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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↗
PubMed1987

Recent views on the pathogenesis of gastro-oesophageal reflux disease.

The pathogenesis of GORD depends on a mix of factors which vary amongst individual patients. The central issue in the pathogenesis of gastro-oesophageal reflux is understanding of the mechanisms that lead to reflux, since the effects of all other factors depend on this event. Consequently, new information and views about the mechanisms of gastro-oesophageal reflux have been presented in detail. This information suggests that defective lower oesophageal sphincter motility is the most important abnormality that underlies pathological gastro-oesophageal reflux. Two major forms of LOS dysfunction have been identified as responsible for pathological gastro-oesophageal reflux in the horizontal position: (1) an excessively frequent rate of occurrence of transient LOS relaxations; and (2) defective basal LOS tone. Both of these dysfunctions appear to arise from abnormal neural control of the LOS, probably by the central nervous system. The effect of these LOS dysfunctions on gastro-oesophageal competence is probably significantly influenced by non-sphincteric factors, the most important of these apparently being hiatus hernia. Though there is currently poor understanding about the ways in which hiatus hernia impairs gastro-oesophageal competence, measurement techniques have now advanced sufficiently to allow significant accrual of knowledge in this field. Once reflux has occurred, the efficiency of oesophageal acid clearance plays a major role in determining the impact of reflux on the oesophageal mucosa. Recent studies have shown that oesophageal acid clearance depends on both effective volume clearance and neutralization by saliva of residual acid in the oesophageal lumen. The efficiency of oesophageal volume clearance of both stimulated and real reflux has not been studied formally in GORD patients, but the high incidence of peristaltic dysfunction in reflux disease suggests that volume clearance will be defective in some patients. The limited information available about salivation in GORD patients suggests that salivary secretion is no different from that of age-matched controls, but that there is an age-dependent loss of the salivary response to oesophageal acidification. This impairment of salivary response may produce an age-dependent decline of the efficiency of oesophageal acid clearance. Unusually aggressive refluxate and impaired mucosal resistance to injury have been proposed as significant variables which contribute to pathogenesis of reflux disease. The evidence for these factors is circumstantial and scanty. Their importance has probably been overestimated.(ABSTRACT TRUNCATED AT 400 WORDS)

Abdomen↗
PubMed1994

Pathogenesis of tuberculosis: pathway to apical localization.

We have examined the published work of investigators which dealt with the pathogenesis of tuberculosis, especially the following: the infective dose, the yield of bacilli from the primary lesion and primary complex, the predominant location of the minimal lesion, the hypotheses of a vulnerable region in the lung and the specific pathways (endogenous or exogenous) by which tubercle bacilli cause disease. More knowledge of the pathogenic pathway to tuberculosis would provide clues to the development of new vaccines and drug regimens that can intervene at a specific stage in the pathogenesis. Based on the examination of the literature on pathogenesis of human tuberculosis and our findings in a guinea-pig model of experimental airborne tuberculosis, we have proposed an hypothesis which integrates the endogenous and exogenous pathways to tuberculosis. This hypothesis is based on the following observations: 1. The infectious dose is very low, usually 1-5 tubercle bacilli. 2. The first implant can occur anywhere in the lungs. 3. The cavitary lesion, characteristic of tuberculous disease, is often located in the apical regions in the lungs. 4. Whereas the primary implant can occur anywhere in the lungs, for the progression from infection to disease, the tubercle bacilli must gain access to the 'vulnerable' regions in the apex of the lungs. Our hypothesis states that in areas of the world where there is a low risk of infection with tubercle bacilli low incidence of vaccination or sensitization to environmental mycobacteria, or high incidence of high virulent isolates, the virulent tubercle bacilli reach the vulnerable region via a bacillemia during the first infection. In areas of the world where there is a high risk of infection with tubercle bacilli, high incidence of vaccination or sensitization to environmental mycobacteria or a high incidence of low virulent isolates, the tubercle bacilli reach the vulnerable region via the airway, which requires repeated episodes of infection as the probability of a first implant occurring in the vulnerable regions is low.

