| My once little baby, who could probably beat me up now. |
BBC’s Passive Voice
1 day ago
A personal blog, named in honor of the novel Petticoat Government by a favorite author, Emma Orczy. The novel is about a fictional woman, Lydie d'Aumont, who attempts to inject some fairness and good governance into the court of France's Louis XVth despite the corruption and selfishness there.
| My once little baby, who could probably beat me up now. |
| A kilt-wearing wisp playing the harp with two wisps dancing to its sides. |
Secretory Diarrhea
Large volumes of water are normally secreted into the small intestinal lumen, but a large majority of this water is efficienty absorbed before reaching the large intestine. Diarrhea occurs when secretion of water into the intestinal lumen exceeds absorption.
Many millions of people have died of the secretory diarrhea associated with cholera. The responsible organism, Vibrio cholerae, produces cholera toxin, which strongly activates adenylyl cyclase, causing a prolonged increase in intracellular concentration of cyclic AMP within crypt enterocytes. This change results in prolonged opening of the chloride channels that are instrumental in secretion of water from the crypts, allowing uncontrolled secretion of water. Additionally, cholera toxin affects the enteric nervous system, resulting in an independent stimulus of secretion.
Exposure to toxins from several other types of bacteria (e.g. E. coli heat-labile toxin) induce the same series of steps and massive secretory diarrhea that is often lethal unless the person or animal is aggressively treated to maintain hydration.
In addition to bacterial toxins, a large number of other agents can induce secretory diarrhea by turning on the intestinal secretory machinery, including:
- some laxatives
- hormones secreted by certain types of tumors (e.g. vasoactive intestinal peptide)
- a broad range of drugs (e.g. some types of asthma medications, antidepressants, cardiac drugs)
In most cases, secretory diarrheas will not resolve during a 2-3 day fast.
- certain metals, organic toxins, and plant products (e.g. arsenic, insecticides, mushroom toxins, caffeine)
The immune response to inflammatory conditions in the bowel contributes substantively to development of diarrhea. Activation of white blood cells leads them to secrete inflammatory mediators and cytokines which can stimulate secretion, in effect imposing a secretory component on top of an inflammatory diarrhea. Reactive oxygen species from leukocytes can damage or kill intestinal epithelial cells, which are replaced with immature cells that typically are deficient in the brush border enyzmes and transporters necessary for absorption of nutrients and water. In this way, components of an osmotic (malabsorption) diarrhea are added to the problem.
Acute gastroenteritis is a common cause of morbidity and mortality worldwide. Conservative estimates put diarrhea in the top 5 causes of deaths worldwide, with most occurring in young children in nonindustrialized countries.
In the last years, a clear link between the endocrine signalling also influenced by Western diet and the pathogenesis of acne has emerged. In this context, a crucial role has been attributed to the hyperactivity of the conserved serine/threonine kinase mTORC1. mTOR is a nutrient-sensitive regulator of cellular growth, proliferation, lipid synthesis and protein translation, exerting its effects through two distinct signalling complexes: mTORC1 and mTORC2. In particular, the rapamycin-sensitive mTORC1 promotes cell growth and proliferation whereas mTORC2, rapamycin-non-sensitive, is involved in the regulation of cell polarity and in the functional phosphorylation of cytoskeleton actin fibres. mTORC1 is able to integrate multiple intra- and extracellular mediators such as growth factors (insulin, IGF-1) and energy-sensing signals (glucose, AMP/ATP-ratio), controlling the adequate availability of amino acids, especially the BCAA leucine, necessary for its own activation. Multiple diseases, either neoplastic, dysmetabolic or inflammatory, show dysregulation of mTOR pathway, which might be also involved in inflammatory skin diseases such as psoriasis, atopic dermatitis and allergic contact dermatitis. Enhanced levels of leucine [peanut butter is really high in leucine] and other amino acids, insulin, IGF-1 and glucose, deriving from meat, milk/dairy intake and high glycaemic load, permit mTORC1 activation through specific mechanisms. Consequently, by the phosphorylation of 4E-BP1, the lipin1 activator of SREBP-1 and S6K1, mTORC1 is able to enhance protein and lipid synthesis, as well as growth and cell proliferation. This could be translated into proliferation of acroinfundibular keratinocytes and increased lipid biosynthesis in sebaceous glands, responsible for seborrhoea. In two recent elegant papers, Melnik integrated mTORC1 signalling into the complex scenario of acne pathogenesis, highlighting the antagonistic interaction between the metabolic transcription factor FoxO1 and the nutrient-sensitive kinase mTORC1 . Nevertheless, either for the role of FoxO1 or for the modulation of mTOR in the pathophysiology of acne, direct evidences in humans are lacking.
There is a 90% probability that life expectancy at birth among South Korean women in 2030 will be higher than 86·7 years, the same as the highest worldwide life expectancy in 2012, and a 57% probability that it will be higher than 90 years. Projected female life expectancy in South Korea is followed by those in France, Spain, and Japan.
“The human mind and body contains a myriad of secrets awaiting discovery.”
“Sickness is the motivator for research by those that recognize improved health is just a discovery away.”
“Curiosity is what powers discovery.”
“When walking alone on the path of discovery, have faith that you are illuminating the way for others to follow.”
“Research is an endless loop of failures interspersed with occasional profound discoveries.”
As I've thought about the possible uses of cell phones and similar technology to affect us and our children for good or ill, I've lo...