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After weeks of struggle, we were still unable to recover our own domain. Long story short, our domain registrar called has PUT OUR DOMAIN ON HOLD because of a decision made by a site called who put our site in their list of so called “rogue pharmacies” due to some ridiculous claims (their site list 98 percent of any site related to health or beauty as rogue pharmacy). Our losses are huge. We have lost our great results is search engihnes and our daily visit has dropped hugely. Obviously, people think that we had to shut down the business. Well, fortunately, we only had to move to a different domain until we sort out things, so all you have to do is take out a letter at the end, instead of .com we are .co – WWW.SUPERHUMANGEAR.CO

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The beta-thymosins are a family of highly conserved polar 5 kDa peptides originally thought to be thymic hormones. About 10 years ago, thymosin beta(4) as well as other members of this ubiquitous peptide family were identified as the main intracellular G-actin sequestering peptides, being present in high concentrations in almost every cell. beta-Thymosins bind monomeric actin in a 1:1 complex and act as actin buffers, preventing polymerization into actin filaments but supplying a pool of actin monomers when the cell needs filaments. Changes in the expression of beta-thymosins appear to be related to the differentiation of cells. Increased expression of beta-thymosins or even the synthesis of a beta-thymosin normally not expressed might promote metastasis possibly by increasing mobility of the cells. Thymosin beta(4) is detected outside of cells in blood plasma or in wound fluid. Several biological effects are attributed to thymosin beta(4), oxidized thymosin beta(4), or to the fragment, acSDKP, possibly generated from thymosin beta(4). Among the effects are induction of metallo-proteinases, chemotaxis, angiogenesis and inhibition of inflammation as well as the inhibition of bone marrow stem cell proliferation. However, nothing is known about the molecular mechanisms mediating the effects attributed to extracellular beta-thymosins.

[PubMed – indexed for MEDLINE]

A number of studies have shown that it is possible to lengthen the average life of individuals of many species, including mammals, by acting on specific genes. To date, however, this has meant altering the animals’ genes permanently from the embryonic stage – an approach impracticable in humans. Researchers at the Spanish National Cancer Research Centre (CNIO), led by its director María Blasco, have proved that mouse lifespan can be extended by the application in adult life of a single treatment acting directly on the animal’s genes. And they have done so using gene therapy, a strategy never before employed to combat ageing. The therapy has been found to be safe and effective in mice.

The results are published today in the journal EMBO Molecular Medicine. The CNIO team, in collaboration with Eduard Ayuso and Fátima Bosch of the Centre of Animal Biotechnology and Gene Therapy at the Universitat Autònoma de Barcelona (UAB), treated adult (one-year-old) and aged (two-year-old) mice, with the gene therapy delivering a “rejuvenating” effect in both cases, according to the authors.

Mice treated at the age of one lived longer by 24% on average, and those treated at the age of two, by 13%. The therapy, furthermore, produced an appreciable improvement in the animals’ health, delaying the onset of age-related diseases – like osteoporosis and insulin resistance – and achieving improved readings on ageing indicators like neuromuscular coordination.

The gene therapy utilised consisted of treating the animals with a DNA-modified virus, the viral having been replaced by those of the telomerase enzyme, with a key role in ageing. Telomerase repairs the extremes of chromosomes, known as telomeres, and in doing so slows the cell’s and therefore the body’s biological clock. When the animal is infected, the virus acts as a vehicle depositing the telomerase gene in the cells.

This study “shows that it is possible to develop a telomerase-based anti-ageing gene therapy without increasing the incidence of cancer”, the authors affirm. “Aged organisms accumulate damage in their DNA due to telomere shortening, [this study] finds that a gene therapy based on telomerase production can repair or delay this kind of damage”, they add.

‘Resetting’ the biological clock

Telomeres are the caps that protect the end of chromosomes, but they cannot do so indefinitely: each time the cell divides the telomeres get shorter, until they are so short that they lose all functionality. The cell, as a result, stops dividing and ages or dies. Telomerase gets round this by preventing telomeres from shortening or even rebuilding them. What it does, in essence, is stop or reset the cell’s biological clock.

But in most cells the telomerase gene is only active before birth; the cells of an adult organism, with few exceptions, have no telomerase. The exceptions in question are adult stem cells and cancer cells, which divide limitlessly and are therefore immortal – in fact several studies have shown that telomerase expression is the key to the immortality of tumour cells.

It is precisely this risk of promoting tumour development that has set back the investigation of telomerase-based anti-ageing therapies.

