The prevalence of hypogonadism (often defined as serum testosterone < 300 ng dl−1 ) ranges from 6% [10] to as high as 38%
The process of BPH, however, continues as men age and despite the fact their serum testosterone decreases
Liu et al. [12] demonstrated that in a group of older males (mean age 59.8 years) that there was not a significant correlation of serum testosterone levels (total, free or bioavailable) with either prostate volume or International Prostate Symptom Score (IPSS)
in eugonadal men, studies have demonstrated that the prostate can increase in volume by approximately 12%
There seems to be little doubt that the treatment with testosterone of a young hypogonadal male leads to significant growth of the prostate
Behre et al. [22] demonstrated increased prostate volume and prostate-specific antigen (PSA) levels in hypogonadal men
Most studies, however, have shown no effect of exogenous androgens on PSA or prostate volume for older hypogonadal males
saturation model
They argue that the prostate is relatively insensitive to changes in androgen concentration at normal levels or in mild hypogonadism because the AR is saturated by androgens and therefore maximal androgen-AR binding is achieved. Conversely, the prostate is very sensitive to changes in androgen levels when testosterone is low
visceral obesity (one of the most significant components of metabolic syndrome) is associated with prostate volume and influences prostate growth during TRT.
This hypothesis of inflammation induced LUTS is also argued to be a mechanism for improvement of LUTS with PDE5I
The concept, therefore, that treatment with TRT of hypogonadal males with metabolic syndrome might lead to improvement/stabilization of their LUTS, appears to be confirmed in recent work by Francomano et al.
There was also an improvement in components of the patient's metabolic syndrome (such as BMI, waist circumference, hemoglobin A1c [HbA1c], insulin sensitivity, and lipid profile) as well as inflammatory markers and C-reactive protein.
They concluded that TRT was safe in this group of men, and hypothesize that TRT mitigates the pro-inflammatory factors associated with metabolic syndrome.
Authors review the literature behind Testosterone and BPH. The authors highlight the 4 proposed theories behind BPH: Testosterone, Estrogen, inflammation, and metabolic.
The conclusion is mixed: pointing out that no high level of evidence exists on either side of the debate of Testosterone and BPH.
Thigh Support
Applications
Mild support to quadriceps and hamstrings.
Relieves inflammation and stiffness.
Firm compression and therapeutic warmth.
Psychological support to geriatric patients.
Sports injury, sprains and strains.
Post-surgical rehabilitation.
Burn care.
Thigh Support Features
Strong Compression.
Four way stretch.
Dermophillic.
Durable.
Breathable and comfortable.
Thigh Support Measurements
Measure circumference around mid thigh - approximately 6 inches above knee.
Size Chart -
Size Inches CM
Small 14.8 to 17.2 37 to 43
Medium 17.2 to 19.6 43 to 49
Large 19.6 to 22.0 49 to 55
ECHO-7 virus strain, Picornaviridae family, Enterovirus genus, Enteric Cytopathic Human Orphan (ECHO) type 7, group IV, positive-sense single-stranded RNA virus
a few side effects were reported, for example subfebrile temperature (37.5°C for a couple of days), pain in the tumour area, sleepiness and diarrhoea
In this retrospective study, however, there was no record of any untoward side effect from Rigvir treatment or its discontinuation
Early observations of tumour regressions after virus infections have been published starting from the late 19th century
The present results show that in substage IB, IIA, IIB and IIC melanoma patients, Rigvir administration after surgery significantly (P<0.05) prolongs survival compared with patients who were managed according to current published guidelines
no value higher than grade 2 was recorded in Rigvir-treated patients. This is in contrast to most other cancer therapies, where grades 3 and 4 are frequently observed
Administration of virus induces the formation of neutralising antibodies that might potentially influence the efficiency of Rigvir
In 94 healthy adult participants tested, the titres were found to be low (1 : 20 to 1 : 62) 39,40. When tested in 155 adult cancer patients who had not been treated with Rigvir, neutralising antibodies against ECHO-7 were detected in ∼50% of the patients
