Referring to AD as type 3 diabetes has its foundation in the fact that the CNS in AD is characterized by a paucity of insulin and resistance of the insulin receptors
Lightweight wheelchairs provide convenience and comfort to the user and caregiver alike and are often built using materials like aluminum and titanium alloy, while foldable wheelchairs allow for easy storage and transport. Merge the two styles, and got a great mobility aid that isn't a pain to lug around. Utilizing small wheels and lighter materials, transport wheelchairs can tip the scale at as little as 19 lbs, ideal for those looking for a highly portable option. Transport chairs also tend to be more affordable and offer the benefit of increased mobility without breaking the bank.
This type of lightweight wheelchair is often referred to as a "transfer chair" and is typically used for shorter trips. Since it's geared towards storability and portability, it features four smaller wheels and dispenses with the larger, rear-mounted wheels that characterize standard wheelchairs. Its construction ensures that it's always foldable and portable, but does so at the expense of self-propulsion. Instead, a transport chair is built so that a caregiver can easily push the user. Transport wheelchairs or companion chairs are companion wheelchairs where the purpose is for a companion to push the user. Most transporters have swing-away leg rests, fixed armrests, and side panels. Instead of the usual 'large back - small front' wheels typical of most wheelchairs, light travel chairs have four small wheels providing much easier maneuverability of the chair.
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: 100
Transport chairs, also known as companion wheelchairs, have four small wheels instead of two small and two large. A transport chair is designed to only be push by caregiver, other common names are 'companion chair' or 'rollabout chair'. A huge variety of different widths and weight capacities are available. A transport wheelchair is a mobility chair designed for convenience, short-distance use and easy handling by a caregiver. Lightweight and foldable, these wheelchairs are easily moved and typically fit in the trunk of most vehicles. There is even a model designed to fold into a bag to be carried over the shoulder. They are much smaller than standard manual wheelchairs and similar in size to the front wheels. Without large rear wheels, the user must rely on someone else to push the chair, which is why the transport chair is often referred to as a companion wheelchair.
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 Depth (inches): 13"
Back height (inches): 16"
Total height (inches): 35"
Max User Weight Capacity (kgs): 80 k.g.
Net Weigh
Heat exposure (40 °C to 43 °C) of cancer cells in preclinical studies, and hyperthermia regionally applied to patients in early randomized clinical studies, have shown synergistic activity with ionizing radiation and chemotherapy
For the combination of hyperthermia with chemotherapy, the study group at Munich7 was the first to demonstrate the safety and efficacy of regional hyperthermia (RHT) in patients with high-risk sarcoma.
delayed hemolytic events occur in ≈20% of patients with severe imported malaria, and 60% of these patients require blood transfusion
Delayed-onset anemia (herein referred to as postartesunate delayed-onset hemolysis [PADH] pattern of anemia) has been observed to occur 2–3 weeks after initiation of IV artesunate
The mechanism of this anemia is hemolytic, as demonstrated by high serum lactate dehydrogenase (LDH) and low plasma haptoglobin levels
PADH occurred in 27% of patients in this study, but it was rarely associated with severe anemia and was never fatal
median delayed drop in hemoglobin levels was 1.3 g/dL
This transfusion rate (<5%) is markedly lower than that previously reported for patients with severe imported malaria and delayed-onset anemia (≈60%)
Side effects of artesunate frequently include gastrointestinal disturbances, neutropenia (1.3%), reticulocytopenia (0.6%), and elevated liver enzymes (1.1%)
The avermectins are known to possess pronounced antitumor activity
Over the past few years, there have been steadily increasing reports that ivermectin may have varying uses as an anti-cancer agent, as it has been shown to exhibit both anti-cancer and anti-cancer stem cell properties
In human ovarian cancer and NF2 tumor cell lines, high-dose ivermectin inactivates protein kinase PAK1 and blocks PAK1-dependent growth
PAK1 is essential for the growth of more than 70% of all human cancers, including breast, prostate, pancreatic, colon, gastric, lung, cervical and thyroid cancers, as well as hepatoma, glioma, melanoma, multiple myeloma and for neurofibromatosis tumors
Ivermectin suppresses breast cancer by activating cytostatic autophagy, disrupting cellular signaling in the process, probably by reducing PAK1 expression
Cancer stem cells are a key factor in cancer cells developing resistance to chemotherapies and these results indicate that a combination of chemotherapy agents plus ivermectin could potentially target and kill cancer stem cells, a paramount goal in overcoming cancer
Triple-negative breast cancers, which lack estrogen, progesterone and HER2 receptors, account for 10–20% of breast cancers and are associated with poor prognosis
Ivermectin addition led to transcriptional modulation of genes associated with epithelial–mesenchymal transition and maintenance of a cancer stem cell phenotype in triple-negative breast cancers cells, resulting in impairment of clonogenic self-renewal in vitro and inhibition of tumor growth and metastasis in vivo
ivermectin synergizes with the chemotherapy agents cytarabine and daunorubicin to induce cell death in leukemia cells
Ivermectin-induced cytostatic autophagy also leads to suppression of tumor growth in breast cancer xenografts, causing researchers to believe there is scope for using ivermectin to inhibit breast cancer cell proliferation and that the drug is a potential treatment for breast cancer
Ivermectin inhibits proliferation and increases apoptosis of various human cancers
Activation of WNT-TCF signaling is implicated in multiple diseases, including cancers of the lungs and intestine,
A new screening system has found that ivermectin inhibits the expression of WNT-TCF targets
It represses the levels of C-terminal β-catenin phosphoforms and of cyclin D1 in an okadaic acid-sensitive manner, indicating its action involves protein phosphatases
In vivo, ivermectin selectively inhibits TCF-dependent, but not TCF-independent, xenograft growth without side effects
ivermectin has an exemplary safety record, it could swiftly become a useful tool as a WNT-TCF pathway response blocker to treat WNT-TCF-dependent diseases, encompassing multiple cancers.117
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 harmful effects of chicken papilloma disease not only stop at physical health but also the spirit of patients is seriously affected. Patients may be depressed, mentally in crisis when they know that they can follow them all their lives.
