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PubMed2005

Pathogenesis of prion diseases.

Prion diseases are rare neurological disorders that may be of genetic or infectious origin, but most frequently occur sporadically in humans. Their outcome is invariably fatal. As the responsible pathogen, prions have been implicated. Prions are considered to be infectious particles that represent mainly, if not solely, an abnormal, protease-resistant isoform of a cellular protein, the prion protein or PrP(C). As in other neurodegenerative diseases, aggregates of misfolded protein conformers are deposited in the CNS of affected individuals. Pathogenesis of prion diseases comprises mainly two equally important, albeit essentially distinct, topics: first, the mode, spread, and amplification of infectivity in acquired disease, designated as peripheral pathogenesis. In this field, significant advances have implicated an essential role of lymphoid tissues for peripheral prion replication, before a likely neural spread to the CNS. The second is the central pathogenesis, dealing, in addition to spread and replication of prions within the CNS, with the mechanisms of nerve cell damage and death. Although important roles for microglial neurotoxicity, oxidative stress, and complement activation have been identified, we are far from complete understanding, and therapeutic applications in prion diseases still need to be developed.

Animals↗

PubMed2002

Pathology, diagnosis and pathogenesis of AA amyloidosis.

Amyloid is defined as a proteinaceous tissue deposit that shows a typical green birefringence in polarised light after staining with Congo red, the presence of non-branching linear fibrils of indefinite length with an approximate diameter of 10-12 nm and a distinct X-ray diffraction pattern consistent with Pauling's model of a cross-beta fibril. Approximately 45% of generalised amyloidoses are secondary or reactive (AA) amyloidosis. Among the causes of AA amyloidosis are rheumatic diseases, idiopathic diseases, inherited diseases, infectious diseases and malignant tumours. Recent decades have provided significant advances in our understanding of the pathology and pathogenesis of AA amyloidosis. Its pathogenesis is multifactorial involving many variables such as primary structure of the precursor protein, acute phase response, the presence of non-fibril proteins (e.g. amyloid P component, apolipoprotein E, glycosaminoglycans, proteoglycans and basement membrane proteins), receptors, lipid metabolism and proteases. Study of the pathogenesis of AA amyloidosis has provided many insights into the nature of conformational diseases, which may help in the understanding of other members of this particularly heterogeneous group of diseases, such as Alzheimer's disease and transmissible spongiform encephalopathies.

Amyloidosis↗

PubMed1997

Pathogenesis of myasthenia gravis.

Various studies over the last 25 years in Man and animal models have revealed many steps in the pathogenesis of myasthenia gravis (MG) which is now considered the classical organ specific, autoantibody mediated and T cell dependent human autoimmune disease. Though not a disease entity, MG is associated with pathological alterations of the thymus in about 80% of cases. These are described here with reference to distinct models of autoimmunization against the acetylcholine receptor (AChR). In MG with thymitis, intrathymic production of AChR-specific autoantibodies is the result of a classical antigen-driven immune reaction that occurs completely inside the thymus and probably involves AChR on myoid cells as the triggering (myasthenogenic) antigen. Genetic factors contribute essentially to the pathogenesis of this form of MG. In thymoma-associated MG genetic factors are probably of marginal significance. Neither intratumour autoantibody production nor T cell activation seem to occur and the AChR is not the myasthenogenic antigen. Instead, abnormal neurofilaments that share epitopes with the AChR and other auto-antigen targets in paraneoplastic MG are expressed in thymomas and may trigger autoantigen-specific, non-tolerogenic T cell selection by molecular mimicry. These data support the hypothesis that initial steps in the pathogenesis of most MG cases take place within abnormal thymic microenvironments, be they inflammatory or neoplastic. Where these initial steps occur in MG cases without thymic pathology is not known. Likewise, the factors involved in the initial triggering of MG remain enigmatic in all MG subtypes.

Adolescent↗

PubMed2006

Pathogenesis of tendinous xanthoma: histopathological study of the extremities of Watanabe heritable hyperlipidemic rabbits.

