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PubMed2004

The immunobiology of Th1 polarization in high-pathology schistosomiasis.

Schistosomiasis is a serious global helminthic disease, in which the main immunopathology consists of a granulomatous and fibrosing reaction against tissue-trapped parasite eggs. The severity of this inflammatory process, the product of a CD4(+) T-cell-mediated immune response against parasite egg antigens, is, however, markedly uneven, both in human patients and among mouse strains in an experimental model. Severe schistosomiasis is associated with persistently elevated pro-inflammatory T-helper-1 (Th1)-type cytokines, whereas milder pathology is present when Th2 cytokines dominate. This scenario is supported by the pronounced pathology resulting from the obliteration of pathways that facilitate Th2 differentiation and by the development of more intense lesions in mouse strains that fail to downregulate the Th1 response. Genetically prone high-pathology mice have a higher proportion of CD4(+) T cells in lymph nodes and granulomas, in which the Th1 phenotype is driven by interleukin-12; they also develop a dominant repertoire against peptide 234-246 of the major Sm-p40 egg antigen, utilizing a strikingly restricted T-cell receptor structure that involves Valpha11.3beta8. In turn, low-pathology mice exhibit enhanced CD4(+) T-cell apoptosis, which contributes to limit pathology. The definition of distinctive immune profiles associated with polar forms of schistosomiasis opens opportunities for targeted immuno-intervention in individuals suffering from or at risk of severe disease.

Animals↗
PubMed2004

Dendritic spine pathology and deficits in experience-dependent dendritic plasticity in R6/1 Huntington's disease transgenic mice.

Huntington's disease (HD) is a fatal neurodegenerative disease caused by a CAG repeat expansion coding for an expanded polyglutamine tract in the huntingtin protein. Dendritic abnormalities occur in human HD patients and in several transgenic mouse models of the disease. In this study, we examine, for the first time, dendrite and spine pathology in the R6/1 mouse model of HD, which mimics neurodegeneration seen in human HD. Enriching the environment of HD transgenic mice delays the onset of symptoms, so we also examine the effects of enrichment on dendrite pathology. Golgi-impregnated tissue from symptomatic R6/1 HD mice reveals a decrease in dendritic spine density and dendritic spine length in striatal medium spiny neurons and cortical pyramidal neurons. HD also causes a specific reduction in the proportion of bifurcated dendritic spines on basal dendrites of cortical pyramidal neurons. No differences in soma size, recurving distal dendrites, or dendritic branching were observed. Although home-cage environmental enrichment from 1 to 8 months of age increases spine density in wild-type mice, it has no effect on the spine pathology in HD mice. These results show that dendritic spine pathology in R6/1 HD mice resembles degenerative changes seen in human HD and in other transgenic mouse models of the disease. We thus provide further evidence that the HD mutation disrupts the connectivity in both neostriatum and cerebral cortex, which will contribute to motor and cognitive disease symptoms. Furthermore, we demonstrate that Huntington's disease pathology interferes with the normal plastic response of dendritic spines to environmental enrichment.

Animals↗
PubMed2006

Clinical and pathological study of lichen-planus-like keratosis in China.

Lichen-planus-like keratosis is usually diagnosed pathologically; rarely, a definitive diagnosis can be made grossly in the clinic. Only a few cases of lichen-planus-like keratosis have been reported in China. The purpose of this study was to investigate the clinical and pathological features of lichen-planus-like keratosis in China. Fifty cases of lichen-planus-like keratosis patients diagnosed pathologically during a 5-year period in our clinic were analyzed. Clinical features were recorded. Sectioned specimens were subjected to hematoxylin and eosin staining to observe pathological changes. Results showed that there were 34 males and 16 females (ratio 2:1) with an average age of 61.2 years. Most of the lesions were single papules or plaques with rough surfaces. They were distributed on the face, larger than 1 cm, and dark red to brown in color. Only one case (2%) was considered to be lichen-planus-like keratosis clinically. By hematoxylin and eosin staining, solar lentigo and solar elastosis could be found in 68% and 32% of lichen-planus-like keratosis lesions, respectively. Eosinophil (42%) and plasma cell (36%) infiltration was also found frequently. Exoerythrocytes could be detected in 50% of the cases. Lichen-planus-like keratosis is not uncommon in clinical practice in China, the diagnosis of lichen-planus-like keratosis should be made by a combination of clinical manifestations and pathological changes. It is better to classify lichen-planus-like keratosis as a benign skin tumor. More attention should be paid to lichen-planus-like keratosis in China.