Animals↗
PubMed2024

Acute MeCP2 loss in adult mice reveals transcriptional and chromatin changes that precede neurological dysfunction and inform pathogenesis.

Mutations in the X-linked methyl-CpG-binding protein 2 (MECP2) gene cause Rett syndrome, a severe childhood neurological disorder. MeCP2 is a well-established transcriptional repressor, yet upon its loss, hundreds of genes are dysregulated in both directions. To understand what drives such dysregulation, we deleted Mecp2 in adult mice, circumventing developmental contributions and secondary pathogenesis. We performed time series transcriptional, chromatin, and phenotypic analyses of the hippocampus to determine the immediate consequences of MeCP2 loss and the cascade of pathogenesis. We find that loss of MeCP2 causes immediate and bidirectional progressive dysregulation of the transcriptome. To understand what drives gene downregulation, we profiled genome-wide histone modifications and found that a decrease in histone H3 acetylation (ac) at downregulated genes is among the earliest molecular changes occurring well before any measurable deficiencies in electrophysiology and neurological function. These data reveal a molecular cascade that drives disease independent of any developmental contributions or secondary pathogenesis.

Animals↗
PubMed1996

The pathogenesis of Staphylococcus aureus in the trauma patient and potential future therapies.

BACKGROUND: Staphylococcus aureus is the most frequently isolated pathogen in the trauma patient and uses multiple virulent factors to cause infection. At the cellular level, infection begins with the prokaryotic bacterial cell manipulating the eukaryotic host cell through its virulent factors. Researching this cellular interaction by describing the mechanisms of actions of various virulent factors may lead to new preventive therapies which will make the trauma patient less susceptible to S aureus infections. METHODS: Surgical, medical, and microbial literature was reviewed to provide an update on S aureus pathogenesis. RESULTS: Novel future therapies, in addition to antibiotics, are being devised based on understanding the molecular nature of S aureus pathogenesis. CONCLUSION: The impact of S aureus on trauma will increase as S aureus develops more antibiotic resistance and as the trauma population becomes older and includes an increasing proportion of immunocompromised patients. To meet the challenge of increased virulence, trauma surgeons should be directly involved in the research of microbial pathogenesis.

Bacterial Adhesion↗
PubMed2002

The role of macrophage/microglia and astrocytes in the pathogenesis of three neurologic disorders: HIV-associated dementia, Alzheimer disease, and multiple sclerosis.

Macrophage/microglia (M phi) are the principal immune cells in the central nervous system (CNS) concomitant with inflammatory brain disease and play a significant role in the host defense against invading microorganisms. Astrocytes, as a significant component of the blood-brain barrier, behave as one of the immune effector cells in the CNS as well. However, both cell types may play a dual role, amplifying the effects of inflammation and mediating cellular damage as well as protecting the CNS. Interactions of the immune system, M phi, and astrocytes result in altered production of neurotoxins and neurotrophins by these cells. These effects alter the neuronal structure and function during pathogenesis of HIV-1-associated dementia (HAD), Alzheimer disease (AD), and multiple sclerosis (MS). HAD primarily involves subcortical gray matter, and both HAD and MS affect sub-cortical white matter. AD is a cortical disease. The process of M phi and astrocytes activation leading to neurotoxicity share similarities among the three diseases. Human Immunodeficiency Virus (HIV)-1-infected M phi are involved in the pathogenesis of HAD and produce toxic molecules including cytokines, chemokines, and nitric oxide (NO). In AD, M phis produce these molecules and are activated by beta-amyloid proteins and related oligopeptides. Demyelination in MS involves M phi that become lipid laden, spurred by several possible antigens. In these three diseases, cytokine/chemokine communications between M phi and astrocytes occur and are involved in the balance of protective and destructive actions by these cells. This review describes the role of M phi and astrocytes in the pathogenesis of these three progressive neurological diseases, examining both beneficent and deleterious effects in each disease.

AIDS Dementia Complex↗
PubMed1997

Interstitial cystitis: a critique of current concepts with a new proposal for pathologic diagnosis and pathogenesis.