Chicken ridge is considered the undeniable obsession of men. Referring to this disease, many boys are bored, because once they get sick, the chicken's neck often hangs and leaves many harms.
Dr. Vo Duy Tam said, "The chicken's crest is a sexually transmitted disease caused by HPV (Human Papilloma Virus) - The virus causes human papilloma.
Currently there are more than 130 HPV types that have been discovered, among them, the ones that often cause genital warts are types 6, 11, 16, and 18.
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.
pharmacokinetic data indicate that intravenous administration of ascorbate can bypass this tight control resulting in highly elevated plasma levels
ascorbate readily oxidizes to produce H2O2, pharmacological ascorbate has been proposed as a prodrug for the delivery of H2O2 to tumors
Ascorbate is an excellent reducing agent and readily undergoes two consecutive, one-electron oxidations to form ascorbate radical (Asc•−) and dehydroascorbic acid (DHA)
Ascorbate oxidizes readily. The rate of oxidation is dependent on pH and is accelerated by catalytic metals
In near-neutral buffers with contaminating metals, the oxidation and subsequent loss of ascorbate can be very rapid
Ascorbate is required for maintaining iron in the ferrous state
In the presence of catalytic metal ions, ascorbate can also exert pro-oxidant effects
Ascorbate is an excellent one-electron reducing agent that can reduce ferric (Fe3+) to ferrous (Fe2+) iron, while being oxidized to ascorbate radical
In a classic Fenton reaction, Fe2+ reacts with H2O2 to generate Fe3+ and the very oxidizing hydroxyl radical
e presence of ascorbate can allow the recycling of Fe3+ back to Fe2+, which in turn will catalyze the formation of highly reactive oxidants from H2O2
Depending on concentrations, the effects of ascorbate on models of lipid peroxidation can be pro- or antioxidant
ferritin released enhanced pharmacologic ascorbate induced-cytotoxicity, indicating that ferritin with high iron-saturation could be a source of catalytic iron. Consistent with this, ascorbate has also been shown to be capable of releasing iron from cellular ferritin
not well understood, but it is felt to be a combination of both heat-induced necrosis and of protein inactivation (e.g., repair enzymes) as opposed to DNA damage
alterations in tumor cytoskeletal and membrane structures, which disrupt cell motility and intracellular signal transduction
A common explanation for HT-enhancement of RT and CT involves inhibition of homologous recombination repair of double-strand DNA breaks, preventing cells from repairing sub-lethal damage
it does appear to inhibit rejoining of RT-induced DNA breaks more than is commonly observed after RT alone
HT damages cells and enhances RT and CT sensitivity as a function of both temperature and duration of treatment
as temperature or duration increase, the rate of cell killing also increases
At temperatures above 42 °C, tumor vasculature is damaged, resulting in decreased blood flow
Cancer cells are particularly vulnerable to heating; in vivo studies have shown that temperatures in the range of 40–44 °C cause more selective damage to tumor cells
cancerous blood vessels are chaotic, leaky, and inefficient
selective cytotoxic effect on tumor cells include inhibition of key cancer cell-signaling pathways such as AKT, inducing apoptosis, suppression of cancer stem cell proliferation, and others
increase in immunological attacks against tumors after HT, which were believed to be achieved through activation of HSPs and subsequent modulation of the innate and adaptive immune responses against tumor cells
HT does lead to activation of the immune system and HSP-induced cell death through modification of the tumor cell surface
These HSPs and tumor antigens are taken up by dendritic cells and macrophages and go on to induce specific anti-tumor immunity
In vivo studies demonstrate HT-enhancement of NK cell activity, and HT has been shown to increase neutrophilic granulocytes with anti-tumor activity
it has become increasingly clear that HT results in immune stimulation, through both direct heat-mediated cell killing as well as innate and adaptive immune system modulation
The term hyperthermia is used in this review to refer to heating within the clinically accepted range of 40–45 °C
temperatures above 42.5–43 °C the exposure time can be halved with each 1 °C increase while maintaining equivalent cell killing
gradual heating at 43 °C for 1 h worked through an apoptotic pathway
glucose deprivation triggers apoptosis47 and vitamin C treatment kills RAS-oncogene expressing tumor cells, but not wild-type RAS containing cells, by inhibition of GAPDH
New study out of the UK supports the role of glucose in cancer growth and aggressiveness. This research found that high influx of glucose into the glycolysis pathway upregulated the RAS oncogene via accumulation of the Fructose 1,6 bisphosphonate through the enzyme phosphofructokinase..
