Dr Jennifer Martinick is a well known hair transplant surgeon who is credited for developing the advanced and outstanding hair transplant technology - The Martinick TechniqueTM.
Developed and perfected with over three decades of knowledge and expertise of renowned surgeon Dr Jennifer Martinick, the Martinick Technique™ is a patent technology. Along with this technique, the clinic follows a multi-therapy approach to ensure better and superior results for its patients.
Dr Jennifer Martinick is a renowned name in the hair transplant fraternity. With her hard work and dedication towards providing excellent hair transplant results, Dr Jennifer Martinick has developed a unique and superior technique for hair transplantation.
The Martinick Technique is developed and perfected by Dr Jennifer Martinick. This technique is globally recognised and proven to be superior than the earlier transplantation techniques used.
methylmercury mediates neurotoxicity via mitochondrial damage, inflammation, and oxidative stress. Astrocytes accumulated the methyl mercury. The destruction of the astrocytes will result in an increase in glutamate. Methylmercury is synergistic with other toxins in the development of immunoexcitotoxicity.
New study suggests that intra-uterine exposure effects prefrontal cortex development that leads to autism. This study was conducted of postmortem samples of children with autism ranging from 2 to 15. Intra-pregnancy exposure of what? That is the question. Environmental toxins: whether it is all the xenoestrogens (autism at rate of 5:1 in boys), PCBs, heavy metals, and yes (lead author) preservatives, metals (Al and thermeresol) in vaccines--particularly the flu vaccine which ACOG is almost mandating during pregnancy.
This study's conclusion is to evaluate clotting factor i.e. factor V leiden, Factor VIII, and prothrombin prior to giving Testosterone. This small study found increased clotting in some men on Testosterone. The problem here is the dosing of Testosterone in these men was 50-160 mg. Physiologic dosing is 5-10 mg. The problem is doping. One wonders if physiologic dosing was undertaken if any of the men in this study would develop clotting problems, even though they had undiagnosed hypercoagulabitliy.
Studies have shown pharmacological doses of testosterone to relax coronary arteries when injected intraluminally [39] and to produce modest but consistent improvement in exercise-induced angina and reverse associated ECG changes [40]. The mechanism of action is via blockade of calcium channels with effect of similar magnitude to nifedipine
Testosterone acts as a calcium channel blocker inducing vasodilation.
men with chronic stable angina pectoris, the ischaemic threshold increased after 4 weeks of TRT and a recent study demonstrates improvement continuing beyond 12 months [
Exercise capacity in men with chronic heart failure increased after 12 weeks
Studies have shown an inverse relationship between serum testosterone and fasting blood glucose and insulin levels
Medications such as chronic analgesics, anticonvulsants, 5ARIs, and androgen ablation therapy are associated with increased risk of testosterone deficiency and insulin resistance
Women with T2D or metabolic syndrome characteristically have low SHBG and high free testosterone
Hypogonadism is a common feature of the metabolic syndrome
The precise interaction between insulin resistance, visceral adiposity, and hypogonadism is, as yet, unclear but the important mechanisms are through increased aromatase production, raised leptin levels, and increase in inflammatory kinins
levels of testosterone are reduced in proportion to degree of obesity
Men should be encouraged to combine aerobic exercise with strength training. As muscle increases, glucose will be burned more efficiently and insulin levels will fall. A minimum of 30 minutes exercise three times weekly should be advised
Testosterone increases levels of fast-twitch muscle fibres
By increasing testosterone, levels of type 2 fibres increase and glucose burning improves
Weight loss will increase levels of testosterone
studies now clearly show that low testosterone leads to visceral obesity and metabolic syndrome and is also a consequence of obesity
In the case of MMAS [43], a baseline total testosterone of less than 10.4 nmol/L was associated with a greater than 4-fold incidence of type 2 diabetes over the next 9 years
There is high level evidence that TRT improves insulin resistance
Low testosterone predicts increased mortality and testosterone therapy improves survival in 587 men with type 2 diabetes
A similar retrospective US study involved 1031 men with 372 on TRT. The cumulative mortality was 21% in the untreated group versus 10% (
) in the treated group with the greatest effect in younger men and those with type 2 diabetes