In 2007, Blasco’s group proved that it was feasible to prolong the lives of transgenic mice, whose genome had been permanently altered at the , by causing their cells to express telomerase and, also, extra copies of cancer-resistant genes. These animals live 40% longer than is normal and do not develop cancer.

The mice subjected to the gene therapy now under test are likewise free of cancer. Researchers believe this is because the therapy begins when the animals are adult so do not have time to accumulate sufficient number of aberrant divisions for tumours to appear.

Also important is the kind of virus employed to carry the telomerase gene to the cells. The authors selected demonstrably safe viruses that have been successfully used in gene therapy treatment of haemophilia and eye disease. Specifically, they are non-replicating viruses derived from others that are non-pathogenic in humans.

This study is viewed primarily as “a proof-of-principle that telomerase is a feasible and generally safe approach to improve healthspan and treat disorders associated with short telomeres”, state Virginia Boccardi (Second University of Naples) and Utz Herbig (New Jersey Medical School-University Hospital Cancer Centre) in a commentary published in the same journal.

Although this therapy may not find application as an anti-ageing treatment in humans, in the short term at least, it could open up a new treatment option for ailments linked with the presence in tissue of abnormally short telomeres, as in some cases of human pulmonary fibrosis.

More healthy years

As Blasco says, “ageing is not currently regarded as a disease, but researchers tend increasingly to view it as the common origin of conditions like insulin resistance or cardiovascular disease, whose incidence rises with age. In treating cell ageing, we could prevent these diseases”.

With regard to the therapy under testing, Bosch explains: “Because the vector we use expresses the target gene (telomerase) over a long period, we were able to apply a single treatment. This might be the only practical solution for an anti-ageing therapy, since other strategies would require the drug to be administered over the patient’s lifetime, multiplying the risk of adverse effects”.

Provided by Centro Nacional de Investigaciones Oncologicas (CNIO)



Intraarticular hyaluronic acid is indicated for patients with osteoarthritis of the knee. However, clinical experience, especially efficacy and adverse events, with repeated injection series in the long term are limited.


Patients were referred to a large primary care center for management of osteoarthritis of the knee. All were naive to intraarticular hyaluronic acid therapy and met our entry criteria, including resting visual analog scale pain of > 45 mm, radiographic confirmation of unilateral knee grade 1-3 osteoarthritis, and willingness to receive intraarticular therapy. Patients received a three-intraarticular injection series with Suplasyn (10 mg/ml, 2-ml injection) over 3 wks. Patients were instructed to return for consideration of repeat injection series based on their perception of pain restricting daily activity and a resumption of severity similar to their initial presentation. This prospective naturalistic cohort was followed for 6.7 yrs. Patients completed baseline assessment of rest and walking visual analog scale pain (primary efficacy variable), completed a 5-point categorical global satisfaction score, and recorded adverse events and concomitant therapeutic modality use at each study visit. Patients returned for consideration of a repeat injection series based on their perception of symptom severity and were eligible if their resting visual analog scale pain was > 45 mm. The three-injection series and data collection were repeated, and again, patients were given similar instructions regarding consideration of a third injection series.


Of 897 referral patients, 537 (mean age, 68 +/- 8 yrs; mean duration of symptoms, 7.4 +/- 4.1 yrs) met our criteria, and only 21 patients did not return for a second injection series. The mean time between first and second series was 27 +/- 7 wks. The change in walking visual analog scale pain was significantly improved from baseline after the first series (81.3%, P < 0.001) and second series (86.7%, P < 0.0001). Similarly, resting visual analog scale pain was significantly decreased from baseline after the first (P < 0.001) and second (P < 0.001) series, and patient satisfaction was significantly improved with each injection series (P < 0.03 and P < 0.01). Very few adverse events were recorded and were limited to local pain and swelling. Use of concomitant therapeutic modalities at presentation for a second injection series included: nonsteroidal anti-inflammatory drugs/cyclooxygenase-2 medications (37%), acetaminophen (31%), oral nutraceuticals (12%), and physical therapy and bracing (12%).


Intraarticular hyaluronic acid injections were highly effective in improving resting and walking pain in patients with osteoarthritis of the knee on a first and a second treatment series. Duration of symptom control was about 6 mos, and the therapy was highly satisfactory to patients and was associated with very few local adverse events and limited use of concomitant therapeutic modalities. These data support the potential role of intraarticular hyaluronic acid as an effective long-term therapeutic option for patients with osteoarthritis of the knee.

