Ricki Lewis

As drugstore chains embrace products with traces of CBD, two recent reports in prominent medical journals point out the dangers of the other familiar component of cannabis, THC.

 

An article in Lancet Psychiatry strengthens the link of THC to psychosis, and one in Annals of Internal Medicine chronicles people ending up in the emergency departments of hospitals after indulging in edibles. The news media picked up the edible-ED story, the psychosis one not so much.

 

From 2012 through 2016, the University of Colorado Hospital saw a more than 3-fold increase in cannabis-associated ED visits. Edibles, which became available there in 2014, were disproportionately represented in those visits – 10.7 percent due to edibles, despite making up only 0.32 percent of total cannabis sales.

 

I can relate.

 

A short, strange trip

 

To continue reading, go to Genetic Literacy Project, where this post first appeared.

 

 

"Do you mind if we take one more sample?" asked the endocrinologist who had already stuck six needles into the bulge in my neck that would turn out to be thyroid cancer. "It's for a research study."

 

"On what?"

 

"Something called p53."

 

That's a tumor suppressor, a gene that lies at the crux of cancers triggered by environmental factors, like the 5 years of unprotected dental x-rays I'd had as a kid.

 

"I know what that is and hope I don't have a mutation. When will I get the results?"

 

"I'm afraid you won't. That's part of the protocol." My sample would be de-identified.

 

I forgot about it. Years later, I had genetic testing again, this time for breast cancer, from a blood sample sent to Invitae, a clinical testing lab. They applied their 80-gene cancer panel and threw in probes for another two dozen genes they were developing.

 

To continue reading, go to Genetic Literacy Project, where this post first appeared.

 

I'll admit that I have long admired the beauty of the large milkweed bug Oncopeltus fasciatus, without knowing anything about it. So I was pleased to read of the recent publication of its genome sequence, an effort undertaken by 83 researchers working as 27 teams in 10 nations. The findings are reported in Genome Biology.

 

Most of the 100+ insect species that have had their genomes sequenced are homometabolous, which means that they develop through several stages of larvae, metamorphose, and then burst from their cocoons looking completely different. (See "The Making of a Mutant" for a scintillating view of fruit fly larvae living in goop in a milk bottle.) Flies, beetles, wasps, and butterflies are among the homometabolous.

 

In contrast, milkweed bugs are hemimetabolous. The species of this group are less well represented among the sequenced, although they are more numerous. The juvenile stages of milkweed bugs are tiny, flightless versions of the adults, called nymphs, that have more orange.

 

The hemimetabolous insects have trademark mouthparts that pierce and suck, and include agricultural pests and vectors of human disease, like the kissing bugs that deliver Trypanosoma cruzi, the cause of Chagas' disease. A more familiar hemimetabolous insect is the bed bug Cimex lectularius.

 

The milkweed bug, so-named because it eats the bitter seeds of the milkweed plant Asclepias syriaca, joins many other insects and their arthropod cousins in having their genetic selves laid bare as part of the i5k project. The international consortium is sequencing the genomes of 5,000 arthropod species.

 

So far partial or complete genomes have been unveiled for, in alphabetical order, ants, aphids, bedbugs, bees, beetles, borers, cockroaches, crabs, crayfish, fleas, flies, lice, locusts, mealybugs, midges, mites, mosquitoes, pillbugs, psyllids, scorpions, shrimp, spiders, stinkbugs, ticks, wasps, weevils, worms, the delightful-sounding snowberry maggot and meadow spittlebug, and a pretty butterfly called a Glanville fritillary.

 

To continue reading, go to DNA Science, my blog at Public Library of Science.

 

 

I've just had cataract surgeries, so I wasn't thrilled to find a new report in the Proceedings of the National Academy of Sciences comparing the protein glitch behind them to the one behind Alzheimer's. Fortunately the similarity is only in how the proteins fold.

 

The amyloid beta buildup of cataracts could be an early marker that might eventually allow drug treatment to replace surgery. Too late for me, but that could be great news for the more than 18 million people worldwide  blinded by cataracts because they can't get surgery.

 

Cataracts develop as proteins coalesce in the lens, triggering spreading of patches of blurriness. They are the leading cause of blindness globally and affect half of people over age 50. My fellow PLOS blogger Hilda Bastian recently recounted the compelling story of the origin of cataract surgery.

 

A human lens is fascinating, in terms of biochemistry, cell biology, and evolution.

 

To continue reading go to my DNA Science DNA Science blog at Public Library of Science, where this post first appeared.