steroid hormones typically interact with their cognate receptor in the cytoplasm for AR, glucocorticoid receptor (GR) and PR, but may also bind receptor in the nucleus as appears to often be the case for ERα and ERβ
This ligand binding results in a conformational change in the cytoplasmic NRs that leads to the dissociation of HSPs, translocation of the ligand-bound receptor to the nucleus
In the nucleus, the ligand-bound receptor dimerizes and then binds to DNA at specific HREs to regulate gene transcription
some steroid hormone-induced nuclear events can occur in minutes
the genomic effects of steroid hormones take longer, with changes in gene expression occurring on the timescale of hours
Classical steroid hormone signaling occurs when hormone binds nuclear receptors (NR) in the cytoplasm, setting off a chain of genomic events that results in, among other changes, dimerization and translocation to the nucleus where the ligand-bound receptor forms a complex with coregulators to modulate gene transcription through direct interactions with a hormone response element (HRE)
NRs have been found at the plasma membrane of cells, where they can propagate signal transduction often through kinase pathways
Membrane-localized ER, PR and AR have been reported to modulate the activity of MAPK/ERK, phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), nitric oxide (NO), PKC, calcium flux and increase inositol triphosphate (IP3) levels to promote cell processes including autophagy, proliferation, apoptosis, survival, differentiation, and vasodilation
ERα36, a 36kDa truncated form of ERα that lacks the transcriptional activation domains of the full-length protein. Membrane-localized ERα36 can activate pathways including protein kinase C (PKC) and/or mitogen activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) to promote the progression of various cancers
G protein-coupled receptor 30 (GPR30), also referred to as G protein-coupled estrogen receptor (GPER), is a membrane-localized receptor that has been observed to respond to estrogen to activate rapid signaling
hormone-responsive G protein coupled receptor is Zip9, which androgens can activate
GPRC6A is another G protein-coupled membrane receptor that is responsive to androgen
androgen-mediated non-genomic signaling through this GPCR can modulate male fertility, hormone secretion and prostate cancer progression
non-NR proteins located at the cell surface can bind to steroid hormones and respond by eliciting rapid signaling events
Estrogens have been shown to induce rapid (i.e. seconds) calcium flux via membrane-localized ER (mER)
ER-calcium dynamics lead to activation of kinase pathways such as MAPK/ERK which can result in cellular effects like migration and proliferation
17β-estradiol (E2) has been reported to promote angiogenesis through the activation of GPER
Membrane NRs may also mediate rapid signaling through crosstalk with growth factor receptors (GFR)
A similar crosstalk occurs between the receptor tyrosine kinase insulin-related growth factor-1 receptor (IGF-IR) and ERα. Not only does IGF-IR activate ERα, but inhibition of IGF-IR downregulates estrogen-mediated ERα activity, suggesting that IGF-IR is essential for maximal ERα signaling
This is a bombshell that shatters the current right brain approach to ER. It completely shatters the concept of eat sugar, whatever you want, with cancer treatment in ER+ or hormonally responsive cancer!
Further, ER activates IGF-IR pathways including MAPK
GPER is involved in the transactivation of the EGFR independent of classical ER
tight interconnection between genomic and non-genomic effects of NRs.
non-genomic pathways can also lead to genomic effects
androgen-bound AR associates with the kinase Src at the plasma membrane, activating Src which then leads to a signaling cascade through MAPK/ERK
However, Src can also increase the expression of AR target genes by the ligand-independent transactivation of AR
extranuclear steroid hormone actions can potentially reprogram nuclear NR events
estrogen modulated the expression of several genes including endothelial nitric oxide synthase (eNOS) via rapid signaling pathways
epigenetic changes can then mediate genomic events in uterine tissue and breast cancer cells