Endometriosis Pathogenesis

Endometriosis Pathogenesis
Endometriosis is a benign chronic gynaecological disease characterized by the presence of
endometrium– like tissue–glands and stroma– outside the uterine cavity [1]. This condition may
affect up to 10–15% of women in childbearing–age, causing pelvic pain [2], and infertility [3].
Although endometriosis was first reported by Carl von Rokitansky more than a hundred years ago
[4], the pathogenesis of this condition is still not clear [5]. Sampson's theory of retrograde
menstruation is probably the most accepted among scientific community, though this explanation
cannot adequately account for all the pathogenesis of the disease [6]. Previous studies report that
retrograde menstruation occurs in >90% of women [7], nevertheless, the incidence of ... Show more
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Abundant bulk of evidence suggests that patients with endometriosis have an immunity dysfunction
that enables ectopic endometrial cells to implant and proliferate [8–11]. Notwithstanding, the onset
and progression of the disease is probably not only an immune issue, but the result of a complex
series of processes that lead to the attachment of endometrial cells to the peritoneal surface [12],
invasion and estrogen–related proliferation [13], vasculogenesis [14], angiogenesis and finally
chronic inflammation [15,16]. Chronic inflammation is associated with an overproduction of
prostaglandins [17], metalloproteinases, cytokines and chemokines, creating a self–supporting loop
that mantains and amplificates the progression of the disease [18–20]. Once the process is started,
many profibrotic mediators also play a role in the fibrogenesis associated with endometriosis [21].
From an immunological point of view, it has been shown that circulating natural killer (NK) cells
are capable of destroying endometrial cells [22]. Thus, it has been proposed that NK cells may have
a pivotal role in the immune control of endometriosis [23,24].
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OSA Pathogenesis
Though overweight and an excess of regional adipose tissue are considered major risk factors for
OSA, there are also other interacting elements in OSA pathogenesis, such as craniofacial
abnormalities and an altered UA structure. The results obtained in Lee et al. [3, 4] and Davidson et
al. [5] suggest that the appearance of OSA is connected to physiological changes in craniofacial
morphology or acquisition of speech. First studies used cephalometry and computed tomography
(CT) to examine possible abnormalities within craniofacial structures. Both techniques are very
common in medical imaging procedures. In [6] authors applied sophisticated volumetric analysis on
magnetic resonance imaging (MRI) of the upper airway soft tissue structures in

Essay On Pathogenesis Of Arthritis
Discussion Over five decades of research, have shown complex pathogenesis of RA. Variable
clinical responses to targeted therapies, such as TNF blockers, T–cell costimulation inhibitors, and
B–cell depletors, demonstrate that the disease is heterogeneous and probably lacks a single
mechanism that applies to all patients (21). Inhibition of adjuvant–induced arthritis (AIA) in rats is
one of the most suitable test procedures to screen anti–arthritic agents since it closely resembles
human arthritis (22). The present study was designed to evaluate the efficacy of the use of MPEE for
one and two weeks on ankle diameter, serum levels of RF, pro–inflammatory biomarkers (IL–1 β
and TNF–α), anti–inflammatory cytokines (IL–4 and IL–10), ... Show more content on
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Moreover, previous study demonstrated that the effect of thymol, a natural monoterpene phenol
primarily found in mandarin peel, on anti–inflammation not only comes from the expression of
inflammatory cytokines but also from the iNOS and COX–2 pathway. The promising anti–
inflammatory effect of thymol may involve in the inhibition of NF–κB and MAPK signaling
pathways (26). TNF–α being a key inflammatory mediator triggers an increase in synovial
proliferation and also production of other secondary mediators. TNF–α also induces osteoclast
differentiation. Overproduction of TNF–α in affected joint causes a cascade of secondary mediators
involved in the recruitment of inflammatory cells which leads to joint destruction (27). The actions
of IL–1β include induction of knee joint inflammation, cartilage damage and bone resorption (28).
Cyclooxygenase (COX) is strongly induced by IL–1β and plays an important role in the
pathophysiology of rheumatoid arthritis. Therefore, down–regulation of pro–inflammatory cytokines
and NF–κB may be an appropriate therapeutic strategy for rheumatoid arthritis (29). The current
study revealed increased serum levels of both IL–1β and TNF–α in the RA control groups. These
results run parallel to several reports showed that progression of RA is accelerated by pro–
inflammatory cytokines and chemokines. TNF–α and IL–1β are reported to be associated with the
progression of RA (30). Also, it was observed significantly high levels of IL–1β

A Study Of Aneurysm Pathogenesis And Progression
Over the past 30 years, the study of aneurysm pathogenesis and progression has become a
multidisciplinary e ort involving a wide range of areas spanning from molecular cell biology to solid
and fluid mechanics. The studies have been motivated by the need of providing an– swers to the
following questions [12]:
1. Formation:Whatcausesarterialaneurysmstoform?Whydoonlysomepeopledevelop aneurysms and
others don't? Why do aneurysms dominantly form at specific locations in certain arteries?
2. Growth: Which factors a ect aneurysm growth, once it has formed? Can aneurysm growth rate be
predicted?
3. Rupture: Is there a way to quantify the risk of rupture at any given moment during aneurysm
growth?
4. ... Show more content on Helpwriting.net ...
Therefore, it is standing to reason to assume, that aging plays an important role in AAA
pathogenesis. The assumption is, that
18
specific changes in the geometry of the vessel (length, diameter, and wall structure/sti ness)
resulting from the natural aging process combined with changes they induce in the hemo– dynamics,
are the primary cause of aneurysm formation. This assumption postulates, that the mentioned
coupling induces a segment of the aortic wall to degrade and simultaneously leads to a gradually
increase of its diameter.
A lot of research has been devoted to the fundmental mechanisms of aging in the arteries. Generally
spoken, the aging process leads to an increase in the arterial diameter and a sti ening as well as
thickening of the arterial wall. The median layer undergoes the bigger changes thinning out and
losing its orderly arrangement of elastin laminas and fibers. The elastin laminas and fibers become
fragmented and unorganized leading to decreasing elastic properties and increasing the sti ness [16].
From fluid mechanical viewpoint, the speed of the pulse wave in the artery increases, as sti ness
goes up with age. It was shown, that the wave speed nearly doubles for a 60–year old adult
compared to a 10–year old child (from 6.5 m/s to upwards of 11 m/s) [17].
Studies found out, that the aging iliac

Describe The Pathogenesis Behind Osteoporosis
Osteoporosis is a disease in which bones become brittle and lose their durable architecture. This
condition can be caused as a side effect of some drugs such as corticosteroids, hormonal changes or
due to nutritional deficiencies. The pathogenesis behind osteoporosis is an imbalance between bone
catabolism and anabolism; which nutrition contributes greatly to. The two main nutrients that are
implicated with bone turnover are calcium and vitamin D, and a deficiency in either of them can
result in impaired bone matrix deposition. Calcium and vitamin D are tightly linked; the body
cannot benefit from either if they are not present together. Calcium is one of the major components
of bone and regardless of the amount of intake, it cannot be absorbed

