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Pathological Lesions (pathological + lesion)
Selected AbstractsModerate Alcohol Consumption Aggravates High-Fat Diet Induced Steatohepatitis in RatsALCOHOLISM, Issue 3 2010Yan Wang Background:, Nonalcoholic steatohepatitis (NASH) develops in the absence of chronic and excessive alcohol consumption. However, it remains unknown whether moderate alcohol consumption aggravates liver inflammation in pre-existing NASH condition. Methods:, Sprague-Dawley rats were first fed ad libitum with Lieber-DeCarli high-fat diet (71% energy from fat) for 6 weeks to induce NASH, as demonstrated previously. Afterwards, these rats were continuously fed with high-fat diet (HFD, 55% total energy from fat) or high fat plus alcohol diet (HFA, 55% energy from fat and 16% energy from alcohol) for an additional 4 weeks. Pathological lesions including fat accumulation and inflammatory foci in liver were examined and graded. Lipid peroxidation and apoptotic hepatocytes in the liver were assessed. The mRNA expressions of tumor necrosis factor-, (TNF,) and TNF receptor 1 (TNF-R1), Fas death receptor (Fas) and Fas ligant (FasL), IL-1, and IL-12 were determined by real-time PCR. Protein levels of total and cleaved caspase-3, CYP2E1, Bax, and Bcl-2 were measured by western blotting. Results:, The number of hepatic inflammatory foci and apoptotic hepatocytes were significantly increased in rats fed with HFA as compared with those in HFD-fed rats. The aggravated inflammatory response and cellular apoptosis mediated by HFA were associated with elevated mRNA expression of Fas/FasL and cleaved caspase-3 protein. Although no significant differences were observed between HFD and HFA groups, the levels of lipid peroxidation, Bax and Bcl-2 protein concentration, and mRNA levels of other inflammatory cytokines were significantly higher in these 2 groups than those in the control group. Conclusions:, These data suggest that even moderate alcohol consumption can cause more hepatic inflammation and cellular apoptosis in a pre-existing NASH condition. [source] Prevalence rates of spondylolysis in British skeletal populationsINTERNATIONAL JOURNAL OF OSTEOARCHAEOLOGY, Issue 3 2005L. Fibiger Abstract As an activity-related pathological lesion, spondylolysis and its prevalence rates are indicative of relative diachronic activity levels in different populations. In this paper we document the prevalence of spondylolytic defects in a series of time-successive populations with special reference to the recording methods employed, and compare the findings with modern clinical studies. We identify epidemiological trends in expression of the condition through 1500 years in a series of skeletonised human remains from England. This includes a 5th,6th-century settlement, a 15th-century mass grave, a 14th to 17th-century rural parish, a medieval Dominican friary, a medieval leper hospital and an 18th to 19th-century crypt collection. These skeletal populations sample human groups experiencing considerable social change from an agrarian, non-centralised early medieval period through the development of the medieval state to the earliest phases of industrialisation in England. A detailed study of all lumbar vertebrae in one of the assemblages highlights discrepancies between clinical prevalence rates for spondylolysis established through radiography, and those resulting from direct osteological analysis of the lumbar region of the vertebral column. Current prevalence rates cited in the osteological as well as the clinical literature are greatly dependent upon the recording methods employed, and the effects of several methods for osteological remains are considered in this treatment. For the populations reported on here, prevalence rates vary from considerably less than 1% to as much as 12%, depending on the method selected. A standardised recording method for spondylolytic lesions is suggested to facilitate accurate prevalence reporting and comparison of activity levels between different populations. Copyright © 2005 John Wiley & Sons, Ltd. [source] Unresolved issues relating to the Shaking Palsy on the celebration of James Parkinson's 250th birthdayMOVEMENT DISORDERS, Issue S17 2007Andrew J. Lees MD Abstract James Parkinson's Essay on the Shaking Palsy published in 1817 provided the first clear clinical description for the disorder now known throughout the world by his