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For thousands of years, humans have used honey, propolis, and venom from the European honeybee Apis mellifera as medicines.

More recently, scientists have discovered that honeybee venom and its active component, melittin, are toxic to a wide range of tumors — including melanoma, lung, ovarian, and pancreatic cancers — in laboratory tests.

Melittin is the molecule that creates the painful sensation of a bee’s sting. Scientists do not fully understand how it kills cancer cells, however.

Engineers have designed a computer processor that thwarts hackers by randomly changing its microarchitecture every few milliseconds. Known as Morpheus, the puzzling processor has now aced its first major tests, repelling hundreds of professional hackers in a DARPA security challenge.

In 2017, DARPA backed the University of Michigan’s Morpheus project with US$3.6 million in funding, and now the novel processor has been put to the test. Over four months in 2020, DARPA ran a bug bounty program called Finding Exploits to Thwart Tampering (FETT), pitting 525 professional security researchers against Morpheus and a range of other processors.

The goal of the program was to test new hardware-based security systems, which could protect data no matter how vulnerable the underlying software was. Morpheus was mocked up to resemble a medical database, complete with software vulnerabilities – and yet, not a single attack made it through its defenses.

Circa 2010


Medical researchers use laboratory-grown human cells to learn the intricacies of how cells work and test theories about the causes and treatment of diseases. The cell lines they need are “immortal”—they can grow indefinitely, be frozen for decades, divided into different batches and shared among scientists. In 1951, a scientist at Johns Hopkins Hospital in Baltimore, Maryland, created the first immortal human cell line with a tissue sample taken from a young black woman with cervical cancer. Those cells, called HeLa cells, quickly became invaluable to medical research—though their donor remained a mystery for decades. In her new book, The Immortal Life of Henrietta Lacks, journalist Rebecca Skloot tracks down the story of the source of the amazing HeLa cells, Henrietta Lacks, and documents the cell line’s impact on both modern medicine and the Lacks family.

HeLa (/ ˈ h iː l ɑː / ; also Hela or hela) is an immortal cell line used in scientific research. It is the oldest and most commonly used human cell line.[1] The line is named after and derived from cervical cancer cells taken on February 8, 1951,[2] from Henrietta Lacks, a 31-year-old African-American mother of five, who died of cancer on October 4, 1951.[3] The cell line was found to be remarkably durable and prolific, which allows it to be used extensively in scientific study.[4][5]

Scanning electron micrograph of an apoptotic HeLa cell. Zeiss Merlin HR-SEM.

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The research team of Gero, a Singapore-based biotech company in collaboration with Roswell Park Comprehensive Cancer Center in Buffalo NY, has presented a study in Nature Communications on associations between aging and the loss of the ability to recover from stresses.

Recently, scientists have reported the first promising examples of reversal by experimental interventions. Indeed, many biological clock types properly predict more years of life for those who choose or quit unhealthy ones, such as smoking. Still unknown is how quickly biological age is changing over time for the same individual, and distinguishing between the transient fluctuations and the genuine bioage change trend.

The emergence of big biomedical data involving multiple measurements from the same subjects brings about a whole range of novel opportunities and practical tools to understand and quantify the in humans. A team of experts in biology and biophysics presented results of a detailed analysis of dynamic properties of the fluctuations of physiological indices along individual aging trajectories.

Is this the reason why the general public view the emerging field of regenerative medicine with such scepticism? Has a combined cultural history of being bombarded with empty promises of longevity made us numb to such a prospect? Possibly, although I believe it might go deeper than old fashioned scepticism. After all, our species is hardly a stranger to believing something if we desire for it to be true, regardless of how much evidence is presented to us.

Maybe we are simply experiencing just another example of humans finding dramatic change to our way of life hard to comprehend and accept. After all, practically every major change in our recent history was largely believed to be an impossibility by the general public, right up until the point that it became the norm. Everything from the aeroplane to the internet was seen as science fiction, but yet today they are integral parts of our lives. Now, this is not to say that everything the general public is sceptical of will inevitably turn out to prove them wrong, but lessons from our history do show that when it comes to scientific progress, the public will not believe it until they can see it.

Some would believe that scepticism towards regenerative medicine strikes at something much deeper in our psych, as it threatened to fundamentally change our entire outlook on the world. For our entire lives, we have been taught by our interactions with others exactly how life is supposed to progress. You are supposed to suffer a gradual decay of mental and physical abilities, until eventually you die. That is just how it is, and if that were to ever change then we would all have to change how we think about the world. The concept of a 125 year old with the appearance of a 25 year old seems bizarre to us right now, and to many the idea of ever lasting health just goes against their fundamental beliefs of how the world functions to such an extent that they cannot comprehend anything different. Some would even go far as to defend the ageing process as being an integral part of life, displaying what can only be described as ‘Stockholm syndrome with extra steps’.

Of 25000+ people who tested positive for #COVID19 in Germany, 8% had very high viral loads; about a third of these had little to no symptoms. The results suggest asymptomatic people can be expected to be as infectious as hospitalized patients.

Read more from Science:


Two elementary parameters for quantifying viral infection and shedding are viral load and whether samples yield a replicating virus isolate in cell culture. We examined 25381 German SARS-CoV-2 cases, including 6110 from test centres attended by pre-symptomatic, asymptomatic, and mildly-symptomatic (PAMS) subjects, 9519 who were hospitalised, and 1533 B.1.1.7 lineage infections. The youngest had mean log10 viral load 0.5 (or less) lower than older subjects and an estimated ~78% of the peak cell culture replication probability, due in part to smaller swab sizes and unlikely to be clinically relevant. Viral loads above 109 copies per swab were found in 8% of subjects, one-third of whom were PAMS, with mean age 37.6. We estimate 4.3 days from onset of shedding to peak viral load (8.1) and cell culture isolation probability (0.75). B.1.1.7 subjects had mean log10 viral load 1.05 higher than non-B.1.1.7, with estimated cell culture replication probability 2.6 times higher.

