Necrosis Research 40

Necrosis Research Paper
The Flesh Fating Disease Necrosis is abnormal death of cells that are likely caused by disease or
infection. Necrotizing fasciitis "the flesh eating disease" is caused by several bacteria (mixed flora,
aerobic and anaerobic), the most common and deadly is Streptococcus pyogenes (S. pyogenes) or
group A streptococcus. Characteristics are Gram positive, nonmotile, nonsporeforming, beta
hemolytic catalase negative, cocci that are spherical bacterium that appears in chain–like formations.
S. pyogenes are considered a facultative anaerobic bacterium; it can grow in the presence or absence
of oxygen. Growth is stimulated by incubating in an environment with increased carbon dioxide.
Type I caused by anaerobic bacteria with or without the presence ... Show more content on
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It begins with a harmless cut in the skin and spreads rapidly into nearby tissue. When streptococci
on the skin are introduced to the cut, strains of group A release enzymes and toxins that greatly
increase invasiveness and virulence. Invasive bacteria are pathogens that can invade parts of the
body where bacteria are not normally present, such as the bloodstream, and soft tissues like muscle
or fat. Virulence is the degree of pathogenicity determined by its ability to establish itself in a host
and survive the host defense. Virulence factors of group A streptococci include (1) M protein and
lipoteichoic acid for attachment; (2) a hyaluronic acid capsule that inhibits phagocytosis; (3) other
extracellular products, such as pyrogenic (erythrogenic) toxin, which causes the rash of scarlet
fever; and (4) streptokinase, streptodornase (DNase B), and streptolysins. Some strains are
nephritogenic. Immune–mediated sequelae do not reflect dissemination of bacteria. Nongroup A
strains have no defined virulence factors. Antibody to M protein gives type–specific immunity to
group A streptococci. Antibody to erythrogenic toxin prevents the rash of scarlet fever. Immune
mechanisms are important in the pathogenesis of acute rheumatic fever. S. pyogenes produce several
virulence factors that lend to its pathogenicity, or disease–causing capabilities. It contains a capsule
that helps allow the bacteria to disguise it from getting engulfed by white blood cells (phagocytosis).
It also contains proteins on its cell wall that allows it to adhere to epithelial cells, which allows it to
produce disease. S. pyogenes also produces several enzymes that give the bacteria the ability to
destroy tissue and spread. The enzymes digest the connective tissue in the skin. Lastly, it produces a
wide variety of toxins that can produce
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How Does Nitroglycerin Affect Myocardial Infarctions
Nitroglycerin's Effects on Myocardial Infarctions and the incurring results vary greatly depending
on the location of the infarct. In the following paper I will attempt to explain and answer the
following topically related questions: "Why to use caution with nitro in the inferior wall MI? What
is happening to the heart in this event? What treatments can instead be administered and how do
they slow tissue damage?" Defining Nitro, Inferior MI's, and their relationship As stated in the
European Heart Journal1," Myocardial Infarction is defined in pathology as myocardial cell death
due to prolonged ischemia". In the pre–hospital setting, the main goal of paramedic's is to counter
act the ischemia and prevent further cell death. One of the paramedic's drugs of choice will ... Show
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In short, Nitroglycerin is a vasodilator by action of smooth muscle relaxation. The goal when
administering this nitrate is to decrease cardiac work via decreased vascular resistance, improve
blood flow within the heart, and maintaining adequate systemic circulation or blood pressure. In the
case of a right sided inferior MI, the right coronary artery has developed a clot and the right side of
the heart is affected, most notably the right ventricle. Due to the anatomical fact that the right
ventricle fills during preload as a direct dependent of left ventricle stroke volume and its resulting
systolic pressure, vasodilation and constriction is a key factor in maintaining adequate circulation
back through the heart. Also, the heart itself relies on the coronary arteries for its own perfusion. The
coronary arteries are filled during diastole; therefore, decreased vascular resistance and inadequate
stroke volume will result in a low blood pressure and overall decreased cardiac output and perfusion
of the cardiac muscle. If the left ventricle cannot sufficiently pump to the back to the right side of
the heart, then overtime the right ventricle will not adequately supply the left

Case Study Of Kerosene
Background: Kerosene is one of the most widely used sources of energy in developing countries.
Modes of accidental exposure include inhalation, ingestion and through skin or eye contact. There
have been few cases reported in literature where kerosene was injected intravenously and
subcutaneously with differing outcomes ranging from mild irritation to serious necrotizing fasciitis.
It remains challenging to predict the outcome of patients who inject kerosene via non–venous route
as it is difficult to establish the accuracy of tissue layer affected by the injection
Objective: To establish methods of management available in the rare presentation of attempted
suicide by self–injection of kerosene.
Design: An analysis of Case Studies
Setting: Training ... Show more content on Helpwriting.net ...
Most reported cases are in Arab countries (KSA, Jordan, Iraq) (15 cases) [2–6]. Iraq is the highest of
Arab countries (11 cases) [4]. The difficulty arises in management as cases are unique to each
exposure in terms of dose injected, site of intended versus actual injection and quantification of the
exact dose of exposure. The lethal dose of kerosene for 70 kg adult is 100 ml [7]. Only 12.9% (4
cases) had reported the exact dose of kerosene that was used. Routes of kerosene exposure included:
intradermal, subcutaneous and intravenous. Superficial skin contact with kerosene may cause
dryness scaling and dermatitis [8]. Injection of kerosene presents with a more severe clinical
presentation in the form of local unspecified inflammation, aggregation of neutrophils and soft
tissue necrosis. This was demonstrated in two histopathology specimens of debrided necrotic tissue
in two reported cases [2,3]. Intradermal injection has been reported in 32% of cases (10 cases) [4].
All treated medically as a case of panniculitis and skin ulceration. Patients recovered without
complications except one who has developed injection site fibrosis and contracture in the wrist and

Skin Flap Necrosis Research Paper
Skin flaps are commonly used in plastic and reconstructive surgery to repair defects resulting from
trauma, congenital anomalies, or after tumor resection. Partial necrosis of the flap can be
encountered postoperatively as a result of inadequate blood supply (Lu et al., 2008). Subsequent
management of flap necrosis usually includes time–consuming and repetitive dressing changes
aimed at promoting secondary intention healing or even secondary reconstructive procedures
(Lubiatowski et al., 2002). To overcome this potential problem, numerous studies have investigated
methods for improving skin flap survival. Many have focused on enhancing flap viability with
pharmacological agents as glucocorticoids and vasodilators to preserve the existing ... Show more
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Mesenchymal stem cells can be isolated from various sites, including bone marrow and adipose
tissue (Ko et al., 2011). A set of standards were proposed by the Mesenchymal and Tissue Stem Cell
Committee of the International Society for Cellular Therapy to define human mesenchymal stem
cells. First, cells must be plastic adherent when maintained in standard culture conditions. Second,
they express specific surface antigens. Third, the cells are capable of differentiation into osteoblasts,
adipocytes and chondroblasts in vitro (Dominici et al.,