name. His primary reason for publishing his monograph shortly before his retirement from medical practice was to draw the medical profession's attention to a malady, which had not yet been defined as a nosological entity. He also hoped that the eminent anatomists of the day would be stimulated to elucidate the pathological lesion responsible for the clinical picture and that this in turn might lead to a rational cure. The concept of Parkinson's disease remains clinically based and successive generations of neurologists have refined and embellished Parkinson's seminal descriptions. Narrative accounts by affected individuals have also helped physicians understand what it is like to live with Parkinson's disease. For many years, the pathological hallmarks of Parkinson's disease were disputed and there were few clinico-pathological reports with adequate clinical description. However, most neurologists now link severe loss of nigral cells in the ventrolateral tier of the pars compacta of the substantia nigra with bradykinesia and the presence of Lewy bodies in a number of discrete brain stem and cortical regions with Parkinson's disease. There are many unanswered clinical questions relating to Parkinson's disease including the striking heterogeneity and frequent limb asymmetry. It also remains somewhat uncertain whether Parkinson's disease is ever truly unilateral by the time of clinical presentation and whether the hand rather than the foot is the most common site of onset. Hyposmia and visual hallucinations are helpful pointers in distinguishing Parkinson's disease from atypical Parkinsonism and should be specifically enquired about in the history. Simple reliable cultural-specific smell identification batteries are an urgent need and target of clinical research. It remains to be determined whether Alzheimer type dementia as opposed to a dysexecutive syndrome should be considered a part of Parkinson's disease and further detailed clinico-pathological correlative studies are needed. It is also unclear whether autosomal dominant monogenetic Parkinsonism due to synuclein or LRRK-2 mutations will prove to be identical clinically with Parkinson's disease and for the present it is wiser to regard Parkinson's disease as a sporadic disorder. Parkinson was an active political reformer and if alive today would certainly be campaigning to translate more effectively the rich seam of neuroscientific research of the last decade into therapeutic benefits for the rising number of people who are developing the shaking palsy as a result of increasing longevity in the developed world. © 2007 Movement Disorder Society [source] Non-traumatic pulmonary haematoma complicating oral anticoagulation therapyRESPIROLOGY, Issue 4 2007Moussa RIACHY Abstract: Several cases of non-traumatic pulmonary haematoma have been reported in the literature. However, very few of them are related to anticoagulation therapy. The authors report two cases of pulmonary haematoma caused by oral anticoagulant therapy without any underlying pathological lesion. The evolution was fatal in the first case, whereas a slow spontaneous resolution of the haematoma was noted in the second. Non-traumatic pulmonary haematoma can be a complication of oral anticoagulation and should be considered in the differential diagnosis of pulmonary densities in this setting. [source] Fine needle aspiration cytology in a case of fibrous dysplasia of jawDIAGNOSTIC CYTOPATHOLOGY, Issue 12 2009Nalini Gupta M.D. Abstract Fibro-osseous lesions of the jaw comprise of a spectrum of diseases which include osseous dysplasia, fibrous dysplasia, and ossifying fibroma. The differentiation amongst these individual pathological lesions is difficult and a combined clinico-radiological and histological correlation is essential for exact categorization. Fine needle aspiration cytology (FNAC) is frequently carried out to distinguish between benign and malignant lesions of the jaw as is a quick and reliable modality of investigation which guides in further management. We report, a case of a jaw swelling in a young male, diagnosed as fibrous dysplasia on FNAC. Diagn. Cytopathol. 