Pathogenesis And Endocytosis
The proposed mechanism is that the mutated α–synuclein binds directly to the ER–Golgi SNARE
complex inhibiting its assembly (Gitler et al., 2008). Altering vesicle trafficking at any point inside
the cell can lead to an accumulation of proteins, which can have severe consequences for
dopaminergic neurons. The endocytic pathway is also important in the pathogenesis of Prkinson's
disease. Mutations in the cyclin G associated kinase (GAK) are important for endocytosis. Single
nucleotide polymorphisms (SNPs) have actually been identified that can be associated with risk
factors for sporadic Parkinson's disease (Nalls et al., 2014). A relationship between one GAK SNPs
and increased levels of the protein α–synuclein has been demonstrated on a ... Show more content
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It is possible that α–synuclein causes the ER stress by interrupting the vesicular protein trafficking
and causing the ER to be overworked. It is also found that mutations in the parkin gene end up
forming aggregations of its own substrates in the ER, which leads to stress and death of dopamine
neurons (Imai et al., 2001). Other than the stress on the ER created by clusters of incorrectly folded
α–synuclein proteins, mitochondria that are functioning improperly can also induce stress on the ER.
Parkin is an E3 ubiquitin ligase responsible for regulating many cellular processes by tagging
proteins with ubiquitin for their destruction (Dawson and Dawson 2010). A loss of function
mutation in the parkin gene is seen to play a major role in altering the function of mitochondria
leading to stress on the ER (Bouman et al., 2011). Mutations in PINK1 (PTEN induced putative
kinase 1) affect pakin translocation and cause mitochondria to accumulate which increases the
vulnerability of dopamine neurons (Song et al., 2013). Along with this, muations in both the parkin
gene and PINK1 cause ER stress by increasing contacts between ER and dysfunctional
mitochondrial, which can lead to neurodegeneration (Celardo et al., 2016). In rare forms of heredity
Parkinson's disease, mutations in

Alzheimer's Disease: AD Pathogenesis
ALZHEIMER'S DISEASE – A COMPLEX MULTIFACETED DISORDER In spite of significant
improvements in our knowledge of the pathogenesis of AD over recent decades, the precise
mechanisms leading to AD development remain elusive. Over the years, several different
hypotheses have been postulated to address the pathological lesions observed in AD. Indeed,
oxidative stress has been consistently observed as an underlying biochemical anomaly in several
neurodegenerative diseases including AD. However, whether oxidative stress presents a causal role
or is secondary to AD pathogenesis remains unclear.[39] Markers for oxidative stress have been
reported during early development of the disease and in patients with mild cognitive impairment
well before the onset ... Show more content on Helpwriting.net ...
In lower organisms such as bacteria or fungi, resveratrol acts as a phytoalexin with potent
antimicrobial activity against these pathogens [62]. One epidemiological study reported a positive
association between low to moderate red wine consumption and a reduced incidence of
cardiovascular disease. This phenomenon is known as the "French Paradox" [63, 64]. Resveratrol is
naturally found in both cis– and trans– isomers (Figure 1). The trans– isomer is the most common
and highly active form. Resveratrol is highly vulnerable to isomerisation due to UV. With at least
80% of trans–resveratrol being transformed to cis–resveratrol after exposure to just 1 hour of
ordinary light

Pathogenesis Of Asthma
A plethora of both genetic and environmental triggers contribute to the pathogenesis of asthma, one
of the most prevalent respiratory diseases in the world (Burney et al, 2015). Studies have found
environmental, physical and allergic triggers lead to exacerbation of disease in suffering
populations. Similarly, in the last decade, advances in genetic research has lead to studies linking
variation within specific genes and a vulnerability to developing asthma. Understanding asthma
associated triggers has the potential to contribute to successful disease management and treatment
and is critical to uncovering the pathogenesis and etiology of asthma.
Understanding the genetic etiology of asthma is critical not only to the development of successful

Angiogenic Pathogenesis
The progression from fibrosis to cirrhosis, the end–point of CLDs, is distinguished by a prolonged
inflammatory and fibrogenic process that leads to an abnormal angioarchitecture distinctive for
cirrhosis. Several mechanisms are responsible for the angiogenic switch during the pathogenesis of
CLDs. First, CLDs are characterised by chronic inflammation. Increased intrahepatic vascular
resistance is primarily caused by anatomical changes, such as fibrotic scar tissue compressing portal
and central venules. In addition, the formation of fibrotic septa, as well as sinusoidal capillarisation,
can result in an increased resistance to blood flow and oxygen delivery. This results in hypoxia and
the transcription of hypoxia–sensitive pro–angiogenic ... Show more content on Helpwriting.net ...
The characteristic fenestrated phenotype of the sinusoidal ECs is lost and an organised basement
membrane is established, which leads to an impairment of oxygen diffusion even though the
increased arterial flow provides a high supply of oxygenated blood . The deposition of collagen in
the space of Disse accentuates the narrowing and distortion of the sinusoidal lumen, further
restricting microvascular blood flow. This is aggravated by leucocytes, either mechanically trapped
in the narrowed sinusoids or adhering to the endothelium, as a result of activation of a hepatic
microvascular inflammatory response. The hypoxic liver tissue causes an up–regulation of VEGF,
Ang and their receptors in HSCs, not only enhancing the hypoxia–induced angiogenesis but also
stimulating activation and migration of HSC. As stated previously, activated HSCs induce an
inflammatory response and enhance angiogenesis. New vessels themselves can significantly
contribute to the perpetuation of the inflammatory response by expressing chemokines and adhesion
molecules promoting the recruitment of inflammatory cells. Furthermore, angiogenesis, early in the
course of a CLD, may contribute to the transition from acute to chronic

Aureus: Opportunistic Pathogenesis
Staphylococcus aureus is an opportunistic pathogen found mainly on skin, nose and respiratory tract
1 The gram positive facultative anaerobe is round. Transmission occurs through humans or animals,
exposure to contaminated surfaces or enterotoxins presence in food 2 . Most susceptible are
newborns, young children and the elderly due to reduced immune function 3, 4.
Immunocompromised individuals diagnosed ( ie. AIDS, HIV, Crohn's etc.) assume greater risk of
infection 3, 5 . S. aureus causes many diseases including food poisoning, endocarditis, skin/soft
tissue (enterotoxin caused scaled skin and abscess) and pleuropulmonary infections (ex.
pneumonia), osteomyelitis, septic arthritis and bacteremia 2, 3. In health care settings S. aureus
colonies ... Show more content on Helpwriting.net ...
S.aureus skin infection is often diagnosed visually 9. Respiratory tract and sometimes external
infections require collections of swabs from invaded site, Gram–staining and selective culturing for
confirmation of diagnosis; additional tests are coagulase and catalase test (S.aureus positive for
both) 9, 10. For detection of bacteremia, blood sample is taken and selectively cultured. More rapid
detection is possible with use of real time quantitative PCR. Specifically, nuc and sodA assays allow
for detection/monitoring the presence/increase of S.aureus cells and genomic DNA in patient's blood
11. As of 2015, there were 740 cases of S.aureus infection in Canada, 210 cases (53 new), occurred
in Ontario 12. Mortality is 20%, majority of deaths occurring within 30 days of infection 21,22, 23.
Community acquired S.aureus is ~$7070–20500 per case; 27% of those who acquire CA–MRSA
nosocomially die 17,20. MRSA also makes up nearly 1% of all SSTIs in America 19. S.aureus is
equipped with a battery of virulence factors; Its enterotoxins, and toxic syndrome toxin are harmful
to gastroenteric and endothelial tissues

