When it comes to wheelchairs, 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. That's why kids wheelchair category offers models that feature seat width and depth adjustability, elevating legrests, and other versatile features.
Pediatric walkers differ from adult walkers in several ways. For one, walking aids for children are usually adjustable, taking growth patterns into account; but many models also provide gait training and postural correction. Those caring for kids in their formative years must be concerned about more than just the young person's mobility, they must also consider their development.
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 provided
Safety belt provided
Maintenance free rear solid wheels
Cerebral Palsy Wheelchair Recline system:
Recline system provides kids with the most comfortable resting environme
both 2- and 4-catechol estrogen metabolites bind to the ER with affinities comparable
with estradiol, 4-catechol estrogen metabolites have lower dissociation rates than estradiol and an enhanced ability to upregulate
ER-dependent processes
2-catechol estrogen metabolites act as either weak mitogens (39) or weak inhibitors of cell proliferation
While 16α-hydroxyestrone binds to the ER with lower affinity than estradiol, it binds covalently (41) and leads to a constitutively activated ER
4-hydroxyestradiol
and 16α-hydroxyestrone increasing proliferation and decreasing apoptosis in a manner similar to estradiol; however, these
effects were achieved only at concentrations 10-fold higher than estradiol (39). In contrast, 2-hydroxyestradiol did not have substantial proliferative or antiapoptotic effects
In our study, the associations with both 2-hydroxyestrone and 16α-hydroxyestrone were nonsignificantly inverse and
we did not observe a consistent trend or significant associations between the 2-hydroxyestrone:16α-hydroxyestrone ratio and
breast cancer risk
Ratios of the 3 hydroxylation pathways
were not significantly associated with risk although the 2:16-pathway and 4:16-pathway ratios were suggestively inversely
associated
a significant inverse association with the ratio of parent estrogens to estrogen metabolites
several potentially estrogenic and genotoxic mechanisms
Estrogen metabolites also can be genotoxic
Catechol estrogens can be oxidized into quinones and induce DNA damage directly through the formation of DNA adducts, or indirectly
via redox cycling and generation of reactive oxygen species
the oxidized forms of the catechol estrogens differ in their ability to damage DNA through adducts, with oxidized
2-catechols forming stable and reversible DNA adducts and oxidized 4-catechols forming unstable adducts, which lead to depurination
and mutations
2- and 4-catechols have been shown to produce reactive oxygen species and induce oxidative
DNA damage
act independently from the ER
16α-Hydroxyestrone also may be genotoxic
While the catechol estrogens have estrogenic and genotoxic potential, the methylated catechol estrogens, which are catechol
estrogens with one hydroxyl group methylated, have been hypothesized to lower the risk of breast cancer
The suggested mechanisms
are indirect, by decreasing circulating levels of catechol estrogens and thereby the opportunity for catechols to exert genotoxic
or proliferative effects, or direct, by inhibiting tumor growth and inducing apoptosis
the balance between phase I (oxidation) and phase II (methylation) metabolism of estrogen may be important in hormonally
related cancer development.
Despite the estrogenic and genotoxic potential of many of the estrogen metabolites, we only observed a significantly increased
breast cancer risk with one estrogen metabolite, 17-epiestriol, which has particularly strong estrogenic activity and binds
to both ERα and ERβ with an affinity comparable with estradiol
Inflammatory processes are now recognized to play a central role in the pathogenesis of atherosclerosis and its complications. Plasma levels of several markers of inflammation have been found to be associated with future cardiovascular risk in a variety of clinical settings.
glutamate antagonists or agents that improve energy metabolism may slow the degenerative process and offer a therapeutic approach for temporarily retarding the progression of these disabling disorders.
High serum rT3 may result from a decreased peripheral metabolism of thyroid hormones due to the aging process itself and/or disease and may reflect a catabolic state.