2009. © 2009 Wiley-Liss, Inc. [source] DIAGNOSIS AND CLINICAL COURSE OF ULCERATIVE GASTRODUODENAL LESION ASSOCIATED WITH ULCERATIVE COLITIS: POSSIBLE RELATIONSHIP WITH POUCHITISDIGESTIVE ENDOSCOPY, Issue 4 2010Takashi Hisabe Background and Aim:, Ulcerative colitis (UC) is not only characterized by pathological lesions localized to colonic mucosa, but also to various complications involving other organs, including postoperative pouchitis. Among these complications, diffuse gastroduodenitis with lesions resembling colonic lesions has been reported, albeit rarely. The aim of the present study was to attempt to characterize the lesions of the upper gastrointestinal tract occurring as a complication of UC, and to assess the frequency and clinical course of these lesions. Methods:, A total of 322 UC patients who had undergone upper gastrointestinal endoscopy were retrospectively analyzed. We assessed the frequency of endoscopic findings, including diffuse gastroduodenal lesions resembling colonic lesions. Ulcerative gastroduodenal lesion (UGDL) associated with UC was diagnosed if lesions satisfied the following criteria: (i) improvement of the lesions with treatment of UC; and/or (ii) resemblance to UC in pathological findings. Results:, UGDL satisfying the aforementioned criteria was found in 15 (4.7%) of 322 patients. All the 15 patients had UGDL accompanied by pancolitis or after proctocolectomy. Frequency in 146 patients with pancolitis was 6.2% (nine patients) and that in 81 patients who had undergone proctocolectomy was 7.4% (six patients). Four patients with diffuse ulcerative upper-gastrointestinal mucosal inflammation (DUMI) had pouchitis. In all patients except one, the lesions resolved easily with medical treatment. Conclusions:, In more than half of the post-proctocolectomy patients, UGDL was related to the occurrence of pouchitis. The existence of characteristic UGDL must be taken into account in the diagnosis and treatment of UC, and UGDL is possibly related to the occurrence of pouchitis. [source] Distribution and signaling of TREM2/DAP12, the receptor system mutated in human polycystic lipomembraneous osteodysplasia with sclerosing leukoencephalopathy dementiaEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 10 2004Giuseppina Sessa Abstract Together with its adaptor protein, the adaptor protein of 12 kDa also known as KARAP and TYROBP (DAP12), triggering r (TREM2) is a stimulatory membrane receptor of the immunoglobulin/lectin-like superfamily, well known in myeloid cells. In humans, however, loss-of-function mutations of TREM2/DAP12 leave myeloid cells unaffected but induce an autosomal recessive disease characterized, together with bone cysts, by a spectrum of pathological lesions in the cortex, thalamus and basal ganglia with clinical symptoms of progressive dementia (polycystic lipomembraneous osteodysplasia with sclerosing leukoencephalopathy). Nothing was known about the role of TREM2/DAP12 in brain cell biology and physiology. By confocal immunocytochemistry we demonstrate that, in both human and mouse cerebral cortex, TREM2/DAP12, strongly expressed by microglia, is also present in a fraction of neurons but not in astrocytes and oligodendrocytes. In contrast, in the hippocampal cortex TREM2-expressing neurons are rare. Both in neurons and microglia the receptor appears to be located mostly intracellularly in a discrete compartment(s) partially coinciding with (or adjacent to) the Golgi complex/trans-Golgi network. Four nerve cell lines were identified as expressing the intracellular receptor system. In living human microglia CHME-5 and glioblastoma T98G cells, activation of TREM2 by its specific antibody induced [Ca2+]i responses, documenting its surface expression and functioning. Surface expression of TREM2, low in resting CHME-5 and T98G cells, increases significantly and transiently (60 min) when cells are stimulated by ionomycin, as revealed by both surface biotinylation and surface immunolabeling. Our results provide the first information about the expression, distribution (mostly intracellular) and functioning of TREM2/DAP12 system in nerve cells, a necessary step in the understanding of the cellular mechanisms affected in polycystic lipomembraneous osteodysplasia with sclerosing leukoencephalopathy. [source] Frequency and type of canal isthmuses in first molars detected by endoscopic inspection during periradicular surgeryINTERNATIONAL ENDODONTIC JOURNAL, Issue 3 2005T. Von Arx Abstract Aim, To analyse the occurrence of canal isthmuses in molars following root-end resection. Methodology, The material consisted of 56 mandibular and 32 maxillary first molars subjected to periradicular surgery. Based