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At least 415 records · Page 23Linked to original sources
PubMed2006

Quantitative determination of gland mucous cells-type mucin using a monoclonal antibody, HIK1083: its pathophysiological changes in human gastric juice.

BACKGROUND: Pathological alteration in gastric mucosa is caused by Helicobacter pylori infection and is detectable by histological analysis. In particular, the alteration of gland mucous cells (GMCs)-type mucin, which plays a protective role against H. pylori infection, is critical in the pathogenesis of H. pylori-related gastritis. We established an assay for GMCs-type mucin and quantitatively assessed the pathophysiological changes in its content in human gastric juice samples. METHODS: The assay method for GMCs-type mucin was based on ELISA using a monoclonal antibody (HIK1083), and was used it to measure GMCs-type mucin in gastric juice obtained from patients with or without H. pylori infection. RESULTS: All the basic characteristics of the current method were satisfactory to quantify the GMCs-type mucin content in gastric juice. The GMCs-type mucin content, but not total mucin content, was significantly higher in patients with H. pylori infection (n=17; 437+/-476 U, mean+/-SD) than in those without H. pylori infection (n=55; 168+/-322 U, p<0.05). CONCLUSIONS: The current method is suitable for the quantitative analysis of GMCs-type mucin in gastric juice. The change in GMCs-type mucin content in gastric juice may be possibly implicated in the pathophysiology of the gastric mucosa and in the patient's gastric mucosal lesions.

Animals↗
PubMed2005

Abnormal H-reflexes in periodic limb movement disorder; impact on understanding the pathophysiology of the disorder.

OBJECTIVE: To get more insight in the pathophysiological basis of periodic limb movement disorder (PLMD) with or without restless legs syndrome (RLS), we investigated whether these patients have spontaneous changes in H-reflexes or show altered reflex patterns after (external) inhibition or excitation of the relevant spinal segment. METHODS: The ratio of the peak-to-peak values of the maximal soleus H-reflex and the maximal direct muscle potential (H/M ratio), H-reflex recruitment curves, vibratory inhibition and recovery curves of the soleus H-reflex in double stimulus experiments were measured in 9 PLMD patients and 11 controls. RESULTS: In comparison to controls the vibratory inhibition, predominantly reflecting pre-synaptic inhibitory action, was depressed in PLMD patients. The soleus H-reflex recovery curves showed increased late facilitation and depressed late inhibition, both reflecting diminished inhibition due to post-synaptic central activity. CONCLUSIONS: Our data indicate diminished inhibition at spinal level in PLMD patients. This is probably due to altered function of the descending spinal tracts, peripheral influence or changes at the inter-neural circuitry at spinal level itself, or combinations of these 3 possibilities. SIGNIFICANCE: The results of this study give further insight in the pathophysiology of PLMD and RLS by stressing the importance of diminished central inhibition.

Adult↗
PubMed2006

Influence of peer review medical audit on pathophysiological interpretation of nerve conduction studies in polyneuropathies.

OBJECTIVE: To evaluate the possible influence of peer review medical audit on experienced physicians' pathophysiological interpretation of nerve conduction studies in polyneuropathy patients. METHODS: Since 1992, 7 European neurophysiologists have collected samples of their patient examinations for regular review where the physicians interpret each other's cases electronically and subsequently discuss them at regular workshop meetings (i.e. a form of medical audit). Two sets of 100 polyneuropathy examinations interpreted with an interval of 4-6 years were selected. The sets contained 1456 and 1719 nerve conduction studies, each given a pathophysiological test conclusion by each individual physician. Inter-physician agreement on interpretation of demyelination and axonal loss of the nerve, as well as neuropathic and unspecific findings, was estimated using kappa statistics. RESULTS: Increased agreement from set 1 to set 2 was found on interpretation of demyelination of the nerve (set 1: kappa=0.22; set 2: kappa=0.45), and of neuropathic (set 1: kappa=0.46; set 2: kappa=0.64) and unspecific findings (set 1: kappa=0.35; set 2: kappa=0.54). No changes were found on interpretation of axonal loss (set 1: kappa=0.26; set 2: kappa=0.31) and normal findings (set 1 and set 2: kappa=0.90). CONCLUSIONS: Participation in regular peer review medical audit resulted in increased agreement on interpretation of nerve conduction studies for 6 of the 7 participants. The study further highlights the need for better definition of criteria for identification of demyelinating, and in particular, axonal peripheral neuropathies. SIGNIFICANCE: International collaboration involving peer review medical audit may contribute to development of practice guidelines and, in turn, to increased quality of electrodiagnostic medicine.

