bacteriostatic