Osteoporosis and Osteoarthritis Case Studies

Osteoporosis and Osteoarthritis Case Studies The main aim of this essay is to understand different aspects of medical conditions ranging from pathophysiology, symptoms, risk factors, and the management of two case studies. The first case study deals with osteoporosis and osteoarthritis. The second case deals with peptic ulcers and gastric esophageal reflux disease. To address both patients’ medical condition, knowing the condition’s pathophysiology is quintessential. Osteoarthritis is a disease of the joints, which affects the slippery tissue called cartilage which covers the joints (Kapoor, Martel-Pelletier, Lajeunesse, Pelletier Fahmi, 2010). The cartilage in healthy individuals ensures smooth sliding of bones over each other and better shock absorbance. In osteoarthritic patients, wearing of the top layer of cartilage leads to rubbing of bones against one another (Swift, 2012). This causes inflammation of the joint evident from swelling, pain and limited joint activity as time progresses (Kapoor et al, 2010). Excessive rubbing leads to gradual decrease in bone mass with loss in shape, bone spurs growing at edges of joints and a more painful condition manifested by floating of broken bones at joints in joint spaces (Swift, 2012). Osteoporosis on the other hand is marked by an imbalance between bone resorption and bone formation causing loss of skeletal mass (Huether McCance, 2012). In the normal physiological condition, bone resorption and formation are always in balance, thus maintaining the bone strength and mass. Any disorder in these two processes such as increased resorption or decreased formation can lead to osteoporosis (Huether McCance, 2012). In the above case Claire reported a fall and trauma which is a common symptom in an osteoporosis case. The common modifiable risk factors associated with osteoporosis are vitamin D and calcium deficiency (Wickham, 2011). Similarly cola, alcohol intake and smoking are three modifiable factors which can increase the chances or severity of the disease. Excessive alcohol or cola drinks intake leads to secondary osteoporosis by affecting bone formation, absorption of calcium and vitamin D, and disorder in calcium regulating hormone (Metcalfe, 2008). Estrogen deficiency can lead to post menopause condition where bone resorption is faster than bone formation (Marini Brandi, 2010). Lack of physical activity can make Claire prone to osteoporosis (Metcalfe, 2008). Along with the above mentioned modifiable factors there are certain non-modifiable factors on which the control is less. Aging is the first factor which can lead to such disease (Barreiro, Acosta, Marquez, Rodriguez, Arriaga, 2013). In ageing, the supply of osteoblasts decreases against the demand of the body. Similarly genetic predisposition and epigenetic are non-modifiable factors, the mother’s health status during pregnancy, child birth weight and weight at 1 year are predictive of bone mass till 70 years in female (Marini Brandi, 2010). The bone diseases like rheumatoid arthritis can also leads to osteoporosis (Huether McCance, 2012). Experiencing pain may be the first factor Claire experiences with her osteoarthritis (Swift, 2012). The drying of synovial fluid leads to stiffness of joints which may have been felt by Claire in her hip and knee joints (Swift, 2012). The constant presence of stiffness may lead to muscle weakness in that area. The weakening of muscles, drying of fluid, and inflammation combined effect may restrict her movements such as bending, flexing and extending of joints (Goldring Otero, 2011). Osteoporosis often goes unnoticed until a fracture occurs (Brown, 2009). Claire was diagnosed with osteoporosis thus she may have experienced certain clinical manifestations which are common in osteoporosis. Since Claire has sustained fractures in her left colle’s and right tibia/fibula she may experience acute pain during movement of her hands and legs (Brown, 2009). The fractures she received due to osteoporosis may limit her movement and affect the weight bearing capacity of her legs (Brown, 2009). With constant loss of bone at area of fractures, Claire may find it hard to stand erect and may stand in a stoop posture. Loss of height may occur due to increased bone loss (Brown, 2009). Post-operative nursing management of Claire involves a number of interventions to address the issues faced by Claire. In osteoarthritis and osteoporosis, the most common symptom experienced by patient is pain (Swift, 2012). Thus, the nurse’s interventions must be to reduce the pain, by doing a pain assessment through a recommended scale. The pain must be measured for areas affected, severity and Claire’s reporting of pain. The PRN medications must be administered to Claire as per prescription and timing must be noted for each medication and dose (Colon, 2012). The nurse should take care of any of Claire’s wounds through proper wound management interventions, in order to prevent inflammation and infection (Brown, 2009). Possibilities, of the