Tumour Necrosis Factor Alpha Case Study
Tumour necrosis factor–alpha (TNFa) is a pro–inflammatory monocyte derived cytokine identified
as initiating a number of crucial cell mechanisms, largely within the regulation of immune cells and
host defence. It is secreted primarily by macrophages and monocytes in response to a bacterial
challenge or tumour. Although TNFa is mainly produced by macrophages, it is also produced by a
broad variety of other tissues including (but not limited to) endothelial cells, mast cells, fibroblasts
and lymphoid cells.
TNFa is an endogenous pyrogen, thus is capable of inducing inflammation, fever, apoptotic cell
death and, inhibition of tumorigenesis. (Kleef and Hager, 2000) One of the most potent stimuli for
TNFa is a bacterial endotoxin (lipopolysaccharide) or (LPS) which is derived from the outer cell
wall of gram–negative bacteria. (Verhoef et al., 1999) LPS is a major component of the outer
membrane of gram–negative bacteria, and contributes greatly to the structural integrity of the
bacteria. (Kaszowska, 2004) Large amounts of TNFa are released in ... Show more content on
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These cells are present as monocytes within original culture, however were differentiated to form
macrophage cells using PMA, a plant ester (and toxin) which is used in many cell models. PMA
produces macrophages from the monocytic U937, through the promotion and activation of protein
kinase C. PMA is detected by tyrosine kinase receptors found upon the surface of monocytic cells
and initiates a cascade of changes within the U937 cells. The activation of Phospholipase C is a
crucial change within the monocytic cell as this in turn activates diacylglycerol, which results in the
activation of Protein Kinase C. This PKC molecule will be transported to the nucleus where it will
initiate the differentiation process. (Vrana and Grant, 2001), (Signal transduction, no

Gastrointestinal Lesions
Gastrointestinal lesions involved the distal colon or rectum, gastric cardia, ileum, cecum, and
esophagus. With the exception of the esophagus, lesions were characterized by mucosal necrosis
that had progressed to erosion or ulceration in more advanced lesions, proliferation of underlying
fibroblasts, and infiltration by low numbers of neutrophils and macrophages. Necrosis of the GALT
appeared to precede mucosal involvement in many of the lesions (Fig. 6D). There were very few
syncytia. Antigen was detected in glandular or crypt epithelium of the stomach, colon, cecum, and
ileum; in stratified squamous epithelium of the gastric cardia; in fibroblasts in the submucosa or
lamina propria of the cecum, ileum, stomach, and colon; and in macrophages or dendritic cells
within associated GALT. As described for oral mucosa, there were weakly immunopositive
mononuclear cells rarely in association with otherwise unaffected stratified squamous epithelium of
the stomach. Minimal antigen was present within smooth muscle of the muscularis mucosa of more
severely affected sections of colon, cecum, and stomach. Esophagitis, observed only in one animal,
was ... Show more content on Helpwriting.net ...
Vaginitis and superficial uterine lesions were similar to epithelial lesions in other organ systems,
with epithelial degeneration, necrosis, and hyperplasia. There were also necrotic foci in the uterine
stroma and myometrium. Antigen was detected in vaginal and uterine epithelium, uterine stroma,
myometrium, and submucosal fibroblasts. Ovaries of affected animals exhibited foci of necrosis
involving secondary follicles and stroma, with antigen present in mpinge s and thecal cells of
follicles and in stromal spindle cells. Mild necrotizing lesions of the testes and epididymis contained
viral antigen within interstitial spindle cells of both structures and within tubular epithelium of the

Persuasive Essay On Cosmetic Surgery
Cosmetic Surgery: Liposuction Contemporary society is more widely accepting of cosmetic surgery
as normal compared to the past. In the modern–world, people are highly concerned with
appearances, features, attractiveness and insecurities, and believe the solution to these problems is
cosmetic surgery. People are willing to undergo cosmetic procedures despite many of the possible
complications. Liposuction is one most common cosmetic procedures patients choose to undergo in
the U.S. Liposuction, or lipoplasty, is the removal of fat from the body. Patients elect to undergo this
surgery because they are seeking more aesthetically pleasing body shapes, and it is important to
know that it is not a substitute for weight–loss. Liposuction is simply the reshaping or molding of
body parts. The abdomen, butt, and thighs are some of the most common areas of the body that
liposuction is performed on. The best candidates for liposuction are people who have good elasticity
and skin tone, "where the skin molds itself into new contours" (Nordqvist). The procedure includes
an anesthesia, general or local, depending on the amount of fat that is being removed. Then, small
incisions are made in discreet spots of the targeted area of fat removal (Jones). The incisions are
typically less than an inch in length. Next, a cannula, a small tube, is inserted into the incisions to
loosen the fat by moving it back and forth, and it is then suctioned out using a "surgical vacuum or
syringe attached to

A Hub Of Cellular Adaptive Response
1.2.4 ATF3: a hub of cellular adaptive response The wide use of the DNA microarray technique to
study systemic gene expression (mRNA) profiles has rapidly contributed to the growing list of
signals that can induce ATF3 expression. ATF3 is induced by tissue–injury, infection, oxidative
stress, chemicals, alcohol, chemotherapeutic agents, hypoxia, genotoxic agents and others (see
reviews). In addition to the above mentioned stresses, ATF3 is also induced by stimuli that are
typically not considered as stress stimuli such as serum, cytokines, chemokines, growth factors and
others. Thus, ATF3 is more accurately characterized as an "adaptive response" gene that helps cells
to adapt to extra– and/or –intra–cellular changes. Extra–cellular stimuli trigger intra–cellular
signaling pathways, which in turn upregulate ATF3. For instance, the p38 MAPK pathway is
necessary for various signals (such as anisomycin, IL–1β (interleukin 1β), TNFα (tumour necrosis
factor α) and H2O2 to induce ATF3. Prostaglandin induction of ATF3 in the bovine corpus luteum is
inhibited by inhibitors of the ERK, JNK and p38 MAPK pathways. Various other pathways are also
linked with ATF3 induction such as the Smad, Myc, Ras and NF– pathways (Review). In fact, a
review of existing literature clearly underlines one feature of ATF3 induction: it is neither tissue–
specific nor stimulus specific. ATF3 is induced in many different cell types, both in vivo and in
vitro, by many different extra–cellular and

Muscular Dystrophy Case Study
Duchenne's Muscular Dystrophy (DMD) is caused by recessive mutations in the dystrophin gene on
the X–chromosome affecting 1 in every 3,500 –5,000 male births. As shown in Fig. 1, dystrophin
protein anchors the actin cytoskeleton to the extracellular matrix, playing critical roles in stabilizing
and protecting the muscle fibers against strain related injuries. As outlined in Fig. 2, dystrophin
mutations lead to myocyte fragility and membrane damages with repeated contractions, resulting in
increased cell permeability. Consequently, calcium ions diffuse into the myocytes, activating
calcium–dependent proteases to cause further cell necrosis. , Additionally, creatine kinase (CK), a
myocyte enzyme that stores energy for contraction, leaks out ... Show more content on
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Treatments are aimed to control symptoms, preserve muscle functions and improve quality of life.
Prednisone is a type of commonly prescribed corticosteroid known for its anti–inflammatory and
immunosuppressive properties through direct gene expression regulations. The precise mechanism
by which prednisone increases muscle strength in DMD patients is unknown, but hypothesises have
been made based on its modulatory effects in the myocyte inflammation, degeneration and
regeneration pathways following damage. As illustrated in Fig. 3, under healthy physiology
condition, myocyte damage stimulates signaling pathways that promotes both degeneration and
regeneration of the damaged tissue to promote healing. The extend of muscle healing is dependent
on the balance between the two processes. As outlined in Fig. 4, initial myocyte damage activates
inflammatory cells such as neutrophils and macrophages to inflict further necrosis through the
release of free radicals and proteases. The damaged myocytes are then removed via phagocytosis to
provide space for healthy tissue regeneration. The regeneration process is initiated through the
activation of myocyte precursor cells called satellite cells to differentiate and fuse at the site of
damage. However the proliferating abilities of satellite cells are reduced in DMD patients due to the
absence of dystrophin proteins, resulting in impaired muscle regeneration capacities. As a result,
inflammation