The NAD+-dependent protein deacetylase family, Sir2 (or sirtuins), is important for many cellular processes including gene silencing,
regulation of p53, fatty acid metabolism, cell cycle regulation, and life span extension
resveratrol was shown to increase life span in three model organisms through a Sir2-dependent pathway.
hypothalamic AMP-activated protein kinase plays a key role in regulating these processes. Leptin, insulin, glucose and alpha-lipoic acid have been shown to reduce food intake by lowering hypothalamic AMP-activated protein kinase activity,
in addition to the type of diet being a modulator of microbiota composition, the timing of food intake plays a critical role in shaping intestinal microbial ecology.
the microbiota rhythms are influenced by the host clock and perform critical functions in the adaptation of metabolic processes to the diurnal fluctuations in the environment
Our study reveals that dysbiosis has a temporal dimension and that static microbiota comparisons might not be fully conclusive unless samples were taken in a controlled manner with respect to this important additional variable
This is a really nice study. Altered sleep-wake cycles result in altered food consumption which leads to altered gut microbiota diurnal oscillations. Gut microbiota have a normal diurnal oscillation. This altered gut flora then leads to increase insulin resistance, metabolic syndrome, diabetes...
In a cohort of well-trained athletes, we demonstrated that intense endurance exercise causes an acute reduction in RV function that increases with race duration and correlates with increases in biomarkers of myocardial injury
no relationship between LV function and biomarker levels
focal gadolinium enhancement and increased RV remodelling were more prevalent in those athletes with a longer history of competitive sport, suggesting that repetitive ultra-endurance exercise may lead to more extensive RV change and possible myocardial fibrosis
he cardiac impact of both acute and cumulative exercise is greatest on the RV.
Greater reductions in RV function occurred in those athletes competing for a longer duration, suggesting that the heart has a finite capacity to maintain the increased work demands of exercise
cardiac injury is greatest in the least trained
Previous investigators have documented reductions in RV function in less trained subjects over the marathon distance
We enrolled elite and subelite athletes and found a significant association between fitness (VO2max) and the reduction in post-race RVEF
Even after many years of detraining, cardiac dilation may not completely regress in elite athletes
The focus on well-trained athletes may be of particular relevance, given that they perform exercise of highest intensity and duration most frequently, and, thus, may be at a greater risk of cumulative injury.
The lack of correlation between increases in troponin and changes in LV function seen in this study has been previously interpreted as evidence that post-exercise elevations in cardiac biomarkers are benign.
a significant correlation between changes in RVEF and post-race biomarker levels and this relationship was even stronger in the athletes who completed the race of longest duration, the ultra-triathlon
The correlations with RVEF, but not LVEF, provide further evidence of the differential effects of intense exercise on RV and LV function
BNP release during intense exercise is associated with greater relative increases in RV systolic pressures, but not LV pressures
BNP may provide a measure of both acute RV load and the resultant fatigue which occurs when this load is sustained
It has been demonstrated that ventricular load increases with exercise intensity and is greater for the RV than the LV,29 thus potentially explaining why the RV is more susceptible to fatigue after prolonged exercise.
This study demonstrates, for the first time, an association between endurance exercise of increasing duration and structural, functional, and biochemical markers of cardiac dysfunction in highly trained athletes
Functional abnormalities were confined to the RV and were largely reversible 1 week following the event
there remained a significant minority of athletes in whom there was evidence of myocardial fibrosis in the interventricular septum
RV abnormalities may be acquired through cumulative bouts of intense exercise and provides direction for prospective investigations aimed at elucidating whether extreme exercise may promote arrhythmias in some athletes.
the acute injury and chronic remodelling of the myocardium both disproportionately affect the RV and it remains possible that the two are linked.
focal DGE was confined to the interventricular septum and commonly at the site of RV attachment
emerging evidence that intense endurance exercise may be associated with an excess in arrhythmic disorders, the mechanisms for which remain unexplained
RVEF (and not LVEF) was reduced in athletes with complex ventricular arrhythmias when compared with healthy athletes and non-athletes without arrhythmias
it is premature to conclude that these changes may represent a proarrhythmic substrate
Study finds endurance racing results in reduce Right ventricle ejection fraction even in elite athletes. This post-race RVEF reduction is associated with VO2max.
