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Local intracoronary infusions of bradykinin profoundly reduce the severity of ischaemia-induced
arrhythmias in anaesthetized dogs. Bradykinin protects the rabbit heart after cardioplegic ischemia
via NO-dependent pathways. Bradykinin enhances insulin receptor tyrosine kinase in 32D cells
reconstituted with bradykinin and insulin signaling pathways. Campbell DJ, Anastasopoulos F,
Duncan AM, James GM, Kladis A, Briscoe TA. Pittis M, Zhang X, Loke KE, Mital S, Kaley G,
Hintze TH. The identity of the EDHF is not clearly defined and the term may represent a category
of various compounds with the common denominator that they all cause hyperpolarization of
vascular SMCs, thereby inducing blood vessel dilation. Calcium signaling in endothelial cells
involves activation of tyrosine kinases and leads to activation of mitogen-activated protein kinases.
Arcaro G, Solini A, Monauni T, Cretti A, Brunato B, Lechi A, Fellin R, Caputo M, Cocco C, Bonora
E, Muggeo M, Bonadonna RC. In a mouse model, knocking out G?i2, one of the two major G. Varin
R, Mulder P, Tamion F, Richard V, Henry JP, Lallemand F, Lerebours G, Thuillez C. Purification of
bradykinin by ion exchange chromatography. Role of bradykinin in insulin sensitivity and blood
pressure regulation during hyperinsulinemia. The current treatment is also aimed at treating the
condition of the patient. Autoradiographic visualization of B1 bradykinin receptors in porcine
vascular tissues in the presence or absence of inflammation. BNP inhibits renin and aldosterone
release and, therefore. It is however important to note that drug interaction of metoprolol with
digoxin and calcium channel blockers would result in excessive reduction of blood pressure. Agonist-
specific alterations in receptor-phospholipase coupling following inactivation of Gi2alpha gene.
Exercise-induced increase in glandular kallikrein activity in human plasma and its significance in
peripheral glucose metabolism. Species variation in pulmonary endothelial aminopeptidase P activity.
Inducible expression of the kinin B1 receptor in the endotoxemic heart: mechanisms of des-
Arg9bradykinin-induced coronary vasodilation. Insulin enhances the bradykinin response in L8 rat
skeletal myoblasts. Campbell WB, Harder DR. Endothelium-derived hyperpolarizing factors and
vascular cytochrome P450 metabolites of arachidonic acid in the regulation of tone. The effects of
kinins on myocardial physiology during ischemia and reperfusion The positive effects of kinins on
recovery from MI were found by infusing BK into animals with MI. Incidence of heart failure in
eastern Finland: a population-based surveillance study. The inclusion criteria were age- 55 years or
more, about to be discharged home, Congestive Heart Failure with left ventricular ejection fraction
less than 55% and New York Heart Association Class 2, 3 or 4 and at least one previous admission
for acute heart failure. While the classical PC lasts 2 to 3 hours after the stimulus and protects against
infarction but not against stunning, late PC lasts 3 to 4 days and protects against both infarction and
stunning. Angiotensin-converting enzyme inhibition modifies angiotensin but not kinin peptide levels
in human atrial tissue. Data were analysed in several ways to comply with the objectives of this
thesis. Mitral valve replacement in ischemic mitral regurgitation. Amann K, Gassmann P, Buzello M,
Orth SR, Tornig J, Gross ML, Magener A, Mall G, Ritz E.