Cancer Pathogenesis Of Cancer
There has been a spontaneous advancement in the understanding the pathogenesis of cancer over the
last two decades. Even though there has been a significant success in the knowledge of tumor, there
still a wide gap in the treatment of tumors. There is a little treatment information available on cancer
making it difficult to control it. Chemotherapy remains the only effective treatment method used.
This study aims at examining the possible roles of the p53 gene in leukemia and how that data can
be utilized for diagnosis and treatment of cancer.
Due to its potent tumor suppressive activity, a molecular understanding of p53 action will create
significant experiences into specific procedures that limit tumor growth and may identify key ...
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There are essentially two pathways that transduce signs to start apoptosis in leukemia. The primary
route is the extrinsic pathway. It includes the trimerization of death factors like CD95/Fas/APO–1 or
TNF receptor one which initiates caspase 8, which initiates the apoptotic machinery. The second
pathway is the intrinsic pathway. This pathway involves the p53 gene and is subsequently of more
concern. The p53 gene initiates the arrival of cytochrome C from the mitochondrial intermembrane
space into the cytosol. The cytochrome C in the presence of ATP reasons the oligomerization and
activation of Apaf–1 and caspase 9 as per Schuler, (2000).
Therefore, then prompt caspase three and other effector caspases that cause apoptosis. By utilizing
this data, experiments have been carried out that try to induce apoptosis in cancer cells by activation
of the p53 gene. One particular examination was done on the human osteosarcoma cell line Saos–2,
which is deficient in p53. According to Schuler (2000), an introduction of the p53 gene led to
apoptosis through an intrinsic pathway. Subsequently subjecting p53 to gene treatment might be of
enormous importance in the battle against leukemia.
According to Liu (1994), it has additionally been discovered that p53 mutant tumors are more
unstable genetically and this state of instability may enable the tumors to become more rapidly
resistant to drug treatments.
Since p53

LF Disease Pathogenesis Paper
Pathogenesis of LF disease:
There are several important progress have been achieved in understanding of pathogenesis of LF
disease, which primarily based on animal experiments and biopsy from the patients.
Figure: Pathogenesis of LF disease (lymphedema, hydrocele, elephantiasis).
Adapted from Nutman, 2013.
The Filarial worm and their products have direct effect on lymphatic endothelial cells, and cells of
adaptive and innate immune system. The interaction of inflammatory/immune mediators, molecules
of parasite, Wolbachia and other factors contribute to pathogenesis and development of LF disease.
The secondary bacterial infections further complicate the pathology.
The adult and developing worm of Wuchereria bancrofti, ... Show more content on Helpwriting.net
...
Worms produces small reaction when they are alive. However, after death of adult worm, a
granulomatous reaction started (Dreyer et al., 2000; Figueredo–Silva et al., 2002)
The host adaptive immune response produces an inflammatory reaction to the death or dying
parasites. The subsequent release of parasite molecules and inflammatory mediators results an
irreversible lymphatics dysfunction. (Figueredo–Silva et al., 2002; Nutman, 2013). The lymphatic
dysfunction predispose a suitable environment for secondary bacterial or fungal infection, initiate
inflammatory reaction in the skin and subcutaneous tissue, and enhance progression of lymphedema
and precipitate the development of elephantiasis (Nutman, 2013)
The role of inflammatory cytokines of innate origin have been shown to have vital role in
pathogenesis of lymphedema. Individuals having chronic LF disease, contain elevated level of pro
inflammatory cytokines and C–reactive protein.
An important factor associated with the inflammatory response and increase release of C–reactive
protein plus vascular endothelial growth factor might be the Wolbachia, an endosymbiotic,
intracellular bacteria live in the most filarial nematodes (Pfarr et al., 2009; Nutman,

Aetiology And Pathogenesis Essay
Aetiology and Pathogenesis
Multiple Sclerosis (MS) is a non–preventable inflammatory neurodegenerative demyelinating
disease. The pathogenesis of MS is a debatable topic and still needs to be better understood. (1,3) .
In histological assessments, both the myelin sheath and oligodendrocytes are damaged and attacked
by cells of the immune system. Both, the humoural and cellular immune responses, are present. First
a T cell phagocytic reaction by macrophages and targets the myelin sheath and oligodendrocytes.
this is followed by the secretion of anti–myelin antibodies from B cells, opsonisation of the myelin
sheath and activation of the complement cascade (1,3,4).
There are several theories used to explain the mechanisms of demyelination. ... Show more content
compared to the general population risk rate of 0.1%
The disease is not a worldwide epidemic (2) Global Distribution of MS
Figure 1: Global Distribution of MS. Darker areas represent high incidence rates (2)
Typical age of onset of signs and symptoms
The age of onset ranges between the ages of 30 and 49 [6]. Prior to the onset of MS, individuals are
likely to begin to develop specific signs and symptoms.
The early clinical signs and signs and symptoms associated with MS (5):
Blurred or double vision.
Lowering of cognitive abilities – this is shown with the shortening attention span, low levels of
concentration, lapses in memory, and poor judgment skills.
Paresthesia which is the development of numbness and tingling. Within MS patients this is
reinforced through the onset of muscle weakness especially within the limbs
Ataxia – characterised by the onset of muscular spasms and problems with weakness, coordination,
balance and functioning of limbs.
Onset of Fatigue
Continence issues – including the lack of bladder control leading to either incontinence and/or

Pathogenesis Of Asthma
Asthma is a chronic disorder of the airways that is characterized by reversible airway obstruction,
cellular infiltration, and airway inflammation. The response involves the interplay of genetic and
environmental factors, as well as the activation of cells in the innate and adaptive immune systems.1
(Hall, S.C et al. 2016) The role of vitamin D in the pathogenesis of asthma has been the focus of
several researches over the last 2 decades. Results from these studies have identified a link between
vitamin D deficiency and poor outcome of lung function and symptoms in patients with asthma.7,
11 Yawn J et al. 2015& Bozzetto et al. 2012
Vitamin D is a pre–prohormone that can be obtained from 2 major sources, skin exposure to UVB
light as well as dietary intake from sources such as fish, fish oils, egg yolk, liver, and dietary
supplements.9, 10 Kerley et al. 2015 &Konstantinopoulou and Tapia 2016 ... Show more content on
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11, 12 Bozzetto et al. 2012 &Thacher and Clarke 2011
Vitamin D, through the activation of vitamin D receptor (VDR), has been shown to have an
immunomodulatory effect on a host of immune cells, including B and T lymphocytes, macrophages
(Mirzakhani, H et al. 2015),5, 6 dendritic cells (DCs),4 (Barragan et al. 2015) as well as structural
cells in the airways (Berraies, A et al.