It is estimated that approximately 30% of children and adolescents in the United States and about 15–30% of those in Europe can be classified as overweight or obese
An increasing body of evidence now suggests that the nutritional environment encountered in utero and the early postnatal life may elicit permanent alterations in adipose tissue structure or function and, thereby, programme the individual’s propensity to later obesity
The composition of fatty acids in the Western diets has shifted toward an increasing dominance of n-6 relative to n-3 LCPUFAs over the past decades.9,10 This shift is also reflected in the fatty acid composition of breast milk
Evidence from animal studies suggests that the n-6 LCPUFA arachidonic acid promotes adipose tissue deposition, whereas the n-3 LCPUFAs eicosapentaenoic acid and docosahexaenoic acid seem to exert an opposite effect
Overall, no effect of supplementation was found on BMI in preschool (<5 years) and school-aged (6–12 years) children
increased adiposity, once established in childhood, tends to track into adulthood
Many studies have shown that even children <2 years with a high BMI are at increased risk of developing obesity later in life
The acquisition of fat cells early in life appears to be an irreversible process
Evidence from cell culture and animal studies suggests that early exposure to n-3 LCPUFAs has the potential to limit adipose tissue deposition mainly by attenuating the production of the arachidonic acid metabolite prostacyclin, which has been shown to enhance adipogenesis
In conclusion, there is currently no evidence to support that maternal n-3 LCPUFA supplementation during pregnancy and/or lactation exerts a favourable programming effect on adiposity status in childhood
our systematic review highlights that most of the trials reviewed were prone to methodological limitations
Literature review finds limited data (9 studies, only 6 RCTs) of omega-3 during pregnancy. No data was found that supported reduced obesity in children by mothers taking n-3 during pregnancy. No harm was found either. Data was sparse.
Take home: not enough data, no harm to pregnancy, children, thus if indications are present for mother, then recommend n-3. At this point not studies have pointed to reduced obesity in children.
increased levels of hydrogen peroxide in exhaled breath condensate from patients with localized breast malignancy, associated with increased clinical severity
Oxidative stress generated by breast cancer cells activates HIF-1α and NFκB in fibroblasts, leading to autophagy and lysosomal degradation of Cav-1
Comparing mitochondrial metabolic activity revealed a difference between stroma and epithelial cells
metalloproteinases (MMP) such as MMP-2, MMP-3, and MMP-9 increase extracellular matrix turnover and are themselves activated by oxidative stress
Overexpression of NOX4 in normal breast epithelial cells results in cellular senescence, resistance to apoptosis, and tumorigenic transformation, as well as increased aggressiveness of breast cancer cells
Lowered expression of Cav-1 not only leads to myofibroblast conversion and inflammation but also seems to impact aerobic glycolysis, leading to secretion of high energy metabolites such as pyruvate and lactate that drive mitochondrial oxidative phosphorylation in cancer cells
Reverse Warburg Effect
secreted transforming growth factor β (TGFβ), insulin-like growth factor (IGF), platelet-derived growth factor (PDGF), fibroblast growth factor 2, and stromal-derived factor 1 (SDF1) are able to activate fibroblasts and increase cancer cell proliferation
oxidative stress has an important role in the initiation and preservation of breast cancer progression
cancer preventive role of healthy mitochondria
the cancer cells produce hydrogen peroxide and by driving the “Reverse Warburg Effect” initiate oxidative stress in fibroblasts. As a result of this process, fibroblasts exhibited reduced mitochondrial activity, increased glucose uptake, ROS, and metabolite production.
Oxidative stress results from an imbalance between unstable reactive species lacking one or more unpaired electrons (superoxide anion, hydrogen peroxide, hydroxyl radical, reactive nitrogen species) and antioxidants
cancer cells are able to induce drivers of oxidative stress, autophagy and mitophagy: HIF-1α and NFκB in surrounding stroma fibro-blasts
Studies show that loss of Cav-1 in adjacent breast cancer stroma fibroblasts can be prevented by treatment with N-acetyl cysteine, quercetin, or metformin
However, diets rich in antioxidants have fallen short in sufficiently preventing cancer
obstructing oxidative stress in the tumor microenvironment can lead to mitophagy and promote breast cancer shutdown is a promising discovery for the development of future therapeutic interventions.
It is widely held that HIF-1α function is dependent upon its location within the tumor microenvironment. It acts as a tumor promoter in CAFs and as a tumor suppressor in cancer cells
It was reported that overexpression of recombinant (SOD2) (Trimmer et al., 2011) or injection of SOD, catalase, or their pegylated counterparts can block recurrence and metastasis in mice
hydrogen peroxide is one of the main factors that can push fibroblasts and cancer cells into senescence
Recent studies show that in the breast cancer microenvironment, oxidative stress causes mitochondrial dysfunction
Really fascinating article on tumor signaling. The article points to a complex signaling between cancer cells and stromal fibroblasts that results in myofibroblast transformation that increases the microenvironment favorability of cancer. This article points to oxidative stress as the primary driving force.
