Saturday, April 26, 2014
Leland Stanford is known as being an early primary investor and then President of Central Pacific Railroads and later founder (with his wife Jane) of the Stanford University. Interesting stories are associated with Leland, including "The Inventor and the Tycoon" by Edward Bell of which initially piqued this writer's interest and this post. This article does not focus however, upon Sanford's association with the "inventor" Eadweard Muybridge. Extensive land grants and bonds were authorized to be issued so that two railroad lines (Central Pacific and Pacific Union) could construct a transcontinental railway. This authorization occurred in 1862 when Abraham Lincoln approved the Pacific Railroad Act of 1862, as a war measure for the preservation of the union. Leland was present at the physical joining of the two railroad lines (Central Pacific from San Francisco and Western Pacific from Omaha/Council Bluffs) meeting at Promontory Summit, Utah in 1869. Leland later commissioned Thomas Hill to make a painting of the event but Stanford did not want the painting particularly accurate (we have photos for that, he said in effect). Stanford advised Hill that only he should be depicted with a hammer and he further instructed Hill that people to be painted about him were to be of his friends and business partners whether they were actually there or not at the event . Stanford "told Hill who would appear and where they might be placed-seventy one people altogether and they had to be recognizable" "Inventor and Tycoon, p. 102. However, later Leland changes his mind as to some of the painted individuals and makes Thomas Hill paint over some of the figures and turn them into other favored people. However, one of Stanford's partners, Charles Crocker was not near enough to the center of the painting and so when Crocker saw the painting, Crocker became enraged! So.....Stanford never paid Thomas Hill for his (year's long worth) work. No depiction of the Chinese men who had been imported to build the railroad are in the painting. Another story is that Leland and his wife had been childless for eighteen years of their marriage but suddenly, at the age of thirty nine, Jane was pregnant with a boy which would be named after his father! However, Leland Stanford Jr. however caught typhoid in Athens, Greece shortly before his 16th birthday when on a trip abroad with his family and was then rushed to Italy for medical treatment. Leland Stanford Jr. died from typhus in Florence, Italy. Later, in his memory, Leland and his wife, Jane founded Sanford University which was built on the grounds that had been Leland Stanford Sr.'s horse stock farm where he bred horses in Palo Alto. Leland Stanford died in 1893 and thereafter Jane oversaw Stanford University with the attentive care and concern of a mother. David Starr Jordan had been chosen based upon a recommendation by the Stanfords to be the President of Stanford University. However, Jane became concerned about Jordan's conduct and asked professor Goebel (her friend and confident) to keep a paper trail re Jordan's conduct. Finally, it was concluded by Jane that she would remove Jordan from his position as President of Sanford. Meanwhile (1905), there was an incident wherein she was poisoned by strychnine when she drank some spiked Poland mineral water in her home. The taste of the water had been bitter so she only had had a sip but fell sick but survived the ordeal. It was undetermined how that had happened. Shortly thereafter, she went to Hawaii for rest and further recovery (also had a chest cold) only to find her tummy troubled and thus she asked for and received by her trusted personal secretary of Bertha Berner, a bottle of bicarbonate soda only to find herself poisoned once again. Several physicians were called to her aid but she was not saved: "As Humphris tried to administer a solution of bromine and chloral hydrate, Mrs. Stanford, now in anguish, exclaimed, “My jaws are stiff [Humphris confirmed the contraction of her jaw muscles by palpation]. This is a horrible death to die.” Whereupon she was seized by a tetanic spasm that progressed relentlessly to a state of severe rigidity: her jaws clamped shut, her thighs opened widely, her feet twisted inwards, her fingers and thumbs clenched into tight fists, and her head drew back. Finally, her respiration ceased." Source: The Mysterious Death of Jane Stanford (Stanford University Press, 2003), Stanford physician Robert W.P. Cutler. Strychnine was found in the bicarbonate soda just as it had been found in the mineral water. An autopsy and an inquiry by a