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Another area osteology can cover is the trama a person suffered from throughout their life.  Because osteology only deals with bones, there are likely some sufferings that go missed during this analysis.  For example, if a person was stabbed but the knife did not come in contact with any bones, this trauma would be missed in osteologic analysis of the individual.  Traumas to bones can be identified in three different timing ranges, premortem, perimortem or postmortem.  Premortem traumas occur before the person died.  These traumas would often show signs of healing the the rough formation of bony tissue to heal the bone or the smoothing of this tissue indicating the injury had time to heal properly before the individual died.  Traumas that occur perimortem, at the time of death, show no signs of healing.  One type of trauma that can only occur perimotem is a hinge fracture.  Postmortem traumas vary in their appearance with how long the bones have been exposed to the elements.  Breaks in the bone will often appear lighter than the rest of the bone and depending how dry the bones are will look like the bone shattered.

Osteolgoy, the study of bones, can reveal a lot about how an individual lived their life but there are also many limitations to the kind of information that can be produced by osteology.  For example, when aging a skeleton, the most tool in age determination is the ossification or fusion of growth plates in the bone.  Each bone in the body has one or more centers of ossification which happens during a particular age range in a human's life.  By analyzing an assortment of bones, an approximate age of an individual can be determined only if the bones are still maturing.  Once all the bones are ossified, around the age of 27 when the S1 suture closes, determining the age gets mroe difficult and less precise to narrow down.  From here, the breakdown and wear and tear of the bones are used to determine age.  One of the most useful bones to have with this type of age determination is the ox coxa which contains both the aricular surface and public symphysis which gives an relatively accurate range of the individual's age.  

In class on September 12th  of 2019 and September 19th, 12 different adult tree species were measured into 8, 20 by 20m areas. Multiple groups measured out two 10m  x 10m plots within the area. Inside each 10 x 10 plot, a 4x4m subplots was measured out. These plots were measured out in 3 different locations; the North Slope, South Slope and the Notch in the Holyoke Range. Before the groups began measuring out plots, they were placed 10 meters apart. The groups purpose was to measure the amount of tree species in two stages of development, sapling and adult.

Differences in air temperature, and solar radiation are also functions of elevation, specifically “photosynthetically active radiation” as these are expected to vary with along a gradient due to differences in topography of a region (Alves, et al 2010).  Based off of this research, it was hypothesized steepness of slopes impacts vegetation in an area, where slopes that receive more sun have higher productivity. If this hypothesis is true, it was predicted that there will be a higher density of adults on the south slope and the lowest density on the north slope, the flat slope density will be in-between. Total biomass of all species, based on basal area, will be highest on south and lowest on the north slope. There will also be a higher density of saplings on the south slope and the lowest density on the north slope, the flat slope density will be in-between. 

    First documented in the early 1950s, Kuru is a rare and incurable disease that was common to the Fore people of Papua New Guinea. It was the first chronic degenerative disorder in humans to be shown to be transmissible and paved the way for the discovery of prions, an entirely new type of disease vector. This review aims to provide a short overview of the history, demographics, causes, symptoms, and neuropathology of kuru and how it has influenced research into other neurological disorders.

    Kuru is a rare disease, and virtually all cases of the disease have been documented in the tribes inhabiting a subregion of Papua New Guinea. At that, less than 3000 cases were ever documented (Alpers, 2007). In 1957, there were 200 deaths due to kuru reported in the Fore population, and by 2005 only 1 death due to kuru was reported in the population, after which no more kuru-related deaths were reported (Alpers, 2007). Kuru first came under study in 1957 - when Charles Pfarr reported that it had become an epidemic in the Fore people - by a virologist named Daniel Carleton Gajdusek (Alpers, 2007). Gajdusek spent two years in Papua New Guinea examining the disease, after which he performed experiments on chimpanzees (Gajdusek, 1957). In 1960, shortly after his reports about the fact that cannibalism was the most likely cause of the disease, the practice was banned, but research into the disease continued (Alpers, 2007). In his experiments, Gajdusek demonstrated that kuru was transmissible and could cross the human-primate species barrier which he attributed to some unknown disease factor that came from the brain matter of infected humans (Gajdusek, 1966). Prions as the root cause of kuru came later, catalysed by E. J. Field’s work comparing kuru to scrapie and multiple sclerosis and his observation that molecular aggregation was critical to the infection process (Field, 1967).

Nitrogen is one of the most important elements found in fertilizers for plant growth because it is often that soil may be lacking it. When nitrogen is added to soil outdoors, it becomes a part of the complex nitrogen cycle that passes through life on earth. The nitrogen cycle may begin with gaseous nitrogen in the atmosphere. Often unnoticed, nitrogen is at a high concentration in the air we breathe compared to oxygen. The atmospheric nitrogen is in its diatomic form, N2. From here, nitrogen can be deposited by lightning or it is fixed by nitrogen-fixing bacteria and microbes in the soil that turn it into nitrates and ammonium. The ammonium can be made into nitrites by other nitrifying bacteria. From there, plants take up the nitrates and use it in chemical processes and in different molecules. The nitrogen travels up the food chain and gets deposited by different organisms back into the soil by waste products or by decay and decomposition. The decomposers then transform the nitrates back into ammonium in the soil. Denitrifying bacteria then transform nitrates back into atmospheric nitrogen when oxygen levels are low, reducing the mitrogen in the soil and increasing the nitrogen in the atmosphere. The cycle then repeats. 

