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Fast Lean Pro is a natural powder supplement for weight loss that has recently been developed by Japanese scientists.
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What Is Fast Lean Pro?
Fast Lean Pro is a powdered dietary powdery supplement designed to aid in weight loss. It contains a unique combination of ingredients that are believed to activate the body's "fasting switch" to optimize results. This product focuses not only on weight loss but also on promoting cellular rejuvenation, fasting, and a healthy metabolism. The concept behind Fast Lean Pro is that incorporating fasting into one's lifestyle can lead to positive outcomes irrespective of individual food choices and eating habits. To comprehend the mechanism of the Fast Lean Pro process, it is necessary to delve into its specific details.
One of the few weight loss pills on the market that contains Fibersol is Fast Lean Pro. This safe, specialized fiber adds bulk to its weight when combined with water, curbing your appetite before it throws off your meal plan. If you're trying to lose weight or curb your appetite, Fast Lean Pro can help. Supporting substances such as niacin and chromium contribute to this.
The body can further benefit from these nutrients, such as through improved metabolic regulation. Fast lean Pro is non-GMO, vegan friendly, and contains no artificial ingredients or stimulants.
Fast Lean Pro is a weight loss product that promotes the body's natural self-feeding process. The body naturally removes old, damaged cells through a process known as autophagy to encourage cell regeneration and repair. Recent studies by a group
Progesterone has a neuroprotective and promyelinating effects in the nervous system. Progesterone increases BDNF. Progesterone increases proliferation and differentiation of oligodendrocyte progenitor cells which will increase myelin production.
both obesity and low testosterone are linked with promotion of inflammatory pathways [70–72] and exert harmful actions on the central [73–75] and peripheral [29,76] nervous systems
In general, obesity-related changes were worsened by low testosterone and improved by testosterone treatment; however, this relationship was not statistically significant in several instances. Further, our data suggest that a common pathway that may contribute to obesity and testosterone effects is regulation of inflammation
fasting blood glucose levels were independently and additively increased by GDX-induced testosterone depletion and high-fat diet
testosterone treatment significantly reduced fasting glucose under both the normal and high-fat diets, demonstrating potential therapeutic efficacy of testosterone supplementation
fasting insulin, insulin resistance (HOMA index), and glucose tolerance, low testosterone tended to exacerbate and or testosterone treatment improved outcomes.
testosterone status did not significantly affect body weight
testosterone’s effects likely do not indicate an indirect result on adiposity but rather regulatory action(s) on other aspects of metabolic homeostasis
Prior work in rodents has shown diet-induced obesity induces insulin resistance in rat brain [63] and that testosterone replacement improves insulin sensitivity in obese rats [64]. Our findings are consistent with the human literature, which indicates that (i) testosterone levels are inversely correlated to insulin resistance and T2D in healthy [30,65] as well as obese men [66], and (ii) androgen therapy can improve some metabolic measures in overweight men with low testosterone
it has been shown that TNFα has inhibitory effects on neuron survival, differentiation, and neurite outgrowth
Our data demonstrate that low testosterone and obesity independently increased cerebrocortical mRNA levels of both TNFα and IL-1β
Testosterone status also affected metabolic and neural measures
many beneficial effects of testosterone, including inhibition of proinflammatory cytokine expression
neuroprotection [80,81], are dependent upon androgen receptors, the observed effects of testosterone in this study may involve androgen receptor activation
testosterone can be converted by the enzyme aromatase into estradiol, which is also known to exert anti-inflammatory [82] and neuroprotective [83] actions
glia are the primary sources of proinflammatory molecules in the CNS
poorer survival of neurons grown on glia from mice maintained on high-fat diet
Since testosterone can affect glial function [86] and improve neuronal growth and survival [87–89], it was unexpected that testosterone status exhibited rather modest effects on neural health indices with the only significant response being an increase in survival in the testosterone-treated, high-fat diet group
significantly increased expression of TNFα and IL-1β in glia cultures derived from obese mice
testosterone treatment significantly lowered TNFα and IL-1β expression to near basal levels even in obese mice, indicating a protective benefit of testosterone across diet conditions
IL-1β treatment has been shown to induce synapse loss and inhibit differentiation of neurons
Testosterone status and diet-induced obesity were associated with significant regulation of macrophage infiltration
testosterone prevented and/or restored thermal nociception in both diet groups
a possible mechanism by which obesity and testosterone levels may affect the health of both CNS and PNS
Study points to obesity and low Testosterone contribution of neuroinflammation. No effect of body weight was seen with TRT. This animal model found similar positive effects of TRT in insulin sensitivity. Obesity and low T increase inflammatory cytokine production: this study found an increase in TNF-alpha and IL-1beta and TRT reduced TNF-alpha and IL-1beta to near base-line. Testosterone is neuroprotective and this study reviewed the small volume of evaded that pointed to benefit from estradiol. Testosterone's effect on glial survival was positive but not significant. Obesity and low T were found to be associated with increased macrophage infiltration in the PNS with increased TNF-alpha and IL-1beta. Testosterone therapy improved peripheral neuropathy via its positive effects on nocicieption.
