Lifeboat Foundation

The high demand on medical devices and personal protective equipment (PPE) during the COVID-19 crisis left millions of health care professionals unprotected in the middle of this situation, as governments around the world were not prepared for such pandemic. The three-dimensional printing (3DP) community, from universities to 3DP enthusiasts with printers at home, was there to support hospitals from day 1 on this demand by providing PPE and other medical supplies (e.g., face shields and valves for respiratory machines). This editorial covers the importance of 3DP in the fight against COVID-19 and how this can be used to tackle potential pandemics and support the supply chain.

After a series of cases of pneumonia in Wuhan, the capital city of Hubei province (China), the Chinese health authorities announced in January 2020 that a novel coronavirus, officially known as severe acute respiratory syndrome coronavirus (SARS-CoV)-2, was responsible for these cases.¹ SARS-CoV-2, the virus that causes the coronavirus disease (COVID-19), was not detected before the recent pandemic and has been known to be genetically similar to SARS-CoV.¹ The COVID-19 is transmitted mainly through contact with an infected individual, through droplets that are produced when the patient coughs or sneezes or through droplets from the saliva or nasal cavity.^1,2 To avoid transmission, it is very important to implement individual hygiene measures and especially the use of personal protective equipment (PPE). However, the lack of PPE and other key resources during the COVID-19 crisis has been a constant problem, leaving many health care professionals across the world unprotected.

Dealing with a pandemic, such as COVID-19, is an unprecedented situation in this modern globalized word, which has created extraordinary emergency that is particularly affecting the supply chain.³ The supply chain disruptions, in combination with the enormous needs for medical devices and protective health care material, have created the need of new initiatives and the use of emerging technologies such as three-dimensional printing (3DP) to come forward and support the health care professionals and supply chain.

“We expected that the hammer of natural selection also comes down randomly, but that is not what we found,” he said. “Rather, it does not act randomly but has a strong bias, favoring those mutations that provide the largest fitness advantage while it smashes down other less beneficial mutations, even though they also provide a benefit to the organism.”

In other words, evolution is not a multitasker when it comes to fixing problems.

“It seems that evolution is myopic,” Venkataram said. “It focuses on the most immediate problem, puts a Band-Aid on and then it moves on to the next problem, without thoroughly finishing the problem it was working on before.”

Continue reading “To understand the machinery of life, this scientist breaks it on purpose” »

New research supported by the National Institutes of Health delineates how two relatively common variations in a gene called KIF3A are responsible for an impaired skin barrier that allows increased water loss from the skin, promoting the development of atopic dermatitis, commonly known as eczema. This finding could lead to genetic tests that empower parents and physicians to take steps to potentially protect vulnerable infants from developing atopic dermatitis and additional allergic diseases.

Atopic dermatitis is an inflammatory skin condition that affects up to 20% of children in developed countries. This chronic disease is characterized by dry, thickened and intensely itchy skin, particularly in skin folds. People with eczema are more susceptible to bacterial, viral and fungal skin infections and frequently develop additional allergic diseases such as asthma.

KIF3A is a gene that codes for a protein involved in generating signals from the outside to the inside of a cell, part of a complex sensory apparatus. Previously, scientists had identified an association between two genetic variations in KIF3A and asthma in children who also had eczema. In the new study, the researchers found that these variations, or single nucleotide polymorphisms (SNPs), changed parts of the KIF3A gene to a form that can regulate, through a process called methylation, the rate at which a gene is transcribed into the blueprint for protein production. The investigators confirmed that skin and nasal-lining cells from people with the KIF3A SNP variants had more methylation and contained fewer blueprints for the KIF3A protein than cells in which KIF3A lacked the SNPs. In addition, the researchers demonstrated that people with the SNP-created regulating sites had higher levels of water loss from the skin.

The US Food and Drug Administration (FDA) has approved viltolarsen (Viltepso; NS Pharma) for the treatment of patients with Duchenne muscular dystrophy amenable to exon 53 skipping, making it only the second FDA-approved therapy for this specific DMD gene mutation.

The agent from NS Pharma, delivered via weekly intravenous infusion, was granted accelerated approval via its priority review, fast track, orphan drug, and rare disease designations after its new drug application was accepted earlier this year. In March, NS Pharma launched an expanded access program for qualified patients.

The approval was granted based on findings from a phase 2 clinical trial (NCT02740972) and long-term extension study, details of which were recently published in JAMA Neurology. Among 16 participants age 4 to 9, significant drug-induced dystrophin production was observed in both viltolarsen dose cohorts (40 mg/kg per week: mean, 5.7% [range, 3.2–10.3] of normal; 80 mg/kg per week: mean, 5.9% [range, 1.1–14.4] of normal), with 15 (94%) patients achieving dystrophin levels greater than 2% of normal and 14 of 16 (88%) achieving levels greater than 3% of normal.