Group A Streptococcus (GAS) Essay
Streptococcus pyogenes, also known as Group A streptococcus (GAS), is a β–hemolytic, Gram–
positive bacterium that most commonly causes respiratory disease, including pharyngitis or
tonsillitis, as well as skin infections such as impetigo and cellulitis. The organism is transmitted via
respiratory droplets or by contact with fomites, and commonly infects young children. In addition to
the common clinical presentations associated with S. pyogenes, some individuals develop the
postinfectious sequelae of rheumatic fever and glomerulonephritis. Due to the severity of these
medical consequences, prophylactic antibiotic use is often recommended for any patients with
otherwise mild S. pyogenes infections (21).
In addition to its traditional ... Show more content on Helpwriting.net ...
Antibiotic use, particularly with clindamycin and linezolid, may be useful in treating GAS–
associated necrotizing fasciitis, as they target both M–proteins and exotoxins (5). Some cases have
been treated with hyperbaric oxygen therapy, with recent data suggesting prompt surgical therapy
instead is vital for preventing amputations (18). Even after treatment, however, necrotizing fasciitis
mortality has been estimated to range from 24%–60% (10).
In S. pyogenes–associated necrotizing fasciitis, the bacteria first invade host fascia before spreading
and causing more invasive damage. Initial GAS invasion can occur through three primary pathways:
1) preceding superficial infection; 2) direct inoculation; or 3) hematogenous seeding from a previous
injury site. After colonization, GAS spread through the typically sterile fascial planes that separate
muscle groups, which are only loosely held together by connective tissue. The streptococci then
release several proteases and other virulence factors that cause localized tissue damage.
Simultaneously, this dissemination prompts the arrival of acute inflammatory host cells; the
response of polymorphouclear leukocytes (PMNs), in particular, can also contribute to the tissue
damage characteristic of necrotizing fasciitis. Once the

Identification And Characterization Of Soybean Vein...
Abd El–Wahab, A.S. and Manal A. El–Shazly. (2016). Identification and Characterization of
Soybean Vein Necrosis Virus (SVNV): A Newly Isolated Thrips–Borne Tospovirus in Egypt
Egyptian Journal of virology.,13(1):14pp (in press).
Ábrahám R. (2008). Thrips species associated with soybean in Hungary.DOI:
http://dx.doi.org/10.1556/APhyt.43.2008.2.1.
Almeida, A. M. R.; Nakahara, S. and Sosagomez D. R. (1994). Thrips species identified in soybean
fields in Brazil. An. Soc. Entomol. Brasil, v.23, n.2, p.363–365,
Attalla, S. I. (2002). Weed survey in the autumn planting of sugar cane at Esna–District–Qena
Governorate. Bull. Fac. Agric., Cairo Univ., 53(2): 389–410.
Bag, S., S. I. Rondon, K. L. Druffel, D. G. Riley, and Pappu, H. R. (2014). Seasonal dynamics of
thrips (Thrips tabaci) (Thysanoptera: Thripidae) transmitters of Iris yellow spot virus: a serious viral
pathogen of onion bulb and seed crops. J. Econ. Entomol. 107: 75–82.
Carrizo, PI. (1996). Especies de trips (Insecta: Thysanoptera) presentes en flores de malezas en el
área hortícola de La Plata (Prov. Bs. As.Argentina). Rev. Chil. Entomol. 23, 89–95.
Carrizo, PI. (2001). Infestación por trips desde malezas, en almácigo de tomate. Rev. Fac. Agron.
Cuyo, 33, 27–38.
Chappell, T. M., Beaudoin, A.L.P. and Kennedy, G.G. (2013). Interacting virus abundance and
transmission intensity underlie Tomato spotted wilt virus incidence: an example weather–based
model for cultivated tobacco. PLoS One 8.
Chellemi DO, Funderburk JE and

Early Necrosis Case Study
Anna died from a stroke. For starters, blurred vision is a sign of a stroke, which Anna had, according
to her blood vessels in her eyes and to the medical report of external examination that her vision had
been compromised. Another cause for her stroke is her sickle cell anemia. Because Anna has sickle
cell anemia, her red blood vessels would stick together around her arteries (as a result of the shape)
blocking other vessels leading other places in the body, such as the brain. There were also signs of
early necrosis according to the internal examination (2.2.1) because of ketones and her diabetes, her
kidneys were starting to shut down. She had ketones in her urine meaning she wasn't getting enough
insulin. Since Anna wasn't getting enough

Clinical Presentation, Treatment Options, And The...
The general public and even some medical professionals lacks in depth information on Necrotizing
Fasciitis. Most Americans have not heard of it or do not have enough information about it to know
what to do. It is commonly misdiagnosed and is often fatal because it is not caught in time. I will
discuss what it is, what causes it, describe clinical presentation, treatment options, and the prognosis
of this disease. In hopes that more people can be made aware of this deadly disease.
Necrotizing fasciitis (NF) has been called the "flesh eating bacteria" by the media. This past summer
there were a few cases of this on Galveston beaches. Most likely it was caused by the strain Dr.
Edlich talks about in his paper Necrotizing Fasciitis: Background, Pathophysiology, Etiology. He
describes it as "a variant necrotizing Type I, or poly microbial strain known as Type I Saltwater
Necrotizing Fasciitis, in which a minor skin wound is infected with saltwater containing a Vibrio
species." The National Necrotizing Fasciitis Foundation (NNFF) states that in actuality it is the
"decaying infection of the fascia" and not a "flesh eating bacteria." It does not just affect the fascia,
the outer connective tissue bands covering the muscles, and other soft tissues, but it also can destroy
the surrounding soft tissues such as skin, fat, blood vessels and nerves. NF is not easily diagnosed
and it spreads quickly usually using the fascia as an expressway. It is still a relatively rare disease

Gangrene
Gangrene is a term that is used to identify when a large amount of tissue undergoes cell death
(necrosis). Gangrene essentially means death of tissues due to lack of blood supply and invasion of
deeper tissues with infection (Porth & Gaspard, 2015). There are two main classifications of
gangrene, dry type and wet or moist type (Porth & Gaspard, 2015). There are several other types of
gangrene that are rarer, however, all types of gangrene manifest either as dry or wet form (Porth &
Gaspard, 2015).
Dry gangrene, the part becomes dry and shrinks, the skin wrinkles, and its color changes to dark
brown or black (Porth & Gaspard, 2015). Dry gangrene is usually characterized by cold, painless
and dry and shriveled up affected part. There is ... Show more content on Helpwriting.net ...
Some species have been isolated in the stomach, gallbladder, intestine, vagina, and skin of healthy
persons. The bacteria produce toxins that dissolve cell membranes, causing death of muscle cells,
massive spreading edema, hemolysis of red blood cells, hemolytic anemia, hemoglobinuria, and
renal failure. Characteristic of this disorder are the bubbles of hydrogen sulfide gas that form in the
muscle. Gas gangrene is a serious and potentially fatal disease. Antibiotics are used to treat the
infection and surgical methods are used to remove the infected tissue. Amputation may be required
to prevent spreading (Porth & Gaspard,