The SMART Spine Institute & Surgery Center gives you Acupuncture Massage therapy; our doctor monitors the blood flowing through blood vessels and the messages traveling via the nervous system.
A number of the
catabolites produced along this pathway show neurotoxic or neuroprotective activities, and their role in the generation of
central nervous system inflammation is well documented.
Mechanistic studies further showed that such metabolic inflammation is related to the induction of various intracellular stresses such as mitochondrial oxidative stress, endoplasmic reticulum (ER) stress, and autophagy defect under prolonged nutritional excess
intracellular stress-inflammation process for metabolic syndrome has been established in the central nervous system (CNS) and particularly in the hypothalamus
the CNS and the comprised hypothalamus are known to govern various metabolic activities of the body including appetite control, energy expenditure, carbohydrate and lipid metabolism, and blood pressure homeostasis
Reactive oxygen species (ROS) refer to a class of radical or non-radical oxygen-containing molecules that have high oxidative reactivity with lipids, proteins, and nucleic acids
a large measure of intracellular ROS comes from the leakage of mitochondrial electron transport chain (ETC)
Another major source of intracellular ROS is the intentional generation of superoxides by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase
there are other ROS-producing enzymes such as cyclooxygenases, lipoxygenases, xanthine oxidase, and cytochrome p450 enzymes, which are involved with specific metabolic processes
To counteract the toxic effects of molecular oxidation by ROS, cells are equipped with a battery of antioxidant enzymes such as superoxide dismutases, catalase, peroxiredoxins, sulfiredoxin, and aldehyde dehydrogenases
intracellular oxidative stress has been indicated to contribute to metabolic syndrome and related diseases, including T2D [72; 73], CVDs [74-76], neurodegenerative diseases [69; 77-80], and cancers
intracellular oxidative stress is highly associated with the development of neurodegenerative diseases [69] and brain aging
dietary obesity was found to induce NADPH oxidase-associated oxidative stress in rat brain
mitochondrial dysfunction in hypothalamic proopiomelanocortin (POMC) neurons causes central glucose sensing impairment
Endoplasmic reticulum (ER) is the cellular organelle responsible for protein synthesis, maturation, and trafficking to secretory pathways
unfolded protein response (UPR) machinery
ER stress has been associated to obesity, insulin resistance, T2D, CVDs, cancers, and neurodegenerative diseases
brain ER stress underlies neurodegenerative diseases
under environmental stress such as nutrient deprivation or hypoxia, autophagy is strongly induced to breakdown macromolecules into reusable amino acids and fatty acids for survival
intact autophagy function is required for the hypothalamus to properly control metabolic and energy homeostasis, while hypothalamic autophagy defect leads to the development of metabolic syndrome such as obesity and insulin resistance
prolonged oxidative stress or ER stress has been shown to impair autophagy function in disease milieu of cancer or aging
TLRs are an important class of membrane-bound pattern recognition receptors in classical innate immune defense
Most hypothalamic cell types including neurons and glia cells express TLRs
overnutrition constitutes an environmental stimulus that can activate TLR pathways to mediate the development of metabolic syndrome related disorders such as obesity, insulin resistance, T2D, and atherosclerotic CVDs
Isoforms TLR1, 2, 4, and 6 may be particularly pertinent to pathogenic signaling induced by lipid overnutrition
hypothalamic TLR4 and downstream inflammatory signaling are activated in response to central lipid excess via direct intra-brain lipid administration or HFD-feeding
overnutrition-induced metabolic derangements such as central leptin resistance, systemic insulin resistance, and weight gain
these evidences based on brain TLR signaling further support the notion that CNS is the primary site for overnutrition to cause the development of metabolic syndrome.
