A complete guide how to get rid of them. I hope i will never have to use this guide. 2015-05-28: Bed bugs were nearly eradicated in the days of DDT, but have since evolved resistance. They loom large in our fears.
But its dominance went through a hiccup in the 50 years following the Second World War. During this time, the bug was a mere phantom in the United States and parts of Europe, Asia and Australia, wiped out, in part, by DDT and other modern chemical marvels. The pest was so rare that it shrank in our collective memory until it seemed like it didn’t exist at all, save as a bogeyman in a nursery rhyme: Good night, sleep tight. Don’t let the bed bugs bite. Then, starting in the early 2000s or so, bed bugs descended like a plague on New York and other cities across the world. The exact story of their comeback isn’t clear, but the best version is this: not long after the DDT deluge, some of the bugs had evolved resistance to the insecticide – an evolutionary inevitability – and survived in pockets worldwide.
he long struggle to turn medicine from art to science: checklists increase ICU survival rates by 50%. algorithms save lives.
The checklists provided 2 main benefits, Pronovost observed. First, they helped with memory recall, especially with mundane matters that are easily overlooked in patients undergoing more drastic events. (When you’re worrying about what treatment to give a woman who won’t stop seizing, it’s hard to remember to make sure that the head of her bed is in the right position.) A second effect was to make explicit the minimum, expected steps in complex processes. Pronovost was surprised to discover how often even experienced personnel failed to grasp the importance of certain precautions. In a survey of I.C.U. staff taken before introducing the ventilator checklists, he found that 50% hadn’t realized that there was evidence strongly supporting giving ventilated patients antacid medication. Checklists established a higher standard of baseline performance.
Open Prosthetics (OP) is a web-based education and collaboration initiative of the Shared Design Alliance, a 501(c)3 non-profit corporation. We are dedicated to facilitating crowd-sourced curation of information and collaboration in the field of prosthetics and coping with missing body parts in general. OP was created and has been maintained with the hope of producing useful innovations, and of creating an environment conducive to the creation of such innovations: the “adjacent possible”
Virtually all living creatures emit very weak light, which is thought to be a byproduct of biochemical reactions involving free radicals. This suggests cameras that can spot the weak emissions could help spot medical conditions.
Fat, sugar, and salt are the crucial elements for “eatertainment”: Frito-Lay is trying to create “a lot of fun in your mouth”, others to “unlock the code of craveability,” or to “cram as much hedonics as you can in 1 dish.”
The team solved the problem of delivery of siRNAs into cells by making a PTD fusion protein with a double-stranded RNA-binding domain, termed PTD-DRBD, which masks the siRNA’s negative charge. This allows the resultant fusion protein to enter the cell and deliver the siRNA into the cytoplasm where it specifically targets mRNAs from cancer-promoting genes and silences them.
We envisage cancer as the execution of an ancient program pre-loaded into the genomes of all cells. It is rather like Windows defaulting to ‘safe mode’ after suffering an insult of some sort. The new theory predicts that as cancer progresses through more and more malignant stages, it will express genes that are more deeply conserved among multicellular organisms, and so are in some sense more ancient. Genes that are active in the embryo and normally dormant thereafter are found to be switched back on in cancer. These same genes are the ‘ancient’ ones, deep in the tree of multicellular life.
2014-05-17: Measles Virus as a Cancer Fighter. Remarkable: fighting one scourge with another.
1 study of kidney cancers found that no 2 patients had exactly the same set of genetic mistakes; in fact, no 2 tumors within the same patient had the same mutations. Taking it one step further, 1 high-resolution DNA-sequencing study of breast cancer couldn’t find 2 cells within 1 tumor that were genetically identical
2015-08-26: Reprogramming cancer cells. Apply a large grain of salt to the claim, but the mechanism is still very interesting.
miRNAs orchestrate whole cellular programs by simultaneously regulating expression of a group of genes. The investigators found that when normal cells come in contact with each other, a specific subset of miRNAs suppresses genes that promote cell growth. However, when adhesion is disrupted in cancer cells, these miRNAs are misregulated and cells grow out of control. Restoring normal miRNA levels in cancer cells can reverse that aberrant cell growth.
2015-09-23: Dark matter cancer? This is pretty much speculation, but interesting speculation.