Essay On Apoptosis
Given the vital role of caspase activation in apoptotic cell death, blocking their function is a useful
approach to find out whether apoptosis has a causal effect in triggering compensatory proliferation.
In various species tissue regeneration was impaired if cell death was blocked with pan–caspase or
effector caspase inhibitors (Fan and Bergmann 2008; Li et al. 2010; Ryoo and Bergmann 2012;
Tseng et al. 2007). This approach has also been shown to ameliorate loss of neuronal cells and
function after traumatic brain injury and retinal detachment (Hisatomi et al. 2001; Zacks et al.
2003). Following this approach we found that the pan–caspase inhibitor reduced the number of
cleaved CASP3+ cells in cultured retina explants, but not the overall ... Show more content on
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Following our gene expression data we further hypothesized that inhibition of RIPK1 in
combination with CASP8 might be even more specific and therefore similarly effective.
Two distinct signaling pathways trigger programmed apoptosis: the intrinsic pathway activated by
cellular damage and the extrinsic pathway induced by the binding of specific pro–apoptotic ligands,
like TNF, mediated by the initiator CASP8 activating executioner CASP3. CASP8 also has been
shown to negatively regulate necrosis by cleaving RIPK1 and RIPK3 (Festjens et al. 2007).
Apoptosis–induced compensatory proliferation has been shown to either induce generation of
different mitogenic cues, like WNT, SHH or TNF, via initiator or executioner caspases (Bergmann
and Steller 2010; Ryoo and Bergmann 2012). Previous work showed that dying photoreceptors in
fly eyes instruct cell death mediated compensatory proliferation via initiator caspases (Fan and
Bergmann 2008). And in the regenerating zebrafish retina dying photoreceptors, amacrines and
ganglion cells may express TNF that is required for the regeneration response (Nelson et al. 2013).
Inhibition of cell death and MG proliferation was

Systemic Lupus Erythematosus
CS was first described by Dr. David G Cogan in 1945 as a non–syphilitic interstitial keratitis with
vestibuloauditory symptoms (1). CS is rare, with fewer than 250 reported cases in the literature, and
is mostly described in young adult Caucasian patients of both sexes (2). CS is an extremely rare
disorder in Arabic and Middle Eastern countries(3). The novelty of this study is represented by
being the first case reported within Jordanian population that is 7 million people.
The classical form of ocular involvement in CS is characterized by the interstitial keratitis, but also,
iritis or uveitis, scleritis or episcleritis, and conjunctivitis have been also described, and the atypical
CS exists in the absence of interstitial keratitis (2). Some systemic manifestations have been
reported in association with CS, including vasculitis of the aorta leading to aortic aneurysm and/or
aortic valve regurgitation, fever, arthralgia (or arthritis), lymphadenopathy, splenomegaly, skin rash,
and peripheral or central nervous system involvement (2, 4).
The ocular involvement in CS usually gives a good response to topical corticosteroids therapy,
while, systemic corticosteroids are reserved for unresponsive cases or those with posterior uveitis, it
was reported that poor long term ophthalmologic outcomes due to CS are unusual in contrast to
vestibuloauditory affection(4).
Deafness is the most common serious outcome of CS and systemic corticosteroid therapy is
warranted as soon as

Daily Administration Of T. Vulgaris By The Oral Route At A...
3. Results
The study has established that daily administration of T. vulgaris by the oral route at a dose of 500
mg/kg for 10 days did not cause any mortality or any observable toxic effects in mice of GII. Mice
were alert with no alternation of their behavioral pattern, any gastrointestinal tract disorder or
respiratory distress. From the histopathological observations, there were not any observable changes
in the livers at the giving dose compared to the normal controls (Figure 1).
3.1. Histopathological results
Macroscopically, the liver of T. gondii infected group showed a mild degree of enlargement and
focally extensive necrosis, however in T. vulgaris treated mice; the livers appeared more or less
healthy. Microscopically, the livers of T. gondii–infected mice (GIII) showed focal areas of necrosis
with a mild degree of inflammatory cellular infiltrate; mainly lymphocytes that were very obvious in
the portal area and Toxoplasma cysts were observed between the hepatocytes (Figure 2). However,
in the infected immunosuppressed group (GIV), the histopathological features of liver progressed
from moderate to severe, in which there was a dissociation of hepatic cords pattern with generalized
necrosis of the hepatocytes. Also, there was marked dilatation and congestion of the hepatoportal
blood vessels. It was observed that some of Toxoplasma cysts ruptured, releasing tachyzoites to the
sinusoids and invading the other hepatocytes and kupffer cells. Also, there was kupffer

Filler Necrosis
Filler Necrosis
A filler is a material injected by a surgeon to augment volume in certain parts of the body. In non–
surgical rhinoplasty, surgeons use injectable fillers (such as Juvederm, Restylane, and Radiesse) to
modify and alter the shape of a person's nose without using invasive surgery
Even though, these fillers (especially silicone fillers) have been used for decades to fix minor
deformities related to the nose, they are associated with dreaded complications in the long term. For
instance, in some cases, it has been observed that the blood vessel may get blocked from the filler
injection and cause the tissues supplied by that particular blood vessel to die. In pathology, it is
necrosis. As a consequence of this, redness and pain can

Biotechnology Paper
Biotechnology Paper
Biotechnology products are the yield of engineering labors that process biological material and
agents to produce a modified biological substance. Examples of biotechnology drugs are
monoclonal antibodies and recombinant DNA. Monoclonal antibodies are important reagents in the
treatment and diagnosis of disease. They have been used for diagnosis of pregnancy, detection of
presence and concentration of drugs in the blood, histocompatibility assay, and detecting shed tumor
antigens. They are antibodies that are mass produced in a laboratory from a single clone that
recognizes only one epitope of a single antigen. Recombinant DNA is DNA that has been created
artificially and codes for a specific desired protein for ... Show more content on Helpwriting.net ...
Recombinant DNA production also requires a living organism. In 1973 Boyer and Cohen developed
a method to insert DNA from one organism into the DNA of bacteria. The first step in producing a
recombinant DNA protein is to identify what portion of host DNA codes for a desired protein. After
the DNA has been identified, the specified section of host DNA is removed and isolated using
unambiguous DNA cutting proteins. The DNA fragment is inserted into a previously opened
bacteria plasmid. The altered plasmid is inserted back into the bacteria. The plasmid replicates and
produces many copies of the exogenous gene. Finally, the bacteria are stimulated to transcript the
gene for the protein that it codes for and the protein can be harvested.
Infliximab is a monoclonal antibody produced by Centocor Inc. Infliximab is composed of human
constant and murine variable antibody regions. Infliximab is produced by a recombinant cell line
cloned from a single cell isolated by limiting diffusion and is purified by steps that inactivate and
remove viruses. Infliximab binds specifically to Tumor Necrosis Factor ƒÑ (ƒnƒvTNF ¡V ƒÑ)
ƒw TNF ¡V ƒÑ ƒnrelated biological activities include induction of inflammation factors such as
interleukins 1 and 6 (IL–1 and IL–6), enhancement of leukocyte migration by increasing endothelial
layer permeability and expression of adhesion molecules by endothelial cells and leukocytes,
activation of neutrophil and eosinophil functional

Irreversible Cell Injuries
Explain the pathological processes associated with the term "heart muscle died."
Heart muscle died as a results of myocardial infarction (MI) which the main coronary arteries was
blocked, and large part of the heart muscle was affected due to cellular death from lack of blood
flow and oxygen. Cell death is one of the most crucial events in the evolution of MI. A heart attack
or MI is usually caused by a blood clot (thrombosis) that forms inside a coronary artery, or one of its
branches, which suddenly blocks and stops the blood flowing to a part of the heart muscle. When the
blood flow is interrupted necrosis occurs ( McCance & Huether, 2014).
Discuss and contrast reversible and nonreversible cell injury. As per your analysis, what type of cell
injury did Mr. Smith sustain and why? Include pathophysiological processes involved with cell
injury. ... Show more content on Helpwriting.net ...
For example, cellular swelling occurs due to cellular hypoxia, which damages the sodium–
potassium membrane pump; as well as fatty change it can impair cellular function and damage the
cell ability of adequately metabolize fat. Both situations are reversible when the causes are
eliminated. In contrast, irreversible cell injury is the cell death with continuing damage, the injury
becomes irreversible, which the cell cannot recover and dies. There are two types of cell death
necrosis and apoptosis. When damage to membranes is severe, enzymes leak out of lysosomes, enter
the cytoplasm, and digest the cell, resulting in necrosis ( McCance & Huether, 2014). Necrosis is the
major pathway of cell death in many commonly encountered injuries, for example resulting from
ischemia, exposure to toxins, various infections, and