coroner’s jury followed. After reviewing the autopsy report and hearing three full days of testimony, the jury took only two minutes to reach its conclusion: “... Jane Lathrop Stanford came to her death ... from strychnine poisoning, said strychnine having been introduced into a bottle of bicarbonate of soda with felonious intent by some person or persons to this jury unknown.... ” A dispatch in The New York Times of March 11, 1905, stated that the verdict was "written out with the knowledge and assistance of Deputy High Sheriff Rawlins," implying that the jurors may have been coached on what conclusion to reach. By this time, Jordan was en route to Honolulu with a party of his own. Upon his arrival, Jordan quickly hired a local physician, Ernest Coniston Waterhouse, to dispute the cause of death. Waterhouse was paid $7000 to complete a four page document which found that contrary to the earlier reports of poisoning, Mrs. Stanford had died of heart failure. Whether Jordan tried to contradict the findings of the other physicians to protect the University's reputation or to protect his job is still unknown today. Whether the trusted personal secretary was somehow (whether wittingly or not) a part of this poisoning is unclear either ( she was the only party present at both poisonings but she had been a trusted employee of twenty years standing). After Jane's death, Jordan fired Goebel from his position. See also: http://alumni.stanford.edu/get/page/magazine/article/?article_id=36459
Tuesday, February 26, 2013
Born on February 25, 1841 in Limoges, Renoir is one of the leaders of the Impressionist movement. He moved to Paris with his family, where he was apprenticed as a porcelain painter in 1856. Using his meager wages, Renoir attended painting lessons in the atelier of Charles Gleyre, where he met Claude Monet, Alfred Sisley, and Frédéric Bazille. He joined with them to organize the first of the Impressionist exhibitions in 1874 and participated in subsequent shows. Unlike other Impressionists, who worked mainly with landscape and natural light, Renoir preferred to focus on individuals, most of whom he depicted in moments of leisure, indoors and out. Young Girls at the Piano dates from a time of crisis in the artist’s career. By the late 1870s, Renoir felt that he had “wrung Impressionism dry” and, influenced by Raphael’s work on a trip to Italy in 1881, turned away from fleeting effects of light for a more monumental approach to form. Initially, his efforts to use more precise draftsmanship resulted in paintings that were, in his own words, “extraordinarily dry,” but by the end of the decade, he had evolved the approach, seen in Young Girls at the Piano, that combines more exact drawing with the warm tones of his earlier Impressionism. The identity of the girls in the picture is not known, but the painting above shown is displayed in Joslyn Museum in Omaha, Nebraska, and is the first, and most spontaneous, prototype for a painting commissioned by the French government. Coming this summer is the "Renoir to Chagall: Paris and the Allure of Color" exhibit at Joslyn! Now take a gander of this similar painting now on display at the Metropolitan Museum of Art dated as late 1891 or early 1892. Likewise it is called "Two Young Girls at the Piano". Apparently this painting (and its similar ilk) are a result of Renoir being invited by the French government to produce a painting for a new museum in Paris, the Musée du Luxembourg, which was to be devoted to the work of living artists. Up to that time, the French State had never made any official purchase from Renoir. In fact at first there was much derision and scorn from the French artistic establishment as to Impressionism which resulted in Impressionist art not being shown in the Salons at Paris w...resulting in their only being shown in Salaon de Refusés such as in 1863 and separate such showings set apart from the traditional Salons of the time. Traditional paintings such as by Ernest Meissonier (whom, one notes, is no longer remembered as well as impressionists such as Manet, Monet, Degas, Whistler) was at that time the preferred and scucessful artist. As noted above, Renoir had moved away somewhat from the Impressionist style but still employed its influence by the time of the painting of the Girls at the Piano paintings. So again, finally in an attempt to bring newer artist into the lime light with proper official recognition, in 1892 Stépahe Mallarmé helped by a Roger Marx, a member of the Beaux Arts administration in Paris, steps were taken to bring Impressionist and current nontraditional works into the national