on radiographic, clinical, as well as intraoperative status, only roots with associated pathological lesions were treated. In total, 124 roots were resected (80 mandibular and 44 maxillary molar roots). The cut root faces were inspected with a rigid endoscope following apical root-end resection. The number of canals as well as the presence and type of canal isthmuses were recorded. Results, In maxillary first molars, 76% of resected mesio-buccal roots had two canals and an isthmus, 10% had two canals but no isthmus, and 14% had a single canal. All disto-buccal and palatal roots had one canal. In mandibular first molars, 83% of mesial roots had two canals with an isthmus. In 11%, two canals but no isthmus were present, and 6% demonstrated a single canal. Sixty-four per cent of distal roots had a single canal and 36% had two canals with an isthmus. Conclusions, This clinical study during periradicular surgery and intraoperative endoscopic examination of first permanent molars found a high frequency of canal isthmuses at the resection level. Endoscopic inspection also demonstrated that none of the isthmuses were filled, emphasizing the difficulty of orthograde instrumentation and root filling of canal isthmuses. [source] A case of multiple metastasis in Late Holocene hunter-gatherers from the Argentine Pampean regionINTERNATIONAL JOURNAL OF OSTEOARCHAEOLOGY, Issue 5 2008L. H. Luna Abstract Chenque I site is a prehistoric cemetery located in Lihué Calel National Park (La Pampa province) in the Western Pampean region of Argentina. Hunter-gatherer societies made use of this site during the Final Late Holocene for at least 700 years (1030,370,BP). Currently 41 burial structures have been excavated, and more than 150 individuals have been recovered. There is great variability in mortuary patterns at the site (simple, multiple, primary, secondary burials, and also a variant not previously observed in the region). The life-ways of this population have been investigated through the evaluation of several biological and cultural factors. Several pathological conditions have also been identified in this cemetery. Burial no. 12 contains a skeleton of an adult male that shows multiple pathological lesions, compatible with a neoplastic disease. These lesions have been analysed using several methodological strategies: macroscopic, radiological and microscopic. This is the first time that this kind of disease has been identified from a prehistoric burial in Argentina. In this paper the location and characteristics of the lesions are evaluated, and the different neoplastic diseases that could have produced them are discussed. Since the people buried in this cemetery belonged to highly mobile societies, a key issue is to infer the consequences that this disease would have had on the dynamics of the group in which this person lived, because of the gradual deterioration of his health and physical strength. Copyright © 2007 John Wiley & Sons, Ltd. [source] A case study of possible differential diagnoses of a medieval skeleton from Denmark: leprosy, ergotism, treponematosis, sarcoidosis or smallpox?INTERNATIONAL JOURNAL OF OSTEOARCHAEOLOGY, Issue 4 2007M. Lefort Abstract This paper uses macroscopic and radiological examinations to provide differential diagnoses of pathological lesions in the skeleton of a young woman, 20,25 years of age, which triggered the Danish palaeopathologist Vilhelm Møller-Christensen's interest in leprosy. The skeleton was incomplete, but the majority of bones of the upper body, as well as the skull, were present. The pathological changes consisted of medullary and cortical lytic foci, periosteal reaction and enhanced cortical density. The lesions were most extensive on the left side, especially around the elbow, wrist and scapula. Treponematosis, leprosy, smallpox, ergotism, rheumatoid arthritis, tuberculosis and sarcoidosis are all reviewed with regard to bone and joint pathology and their likelihood of being the correct diagnosis. We concluded that the most plausible diagnosis is treponematosis, but neither sarcoidosis nor smallpox can be completely excluded. Copyright © 2007 John Wiley & Sons, Ltd. [source] A comparative experiment in the consolidation of cremated boneINTERNATIONAL JOURNAL OF OSTEOARCHAEOLOGY, Issue 2 2004D. Rossi Abstract This experiment assessed whether consolidation of cremated remains facilitated cross-sectioning and grinding, which