circulating cytokines can limitedly travel to the hypothalamus through the leaky blood-brain barrier around the mediobasal hypothalamus to activate hypothalamic cytokine receptors
significant evidences have been recently documented demonstrating the role of cytokine receptor pathways in the development of metabolic syndrome components
entral administration of TNF-α at low doses faithfully replicated the effects of central metabolic inflammation in enhancing eating, decreasing energy expenditure [158;159], and causing obesity-related hypertension
Resistin, an adipocyte-derived proinflammatory cytokine, has been found to promote hepatic insulin resistance through its central actions
both TLR pathways and cytokine receptor pathways are involved in central inflammatory mechanism of metabolic syndrome and related diseases.
In quiescent state, NF-κB resides in the cytoplasm in an inactive form due to inhibitory binding by IκBα protein
IKKβ activation via receptor-mediated pathway, leading to IκBα phosphorylation and degradation and subsequent release of NF-κB activity
Research in the past decade has found that activation of IKKβ/NF-κB proinflammatory pathway in metabolic tissues is a prominent feature of various metabolic disorders related to overnutrition
it happens in metabolic tissues, it is mainly associated with overnutrition-induced metabolic derangements, and most importantly, it is relatively low-grade and chronic
this paradigm of IKKβ/NF-κB-mediated metabolic inflammation has been identified in the CNS – particularly the comprised hypothalamus, which primarily accounts for to the development of overnutrition-induced metabolic syndrome and related disorders such as obesity, insulin resistance, T2D, and obesity-related hypertension
evidences have pointed to intracellular oxidative stress and mitochondrial dysfunction as upstream events that mediate hypothalamic NF-κB activation in a receptor-independent manner under overnutrition
In the context of metabolic syndrome, oxidative stress-related NF-κB activation in metabolic tissues or vascular systems has been implicated in a broad range of metabolic syndrome-related diseases, such as diabetes, atherosclerosis, cardiac infarct, stroke, cancer, and aging
intracellular oxidative stress seems to be a likely pathogenic link that bridges overnutrition with NF-κB activation leading to central metabolic dysregulation
overnutrition is an environmental inducer for intracellular oxidative stress regardless of tissues involved
excessive nutrients, when transported into cells, directly increase mitochondrial oxidative workload, which causes increased production of ROS by mitochondrial ETC
oxidative stress has been shown to activate NF-κB pathway in neurons or glial cells in several types of metabolic syndrome-related neural diseases, such as stroke [185], neurodegenerative diseases [186-188], and brain aging
central nutrient excess (e.g., glucose or lipids) has been shown to activate NF-κB in the hypothalamus [34-37] to account for overnutrition-induced central metabolic dysregulations
overnutrition can present the cell with a metabolic overload that exceeds the physiological adaptive range of UPR, resulting in the development of ER stress and systemic metabolic disorders
chronic ER stress in peripheral metabolic tissues such as adipocytes, liver, muscle, and pancreatic cells is a salient feature of overnutrition-related diseases
recent literature supports a model that brain ER stress and NF-κB activation reciprocally promote each other in the development of central metabolic dysregulations
when intracellular stresses remain unresolved, prolonged autophagy upregulation progresses into autophagy defect
autophagy defect can induce NF-κB-mediated inflammation in association with the development of cancer or inflammatory diseases (e.g., Crohn's disease)
The connection between autophagy defect and proinflammatory activation of NF-κB pathway can also be inferred in metabolic syndrome, since both autophagy defect [126-133;200] and NF-κB activation [20-33] are implicated in the development of overnutrition-related metabolic diseases
Both TLR pathway and cytokine receptor pathways are closely related to IKKβ/NF-κB signaling in the central pathogenesis of metabolic syndrome
Overnutrition, especially in the form of HFD feeding, was shown to activate TLR4 signaling and downstream IKKβ/NF-κB pathway
TLR4 activation leads to MyD88-dependent NF-κB activation in early phase and MyD88-indepdnent MAPK/JNK pathway in late phase
these studies point to NF-κB as an immediate signaling effector for TLR4 activation in central inflammatory response
TLR4 activation has been shown to induce intracellular ER stress to indirectly cause metabolic inflammation in the hypothalamus
central TLR4-NF-κB pathway may represent one of the early receptor-mediated events in overnutrition-induced central inflammation.