Aged↗
PubMed2006

Should the scope of addictive behaviors be broadened to include pathological gambling?

AIMS: Pathological gambling is currently considered an impulse control disorder in the Diagnostic and Statistical Manual of Mental Disorders (DSM). This paper considers the prospect of reclassifying and broadening the substance use disorders to include non-pharmacological addictions such as pathological gambling. METHODS: Literature reviews were conducted on areas relevant to pathological gambling and its classification and similarities to substance use disorders. RESULTS: The diagnostic criteria for pathological gambling are outlined across the three versions of the DSM since its initial introduction. The paper also describes instruments that have been used to assess the disorder, basic epidemiology and some biological and genetic data, especially in terms of potential overlap with substance use disorders. Similarities and differences with respect to treatments are reviewed as well. CONCLUSIONS: Both advantages and disadvantages should be considered with respect to expanding the classification system to include pathological gambling within the context of addictive disorders.

Comorbidity↗
PubMed1989

Oral pathology and prostheses--are they related? Investigations in an elderly population.

A survey of 233 elderly subjects living in the district served by the Halton Health Authority (Cheshire, England) investigated the relationship between the age of dentures, their need for replacement and the presence of any oral pathological lesions. The retention, stability, occlusion and cleanliness of the dentures were all found to be worse in the older appliances; perceived need for denture replacement was found to increase from 40% in 5-year-old dentures to 84% in dentures over 31 years old. While 41% of the sample had an oral pathological lesion, no significant relationship was found between denture age and pathology or place of residence. People resident in the community with no assistance had the highest incidence of oral pathology and those living in long-stay hospitals the least. The absence of a relationship between denture age and oral pathology is considered to be a powerful indicator of the need for regular oral examination of the edentulous population.

Aged↗
PubMed1996

Prion protein genotype and pathological phenotype studies in sporadic Creutzfeldt-Jakob disease.

A comparative semi-automated morphometric study was performed on the distribution of prion protein, spongiform change and astrocytosis in the brains of nine cases of sporadic Creutzfeldt-Jakob disease of differing genotype at the methionine-valine polymorphism at codon 129 of the prion protein gene. Custom-designed image analysis software was used to produce objective figures for each of the different pathological features throughout 13 different areas of the brain used for analysis. A significant positive correlation was observed between prion protein deposition and astrocytosis in all cases and no significant correlation was observed between spongiform change and prion protein deposition. Different patterns of pathology were found to relate to codon 129 genotype; valine homozygosity favoured the targeting of pathology to deep grey matter structures, while methionine homozygosity favoured cortical targeting of pathology. These results provide evidence that prion protein deposition is closely associated with an astrocytic reaction and suggest that codon 129 genotype may influence the pathological phenotype.

Aged↗
PubMed2005

The impact of argyrophilic grain disease on the development of dementia and its relationship to concurrent Alzheimer's disease-related pathology.