BACKGROUND: Tendinous xanthomas associated with heritable hyperlipidemia are clinically well known. Nevertheless, there have been few basic investigations of the pathogenesis of these xanthomas. To clarify the pathogenesis of these xanthomas, we examined the localization and histopathological features of xanthomatous tissues in the extremities of Watanabe heritable hyperlipidemic (WHHL) rabbits. METHODS: Twenty-six WHHL rabbits at 1-31 months of age were dissected to observe the localization of xanthomas. In the histopathological study, tendons and ligaments that included xanthomatous tissues were sectioned and stained with hematoxylin and eosin, Masson's trichrome, and toluidine blue. Immunohistochemical staining was performed with RAM-11, a monoclonal antibody specific for rabbit macrophages, and CD31, a monoclonal antibody specific for endothelial cells. RESULTS: At necropsy examination, spontaneous development of xanthomas was observed in the plantar side of the plantaris tendon, the flexor retinaculum of the carpus, and around the digital flexor tendons of each joint level. Xanthoma formation was observed from 10 months of age and progressed with advancing age. The histomorphological study revealed that xanthomas had developed in superficial paratenon of the tendons that wrap around bony or fibrous pulleys. Many fibrocartilage cells were observed in the deep side of affected tendons. A large number of blood vessels were seen in the xanthomatous tissues of these WHHL rabbits. Immunohistochemical evaluation revealed that the xanthoma plaques contained endothelial cells and macrophages. CONCLUSIONS: It is likely that mechanical stress and extensive vascularization are essential factors for xanthoma formation. Moreover, endothelial cells and macrophages cells are principal contributors to the pathogenesis of tendinous xanthomas and to atherogenesis.

Animals↗

PubMed2003

Platelet-activating factor, a critical mediator in the pathogenesis of dextran sulfate sodium-induced colitis in rats.

PURPOSE: Disorder of mucosal immunity based on an imbalance between proinflammatory and anti-inflammatory cytokines is believed to be a major factor in the pathogenesis of ulcerative colitis. Platelet-activating factor potentially stimulates the production of proinflammatory cytokines and recruits inflammatory cells. The aim of this study was to determine whether and to what extent platelet-activating factor plays a role in the pathogenesis of ulcerative colitis. METHODS: Using dextran sulfate sodium-induced colitis in rats as a model of ulcerative colitis, we analyzed the composition of cellular infiltrates and the local tissue expression of messenger ribonucleic acid for cytokine-induced neutrophil chemoattractant and tumor necrosis factor-alpha. To directly assess the impact of platelet-activating factor on the development of colitis, we also determined the efficacy of a specific platelet-activating factor receptor antagonist for preventing dextran sulfate sodium-induced colitis. RESULTS: The activity of colitis was well correlated with the upregulation of cytokine-induced neutrophil chemoattractant and tumor necrosis factor-alpha messenger ribonucleic acid in local tissues and infiltration of cytokine-induced neutrophil chemoattractant-positive neutrophils and ED1-positive macrophages. The platelet-activating factor receptor antagonist effectively ameliorated colitis, along with causing a decrease in the tissue cytokine-induced neutrophil chemoattractant messenger ribonucleic acid level and a decline in neutrophil and macrophage infiltration. However, the antagonist did not alter tissue levels of tumor necrosis factor-alpha messenger ribonucleic acid. CONCLUSION: Platelet-activating factor plays a critical role in the pathogenesis of dextran sulfate sodium-induced colitis through recruitment of cytokine-induced neutrophil chemoattractant-positive neutrophils and macrophages and/or stimulation of cytokine-induced neutrophil chemoattractant release from activated neutrophils. The tissue level of tumor necrosis factor-alpha messenger ribonucleic acid does not closely reflect the activity of colitis.

Analysis of Variance↗

PubMed2005

Arcanobacterium pyogenes: molecular pathogenesis of an animal opportunist.

Arcanobacterium pyogenes is a commensal and an opportunistic pathogen of economically important livestock, causing diseases as diverse as mastitis, liver abscessation and pneumonia. This organism possesses a number of virulence factors that contribute to its pathogenic potential. A. pyogenes expresses a cholesterol-dependent cytolysin, pyolysin, which is a haemolysin and is cytolytic for immune cells, including macrophages. Expression of pyolysin is required for virulence and this molecule is the most promising vaccine candidate identified to date. A. pyogenes also possesses a number of adherence mechanisms, including two neuraminidases, the action of which are required for full adhesion to epithelial cells, and several extracellular matrix-binding proteins, including a collagen-binding protein, which may be required for adhesion to collagen-rich tissue. A. pyogenes also expresses fimbriae, which are similar to the type 2 fimbriae of Actinomyces naeslundii, and forms biofilms. However, the role of these factors in the pathogenesis of A. pyogenes infections remains to be elucidated. A. pyogenes also invades and survives within epithelial cells and can survive within J774A.1 macrophages for up to 72 h, suggesting an important role for A. pyogenes interaction with host cells during pathogenesis. The two component regulatory system, PloSR, up-regulates pyolysin expression and biofilm formation but down-regulates expression of proteases, suggesting that it may act as a global regulator of A. pyogenes virulence. A. pyogenes is a versatile pathogen, with an arsenal of virulence determinants. However, most aspects of the pathogenesis of infection caused by this important opportunistic pathogen remain poorly characterized.