museums ( The preceding painting apparently is from the Lehman collection and now at the Metropolitain Museum of Art in NYC.) Now, the above painting, of which you will note is trés similar to the above two paintings and this one hangs in the Musee d'Orsay in Paris. So which paiting actually hung in the Musée du Luxembourg originally? Apparently not the one at Joslyn as it is claimed as one of the first prototypes. Apparently four finished versions using the same composition (the one at the Musee d'Orsay and the one in the Metropolitan Museum de New York (see above) and two others in private collections apparently including that of Gustave Caillebotte (or his descendants rather as he was a collector but artist in his own right at the time (see Paris Street; Rainy Day 1877 (Chicago Institute of Art)(Caillebotte also was responsible (organizer/financier/promoter) for exhibits of Impressionism especially in the late 1870s/early 1880s). There also exists a sketch of the Two Girls at the Piano in oils (Paris, Musée de l'Orangerie) and a pastel of the same size (private collection). The repetition of this motif shows Renoir's concentrated effort in this attempt. Actually there is so much regarding Renoir..how he employed Susan Valadon as a model in the 1880s (She is an artist herself and mother of Utrillo, yet another artist). But the above shall ponder only one of his masterpieces....a mystery of work of which I had pondered heretofore.
Wednesday, March 14, 2012
Alzheimers was not a word used in instances of "senile dementia" situations until more recent decades as it had been supposed such dementia was not so much a distinct disease but rather a matter of aging (albeit age remains a factor). However, now the term is also used in situations of non early onset and the diagnosis is validated by both clinical findings of behavior as well as amyloid plaques and neurofibrillary tangles. Futhermore, while "normal" persons (no behavioral disturbances) may have these same findings of amyloid plaques and neurofibrillary tangles, it may be a matter of degree especially of neurofibrillary tangles (as number of plaques are not necessarily indicative of degree of apparent dementia as evidenced by behavior). While past treatments have been aimed at reducing the amyloid plaques, this may have been misdirected. Amyloid plaques are extracellular whilst neurofibrillary tangles are intracellular. It is thought the the amyloid-beta peptide 42(a soluble protein) may be the major or causative element in the neurodegenerative process . Either too much amyloid-beta 42 is made or not cleared away. When too much is present, the individual little peptides stick together and cause oligomers. These gluey oligomers of amyloid-beta 42 lodge in synapses between neurons and interfere with synaptic transmission. Eventually the neurons atrophy from non-use and/or inflammation. Possibly the heap of amyloid-beta (e.g. 40 and 42) results in the plaques. Beta-amyloid gets released when the amyloid precursor protein (APP)* on a brain cell is cut by two enzymes: Beta-secretase and gamma-secretase. (A third enzyme that snips it, alpha-secretase, actually prevents Alzheimer's-related plaques from forming). (*APP is best known as the precursor molecule whose proteolysis** (**i.e. breakdown of protein into smaller units) generates beta amyloid 37 to 49 peptides whose amyloid fibrillar form is the primary component of amyloid plaques as found in Alzheimer). The secretase can cut APP at several points within a small region of the protein which results in alpha beta of various lengths. The length associated with Alzheimer's are 40 and 42 amino acids long. Alpha beta 42 is more likely to aggregate. In the less common heredity type of Alzheimers (fn A), it has been found that mutations found in presenilin* (*subcomponent of gamma secretase (multi pass transmembrane protein that functions as part of gamma secretase)) lead to an increase in the ratio of alpha beta 42 produced compared to Alpha Beta 40, albeit total quantity of alpha beta remains constant. As for Alzheimers in general, Aβ, which are unstructured in the monomeric state, go on to form characteristic beta-hairpin like structures in the fibrillar aggregates through a ‘misfolding’ step. On the way of transition from the monomeric peptide to fibrils* (*abnormal protein assembly) Aβ forms a wide variety of species of different sizes and some of them are related to the toxicity. The hairpin like ‘misfolding’ of the peptide seems to a critical phenomenon for the aggregation and may also be strongly related to the toxicity. When does this misfolding