often are required for microstructural analyses such as the histomorphometric estimation of age and the examination of pathological lesions. Green, bovine femoral diaphyses were cremated at three temperature ranges (346,357°C; 610,755°C; 684,838°C) in an electric furnace and then consolidated with Acryloid B-72 or Butvar B-98 using simple brushing and immersion techniques. After consolidation was complete, bone pieces were cross-sectioned and ground to a thickness of 100,120,,m. Results indicate that specimens treated with Acryloid B-72 are harder and stronger than Butvar treated and untreated control specimens. Acryloid B-72 is, therefore, recommended for the consolidation of cremated remains in preparation for microstructural analysis. Copyright © 2004 John Wiley & Sons, Ltd. [source] Renal malakoplakia as a pseudotumoral lesion in a renal transplant patient: A case reportINTERNATIONAL JOURNAL OF UROLOGY, Issue 7 2007Isidro Machado Puerto Abstract: Malakoplakia is a rare chronic inflammatory disease associated with gram-negative bacterial infections frequently caused by Escherichia coli. Malakoplakia usually affects the lower urinary tract (bladder) but there are cases described in the kidney as well as in the respiratory and digestive organs. We report on a case with renal parenchymal malakoplakia in a renal transplant patient and describe the pathological lesions of malakoplakia: histiocytic proliferation with scarce inflammatory infiltrate, histiocytes with acidophilic cytoplasm and the presence of characteristic Michaelis-Gutmann bodies. The authors in this study review the updated reports related to the entity in this uncommon localization, the association with an immunocompromised patient, the macroscopic presentation as a pseudotumoral lesion and the possible relationship with the xanthogranulomatous pyelonephritis as a form of a histopathological spectrum in patients affected with gram negative urinary tract infection. [source] Expression of transforming growth factor-beta isoforms and their receptors in chronic tendinosisJOURNAL OF ANATOMY, Issue 3 2001S. A. FENWICK Chronic tendon lesions are degenerative conditions and may represent a failure to repair or remodel the extracellular matrix after repeated micro-injury. Since TGF-, is strongly associated with tissue repair, we investigated the expression of TGF-, isoforms (,1, ,2 and ,3) and their 2 signalling receptors (TGF-,RI and TGF-,RII) in normal and pathological Achilles tendons. In all tissues, all 3 TGF-, isoforms and the 2 receptors were present at sites of blood vessels. Cells in the matrix showed no staining for TGF-,1 or ,3, while TGF-,2 was associated with cells throughout the normal cadaver tendon. Tissue from tendons with pathological lesions showed an increase in cell numbers and percentage TGF-,2 expression. TGF-,RII showed a wide distribution in cells throughout the tissue sections. As with TGF-,2, there was an increase in the number of cells expressing TGF-,RII in pathological tissue. TGF-,RI was restricted to blood vessels and was absent from the fibrillar matrix. We conclude that despite the presence and upregulation of TGF-,2, TGF-, signalling is not propagated due to the lack of TGF-,RI. This might explain why chronic tendon lesions fail to resolve and suggests that the addition of exogenous TGF-, will have little effect on chronic tendinopathy. [source] Experimental transmission of sleeping disease in one-year-old rainbow trout, Oncorhynchus mykiss (Walbaum), induced by sleeping disease virusJOURNAL OF FISH DISEASES, Issue 5 2006S Kerbart Boscher Abstract Sleeping disease (SD) is a serious disease of rainbow trout, Oncorhynchus mykiss, reared in fresh water caused by sleeping disease virus (SDV). In this study a detailed clinical, histological, virological and serological description of the experimental reproduction of SD in 1-year-old rainbow trout exposed to SDV was carried out. Two hundred disease-free fish were intraperitoneally inoculated with a SDV isolate and 100 fish were inoculated with an uninfected cell culture lysate as a negative control. Infected and control fish were randomly removed at days 4, 7, 14, 21, 42 and 70 post-infection. Blood and tissues were collected for virus isolation, histopathological examination and serum neutralization. SDV was detected in serum, kidney and brain of infected fish from 4 to 21 days post-infection (dpi). Characteristic