Actinomycetaceae↗

PubMed2005

Isolation of virus from a SARS patient and genome-wide analysis of genetic mutations related to pathogenesis and epidemiology from 47 SARS-CoV isolates.

Severe acute respiratory syndrome (SARS) caused by SARS-associated coronavirus (SARS-CoV) is a fatal disease. Prevention of future outbreaks is essential and requires understanding pathogenesis and evolution of the virus. We have isolated a SARS-CoV in China and analyzed 47 SARS-CoV genomes with the aims to reveal the evolution trends of the virus and provide insights into understanding pathogenesis and SARS epidemic. Specimen from a SARS patient was inoculated into cell culture. The presence of SARS-CoV was determined by RT-PCR and confirmed by electron microscopy. Virus was isolated followed by the determination of its genome sequences, which were then analyzed by comparing with other 46 SARS-CoV genomes. Genetic mutations with potential implications to pathogenesis and the epidemic were characterized. This viral genome consists of 29,728 nucleotides with overall organization in agreement with that of published isolates. A total of 348 positions were mutated on 47 viral genomes. Among them 22 had mutations in more than three genomes. Hot spots of nucleotide variations and unique trends of mutations were identified on the viral genomes. Mutation rates were different from gene to gene and were correlated well with periodical or geographic characteristics of the epidemic.

Adolescent↗

PubMed2005

Pathogenesis and therapy for idiopathic dyspepsia.

Functional dyspepsia (FD) is one of the most common gastrointestinal disorders. This review summarizes recent progress in our understanding of the pathogenesis and therapy for FD. Although distinction among FD, irritable bowel syndrome, and reflux disease is difficult in population-based studies, separate entities can be recognized in patients who seek medical attention. The pathogenesis of FD remains unclear, but recent studies have demonstrated a role for acute gastrointestinal infection in triggering FD and in genetic polymorphisms of G-proteins in predisposing to FD. The role of abnormalities in gastric motor function, visceral hypersensitivity, and psychosocial factors in the pathophysiology of dyspeptic symptoms has been the topic of multiple studies. Treatment options for FD remain limited. Recent studies have focused on acid-suppressive drugs and on novel prokinetics. Progress in our understanding of the pathogenesis and pathophysiology of FD may lead to new or improved treatment modalities. Areas of major advances are the role of infection and genetic predisposition and studies on the role of abnormalities in gastric motility and sensitivity.

Dyspepsia↗

PubMed2000

The role of cytokines, chemokines, and adhesion molecules in the pathogenesis of idiopathic inflammatory myopathies.

Cytokines, chemokines, and adhesion molecules are important mediators in chronic inflammation and in immune regulation. In idiopathic inflammatory myopathies (IIM), increased expression of proinflammatory cytokines particularly interleukin (IL)-1alpha and IL-1beta, tumor necrosis factor (TNF)-alpha and macrophage inflammatory proteins (MIP)-1alpha, as well as of the inhibitory cytokines transforming growth factor (TGF)-beta was observed in muscle. There was no difference in cytokine and chemokine pattern between polymyositis, dermatomyositis, and inclusion body myositis, which could indicate that similar pathogenetic mechanisms are involved in these subsets of myositis. A prominent finding of IL-1alpha expression in endothelial cells, both in patients with active inflammation and in patients with chronic persisting muscle weakness without inflammation, makes this an interesting molecule in understanding the mechanisms for the pathogenesis of muscle weakness. Involvement of the blood vessels in the pathogenesis of myositis was further supported by increased expression of adhesion molecules and by a phenotypical expression of endothelial cells, resembling high endothelium venules in all three subsets of IIM. The molecular studies to date indicate a role of the microvessels in the pathogenesis of IIM not only in DM, as was previously suggested, but also in PM and IBM. The studies also indicate that IL-1alpha could be a target molecule for new therapeutical interventions.