occur? A study of the lifetime of the fluorophore reports the end to end distance of this peptide in the monomeric as well as in the aggregated state reveals a major conformational transition between the monomer/small oligomer species (~1nm) and the larger oligomeric species (>2 nm) This perspective as to how Alzheimers may be initiated (and thus possibly prevented) appears circumstantially expressed by findings in the Nature study (2012) which suggest that when people have a newly discovered mutation on the APP gene, they naturally experience less cutting from beta-secretase, resulting in lower amounts of beta-amyloid getting into the brain from birth thus providing apparent protection from Alzheimers. (albeit this mutation has only thus far been found in Iceland) It is now believed that certain misfolded oligomers (known as seeds)can induce other amyloid beta molecules to take misfolded oligomer form, leading to a chain reaction akin to prion infection. There is some evidence the misfiled amyloid beta can induce tau to misfold as well. Such may result in the inception of toxic protein species due to nonproductive templating (e.g. where the substrate exceeds amyloid conversion or if amino acid sequences are incompatible) and such may give rise to abnormal conformation of species that may go on to form toxic oligomers (e.g. soluble oligomer of the amyloid-beta peptide 42) and amorphous aggregates. Prefibrillar oligomers may disassemble tau dependent microtubules (resulting in the neurofibrillary tangles) and thus may cause and or contribute to the disruption of axonal transport (i.e. specific oligomeric form of amyloid-beta (esp # 42) is a trigger for loss of synapses and neuronal damage) Questions remain as to whether the over expression of the precursor protein (APP) is sufficient to cause pathology. Thus the thinking is changing to that it may be the poorly defined pre-amyloid species rather than the plaques that are the true toxic conformations. The subsequent amyloid plagues themselves also seem to be a protection against Alzheimer's. More recent studies have found that these plaques as well as inclusion bodies may circumvent the formation of more toxic species such as pre fibrillar oligomers and thus are actually a reaction and/or protection devise as opposed to pathogenic: plaque formation being an attempt to protect cells from the effect of toxic misfolded proteins. Rather than cellular dysfunction and neuronal loss itself, amyloid plaques may be the product of a cellular process enabling cells to cope with the accumulation of misfolded and damaged proteins. It is suggested that the plaques and inclusion bodies may become inefficient from accumulating protein damage. (Much still needs to be understood but long past are the days when researchers peered into the brains that had evidenced dementia and found mysterious items...and pondered....were they alive? Past researchers pondered whether the mysterious findings were of fungal nature (mycotic?)). Much more is known now; much more needs to be gleaned. Interesting studies show for example that small poisonous Aβ assemblies, called oligomers, bind strongly to vulnerable neurons in the brain, but in the presence of collagen VI, this binding was blocked. Studies showed that collagen VI and Aβ form large aggregates with each other that may sequester the smaller, more toxic Aβ complexes away from neurons. Important clues such as the presence/effect of collagen VI (made in the brain itself!) provide possible solutions against AD. Also some researchers have found that the Aβ oligomers induce some of the symptoms of Alzheimer's Disease by competing with insulin for binding sites on the insulin receptor, thus impairing glucose metabolism in the brain. There are also studies regarding the positive effect of acid DHA in relation to alzheimers. Also another approach is one by Biogen which is researching an antibody called "adu" which appears to target amyloid protein and which has shown some evidence of promise in patients with mild and even incipient Alzheimers (evidenced by clinical findings (e.g. cognitive tests) as well as by emerging technology of imaging equipment that allows clinicians to pin point amyloid deposits and tau in the brain) (Aducanumab antibody derived from elderly patients in Switzerland who were especially mentally quick and healthy). So fingers are crossed and one can be cautiously optimistic for the future. A new avenue of study regards C1q which is a protein that normally does synaptic pruning (essential for the brain) but if in conjunction with the toxic soluble Aβ, it may cause synaptic destruction. Fn A(Re hereditary alzheimers, dominant mutations in genes that encode presenilin proteins are the most common cause of familial early onset Alzheimers)