Argyrophilic grain disease (AGD) constitutes a neurodegenerative disorder that occurs in the brains of the elderly and affects 5% of all patients with dementia. Tau protein-containing lesions known as argyrophilic grains and located predominantly in limbic regions of the brain characterize this disease. Dementia is encountered in only a subset of cases that display the morphological pattern of AGD. The aim of this study is to determine the role of concurrent Alzheimer's disease (AD)-related pathology for the development of dementia in AGD patients. A total of 204 post-mortem brains from 30 demented and 49 nondemented AGD patients, 39 AD patients, and from 86 nondemented controls without AGD were staged for AD-related neurofibrillary tangles (NFTs) as well as amyloid beta-protein (Abeta) deposition. To identify differences in AD-related pathology between demented and nondemented AGD cases, and to differentiate the pattern of AD-related changes in demented and nondemented AGD cases from that seen in AD and nondemented controls, we statistically compared the stages of Abeta and NFT distribution among these groups. Using a logistic regression model, we showed that AGD has a significant effect on the development of dementia beyond that attributable to AD-related pathology (P < 0.005). Demented AGD cases showed lower stages of AD-related pathology than did pure AD cases but higher stages than nondemented AGD patients. AGD associated dementia was seen in the presence of NFT (Braak)-stages II-IV and Abeta-phases 2-3, whereas those stages were not associated with dementia in the absence of AGD. In conclusion, AGD is a clinically relevant neurodegenerative entity that significantly contributes to the development of dementia by lowering the threshold for cognitive deficits in the presence of moderate amounts of AD-related pathology.

Aged↗
PubMed2006

Alpha-synuclein pathology of the spinal and peripheral autonomic nervous system in neurologically unimpaired elderly subjects.

Studies on cases with incidental Lewy body disease (ILBD) suggest that alpha-synuclein (alphaSN) pathology of Parkinson's disease (PD) starts in lower brainstem nuclei and in the olfactory bulb. However, medullary structures as the induction site of alphaSN pathology have been questioned as large parts of the nervous system, including the spinal cord and the peripheral autonomic nervous system (PANS), have not been examined in ILBD. Thus, the time course of PD lesions in the spinal cord or PANS in relation to medullary lesions remains unknown. We collected 98 post mortem cases with no reference to PD-associated symptoms on clinical records. alphaSN pathology was found in the central nervous system, including the spinal cord, and in the PANS in 17 (17.3%) cases. alphaSN pathology was encountered in autonomic nuclei of the thoracic spinal cord, brainstem and olfactory nerves in 17/17, in sacral parasympathetic nuclei in 15/16, in the myenteric plexus of oesophagus in 14/17, in sympathetic ganglia in 14/17, and in the vagus nerve in 12/16 cases. In addition to the thoracic lateral horns, a high number of alphaSN lesions was also found in non-autonomic spinal cord nuclei. Considering supraspinal structures our cases corresponded roughly to the recently described sequential order of alphaSN involvement in PD. Our study indicates, however, that the autonomic nuclei of the spinal cord and the PANS belong to the most constantly and earliest affected regions next to medullary structures and the olfactory nerves. A larger cohort of ILBD cases will be needed to pinpoint the precise induction site of alphaSN pathology among these structures.

Aged↗
PubMed2006

Differential microglial regulation in the human spinal cord under normal and pathological conditions.

As the primary intrinsic immune effector cells of the central nervous system, microglia are involved in virtually all pathological processes of the brain and spinal cord including inflammatory, neurodegenerative, traumatic, neoplastic and vascular diseases. Despite this important role, there is a lack of data concerning microglial distribution and protein expression in the human spinal cord. In this study, we immunohistochemically investigated 10 normal human spinal cords to establish reference data and compared these results with 15 pathological human spinal cords deriving from distinct pathologies. Each spinal cord was evaluated at eight different levels for three white and two grey matter areas for both constitutive (MHC-II, CD68, IL-16, AIF-1, LCA, CD4) and reactive (MRP-8, MRP-14) microglial antigens. Whereas previous studies revealed significant regional differences in microglial distribution and protein expression in human brain, normal spinal cord displayed a uniform expression pattern, reaching levels of up to 17% MHC-II positive cells of the total cell population. This datum formed the basis for the further evaluation of microglia expression levels in pathological spinal cords, where levels of up to 45% positive cells were observed. Our results represent important reference values for future neuropathological diagnostic and therapeutical approaches in spinal cord pathologies.

Adult↗
PubMed2005

Preoperative prediction of final pathological features is not improved by the free-to-total prostate-specific antigen ratio in Japanese men with clinically localized prostate cancer.