Inducible expression of the kinin B1 receptor in the endotoxemic heart: mechanisms of des-
Arg9bradykinin-induced coronary vasodilation. The present results, showing a differential
expression of BK-2R in normal and failing hearts, are the first to suggest that BK-2Rs may be
involved in the pathogenesis of human HF. Alterations in diastolic function in response to
progressive left ventricular hypertrophy. Dendorfer A, Wolfrum S, Wagemann M, Qadri F, Dominiak
P. GERIATRIC PHARMACOLOGY Geriatric pharmacology is a specialized field focusing. Its
activity is highest in the epithelial cells of kidneys (Gafford et al., 1983). NEP activity has also been
found in the cardiovascular system; particularly on the plasma membranes of cultured rat CMCs
(Piedimonte et al., 1994). In parallel with our report several others have appeared showing NEPi-
induced cardioprotection through the kinin system. Kinins, receptors, kininases and inhibitors--where
did they lead us. Importantly, the effect can be reproduced pharmacologically with clinically relevant
agents, such as NO donors, adenosine receptor agonists and opioid agonists, enabling
pharmacological exploitations (Bolli et al., 1998 and 2000). The first study linking BK to late PC
was that by Kim et al. (1997), showing that a 10-minute PC in chronically instrumented dogs
induced an increase in the response to acetylcholine and BK after 6 hours, reaching a maximal
response at 1-2 days. When someone has a heart attack the cause of the heart attack cannot always
be determined. Jeserich M, Pape L, Just H, Hornig B, Kupfer M, Munzel T, Lohmann A, Olschewski
M, Drexler H. Proc Assoc Am Physicians 111: 417-22. 1999. Sanchez R, Gimenez MI, Ramos F,
Baglivo H, Ramirez AJ. Ceramide reduces endothelium-dependent vasodilation by increasing
superoxide production in small bovine coronary arteries. Wollert KC, Studer R, Doerfer K, Schieffer
E, Holubarsch C, Just H, Drexler H. Alternatively, the dosage of the captopril would be used as the
doctor finds appropriate. MAP-kinase dependent activation of kinin B1 receptor gene transcription
after heat stress in rat vascular smooth muscle cells. Additionally, a cohort of 8399 patients with
chronic symptomatic heart failure with reduced ejection fraction from PARADIGM-HF was
examined. As a result of the BK-2R-initiated phosphorylation steps, STAT3 is translocated to the cell
nucleus (Ju et al., 2000). NF-?B activation BK-2Rs are also known to activate the nuclear factor-?B
(NF-?B) pathway. The ageing spontaneously hypertensive rat as a model of the transition from
stable compensated hypertrophy to heart failure. My father has had two heart attacks in his lifetime.
Rifo J, Pourrat M, Vavrek RJ, Stewart JM, Huidobro-Toro JP. The results of studies on the
enzymatic degradation of BK in human plasma or serum have been controversial. Chronic
bradykinin infusion and receptor blockade in angiotensin II hypertension in rats. These blockages are
usually cause by atherosclerosis. Only then it is possible to find use of their potential as
cardioprotective effector molecules. Page 72. Bradykinin blocks angiotensin II-induced hypertrophy
in the presence of endothelial cells. Location of the disulfide bonds in human plasma prekallikrein:
the presence of four novel apple domains in the amino-terminal portion of the molecule. Role of
carboxypeptidase, angiotensin-converting enzyme and determination of final degradation products.
There are various symptoms of Congestive Heart Failure, but the common ones are tiredness,
reduced exercise capacity, shortness of breath and swelling. Moreover, other major organs such as
the kidney and liver may be permanently injured before the patient has cardiac transplantation. Late
PC requires activation of multiple stress-response genes and a complex intracellular signaling
cascade, including PKC, Src protein tyrosine kinases, NF-?B, ending in an increase in, for example
inducible nitric oxide synthase (iNOS), COX-2, and aldose reductase.
Miki T, Miura T, Ura N, Ogawa T, Suzuki K, Shimamoto K, Iimura O. In the short term, these
compensatory mechanisms protect the heart by balancing the cardiac output with the demands.
Immunoaffinity purification and activation to alpha- and beta-kallikrein. Nitric oxide mediates
protein kinase C isoform translocation in rat heart during postischemic reperfusion. In the circulation,
stimulation of BK-1R has been shown to cause vasodilatation. My grandfather passed away after
having a heart attack as well. Jorma taught me the basics of science and gave only clear lessons on
many different aspects of science and medicine. As the pressure in the pulmonary artery increases,
gradually it results in right-sided failure which is characterized by increased JVP (Jugular Venous
Pulse); hepatomegaly, pedal edema, etc. Menke JG, Borkowski JA, Bierilo KK, MacNeil T, Derrick
AW, Schneck KA, Ransom RW, Strader CD, Linemeyer DL, Hess JF. The illness in my family that I
feel poses the greatest threat to me is heart disease. Moore AF, Heiderstadt NT, Huang E, Howell
NL, Wang ZQ, Siragy HM, Carey RM. Ito H, Hirata Y, Hiroe M, Tsujino M, Adachi S, Takamoto T,
Nitta M, Taniguchi K, Marumo F. Regular taking of patient vitals and blood pressure measurement.