Interstitial cystitis (IC) has continued to be an unresolved problem in clinical urology despite intense investigation over the past 16 or more years. Its etiology and pathogenesis are still undetermined, and its pathologic diagnosis is essentially one of exclusion, with no specific or clear criteria. In this review, current concepts of the etiology/pathogenesis and pathology are critically analyzed, new pathologic observations summarized, and a proposal of neurogenic inflammation as the primary pathogenetic factor is presented in the context of all currently available information. The popular postulate attributing IC to a deficient or defective glycosaminoglycan urothelial surface layer is not substantiated by morphologic, experimental, clinical, or therapeutic observations. Although the consensus seems to discount an infectious etiology, there is sufficient evidence that a microbial factor-short of a bona fide clinical infection-may have a role. Both autoimmunity and mast cell infiltration also appear to have a role, despite the lack of evidence that either is involved as the primary etiologic factor. Claims that the so-called feline urologic syndrome may represent a natural animal model of IC are shaky. As it now stands, there is no natural or induced animal model that duplicates IC as it occurs in humans. No specific or diagnostic light microscopic pathologic features are provided by either routine histopathology or immunohistochemistry. Increasingly, it has been recognized that detrusor mast cell count has little or no diagnostic value. On the other hand, electron microscopy has provided important new observations: (a) presence of mast cells, activated by piecemeal degranulation, in close proximity to intrinsic nerves-particularly in suburothelium: (b) distinctive pathologic changes in urothelium, suburothelium, and muscularis in biopsy samples obtained after diagnostic bladder hydrodistension; (c) constant associated changes in venules, capillaries, and neural elements in the same biopsy samples; and (d) diffuse involvement of bladder wall, with the most evident and profound pathologic changes in posthydrodistension biopsy samples obtained from cystoscopically obvious lesions (glomerulations). These features are sufficiently distinctive to allow definitive pathologic diagnosis of IC, and provide a firm basis for primary involvement of neurogenic inflammation in its pathogenesis. A proposal is presented regarding the mechanisms invoked by neurogenic inflammation. This proposal revolves around sensory nerve excitation, the release of neuropeptides, and activated differential secretion of potent mast cell mediators. This proposal can account for the heterogeneity and variability of observed pathologic features, and upholds the tacit acceptance of IC as a disease of pluricausal etiology and multifactorial pathogenesis.

Animals↗
PubMed1995

A role for eosinophils in the pathogenesis of skin lesions in patients with food-sensitive atopic dermatitis.

BACKGROUND: Atopic dermatitis is associated with skin and blood eosinophilia, but the role of eosinophils in the pathogenesis of the skin lesions is poorly understood. METHODS: To determine whether eosinophils play a role in the pathogenesis of the skin lesions in atopic dermatitis, we studied the relationship between the severity of the disease and both the number and the extent of activation of eosinophils in 15 patients with food-sensitive atopic dermatitis. Furthermore, this relationship was re-evaluated in eight of these patients who, after a period of elemental diet or total parenteral nutrition, showed significant clinical improvement. RESULTS: A clear relationship was found between the number of light-density eosinophils and the severity of the disease both during the active disease and after clinical improvement. Furthermore, we describe an adhesion-stimulating activity for eosinophils in patients' plasma, which does not change after recovery. CONCLUSIONS: Taken together, these observations strongly indicate that eosinophils play a pivotal role in the pathogenesis of the skin lesions in atopic dermatitis. In particular, the light-density phenotype seems to be an essential feature of eosinophils involved in this process. The adhesion-promoting activity that we observed in the patients' plasma could be important in the recruitment of eosinophils from the blood into the skin.

Adult↗
PubMed1999

Inflammatory pathogenesis in Alzheimer's disease: biological mechanisms and cognitive sequeli.

Experimental evidence from molecular biology, biochemistry, epidemiology and behavioral research support the conclusion that brain inflammation contributes to the pathogenesis of Alzheimer's disease and other types of human dementias. Aspects of neuroimmunology relating to the pathogenesis of Alzheimer's disease are briefly reviewed. The effects of brain inflammation, mediated through cytokines and other secretory products of activated glial cells, on neurotransmission (specifically, nitric oxide, glutamate, and acetylcholine), amyloidogenesis, proteolysis, and oxidative stress are discussed within the context of the pathogenesis of learning and memory dysfunction in Alzheimer's disease. Alzheimer's disease is proposed to be an etiologically heterogeneous syndrome with the common elements of amyloid deposition and inflammatory neuronal damage.