BACKGROUND: The objective of the present study was to determine whether the percentage of free/total prostate-specific antigen (f/tPSA) in patients scheduled to undergo radical prostatectomy for clinically localized prostate cancer can preoperatively predict organ-confined versus extraprostatic disease. METHODS: Serum levels of fPSA and tPSA were measured in 97 patients with clinically organ-confined disease before they underwent radical prostatectomy. The relationships of tPSA, f/tPSA and the pathological stage of the prostatectomy specimens were analyzed. Furthermore, the ability of f/tPSA to predict the pathological features was compared with those of tPSA and systematic biopsy findings. RESULTS: Organ-confined and extraprostatic extension diseases were present in 51 and 46 men, respectively. tPSA in patients with extraprostatic diseases was significantly higher than that in those with organ-confined diseases; however, there was no significant difference in f/tPSA between these two groups. There was also a significant difference in tPSA levels at each pathological stage, while f/tPSA did not parallel the pathological stage. Furthermore, there was no additional information concerning the extent of prostate cancer obtained when f/tPSA was combined with tPSA or with the percent of positive biopsy cores, which is the most significant predictor of the extent of prostate cancer among factors associated with systematic biopsy. CONCLUSION: f/tPSA could not predict the final pathological features in patients with clinically localized prostate cancer before radical prostatectomy. Moreover, the predictive value provided by tPSA or systematic biopsy findings was not improved by combined analysis with f/tPSA.

Aged↗
PubMed2004

The total percentage of biopsy cores with cancer improves the prediction of pathological stage after radical prostatectomy.

OBJECTIVE: To examine whether the simple variable 'percentage of cancer-positive biopsy cores' is a significant predictor of true pathological stage after radical prostatectomy and can be used to improve pathological stage prediction by simple means. PATIENTS AND METHODS: In all, 375 patients had a radical prostatectomy for localized prostate cancer in two UK centres; 260 had complete preoperative staging information. Logistic regression was used and predicted probability graphs constructed to assess predictors of pathological stage. RESULTS: In this study, only PSA (P = 0.004) and percentage cancer-positive biopsy cores (P < 0.001) were significant predictors of pathological stage. The final model was an acceptable classifier for pathological stage (area under the receiver operating characteristic curve 0.76, specificity 85%, sensitivity 47%). A patient with a PSA of 10 ng/mL and one of six cores positive for cancer would have a predicted probability of extraprostatic disease of 20%, whereas the same patient with all six biopsy cores positive would have a predicted probability of extraprostatic disease of 80%. CONCLUSIONS: The percentage of cancer-positive biopsy cores significantly predicts the disease stage after radical prostatectomy. This variable is easy to obtain by the clinician and avoids the need to estimate the percentage of biopsy tissue infiltrated by cancer. This readily available information can easily be computed and may help to counsel patients about realistic expectations of organ-confined disease in relation to surgery as a treatment option.

Aged↗
PubMed2005

Correlation between clinical and pathological staging in a series of radical cystectomies for bladder carcinoma.

OBJECTIVE: To analyse the rate of concordance between the clinical and pathological Tumour-Nodes-Metastasis staging systems in a homogeneous series of patients who had undergone radical cystectomy for locally advanced or recurrent multifocal superficial bladder carcinoma. PATIENTS AND METHODS: The clinical data of 156 patients who had undergone radical cystectomy and bilateral iliaco-obturator lymphadenectomy for bladder cancer in our department were analysed retrospectively. RESULTS The clinical stage of the primary tumour was carcinoma in situ in three patients (1.9%), cT1 in 67 (42.9%), cT2 in 70 (44.9%), cT3 in five (3.2%) and cT4 in nine (5.8%). Clinical lymph node involvement was detected in 19 patients (12.2%). The differences between clinical and pathological stages were statistically significant (P < 0.001), the concordance was moderate (kappa = 0.27, P < 0.001). Of the 70 patients with < or = cT1, 40 (57%) were reconfirmed as having pathological stage < or = T1; of the 70 with cT2, 16 (23%) had pT2 carcinoma. Of the 140 patients with clinically organ-confined (< or =T2) neoplasms, 70 (50%) had been understaged after radical cystectomy. The clinical and pathological systems were statistically overlapping for locally advanced cases only. Pathological lymph node involvement was diagnosed in 45 patients (28.8%); this was foreseen with pelvic computed tomography in 19 (12%) only (P < 0.001). All patients designated cN+ were also pN+. CONCLUSION: These data confirm the high risk of clinical understaging of both local extension of the primary tumour and lymph node involvement.