Pathogenesis Of Depression
Depression is a common psychiatric disorder which has a long lasting effect on the mind as well as
the body and is the fastest growing cause that tends to decrease productivity, disability, work
absistence and high suicide rates among the individuals. Around one in ten patients usually treated
in primary health care settings encountered some forms of depression. It can reoccur, tends to be
chronic and can be worsen with increasing disability over time if not treated. In recent report 56
million Indians suffer from depression. In worldwide the prevalence of depression is increase 18%
from 2005 to 2015. Major depression is less common in older than younger adult which are living in
community. The pathogenesis of depression is depending on various

The Genetic Pathogenesis Of Migraine
Genetics has been shown to play a crucial role in the pathogenesis of migraine. The studies in the
field of migraine has advanced tremendously in the last two decades resulting in the development of
the existing knowledge about genetic inheritance of this debilitating disease. However, there is a
need to expand this knowledge in the areas of treatment. Approximately 70% of patients with
migraine reported to have a first–degree relative who is also suffering from migraine. The relatives
of migraine patients with aura has a four times increased risk of developing migraine (Medscape).
The studies conducted among the twins and families of migraine patients have shown that migraine
with aura (MA) and migraine without aura (MO) have a heritability ... Show more content on
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The hemiplegia associated with FHM typically resolves. It is also accompanied with cerebellar
ataxia that is related to the 19p locus. So far three genes are recognized as causing FHM. The type I
FHM is caused by mutations in theCACNA1A gene located on 19p13. FHM type 2 is linked to
mutations in the ATP1A2 gene and the type 3 is attributed to the mutations in the SCN1A gene.
Migraine is also associated with other inherited disorders such as mitochondrial myopathy,
encephalopathy, lactic acidosis, and stroke like episodes (MELAS) as well as cerebral autosomal
dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Migraine is
also a common clinical manifestation of various genetic vasculopathies such as retinal vasculopathy
with cerebral leukodystrophy (RVCL) and hereditary infantile hemiparesis, retinal arteriolar
tortuosity, and leukoencephalopathy (HIHRATL). These two vasculopathies are autosomal dominant
disorders. However the process by which these genetic vasculopathies causing migraine is still not

Mucormycosis And Pathogenesis Essay
Mucormycosis is an emergent and lethal infection caused by Mucoralean species. Using Mucor
circinelloides as a model of mucormycosis to identify new genetic determinants of virulence is the
aim of this work. First strategy parts from identification of genes differentially expressed during
pathogenesis, choosing zebra fish as an infection model (Fig. 1).
Figure 1. Transcriptomic analysis during infection with M. circinelloides virulent and avirulent
strains revealed several genes either induced (green) or repressed (red) during zebrafish infection, in
both avirulent and virulent strains.
The most induced gene during infection encodes a multicopper ferroxidase, which shares high
homology with Fet3 protein sequence from other fungi. This gene, named fet3a, could be involved
in the reductive iron uptake mechanism during infection as a virulence determinant. ... Show more
(A) Expression of fet3 genes in M. circinelloides in low iron conditions. Iron–depleted media were
obtained by adding Fetal Bovine Serum or 1,10–Phenanthroline to control media. (B) Densitometric
analysis of hybridization signals showed in (A).
Bioinformatic analysis revealed the presence of two fet3a homologs, fet3b and fet3c, in M.
circinelloides genome. Northern blot hybridization validated fet3a RNA–seq results, and showed an
upregulation of the three fet3 genes triggered by low iron availability (Fig. 3). These results imply
that fet3 genes are functionally redundant, suggesting that fet3b and fet3c are complementing fet3a
deletion during infection on the host Galleria

Thyroid Pathogenesis Lab Report
Thyroid Disorder27
Pathogenesis: both hyperthyroidism and hypothyroidism can lead to amenorrhea, though most
commonly it present as primary amenorrhea in patients with hypothyroidism. Low levels of thyroid
hormones, T3 and T4, stimulate the hypothalamus to produce thyrotropin–releasing hormone
(TRH), which stimulates both thyroid stimulating hormone (TSH) and prolactin production in the
anterior pituitary. High prolactin levels inhibit GnRH production in the hypothalamus, which is
needed for LH and FSH activation in the anterior pituitary. Without LH and FSH, ovarian follicles
cannot mature and menstruation does not occur.
Diagnosis: patients who present with signs and symptoms of hypothyroidism, such as low energy,
weight gain, cold intolerance, and amenorrhea, should be tested for the disorder with serum
measurements of TSH and free T4. High TSH and low free T4 levels suggest hypothyroidism.
Conversely, measurement of anti–thyroid antibodies may also be tested, such as anti–thyroglobulin,
anti–thyroid peroxidase, and anti–TSH receptor. Clinical suspicion should still be present when
patients do not have these characteristic hypothyroid symptoms, but present with primary
amenorrhea in the ... Show more content on Helpwriting.net ...
Imaging may show the presence of testes, karyotype analysis demonstrates a 46XY karyotype, and
serum testosterone concentrations in the normal adult male range. CAIS should also be suspected in
females with inguinal hernias or inguinal or labial masses as about 1–2% of these individuals may
have CAIS. Newborns with a female phenotype can also be diagnosed if prenatal karyotyping
identifies a 46,XY karyotype. In CAIS, testes may be located in the abdomen or inguinal region. If
the site and size of the testes cannot be elucidated by ultrasonography then MRI may be more

Pathogenesis Essay
Pathogenesis It is known that cancer, in general, is a group of diseases that is characterized by the
out–of–control growth and spread of a group of abnormal cells, which can often times result in
death. More specifically, breast cancer is a hormonally dependent disease, which causes malignancy
in the epithelial cells of the ducts and/or lobules of the breast (Lippman, 2012). Therefore, "women
without functioning ovaries, who never receive estrogen–replacement therapy, do not develop breast
cancer" (Lippman, 2012). Genomic profiling has furthered research and understanding of this
complex disease process by identifying further tumor subtypes and molecular alterations of the
disease. (Stopeck, 2009). Based upon the specific gene ... Show more content on Helpwriting.net ...
They tend to be less responsive to chemotherapy" (Lippman, 2012).
The second identified subtype is Luminal B. Luminal B tumor cells are epithelial in origin, have a
different gene expression pattern than that of Luminal A, and have a worse prognosis than Luminal
A (Lippman, 2012). The third subtype is known as normal breast–like subtype, which express genes
similar to that of normal breast epithelium and appears somewhat nonmalignant, with a prognosis
similar to that of Luminal B (Lippman, 2012).
The fourth subtype is known as HER2 amplified, which means that these have an increase in the
HER2 gene found on chromosome 17q and often have overexpression of genes that are adjacent to
the HER2 (Lippman, 2012). Before recent research and studies, the prognosis of a patient with such
subtype was quite poor however, with the recent advances in therapy designed to directly target
such, the clinical outcome for these patients is improving dramatically (Lippman, 2012).
Lastly is the basal type. These are typically called the "triple negative" type in that they are
estrogen–receptor, progesterone receptor, and HER2 negative tumors. They are characterized by
basal/myoepithelial cells and tend to be "high–grade, and express cytokeratins 5/6 and 17 as well as
vimentin, p63, CD10, and alpha–smooth muscle actin, and epidermal growth factor receptor
(EGFR)" (Lippman, 2012). Patients with BRCA mutations also fall within this molecular subtype.

Pathogenesis of Menstural Migraines Essay
A migraine is a common, chronic, and debilitating neurovascular disorder. It is characterized by
attacks of serve headache along with autonomic nervous system dysfunction and some patients an
aura neurological symptom (Goadsby, Lipton, & Ferrari, 2002). Migraine attacks start at any age but
they peak in the early to mid adolescence age. Migraines rates were observed for a year and the
results showed the prevalence of migraines being 11% overall, 6% among men and 15–18% in
women(Stewart WF, Lipton RB, Celentano DD, & Reed ML, 1992). Although prevalence of
migraine is similar in preadolescent boys and girls, when the onset of the menstrual cycle occurs, it
changes. After onset, migraine attacks are two to three times higher in girls ... Show more content on
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If there is menstrual association with migraines they are subdivided by a more menstrual cycle
related frequency.
Characteristics of menstrual migraines are usually that they are more resistant to treatment, not
associated with aura, of longer duration than other migraine types and have more functional
disability compared to migraine attacks other times of the month (Headache Classification
Subcommittee of the International Headache Society, 2004). The International Headache Society
characterizes menstrual migraines as ones that occur without aura but they may also occur with aura.
Migraine without Aura
These migraines last as long 4–72 hours. They are characterized by one–sided location, moderate to
severe pain strength, pulsating or provoked by routine physical activity. They are associated with at
least 2 of the following: nausea, vomiting, photophobia (sensitivity to light), phonophobia(fear of
loud sounds) or osmophobia(fear of odors) (Headache Classification Subcommittee of the
International Headache Society, 2004)
Catamenial Migraine
Migraines that have a temporal associate with menses are referred to as catamenial migraines and
can be either pure menstrual or menstrual related migraine. Precise diagnosis of catamenial migraine
can be known by using headache diary recoding of at least 3 months to determine if there is any
temporal associated between headache and menstruation cycle