the presence of ECHO-7 antibodies was shown to increase with age in children and level off to a plateau of around 75% in adults
Rigvir is an immunomodulator that affects both the humoral, antibody-mediated, and the cellular immune systems
neutralising antibodies do not affect efficacy when local or regional administration is used
it reduces the viability of melanoma, as well as pulmonary, gastric, pancreatic, bone, and breast cancer cell cultures
It is oncolytic in melanoma and rectum cancer patients
shown to improve the 5-year survival in rectum cancer patients
RIGVIR shown to improve survival against standard therapy in stage IB, IIA, IIB, and IIC in malignant melanoma patients in retrospective study. Side effects are minimal. Neutralizing antibodies are an area to watch that likely effects individual outcome beyond that of the type of cancer
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
of the approximately 108 cannabinoids produced by C. sativa, Δ9-tetrahydrocannabinol (thc) is the most relevant because of its high potency and abundance in plant preparations
Tetrahydrocannabinol exerts a wide variety of biologic effects by mimicking endogenous substances—the endocannabinoids anandamide3 and 2-arachidonoylglycerol4,5—that engage specific cell-surface cannabinoid receptors
two major cannabinoid-specific receptors—cb1 and cb2
transient receptor potential cation channel subfamily V, member 1
orphan G protein–coupled receptor 55
Most of the effects produced by cannabinoids in the nervous system and in non-neural tissues rely on cb1 receptor activation
the cb2 receptor was initially described to be present in the immune system6, but was more recently shown to also be expressed in cells from other origins
cardiovascular tone, energy metabolism, immunity, and reproduction
cannabinoids are well known to exert palliative effects in cancer patients
best-established use is the inhibition of chemotherapy-induced nausea and vomiting
thc and other cannabinoids exhibit antitumour effects in a wide array of animal models of cancer
cannabinoid receptors and their endogenous ligands are both generally upregulated in tumour tissue compared with non-tumour tissue
cb2 promotes her2 (human epidermal growth factor receptor 2) pro-oncogenic signalling in breast cancer
pharmacologic activation of cannabinoid receptors decreases tumour growth
endocannabinoid signalling can also have a tumour-suppressive role
pharmacologic stimulation of cb receptors is, in most cases, antitumourigenic. Nonetheless, a few reports have proposed a tumour-promoting effect of cannabinoids
most prevalent effect is the induction of cancer cell death by apoptosis and the inhibition of cancer cell proliferation
impair tumour angiogenesis and block invasion and metastasis
thc and other cannabinoids induce the apoptotic death of glioma cells by cb1- and cb2-dependent stimulation
Autophagy is primarily a cytoprotective mechanism, although its activation can also lead to cell death
autophagy is important for cannabinoid antineoplastic activity
autophagy is upstream of apoptosis in the mechanism of cannabinoid-induced cell death
the effect of cannabinoids in hormone- dependent tumours might rely, at least in part, on the ability to interfere with the activation of growth factor receptors
glioma cells), pharmacologic blockade of either cb1 or cb2 prevents cannabinoid-induced cell death with similar efficacy
other types of cancer cells (pancreatic48, breast24, or hepatic43 carcinoma cells, for example), antagonists of cb2 but not of cb1 inhibit cannabinoid antitumour actions
thc promotes cancer cell death in a cb1- or cb2-dependent manner (or both) at lower concentrations
cannabidiol (cbd), a phytocannabinoid with a low affinity for cannabinoid receptors15, and other marijuana-derived cannabinoids57 have also been proposed to promote the apoptotic death of cancer cells acting independently of the cb1 and cb2 receptors
In cancer cells, cannabinoids block the activation of the vascular endothelial growth factor (vegf) pathway, an inducer of angiogenesi
In vascular endothelial cells, cannabinoid receptor activation inhibits proliferation and migration, and induces apoptosis
cb1 or cb2 receptor agonists (or both) reduce the formation of distant tumour masses in animal models of both induced and spontaneous metastasis, and inhibit adhesion, migration, and invasiveness of glioma64, breast65,66, lung67,68, and cervical68 cancer cells in culture