Agonist stimulation of B1 and B2 kinin receptors causes activation of the MAP kinase signaling
pathway, resulting in the translocation of AP-1 in HEK 293 cells. Stimulation of bradykinin B(1)
receptors induces vasodilation in conductance and resistance coronary vessels in conscious dogs:
comparison with B(2) receptor stimulation. Blais C Jr, Lapointe N, Rouleau JL, Clement R, Gervais
N, Geadah D, Adam A. Improvement of bradykinin endothelium-mediated vasodilation of forearm
resistance circulation by quinaprilat in patients with coronary artery disease with or without left
ventricular dysfunction. Costenbader K, Ardaillou N, Marchetti J, Placier S, Ardaillou R. Chronic
effects of early started angiotensin converting enzyme inhibition and angiotensin AT1-receptor
subtype blockade in rats with myocardial infarction: role of bradykinin. Acetylcholine, bradykinin,
opioids, and phenylephrine, but not adenosine, trigger preconditioning by generating free radicals
and opening mitochondrial K(ATP) channels. This initial event may be induced by an acute incident,
such as myocardial infarction (MI) myocarditis, or by a chronic disease, such as hypertension,
diabetes, or VHD. Jeserich M, Pape L, Just H, Hornig B, Kupfer M, Munzel T, Lohmann A,
Olschewski M, Drexler H. Although some doctors may not bring up issues concerning lifestyle with.
Am J Physiol Heart Circ Physiol 278: H507-14, 2000. Nitric oxide attenuates cardiac myocyte
contraction. Harris MB, Ju H, Venema VJ, Liang H, Zou R, Michell BJ, Chen ZP, Kemp BE,
Venema RC. FXII levels, FXIIa-like activities and kallikrein activities in normal subjects and
patients undergoing cardiac surgery. Role of endothelium-derived nitric oxide in the modulation of
canine myocardial mitochondrial respiration in vitro. Editors: Braunwald E, Zipes DP, Libby P. W.B.
Saunders company, Philadelphia, Pennsylvania, United States of America: 1114-219, 2001. Antonio
A. The relaxing effect of bradykinin on intestinal smooth muscle. Harvey TJ, Hooper JD, Myers SA,
Stephenson SA, Ashworth LK, Clements JA.
Congestive Heart Failure: Current Research and Clinical. Reduced gene expression of vascular
endothelial NO synthase and cyclooxygenase-1 in heart failure. Selective inhibition of the renal
angiotensin type 2 receptor increases blood pressure in conscious rats. Interestingly, as a result of the
aggressive treatment of hypertension, the relative importance of these etiologies changed
dramatically between the 1950s and the 1980s. Genomic DNA sequence, expression, and
chromosomal localization of the human B1 bradykinin receptor gene BDKRB1. Dietary
recommendation for the patient’s congestive heart failure includes a reduction in the amount of
sodium in the diet. Douillet CD, Velarde V, Christopher JT, Mayfield RK, Trojanowska ME, Jaffa
AA. Effect of low-dose bradykinin on glucose metabolism and nitrogen balance in surgical patients.
Newer aspects of kinin research. I. Potentiation and blockade of the biological action of kinins.