fracture would mean Claire may stay in bed for a prolonged period, thus chances of having pressure ulcer increases. The same would apply for deep vein thrombosis which nurses can prevent by applying TED stockings (Brown, 2009) . Nurses must change her position every 2 hours and a pillow can be provided at pressure areas to Claire. Nutrients, fluid and diet management should be prepared with consultation with a dietician or a nutritionist (Brown, 2009). Physiotherapist interventions are required to assist her with walking and simultaneously the neurovascular assessment must be assessed by nurses to prevent neurovascular degeneration (colon, 2012). The immediate nursing interventions for Claire would be a primary assessment for immediate danger. The nurse should take a physical assessment on Claire, including assessing her airway patency and circulation. A pain assessment is essential as it provides the only way to ensure that management methods are appropriate and effective (Elliott Coventry, 2012). The nurse should carry out a pain assessment on Claire using the â€Å"PQRST† model. This type of pain assessment gives a detailed account of pain helping nurses to administer pain reduction medications keeping in mind the allergic reactions and six rights (Elliott Coventry, 2012). The nurse should document when analgesia was administered to Claire so other care team members will have a clear understanding of Claire’s pain (Brown, 2009). Claire must be assessed often for her presence of pain and she must be treated promptly and effectively (Elliott Coventry, 2012). A number of factors play an important role in eliciting complications (early and later) post fracture surgery. Complications which may be associated with Claire’s fracture surgery are; during surgery the skin and soft tissues are cut down to reach to the bones, thus chances of bacterial infections exist which can lead to fatal situations if not prevented properly (Brown, 2009). Another serious complication of fracture is compartment syndrome where it causes decreased capillary perfusion below the level necessary for tissue viability (Brown, 2009). Presence of other co morbidities can prolong the recovery stage. Venous thrombosis can also lead to a complication after fracture (Brown, 2009). Precipitating factor is venous stasis which can be caused by incorrectly applied casts to Claire (Brown, 2009). Another contributing factor for the fracture complication on Claire if not treated properly would be fat embolism syndrome where presence of systemic fat globules is distributed in to tissues and organs after a traumatic skeletal injury (Brown, 2009). Case study 2 Pathophysiology of gastro esophageal reflux disease is when the lower esophageal sphincter (LES) is attached to the stomach in the form of a plumbing circuit (Huether McCance, 2012). Any structural changes occurring in between the stomach and esophageal barrier associated with abnormal relaxation of LES can lead to gastro esophageal reflux disease (Huether McCance, 2012). Peptic ulcers occur with excess secretion of hydrochloric acid and pepsin, this impairs the balance between gastric luminal factors and the action of the gastric mucosal barrier, (Huether McCance, 2012). The main functions of gastric mucosal barrier are; secretion of bicarbonate, defense of epithelial cells and mucosal blood flow. With increased secretion of acid, the mucosal barriers are affected and thus histamine is released. This activates the parietal cells to release more acids causing ulcers (Huether McCance, 2012). A clinical manifestation of peptic ulcers and gastro esophageal disease is heart burn, caused by acid reflux thus causing an inflamed esophagus (Huether McCance, 2012). Regurgitation occurs due to the loss of the mechanical barrier between the stomach and esophagus and is aggravated by gastric acid reflux. Justin may experience upper abdominal pain within an hour of eating meals (Huether McCance, 2012). Due to excessive diarrhea, skin may get irritated, red and swollen. The stool with blood in it may be black and have an offensive smell due to oxidation of hemoglobin (Huether McCance, 2012). The dysphagia experienced by Justin could be due intake of alcohol or acid containing food which leads to esophageal spasms (Huether McCance, 2012). Due to excessive fluid loss, nurses may have noted that Justin presented as dehydrated. One common cause of Justin’s peptic ulcer could be his lifestyle of takeaway meals such as fried food, eating spicy and junk foods which has been hypothesized as a causal factor for ulceration (Huether McCance, 2012). Another major cause could be infection of the gastric and duodenal mucosa with Helicobacter pylori and regular use of non-steroidal anti-inflammatory drugs (NSAIDs), especially those that are classified as COX-1 inhibitors (Huether McCance, 2012). In Justin’s case, he has been buying over the counter medications for his chronic back pain which may increase the risk factor of gastric ulceration. The other associated factor would be alcohol consumption (Huether