Axons↗
PubMed2005

Multi-dysfunctional pathophysiology in ITP.

Idiopathic thrombocytopenic purpura (ITP) is an organ-specific autoimmune disorder characterized by a low platelet count and mucocutaneous bleeding. The decrease of platelets is caused by increased autoantibodies against self-antigens, particularly IgG antibodies against GPIIb/IIIa. The production of these autoantibodies by B cells depends on a number of cellular mechanisms that form a network of modulation, with T cells playing a pivotal role in pathophysiology. Delineation of the dysfunction of cellular immunity has recently been attempted. This review will focus on these recent advances applicable to ITP and to highlight how these may translate into novel approaches to treatment in the future. Multi-dysfunction in these networks may include a failure of self-antigen recognition and tolerance, involvement of abnormal cell surface molecules, altered Th1/Th2 cytokine profiles, impaired megakaryocytopoiesis and impaired cell-mediated cytotoxicity. In ITP, multi-step dysfunctions in these networks may take place that finally lead to the occurrence of the disease. Therefore, unveiling these dysfunctions is vital in understanding the pathophysiology of ITP and will finally lead to the development of new therapies to fight the disease.

Cell Communication↗
PubMed2005

Pathophysiology of newborn hypotension outside the transitional period.

Hypotension is a common diagnosis in neonatal intensive care units. Although there are epidemiological data for normative blood pressure values in preterm and term infants, the ranges of normal blood pressure where adequate organ perfusion is ensured for different gestational and postnatal ages remain unclear. An understanding of the developmentally regulated differences in the physiology and pathophysiology of the neonatal cardiovascular system in comparison to that of mature subjects is important to formulate an appropriate treatment strategy in neonates with circulatory compromise. This article reviews the current understanding of pathophysiology of hypotension and shock in the neonate beyond the transitional period, focusing on hypovolemia, myocardial dysfunction, abnormal peripheral vasoregulation, and relative or absolute adrenal insufficiency with potentially associated down regulation of adrenergic receptors.

Blood Pressure↗
PubMed2005

Effect of celecoxib, a cyclooxygenase-2 inhibitor, on the pathophysiology of adjuvant arthritis in rat.

We investigated the efficacy of celecoxib, a specific cyclooxygenase (COX)-2 inhibitor, on arthritic pathophysiology and confirmed its gastric safety in adjuvant-induced arthritis rats. Results were compared with those for loxoprofen, a non-selective COX inhibitor. Arthritis was induced by injection of 1 mg of Mycobacterium butyricum in 50 microl of liquid paraffin into the left footpad of Lewis rats. The drugs were given by twice daily oral administration for 10 days beginning 15 days after adjuvant injection, with celecoxib at 0.01-3 mg/kg/day and loxoprofen at 0.01-3 mg/kg/day. Celecoxib significantly inhibited paw swelling, hyperalgesic response, and joint destruction (radiographic and histopathological findings) in these arthritic rats. These effects of celecoxib were superior to those of loxoprofen. Further, the administration of loxoprofen (3 mg/kg/day) caused significant gastric lesions, whereas celecoxib at the same dose did not. These results suggest that COX-2-mediated prostaglandins may play an important role in the progression of pathophysiology in this model and that celecoxib may be a useful therapeutic agent for the treatment of rheumatoid arthritis, with greater safety than non-selective COX inhibitors.

Animals↗
PubMed2005

Tako-Tsubo cardiomyopathy: new insights into the possible underlying pathophysiology.