Summary: Tumor Necrosis Factor Receptor
There are two receptors in which TNF has the ability to bind to. The first is Tumor Necrosis Factor
receptor type 1 (TNF–R1 or CD120a). The gene that codes for TNF–R1 is TNFRSF1A (TNF
receptor superfamily – member 1A), which is located on chromosome 12 (12p13.21)(Schall, 1990).
TNF–R1 has a mass of 55 kilodaltons. The second receptor is Tumor Necrosis Factor receptor type
2 (TNF–R2 or CD120b). The coding gene for TNF–R2, TNFRSF1B (TNF receptor superfamily –
member 1B), is located on chromosome 1 (1p36.22)(Schall, 1990). TNF–R2 has a mass of 55
kilodaltons (Theiss, 2005). TNF–R1 can be conveyed in most epithelial, nervous, connective,
muscular, and vascular tissue, and is capable of being entirely activated by the two forms of TNF (
trimeric and dissolved membrane–contained). On the contrary, TNF–R2 is primarily located in cells
specific to the immune system. These TNF–R2 receptors respond to the membrane–contained
trimeric structure of TNF. Figure 1.2 Shows the Signaling pathways in which a TNF Protein engages
with a TNFR leading to the Survival or Death of a cell (Olivier and Tschopp, 2003). ... Show more
Simultaneous to this contact, TNFRs create trimeric tips that slide into the gaps of the singular TNF
structures. The contact between the TNF ligand and the TNFR causes a conformational change in
the receptor ––– as an effect, the inhibitory protein (IP) uncouples from the death domain located
within the cell (Wajant and Pfizenmaier, 2003). The uncoupling of the IP creates an opportunity for
a signal transducing adapter protein known as, "TNFR–type 1–associated Death domain protein"
(TRADD), to react with the death domain and act as a location for consecutive binding of proteins.
Ensuing the reaction between TRADD and the death domain, several new reactions can

Hypoxia-mediated Selection of Cells with Diminished...
Cancer: Necrosis vs. Apoptosis
Cancer is the second leading cause of death in humans. A cancer cell is a cell that has mutated from
its original form and will often grow at a more rapid rate than normal. The body has built certain
mechanisms to protect itself from these types of cells. One of the physiological processes the body
uses to kill off these cells is apoptosis. Apoptosis is sometimes called "cell suicide". When the body
detects that a cell's DNA has mutated and cannot be repaired, the cell will somehow trigger itself to
self destruct. Up until 1972, scientists hadn't really looked carefully at how cells die. Once they did,
it was apparent that two things could happen: necrosis or apoptosis. Necrosis was the term used to ...
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Bcl–2 also seems to play a role in this process. Cells that seem to have an over expression of bcl–2
are also resistant to to going through apoptosis. Because the over–expression of bcl–2 inhibits
apoptosis, it is said to be an apoptotic suppressor protein, whereas p53 can be an apoptosis–
promoting gene.
Hypoxia
The article then looks at the role, in solid tumours, of areas of low oxygen (hypoxia) in selecting for
those cells that have mutations in the p53 tumour supressing gene. A common feature inside solid
tumours is hypoxia and an increase of cell death. This happens because often the rate of growth in a
solid tumour outstrips the supply of oxygen to the cells. The normal reaction of a group of cells,
expressing the normal p53 gene, when exposed to an hypoxic region, is an increase in the rate of
apoptosis. However, in a solid tumour there are many cells with many different types of mutations.
In the battle against solid tumours, some tumours resistant to treatment have cropped up. The article
takes a look at the role of hypoxia possibly selecting for those cells resistant to apoptosis.
Rate of Apoptosis
Using the cells of mice the authors selected cells that expressed the normal p53 gene and those that
lacked the expression of p53 (p53 deficient). They then went through a series of tests trying to
determine the effects of low oxygen on the rate of cell death in the different cells. In the

Crush Syndrome Case Studies
Crush syndrome is a life–threating medical emergency in which rhabdomyolysis develops after
prolonged compression of the limbs.7 It is most frequently characterized by hemodynamic shock,
hyperkalemia, metabolic acidosis, and myoglobinuric acute renal failure. 7 Direct traumatic pressure
initiates cell death through mechanical disruption of myocytes, followed by ischemic injury.7 After
the release of pressure, ischemia reperfusion injury combined with an increase in vascular
permeability cause edema of the skeletal muscles.4 A rapid rise in intracompartmental pressures
(ICP) ensues leading to Acute Compartment Syndrome.10 Prolonged elevation of ICP greater than
35–40 mmHg can lead to cellular ischemia and widespread muscle necrosis.11 ... Show more
Finkelstein et al. cautions the use of fasciotomies when the recognition of an established
compartment syndrome is delayed more that 8 to 10 hours.3 A missed compartment syndrome will
result in widespread muscle necrosis that can be prone to severe infection if the compartment is
opened.10,8 Despite aggressive treatment of infections, sepsis is still a major factor in mortality due
to crush injuries.6 The University of Toronto has thus changed the management plan for crush
patients presenting with an established compartment syndrome longer than 8–10 hours. Care for
acute renal failure is provided and skin left intact for fear of converting a closed injury into an open
wound prone to

Necrotizing Facsiitis Essay
Necrotizing Fasciitis Necrotizing fasciitis is a bacterial infection that attacks the soft tissue and the
fascia. It is commonly known as the "flesh–eating bacteria". The term flesh– eating bacteria is not
really the word for the disease, as the bacteria does not actually eat the tissue. It also progresses very
quickly, greater risk of developing in immunocompromised patients due to conditions such as
diabetes and cancer. As the bacterial can be developed in many ways, after abdominal surgery, tiny
scratch, C–section, simple cut, or rash, to even a simple blood draw. To get the bacteria it must be
introduced into the body, by either direct contact with a person carrying the bacteria or because that
person is carrying the bacteria ... Show more content on Helpwriting.net ...
The disease occurs more frequently in diabetics, alcoholics, and immunosuppressed patients. There
are .40 cases per 100,000 that get necrotizing fasciitis in a population and only .08 cases in children
per 100,000. The mortality also varies with age, 50 year olds have a mortality of about 37% and
over 60 years of age a 62% mortality rate. "Statistics vary, and are not entirely accurate. A 1996
CDC Report estimates from 500 to 1500 cases per year of necrotizing fasciitis of which 20% die".
In 1998 The estimates were figures to be higher which were based on the cases reported.
Microorganisms that are cultured from the wounds have two types that exist. Type 1 necrotizing
fasciitis is a polymicrobial infection which consist of infection with aerobic and anaerobic bacteria.
Which consists of clostridium and bacteroides species, these work synergistically in the progression
of necrotizing fasciitis. Type 2 necrotizing fasciitis consists of group A streptococcus and with or
without a coexisting staphylococcal infection. The Type 2 also consists of staphylococcus aureus,
clostridium perfringens, bacteroides fragilis, and aeromonas hydrophila. The microscopic level
would include the laboratory of necrotizing fasciitis the bacteria that is seen with a microscope.
"The micrograph of necrotizing fasciitis shows necrosis of the dense connective tissues and fascia
interposed between fat lobules". The gross anatomy is the structures visible to the naked eye, such as
the