McCance, 2012). The medications commonly used to treat peptic ulcers are acid suppressor’s antacids such as ranitidine and famotidine; they form a foam barrier between the stomach and esophagus thus preventing acid reflux (Brown, 2009). Similarly the H2 antagonists help in reducing the acid secretion in the stomach leading to healing of ulcers (Brown, 2009). Proton pump inhibitors such as omeprazole are effective in decreasing acid secretion from the stomach. PPIs are used in combination with antibiotics to treat ulcers caused by H. pylori (Brown, 2009). Bowel preparation is the artificial method of removal of faeces from the colon in order to prepare Justin for any type of surgical procedure such as colonoscopy. The colons may have indigested food and fecal matters attached to them (Beck, 2010). The chances of infection increases if any surgical procedures are carried out nearby the colon area. Based upon Justin’s bowel movement patterns and stool characteristics he must be advised to go for a colon cleansing solution drink or laxative drink (Beck, 2010). This procedure can be done the day before scopes or some days before depending upon Justin’s condition. Enemas can also be administered based upon surgeons and specialists prescription. During the bowel preparation, nurses must keep in mind that Justin’s privacy must be maintained and hospital’s policies and procedures are followed. Documentation must be written in clear hand writing for other team members to read about Justin’s treatment (Blair Smith, 2012). Peptic ulcers are characterized by tarry and bloody stools due to ulcerations in gastrointestinal tract. Excessive blood loss can be fatal for Justin leading to unconsciousness and other complications, thus it is advised for nurses to check the amount of blood and blood type (clots) (Brown, 2009). This can help to determine the severity of the disease and further diagnosis. The nurse should help Justin to return to his bed as heavy loss of blood leads to fluid deficiency and lowering of blood pressure. Justin’s vital signs must be assessed and fluids must be provided to manage the deficiency (Brown, 2009). While checking Justin’s abdomen for firmness, tenderness and pain, curtains must be pulled to maintained Justin’s privacy. The findings must be documented and reported to the ward in charge doctor for further processing (Blair Smith, 2012). Post colonoscopy the nurse should manage Justin’s pain through an assessment of pain, using a severity scale on a specified area and administering PRN medications (Brown, 2009). In order to recover from injury caused by his condition and address other complications associated with the disease, Justin’s nutritional status and fluid balance should be maintained (Brown, 2009). Due to heavy blood loss and pain, the patient may feel frustrated and anxiety symptoms may develop. The nurse should calm Justin, establish effective communication and allow him to express his feelings (Brown, 2009). In conclusion, the conditions such as osteoarthritis and osteoporosis can be disastrous to Claire as it can affect the quality of her life to a high degree. The case remains the same for peptic ulcer and gastro oesophageal disease and can affect the eating habits of Justin. Thus, it is important to address both patient’s pain level and other complications in order for them to be comfortable. The disease process can be controlled through nursing interventions along with other medical interventions such as surgery and pharmacological management. It is essential for nurses to know pathophysiology of conditions of both cases described above in order to best manage both patients’ issues.

Cell and Molecular Biology

Cell and Molecular Biology Final Name: Hadeel Binomar30 pts. Protein misfolding can be an aspect of several different human disorders, including cystic fibrosis, Alzheimer's disease, and atherosclerosis. Many times, the misfolded protein is a membrane protein. In fact, a type of diabetes insipidus results from a mutation in the G-protein-coupled vasopressin 2 receptor that prevents the protein from making it to the cell membrane A) Describe how this type of receptor would normally get targeted to the membrane (from the beginning of translation) and B) then propose one mechanism by which the mutation could cause a lack of proper targeting. One of the most important protein's target is G protein-coupled receptors, several signaling mechanisms depend on this type of receptor to change both internal and external stimuli to the intracellular responses. Basically, one of the G couple receptor subfamilies is G-coupled Vasopressin-2- Receptor (V2R), and this receptor is going through a strict quality control process at the endoplasmic reticulum, which presents the only correctly folded protein to gets through the secretory pathway. The primary function of the V2 receptor is to activate the attached G protein that bound to the ? subunit then phosphorylated to GTP. The G protein couple receptor then activates the enzyme adenylate cyclase that catalyzes the