Jean-Baptiste Lamarck
Jean-Baptiste Pierre Antoine de Monet, Chevalier de Lamarck (1 August 1744 – 18 December 1829), often known simply asLamarck (/ləˈmɑrk/;[1] French: [lamaʁk]), was a French naturalist. He was a soldier, biologist, academic, and an early proponent of the idea that evolution occurred and proceeded in accordance with natural laws. He gave the term biology a broader meaning by coining the term for special sciences, chemistry, meteorology, geology, and botany-zoology.[2]
Lamarck fought in the Pomeranian War (1757-1762) with Prussia, and was awarded a commission for bravery on the battlefield.[3] At his post in Monaco, Lamarck became interested in natural history and resolved to study medicine.[4] He retired from the army after being injured in 1766, and returned to his medical studies.[4] Lamarck developed a particular interest in botany, and later, after he published a three-volume work Flore française (1778), he gained membership of the French Academy of Sciences in 1779. Lamarck became involved in the Jardin des Plantes and was appointed to the Chair of Botany in 1788. When the Muséum national d'Histoire naturelle was founded in 1793, Lamarck was appointed as a professor of zoology.
In 1801, he published Système des animaux sans vertèbres, a major work on the classification of invertebrates, a term he coined. In an 1802 publication, he became one of the first to use the term biology in its modern sense.[5][Note 1] Lamarck continued his work as a premier authority on invertebrate zoology. He is remembered, at least in malacology, as a taxonomist of considerable stature.
In the modern era, Lamarck is widely remembered for a theory of inheritance of acquired characteristics, called soft inheritance,Lamarckism or use/disuse theory.[6] However, his idea of soft inheritance was, perhaps, a reflection of the wisdom of the time accepted by many natural historians. Lamarck's contribution to evolutionary theory consisted of the first truly cohesive theory of evolution,[7] in which an alchemical complexifying force drove organisms up a ladder of complexity, and a second environmental force adapted them to local environments through use and disuse of characteristics, differentiating them from other organisms.[8]Scientists have debated whether advances in the field of transgenerational epigenetics mean that Lamarck was to an extent correct, or not.[9]
Biography
Jean-Baptiste Lamarck was born in Bazentin, Picardy, northern France,[4] as the eleventh child in an impoverished aristocratic family.[Note 2] Male members of the Lamarck family had traditionally served in the French army. Lamarck's eldest brother was killed in combat at the Siege of Bergen op Zoom, and two other brothers were still in service when Lamarck was in his teenage years. Yielding to the wishes of his father, Lamarck enrolled in a Jesuit college in Amiens in the late 1750s.[4]
After his father died in 1760, Lamarck bought himself a horse, and rode across the country to join the French army, which was in Germany at the time. Lamarck showed great physical courage on the battlefield in the Pomeranian War with Prussia, and he was even nominated for the lieutenancy.[4] Lamarck's company was left exposed to the direct artillery fire of their enemies, and was quickly reduced to just fourteen men – with no officers. One of the men suggested that the puny, seventeen-year-old volunteer should assume command and order a withdrawal from the field; but although Lamarck accepted command, he insisted they remain where they had been posted until relieved.
When their colonel reached the remains of their company, this display of courage and loyalty impressed him so much that Lamarck was promoted to officer on the spot. However, when one of his comrades playfully lifted him by the head, he sustained an inflammation in the lymphatic glands of the neck, and he was sent to Paris to receive treatment.[4] He underwent a complicated operation, and continued his treatment for a year.[10] He was awarded a commission and settled at his post in Monaco. It was there that he encounteredTraité des plantes usuelles, a botany book by James Francis Chomel.[4]
With a reduced pension of only 400 francs a year, Lamarck resolved to pursue a profession. He attempted to study medicine, and supported himself by working in a bank office.[4] Lamarck studied medicine for four years, but gave it up under his elder brother's persuasion. He was interested in botany, especially after his visits to the Jardin du Roi, and he became a student under Bernard de Jussieu, a notable French naturalist.[4] Under Jussieu, Lamarck spent ten years studying French flora.
After his studies, in 1778, he published some of his observations and results in a three-volume work, entitled Flore françoise. Lamarck's work was respected by many scholars, and it launched him into prominence in French science. On August 8, 1778, Lamarck married Marie Anne Rosalie Delaporte.[11] Georges-Louis Leclerc, Comte de Buffon, one of the top French scientists of the day, mentored Lamarck, and helped him gain membership to the French Academy of Sciences in 1779 and a commission as a Royal Botanist in 1781, in which he traveled to foreign botanical gardens and museums.[12] Lamarck's first son, André, was born on April 22, 1781, and he made his colleague André Thouin the child's godfather.