There are three parts to the small intestine; the duodenum, the jejunum, and the ileum. In the small intestine, Carbohydrates are broken down into monosaccharides, Lipids are broken down into individual fatty acids, and Proteins are broken down into individual amino acids. All of these macronutrients are broken down into their simplest forms and absorbed through the walls of the small intestine, made up of simple columnar epithelial tissue. The Pyloric sphincter regulates passage of chyme into the small intestine, where chyme is the acidic fluid that passes from the stomach to the small intestine, consisting of gastric juices and partly digested food. The pyloric sphincter is a smooth muscle sphincter that regulates passage of contents through the stomach to the small intestine. When it is constricted: nothing passes, and when it is relaxed: allows small amounts of chyme to enter the small intestine. This is an important regulation because you pepsin is required to cleave proteins before they enter the small intestine, and will prevent the small intestine from being overwhelmed.

In the small intestine those acidic contents from the low pH of the stomach get passed here (chyme). It’s regulated at the pyloric sphincter. Pancreatic juices get secreted here which have those enzymes for each macronutrient that breaks it down to individual molecules so that it can move on. For carbs we have pancreatic amylase breaking carbs down and brush border enzymes lactase sucrase and maltase which break them down even further from disaccharides into monosaccharides. If the disaccharides can’t be broken down they can’t be absorbed! They’ll remain in the gut and create osmotic pressure which makes you bloated. They need to be broken into individuals. Their transport across the membrane is by secondary active transport and facilitated diffusion. They are also broken down prior to transport. For protein we have those proteases. Pepsin cleaves the protein, trypsin and chymotrypsin cleave them more, and FINALLY and carboxypeptidase cleaves then even more and makes them individual amino acids. Transport here is also through secondary active transport and facilitated diffusion. Amino acids then get secreted into the interstitial fluid and enter the bloodstream. Last- lipids are cleaved by the lipases to become individual fatty acids. This starts with emulsification. The globule of fat is emulsified by bile salts to be able to enter aqueous solutions. Otherwise, without these bile salts, it cannot enter. The bile salts act like detergent and break down the globule into smaller pieces. NOW, lipases can break them down into their individual forms. Once they’re individual fatty acids, they get packaged in these molecules called micelles, which diffuse into enterocytes. After this, the micelle’s get packaged into molecules called chylomicrons. So it’s like a box filled with something going into another box. So now the individual fatty acids packaged in the chylomicrons get secreted into the interstitial space and travel in lymphatics to the bloodstream because they’re too large.

The effects of ADH, Aldosterone, and Angiotensin II all increase blood pressure. AntiDiuretic Hormone (ADH) increases reabsorption of water, plasma volume, and cardiac output e.g. EDV and therefore blood pressure increases. In the Distal convoluted tubule, aldosterone determines the final rate of sodium reabsorption and therefore adjusts the sodium concentration in the bloodstream It’s a hormone so it’s regulated by the endocrine system. Aldosterone is secreted by the adrenal cortex of the kidney. High aldosterone means increased sodium reabsorption. Because water follows solutes, if we increase sodium reabsorption, water reabsorption also occurs. Though, this ultimately depends on expression of ADH, which we will get into...but for now, just assume if everything else is “normal,” increased aldosterone release increases sodium reabsorption and water as well. The increased sodium reabsorption would increase blood volume, blood pressure, cardiac output, increases EDV, and increases SV. It is important to know that blood pressure increases in response to more reabsorption of fluid, and the reabsorption of fluid is driven by the reabsorption of sodium.
In the collecting duct, we know that final reabsorption of water occurs here and is dependent on ADH. ADH adjusts the osmolarity of the extracellular fluid by reabsorbing water, and is secreted by the pituitary gland of the hypothalamus. If ADH is secreted, this will signal the insertion of aquaporins, which are the channels that allow water to pass and be reabsorbed in the medulla when it follows down its concentration gradient. Side note - but remember that the gradient water follows is basically anything with a lot of salt. Deep in the medulla, as discussed, is a highly concentrated area. So water follows salt as it reaches down there when its traveling in the collecting duct, and gets reabsorbed into the blood. But like I said, this is only if ADH is secreted and signals aquaporin insertion.

 There are many elements vital to sustaining life. These elements, like energy itself, and not created or destroyed, but transfered from form to form and travel through cycles in the environment. Such elements include phosphorus which cycles through forms and life and is used and wasted and restored over and over. The phosphorus cycle may start in the form of solid rocks and geological formations. The phosphorus is present in rocks in the chemical form of phosphates. The rock, deep underground, rises from plate movements and volcano activations can pump it into the air and then it settles on the ground surfaces. When the rock rises to the surface, the phosphorus is exposed to weather. Here, the phosphorus is weathered from the rocks by wind, rain, and other disturbances. The phosphorus is now dissolved in solution and can leach into soil or run off into water pools. From the soil, the phosphorus gets used by plants to form different molecules. These plants are consumed by primary consumers and the molecules travel up the food chain. Eventually, the phosphorus returns to the soil by decomposers like fungi and certain bacteria. In cases of high run off, the phosphorus leaches out of the soil into the water pools. Here the phosphorus settles to the bottom and eventually forms new sediments and compresses down into rocks and other formations as phosphates once again.