reaction in the ER and forms cAMP from ATP. After that, cAMP acts as a second messenger and activates a protein kinase that phosphorylates the integral membrane proteins on the cell surface. Moreover, the secretory pathway organelles' and the plasma membrane both are first introduced into the Endoplasmic reticulum, and the co-translationally proteins that can cross the ER are synthesized by the ribosome first then binds by chaperones to gets moves to the ER surface using GTP that allows them to move toward the receptor then release it. The soluble proteins and the integral membrane proteins as I mentioned above, can be targeted through the ER and then translocated by the same mechanism.Further, several mutations occurring in the transmembrane region which affect the structure of the protein. These are multiple mutation sites, such as mutations occurring in the amino acid residues which was acting as a causative agent for human disease. Also, there are other mutations occurring on the single site position that will affect the translation mechanism and cause many human diseases like: cystic fibrosis, Alzheimer's disease, and atherosclerosis that proves the function of V2R protein which plays important role in the translation during the protein folding process. One of the mechanism that may a reason for lacking the proper target protein is when the mutations of the CFTR gene occurring and affect the function of the chloride ion channels and cause defect in the protein sequences which lead to the production of diseases and misfolded of the proteins that are unable to recognize their functional destinations. Otherwise, Lack of the stop signals is another issue that prevents the protein from getting into the surface of the ER, also called the non-stop decay cellular pathway, because lack of this stop signals prevents mRNA from synthesis and translate the proteins, these consider as a point mutation that inhibits the essential stop codons. 30 pts. Describe the experiment shown in figure 3 from the paper we discussed in class (Miller et al, 2003). (A) In your description, consider the following questions: Why did they do it? How did they do it? What did they learn? (B) Diagram the results that you would expect to see in Lanes T, 1, 2, 3, and 4, if the amino acid signal DID in the protein Gap1p was mutated to random amino acids and tell why; and (C) Give two possible (different) results that might occur if the amino acid signal LxxLE in Bet1p was mutated to the amino acids DID (which are the signal in Gap1p). Diagram the results expected in Lanes T, 1, 2, 3, and 4 and explain why you predicted this result for each case.left20840701.A001.A4467225201739500The experiment was performed to study the role of cargo binding domain of Sec24p in the process of protein sorting. To perform this study, both mutant and wild types subunit Sec23/24p and Sec23/24L616W were harvested from microsomal membranes. The immunoblotting assay performed to quantify cargo molecules using radio-labeled secondary antibodies. Comparison of the mutant subunit with wild type illustrated omission of some molecules in mutant one, these molecules were cargo protein molecules. While some of them are packed in a way that similar to the wild-type. It meant that there were some signals that remained unaffected although mutation was there. Unexpectedly, it was found that in these unaffected molecules of mutation in Sec23/24p, packaging was better than the wild type. Further, they found the proteins that were highly affected had Bet1p and Gap1p/Sys1p chimera, because they completely depending on the Sys1p di-acidic of COPII vesicles. If the amino acid signal DID in the protein Gap1p was mutated to random amino acids, the resulting bands would be seen as in figure 1. A because the amino acids might be present in all the lanes. And Gap1p is required for di-acidic motifs to fuse together with the COPII vesicles at the mutated domain. Also, Sys1 peptide is not involved in Sec 23/24p hence its mutation is not contained in a di-acidic motif. If the signal LxxLE was mutated to the DID, the expected Bet1p packaging would be shown in figure 2. A as not be seen in lanes containing Bet1p because the amino acid signal LxxLE does not exit after mutating to amino acids DID. The second probability for the Bet1p would be expected to bind with the vesicle for packaging when it interacts with di-acidic motifs which is needed as shown in figure 2.B290512515621000581025113030004781550412752.B002.B6286501346202.A002.A20 pts. Explain the experiment shown in Figure 5C from the Shen et al. (2018) paper on the phosphorylation of CDC25 that we discussed in class. In addition, be sure to also address the following: A) why did they do this experiment (the central issue); B) what did they learn; and C) what is another control experiment they could have done? D) Would these results change if you added a constitutively active form of LKB1 to the reaction? If so, how and why? A) Overall, the main purpose of this paper is to explain how the division of cells is highly