cytokines and their receptors are both upstream activating components and downstream transcriptional targets of NF-κB activation
central administration of TNF-α at low dose can mimic the effect of obesity-related inflammatory milieu to activate IKKβ/NF-κB proinflammatory pathways, furthering the development of overeating, energy expenditure decrease, and weight gain
the physiological effects of IKKβ/NF-κB activation seem to be cell type-dependent, i.e., IKKβ/NF-κB activation in hypothalamic agouti-related protein (AGRP) neurons primarily leads to the development of energy imbalance and obesity [34]; while in hypothalamic POMC neurons, it primarily results in the development of hypertension and glucose intolerance
the hypothalamus, is the central regulator of energy and body weight balance [
crucial role of the RAS in the development and maintenance of cancer
kidneys, which produce renin in response to decreased arterial pressure, reduced sodium in the distal tubule, or sympathetic nervous system activity via the β-adrenergic receptors
Renin is secreted from the juxtaglomerular cells into the bloodstream where it encounters angiotensinogen (AGN), normally produced by the liver
Renin catalyses the conversion of AGN to angiotensin I (ATI), which is quickly cleaved by angiotensin converting enzyme (ACE) to form angiotensin II (ATII)
ATII triggers the release of aldosterone from the adrenal glands, which stimulates reabsorption of sodium and water and thereby increases blood volume and blood pressure
ATII also acts on smooth muscle to cause vasoconstriction of the arterioles
ATII promotes the release of antidiuretic hormone from the posterior pituitary gland, which results in water retention and triggers the thirst reflex
ability of non-CSCs to ‘de-differentiate’ into CSCs due to epigenetic or environmental factors, which further increases the complexity of tumour biology and treatment
efficacy of RAS modulators on cancer in both cancer models and cancer patients
A localised (‘paracrine’) RAS mechanism has been identified in many types of cancers, and interruption of the control of the RAS is thought to be the basis for its role in cancer
Components of the RAS are expressed by these CSCs, supporting the hypothesis of the presence of a ‘paracrine RAS’ in regulating these CSCs
Renin is an enzyme normally released by the kidneys in response to falling arterial pressure
a study of GBM demonstrating overexpression of PRR coupled with the observation that inhibition of renin reduces cellular proliferation and promotes apoptosis
PRR has been found to be vital for normal Wnt signalling
A major focus of PRR research is its relationship with Wnt signalling
suggest a crucial role for PRR activation on the proliferation of CSCs, possibly via Wnt/β-catenin signalling, leading to carcinogenesis.