Aged↗
PubMed1981

Alterations in blood elements in the pathogenesis of diabetic retinopathy.

The role of altered blood elements in the pathogenesis of retinal ischemia and diabetic retinopathy and the relationship to abnormal carbohydrate metabolism and to elevated levels of growth hormone are discussed. These changes involve red blood cells, platelets, plasma proteins, fibrinolytic response, and vascular endothelium. The significance of blood elements mediated by plasma is noted with aggregation of normal red cells when cross-matched with diabetic plasma and with intensive plasmapheresis, which caused red cell disaggregation and improvement of retinopathy. The relationship of metabolic control to diabetic retinopathy is reviewed and is evident by improvement of retinopathy occurring eight weeks after continuous subcutaneous infusion of insulin. A hypothesis is presented which integrates the multifactorial processes involved in the pathogenesis of diabetic retinopathy. Only through future research can one prove the implicated mechanisms in the pathogenesis of diabetic retinopathy and the role of strict metabolic control in altering the progression of retinopathy.

Blood Proteins↗
PubMed1999

Pathogenesis of Guillain-Barré syndrome.

Recent neurophysiological and pathological studies have led to a reclassification of the diseases that underlie Guillain-Barré syndrome (GBS) into acute inflammatory demyelinating polyradiculoneuropathy (AIDP), acute motor and sensory axonal neuropathy (AMSAN) and acute motor axonal neuropathy (AMAN). The Fisher syndrome of ophthalmoplegia, ataxia and areflexia is the most striking of several related conditions. Significant antecedent events include Campylobacter jejuni (4-66%), cytomegalovirus (5-15%), Epstein-Barr virus (2-10%), and Mycoplasma pneumoniae (1-5%) infections. These infections are not uniquely associated with any clinical subtype but severe axonal degeneration is more common following C. jejuni and severe sensory impairment following cytomegalovirus. Strong evidence supports an important role for antibodies to gangliosides in pathogenesis. In particular antibodies to ganglioside GM1 are present in 14-50% of patients with GBS, and are more common in cases with severe axonal degeneration associated with any subtype. Antibodies to ganglioside GQ1b are very closely associated with Fisher syndrome, its formes frustes and related syndromes. Ganglioside-like epitopes exist in the bacterial wall of C. jejuni. Infection by this and other organisms triggers an antibody response in patients with GBS but not in those with uncomplicated enteritis. The development of GBS is likely to be a consequence of special properties of the infecting organism, since some strains such as Penner 0:19 and 0:41 are particularly associated with GBS but not with enteritis. It is also likely to be a consequence of the immunogenetic background of the patient since few patients develop GBS after infection even with one of these strains. Attempts to match the subtypes of GBS to the fine specificity of anti-ganglioside antibodies and to functional effects in experimental models continue but have not yet fully explained the pathogenesis. T cells are also involved in the pathogenesis of most or perhaps all forms of GBS. T cell responses to any of three myelin proteins, P2, PO and PMP22, are sufficient to induce experimental autoimmune neuritis. Activated T cells are present in the circulation in the acute stage, up-regulate matrix metalloproteinases, cross the blood-nerve barrier and encounter their cognate antigens. Identification of the specificity of these T cell responses is still at a preliminary stage. The invasion of intact myelin sheaths by activated macrophages is difficult to explain according to a purely T cell mediated mechanism. The different patterns of GBS are probably due to the diverse interplay between antibodies and T cells of differing specificities.

Animals↗
PubMed2000

Energetics in the pathogenesis of neurodegenerative diseases.