Adult↗
PubMed2005

Relationship between Lens culinaris agglutinin-reactive alpha-fetoprotein and pathologic features of hepatocellular carcinoma.

AIM: We investigated pathological features of Lens culinaris agglutinin-reactive alpha-fetoprotein (AFP-L3)-positive hepatocellular carcinoma (HCC) in order to seek a pathological basis of poor prognosis of HCC patients with elevated AFP-L3. METHODS: A total of 111 patients with HCC < or =5 cm in diameter who underwent hepatic resection were studied. Serum AFP-L3 concentration was measured within a month prior to surgery by lectin-affinity electrophoresis coupled with antibody-affinity blotting, and expressed as AFP-L3 percentage of total AFP. AFP-L3 of 10% or higher was judged to be positive. Pathologic features of resected HCC specimens were evaluated and classified concerning growth pattern (expansive or infiltrative growth), capsule formation, capsule infiltration, septal formation, portal vein invasion, hepatic vein invasion, bile duct invasion, and intrahepatic metastasis. These macroscopic and microscopic findings were compared between AFP-L3-positive and negative HCC specimens. RESULTS: Thirty-three (29.7%) were positive for AFP-L3. The prevalence of HCC with infiltrative growth, with capsule infiltration, with septum formation, with portal vein invasion, and with hepatic vein invasion was significantly higher in AFP-L3-positive group (P=0.0121, 0.0290, 0.0442, 0.0314, and 0.0433, respectively). These pathologic features reportedly indicate the progression of the tumor. CONCLUSIONS: AFP-L3-positive HCC had several pathologic features of progressed state of HCC, which accounted for the AFP-L3 as an indicator of poor prognosis of HCC.

Adult↗
PubMed2000

The pathological substrate of limbic epilepsy: neuronal loss in the medial dorsal thalamic nucleus as the consistent change.

PURPOSE: The focus of research in limbic epilepsy has been the hippocampus because of its well-known pathology of hippocampal atrophy and sclerosis as well as the strong propensity for this structure to seize under a variety of circumstances. There is ample evidence, however, for pathological alterations in other regions of the limbic system in limbic/mesial temporal lobe epilepsy, including the amygdala, the entorhinal cortex, and, in some cases, the thalamus. In this preliminary evaluation of the pathological substrate for limbic epilepsy, we wished to determine if there was consistent anatomic change at extrahippocampal sites. METHODS: We compared paraffin sections of brains from rats with chronic spontaneous limbic epilepsy and age-matched controls to determine the consistency of the pathology at five sites: the hippocampus, amygdala, entorhinal cortex, piriform cortex, and medial dorsal thalamus. RESULTS: In a qualitative evaluation of these sections taken from standardized positions, we found that the medial dorsal thalamic nucleus in the epileptic animals was the site that was consistently involved with neuronal loss. With all other sites, at least several animals had qualitatively normal tissue. CONCLUSIONS: This finding suggests that neuronal loss in the medial dorsal thalamus may be the consistent pathology in limbic epilepsy, at least in an animal model of the disorder. The presence of a structurally abnormal subcortical region with broad connections to the limbic sites involved with chronic epilepsy may have implications for our understanding of the pathophysiology of this disorder.

Animals↗
PubMed2005

Parenchymal lesions in pharmacoresistant temporal lobe epilepsy: dual and multiple pathology.