Glucocorticoids inhibit the bradykinin B2 receptor increase induced by interleukin-1beta in human
bronchial smooth muscle cells. Role of bradykinin in insulin sensitivity and blood pressure regulation
during hyperinsulinemia. Molecular and pharmacological evidence for modulation of kinin B(1)
receptor expression by endogenous glucocorticoids hormones in rats. Racial differences in response
to therapy for heart failure. These seemingly discrepant findings may be explained as follows: PKLK
acts locally at the luminal surface of the endothelium and therefore the highest concentration of BK
produced by pKLK is that by the endothelial surface inside the vessel (also the location of the BK-
2R). The results clearly support a role for BK-2Rs in the pathogenesis of HF. Page 73. Phagoo SB,
Yaqoob M, Herrera-Martinez E, McIntyre P, Jones C, Burgess GM. Meini S, Lecci A, Cucchi P,
Catalioto RM, Criscuoli M, Maggi CA. Its induction is at least partly a result of activation of all the
previous signaling cascades. Regulation of nitric oxide production in human coronary microvessels
and the contribution of local kinin formation. Am J Physiol Heart Circ Physiol 279: H2829-37,
2000. Similar results have previously been shown for the other mediator of BK-2R, the
prostaglandins, i.e. that prostaglandins can substitute NO for BK-2R-induced vasodilatation in the
coronary circulation (Puybasset et al., 1996). Page 29. Differences in the properties and enzymatic
specificities of the two active sites of angiotensin I-converting enzyme (Kininase II). Role of
calcitonin gene-related peptide and kinins in post-ischemic intestinal reperfusion. Cardioprotective
effects by ramipril after ischemia and reperfusion in animal experiment studies. The effects of kinins
on myocardial physiology during ischemia and reperfusion The positive effects of kinins on recovery
from MI were found by infusing BK into animals with MI. Am J Physiol Heart Circ Physiol 281:
H1648-56, 2001. ACE activity in cardiac membranes can be measured specifically with
furanacryloyl-Phe-Gly-Gly (FAPGG) as substrate (Kokkonen et al., 1997). As shown in table 4 (I)
the cardiac ACE activities of patients receiving ACEis were not lower than those of patients not
receiving ACEis or those of normal subjects. Some side effects are appetite loss, diarrhea, low
energy, headaches, nausea and vomiting, vision trouble, and weakened muscles (Understanding
Congestive Heart Failure, 1995). Hosoya K, Takeda K, Nishikimi T, Ishimitsu T, Matsuoka H.
Moreover the half life of BK is very short (10-15 seconds in the plasma alone) and, because the
myocardial demand for oxygen is so great, the blood passes through the myocardial vessels quickly.
Newer aspects of kinin research. I. Potentiation and blockade of the biological action of kinins.
PLA2 phosphorylation and cyclooxygenase-2 induction, through p38 MAP kinase pathway, is
involved in the IL-1beta-induced bradykinin B2 receptor gene transcription. Collagen remodeling of
the pressure-overloaded, hypertrophied nonhuman primate myocardium. Dual natriuretic peptide
system in experimental heart failure. Shiota N, Fukamizu A, Okunishi H, Takai S, Murakami K,
Miyazaki M. Experiments performed in 1) kininogen-deficient Brown-Norway-Katholiek rats
(BNK), 2) rats inbred for low KLK excretion, 3) BK-2R-KO mice, 4) Dahl salt-resistant rats with
BK-2R blockade and 5) normal rats treated with anti-KLK antibody consistently showed that a salt
challenge, on top of an impaired KKK system, makes these animals hypertensive. If the patient has
abnormal heartbeats then they may need electric shocks in an attempt to fix these (G, 57-62).
Stimulation of phosphatidylinositol hydrolysis, protein kinase C translocation, and mitogen-activated
protein kinase activity by bradykinin in rat ventricular myocytes: dissociation from the hypertrophic
response. Cardiac interstitial bradykinin release during ischemia is enhanced by ischemic
preconditioning. Paolocci N, Pagliaro P, Isoda T, Saavedra FW, Kass DA. Rocha e Silva M.
Bradykinin, occurrence and properties. Urinary and renal tissue kallikrein in the streptozocin-diabetic
rat. Cardiovascular abnormalities with normal blood pressure in tissue kallikrein-deficient mice. In a
similar experiment, insulin dose-dependently corrected both prokallikrein and kininogen levels in
STZ rats. References Berger, A. (2009). Heart Failure. Medline Plus Medical Encyclopedia. Role of
the Rho GTPase in bradykinin-stimulated nuclear factor-kappaB activation and IL-1beta gene
expression in cultured human epithelial cells. Barabe J, Marceau F, Theriault B, Drouin JN, Regoli D.
Dietary recommendation for the patient’s congestive heart failure includes a reduction in the amount
of sodium in the diet. Coronary angiography is “an invasive test that evaluates the heart arteries
under x-ray” (C, 29). Chao J, Chao L. Experimental kallikrein gene therapy in hypertension,
cardiovascular and renal diseases. Calcium signaling in endothelial cells involves activation of
tyrosine kinases and leads to activation of mitogen-activated protein kinases. Several treatments have
been effective in reducing some or all of these, however, each approach has possible side effects,
hence, cautious observation is necessary to capitalize on benefits and lessen unpleasant consequences
(Management of Chronic Heart Failure, 2007). High molecular weight kininogen regulates
prekallikrein assembly and activation on endothelial cells: a novel mechanism for contact activation.