[PubMed – indexed for MEDLINE]
Researchers at Columbia University Medical Center have discovered the biological mechanism behind age-related loss of muscle strength and identified a drug that may help reverse this process. Their findings were published in the August 2 online edition of Cell Metabolism.
As we grow older, our skeletal muscles tend to wither and weaken, a phenomenon known as sarcopenia. Sarcopenia, which begins to appear at around age 40 and accelerates after 75, is a major cause of disability in the elderly. Exercise can help counter the effects of age-related muscle loss. Otherwise, there are no established treatments.
According to the new study, conducted in mice, sarcopenia occurs when calcium leaks from a group of proteins in muscle cells called the ryanodine receptor channel complex. These leaks then trigger a chain of events that ultimately limits the ability of muscle fibers to contract, reports study leader Andrew R. Marks, M.D., chairman and professor of physiology and cellular biophysics, the Clyde and Helen Wu Professor of Medicine, and director of the Wu Center for Molecular Cardiology at Columbia University Medical Center (CUMC).
Ryanodine receptors, which are calcium channels found in most body tissues, have been the focus of Dr. Marks’ research since 1989. After cloning the ryanodine receptor gene, he later discovered, in studies of mice, that leaky ryanodine receptors are involved in the development of heart failure and arrhythmias. In 2009, he showed that leaks in these channels also contribute to Duchenne muscular dystrophy, a genetic disorder characterized by rapidly progressing muscle weakness and early death.
Since muscular dystrophy and sarcopenia have some commonalities, Dr. Marks suspected that ryanodine receptor leakage may also be involved in age-related muscle loss, which the present study shows is the case.
“This is a completely new concept — that the damage that occurs in aging is very similar to what happens in muscular dystrophy,” says Dr. Marks, “thus as we age we essentially develop an acquired form of muscular dystrophy.”
Both the aging process and the genetic defect responsible for muscular dystrophy cause an increase in the production of oxygen free radicals, highly reactive and harmful molecules. “Our data suggest that this sets up a vicious cycle, in which the free radicals cause ryanodine receptors to leak calcium into the cell. The calcium poisons mitochondria — organelles that power the cell — leading to the release of even more free radicals. This, in turn, causes more calcium leakage. With less calcium available for contraction, the muscles get weaker,” says first author Daniel C. Andersson, M.D., Ph.D., a postdoctoral fellow in physiology and cellular biophysics at CUMC.
The study also points to a possible therapy for sarcopenia: an experimental drug called S107, developed by Dr. Marks and his colleagues. The drug acts by stabilizing calstabin1, a protein that binds to ryanodine receptors and prevents calcium leakage.
In the study, 24-month-old mice (roughly the equivalent of 70-year-old humans) were given S107 for four weeks. The mice showed significant improvements in both muscle force and exercise capacity, compared with untreated controls. “The mice ran farther and faster during voluntary exercise,” says Dr. Andersson. “When we tested their muscles, they were about 50 percent stronger.” The drug had no effect on younger mice with normal ryanodine receptors.
A similar drug is now in phase II clinical trials for the treatment of heart failure.
“Most investigators in the field of aging have been saying that the way to improve muscle strength is to build muscle mass, using such therapies as testosterone, growth hormone, and insulin-like growth factor-1,” says Dr. Marks. “But an increase in muscle mass is not necessarily accompanied by an increase in muscle function. Our results suggest that you can improve muscle function by fixing leaky calcium channels. And in fact, treating aged mice with S107 enhanced muscle strength without increasing muscle size, at least during the four-week treatment period.”
Dr. Marks’ paper is titled, “Ryanodine Receptor Oxidation Causes Intracellular Calcium Leak and Muscle Weakness in Aging.” In addition to Dr. Andersson, his coauthors include Mathew J. Betzenhauser, Steven Reiken, Albano C. Meli, Alisa Umanskaya, Wenjun Xie, Takayuki Shiomi, and Ran Zalk at CUMC, and Alain Lacampagne at Universités Montpellier, Montpellier, France.
A.R. Marks is a consultant for a start-up company, ARMGO Pharma, Inc., which is targeting ryanodine receptors to improve exercise capacity in muscle diseases.
This research was supported by grants from the National Heart, Lung, and Blood Institute and the Swedish Research Council