the presence of ED has been shown to be an independent risk factor, particularly in hypogonadal men, increasing the risk of cardiac events by over 50%
A recent online publication on ischaemic heart disease mortality in men concluded optimal androgen levels are a biomarker for survival
inverse associations between low TT or FT (Table 2) and the severity of CAD
A recent 10 year study from Western Australia involving 3690 men followed up from 2001–2010 concluded that TT and FT levels in the normal range were associated with decreased all-cause and cardiovascular mortality, for the first time suggesting that both low and DHT are associated with all-cause mortality and higher levels of DHT reduced cardiovascular risk
TDS is associated with increased cardiovascular and all-cause mortality
The effect of treatment with TRT reduced the mortality rate of treated cohort (8.4%) to that of the eugonadal group whereas the mortality for the untreated remained high at 19.2%
hypogonadal men had slightly increased triglycerides and HDL
Men with angiographically proven CAD (coronary artery disease) have significantly lower testosterone levels [29] compared to controls (
) and there was a significant inverse relationship between the degree of CAD and TT (total testosterone) levels
TRT has also been shown to reduce fibrinogen to levels similar to fibrates
men treated with long acting testosterone showed highly significant reductions in TC, LDL, and triglycerides with increase in HDL, associated with significant reduction in weight, BMI, and visceral fat
Low androgen levels are associated with an increase in inflammatory markers
In the Moscow study, C-reactive protein was reduced by TRT at 30 weeks versus placebo
In some studies, a decline in diastolic blood pressure has been observed, after 3–9 months [24, 26] and in systolic blood pressure
A decline was noted in IL6 and TNF-alpha
No studies to date show an increase in LUTS/BPH symptoms with higher serum testosterone levels
TRT has been shown to upregulate PDE5 [65] and enhance the effect of PDE5Is (now an accepted therapy for both ED and LUTS), it no longer seems logical to advice avoidance of TRT in men with mild to moderate BPH.
What about just starting with normalization of Testosterone levels first.
Several meta-analyses have failed to show a link between TRT and development of prostate cancer [66] but some studies have shown a tendency for more aggressive prostate cancer in men with low testosterone
And if one would have looked at their estrogen levels, I guarantee they would have been found to be elevated.
low bioavailable testosterone and high SHBG were associated with a 4.9- and 3.2-fold risk of positive biopsy
Current EAU, ISSAM, and BSSM guidance [1, 2] is that there is “no evidence TRT is associated with increased risk of prostate cancer or activation of subclinical cancer.”
Men with prostate cancer, treated with androgen deprivation, develop an increase of fat mass with an altered lipid profile
Erectile dysfunction is an established marker for future cardiovascular risk and the major presenting symptom leading to a diagnosis of low testosterone
Study finds higher Pb levels in young girls is associated with delayed puberty onset. This occurs through an inverse relationship with inhibin B and follicular development. This relationship was also found with Cadmium. Both of these heavy metals are toxic to the ovaries.
Powerchair, is more compact and has a better turning radius, making it is easier to navigate narrow doorways and tight turns. Another advantage of the powerchair wheelchair is that its armchair joystick does not require an upright posture like an electric scooter's handlebars. Most powerchair wheelchairs can also be taken apart and stowed, while scooters usually can't. Powerchair wheelchairs are also usually less.
Power Wheelchairs/Electric Wheelchairs is specially designed for Disabled and Handicapped People. They are recognized as the prominent manufacturer and supplier of a wide array of Power Wheelchairs. Variety of Power Wheelchairs for handicapped and disability product like:
Variety of Power Wheelchairs:
Karma KP 10-2 Power Wheelchair
Karma KP 10-3 Power Wheelchair
Karma KP 80 Power Wheelchair
GM Lite Power Wheelchair
Bronco Wheelchair
Angel Wheelchair
Bronco Wheelchair:
Bronco Reclining Power Wheelchair Description:
Comfort mobility is a professional Bronco Wheelchair and power scooter manufacturer established in 1978 in Taiwan. It operates with the policy of combining high quality with innovation. With dedication to research and development, Bronco wheelchair are exported around the world and earned solid reputation for its superior quality, comfort and convenience.
Bronco wheelchair - comfortable, durable, designed for easy and healthy movement with full precautions.