pathological lesions were observed in infected fish as early as 7 dpi. Lesions were first detected in exocrine pancreas and subsequently observed in heart and skeletal muscle. Neutralizing antibodies to SDV were detected in infected fish from 14 to 70 dpi. Infected fish displayed typical signs of SD 1-month pi and the mortality reached 18.7% within 44 days. This study experimentally reproduced all the pathognomonic features of natural outbreaks of SD in 1-year-old rainbow trout. [source] Identification of a unique BK virus variant in the CNS of a patient with AIDS,JOURNAL OF MEDICAL VIROLOGY, Issue 1 2003Gunn Eli Kimo Jørgensen Abstract Human polyomavirus BK (BKV; GenBank or EMBL or DDBJ accession no. NC001538) is often reactivated in immunosuppressed patients. Reactivation has been associated primarily with excretion of the virus in the urine, and there have been few reports of renal and/or neurological disease caused by BKV in patients with acquired immunodeficiency syndrome (AIDS). Polymerase chain reaction, Southern blotting, and sequencing were used to detect and identify the noncoding control region (NCCR) of BKV in different tissues in an AIDS patient with meningoencephalitis, retinitis, and nephritis. An undescribed reorganized NCCR variant of the virus, completely different from the variants detected in peripheral blood leukocytes (PBLs) and urine, was identified in the cerebrospinal fluid (CSF) and CNS tissues. These results suggest that rearrangements in the NCCR of the virus have resulted in a BKV variant, which is better adapted to the host cell machinery of the cells in CNS tissue. The rearranged variant (BKV CNS) might have been involved in the initiation and/or development of the pathological lesions observed in the CNS-related tissues of this patient. J. Med. Virol. 70: 14,19, 2003. © 2003 Wiley-Liss, Inc. [source] Incidence and significance of microscopic pathological lesions found in pedicle and recipient vessels used in microsurgical breast reconstructionMICROSURGERY, Issue 1 2003H.H. El-Mrakby M.D. The purpose of this study was to assess the incidence of abnormal vascular histology and to determine whether or not this was correlated with the incidence of postoperative microvascular problems. The microvascular histology of both donor and recipient vessels was studied in 38 patients (40 flaps) undergoing breast reconstruction with free TRAM flaps. Preoperative risk factors were assessed and correlated with histological changes in vessels, and both were tested against anastomotic complications. Thrombosis of either the artery or the vein of the flap was seen in 6 cases (15%), and of these, two flaps failed completely and one suffered partial necrosis. The occlusion affected the arterial anastomosis in 3 patients, and the venous anastomosis in 2 patients, while both the artery and the vein were thrombosed in one case. Preoperative risk factors such as smoking, obesity, radiotherapy, and chemotherapy were not associated with a significantly higher incidence of thrombosis or with significant histological abnormalities in vessels (P value varied between 0.3,0.06). Microvascular histology showed variable degrees of pathological changes in six flaps (15%); nevertheless, in this group, only one flap suffered a venous thrombosis, which ended in total flap loss. Among those with one or more risk factors (24 patients), only 2 had some evidence of histological abnormality of the blood vessels used for the microvascular anastomosis (P = 0.2). © 2003 Wiley-Liss, Inc. MICROSURGERY 23:6,9 2003 [source] Neuropathology of Alzheimer's DiseaseMOUNT SINAI JOURNAL OF MEDICINE: A JOURNAL OF PERSONALIZED AND TRANSLATIONAL MEDICINE, Issue 1 2010Daniel P. Perl MD Abstract Alois Alzheimer first pointed out that the disease which would later bear his name has a distinct and recognizable neuropathological substrate. Since then, much has been added to our understanding of the pathological lesions associated with the condition. The 2 primary cardinal lesions associated with Alzheimer's disease are the neurofibrillary tangle and the senile plaque. The neurofibrillary tangle consists of abnormal accumulations of abnormally phosphorylated tau within the perikaryal cytoplasm of certain neurons. The senile plaque consists of a central core of beta-amyloid, a 4-kD peptide, surrounded by abnormally configured neuronal processes or neurites. Other neuropathological lesions are