In his two years of travel, Lamarck collected rare plants that were not available in the Royal Garden, and also other objects of natural history, such as minerals and ores, that were not found in French museums. On January 7, 1786, his second son, Antoine, was born, and Lamarck chose Antoine Laurent de Jussieu, Bernard de Jussieu's nephew, as the boy's godfather.[13] On April 21 of the following year, Charles René, Lamarck's third son, was born. René Louiche Desfontaines, a professor of botany at the Royal Garden, was the boy's godfather, and Lamarck's elder sister, Marie Charlotte Pelagie De Monet was the godmother.[13] In 1788, Buffon's successor at the position of Intendant of the Royal Garden, Charles-Claude Flahaut de la Billaderie, comte d'Angiviller, created a position for Lamarck, with a yearly salary of 1,000 francs, as the keeper of the herbarium of the Royal Garden.[4]
In 1790, at the height of the French Revolution, Lamarck changed the name of the Royal Garden from Jardin du Roi to Jardin des Plantes, a name that did not imply such a close association with King Louis XVI.[14] Lamarck had worked as the keeper of the herbarium for five years before he was appointed curator and professor of invertebrate zoology at the Muséum national d'histoire naturelle in 1793.[4] During his time the herbarium, Lamarck's wife gave birth to three more children before dying on September 27, 1792. With the official title of "Professeur d'Histoire naturelle des Insectes et des Vers", Lamarck received a salary of nearly 2,500 francs per year.[15] The following year on October 9, he married Charlotte Reverdy, who was thirty years his junior.[13] On September 26, 1794, Lamarck was appointed to serve as secretary of the assembly of professors for the museum for a period of one year. In 1797, Charlotte died, and he married Julie Mallet the following year; she died in 1819.[13]
In his first six years as professor, Lamarck published only one paper, in 1798, on the influence of the moon on the Earth's atmosphere.[4] Lamarck began as an essentialist who believed species were unchanging; however, after working on the molluscs of the Paris Basin, he grew convinced that transmutation or change in the nature of a species occurred over time.[4] He set out to develop an explanation, and on 11 May 1800 (the 21st day of Floreal, Year VIII, in the revolutionary timescale used in France at the time), he presented a lecture at the Muséum national d'histoire naturelle in which he first outlined his newly developing ideas about evolution.
Rabies
Rabies is a viral disease that causes acute inflammation of the brain in humans and other warm-blooded animals.[1] Early symptoms can include fever and tingling at the site of exposure.[1] These symptoms are followed by one or more of the following symptoms: violent movements, uncontrolled excitement, fear of water, an inability to move parts of the body, confusion, and loss of consciousness.[1] Once symptoms appear it nearly always results in death.[1] The time period between contracting the disease and the start of symptoms is usually one to three months; however, this time period can vary from less than one week to more than one year.[1] The time is dependent on the distance the virus must travel to reach the central nervous system.[2]
Rabies is caused by lyssaviruses including: rabies virus and Australian bat lyssavirus.[3] Rabies is spread when an infected animal scratches or bites another animal or human.[1] Saliva from an infected animal can also transmit rabies if the saliva comes into contact with the mouth, nose, or eyes.[1] Overall dogs are the most common animal involved.[1] More than 99% of rabies cases in countries where dogs commonly have the disease are caused by dog bites.[4] In the Americas, bat bites are the most common source of rabies infections in humans, and less than 5% of cases are from dogs.[1][4] Rodents are very rarely infected with rabies.[4] The rabies virus travels to the brain by following the peripheral nerves. The disease can only be diagnosed after the start of symptoms.[1]
Animal control and vaccination programs have decreased the risk of rabies from dogs in a number of regions of the world.[1]Immunizing people before they are exposed is recommended for those who are at high risk. The high-risk group includes people who work with bats or who spend prolonged periods in areas of the world where rabies is common.[1] In people who have been exposed to rabies, the rabies vaccine and sometimes rabies immunoglobulin are effective in preventing the disease if the person receives the treatment before the start of rabies symptoms.[1] Washing bites and scratches for 15 minutes with soap and water,povidone iodine, or detergent may reduce the number of viral particles and may be somewhat effective at preventing transmission.[1][5] Only a few people have survived a rabies infection after showing symptoms and this was with extensive treatment known as the Milwaukee protocol.[6]
Rabies causes about 26,000 to 55,000 deaths worldwide per year.[1][7] More than 95% of these deaths occur in Asia and Africa.[1]Rabies is present in more than 150 countries and on all continents but Antarctica.[1] More than 3 billion people live in regions of the world where rabies occurs.[1] A number of countries including Australia, Canada, Japan, Malaysia, the United States, and Western Europe do not have rabies among dogs.[8] Many small island nations do not have rabies at all.[9]
Signs and symptoms
The period between infection and the first flu-like symptoms is typically 2 to 12 weeks in humans. Incubation periods as short as four days and longer than six years have been documented, depending on the location and severity of the contaminated wound and the amount of virus introduced. Signs and symptoms may soon expand to slight or partial paralysis, anxiety, insomnia, confusion, agitation, abnormal behavior, paranoia, terror, and hallucinations, progressing to delirium.[2][10] The person may have hydrophobia.