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.
mechanical tension, muscle damage and metabolic stress are the three primary factors that promote hypertrophy from exercise
The mechanical tension is directly related to intensity of the exercise, which is the key to stimulating muscle growth
Muscle damage, that leads to muscle soreness, from exercise training initiates an inflammatory response, which activates satellite cells growth processes
metabolic stress that is a result of the byproducts of anaerobic metabolism (i.e., hydrogen ions, lactate, inorganic phosphates) is now also believed to promote hormonal factors leading to muscle hypertrophy
The upper extremities tend to show more growth earlier then the lower body
Maximal growth occurs with loads between 80-95% of 1 repetition maximum
weightlifters and powerlifters show more favorable hypertrophy of type II (fast twitch) muscle fibers
body builders appear to have comparable hypertrophy in both the type I (slow twitch) and type II muscle fibers
Multi-joint exercises have been shown to produce larger increases of anabolic hormones than single-joint exercises
Review of the physiology of muscle building. The authors review the evidence behind the types of muscle building exercises and the physiology responsible for muscle hypertrophy. The authors point to Schoenfeld's description of mechanical tension, muscle damage, and metabolic stress to build muscle.
Long-chain polyunsaturated fatty acids, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are highly enriched in neuronal synaptosomal plasma membranes and vesicles
The predominant CNS polyunsaturated fatty acid is DHA
effective supplementation and/or increased ingestion of dietary sources rich in EPA and DHA, such as cold-water fish species and fish oil, may help improve a multitude of neuronal functions, including long-term potentiation and cognition.
multiple preclinical studies have suggested that DHA and/or EPA supplementation may have potential benefit through a multitude of diverse, but complementary mechanisms
pre-injury dietary supplementation with fish oil effectively reduces post-traumatic elevations in protein oxidation
The benefits of pre-traumatic DHA supplementation have not only been independently confirmed,[150] but DHA supplementation has been shown to significantly reduce the number of swollen, disconnected and injured axons when administered following traumatic brain injury.
DHA has provided neuroprotection in experimental models of both focal and diffuse traumatic brain injury
potential mechanisms of neuroprotection, in addition to DHA and EPA's well-established anti-oxidant and anti-inflammatory properties
Despite abundant laboratory evidence supporting its neuroprotective effects in experimental models, the role of dietary DHA and/or EPA supplementation in human neurological diseases remains uncertain
Several population-based, observational studies have suggested that increased dietary fish and/or omega-3 polyunsaturated fatty acid consumption may reduce risk for ischemic stroke in several populations
Randomized control trials have also demonstrated significant reductions in ischemic stroke recurrence,[217] relative risk for ischemic stroke,[2] and reduced incidence of both symptomatic vasospasm and mortality following subarachnoid hemorrhage
Clinical trials in Alzheimer's disease have also been largely ineffective
The clinical evidence thus far appears equivocal
curcumin has gained much attention from Western researchers for its potential therapeutic benefits in large part due to its potent anti-oxidant[128,194,236] and anti-inflammatory properties
Curcumin is highly lipophilic and crosses the blood-brain barrier enabling it to exert a multitude of different established neuroprotective effects
in the context of TBI, a series of preclinical studies have suggested that pre-traumatic and post-traumatic curcumin supplementation may bolster the brain's resilience to injury and serve as a valuable therapeutic option
Curcumin may confer significant neuroprotection because of its ability to act on multiple deleterious post-traumatic, molecular cascades
studies demonstrated that both pre- and post-traumatic curcumin administration resulted in a significant reduction of neuroinflammation via inhibition of the pro-inflammatory molecules interleukin 1β and nuclear factor kappa B (NFκB)
no human studies have been conducted with respect to the effects of curcumin administration on the treatment of TBI, subarachnoid or intracranial hemorrhage, epilepsy or stroke
studies have demonstrated that resveratrol treatment reduces brain edema and lesion volume, as well as improves neurobehavioral functional performance following TBI
green tea consumption or supplementation with its derivatives may bolster cognitive function acutely and may slow cognitive decline
At least one population based study, though, did demonstrate that increased green tea consumption was associated with a reduced risk for Parkinson's disease independent of total caffeine intake
a randomized, placebo-controlled trial demonstrated that administration of green tea extract and L-theanine, over 16 weeks of treatment, improved indices of memory and brain theta wave activity on electroencephalography, suggesting greater cognitive alertness