Bronco Reclining Power Wheelchair Specifications:
Anchorage points
Adjustable footplates
LED front lights
Detachable backrest
Flip-back armrests
Adjustable headrest
Mechanic repairs
Optional handbrake
Power Wheelchair Features:
Battery Power Wheelchair.
Seat, base & battery quickly detach for easy storage and transportation
Come with captain seat.
With seat platform, the captain seat can be moved forward or backward using tools which is included.
Adjustable armrest width and height.
Footrests can be moved forward or backward for optimum placeme
The intra-testicular level of testosterone in GF mice was found to be significantly lower than in SPF and CBUT mice
This study establishes a novel role for the commensal gut microbiota in the regulation of testicular development and function
Absence of the normal microbiota influences the formation and the integrity of the BTB as well as the intra-testicular levels of testosterone and serum levels of LH and FSH.
Nutritional, socioeconomic, lifestyle and environmental factors (among others) are involved in the regulation of normal spermatogenesis.
he gut microbiota is one such potential source of environmental factors/products that has developed an intimate symbiotic relationship with host's physiology.
Manipulation of the gut microbiotia through dietary modification, pre- and probiotics can therefore be beneficial for the host's reproductive health.
In the current study, colonizing GF mice with CBUT resulted in an increased sperm production, suggesting that bacterial products, e.g. of fermentation, directly or indirectly, can affect the testis.
the absence of gut microbiota influenced testosterone levels
A recent study demonstrated that dietary supplementation of the probiotics Lactobacillus reuteri increased and restored testosterone levels in aging mice
bacterial metabolites such as butyrate have been shown to increase the levels of LH [43] and FSH
This suggests that butyrate most likely regulates testosterone production at the testicular level by stimulation of gene expression in Leydig cells and with little or no effect at the pituitary- hypothalamic levels.
The tricycles are individually designed to meet the needs of each disabled child and help provide physiotherapy, build muscle tone and promote play. Italso help benefit growth and development in children with disabilities, enabling them to keep active and retain their independence. Disabled children get huge physical and emotional benefits from having the specially tricycles, which are each custom made to suit the individual child's needs. Riding a tricycle provides both fun and fitness, and is a therapeutic activity that allows children to exercise their lower extremities. As the muscles move through cycling motions, they are flexed, extended and stretched. This range of motion is crucial for children with disabilities, because muscles are incapable of keeping up with bone growth unless fully extended.
Tricycles are provided to severely disabled children and adults and come in two sizes, 20 inch and 24 inch models. These trikes are grant funded and to qualify for one of these, an individual must suffer from a condition such as, but not limited to, Cerebral Palsy, Down Syndrome, Traumatic Brain Injury or Autism.
Trunk support system is ideal for riders who have trouble remaining upright while seated. An optional headrest is available. A headrest can be purchased with either a flat or contoured headpiece, and adjusts both horizontally and vertically for optimum positioning. The Front Pulley System maintains a level pedal position for children whose extreme tone forces the front of the pedal downward. Turn the oval knob to raise and lower the handlebar. A handbrake for the conventional handlebar will arrive installed on Large tricycle. Open access combined with a low transfer step makes it easy to get on and off trikes.
Tricycle Deluxe Double Hand Drive:
Frame : Made by E.R.W. Tubes 38.0 mm-16 G. 25.4 mm & 22.22 mm- 18 G.
Seat & Back : M S, C.R.C. Sheet. Seat Size 18"x 16"
Wheel Size : Wheel Diameter 24"x 1 1/2" Tyre and Tube Standard Company.
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The gut microbiota participates in the body’s metabolism by affecting energy balance, glucose metabolism, and low-grade inflammation associated with obesity and related metabolic disorders
Firmicutes and Bacteroidetes represent the two largest phyla in the human and mouse microbiota and a shift in the ratio of these phyla has been associated with many disease conditions, including obesity
In obese humans, there is decreased abundance of Bacteroidetes compared to lean individuals
weight loss in obese individuals results in an increase in the abundance of Bacteroidetes
there is conflicting evidence on the composition of the obese microbiota phenotype with regards to Bacteroidetes and Firmicutes ratios
Bifidobacteria spp. from the phyla Actinobacteria, has been shown to be depleted in both obese mice and human subjects
While it is not yet clear which specific microbes are inducing or preventing obesity, evidence suggests that the microbiota is a factor.