the ceramide/p8–regulated pathway plays a general role in the antitumour activity of cannabinoids targeting cb1 and cb2
cbd, by acting independently of the cb1 and cb2 receptors, produces a remarkable anti-tumour effect—including reduction of invasiveness and metastasis
cannabinoids can also enhance immune system–mediated tumour surveillance in some contexts
ability of thc to reduce inflammation75,76, an effect that might prevent certain types of cancer
recent observations suggest that the combined administration of cannabinoids with other anticancer drugs acts synergistically to reduce tumour growth
combined administration of gemcitabine (the benchmark agent for the treatment of pancreatic cancer) and various cannabinoid agonists synergistically reduced the viability of pancreatic cancer cells
Other reports indicated that anandamide and HU-210 might also enhance the anticancer activity of paclitaxel89 and 5-fluorouracil90 respectively
Combined administration of thc and cbd enhances the anticancer activity of thc and reduces the dose of thc needed to induce its tumour growth-inhibiting activity
Preclinical animal models have yielded data indicating that systemic (oral or intraperitoneal) administration of cannabinoids effectively decreases tumour growth
Combinations of cannabinoids with classical chemotherapeutic drugs such as the alkylating agent temozolomide (the benchmark agent for the management of glioblastoma80,84) have been shown to produce a strong anticancer action in animal models
pharmacologic inhibition of egfr, erk83, or akt enhances the cell-death-promoting action of thc in glioma cultures (unpublished observations by the authors), which suggests that targeting egfr and the akt and erk pathways could enhance the antitumour effect of cannabinoids
Aside from THC, C. sativa produces approximately 70 other cannabinoids, although, unlike THC, many of them exhibit little affinity for CB receptors (10, 20). Of interest, at least one of these components, namely, cannabinol (CBD; Supplementary Fig. 1), has been shown to reduce the growth of different types of tumor xenografts including gliomas
the combined administration of THC and CBD is being therapeutically explored (10, 20, 26), although its effects on the proliferation and survival of cancer cells have only been analyzed in vitro
Nathan healthy skin Growing up is something, everybody. You go through а lot of chаnges in your selection preference in clothes, of music, аnd so on аs you get older. However, your body undergoes а rаnge of chаnges thаt require the greаtest аmount of cаre аnd аttention. This is becаuse аt the stаrt of puberty, usuаlly between sixteen
mean serum testosterone concentrations were found to be lower in men with GG than in those with TT genotype for rs12150660
men with the CT genotype for rs6258 had lower serum testosterone concentrations than those with CC genotype.
The two autosomal SNPs identified by GWAS had a significant influence on the risk of having low serum testosterone (serum testosterone <300 ng/dl) in both the discovery and the replication cohorts with a combined odds ratio (OR) per minor allele of 0.72 (95% CI, 0.65 – 0.79) and 2.7 (95% CI, 2.1 – 3.5) for rs12150660 and rs6258, respectively
The risk of having low serum testosterone concentrations increased by the number of risk alleles with an OR of 1.62 (95% CI, 1.41 – 1.86) for each risk allele (Figure S4). Low serum testosterone concentrations were 6.5-times more prevalent in men with ≥3 risk alleles (30.1% prevalence of low serum testosterone) compared to men without any risk allele (4.6% prevalence of low serum testosterone;
SNP rs5934505 was associated with serum testosterone without SHBG-adjustment (combined p-value of 1.7×10−9) and with free testosterone (combined p-value of 6.7×10−15), but not with SHBG
The mean serum testosterone and calculated free testosterone but not SHBG concentrations were lower in men with T genotype than in those with C genotype for rs5934505
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
Axiva Hydrophobic Edge CN Membrane Filters are used for sterility testing of antibiotics and drugs containing bacteria-stats. The hydrophobic edge does not allow the drug to seep under the rim of filter holder.
In most cancers, oncogenic driver mutations such as activation of K-ras, c-Myc and phosphatidylinositol-3 (PI3) kinase or loss of phosphatase and tensin homolog (Pten) and p53, not mutations that inactivate mitochondrial respiration complexes, promote glycolysis