Angiotensin converting enzyme (ACE), also known as CD143, is the endothelial-bound peptidase which physiologically converts ATI to ATII
ACE is crucial in the regulation of blood pressure, angiogenesis and inflammation
results suggest that an overactive ACE promotes cancer growth and progression, and an inhibited or low-activity ACE may have cancer-protective effects
When bound to ATII or ATIII it causes vasoconstriction by stimulating the release of vasopressin, reabsorption of water and sodium by promoting secretion of aldosterone and insulin, fibrosis, cellular growth and migration, pro-inflammation, glucose release from the liver, increased plasma triglyceride concentration, and reduced gluconeogenesis
ATIIR1 is a G-protein-coupled receptor, with downstream signalling involved in vasodilation, hypertrophy and NF-κB activation leading to TNF-α and PAI-1 expression
ATIIR1 has well-documented links with cancer, with one study demonstrating its overexpression in ~20% of breast cancer patients
the effect of RAS dysregulation has been associated with increased VEGF expression and angiogenesis in cancers
In ovarian and cervical cancer, ATIIR1 overexpression has been shown to be an indicator of tumour invasiveness
administration of ATIIR1 blockers (ARBs) have been associated with reduced tumour size, reduction in tumour vascularisation, lower occurrence of metastases, and lower VEGF levels
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
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
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
two major cannabinoid-specific receptors—cb1 and cb2
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
young children have a different set of needs than adults. Aesthetically, devices designed for kids are often sleek and colorful, and functionally, they are typically lightweight and adjustable. As any parent knows, young people don't stay the same size for long and since a wheelchair is a major purchase -- don't want a simple growth spurt to render it useless. Wheelchair category offers models that feature seat width and depth adjustability, elevating legrests, and other versatile features. As a weight-bearing activity is critical to proper physical and mental function-which is why children with cerebral palsy, who may sit for stretches in a wheelchair and typically are unable to stand on their own, can benefit greatly from pediatric standers as part of a comprehensive pediatric rehabilitation program. Pediatric standers are offered in passive, active and mobile formats: Passive standers stay in one place and feature a support surface, active standers allow reciprocal movement of the extremities while in a standing position, and mobile standers enable users to self-propel.
Cerebral Palsy Wheelchair:
Cerebral Palsy Wheelchair Description:
The model designed for cerebral palsy child only.
Ultra light weight aluminium alloy frame.
Seat Width 38 cms (15").
Net Weight: 18.5 kgs.
Epoxy powder coated frame.
Detachable arm rest & foot rest provided.
Elevated and swinging foot rest.
Elevated foot rest provided to elevate leg angle.
Height adjustable and detachable head rest.
Hydraulic reclining high back for a comfortable posture.
Hydraulic adjustable seat angle.
Detachable back and seat pad.
Extra cushion upholstery provided to under arm, head & calg Foldable.
Lever and paddle brakes provided.
Safety belt provided.
Maintenance free rear solid wheels.
Cloth look like water proof upholstery.
Anti wheels for better safety and stability.
Extra cushion upholstery provided to under arm, head & leg.
Folding action.
Lever and paddle brakes provide
Cerebral palsy (CP) is a group of conditions caused by medical abnormalities in the development of a fetus or the early life of a child. These lead to damage or delayed development in the brain. The disorder is permanent and, though it does not worsen with age, the level of functionality of a person with cerebral palsy varies widely: in some cases, effects may be very minor, while in others, movement is impaired to the extent that a wheelchair is required. Common complications associated with CP vary by the type of CP disorder but can include vision problems, seizures, learning disabilities, and issues speaking, writing, and performing other tasks. Cerebral palsy causes problems with muscle tone, movement, balance and/or coordination. Symptoms and effects range from mild to severe. In some infants, problems are evident soon after birth. In others, diagnosis comes in later infancy or toddlerhood.
Cerebral Palsy Wheelchair Description:
The model designed for cerebral palsy child only.
Ultra light weight aluminium alloy frame.
Seat Width 38 cms (15").
Net Weight: 18.5 kgs.
Epoxy powder coated frame.
Detachable arm rest & foot rest provided.
Elevated and swinging foot rest.
Elevated foot rest provided to elevate leg angle.
Height adjustable and detachable head rest.
Hydraulic reclining high back for a comfortable posture.
Hydraulic adjustable seat angle.
Detachable back and seat pad.
Extra cushion upholstery provided to under arm, head & calg Foldable.
Lever and paddle brakes provided.
Safety belt provided.
Maintenance free rear solid wheels.
Cloth look like water proof upholstery.
Anti wheels for better safety and stability.
Extra cushion upholstery provided to under arm, head & leg Folding action.
Lever and paddle brakes provided.
Safety belt provided.
Maintenance free rear solid wheels.
Cerebral Palsy Wheelchair Recline system:
Recline system provides kids with the most comfortable resting environment.
It also allows stretching abdomin
High dose vitamin E, in doses up to 2,000 IU, in patients with Parkinson, Alzheimers and tar dive dyskinesia found to be safe and somewhat effective in these disease states in older individuals. The length of the studies reviewed were up to 2 years.