targeted manipulation of the microbiota results in divergent metabolic outcomes depending on the composition of the diet
The microbiota has been linked to insulin resistance or type 2 diabetes (T2D) via metabolic syndrome and indeed the microbiota of individuals with T2D is also characterized by an increased Bacteroidetes/Firmicutes ratio, as well as an increase in Bacillus and Lactobacillus spp
It was also observed that the ratio of Bacteriodes-Prevotella to C. coccoides-E. rectale positively correlated with glucose levels but did not correlate with body mass index [80]. This suggests that the microbiota may influence T2D in conjunction with or independently of obesity
In humans, high-fat Western-style diets fed to individuals over one month can induce a 71% increase in plasma levels of endotoxins, suggesting that endotoxemia may develop in individuals with GI barrier dyfunction connected to dysbiosis
LPS increases macrophage infiltration essential for systemic inflammation preceding insulin resistance, LPS alone does not impair glucose metabolism
early treatment of dysbiosis may slow down or prevent the epidemic of metabolic diseases and hence the corresponding lethal cardiovascular consequences
increased Firmicutes and decreased Bacteroidetes, which is the microbial profile found in lean phenotypes, along with an increase in Bifidobacteria spp. and Lactobacillus spp
mouse and rat models of T1D have been shown to have microbiota marked by decreased diversity and decreased Lactobacillus spp., as well as a decrease in the Firmicutes/Bacteroidetes ratio
microbial antigens through the innate immune system are involved in T1D progression
The microbiota appears to be essential in maintaining the Th17/Treg cell balance in intestinal tissues, mesenteric and pancreatic lymph nodes, and in developing insulitis, although progression to overt diabetes has not been shown to be controlled by the microbiota
There is evidence that dietary and microbial antigens independently influence T1D
Lactobacillus johnsonii N6.2 protects BB-rats from T1D by mediating intestinal barrier function and inflammation [101,102] and a combination probiotic VSL#3 has been shown to attenuate insulitis and diabetes in NOD mice
breast fed infants have higher levels of Bifidobacteria spp. while formula fed infants have higher levels of Bacteroides spp., as well as increased Clostridium coccoides and Lactobacillus spp
the composition of the gut microbiota strongly correlates with diet
In mice fed a diet high in fat, there are many key gut population changes, such as the absence of gut barrier-protecting Bifidobacteria spp
diet has a dominating role in shaping gut microbiota and changing key populations may transform healthy gut microbiota into a disease-inducing entity
“Western” diet, which is high in sugar and fat, causes dysbiosis which affects both host GI tract metabolism and immune homeostasis
Five branched chain and aromatic amino acids (isoleucine, leucine, valine, tyrosine, and phenylalanine) showed significant associations with future diabetes
there is increasing evidence that longer term high-protein intake may have detrimental effects on insulin resistance [68, 117–123], diabetes risk [69], and the risk of developing cardiovascular disease
high-protein and the high GI diets significantly increased markers of low-grade inflammation
significant and clinically relevant worsening of insulin sensitivity with an isoenergetic plant-based high-protein diet
healthy humans that are exposed to amino acid infusions rapidly develop insulin resistance
longer term high-protein intake has been shown to result in whole-body insulin resistance [68, 118], associated with upregulation of factors involved in the mammalian target of rapamycin (mTOR)/S6K1 signalling pathway [68], increased stimulation of glucagon and insulin within the endocrine pancreas, high glycogen turnover [118] and stimulation of gluconeogenesis [68, 118].
it was recently shown in a large prospective cohort with 10 years followup that consuming 5% of energy from both animal and total protein at the expense of carbohydrates or fat increases diabetes risk by as much as 30% [69]. This reinforces the theory that high-protein diets can have adverse effects on glucose metabolism.
Another recent study showed that low-carbohydrate high-protein diets, used on a regular basis and without consideration of the nature of carbohydrates or the source of proteins, are also associated with increased risk of cardiovascular disease [70], thereby indicating a potential link between high-protein Western diets, T2DM, and cardiovascular risk.
Premature ovarian failure shown to be autoimmune. This study from '97 describes the mechanism of the autoimmune ovarian failure. Now, case studies are emerging of young women developing premature ovarian failure following the HPV vaccine.