Haring HU, Tippmer S, Kellerer M, Mosthaf L, Kroder G, Bossenmaier B, Berti L. These seemingly
discrepant findings may be explained as follows: PKLK acts locally at the luminal surface of the
endothelium and therefore the highest concentration of BK produced by pKLK is that by the
endothelial surface inside the vessel (also the location of the BK-2R). Requirement of
phosphatidylinositol 3-kinase activity for bradykinin stimulation of NF-kappaB activation in cultured
human epithelial cells. Bradykinin directly triggers GLUT4 translocation via an insulin-independent
pathway. Ischemic preconditioning in pigs: a graded phenomenon: its relation to adenosine and
bradykinin. Effects of bradykinin on prostaglandin I2 synthesis in human vascular endothelial cells.
Neutral endopeptidase inhibition prevents isoproterenol-induced myocardial hypoperfusion in rats by
reducing bradykinin degradation.
Diabetes is the leading cause of kidney failure among the United States population. A cohort of 3830
men and women with LVEF (left ventricular ejection fraction) ?35% who participated in the
Controlled Rosuvastatin Multinational Trial in Heart Failure (CORONA) was examined. Opposing
effects of a ras oncogene on growth factor-stimulated phosphoinositide hydrolysis: desensitization to
platelet-derived growth factor and enhanced sensitivity to bradykinin. Malmsjo M, Bergdahl A,
Zhao XH, Sun XY, Hedner T, Edvinsson L, Erlinge D. Am J Physiol Heart Circ Physiol 281:
H1778-83, 2001. Bradykinin accounts for improved postischemic function and decreased
glutathione release of guinea pig heart treated with the angiotensin-converting enzyme inhibitor
ramiprilat. The results show that at this concentration NEP was still the major BK-degrading
enzyme, ACE playing a minor role (data not shown). Late treatment with ramipril increases survival
in old spontaneously hypertensive rats. The first page of the PDF of this article appears above.
Contribution of bradykinin receptor dysfunction to abnormal coronary vasomotion in humans.
Bradykinin-induced preconditioning in patients undergoing coronary angioplasty. Multiple tests must
be done before heart disease can be diagnosed. The growth-regulatory effect of BK on myocardial
cells BK induces different growth-regulating effects in myocardial cells. Blockade of bradykinin B2
receptors prevents the increase in capillary density induced by chronic angiotensin-converting
enzyme inhibitor treatment in stroke-prone spontaneously hypertensive rats. Mechanisms by which
bradykinin promotes fibrosis in vascular smooth muscle cells: role of TGF-beta and MAPK. He did
not speak of any symptoms and had a sudden deadly heart attack. The patients were all under
chronic ACEi therapy, which, in the in vitro assays, may have inhibited the ACE activity in the
cardiac membranes derived from their hearts. Identification of pre- and postsynaptic bradykinin
receptor sites in the vas deferens: evidence for different structural prerequisites. Effects of B1 and B2
kinin receptor antagonists in diabetic mice. The only two mechanisms possibly targeted so far by
medical therapies are the ACEi-induced resensitization of BK-2R and estrogen-induced BK-2R
upregulation. Most importantly, the increase in intracellular calcium results in activation of
endothelial nitric oxide synthase (eNOS). Thus, down-regulation of BK-2R expression in failing
human hearts, as shown in this study, may reflect a maladaptive response in the pathogenesis of HF.
Linz W, Wohlfart P, Scholkens BA, Becker RH, Malinski T, Wiemer G. Long-term effectiveness of
cardiac resynchronization therapy in heart. ACE inhibitors promote nitric oxide accumulation to
modulate myocardial oxygen consumption. Tornel J, Madrid MI, Garcia-Salom M, Wirth KJ, Fenoy
FJ. Rizzoni D, Porteri E, Guelfi D, Muiesan ML, Valentini U, Cimino A, Girelli A, Rodella L,
Bianchi R, Sleiman I, Rosei EA. Ikonomidis JS, Shirai T, Weisel RD, Derylo B, Rao V, Whiteside
CI, Mickle DA, Li RK. The rats were cannulated with PE-50 catheters inserted into the right femoral
and the right carotid arteries for measurement of blood pressures below and above the aortic
banding. Low-salt diet downregulates plasma but not tissue kallikrein-kinin system.