The indication of a chemotherapy is advisable with patients who are suffering from a progressively metastasised, secondarily hormone refractory carcinoma of the prostate. In search of efficient chemotherapy protocols we combined cisplatin with epirubicin (PE scheme) in our clinic. Massive side effects of that aggressive chemotherapy scheme like gastro-intestinal trouble and myelotoxicity are the limiting factors of the scheme. With measures like reducing the dosage, delaying the next cycle, or breaking off the therapy the effective dosage can often not be achieved. The anti-emetics which are usually used today exclusively give anti-emetic protection. The additional administration of xenogenic peptides (Factor AF2) had additionally myeloprotective effect in former studies. In this study we examined whether, by additionally giving Factor AF2, the patients’ subjective condition, and above all their hemogram, could be stabilised in order to achieve the effective dosage or dosage intensity. For that, the patients were prospectively randomised in two groups by means of a random selection board. The analysis of the data gained in the protocol showed that the additional administration of Factor AF2 improves the patients’ subjective conditions significantly. Apart from that, we noticed a considerable reduction of the vomiting frequency. Concerning the objective measured parameters of the leukocytes, thrombocytes, erythrocytes, and the hemoglobin level, the significantly myeloprotective effect of Factor AF2 could be proved. Due to the fact that in the verum group there were considerably fewer cases of breaking off or delays of the treatment than in the control group, the effective dosage intensity could be achieved with a higher number of patients in that group.

[PubMed – indexed for MEDLINE]



Skeletal muscle dysfunction contributes to exercise limitation in patients with chronic obstructive pulmonary disease (COPD). Strength training increases muscle strength and muscle mass, but there is an ongoing debate on the additional effect concerning the exercise capacity. The purpose of this study was to compare the effects of three different exercise modalities in patients with COPD including endurance training (ET), progressive strength training (ST) and the combination of strength training and endurance training (CT).


A prospective randomized trial.


Thirty-six patients with COPD were randomly allocated either to ET, ST, or CT. Muscle strength, cardiopulmonary exercise testing, lung function testing and quality of life were assessed before and after a 12-week training period.


Exercise capacity (Wmax) increased significantly in all three training groups with increase of peak oxygen uptake (VO(2)peak) in all three groups, reaching statistical significance in the ET group and the CT group. Muscle strength (leg press, bench press, bench pull) improved in all three training groups, with a higher improvement in the ST (+39.3%, +20.9%, +20.3%) and the CT group (+43.3%, +18.1%, +21.6%) compared to the ET group (+20.4%, +6.4%, +12.1%).


Progressive strength training alone increases not only muscle strength and quality of life, but also exercise capacity in patients with COPD, which may have implications in prescription of training modality. CLINICALTRIALS.GOV IDENTIFIER: NCT01091623.

Copyright © 2011 Elsevier Ltd. All rights reserved.

[PubMed – as supplied by publisher]

Polydeoxyribonucleotide reduces cytokine production and the severity of collagen-induced arthritis by stimulation of adenosine A(₂A) receptor


University of Messina, Messina, Italy.



Broad antiinflammatory effects following adenosine A(₂A) receptor stimulation have been demonstrated in acute inflammatory diseases, including arthritis. Polydeoxyribonucleotide (PDRN) activates the adenosine A(₂A) receptor. This study was undertaken to investigate the effects of PDRN in collagen-induced arthritis (CIA) in mice.


Arthritis was induced in DBA/1 mice by an intradermal injection of 100 μl of bovine type II collagen in Freund’s complete adjuvant. Mice were immunized a second time 21 days later. Control animals received 100 μl of a saline solution. Animals with CIA were randomized to receive one of the following: vehicle (1 ml/kg); PDRN (8 mg/kg intraperitoneally daily); 3,7-dimethyl-propargylxanthine (DMPX), a specific adenosine A(₂A) receptor antagonist (0.1 mg/kg intraperitoneally daily); or PDRN plus DMPX. The treatment was initiated immediately after the second immunization and continued to day 45. Clinical evaluation of arthritis was performed throughout the study. On day 45, the animals were killed and the severity of arthritis was evaluated histologically. Cartilage expression and circulating levels of high mobility group box chromosomal protein 1 (HMGB-1), tumor necrosis factor α (TNFα), interleukin-6 (IL-6), and IL-10 were investigated. Inflammatory cytokine production was also evaluated in stimulated human chondrocytes treated with PDRN.


PDRN treatment significantly ameliorated clinical signs of arthritis, improved histologic damage, reduced the cartilage expression and circulating levels of HMGB-1, TNFα, and IL-6, and enhanced IL-10 expression. The concomitant administration of DMPX and PDRN ablated the PDRN-induced protective effect in experimental arthritis. PDRN also reduced cytokine production from stimulated human chondrocytes.


Our findings indicate that PDRN may represent a new alternative for the treatment of arthritis.

Copyright © 2011 by the American College of Rheumatology.

[PubMed – in process]