regulated such that cells that fail to pass some specific stage-based tests cannot advance to the proceeding stages. In this particular experiment, HeLa cells were subjected to chemicals that are known to activate the enzyme AMPK. Also, the main catabolic processes that are involved to generate energy for cells to transition from G1/G2 were determined by the application of radiochemical approaches, the experiment required to approve how highly conserved cellular energy sensor can significantly delay mitosis entry and activation of AMP-activated protein kinase (AMPK). Further, Wee 1 family inactivates the cell cycle G2/M Phase which is controlled by Cdc3/cyclic B (mitotic cyclin-dependent kinase complex). They found that AMPK-dependents phosphorylation of CDC25C arranges a metabolic control point for the M-phase transition and the cell cycle phase G2. B) Also, they learned that suppression of Wee 1 or acute induction partially reinstates mitosis ingress in the circumstance of activated protein kinase (AMPK). This experiment showed that when Phosphorylates Cdc25 is in a distributive and disordered state, it results into ultra-sensitivity in protein phosphorylation. C) For another control experiment, they might try exposing the U2OS (cell line) clones conditionally exhibiting Cdc25A etoposide. That will help to test whether Cdc25A degradation is significant for the G2 control point or not.D) If they add an active form of LKB1 to the reaction, the results will not change, because in cells LKBI activity inhibits AMPK activation in response to different stimulations. Also, LKBI is lost upon consistent isolation and therefore no effects of phosphates observed.20 pts. Briefly describe the role of cyclin-CDK in the cell cycle and give an example of positive and negative control in this system. Also, describe how cell cycle regulation links to the stimulation of apoptosis at the molecular level. In the beginning, the cell cycle depends on many basic factors that control the regulation process starting from the signal transcription molecules, growth factors and the Cyclin Dependent Kinases enzymes include the checkpoints which control the transition process between the cell cycle phases by binding to the cyclin proteins CDKs then phosphorylate other proteins to transfer from one phase to another. The role of transcription factors is to turn on the signals for gene expression, DNA replication, and cell divisions. As an example of CDKs, cyclin-dependent kinase 1 CDK1 is a cell division cycle protein homolog 2, that has a primary role in human cancer cells because CDK1 rather than any types of CDKs is fatal to the mutated version of MYC- dependent cancer that leads to a depletion of oncogenes like (Fos and Jun) in human cancer cells. Fos and Jun are combined forms of the transcription factor called AP1 that activates the delayed response genes such as cyclin D and CDK4. Recent studies reveal that the reason for the MYC breast cancer cells duplation is targeting CDF1 exhibit any other CDKs cell lines. Also, CDK1 inhibition can control and target the cancer cells in human and both phosphorylation and expression of MYC during the cell cycle process. To initiate intracellular signaling pathways and stimulate the cell cycle entry, mitogens substance bind to the cell surface receptor with the activation form of GTPase Ras that activates MAP kinase cascade. That will lead to the expression of encoding gene of the transcription regulatory protein like MYC. Moreover, E2F transcription factor is a target for cyclin D and CDKs that stimulate proteins expression to initiate S phase, also E2F regulated by the tumor suppressor gene Rb (Retinoblastoma protein). At early G1 Phase, Rb protein combined with E2f to form the histone deacetylases protein that remains chromatic condensed, then cyclin kinase phosphorylates Rb protein, causing it to disassociate from E2F. That allows recruitment of histone acetylates, which decondense the chromatin and helps transcription complexes to form in G1 and S phase and to form a positive feedback. For the negative control, if there are no growth factors present to stimulate the synthesis of Cyclin D in the new cell, Rb phosphorylated will turn off, and Rb will rebind to E2F, then the cell cycle will stop and that will lead to many negative results like prevent it to bind with DNA, or DNA damage and cells will return to the G0 phase. Apoptosis is a consequence of DNA damage; if the damage is not repaired, the cell cycle will divert towards apoptosis, otherwise, if the cell has DNA defects and fail to undergo apoptosis, that will change to the cancer cell. G1 phase regulators such as P53 and E2F are essential to promote the cell regulations and eliminate any damage or abnormal changes during the cell cycle. P53 has a primary function to prevent any mutation in DNA during cell progression, so any defect in P53 will lead to cancer, and it's usually mutated in cancer cells. Further, Rb protein considers as a tumor suppressor and also promotes apoptosis. Additionally, most human cancers have inactive Rb protein, either mutated Rb or the non-phosphorylated (inactivated form) of Rb protein