Research Paper On Apoptosis And Necrosis
Cell Death
Cell death is when a biological cell stops carrying out is function. Cell death can be due to the
natural process of replacing old cells with new ones, or may result from factors such as disease,
localized injury, or even death of the whole organism.
Apoptosis vs. Necrosis
Apoptosis is a form of cell death that is caused by normal processes of the human body, necrosis on
the other hand is a form of cell death that is caused by disease states or external inputs such as
infection or injury. Apoptosis also known as programmed cell death may also be used as a defence
mechanism for the body in the healing process and is usually normal and beneficial to the organism.
Necrosis is never normal or beneficial, but abnormal and harmful. Necrosis is regarded as an
unprogrammed death of the cell. Apoptosis almost never demands any medical treatment, on the
other hand if necrosis is left untreated it may result in critical injury or death Apoptosis Necrosis
Introduction Apoptosis, or programmed cell death, is a form of cell death that is generally triggered
by normal, healthy processes in the body. Necrosis is the premature death of cells and living tissue.
Though necrosis is being researched as a possible form of programmed cell death, it is considered
an "unprogrammed" cell death process at this time.
Natural Yes ... Show more content on Helpwriting.net ...
Degrading cellular components induces survival of cells during periods of starvation by conserving
cellular energy levels. In this process, certain constituents of the cytoplasm are isolated from the rest
of the cell within a double–membraned vesicle known as an autophagosome. The membranes of the
lysosome and autophagosome fuse and the autophagosome contents are degraded and recycled.
There are three different forms of autophagy that are commonly described, namely macroautophagy,
microautophagy and chaperone–mediated

Exposure In Domestic And Laboratory Animals Lab Report
Exposure in domestic and laboratory animals In among the food crops peanut meal is considered as
the most contaminated feed by aflatoxin. These are consumed by the animal's thus lead those to
hazardous effects. Contaminations of the feeding meals are mainly caused due to mold metabolites.
These metabolites produce carcinogenic effect in rat, ferret, trout and duck. Mainly the organ
affected by aflatoxicosis is liver by both short–term and long–term exposure. Symptoms like
anorexia, icterus, rapid weight loss, exercise tolerance, depression, fever, ataxia, gastrointestinal
damage etc. will prevail in animals by aflaoxicosis. IN BIRDS During the early intoxication caused
by aflatoxin birds die due to venous congestion and sever peri–portal ... Show more content on
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Due the effect in liver cells they are enlarged and later results in fatty depositions and changes that
lead to increase in connective tissue, progressive biliary proliferation and scattered liver necrosis.
The other one effect is the aggregation of lymphocytes and polymorphonuclear leukocytes in the
portal tracts. as a result of this action few weeks after the exposure lymphocytic hyperplasia, fibrosis
and biliary proliferation is occured. Due to the aflatoxin toxicity mitochondrial injury is indicated in
the liver cells where a drastic reduction in activities of enzymes such as succinate dehydrogenase,
malatedehydrogenase and isocitrate dehydrogenase is noticed. This causes the impaired liver
function in chicks due to the Aflatoxin B1 poisoning. So liver mitochondrial injury is considered as
one of the dominant characteristic of aflatoxin toxicity. Not only in chicks but also ducklings also a
lysis of mitochondrial membrane is reported. Broiler chicks more prone to aflatoxicosis than poultry
chicks. IN CATTLE'S Incattle's aflatoxin toxicity had been determined on the basis of consumed
peanut meal and other contaminated feeds by AFB1. Here also the major organ affected is liver.
Venoocclusive disease and fibrosis with biliary proliferation had been exhibited in the affected
hepatic cells. Many pathological alterations had reported through various studies conducted.
Continuous exposure of aflatoxin has also been described about increased connective tissue,

Legg-Calve Perthes Research Paper
Legg–Calve Perthes is a disease that only affects children. Boys are five times more likely to
contract this disease, but girls have found to have more severe cases. It is unknown to why children
get this disease, but the condition tends to be more common to those exposed to second–hand
smoke. Children who have this disease will more than likely to have arthritis in the area when they
are older. It occurs when the blood supply (ischemia) to the head of the femur (the ball) is cut off
and the head begins to die (avascular necrosis). It is a temporary disease, because after the head of
the femur collapses a new one will regenerate back to a normal hip. This disease will cause pain and
can cause a limp in those affected. Doctors can use MRI's, ... Show more content on Helpwriting.net
...
The earliest sign or what a doctor would look for in this disease is that the person will have a limp. It
may even be a painless limp. There could be pain in the anterior part of the thigh or knee. There
have been cases where the child has had pain concentrated only in the hip area and nowhere else in
the leg. An article from the National Osteonecrosis Foundation says, "...often you will first notice
limping during your child's active play". The child usually will not be able to pinpoint the exact
moment when they got injured, or exactly where the pain is if it towards the knee area. The patient
also could experience a limited range of motion or stiffness in the affected area. Symptoms
described to the doctors would also be pain can be experienced with internal rotation and abduction
of the joint, and also in the gluteus medius. Other places other than the hip joint that can experience
pain is the groin, thigh, or knee, but the most common symptom in LCPD is persistent pain in the
hip joint. The pain is usually aggravated during activity, so kids who are very active would
experience more pain than a kid who sits most of the day. A symptom that would be described to the
doctor would also be pain that goes away with rest. Children with LCPD may complain of muscle
spasms of the legs, and the patient could experience the loss of muscle mass in the quadriceps. In
emergency situations the child may even experience a fever

A Short Note On The De La Mano Y Tercer N Desbridarlas
FLICTENAS: ¿DEJARLAS INTACTAS O DESBRIDARLAS? En la literatura científica,
encontramos consenso casi total en lo que a quemaduras y pacientes quemados se refiere.
Prácticamente todos los autores que escriben sobre este ámbito, muestran ecuanimidad casi en todos
los aspectos que este tema engloba: la clasificación de las quemaduras según su profundidad
(primer, segundo y tercer grado), según su extensión (Regla de la palma de la mano y Regla de los
nueves de Wallace), según su agente causal (químicas, eléctricas, biológica, por congelación, por
radiación, térmicas y por fulguración), según su gravedad y según su localización; así como en la
fluidoterapia que se le ha de administrar al paciente quemado en las primeras horas (todos los
autores sin excepción eligen Ringer Lactato). Sin embargo, y aunque en el tratamiento pre y
hospitalario hay casi igualdad por parte de los autores en cuanto las técnicas y protocolos a realizar,
nos encontramos con un punto que causa controversia y la técnica difiere según el manual en el que
busquemos o el autor que lo escriba. Dicho aspecto trata sobre las flictenas o ampollas, tan
características de determinados tipos de quemaduras. Los autores no se ponen de acuerdo sobre si
hay que quitar o no las flictenas en un paciente quemado, y si hacemos una revisión de la literatura
científica sobre quemaduras, vemos que hay argumentos a favor de su retirada y argumentos a favor
de preservarlas. Algunos partidarios de desbridar las flictenas

Bone Formation And Bone Break Down
Bone formation and bone break down is a very important maintenance of the human body. After
tooth eruption teeth move and need new bone to form constantly. Due to the wear of enamel on the
interproximal and occlusal surfaces teeth are constantly moving in the mouth. For that reason,
Osteoclasts are activated and they begin to breakdown old bone. On the opposite side of the tooth
osteoblasts lay down new bone. With age however bone begins to change. When a person is young
they have healthy, dense and smooth bone. When people age bone becomes less dense and jagged.
When this begins to occur it is known as osteoporosis. Osteoporosis is a very common condition
that affects the bone. This condition causes the bone to become very brittle and break down rapidly.
This condition affects men and women worldwide. It is more common to occur in women than in
men. Worldwide an estimated two hundred million women are affected with the debilitated
conditions of osteoporosis (5). Women are diagnosed with this more often than men, it is because of
the effects of menopause. Osteoporosis occurs when certain nutrients levels are not where they are
supposed to be. Estrogen is one of the key nutrients to be low and become an onset for osteoporosis
(7). Although women suffer more frequently from osteoporosis, men however tend to suffer more
fatalities after a hip fracture due to osteoporosis (7). Other factors can play a role in the development
of osteoporosis such as; people who smoke, have eating