UNLABELLED: Tako-Tsubo cardiomyopathy is characterised by an atypical distribution of left ventricular (LV) dysynergy with apical ballooning and compensatory basal hyperkinesis. Coronary angiography is normal. Several substrates have been put forward to explain the underlying pathophysiology such as raised catecholamine levels (due to physical or emotional stress), multivessel epicardial coronary spasm or diffuse microvascular spasm. However, the pathophysiology has not yet been fully clarified. We present a series of cases whose findings could explain the mechanism underlying this syndrome. Four consecutives patients, all female, were admitted with the clinical features typical of Tako-Tsubo syndrome. In all, severe widespread transient LV mid-apical a/dyskinesia was associated with a mid-cavity dynamic obstruction which resolved prior to the resolution of the LV wall motion abnormalities. In all cases the dynamic LV obstruction was related to localised mid-ventricular septal thickening. After improvement in wall motion, a low-dose strain/strain rate dobutamine stress-echocardiography (DSE) was performed to determine the underlying ischaemic substrate. This provoked an LV mid-cavity gradient at peak dose in all. Regional deformation changes during DSE showed the affected myocardium to have the typical response diagnostic of regional stunning. CONCLUSION: We postulate that an important unrecognised factor in the development of Tako-Tsubo cardiomyopathy is the presence of abnormal myocardial functional architecture (such as localised mid-ventricular septal thickening), which in the presence of dehydration and/or raised catecholamine levels due to physical or emotional stress, leads the development of a severe transient LV mid-cavity obstruction. This effectively sub-divides the LV into two functionally different chambers with a marked increase in wall stress in the high pressure distal apical chamber. This, in combination with the abnormal high circulating catecholamine levels, induces widespread sub-endocardial ischaemia which is unrelated to a specific coronary artery territory. With rehydration/fall in catecholamine levels the interventricular gradient resolves and distal function recovers. Low dose SR/S DSE confirms that the distal ischaemic substrate is myocardial stunning.

Aged↗
PubMed2006

Drug addiction: pathways to the disease and pathophysiological perspectives.

Drug addiction is a medical condition, a chronic relapsing disease. As in other domains of experimental medicine, appropriate experimental investigations are needed in order to better understand the disease. However, to understand the diverse facets of drug effects and of the underlying pathophysiology it is necessary to keep in mind the complexity of the psychopathological processes. The main symptoms that characterize addiction correspond to expressions of dysfunctions within specific circuits and regions. Pathways to addiction are numerous and comorbidity and in the real world poly-drug use are common. Some of these aspects will be examined as well as the role of life events and stress. Theoretical considerations will be proposed [see also: Koob, G.F., & Le Moal, M.. 2005a. Neurobiology of Addiction. Elsevier. 570 pp] to account for the stages of the disease from impulse control disorder to compulsive disorders, for affective dynamics and for the relations between the symptoms and pathophysiology.

Humans↗
PubMed2006

The role of IL-12 and TGF-beta1 in the pathophysiology of major depressive disorder.

It has been postulated that major depression may be accompanied by significant changes in cell-mediated and humoral immunity related to the pathophysiology or pathogenesis of that illness. We explored the role of 2 cytokines, IL-12 and TGF-beta1, which represent the cytokines of the Th1 and Th3 types, in the pathophysiology of major depressive disorder (MDD). Cytokine levels were measured in 30 major depressed patients at the time of admission and 6 weeks after effective antidepressant treatment; levels were measured once in 30 normal controls. At the time of admission, TGF-beta1 levels of MDD patients showed no differences from normal controls, but IL-12 was significantly higher than in normal controls. However, the IL-12/TGF-beta1 (Th1/Th3) ratios of depressed patients were not different from those of controls. In MDD patients, IL-12 values were significantly decreased after treatment, while TGF-beta1 levels were significantly increased. IL-12/TGF-beta1 ratios of patients were significantly decreased after treatment compared with before treatment. There were no significant correlations between changes in the cytokine levels and changes in scores representing the severity of depression. These findings suggest that major depression is accompanied by immune activation during the acute depressed state, and antidepressant treatments have anti-inflammatory effects.

Adult↗
PubMed2005

Pathophysiology and clinical presentations of rhabdomyolysis.

Rhabdomyolysis has sparked new interest in recent years. The causes of rhabdomyolysis include drugs and other toxic agents, infections, physical exertion, crush injury, and muscle diseases (dystrophinopathies and metabolic myopathies). Prompt identification of the pathophysiological mechanism is the key to rapid control of the acute episode and to prevention of recurrences. In this update, we discuss the pathophysiological mechanisms and nosology of rhabdomyolysis, as well as diagnostic investigations, with special emphasis on noninvasive methods.