Other animal studies have also demonstrated that theanine, another important component of green tea extract, exerts a multitude of neuroprotective benefits in experimental models of ischemic stroke,[63,97] Alzheimer's disease,[109] and Parkinson's disease
Theanine, like EGCG, contains multiple mechanisms of neuroprotective action including protection from excitotoxic injury[97] and inhibition of inflammation
potent anti-oxidant EGCG which is capable of crossing the blood-nerve and blood-brain barrier,
Epigallocatechin-3-gallate also displays neuroprotective properties
More recent research has suggested that vitamin D supplementation and the prevention of vitamin D deficiency may serve valuable roles in the treatment of TBI and may represents an important and necessary neuroprotective adjuvant for post-TBI progesterone therapy
Progesterone is one of the few agents to demonstrate significant reductions in mortality following TBI in human patients in preliminary trials
in vitro and in vivo studies have suggested that vitamin D supplementation with progesterone administration may significantly enhance neuroprotection
Vitamin D deficiency may increase inflammatory damage and behavioral impairment following experimental injury and attenuate the protective effects of post-traumatic progesterone treatment.[37]
emerging evidence has suggested that daily intravenous administration of vitamin E following TBI significantly decreases mortality and improves patient outcomes
high dose vitamin C administration following injury stabilized or reduced peri-lesional edema and infarction in the majority of patients receiving post-injury treatment
it has been speculated that combined vitamin C and E therapy may potentiate CNS anti-oxidation and act synergistically with regards to neuroprotection
one prospective human study has found that combined intake of vitamin C and E displays significant treatment interaction and reduces the risk of stroke
Pycnogenol has demonstrated the ability to slow or reduce the pathological processes associated with Alzheimer's disease
Pcynogenol administration, in a clinical study of elderly patients, led to improved cognition and reductions in markers of lipid peroxidase
One other point of consideration is that in neurodegenerative disease states like Alzheimer's disease and Parkinson's disease, where there are high levels of reactive oxygen species generation, vitamin E can tend to become oxidized itself. For maximal effectiveness and to maintain its anti-oxidant capacity, vitamin E must be given in conjunction with other anti-oxidants like vitamin C or flavonoids
These various factors might account for the null effects of alpha-tocopherol supplementation in patients with MCI and Alzheimer's disease
preliminary results obtained in a pediatric population have suggested that post-traumatic oral creatine administration (0.4 g/kg) given within four hours of traumatic brain injury and then daily thereafter, may improve both acute and long-term outcomes
Acutely, post-traumatic creatine administration seemed to reduce duration of post-traumatic amnesia, length of time spent in the intensive care unit, and duration of intubation
At three and six months post-injury, subjects in the creatine treatment group demonstrated improvement on indices of self care, communication abilities, locomotion, sociability, personality or behavior and cognitive function when compared to untreated controls
patients in the creatine-treatment group were less likely to experience headaches, dizziness and fatigue over six months of follow-up
CNS creatine is derived from both its local biosynthesis from the essential amino acids methionine, glycine and arginine
Studies of patients with CNS creatine deficiency and/or murine models with genetic ablation of creatine kinase have consistently demonstrated significant neurological impairment in the absence of proper creatine, phosphocreatine, or creatine kinase function; thus highlighting its functional importance
chronic dosing may partially reverse neurological impairments in human CNS creatine deficiency syndromes
Several studies have suggested that creatine supplementation may also reduce oxidative DNA damage and brain glutamate levels in Huntington disease patients
Another study highlighted that creatine supplementation marginally improved indices of mood and reduced the need for increased dopaminergic therapy in patients with Parkinson's disease
Tynor Knee Cap Open Patella
Knee Cap open patella is a compression tubular support used in orthopaedic practice to provide firm compression warmth & support to the limbs and joints, to allay pain and inflammation, generally associated with old age, arthritis, sports injury etc.
Silicon patellar insert
Four way stretch
Freely breathable
Soft and comfortable
Tynor Knee Cap Open Patella Features
Made from high quality nylon
Ensures longer life.
Appealing aesthetics
Offers color fastness.
Four-way stretch ability
Good grip and compression
Snug fitting
No bunching at the back.
Better comfort..
Special interlocking weave and single spiral elastic yarn , double layered
Uniform compression even on uneven limb surface.
Warmth improves healing.
Provides firm support and gentle compression.
Anterior patellar opening
Relieves patellar pressure.
Positions patella in patellar dislocations.
Silicon patellar padding
Propioception.
Massages, increases blood flow, quick healing.
Compresses and supports patellar tendon.