The Use of Stem Cells to Treat Myocardial Necrosis
When an obstruction of a coronary vessel occurs, there is a possibility of myocardial necrosis. In
adults the monocytes located in the cardiac tissue are not able to replicate. There are smooth muscle
and endothelial cells which can replicate, but cause the formation of scar tissue. Using primitive
stem cells, could be a way to regrow the tissue resulting from necrosis. Primitive stem cells are
located on the organs usually of the fetus. They have functional plasticity in which they are able to
move to different areas in the body when needed. In this experiment bone marrow was extracted
from mice and then tested with the c–kit expression, which identifies certain proteins located in the
bone marrow. A side population of cells. or SP cells, were used from the bone marrow and from
these the cells RNA was used and tested using PCR (Polymerase Chain Reaction) and primers. The
SP cells isolated earlier in the experiment were then injected into female mice and after two and a
half months the coronary artery of the female mice was occluded. The hearts were then extracted
after two weeks and the hearts of those mice that were still alive at that time were stained with x–
gal. The x–gal showed that these SP cells migrated to the injured parts of the heart by using the
circulatory system.
This is important for nursing because these primitive stem cells could help to be an alternate therapy
that can be used to help patients. The ability of having the heart to regrow could reduce the

Necrosis Syndrome Essay
Acute Hepatopancreatic Necrosis Syndrome has been known to emanate in shrimp since the year
2010.It is also sometimes referred to as Early Mortality Syndrome (EMS), in which in an expansive
term is used to describe different health problems of shrimp which causes their early death (Nunan,
Redman, & Lightner, 2013). According to Lightner (2013), EMS outbreaks typically occur within
the first 30 days after stocking a newly prepared shrimp pond, and mortality can exceed 70%.
Furthermore, it is caused by a bacterial agent, which is transmitted orally. Also, it colonizes the
shrimp's gastrointestinal tract and produces a toxin that causes the destruction of tissue and
dysfunction of the shrimp's digestive organ which is the hepatopancreas.As stated by Lightners
team, EMS does not affect human. Moreover, they identified the EMS/AHPNS pathogen as a unique
strain of relatively common bacterium which is the Vibrio parahaemolyticus. In conclusion,
V.parahaemolyticus is infected by a ... Show more content on Helpwriting.net ...
monodon and P. vannamei. In china, Penaeus chinensis was also reported to be affected. Presence in
Asia–Pacific AHPNS has been officially reported in China and Vietnam (2010), Malaysia (2011)
and Thailand (2012).While it is apparent that the spread of AHPNS throughout the region, it also
suggests an infectious or at least biological agent may be involved. So far, laboratory challenge tests
have failed to demonstrate that the disease is transmissible and no infectious agent or toxin has been
identified. Apart from that, the histopathology is a suggestive toxicity. Not to mention, the testing of
the feeds from affected farms and two crustaceacides including cypermethrin have similarly failed to
reproduce the disease. Moreover, the disease is not related to any of the known shrimp pathogens
like WSSV, YHV, IMNV, and TSV. In conclusion, at this stage the cause is unknown, and the
possibility of an infectious agent and/or toxin cannot be discounted ( Lightner & Flegel,

Muscular Necrosis Essay
Ultimately, avascular necrosis occurs through one final common pathway, which is decreased blood
flow to the bone that leads to bone ischemia and death (Seamon). The medial femoral circumflex
artery provides the primary blood supply to the femoral head. The MFCA branches off from the
profunda femoris artery and anastomoses, or cross connects, with branches of the lateral femoral
circumflex and inferior gluteal arteries in order to form an extracapsular arterial ring at the base of
the femoral neck (Glynn). Blood is supplied to the femoral head by retinacular vessels that originate
at the arterial ring and travel subsynovially along the capsule of the hip joint. The femoral nutrient
artery has additional intraosseous vessels that travel from the femoral nutrient artery to the femoral
head. The artery of the ligamentum teres derived from the obturator artery and occasionally from the
MFCA also supplies a small yet valuable portion of blood to the medial femoral head (Grose).
Avascular necrosis of the femoral head occurs when any of these blood supplies are affected.
Ischemia of the femoral head can be caused by compression, constriction, vascular disruption or an
intravascular occlusion (Van heil). There are several factors that can contribute to the development
of AVN, but the exact etiology and ... Show more content on Helpwriting.net ...
Multiple studies have attributed the occurrence of AVN to a combination of factors including genetic
predisposition, metabolic factors, alcohol use, steroid use, and local factors that interfere with blood
supply including vascular damage, increased intraosseous pressure, and mechanical stresses (Moya–
Angeler). Leading risk factors for AVN include corticosteroid use, alcohol abuse, sickle cell disease,
systemic lupus erythematosus, renal failure and hematologic disorders (Minkalis). Other cases of
AVN have no identifiable etiological factors and are therefore deemed idiopathic

The Comeback of the Maggot Therapy
The Comeback of the Maggot Therapy
All kinds of arthropods and insects have been and are still employed in many medical treatments
since antiquity. These living organisms are believed to carry myriads of therapeutic benefits, since
they are not biochemically–engineered, perhaps a natural remedy. Despite their medical
significance, many of these practices have ceased to exist in today's society, since there are
insufficient scientific evidences to elicit if they are truly efficient and safe for the human body. In
accordance to today's medical perspective and ideology, these treatments may have also been
terminated due to the disgust that is engendered upon the patients as well as the ethical issues
associated with the use of insects. Furthermore, the shortcomings of some of these ancient therapies
might be largely due to the advancements in medical technologies. In spite of this, modern
technologies are still not completely efficient, safe, applicable, and accessible to everyone, since
some of the patients might be too vulnerable to tolerate the consequences associated with each
therapy as well as prices that could be unaffordable. With these limitations, many clinicians are
turning back towards the "ancient technologies" with tools and wisdoms of the 21st century
(http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2771513/pdf/dst–03–0336.pdf). Among all of the
ancient insect–based therapies that were abolished, the maggot therapy is one of the few that has
now been brought back

The Biotechnology Innovation Organization Defines The...
The Biotechnology Innovation Organization defines the biotech industry as, "technology based on
biology – biotechnology harnesses cellular and bio–molecular processes to develop technologies
and products that help improve our lives and the health of our planet." This Vital sector of the free
market is comprised of many great companies. The five choices that I have selected are, in my
opinion, the best choices to represent the biotechnology industry. My first choice was AbbVie Inc.,
or (ABBV), and on the date of purchase their stock was trading at $64.08 per share. On the date of
purchasing their stock I bought 312 shares equaling a total of $19,992.96. This company is known
for discovering, developing, and marketing both biopharmaceuticals and small molecule drugs. One
drug that is known as the world 's best selling anti–inflammatory medicine is Humira, which was
made by AbbVie. Drugs like Humira and Vicodin have proved to be household names. I chose
AbbVie incorporated because their drugs are some of the best on the market and cater to the needs
of the masses. The second company I selected was Amgen Inc., or (AMGN), and on the date of
purchasing their stock it cost $172.04. I bought 116 shares resulting in a total of $19,956.64. Amgen
Incorporated is a multinational biopharmaceutical company that originated in the United States and
is the world's largest independent biotechnology firm. On their company website, under product
overview, they say, "Amgen's medicines