Humans↗
PubMed2005

Current understanding of gender dimorphism in hepatic pathophysiology.

Studies have shown gender dimorphic response of the liver for various hepatic stresses including ischemia/reperfusion, hemorrhagic shock-resuscitation, hepatectomy, liver cirrhosis, endotoxemia, and chronic alcoholic consumption. The mechanisms responsible for the gender dimorphic response include differences in pro-inflammatory cytokine release, production of reactive oxygen species, and alteration in hepatic vasoregulatory action. These effects were shown to be modulated by circulating sex steroid levels. In this regard, modulation of sex steroid levels by agents/drugs has been proposed as a therapeutic option for preventing hepatic damage in various hepatic stress models. Further elucidation of precise mechanisms responsible for the gender-related differences in the hepatic pathophysiology is essential for the potential clinical application of sex hormone modulation therapy. In this article, current progress in our understanding the gender difference in the hepatic pathophysiology under the condition of hepatic stress is reviewed and discussed.

Estrogens↗
PubMed2004

Pain experienced by lung cancer patients: a review of prevalence, causes and pathophysiology.

BACKGROUND: Lung cancer is one of the commonest cancers to cause pain, but little is known regarding the extent of this complex problem in these patients. METHODS: Medline (1966-June 2002) and Cancerlit (1975-May 2002) were searched to identify studies of lung cancer patients' experience of pain, its prevalence, causes and underlying pathophysiology. RESULTS: Thirty-two studies were identified. Patients were recruited from diverse populations, and the prevalence varied according to study setting. Pain affected 27% of outpatients (range 8-85%), and 76% of patients cared for by palliative care services (range 63-88%). Pain was caused by cancer in 73% (range 44-87%), and cancer treatment in 11% (range 5-17%). Nociceptive pain was the major pathophysiological subtype in lung cancer pain, but neuropathic pain accounted for 30% (range 25-32%) of cases. CONCLUSIONS: The overall weighted mean pain prevalence of pain was 47% (range 6-100%). Cancer patients should be asked about pain at all stages of management. Those with pain should be investigated for disease progression and considered for referral for specialist management.

Humans↗
PubMed2005

Epidemiology, pathophysiology, and treatment of Barrett's esophagus: reducing mortality from esophageal adenocarcinoma.

The definition of BE has evolved over time. BE is the key premalignant lesion for developing EAC. The epidemiology and pathophysiology of BE is outlined, and risk factors for BE and EAC are reviewed. GERD plays a crucial role in the pathophysiology and the clinical identification of BE. Endoscopy with biopsy is the best tool for diagnosing and surveying patients with BE. Detection of early neoplasia is the present approach to reduce EAC mortality. Novel technology should assist in the early detection of dysplasia to enable targeted therapy. Effective chemopreventive strategies may reduce the risk of progression to EAC.

Adenocarcinoma↗
PubMed2004

Induction of apoptosis as a proposed pathophysiological link between glaucoma and Helicobacter pylori infection.

Although apoptosis is equally important both for the development and for the maintenance of homeostasis in some adult tissues, it can also be associated with disease processes. Current studies indicate that apoptosis is a mechanism of cell death in several important ocular and gastrointestinal diseases including glaucoma, and Helicobacter pylori (H. pylori)-induced upper gastrointestinal disorders and/or extraintestinal diseases, including autoimmune and neurodegenerative ones (Sjögren's syndrome, Guillain-Barre syndrome or Parkinson's disease). Glaucoma is also associated with similar autoimmune and neurodegenerative disorders, characterized by apoptotic loss of specific populations of neurons. Recently, a high prevalence of H. pylori infection has been recognized in patients with chronic open-angle glaucoma. In addition, H. pylori eradication may positively influence glaucoma parameters, thereby suggesting a possible causal link between H. pylori and glaucoma. H. pylori infection may influence the pathophysiology of glaucoma by releasing various proinflammatory and vasoactive substances, as well as by influencing apoptotic process; parameters that may also exert their own effects in the induction and/or progression of glaucomatous neuropathy. Importantly, H. pylori infection and glaucoma share the Fas/FasL and the mitochondria-mediated apoptotic pathways, thereby proposing an apoptotic link in the pathophysiology of both diseases.