Saturday, February 18, 2012
France was the center point of fashion in the 1700s and thus the focus herein (i.e. Paris and Versailles). A curious development regarding hair occurred in the 1700s when King Louis XIII, displeased with his male pattern baldness, commenced wearing wigs and such "fashion" was then adopted by others and also wigs were adopted by King Charles II of England, likewise not fond of the thinning of his hair)(1600s)...and such trend continued to and included the time of King Louis XIV of France to King Louis XVI. Also, this provided a tidy solution to ridding one of lice (shaving and wearing a wig instead) or as prevention thereof as such was a problem in the 1700s. Women adopted this, in particular in the latter part of the 1700s, when Marie Antoinette wore increasingly high and elaborate hair, so did the ladies who could afford such hair treatment. This included wigs with wire caging and elaborate adornments. In the latter 1700s, powder was increasingly used to so that this increased hair size could be all uniform in color as one's own hair was insufficient and thus other hair had to be used...and often then could be matched with a person's own hair (if powdered) if visible. Men also felt it made them look wise. Women often opted for pastels as well (light blue, pink or lavender). Obviously the intricacies of such hair made it difficult to be washed frequently...thus "back scratchers" (sticks with tiny claws) were carried by women (e.g. at Versailles) who could then insert the stick carefully into the intricate curls and scratch any itches due to lice! Oh, my! In the 1780s, Marie Antoinette became disgusted with politics and withdrew from the Court and began to (when not dressed for state occasions) wear simpler clothes as did others (this was the time she took to dressing and distracting herself by pretending she was an Alpine shepherdess at Versailles). Simpler styles of England and the United States began to take hold also in France (and thus elsewhere in Europe). Of course, the French Revolution of 1789 made it very uncool to continue this wig/fancy hair trend as it was a sign of aristocracy (not a good thing at the time). Thus the trend stopped.
Sunday, June 22, 2008
June 22, 2008. Having read "Bananas, How the United Fruit Company Shaped the World" by Peter Chapman provided new insight as to this seemingly ubiquitous and inexpensive exotic fruit now consumed by Americans more than apples and oranges combined! The banana is a relatively new to these northern climates, at least in mass amounts. For most of the twentieth century , United Fruit had a monopoly of the banana industry. The fact that the banana is basically a clone/grown from sucklings makes it particularly susceptible to disease and some speculate the banana will perish by 2013, whilst others give it longer (but not much). There are hundreds of bananas. Some are red, some have an apple consistency, some are straight, but only certain ones are marketed. The initial banana that United Fruit sold was "Gros Michel" which is actually bigger than what we enjoy now (the Cavendish). Sadly , the Gros Michel met with disease (Panama disease) so that by around 1960 , the more disease resistant banana (Cavendish) was marketed instead (some claim it is less tastey than the Gros Michel). Sadly there is no current back up banana for the Cavendish, but studies are being done to try to remedy this. Building railroads in the countries that became "banana republics" was a way that United Fruit gained an unique inroad in the business. When governments did not cooperate, invasions and even coups occurred as spearheaded by United Fruit (e.g. Honduras and Guatamela). It is stated that the success of the Guatamela coup encouraged the Bay of Pigs (wherein United Fruit fleet were involved), which ultimately resulted in the Cuban Missile crisis. Beyond political repercussions, branding and propaganda/public relations were pioneered by the multinational company of United Fruit . Critical eyes and earthquakes and hurricanes in the 1970s led to United Fruit's demise. Chiquita is now the remnant of United Fruit (Chiquita being a branding tool used earlier by United Fruit , along with Carmen Miranda).
There is also another book that sounds interesting on this same subject but covers more of the biology of the fruit along with political aspects. It is called "Bananas. The Fate of the Fruit that Changed the World" by Dan Koeppel.