Respiratory disease transmission is highly context dependent and difficult to quantify or predict at the individual level. This is especially the case when transmission from pre-symptomatic, asymptomatic, and mildly-symptomatic (PAMS) subjects is frequent, as with SARS-CoV-2 (1–8). Transmission is therefore typically inferred from population-level information and summarized as a single overall average, known as the basic reproductive number, R0. While R0 is an essential and critical parameter for understanding and managing population-level disease dynamics, it is a resultant, downstream characterisation of transmission. With regard to SARS-CoV-2, many finer-grained upstream questions regarding infectiousness remain unresolved or unaddressed. Three categories of uncertainty are 1) differences in infectiousness among individuals or groups such as PAMS subjects, according to age, gender, vaccination status, etc.

3D printing, also called additive manufacturing, has become widespread in recent years. By building successive layers of raw material such as metals, plastics, and ceramics, it has the key advantage of being able to produce very complex shapes or geometries that would be nearly impossible to construct through more traditional methods such as carving, grinding, or molding.

The technology offers huge potential in the health care sector. For example, doctors can use it to make products to match a patient’s anatomy: a radiologist could create an exact replica of a patient’s spine to help plan surgery; a dentist could scan a patient’s broken tooth to make a perfectly fitting crown reproduction. But what if we took a step further and apply 3D printing techniques to neuroscience?

Stems cells are essentially the body’s raw materials; they are pluripotent elements from which all other cells with specialized functions are generated. The development of methods to isolate and generate human stem cells, has excited many with the promise of improved human cell function understanding, ultimately utilizing them for regeneration in disease and trauma. However, the traditional two-dimensional growth of derived neurones–using flat petri dishes–presents itself as a major confounding factor as it does not adequately mimic in vivo three-dimensional interactions, nor the myriad developmental cues present in real living organisms.

To address this limitation in current neuronal culturing approaches, the FET funded MESO-BRAIN project, led by Aston University, proposed a highly ambitious interdisciplinary enterprise to construct truly 3D networks that not only displayed in vivo activity patterns of neural cultures but also allowed for precise interaction with these cultures. This allows the activity of individual elements to be readily monitored and controlled through electrical stimulation.

The ability to develop human-induced pluripotent stem cell derived neural networks upon a defined and reproducible 3D scaffold that can emulate brain activity, allows for a comprehensive and detailed investigation of neural network development.

The MESO-BRAIN project facilitates a better understanding of human disease progression, neuronal growth and enables the development of large-scale human cell-based assays to test the modulatory effects of pharmacological and toxicological compounds on neural network activity. This can ultimately help to better understand and treat neurological conditions such as Parkinson’s disease, dementia, and trauma. In addition, the use of more physiologically relevant human models will increase drug screening efficiency and reduce the need for animal testing.

Aberrant activation of Wnt/β-catenin pathway is a key driver of colorectal cancer (CRC) growth and of great therapeutic importance. In this study, we performed comprehensive CRISPR screens to interrogate the regulatory network of Wnt/β-catenin signaling in CRC cells. We found marked discrepancies between the artificial TOP reporter activity and β-catenin–mediated endogenous transcription and redundant roles of T cell factor/lymphoid enhancer factor transcription factors in transducing β-catenin signaling. Compiled functional genomic screens and network analysis revealed unique epigenetic regulators of β-catenin transcriptional output, including the histone lysine methyltransferase 2A oncoprotein (KMT2A/Mll1). Using an integrative epigenomic and transcriptional profiling approach, we show that KMT2A loss diminishes the binding of β-catenin to consensus DNA motifs and the transcription of β-catenin targets in CRC. These results suggest that KMT2A may be a promising target for CRCs and highlight the broader potential for exploiting epigenetic modulation as a therapeutic strategy for β-catenin–driven malignancies.

Colorectal cancer (CRC) represents one of the major malignancies and a leading cause of cancer-related death worldwide. Aberrant Wnt/β-catenin pathway plays a pivotal role in colon carcinogenesis (1). Cytoplasmic β-catenin is phosphorylated by a protein complex containing adenomatous polyposis coli (APC), AXIN1 or AXIN2, casein kinase 1α (CK1α), and glycogen synthase kinase-3β (GSK3β), leading to β-catenin destruction through ubiquitin-proteasome system. Wnt binding to the LDL receptor related protein 5/6 (LRP5/6)–frizzled receptors results in the disassembly of the β-catenin–destruction complex and consequent accumulation of β-catenin. β-Catenin then enters into the nucleus and binds to T cell factor/lymphoid enhancer factor (TCF/LEF) transcription factors to initiate the transcription of β-catenin downstream targets (2).

Nearly all colorectal tumors (CRC) harbor genetic mutations that lead to the hyperactivation of β-catenin signaling. For example, germline or spontaneous mutations in tumor suppressor APC may cause constitutive activation of β-catenin in colon stem cells and the development of colonic polyps, which may eventually evolve into colorectal carcinomas. Hyperactivated β-catenin initiates the expression of various downstream targets through binding to the promoter regions via TCF/LEF transcription factors. Studies using transcriptomic approaches have characterized various β-catenin–responsive targets, such as cMYC, AXIN2, ASCL2, LGR5, and CD44. Collectively, these targets promote proliferation (e.g., cMYC) and maintain a stem cell state (e.g., LGR5 and ASCL2), highlighting the potential value of developing treatments that target β-catenin signaling in cancer. However, β-catenin itself is an intractable drug target (6, 7).