encountered in cases of Alzheimer's disease, but the disease is defined and recognized by these 2 cardinal lesions. Other lesions include poorly understood changes such as granulovacuolar degeneration and eosinophilic rodlike bodies (Hirano bodies). The loss of synaptic components is a change that clearly has a significant impact on cognitive function and represents another important morphological alteration. It is important to recognize that distinguishing between Alzheimer's disease, especially in its early stages, and normal aging may be very difficult, particularly if one is examining the brains of patients who died at an advanced old age. It is also noted that instances of pure forms of Alzheimer's disease, in the absence of other coexistent brain disease processes, such as infarctions or Parkinson's disease,related lesions, are relatively uncommon, and this must be taken into account by researchers who employ postmortem brain tissues for research. Mt Sinai J Med 77:32&–42, 2010. © 2010 Mount Sinai School of Medicine [source] Cerebellar metabolic symmetry in essential tremor studied with 1H magnetic resonance spectroscopic imaging: Implications for disease pathologyMOVEMENT DISORDERS, Issue 6 2004Elan D. Louis MD Abstract The pathological basis for essential tremor (ET) is not known; however, metabolic changes in the cerebellum can be observed in positron emission tomography (PET) and 1H magnetic resonance spectroscopic imaging (MRSI) studies. Tremor is relatively symmetric in ET, suggesting that underlying metabolic changes could be also symmetric. The degree of metabolic asymmetry in the cerebellum, however, has not yet been studied in ET, and knowledge about distribution and laterality of metabolic changes might shed some light on basic disease mechanisms. We measured brain metabolism (N -acetylaspartate[NAA]/creatine [tCR]) to obtain an asymmetry index for cerebellar cortical metabolism ET patients compared with that in controls. This index, a percentage, was calculated as |(value right , value left)|/(value right + value left) × 100. Multislice 1H MRSI data were acquired for 20 patients and 11 controls. In ET patients, mean right and left cerebellar cortical NAA/tCR values were 1.61 ± 0.42 and 1.55 ± 0.38, respectively, compared with 1.81 ± 0.62 and 1.87 ± 0.49 in controls. The difference between right and left cerebellar cortical NAA/tCR was also calculated for each subject. In ET patients, the mean right-left difference was 0.14 ± 0.11, compared with 0.32 ± 0.27 in controls (P = 0.016). The mean cerebellar cortical asymmetry index was low in ET (8.8 ± 6.1%), one-half of that in controls (17.0 ± 13.7%, P = 0.027). These data suggest that pathological lesions in ET patients, which remain elusive, might be distributed similarly in each cerebellar cortex. Postmortem studies are needed to confirm these preliminary imaging results. © 2004 Movement Disorder Society [source] What does the study of the spatial patterns of pathological lesions tell us about the pathogenesis of neurodegenerative disorders?NEUROPATHOLOGY, Issue 1 2001Richard A Armstrong Discrete pathological lesions, which include extracellular protein deposits, intracellular inclusions and changes in cell morphology, occur in the brain in the majority of neurodegenerative disorders. These lesions are not randomly distributed in the brain but exhibit a spatial pattern, that is, a departure from randomness towards regularity or clustering. The spatial pattern of a lesion may reflect pathological processes affecting particular neuroanatomical structures and, therefore, studies of spatial pattern may help to elucidate the pathogenesis of a lesion and of the disorders themselves. The present article reviews first, the statistical methods used to detect spatial patterns and second, the types of spatial patterns exhibited by pathological lesions in a variety of disorders which include Alzheimer's disease, Down syndrome, dementia with Lewy bodies, Creutzfeldt,Jakob disease, Pick's disease and corticobasal degeneration. These studies suggest that despite the morphological and molecular diversity of brain lesions, they often exhibit a common type of spatial pattern (i.e. aggregation into clusters that are regularly distributed in the tissue). The pathogenic implications of spatial pattern analysis are discussed with reference to the individual disorders and to studies of neurodegeneration as a