Apoptosis↗
PubMed2004

High altitude sickness. Is acute cortisol deficiency involved in its pathophysiology?

High altitude illness (HAI) affects 42% of individuals climbing above 3000 m. The pathophysiology of HAI, including water retention remains unclear. Although decreased nitric oxide (NO) production is implicated in the pathophysiology, a recent study reported increased NO in breathes of high altitude inhabitants, apparently produced to combat the high altitude hypoxia. NO binds heme generally and impairs cytochrome P450 steroidogenic enzymes. A consequence of increased NO production may be decreased steroidogenesis. An acute cortisol deficiency may thus be the reason for water retention and oedema, and explains why dexamethasone is effective in treating some aspects of HAI.

Altitude Sickness↗
PubMed2006

Retino-hypothalamic-pineal hypothesis in the pathophysiology of primary headaches.

Primary headaches include migraine, tension, cluster headaches, paroxysmal hemicrania and miscellaneous headaches unassociated with structural lesions. A putative role of the retino-hypothalamic-pineal (RHP) axis in the pathophysiology of primary headaches is reviewed in terms of (1) retinal dysfunction, (2) hypothalamic dysfunction and human circadian desynchrony, (3) pineal melatonin dysfunction and (4) rostral limbic dysfunction mediating the human stress response. Unified RHP hypothesis is proposed, suggesting that an acute, periodic or chronic, circadian desynchrony and dysfunction of the whole or part of the RHP axis is implicated in the pathophysiology of primary headaches. Supportive evidence for the RHP hypothesis, including recent PET studies showing changes in dorsal pons, hypothalamus and rostral limbic structures, is presented.

Animals↗
PubMed2005

Pathophysiological basis of therapy of raised intracranial pressure in acute liver failure.

In acute liver failure (ALF) patients that have raised increased intracranial pressure (ICP), mortality remains unacceptably high. There has been an explosion in the knowledge about the pathophysiological basis of raised ICP but treatment modalities are limited. Current therapy is aimed at reducing the circulating ammonia levels and attempts to reduce brain swelling which are only moderately effective. More recently, cerebral hyperemia has been suggested as being of major importance in the pathogenesis of increased ICP providing a new look at interventions such as hyperventilation, N-acetylcysteine, thiopentone sodium and propofol. More recently studies have focused upon the role of systemic inflammatory response in the pathogenesis of increased ICP and support the use of antibiotics prophylactically. The application of moderate hypothermia to treat uncontrolled intracranial hypertension seems promising and its exact place will be decided in a large trial being planned in USA and Europe. Early data from studies in an animal model suggests that albumin dialysis is a promising new tool to treat intracranial hypertension in patients with ALF. The recent advance in our understanding of the pathophysiological basis of intracranial hypertension has provided the platform for the discovery of new treatments.

Ammonia↗
PubMed2005

Homocysteine at pathophysiologic concentrations activates human monocyte and induces cytokine expression and inhibits macrophage migration inhibitory factor expression.

OBJECTIVE: Homocystinemia is an important independent risk factor for atherosclerosis. Inflammatory cytokines play key roles in the development of atherogenesis. This study investigated the effect of homocysteine on inflammatory cytokine expression. METHODS: Human monocytes were treated in vitro with a variety of DL-homocysteine concentrations that ranged from physiologic concentration to higher than pathophysiologic concentration, and we analyzed their expressions of inflammatory cytokines, including tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, interleukin-8, interleukin-12, and migration inhibitory factor. RESULTS: DL-homocysteine at a marginal physiologic concentration of 2 microg/mL (15 microM) activated monocytes. In addition, DL-homocysteine at the pathophysiologic dose of 25 microg/mL (185 microM) induced mRNA and protein expressions of inflammatory cytokines tumor necrosis factor-alpha, IL-1beta, interleukin-6, interleukin-8, and interleukin-12. Moreover, at the larger dose of 50 microg/mL (370 microM) DL-homocysteine decreased expression of migration inhibitory factor at the mRNA and protein levels. CONCLUSION: These findings suggest that homocysteine may contribute to the initiation and progression of vascular disease by activating monocytes, resulting in the secretion of cytokines that amplify the inflammatory response.

Adult↗