Mitochondria have been linked to both necrotic and apoptotic cell death, which are thought to have a major role in the pathogenesis of neurodegenerative diseases. Recent evidence shows that nuclear gene defects affecting mitochondrial function have a role in the pathogenesis of Friedreich's ataxia, Wilson's disease and hereditary spastic paraplegia. There is also accumulating evidence that mitochondrial dysfunction might have a role in the pathogenesis of amyotrophic lateral sclerosis, Huntington's disease, Parkinson's disease and Alzheimer's disease. If this is so, a number of therapeutic targets are implicated that might result in novel treatments for neurodegenerative diseases.

Animals↗
PubMed1986

Cutaneous secondary syphilis: preliminary immunohistopathologic support for a role for immune complexes in lesion pathogenesis.

A circulating immune complex-mediated pathogenesis for lesions of secondary syphilis has been postulated. Textbook descriptions of a lymphoplasmacytic histopathologic picture have contradicted a role for circulating immune complexes in lesion pathogenesis. Four patients with early cutaneous lesions of secondary syphilis were studied. All four patients had serum Raji cell and/or Clq binding assay evidence for circulating immune complexes. Three patients showed a neutrophilic vascular reaction on histologic study of early lesions. The patients studied had immunofluorescence microscopic evidence of immunoreactant deposition in dermal blood vessels (4 hours) and/or a neutrophilic vascular reaction (24 hours) after intradermal histamine injection. Dieterle staining of lesional tissue from all patients showed the presence of treponemal organisms in dermal blood vessels. This new preliminary evidence adds some support to a circulating immune complex-mediated pathogenesis of cutaneous lesions in human secondary syphilis.

Adult↗
PubMed2003

Does an infrasonic acoustic shock wave resonance of the manganese 3+ loaded/copper depleted prion protein initiate the pathogenesis of TSE?

Intensive exposures to natural and artificial sources of infrasonic acoustic shock (tectonic disturbances, supersonic aeroplanes, etc.) have been observed in ecosystems supporting mammalian populations that are blighted by clusters of traditional and new variant strains of transmissible spongiform encephalopathy (TSE). But TSEs will only emerge in those 'infrasound-rich' environments which are simultaneously influenced by eco-factors that induce a high manganese (Mn)/low copper (Cu)-zinc (Zn) ratio in brains of local mammalian populations. Since cellular prion protein (PrPc) is a cupro-protein expressed throughout the circadian mediated pathways of the body, it is proposed that PrP's Cu component performs a role in the conduction and distribution of endogenous electromagnetic energy; energy that has been transduced from incoming ultraviolet, acoustic, geomagnetic radiations. TSE pathogenesis is initiated once Mn substitutes at the vacant Cu domain on PrPc and forms a nonpathogenic, protease resistant, 'sleeping' prion. A second stage of pathogenesis comes into play once a low frequency wave of infrasonic shock metamorphoses the piezoelectric atomic structure of the Mn 3+ component of the prion, thereby 'priming' the sleeping prion into its fully fledged, pathogenic TSE isoform - where the paramagnetic status of the Mn 3+ atom is transformed into a stable ferrimagnetic lattice work, due to the strong electron-phonon coupling resulting from the dynamic 'Jahn-Teller' type distortions of the oxygen octahedra specific to the trivalent Mn species. The so called 'infectivity' of the prion is a misnomer and should be correctly defined as the contagious field inducing capacity of the ferrimagnetic Mn 3+ component of the prion; which remains pathogenic at all temperatures below the 'curie point'. A progressive domino-like 'metal to ligand to metal' ferrimagnetic corruption of the conduits of electromagnetic superexchange is initiated. The TSE diseased brain can be likened to a solar charged battery on continuous charge; where the Mn contaminated/Cu depleted circadian-auditory pathways absorb and pile up, rather than conduct the vital life force energies of incoming ultra violet, acoustic and geomagnetic radiation. Instead of harnessing these energies for the body's own bio-rhythmic requirements, an infrasonic shock induced metamorphosis of the Mn atom intervenes; initiating an explosive pathogenesis that perverts the healthy pathways of darkness and light; Cu prions are replaced by hyperpolarized Mn 3+ prions that seed self perpetuating 'cluster bombs' of free radical mediated neurodegeneration. TSE ensues.

Animals↗
PubMed1999

Towards a greater understanding of the pathogenesis of holoprosencephaly.