OBJECTIVES: Dual pathology is reported in 5-30% of temporal lobe resections performed in pharmacoresistant epilepsy. Dual pathology may be of importance for surgical planning and also for the understanding of the pathogenesis of epilepsy. We describe the frequency of dual or multiple pathology, i.e. more than one histopathological diagnosis, in adults with temporal lobe resections. MATERIAL AND METHODS: Surgical specimens from 33 consecutive patients with resections including mesial as well as neocortical temporal structures were reviewed. All histopathological findings were recorded. Post-mortem specimens from 11 control subjects were also reviewed. RESULTS: Dual or multiple pathology was found in almost half of the epilepsy patients (48%). Hippocampal sclerosis was found in 25 patients (76%), malformations of cortical development in 15 (46%), of which 12 (36%) were microdysgenesis, and low-grade tumours in seven (21%). Apart from mild gliosis, there were no histopathological changes in the control specimens. CONCLUSION: Dual or multiple pathology was a common finding in this group of adults with temporal lobe resections. In order to increase our understanding of how aetiological factors may combine in the development of seizures, we consider it relevant and important to report all histopathological findings in epilepsy surgery series.

Adult↗
PubMed2006

Lysosomal dysfunction, cellular pathology and clinical symptoms: basic principles.

UNLABELLED: Between 40 and 50 lysosomal storage disorders are known at present. Fine details of the pathogenic process involved are in general not known. This overview highlights the basic principles of lysosomal pathogenesis and the clinical consequences of defective genes involved in lysosomal functions. The subject is discussed in the context of the possibility of prevention and reversal of cellular and organ damage by enzyme replacement therapy. Also presented is a mechanical model for the muscle pathology observed in Pompe disease. Direct mechanical effects of the non-contractile inclusions - glycogen-loaded lysosomes - seem to be a key factor in the loss of force during both early and late stages of the disease. CONCLUSION: Each lysosomal storage disorder and each patient with a given lysosomal disorder has unique molecular, pathological and clinical features. But, the order of pathological events is largely the same. Mutations in a gene cause lysosomal dysfunction which, in turn, results in cellular pathology affecting organ structure and function. Clinical symptoms are the ultimate manifestation. The reversibility of symptoms with enzyme replacement therapy will vary according to the disease, as well as the nature and stage of organ pathology.

Animals↗
PubMedDate not supplied

The reification of the "pathological" gambler: an analysis of gambling treatment and the application of the medical model to problem gambling.

PROBLEM: Is the medical model used to reify "pathological" gambling? METHODS: A qualitative field study of 12 subjects with the diagnosis "pathological" gambler. FINDINGS: None of the 12 subjects being treated for "pathological" gambling fit neatly in the category of "pathological" gambler. An examination of the treatment center revealed institutional grounds for the use of this diagnosis. CONCLUSIONS: Rather than a medical diagnosis, "pathological" gambling is a socially constructed phenomenon. Using the medical model serves clients interpersonally and clinicians occupationally.

Adult↗
PubMed1981

Rate-versus-intensity functions and related AP responses in normal and pathological guinea pig and human cochleas.

Cochlear fiber discharge rate-versus-intensity functions, across frequency, have been measured in pathological guinea pig cochleas (ototoxic antibiotic poisoning) and compared with the normal animal. The frequency dependence of the slopes of these functions is reduced in cochlear pathology which results in minimum threshold elevations of more than 50 dB, i.e., there is a reduction in this frequency dependent nonlinearity. The rate functions at characteristic frequency (CF) become abnormally steep (e.g., 4--5 spikes/s/dB compared with a normal 1--2 spikes/s/dB), and comparable to those of the low-frequency tail region of normal cochlear fibers. The CF dynamic range is reduced from 30--40 to 10--15 dB in cochlear pathology. The fiber study has been confirmed by (and has confirmed) a method of indirect measurement of rate functions from AP suppression-versus-intensity functions using a pure-tone forward masking paradigm [Abbas and Gorga, J. Acoust. Soc. Am. 69, 492--499 (1981)]. This method has been used in normal and pathological guinea pigs, and the results parallel the single fiber study. In addition, AP suppression functions, across frequency, have been obtained in human subjects with (near) normal hearing thresholds, and in patients with sensorineural hearing loss of cochlear origin, during transtympanic electrocochleography. The AP suppression curves in pathology indicate, as for the animal studies, a loss of the frequency dependency of the rate function slopes, and predict steep rate functions at CF (and thus reduced dynamic range) in cochlear deafness. The findings are related to loudness recruitment.

Acoustics↗