While satellite imaging lets researchers observe the outer life of plankton populations, the complex genetics in microscopic marine life have made looking inward more challenging. According to a new study published in Nature Methods, researchers from the University of East Anglia were able to deliver and express foreign DNA in 13 species that have never before transformed. They were also able to evaluate the potential cause of non-transformation in 17 other species; in turn, laying the foundation for an expanded understanding of genomes discovered in plankton.

The sheer variety of plankton potential — from antibacterial compounds to antiviral and antifungal solutions — makes this a worthwhile endeavor. If scientists can create reliable methods to modify phytoplankton, it should be possible to reduce their toxic impact, better control their bloom cycle and even increase the photosynthetic output — all critical in the fight to keep our oceans blue and our terra firma green.

As noted by Science Magainze, the international research team used a variety of methods to modify plankton DNA. For some species, shooting tiny gold or tungsten particles covered with DNA through cell walls produced the best result. For others, jolts of electricity made cell walls “leaky” and allowed new DNA to seep through. Specific protist successes included modification of a fish-killing toxic plankton species, and one that infects both mollusks and amphibians. While these discoveries don’t present a complete understanding of the genetics in microscopic marine life, they provide a key testing protocol: By modifying genetic structure and then observing how plankton react, teams could uncover ways to boost antibiotic resistance or lower infectious impact. According to lead UK study author Thomas Mock, “These insights will improve our understanding about their role in the oceans, and they are invaluable for biotechnological applications such as building factories for biofuel or the production of bioactive compounds.”

Before the first oncogene mutations were discovered in human cancer in the early 1980s, the 1970s provided the first data suggesting alterations in the genetic material of tumors. In this context, the prestigious journal Nature published in 1975 the existence of a specific alteration in the transformed cell: an RNA responsible for carrying an amino acid to build proteins (transfer RNA) was missing a piece, the enigmatic nucleotide ‘Y.’

After that outstanding observation, virtually no developments were made for forty-five years on the causes and consequences of not having the correct base in RNA.

In an article published in Proceedings of the National Academy of Sciences (PNAS) by the group of Dr. Manel Esteller, Director of the Josep Carreras Leukaemia Research Institute, ICREA Research Professor and Professor of Genetics at the University of Barcelona has solved this mystery by observing that in cancer cells the protein that generates the nucleotide Y is epigenetically inactivated, causing small but highly aggressive tumors.

Harvard geneticist Dr. George Church is “turning on” youth-promoting genes. In this exclusive interview Dr. Church explains how he expects to achieve human age reversal in the foreseeable future.

Scientifically reviewed by: Dr. Amanda Martin, DC, on August 2020. Written By Dr. Shelly Xuelai Fan.

Last year information was released concerning rejuvenation of the thymus which resulted in a reversal of the epigenetic clock an average of 2.5 years in a small trial of 9 people costing $10,000 per person. You can get this done too. A company has formed called Intervene Immune which will take on volunteers for the process. It is not funded so you would have to pay out pf pocket though eventually the cost may come down and they can provide financing. You do not have to travel to California to get this done. Cost prohibits me, and I may or may not be eligible as I have IBS though that is not on the exclusion list. I emailed them concerning all this which is how I got the information.

http://interveneimmune.com/

https://www.surveymonkey.com/r/TRIIMX

Continue reading “Thymus Regeneration, Immunorestoration, and Insulin Mitigation Extension Trial” »

Hereditary hearing loss is one of the most common disabilities among newborns, affecting approximately 1 in 1000 live-born babies. Most forms of hereditary hearing loss are nonsyndromic; 80% of affected newborns have hearing loss that is inherited in an autosomal recessive pattern, and in the remaining 20%, inheritance shows a dominant pattern.¹

Many forms of hereditary hearing loss are caused by mutations in genes that affect the formation and function of cochlear hair cells — highly specialized sensory cells that play an important role in the detection and processing of sound.¹ The hair cell has bundles of hair-like projections, called stereocilia, on its apical surface ( Fig. 1 ). The deflection of these bundles by sound results in the opening of mechanotransduction ion channels, which are located at the tips of the stereocilia, and consequently, in the depolarization of the hair-cell membrane. Mutations that affect the protein transmembrane channel-like 1 (TMC1), an integral component of the mechanotransduction complex, cause autosomal dominant and autosomal recessive forms of hearing loss.² Correction of the dominant form of hearing loss in a mouse model of Tmc1 (termed “Beethoven”) was recently reported by Gao and colleagues.³