Poliovirus Pathogenesis
Pathogenesis In 99% of poliovirus infections, alpha and beta interferons limit replication of the
poliovirus in nonneural tissues, which causes the infection to end (Racaniello, 2005). There are 1–
2% of poliovirus infections where the interferons do not work as well, and the virus spreads to
extraneural sites and then to the central nervous system causing poliomyelitis (Racaniello, 2005).
Infection with poliovirus causes the inhibition of host cap–dependent translation, DNA– dependent
RNA synthesis, cellular protein secretion of cytokines and antigen presentation, nuclear export, and
the suppression of the nuclear factor kappa–light–chain–enhancer of activated B cells (Racaniello,
2005). Paralysis of the legs due to an infection of ... Show more content on Helpwriting.net ...
Viral replication in the spinal cord is what leads to muscle paralysis and poliomyelitis (Racaniello,
2005). Old world monkeys and chimpanzees can be experimentally infected, and humans are the
natural hosts for poliovirus, because these species have suitable environments and receptors for the
survival of poliovirus, but other species such as mice do not have suitable environments for
poliovirus unless the mice have been experimentally altered to express CD155 (Racaniello, 2005).
Some strains of the poliovirus have been able to replicate in mice due to a process of adaptation, and
some strains of the virus are naturally virulent in the mice (Racaniello, 2005). Scientists were able to
substitute a six amino acid sequence of the P1/Mahoney strain, which is in the VP1 capsid protein
and located near the CD155 binding site, with the corresponding sequence in P2/Lansing strain
(Racaniello, 2005). This caused the mice to have neurovirulence to the poliovirus (Racaniello,
2005). In humans, they have taken samples of tonsillopharyngeal tissue, the wall of the ileum and
mesenteric lymph nodes and been able to isolate poliovirus from each of the samples, but even with
the removal of the tonsils and adenoids there continues to be a multiplication of the poliovirus in the
throat (Racaniello, 2005). CD155 RNA is produced in high levels in human epithelial cells, and
CD155 protein is

Pathogenesis, Prevalence, And Affected Individuals
SLE: Pathogenesis, prevalence, and affected individuals. In general, the term "lupus" is used to
describe a multi–systemic inflammation that results from an abnormal immunological function. It
includes four main types: neonatal and pediatric lupus erythematosus (NLE); discoid lupus
erythematosus (DLE); drug–induced lupus (DIL); and systemic lupus erythematosus (SLE). The
latter is the most common type, and it is referred to simply as "lupus". SLE is a complex rheumatic
disease of an autoimmune origin, with an unknown etiology and thus individuals at risk are unable
to prevent the disease's progression. Genetic, hormonal, environmental factors as well an
immunological abnormalities have been contributed to its pathogenesis. The most agreed upon
theory is that the diseases develop as a consequence of the formation and deposition of
autoantibodies and immune complexes in various organ systems, leading to eventual organ damage.
Studies focusing on SLE as a genetic diseases have shown that there is a genetic predisposition
within families. For example first–degree relatives of patients with SLE are significantly more likely
to have the disease compared to the rest of population (Maidhof & Hilas, 2012).Recent
technological advances have led to breakthroughs in the identification of susceptibility factors
involved in SLE, among which DNA methylation alterations has shown great potential. Incomplete
concordance for SLE has been found in homozygotic twins, suggesting that

A Research Study On Vitiligo Pathogenesis
4. Discussion
Vitiligo is an acquired depigmentation disorder of skin and hair. It is a cosmetically disfiguring
disease caused due to melanocytes destruction [Moretti et al., 2002], however, the pathogenesis of
such disease is still conflicting. Many previous studies tried to explain the pathogenesis according to
many points of view, they showed that it could either be an autoimmune mechanism, a neural
dysfunction, metabolic mechanism, or genetic causes [Moretti et al., 2002, Zhang et al,2005, Yazici
et al., 2006].
In this study, we decided to assess the genetic factor in vitiligo pathogenesis. Our study detected a
non–significant association between IFN–γ +874A/T or +2109A/G gene polymorphism and vitiligo
susceptibility. In line with our finding Dwivedi, et al,2013 couldn 't consider IFN– γ +874 T/A
polymorphism as a genetic risk factor for generalized vitiligo. Also, an Iranian study, couldn't
confirm a relation between IFN– γ +874 T/A gene polymorphism and vitiligo risk [Namian et al.,
2009].
When we studied the different haplotype frequencies of INF–γ (+874A/T) and INF–γ (+2109A/G)
polymorphisms in vitiligo patients and control distributions, we observed a significant elevation of
the haplotype TA in vitiligo patients when compared with control group (P < 0.03), this indicated
increased risk of vitiligo with this haplotype. To the best of our knowledge, no previous studies were
done to assess IFN–γ +2109A/G gene polymorphism in relation to vitiligo and no

Pathogenesis Of Lipodystrophy
Lipodystrophy is a disorder of fat metabolism that may be clinically evident as adipose tissue
accumulation (eg, in intraabdominal, dorsocervical, or breast tissues, and lipomas), lipoatrophy (loss
of fat mass, eg, of the face, limbs, buttocks), and metabolic abnormalities (eg, insulin resistance,
diabetes, dyslipidemia, hypertension, or lactic acidemia). The pathogenesis of lipodystrophy in
HIV–1–infected patients is multifactorial and includes effects of antiretroviral therapy, HIV–1 itself,
and genetics and other host factors. Evidence suggests that the nucleoside analogue, reverse
transcriptase inhibitors (nRTIs) stavudine, didanosine, and zidovudine may cause mitochondrial
toxicity by inhibiting mitochondrial DNA polymerase in fat and ... Show more content on
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By comparison, heterozygous patients with HFE187C/G had a 0.2–kg and 6.1% increase in limb fat,
with 6 (26%) of 23 patients having clinical lipoatrophy (P < .05 for all comparisons). Didanosine,
which is now used infrequently, has been clearly associated with the occurrence of clinical