Cell Adhesion Molecules↗

PubMed1979

The pathogenesis of hyperadrenergic postural hypotension in diabetic patients.

Patients with diabetes generally exhibit normal plasma catecholamine responses to standing. Some have blunted norepinephrine responses and postural hypotension-hypoadrenergic postural hypotension due to classic diabetic adrenergic neuropathy. Others, including some with postural hypotension, have exaggerated norepinephrine responses to standing. In order to clarify the pathogenesis of this hyperadrenergic state which occurs in a subset of diabetic patients, we studied aldosterone secretion, vascular and metabolic responsiveness to the administration of norepinephrine, and intravascular volumes in four diabetic patients who were selected for their exaggerated plasma norepinephrine responses to standing. Three of the four patients also exhibited (hyperadrenergic) postural hypotension. None of the hyperadrenergic diabetic patients had evidence of hypoaldosteronism or vascular resistance to norepinephrine, but all four patients had subnormal red blood cell masses and the mean (+/-SE) red blood cell mass (13.1 +/- 1.0 ml/kg) was approximately half of that of age- and sex-matched diabetic controls (26.5 +/- 2.7 ml/kg, p less than 0.01). Thus, intravascular volume contraction, specifically a reduction in the red blood cell mass, may play an important role in the pathogenesis of hyperadrenergic state observed in a subset of diabetic patients and in the pathogenesis of hyperadrenergic postural hypotension in affected diabetic patients.

Acetoacetates↗

PubMed1984

Host factors in the pathogenesis of urinary tract infections.

Classic animal studies conducted two decades ago provided the basic understanding of the pathogenesis of urinary tract infections. Those studies emphasized the natural resistance of the urinary tract to colonization and infection. Urinary obstruction, stasis, and reflux remain of great importance in all age groups in predisposing to infection. Recent studies of the crucial role of bacterial adherence to epithelial cells lining the genitourinary tract have shed new light on the pathogenesis of urinary infection. Information from adherence studies may have considerable clinical relevance with regard to the development of vaccines that prevent bacterial invasion particularly in the upper urinary tract. The normal defense mechanisms present in the human urinary tract are discussed. Despite progress in our understanding of the pathogenesis of urinary infection, considerable controversy still exists particularly with regard to host susceptibility to recurrent lower urinary tract infections in women with anatomically normal urinary tracts. Recent studies also have emphasized the significance of the host's normal immunologic mechanisms in contributing to intrinsic renal damage after upper urinary tract invasion by bacteria.

Adult↗

PubMed1991

Possible mechanism of the preventive effect of BCG against diabetes mellitus in NOD mouse. II. Suppression of pathogenesis by macrophage transfer from BCG-vaccinated mice.

Our previous reports showed that a single injection of live BCG, one of the biological response modifiers, prevents insulitis and overt diabetes in NOD mice and that the suppression could be due to the generation of some type of suppressor cells in the BCG-treated mice. Furthermore, a more recent study has revealed that macrophages suppressive against a variety of lymphocyte functions can be induced by BCG, which suggests that these macrophages are involved in the suppression of the pathogenesis. To obtain valid evidence for this speculation, the effects of transfer of macrophage and T-cell fractions on the pathogenesis were examined in the present study. Transfer of macrophage-enriched spleen cell fraction harvested from the BCG-treated females to young females abolished the occurrence of spontaneous diabetes up to the age of 25 to 30 weeks. Also, macrophage transfer prevented the progress of insulitis. In contrast, transfer of a T-cell-enriched fraction did not suppress insulitis and overt diabetes. From these results, it could be concluded that the suppression of the autoimmune pathogenesis of diabetes by BCG is due to the generation of suppressor macrophages.

Animals↗

PubMed1996

The pathogenesis of necrotic proliferative colitis in swine is linked to whipworm induced suppression of mucosal immunity to resident bacteria.