whole. [source] Specific association of small heat shock proteins with the pathological hallmarks of Alzheimer's disease brainsNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 2 2006M. M. M. Wilhelmus The small heat shock protein family (sHsp) comprises molecular chaperones able to interact with incorrectly folded proteins. Alzheimer's disease (AD) is characterized by pathological lesions such as senile plaques (SPs), cerebral amyloid angiopathy (CAA) and neurofibrillary tangles (NFTs), predominantly consisting of the incorrectly folded proteins amyloid-, (A,) and tau respectively. The aim of this study was to investigate the association of the chaperones Hsp20, HspB2, ,B-crystallin and Hsp27 with the pathological lesions of AD brains. For this purpose, a panel of well-characterized antibodies directed against these sHsps was used in immunohistochemistry and immunoblotting. We observed extracellular expression of Hsp20, Hsp27 and HspB2 in classic SPs, and Hsp20 expression in diffuse SPs. In addition, extracellular expression of HspB2 was observed in CAA. Both Hsp27 and ,B-crystallin were also observed in astrocytes associated with both SPs and CAA. Furthermore, none of the sHsps were observed in NFTs in AD brains. We conclude that specific sHsp species may be involved in the pathogenesis of either SPs or CAA in AD. [source] The causes of porotic hyperostosis and cribra orbitalia: A reappraisal of the iron-deficiency-anemia hypothesisAMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY, Issue 2 2009Phillip L. Walker Abstract Porosities in the outer table of the cranial vault (porotic hyperostosis) and orbital roof (cribra orbitalia) are among the most frequent pathological lesions seen in ancient human skeletal collections. Since the 1950s, chronic iron-deficiency anemia has been widely accepted as the probable cause of both conditions. Based on this proposed etiology, bioarchaeologists use the prevalence of these conditions to infer living conditions conducive to dietary iron deficiency, iron malabsorption, and iron loss from both diarrheal disease and intestinal parasites in earlier human populations. This iron-deficiency-anemia hypothesis is inconsistent with recent hematological research that shows iron deficiency per se cannot sustain the massive red blood cell production that causes the marrow expansion responsible for these lesions. Several lines of evidence suggest that the accelerated loss and compensatory over-production of red blood cells seen in hemolytic and megaloblastic anemias is the most likely proximate cause of porotic hyperostosis. Although cranial vault and orbital roof porosities are sometimes conflated under the term porotic hyperostosis, paleopathological and clinical evidence suggests they often have different etiologies. Reconsidering the etiology of these skeletal conditions has important implications for current interpretations of malnutrition and infectious disease in earlier human populations. Am J Phys Anthropol 2009. © 2009 Wiley-Liss, Inc. [source] Dynamics of bacterial growth and distribution within the liver during Salmonella infectionCELLULAR MICROBIOLOGY, Issue 9 2003Mark Sheppard Summary Salmonella enterica causes severe systemic diseases in humans and animals and grows intracellularly within discrete tissue foci that become pathological lesions. Because of its lifestyle Salmonella is a superb model for studying the in vivo dynamics of bacterial distribution. Using multicolour fluorescence microscopy in the mouse typhoid model we have studied the interaction between different bacterial populations in the same host as well as the dynamic evolution of foci of infection in relation to bacterial growth and localization. We showed that the growth of Salmonella in the liver results in the spread of the microorganisms to new foci of infection rather than simply in the expansion of the initial ones. These foci were associated with independently segregating bacterial populations and with low numbers of bacteria in each infected phagocyte. Using fast-growing and slow-growing bacteria we also showed that the increase in the number of infected phagocytes parallels the net rate of bacterial growth of the microorganisms in the tissues These findings suggest a novel mechanism underlying growth of salmonellae in vivo with important consequences for understanding mechanisms of resistance and immunity. [source] | ||||||||||||||||