The Pathogenesis Associated With Sle
Immune Mechanisms The pathogenesis associated with SLE is complex and attributed to various
factors. These factors include sex, the imbalance of hormones, and ones' hypothalamus, pituitary,
and adrenal axes. Others have said that it is attributed to the cells in your body that are dying, over
active help of the T cells in the body, defective B cells, and the shifting of the T helper 1(Th1) to T
helper 2 (Th2), which are responsible for the B cells causing them to produce these pathogenic
antibodies that cause SLE. (Cambridge, Teodorescu, et al. 2006.)
Roles of T cells and B cells The immune system is composed of many types of cells, such as T cells
and B cells, which are cells that defend your body from foreign substrates. When ... Show more
B–cells, in particular, play a major role in SLE as then hyperactivity, caused by such cytokines as
IL–10(discussed below) contribute to the pro inflammation of antibodies
IL– 10 gene In Systemic Lupus Erythematosus, expression of the IL– 10 gene located on
chromosome 1 (1q31–q32) is often inhibited. As the gene name implies, the gene encodes the
cytokine IL–10, which is produced by inflammatory cells, such as monocytes and macrophages.
(Yan, Bing, and Yi Liu. 2009). When this gene is inhibited the patient will show the signs of SLE,
which are discoid lesions, and neurological disorder. When these symptoms begin to appear one can
conclude that they have Systemic Lupus Erythematosus. The function of the IL– 10 gene is to
enhance B cell production and the in tissue leading to the production of autoantibodies. This gene
influences many other genes in the body which are associated with inflammation.
Programmed cell death (PDCD1)
Another gene with altered expression in SLE patients is the Programmed Cell death (PDC1), which
encodes for the PD–1 Protein. The PDCD1 over expression has been observed to be in ethnic
groups, such as Mexicans and certain European populations from Sweden. This polymorphism
affects the transcription factors which contribute to the non– tolerance and the hyperactivity of
lymphocyte is a major characteristic in SLE. Under normal expression Levels, the PD–1 protein
helps to regulate T–cell and B–cell

Pathogenesis of Coronary Heart Disease
Introduction Coronary heart disease is caused by the narrowing of the coronary arteries which is
because of the deposition of fats and cholesterol on the inside lining of the arteries. These deposits
which also cause hardening of the walls of the arteries also block the flow of oxygen to the heart.
This deprives the heart of the needed oxygen that is required for its proper functioning. Pathogenesis
of Coronary heart disease Studies have been conducted on the pathogenesis of the Coronary heart
disease and most of these studies have highlighted metabolism mechanism of fats. The studies have
revealed that as there is a need to feed special diets to the patients with Coronary heart disease; these
diets are to be designed in a way that the level of total blood lipid can be maintained within the
healthier limits (Vlodaver, 2012, p. 45). It has been observed that if the daily intake of fat in the
Coronary heart disease patients is limited to 50gm, than the maintenance of total bloody lipid levels
can be assured. Signs and Symptoms One of the most common symptoms in these cases includes
chest pain which is also referred to as angina. It is due to the lack of oxygen in the heart. The pain in
the chest can vary from one person to the other. The pain is generally observed under the breast
bone. It is seen that the pain is mainly triggered with increased motion and activity. In the case of
women, the symptoms can be fatigue, weakness and shortness of breath. Angina is the sign

Pathogenesis Of Arthrosclerosis
The pathogenesis of arthrosclerosis is a progressive disease of the vascular system, it starts while we
are young and progresses throughout our lives. The progression of arthrosclerosis, starts with an
injury to the endothelial lining of the arteries, from such diseases as, hypertension, high cholesterol,
diabetes and smoking. The damage to the endothelial cells causes dysfunction and the area with
endothelial cell inflammation draws leukocytes, cholesterol, vascular smooth muscle cells and other
debris, the buildup creates atherosclerotic plaque deposits in areas on an artery wall causing an
inflammatory process (Hoffman, 2007).
Over time the buildup of plaque on the artery walls produces hardening of the vessel walls and
blockages that slow the flow of blood throughout the body. Arthrosclerosis affects the heart,
peripheral arteries and the carotid and cerebral arteries that supply blood flow to the brain
(Arthrosclerosis, 2014). The effect on the body from arthrosclerosis causes other diseases to form,
peripheral vascular disease, coronary artery disease, hypertension, renal disease and stroke (Story,
2011). If the plaque buildup ruptures or breaks off, it forms a thrombus or blood clot that can cause a
stroke, heart attack or even death. ... Show more content on Helpwriting.net ...
Those over forty–years old have a fifty percent chance of developing arthrosclerosis and the chances
increase as we age. Ways to prevent arthrosclerosis or keeping it from worsening are to stop
smoking, eat a healthier diet, exercise and medications. Diabetics are at a higher risk for developing
arthrosclerosis because of the high levels of glucose in the blood that damages the vessel, which
creates inflammation and gives particles in the blood a place to stick and form plaque

Anthrax Pathogenesis
Anthrax is a deadly disease which can infect millions with the release of one biological weapon or
the melting of decades old permafrost. Anthrax disease is caused by the pathogen Bacillus
Anthracis, which is a bacteria that spreads through the way of spores. Unlike many infectious
diseases Anthrax does not spread from person to person, however, it can be spread widely through
the release and exposure to spores ("Anthrax – Communicable Disease Control and Prevention, San
Francisco Department of Public Health", 2016). The structure of the spores can be seen in figure
2("The pathogenesis of Bacillus anthracis – MicrobeWiki", 2016). If infected anthrax can be a life
threating disease. It most commonly appears in animals especially cows, pigs, ... Show more content
The world has seen many disastrous outbreaks of Anthrax in the past. By implementing preventive
procedures and providing medicine and antibiotics to people who have come into contact with
anthrax spores, outbreaks can be avoided in the future. Therefore, we are doing enough to control
this infectious disease and are preventing the disease from infecting people globally in the future
and ensuring that if people are infected in the future they will know how to accurately treat and
control this infectious disease. Overall society is prepared to help prevent alarming anthrax
outbreaks from occurring in the

The Pathogenesis Of Dnase
In addition to producing these enzymes and toxins, S. pyogenes can produce DNase's. DNase's are
enzymes that will breakdown our genetic material, also known as DNA.(1) If DNA is broken down,
the host cells will lose their ability to produce normal proteins. Each of the virulence factors above
allow the pathogen to harm it's host in one form or another or to subtly evade the hosts adaptive
immune defence. With the help of these virulence factors, the pathogen gains an upper hand and can
initiate an infection. Some of these virulence factors provide assistance in causing a smaller degree
infection and others can be responsible for causing life threatening diseases (1). Many of the
extracellular products S. pyogenes produces such as toxins however ... Show more content on
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pyogenes are not common if treated within an appropriate time period. Some common
complications that could arise however are cervical lymphadenitis, peritonsillar (retropharyngeal
abscess), sinusitis, otitis media, meningitis, bacteraemia, endocarditis and pneumonia. (7) Abscesses
are the accumulation of pus within an inflamed area. Otitis media is when parts of the middle ear are
inflamed causing problems with your auditory abilities. Meningitis is inflammation of the meninges
layer protecting the brain. Bacteraemia is the spread of bacteria within an individuals blood.
Endocarditis occurs when the endocardium layer of the heart is inflamed. (6) Most of these
complications arise when the pathogen spreads into deeper layers within our body through
lymphatic fluid or blood (7). An important complication that is usually caused by a erythrogenic
toxin. This toxin acts as a superantigens and can be present the first time someone encounters this
ifection. Symptoms of Scarlet fever are pink rash on the superficial layers of the skin, strawberry
tongue that is inflamed and a fever. Further complications following scarlet fever are
glomerulonephritis and rheumatic fever. Glomerulonephritis effects the kidneys and causes
inflammation. Rheumatic fever effects the heart and is not infectious. When an individual has
rheumatic fever, antibodies produced to the pathogenic antigen cross react with our own tissues,
specifically heart tissue. This