Necrotizing Fasciitis Research Paper
Necrotizing Fasciitis is a medical infection which requires emergency professional help as soon as it
is indicated. The break down of this name can create an idea of the common symptoms relating to
the bacteria. For example "it is" means inflammation describing how the skin gets due to the dead
skin tissue. This requires medical diagnosis before being able to be treated. Lab tests and/or imaging
are always required. This can be short–term or long–term eventually being deadly. Fewer than
20,000 cases in the United States occur per year. Necrotizing Fasciitis is a bacterial infection which
causes the tissue under the skin to be destroyed. This flesh–eating infection is caused by more than
one type of bacteria making it rare in many cases. Once the bacteria enter the body, it can quickly
spread causing it to be deadly. The fascia, which is the connective tissue surrounding the blood
vessels, nerves, fat, and muscles is infected making the body weak and lack support. In order to
acquire this infection the skin needs to be broken such as getting a cut, scrape, or wound. With small
injuries ... Show more content on Helpwriting.net ...
Signs of inflammation may not be visible within the early stages making it more risky and have a
larger fatality rate. Symptoms will appear after 3 to 4 days. It will start with a fever and the feeling
of being unwell. Unfortunately it will make the skin red and hot with blisters and intense pain in the
areas. Some patients have experienced confusion, dehydration, diarrhea, and vomiting. Once they
are in a bad stage, the affected area of tissue will turn black as a sign of it starting to die. As fast as 5
days, the patient is considered extremely ill. At this time, the infection has now entered the
bloodstream causing them to have high temperature and low blood pressure. Sometimes the pain of
the skin will come to an end due to the nerves being dead

Coral Bleaching In Australia
Coral bleaching occurs when the microscopic plants (zooxanthellae) are expelled by rising ocean
temperature. When there are no microscopic plants such as zooxanthellae, the coral turns white and
die. The studies show that throughout the worlds ocean, from the Florida Keys to the Great Barrier
Reef of the Australia have been evidence of unique coral bleaching caused by the rising of ocean
temperature. In the early 1980s the coral bleaching event has increased because of rapid increase of
sea water temperature. Esther et al., investigates growth of Oculina patagonica at multiple
environmental conditions in the western Mediterranean Sea. The Oculina patagonia is stony coral
specie which is found mostly in the Gulf of Mexico and Caribbean. The coral was basically Atlantic
origin which was transferred to Mediterranean Sea. ... Show more content on Helpwriting.net ...
Esther et al., studied nine live species of O. patagonica in western Mediterranean Sea for the
duration of about of about eighteen months. The nine colonies were marked in the normal location
by the nail on the rock at about 3–5m in February 2010. They took photography of every marked
colony by every 3 month (Esther et al., 2014). They categorized each marked colony into the six
category that is unbleached, paler, the coral surface that is 0–20% bleached, 20–80% bleached coral
surfaces, less than 50–80% bleached and less than 80 percent bleached (Esther et al., They
calculated the Bleaching index and the necrosis of the marked colonies of the O. patagonia to
understand the coral bleaching in the specie(Esther et

Apoptosis
Kerr, Wyllie, and Currie first used the term apoptosis in a paper in 1972 to describe a
morphologically distinct form of cell death, although certain components of the apoptosis concept
had been described years previously. Our understanding of the mechanisms involved in the process
of apoptosis in mammalian cells transpired from the investigation of programmed cell death that
occurs during the development of the nematode Caenorhabditis elegans (Horvitz, 1999). In this
organism 1090 somatic cells are generated in the formation of the adult worm, of which 131 of these
cells undergo apoptosis or "programmed cell death." These 131 cells die at particular points during
the development process, which is invariant between worms, demonstrating the ... Show more
Necrosis is an uncontrolled and passive process that usually affects large fields of cells whereas
apoptosis is controlled and energy–dependent and can affect individual or clusters of cells. Necrosis
is caused by factors external to the cell or tissue, such as infection, toxins, or trauma that result
unregulated digestion of cell components
Some of the major morphological changes that occur with necrosis include cell swelling; formation
of cytoplasmic vacuoles; distended endoplasmic reticulum; formation of cytoplasmic blebs;
condensed, swollen or ruptured mitochondria; disaggregation and detachment of ribosomes;
disrupted organelle membranes; swollen and ruptured lysosomes; and eventually disruption of the
cell membrane. This loss of cell membrane results in the release of the cytoplasmic contents into the
surrounding tissue, sending chemotatic signals with eventual recruitment of inflammatory cells.
Because apoptotic cells do not release their cellular constituents into the surrounding tissue and are
quickly phagocytosed by macrophages or normal cells, there is essentially no inflammatory reaction.
It is also important to note that pyknosis and karyorrhexis are not exclusive to apoptosis (Kurosaka
et al., 2003).
Mechanisms of Apoptosis
The mechanisms of apoptosis are highly complex involving an energy dependent cascade of
molecular events. Research

Acute Renal Failure
Acute renal failure is described as an abrupt reduction in renal function with elevation of both BUN
and plasma creatinine levels. Acute renal failure can be classified as; pre–renal, intra–renal or post–
renal. Moreover, it is often linked to oliguria. However, urine output could still be normal or
increased. When most types of acute renal failure are diagnosed early, it is reversible.
The pathophysiology of pre–renal acute renal failure is due to impaired renal blood flow and is the
most common cause of acute renal failure. Moreover, the GFR decreases due to lowered filtration
pressure. As a result of the poor perfusion, renal vasoconstriction, hypotension, hypovolemia,
hemorrhage, or inadequate cardiac output can occur. Acute pre–renal ... Show more content on
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The three phases include; oliguria, diuresis, and recovery. Oliguria starts within one day after a
hypotensive even and can last between one and three weeks. Moreover, it can regress in several
hours or extend for several weeks. The stent of oliguria depends on the duration of ischemia or the
severity of the toxic injury. Specifically, there is approximately between ten and twenty percent of
cases that have non–oliguric failure. The BUN and plasma creatinine concentrations increase,
however the urine output may vary in volume. Also, other various manifestations are dependent on
the underlying cause of the renal failure. When the renal function improve, the urine volume
increases and is progressive. However, during the beginning of the diuretic phase the tubules are still
impaired. So, both the fluid and electrolyte balance need to be closely monitored due to excessive
urinary losses needing to be replaced. An index of renal function during the recovery phase is
provided my serial measurements of plasma creatinine. In order normal status to return is may take
anywhere from three to twelve months. Furthermore, about thirty percent of individuals do not have
a full recovery of a normal GFR or tubular

The Growth Of Room 40 's Atherosclerosis
The growth of Room 40's atherosclerosis progressed until an acute arterial occlusion was formed,
which stopped blood flow to the tissue. The atherosclerosis consisted of complicated lesions that led
to a decrease in blood flow and the presence of a thrombus, ultimately resulting in thea lack of blood
flow to the right foot and lower leg. Thrombi often appear after a rupture of an atherosclerotic
plaque (Coneliue, 2014). This lack of blood flow led to necrosis of the tissues in the right foot and
lower leg and ultimately resulted in the need for the AKA.
The obstruction in Room 40's leg was discovered using a diagnostic arteriogram. An arteriogram is
an image of the interior of blood vessels, such as arteries, by the use of electromagnetic waves.
During this procedure, a dye is injected into the artery revealing any bulges, weakness, lesions or
occlusions of the blood vessel. The ability to see any evidence of a a plaque formation or obstruction
within a vessel makes an arteriogram an effective method for detecting atherosclerosis (Johns
Hopkins Medicine, 2015).
After the obstruction was detected with the arteriogram, the patient underwent percutaneous
catheter–directed thrombolytic therapy with alteplase in order to regain blood flow and nutrients to
the right foot and lower leg. This choice of therapy is chosen with the goal to quickly dissolve the
arterial obstruction (National Institute of Health, 2014b). Although the TPA in alteplase will not
restore the damaged or

Necrosis Research 40

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