We can thus speculate that the mirror micrometeorite, when interacting with the DNA molecules, can lead to multiple simultaneous mutations and cause disease
Unfortunately, we’re still stuck in dogma. We continue to live in a world where the standard of cancer care is built on the naïve, almost arrogant, assumption that simply understanding the gene is the only important thing. Or that understanding 50 genes or even 500 genes will give us all the information to unlock the secrets of cancer cell metastasis. But our research is beginning to show that this is no longer the case. The bottom-line is that the biology of cancer is extraordinarily complex. It’s so complex that the output of the gene—specifically, the downstream networks of proteins within our bodies—is even more important than the gene itself.
Scientists at Sichuan University have injected a person with aggressive lung cancer with cells modified using the gene-splicing technology in a bid to make the patient’s immune system more effective at combating cancer cells.
cancer death rates continue to fall across most cancer types. From 2010 to 2014, overall death rates decreased by 1.8%. 5-year survival rates for most common types of cancer have increased quite significantly in the past 30-40 years.
Official statistics say we are winning the War on Cancer. Cancer incidence rates, mortality rates, and 5-year-survival rates have generally been moving in the right direction over the past few decades.
More skeptical people offer an alternate narrative. Cancer incidence and mortality rates are increasing for some cancers. They are decreasing for others, but the credit goes to social factors like smoking cessation and not to medical advances. Survival rates are increasing only because cancers are getting detected earlier. Suppose a certain cancer is untreatable and will kill you in 10 years. If it’s always discovered after 7 years, 5-year-survival-rate will be 0%. If it’s always discovered after 2 years, 5-year-survival-rate will be 100%. Better screening can shift the % of cases discovered after 7 years vs. 2 years, and so shift the 5-year-survival rate, but the same number of people will be dying of cancer as ever.
This post tries to figure out which narrative is more accurate.
and another perspective:
Death rates from the disease in the US dropped in the 2016-2017 period by their largest recorded %. This is unequivocally good news, and is attributed to advances in treatment – specifically, the advent of immunotherapies and of various targeted agents for lung and skin cancer. It may come as a surprise to some, but these death rates have actually been falling since the early 1990s at ~1.5% a year, a good part of which can be attributed to the decline in smoking. But the 2016-2017 decline bumped up to 2.2%, which has never been seen before
Aggressive cancers can spread so fiercely that they seem less like tissues gone wrong and more like invasive parasites looking to consume and then break free of their host. If a wild theory recently floated in Biology Direct is correct, something like that might indeed happen on rare occasions: Cancers that learn how to roam between hosts may gradually evolve into their own multicellular species. Researchers are now scrutinizing a peculiar group of marine parasites called myxosporeans to see whether they might be the first known example.
Scientists are unraveling the molecular pathways by which slashing calories or removing a dietary component can bolster the effects of drugs. In mice with cancer, the effects are oftentimes on the same order of magnitude as those from the drugs that we give patients. If those trials show the ketogenic diet helps curb tumor growth for 2 years longer than the PI3K inhibitor otherwise would, the diet could become the standard of care. “That will be what physicians will tell patients to do.”
2022-08-14: Tumors recruit the nervous system to help them spread.
“The nervous system controls everything in normal tissues—growth or atrophy, or anything else”. So there’s a reason to believe that the same is happening with malignancies. “Cancer tissue grows fast so it needs the support of the nervous system”. Moreover, scientists know that certain cancers have a particular predilection for nerves. “For example, breast and prostate tumors have a propensity to look for nerves and kind of invade and travel through those nerves. That suggests that there is synergy there.”
The observational knowledge suggests that a greater amount of nerves bunching up around a tumor signals grimmer prognosis. For example, when pathologists assess the severity of prostate cancer, the number of nerves that surround these tissues factors in. “The pathologist will score that, and if there’s a lot of nerves in the area, it usually means a worse, or a more urgent situation. To us, that seems like a blind spot or a missing link.”
After several decades, therapeutic cancer vaccines now show signs of efficacy and potential to help patients resistant to other standard-of-care immunotherapies, but they have yet to realize their full potential and expand the oncologic armamentarium. Here, we classify cancer vaccines by what is known of the included antigens, which tumors express those antigens and where the antigens colocalize with antigen-presenting cells, thus delineating predefined vaccines (shared or personalized) and anonymous vaccines (ex vivo or in situ). To expedite clinical development, we highlight the need for accurate immune monitoring of early trials to acknowledge failures and advance the most promising vaccines.
Gregor J. Rothfuss 