Carbon Monoxide Pathogenesis
Carbon monoxide, which is essentially produced through the enzymatic actions of heme oxygenase
(HO), appears to have as similar biochemical properties as NO. Activation of guanylyl cyclase
produces high levels of c GMP, and this was attributed to the actions of carbon monoxide. Carbon
monoxide acts as a physiological vasodilator in hepatic microcirculation. In contrast, up–regulated
inducible HO–1 mRNA expression was detected in the right ventricle in animal model of congestive
heart failure. Increased carbon monoxide levels are frequently found in cirrhotic patients.
Experimental evidence also suggests this substance may be implicated in CCM pathogenesis. This is
largely based on the finding of the elevated HO–1 mRNA and protein expression ... Show more
A hallmark in the pathogenesis is the pronounced splanchnic arterial vasodilatation and reduced
systemic vascular resistance (SVR) (Møller and, Henriksen, 2008). In this setting, cardiac pressures
are largely normal, at least in part, because the reduced after–load protects systolic function. This
circulatory state resembles certain high–output states resulting from increased blood volume and
defined as a hyperdynamic unloaded failure of the heart. The distinction is that the hyperdynamic
circulation in cirrhosis is due to the low SVR and increased arterial compliance (Timoh et al., 2011).
Administration of vasoconstrictors, such as angiotensin II and terlipressin, increases the SVR and
thereby the left ventricular afterload unmasking a latent left ventricular dysfunction in cirrhosis. On
the other hand, vasodilators, like angiotensin–converting enzyme inhibitors and other afterload–
reducing agents, should be used cautiously due to the risk of more aggravation of the vasodilatory
state (Krag et al., 2010). Diagnosis and

Pathogenesis Lab Report
The pathogenesis of AD Is not yet fully understood. (H.Break and E.Break,1991)
The neuropathological hallmarks of AD are the presence of plaques and neurofibrillary tangles. (18
–20)
There are two main hypotheses explaining the pathogenesis of AD:
Amyloid cascade hypothesis
The β–amyloid plaques are an extracellular deposition of amyloid beta protein[21]. This protein is
derived from cleavage of the amyloid precursor protein (APP) by the β – and γ– secretase enzymes
[22] .
The accumulated amyloid bet npeptides can aggregatr into oligomer (24) And form plaques (16)
The Aβ deposition and diffused plaque formation lead to local microglial activation, cytokine
release, reactive astrocytosis and a multi–protein inflammatory response (Eikelenboom ... Show
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the pathogenic mechanism of presenilin mutations which alters APP metabolism would be
responsible to elevate levels of Aβ peptides. (Bertram and Tanzi, 2008). followed by APOE, a major
genetic risk factor increase Aβ peptide aggregation and impair Aβ clearance in the brain for the
disorder in the typical late–onset period (Strittmatter and Roses, 1995). The genetic studies suggest
that neurodegenerative processes in AD are the consequences of an imbalance between Aβ peptide
production and clearance. However, physiological functions of APP are poorly understood (Yoshikai
et al., 1990; Ling et al., 2003; Muller and Zheng, 2012). The APP gene is located on chromosome 21
and those individuals suffer from Down's syndrome (trisomy 21) with an extra copy of this
chromosome develops an early–onset familial AD (EOFAD) (Yoshikai et al., 1990; Ling et al.,
2003). There are two proteolytic processing pathways of APP. In the non–amyloidogenic pathway,
APP cleaved by α and γ secretases resulted in the production of soluble form of APP (sAPPα). In
amyloidogenic pathway, APP cleaved by β–secretase generates membrane bound C–terminal
fragment (C99) which subsequently cleaved by γ secretase and produces Aβ peptide (Nunan and
Small, 2000; Selkoe and Schenk, 2003).
Tau hypothesis tau is an intracellular protein, necessary for the stabilization

Opioid Pathogenesis
Emerging evidence indicates that free radicals are involved in the pathogenesis of several digestive
system disorders as well as in the regulation of biological processes such as aging. Previous reports
have indicated that opioids induce apoptosis via stimulating an oxidative stress pathway that is
associated with the production of superoxide and nitric oxide (NO) [11]. NO, together with reactive
oxygen species (ROS), has a pivotal role in the regulation of apoptosis and necrosis in various cells.
Hsiao et al. investigated the role of NO and ROS in the morphine–induced apoptosis. They found
that the morphine treatment enhanced apoptosis through both NO and ROS pathways [12]. The
inducible nitric oxide synthase (iNOS) enzyme is one of the most important enzymes involved in the
generation of NO from the amino acid L–arginine. ... Show more content on Helpwriting.net ...
Moreover, the induction of mu–opioid receptor (MOR1) activity can effectively increase
NADH/NADPH–mediated ROS synthesis via activating the phospholipase D2 (PLD2) [14]. Then,
NADH/NADPH oxidase is a key downstream enzyme responsible for generating opioid–induced
ROS. The role of morphine in the regulating function of NADPH oxidase has been previously
demonstrated [15]. It has been shown that the morphine up–regulates the expression of heme
oxygenase (HO–1) which leads to an induced occurrence of macrophage apoptosis and reduced
macrophage migration [16]. Both ROS and MAPK signaling pathways are required for the full
induction of HO–1 activity [17]. Accordingly, the opioids may increase the expression of HO–1
through a ROS– and MAPK–dependent manner. The function of some other oxidative stress–related
enzymes including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx)
is decreased by opioids [18]. However, Dave et

Effects Of Hiv-1 Pathogenesis
In the absence of a cure for HIV Type 1 (HIV–1) pathogenesis, highly active antiretroviral therapy
(HAART) are designed to suppress viral replication and maintain it at low to undetectable levels
(Prabu–Jeyabalan et al, 2002). Due to their high intrinsic antiviral activity, the introduction of HIV–
1 protease inhibitors (PIs) have led to a dramatic reduction in morbidity and mortality rates of HIV–
1 infected patients (Codoner et al, 2017). HIV–1 protease inhibitors are peptidomimetics, or
substrate or transition state analogs that mimic natural peptides or proteins and retain the ability to
interact with the original protein's biological target, that competitively targets the hydrophobic P2–
P2' domain in the active site (Prabu–Jeyabalan et ... Show more content on Helpwriting.net ...
Proteolytic processing of the Gag polyprotein results mature HIV–1 structural proteins: p17 matrix
(MA), p24 capsid (CA), p7 nucleocapsid (NC), p6 domains, and two spacer peptides, SP1 and SP2.
Each of these HIV–1 structural proteins play a crucial role in the HIV–1 retroviral replication cycle.
MA is responsible for targeting Gag to the plasma membrane and promoting the incorporation of
viral envelop glycoproteins into the forming virions; CA drives Gag multimerization during
assembly to form the Gag lattice that encapsidates the viral RNA genome; NC recruits the viral
RNA genome into the virions; and the p6 domain recruits the endosomal sorting complex required
for transport (ESCRT) apparatus that catalyzes the membrane fission step responsible for the
budding off of new virions from the infected cell (Freed, 2015).
Due to the infidelity of HIV–1 reverse transcriptase, HIV–1 protease, as with all other HIV proteins,
undergoes frequent mutation (Prabu–Jeyabalan et al, 2002). Despite the high genetic barrier, or
sufficient number of critical drug–resistance mutations to overcome the anti–HIV activity of a drug
regimen, of PI, selective pressure induced by PIs have been seen to be associated with drug
resistance mutations at both the active site of HIV–1 protease and Gag polyprotein (Codoner et al,