Mucohemorrhagic enteritis syndrome in swine has a complex etiology with largely unknown pathogenesis. We have observed that inoculation of pigs with swine whipworm, Trichuris suis, initiates an interaction with resident bacterial flora to induce mucohemorrhagic enteritis. The role of bacteria in this mixed infection was demonstrated using 4 treatment groups. One group of pigs was inoculated with 2500 embryonated T. suis eggs alone, while a second group received T. suis eggs along with broad spectrum antibiotic treatment. Two other control groups of pigs were uninoculated and were either treated with antibiotic or untreated. Pigs inoculated with T. suis eggs exhibited diarrhea, mucosal edema, inflammatory cell infiltration, bacterial accumulation at the site of worm attachment in the proximal colon, and intestinal adenomatosis associated with the intracellular Ileal symbiont intracellularis bacteria. In addition, enlarged lymphoglandular complexes (LGCs) containing numerous extracellular bacteria, eosinophils, lymphocytes, macrophages, and neutrophils were observed in the distal colon. The other group of pigs that was inoculated with T. suis but treated with antibiotics had lesions localized to the site of worm attachment and histologically normal LGCs with no invasive bacteria in the distal colon. The groups of uninoculated pigs, with or without antibiotic treatment, exhibited no pathology or bacterial invasion. It appears that the complex pathogenesis of necrotic proliferative colitis in pigs may be linked to worm induced suppression of mucosal immunity to resident bacteria. Further, the association between bacteria,lymphocytes and macrophages in the LGCs of pigs infected with T. suis suggests an antigen-processing role for these structures in the colon. Further, the complex pathogenesis of necrotic proliferative colitis in pigs may be linked to worm induced suppression of mucosal immunity to resident bacteria.

Animals↗

PubMed1987

Raised serum IgA to common cell envelope antigens supports enterobacterial inductive contribution to pathogenesis of secondary ankylosing spondylitis.

Ankylosing spondylitis (AS) is closely associated with the histocompatibility antigen HLA-B27. Pathogenesis of AS is thought to involve interactions between B27 and certain enterobacterial antigens. However, enterobacterial involvement is uncertain and contested by some. The present paper demonstrates raised serum IgA to a common enterobacterial heat modifiable major outer membrane protein (h-momp; Mr 35,000) in active AS (N = 25; IgA = 1485 +/- 20) compared with controls, who were hospital patients without known arthropathies or gastro-intestinal disease (N = 12; IgA = 548 +/- 59). Serum IgG and IgM did not differ statistically. Raised serum IgA to h-momp might indicate enterobacterial antigenic stimulation from the gastro-intestinal tract and thus support an inductive contribution of enterobacterial antigens to the pathogenesis of secondary AS. It does not necessarily imply direct involvement in the pathogenesis of primary AS. H-momp appears to be a convenient tool for serological studies of AS and at present is likely to be more suitable than other bacterial antigens.

Antigens, Bacterial↗

PubMed1991

Pathogenesis of various forms of double outlet right ventricle in mouse fetal trisomy 13.

The pathogenesis of double outlet right ventricle with or without pulmonary infundibular atresia in mouse fetal trisomy 13 was studied at the organ level using microdissection and scanning electron microscopy. Altogether, 394 karyotyped trisomic embryos were collected between 11 days and 16 hours of gestation (presence of a vaginal plug = day 1) and 15 days of gestation at intervals of 8 hours, and at 16 days of gestation. The hearts were perfusion-fixed, microdissected, and prepared to be observed in scanning electron microscope in the following standardized orientations: frontal, right or left profile, septal and parietal halves of the right ventricle and outflow tract (conotruncus). Comparison of 276 trisomic hearts with their normal counterparts described previously has shown that: the first pathognomonic feature is the abnormal anterior position of the proximal part of the parietal outflow tract ridge or of both ridges (at 12 days and 16 hours of gestation); the abnormal anterior fusion of these ridges ("coalescence") results in a mesenchymal mass behind which is deviated the pulmonary part of the outflow tract lumen; from 14 days and 16 hours of gestation on, this lumen is either obstructed, resulting in a supravalvar stenosis of the pulmonary trunk and subsequently evolving into double outlet right ventricle with pulmonary infundibular atresia; or, in a minority of cases, this lumen is not obstructed and the heart develops into double outlet right ventricle without pulmonary infundibular atresia. The pathogenesis of these malformations differs from most of the known hypotheses based on deductions from human malformed hearts, as well as from observations of the pathogenesis of similar outflow tract malformations, such as those found in the Keeshond dog or rats treated with trimethadione.