Death almost always occurs 2 to 10 days after first symptoms. Survival is rare once symptoms have presented, even with the administration of proper and intensive care.[11] Jeanna Giese, who in 2004 was the first patient treated with the Milwaukee protocol,[12]became the first person ever recorded to have survived rabies without receiving successful post-exposure prophylaxis. An intention-to-treat analysis has since found this protocol has a survival rate of about 8%.[13]
Cause
Rabies is caused by a number of lyssaviruses including: rabies virus and Australian bat lyssavirus.[17]
The rabies virus is the type species of the Lyssavirus genus, in the family Rhabdoviridae, order Mononegavirales. Lyssaviruses have helical symmetry, with a length of about 180 nm and a cross-section of about 75 nm.[18] These viruses are enveloped and have a single-stranded RNA genome with negative sense. The genetic information is packed as a ribonucleoprotein complex in which RNA is tightly bound by the viral nucleoprotein. The RNA genome of the virus encodes five genes whose order is highly conserved: nucleoprotein (N), phosphoprotein (P), matrix protein (M), glycoprotein (G), and the viral RNA polymerase (L).[19]
Once within a muscle or nerve cell, the virus undergoes replication. The trimeric spikes on the exterior of the membrane of the virus interact with a specific cell receptor, the most likely one being the acetylcholine receptor, acetyl. The cellular membrane pinches in a procession known as pinocytosis and allows entry of the virus into the cell by way of an endosome. The virus then uses the acidic environment, which is necessary, of that endosome and binds to its membrane simultaneously, releasing its five proteins and single strand RNA into the cytoplasm.[20]
The L protein then transcribes five mRNA strands and a positive strand of RNA all from the original negative strand RNA using free nucleotides in the cytoplasm. These five mRNA strands are then translated into their corresponding proteins (P, L, N, G and M proteins) at free ribosomes in the cytoplasm. Some proteins require post-translative modifications. For example, the G protein travels through the rough endoplasmic reticulum, where it undergoes further folding, and is then transported to the Golgi apparatus, where a sugar group is added to it (glycosylation).[20]
Where there are enough proteins, the viral polymerase will begin to synthesize new negative strands of RNA from the template of the positive strand RNA. These negative strands will then form complexes with the N, P, L and M proteins and then travel to the inner membrane of the cell, where a G protein has embedded itself in the membrane. The G protein then coils around the N-P-L-M complex of proteins taking some of the host cell membrane with it, which will form the new outer envelope of the virus particle. The virus then buds from the cell.[20]
From the point of entry, the virus is neurotropic, traveling quickly along the neural pathways into the central nervous system. The virus usually first infects muscle cells close to the site of infection, where they are able to replicate without being 'noticed' by the host's immune system. Once enough virus has been replicated, they begin to bind to acetyl choline receptors (p75NR) at the neuromuscular junction. [21] The virus then travels through the nerve cell axon via retrograde transport, as its P protein interacts with dynein, a protein present in the cytoplasm of nerve cells. Once the virus reaches the cell body it travels rapidly to the Central Nervous System (CNS), replicating in motor neurons and eventually reaching to the brain. [2] After the brain is infected, the virus travels centrifugally to the peripheral and autonomic nervous systems, eventually migrating to the salivary glands, where it is ready to be transmitted to the next host.
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