OSA Pathogenesis Paper
Though overweight and an excess of regional adipose tissue are considered major risk factors for
OSA, there are also other interacting elements in OSA pathogenesis, such as craniofacial
abnormalities and an altered UA structure. The rationale of using image and speech analysis in OSA
assessment can be found on works such as Lee et al. [3, 4] and Davidson et al. [5], where the
evolutionary changes in physiological characteristics such as craniofacial morphology or acquisition
of speech are connected to the appearance of OSA from an anatomical basis.
First studies looked for abnormalities within craniofacial structures using techniques and processing
common in medical imaging such as cephalometry or computed tomography (CT). In [6] authors
applied sophisticated volumetric analysis on magnetic resonance imaging (MRI) of the ... Show
more content on Helpwriting.net ...
In [7], authors reported differences between control and OSA subjects in craniofacial structures
assessed by lateral cephalometry such as position of mandible (P < 0.05), mandibular plane angle (P
< 0.05), total face height (P < 0.01), upper face height (P < 0.05), and lower face height (P < 0.05).
In addition, they also reported differences in tongue (P < 0.001), soft palate (P < 0.001), and upper
airway (P < 0.01) size determined from computed tomography. In [8], authors studied oropharyngeal
soft tissues profile by means of cephalometric analysis to detect differences between control and
sleep apnea individuals. Significant differences were related to the length of the soft palate (P <
0.001), area of the soft palate (P < 0.001), and distance of close contact between the tongue and soft
palate (P < 0.001). These previous works rely on advanced imaging techniques, allowing a detailed
examination of bony and soft tissue structures. However, these procedures are generally cost–
expensive, time–consuming, and invasive for patients due to radiation exposure.

Pathogenesis of Cervical Cancer
CELL BIOLOGY ESSAY –– PATHOGENESIS OF CERVICAL CANCER
Introduction
According to the Centre for Health Protection of the Department of Health (2011), cervical cancer
becomes the tenth commonest cancer in Hong Kong in 2008. Cervical cancer usually arises from
sexual activity and human papillomavirus (HPV) (Bellentir, 2002). In this essay, Human
papillomavirus would be further discussed. For example, the signal transport pathway of HPV 16
and HPV 18, which many scientists believe that they are closely related of causing cervical cancer,
as well as the HPV vaccine and chemotherapy of cervical cancer, would be discussed.
HPV as the Main Cause of Cervical Cancer
Cervical cancer usually starts from the invasion of HPV to the epidermal ... Show more content on
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PD–ECGF, VEGF) and negative (e.g thrombospondin–1, platelet factor–4) regulatory molecules
(Wei, Kuo, Chen, Chou, Lai, Lee & Hsieh, 2003).
IL–6 Induce Angiogenesis and Tumor Growth
In the cervical cancer cell, VEGF and interleukin–6(IL–6) are commonly found. IL–6 is used to
stimulate the immune response at first. But some research reveals that IL–6 accelerates the tumor
growth and formation of micro vascular network of red blood cell. IL–6 is a kind of pro–
inflammatory cytokine which secreted by T–cells and macrophages. IL–6 would activate VEGF–
dependent angiogenesis process, thus blood vessel can be easily formed the cancer cell and enter
circulatory system through lymph node or capillary. It promotes the development of cervical tumor
through paracrine system or autocrine system. (Wei, Kuo & Chen et al.)
MMP–2 Activity of Degrading Collagen
According to Hardin, Bertoni and Kleinsmith (2011), when the growth factor binds to receptor
protein which located on cell surface, it triggers the complex signal pathway, causes the division of
endothelial cell and secretion of matrix metalloproteinase (MMPs). In the cervical cancer cell,
MMP–2 and MMP–9 play the important roles on tumor invasion and metastasis. MMP–2 acts as a
proteinase for degradation of collagen. Collagen is the main component of basal membrane and
extracellular matrix, which supporting cells structure from outside. For inhibiting the MMP–2
activity, tissue inhibitors of metalloproteinase (TIMPs) are

Pathogenesis Of Rheumatoid
Pathogenesis of rheumatoid arthritis The pathogenesis of RA remains somewhat unclear, which also
contributes to the underlying cause that initiates the process. However, strong clinical researches
associated RA to occurrence of inflammation, and on the role of autoantibodies and immune
complexes in initiation of the pathogenic process (73). Pathogenesis of RA begins with
inflammation of the synovium in small diarthrodial joints in the hands and feet, and in some joints
like elbows, wrists and knees. The initial inflammation leads to progressive bone and cartilage
damage and finally leads to destruction of joint function. In a healthy joint, a thin synovial
membrane containing two basic cell types (73). One of these cells is the synovial ... Show more
For example rheumatoid factor (RF), an antibody directed against the Fc portion of immunoglobulin
G (IgG) molecules. It presents in approximately two thirds of patients with RA (79). Although the
presence RF is used for diagnostic purposes, 10% of healthy individuals and many patients with
other autoimmune disorders, involving Sjogren,s syndrome, systemic lupus erythematous (SLE),
and mixed connective tissue disease, also express RF(80). In addition, about 70% of hepatic patients
with chronic hepatitis C virus are RF positive (81). The diagnostic protocol for RA has included
laboratory testing for RF for more than 50 years, but the presence of RF as a marker for RA in
patients is considered unreliable as it presents in the general population and in other autoimmune
and infectious diseases. However, decline in RF levels indicates regression in RA activity, as it is an
indicator of a given patient's response to treatment when various disease–modifying anti–rheumatic
drugs and other biologics, such as infliximab or rituximab, are administered

Pathogenesis Research Paper
Pathogenesis The intestinal tract is responsible for the secretion and reabsorption of fluids and
electrolytes, handling approximately 6,500 mL of fluid / day in an adult. Of this fluid only 2,000 mL
to 3,000 mL comes from fluid consumption. The remaining portion comes from a combination of
the foods we eat, gastric, pancreatic, biliary, and upper intestinal secretions. (Center for Disease
Control and Prevention, 2003) In acute gastroenteritis the re–absorptive capacity of the
gastrointestinal (GI) tract is overwhelmed, causing diarrhea and leading to dehydration if left
untreated. To prevent or correct dehydration it is important to replace the lost fluids. Due to the
overwhelmed GI tract water alone will not be absorbed and therefore

Nf1's Pathogenesis Essay
On the one hand, it is critically important to itemize and understand the inter– relationships of the
various elements of NF1 on their own. On the other hand, realizing how those elements relate to the
respective ages of the persons with each of the several NF disorders, may also contribute to their
individual health care and to the understanding of the disorder's pathogenesis in more general terms.
For example, virtually everyone with NF1 will manifest café–au–lait spots (CLS) in the first year of
life, while an NF2 vestibular schwannoma may not be obvious until the affected person's3rd decade
or later. And persons affected by Schwannomatosis may only develop problems that appear well
beyond childhood and are much more non–specific, such as pain without an otherwise apparent
cause. Reliance on clinical symptoms and signs is at least laudable, and, I would say, commendable.
Nonetheless, in at least some problem cases, resort to genetic analyses may be especially
contributory, specifically assessing mutations in or deletions (loss) of the NF1 locus on the long arm
of human chromosome 174 , the NF2 locus on the long arm of human ... Show more content on
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In addition, somatic mosaicism – especially when there are minimal or topographically limited signs
and symptoms – may be a factor in both diagnosis and prognosis, a consideration numerically most
important for NF2. And beyond mutational heterogeneity and mosaicism there is also the matter of
overlap with disorders utterly distinct from NF1, NF2 and Schwannomatosis. For example, for a
very young child with CLS as the sole or primary finding, identifying or discounting a mutation of
the SPRED1 locus on the long arm of human chromosome 15 may be very helpful for both the
child's parents and the concerned

Endometriosis Pathogenesis

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