Animals↗

PubMed1989

Pathogenesis of scrapie in mice after intragastric infection.

Infection via the gastrointestinal tract is likely to be a natural route of scrapie infection in sheep. This paper describes the pathogenesis of the 139A strain of scrapie introduced intragastrically (i.g.) into CW mice. There was an almost immediate uptake of infectivity and onset of replication in Peyer's patches which preceded replication in spleen. Splenectomy had no effect on incubation period suggesting that, in contrast to the intraperitoneal route, the spleen plays little or no role in the pathogenesis of 139A scrapie administered intragastrically. Replication in the CNS was first detectable in the thoracic spinal cord and later in brain. The evidence is consistent with neural spread of infection from the gastrointestinal tract, via the enteric and sympathetic nervous systems to spinal cord. Neuroinvasion may be initiated either via infection of Peyer's patches or directly by infection of nerve endings in the gut wall. The latter possibility means that pathogenesis may be completely independent of the lymphoreticular system.

Animals↗

PubMedDate not supplied

Pathogenesis of viral infections: the role of the immune response.

The replication and spread of viral infections in the human host occurs by a variety of mechanisms. Replication of genetic sequences varies with the initial starting material (DNA or RNA). Proliferation in the host may be by direct cell-to-cell spread, cell lysis, or budding from the infected cell's membrane. Various viremic or localized stages have been demonstrated. Particular tropisms are thought to be due to the presence of particular receptors. Recent advances in molecular biology, which will be reviewed, have expanded our capacity to detect the genetic footprints of viruses, and our understanding of viral pathogenesis. The host immune system must be prepared for an array of mechanisms to prevent or ameliorate virus infection. These may take the form of specific and nonspecific antibody formation, or the generation of specific cytotoxic lymphocytes that are restricted by the HLA system. In addition, nonspecific mediators, such as the complement system, interferon, and other lymphokines, play a significant role in the pathogenesis of viral infections. While the greatest portion of these cellular efforts are aimed at the destruction or elimination of viral infection, the immune response may augment the pathogenic effect under some circumstances. The formation of immune complexes may also contribute to the pathogenesis of some infections.

Antibody Formation↗

PubMed1995

Bioenergetics in the pathogenesis, progression and treatment of cardiovascular disorders.

The aim of this manuscript is to review perturbations in bioenergetics that are redundant denominators in the diversity of factors mediating the pathogenesis and progression of coronary heart disease (CHD), congestive heart failure (CHF), hypertension and arrhythmias. This paper likewise assesses the pharmacodynamics of widely prescribed drugs that enhance cellular respiration, maintain positive inotropic, chronotropic, dromotropic cardiac effects, sustain myocardial biosynthesis, reverse the morbidity of heart disease, and assure low levels of toxicity commensurate with the agent's biocompatability. Conversely, it is essential to delineate the modality of xenobiotic drugs that inhibit energy transformations, enhance the pathogenesis of CHD, worsen survival in CHF, provoke arrhythmogenic effects, and induce serious side-effects. Documented evidence, derived from biochemical, physiological and pharmacological data sources, consistently links inhibited mitochondrial decarboxylation to aberrations in cholesterol metabolism, biosynthesis, and calcium balance. Underutilized citrates evolved from inhibited decarboxylation are degraded to acetyl CoA. The acetate is the source of steroid synthesis; its carbon atoms form the molecular basis for all endogenous cholesterol. Myocardial anoxia, a consequence of the atheromatous plaque, inhibits ATP production, impairs biosynthesis, induces negative cardiac inotropic and chronotropic effects, and enhances the pathogenesis of CHF. Inhibited decarboxylation is likewise a factor in the mobilization of in situ cardiac Ca2+, resulting in arrhythmias provoked by the cation's deficiency. The restoration of calcium homeostasis decreases peripheral vasotension, reducing hypertension. Parameters drawn from endocrinopathies and the new physiological dimension of microgravity are developed to illustrate the detrimental effect of inhibited bioenergetics on cardiac pathomorphism and cardiovascular dysfunction. In conclusion, anabolic agents, adjunctive to a productive life-style, can provide the rational basis for the prevention and treatment of cardiac diseases. Failure to understand mechanisms generating cardiovascular morbidity eventuates in ineffective and empirical treatment.

Acetyl Coenzyme A↗