Life and Art of Charles Demuth, Precisionist Painter

Charles Demuth (November 8, 1883 – October 23, 1935) was an American Modernist painter best known for his use of watercolor to portray the industrial and natural landscapes of his Pennsylvania hometown. His paintings emerged out of the abstract Cubist style and ultimately led to a new movement called Precisionism. Fast Facts: Charles Demuth Occupation: Artist (painter)Known For: Abstract Cubist style and involvement in the Precisionist movementBorn:  November  8, 1883 in Lancaster, PennsylvaniaDied:  October  23, 1935  in Lancaster, PennsylvaniaEducation: Franklin Marshall College and Pennsylvania Academy of Fine Arts Selected Paintings: My Egypt (1927);  I Saw the Figure 5 in Gold (1928);  Roofs and Steeple (1921) Early Years and Training Demuth was born and raised in Lancaster, Pennsylvania, whose urban landscape and emerging industrial setting served as an inspiration for several of his paintings. Demuth was ill and often bedridden as a child. During those times, his mother kept him entertained by providing him with watercolor supplies, thus giving the young Demuth his start in the arts. He eventually portrayed the agricultural portraits he knew best: flowers, fruit and vegetables. Demuth graduated from Franklin Marshall Academy, which later become Franklin Marshall College, in Lancaster. He also studied at Pennsylvania Academy of Fine Arts in Philadelphia and in the arts scenes of New York, Provincetown, and Bermuda. He socialized with and was photographed by Alfred Stieglitz, who was working at the time to organize exhibits of modernist art for his American Place Gallery in New York. Demuth spent time studying art in Paris, where he was part of the avant garde scene. His contemporaries included  Georgia OKeeffe, Marcel DuChamp, Marsden Hartley and Alfred Steiglitz. Painting in His Own Backyard Though he traveled to and was influence by exotic locales, Demuth painted most of his art in the second-story studio of his Lancaster home, which overlooked a garden. In the painting My Egypt (1927), Demuth depicted a grain elevator, a massive structure used to store the harvest, next to row house rooftops. Both structures are common in the rich agriculture economy and historic urban setting of Lancaster County. Like many of his contemporaries in the arts, Demuth was fascinated with Americas landscape, which was being altered at the hands of industrialism. He saw firsthand the smokestacks and water towers in cities such as Philadelphia, New York and Paris. He painted those skylines and contrasted them with grain elevators that were common in his hometown. The Precisionist Style The movement to which Demuth belonged, Precisionism, stressed visual order and clarity in the visual arts and combined those facets with a celebration of technology and expression of speed through dynamic compositions, according to the Metropolitan Museum of Art. Demuth and his fellow Precisionists painted distinctly American landscapes in an intentional move to distance themselves from European artists. Demuths most famous work is a 1928 oil painting called I Saw the Figure 5 in Gold, which has been described as a masterpiece of the Precisionism movement. The painting was inspired by the poem The Great Figure by William Carlos Williams. Williams, who had met Demuth at Philadelphias Pennsylvania Academy of Fine Arts, wrote the famous poem after watching a fire engine speed by on a Manhattan street. Demuth tried to capture the following lines in his painting: Among the rainand lightsI saw the figure 5in goldon a redfiretruckmovingtenseunheededto gong clangssiren howlsand wheels rumblingthrough the dark city I Saw the Figure 5 in Gold, as well as other Demuth paintings, served as an influence on commercial artists who later designed movie posters and book covers. Later Life and Legacy Demuth was diagnosed with diabetes at a relatively young age, and the condition made him weak before he turned 40. He spent his final years confined to his mothers home in Lancaster, away from his fellow artists working in Paris, and died at age 51. Demuth made a significant impact on the art world with the development of the Precisionist movement. His emphasis on geometrical forms  and industrial  subject matter came to exemplify the ideals of Precisionism. Sources Further Reading Johnson, Ken. â€Å"Chimneys and Towers: Charles Demuths Late Paintings of Lancaster - Art - Review.† The New York Times, The New York Times, 27 Feb. 2008, www.nytimes.com/2008/02/27/arts/design/27demu.html.Murphy, Jessica. â€Å"Precisionism.† In Heilbrunn Timeline of Art History. New York: The Metropolitan Museum of Art, 2000–. http://www.metmuseum.org/toah/hd/prec/hd_prec.htmSmith, Roberta. â€Å"Precisionism And a Few Of Its Friends.† The New York Times, The New York Times, 11 Dec. 1994, www.nytimes.com/1994/12/11/arts/art-view-precisionism-and-a-few-of-its-friends.html?ftay.

Fern Reproduction and Life Cycle