Holoprosencephaly is a malformation of the cerebral hemispheres resulting in the absence of the inter-hemispheric fissure along with other defects of brain development. Frequently midline defects of the craniofacial structures are also present. This malformation sequence has been of interest for many years because of the well recognized genetic and environmental pathogeneses, although the molecular pathogenesis remained elusive. Recent studies have begun clarifying the molecular pathogenesis of holoprosencephaly. Herein is reviewed the syndromes associated with holoprosencephaly, the pathology of this disorder, genetic and environment factors, and a current understanding of the molecular pathogenesis of this disorder.

Animals↗
PubMed2002

Comparison of anti 60 and 52 kDa SS-A/Ro antibodies in the pathogenesis of cutaneous lupus erythematosus.

Anti SS-A/Ro antibodies are involved in the pathogenesis of cutaneous lupus erythematosus (CLE) in a part through antibody dependent cellular cytotoxicity (ADCC). However, it is still obscure which and how anti 60 and anti 52 kDa Ro antibodies are involved. To address the issue, we examined both types of anti Ro antibodies of sera from patients with systemic LE (SLE) or discoid LE (LE). The titer of anti 60 kDa antibody in SLE was significantly much higher than that of DLE or control. The positive ratio of DLE showed more higher tendency than control, but it was not statistically significant. The similar tendency was observed in the titer of anti 52 kDa antibody. An association between the anti 60 kDa antibody and the anti 52 kDa antibody was statistically significant in SLE patients. Although the relative index (RI) was statistically significant in DLE, they included many negative sera, which biased the statistics. Both anti 60 kDa antibody and anti 52 kDa antibody could induce significant ADCC of ultraviolet B (UVB) light-irradiated keratinocytes from neonatal foreskins and/or normal adults, in which anti 60 kDa antibody showed higher cytotoxicity than anti 52 kDa antibody. The autologous combination studies (keratinocytes and monospecific anti 60 or anti 52 kDa antibody from patients) suggested anti 60 kDa antibody was more potent to induce ADCC activity than anti 52 kDa antibody. Taken together, it is likely that anti 60 kDa antibody dependent keratinocyte damage plays more significant role in the pathogenesis of SLE skin lesions than anti 52 kDa dependent damage. However, both type antibodies seemed to have little contribution to the pathogenesis of DLE skin lesion.

Adult↗
PubMed1998

Role of free oxygen radicals and prostanoids in the pathogenesis of Henoch-Schönlein Purpura.

The pathogenesis of Henoch-Schonlein Purpura (HSP) is still controversial. The aim of our study was to investigate the role of oxidative stress and cyclooxygenase (CO) pathway products in the pathogenesis of HSP. In order to investigate this, malondialdehyde (MDA) levels, indicating lipid peroxidation, prostaglandin E (PGE)-like activity as inflammatory mediator and vitamin E (vit-E) levels indicating anti-oxidant status were studied in a group of 10 children with HSP (five girls and five boys, aged 6-21 years, mean 10.7 years), both in the acute and recovery phase of the disease and in five age and sex-matched healthy children as a control group. The patients were also grouped into low and high clinical score groups. Plasma levels of MDA and PGE-like activity were significantly elevated in the active phase of HSP compared to the recovery phase. Vit-E levels were significantly reduced in the active phase compared to the recovery phase. The plasma levels of PGE-like activity of the patients obtained in the active phase were significantly higher than the levels of the control group, whereas the levels of the recovery phase were significantly lower than in the control group. No such difference between the controls and MDA and vit-E levels in the patient group was shown. No correlation between the clinical scores and the parameters studied could be found. Our findings indicate that oxidant stress and CO pathway products may play a role in the pathogenesis of HSP.

Child↗
PubMed2002

The use of animal infection models to study the pathogenesis of melioidosis and glanders.

The use of animal infection models is central to the study of microbial pathogenesis. In combination with genetic, immunological and antigen purification techniques, much can be learned regarding the pathogenesis of diseases caused by microorganisms. This update focuses on the recent use of animal infection models to study the pathogenesis of melioidosis and glanders.

Animals↗