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PubMed1997

LAD-1 is absent in a subset of junctional epidermolysis bullosa patients.

The anchoring filament protein LAD-1 has been recently identified as the target of autoantibodies in the acquired blistering disorder linear IgA bullous dermatosis. Because this protein appears to be involved in the process of dermal-epidermal cohesion, this study sought to determine the involvement of LAD-1 in the pathology of junctional epidermolysis bullosa (JEB). To this end, 44 patients with a variety of subtypes of JEB were analyzed by indirect immunofluorescence microscopy with antibodies to LAD-1, BP180, and laminin-5. We found that only patients with generalized atrophic benign epidermolysis bullosa (GABEB) contained LAD-1 defects. Of the 16 GABEB patients studied, 13 showed absent or greatly reduced expression of LAD-1 (including 2 patients with a peculiar interrupted staining pattern) and 3 patients showed defects of laminin-5 expression with normal LAD-1 expression. Patients who showed LAD-1 defects also showed abnormal expression of BP180. Keratinocytes were cultured from the skin of two GABEB patients and analyzed by indirect immunofluorescent microscopy. One culture demonstrated defects of BP180 and LAD-1 expression (which was also verified by radioimmunoprecipitation assay), and one culture showed decreased laminin-5 expression but normal BP180 and LAD-1 expression. Thus, these studies demonstrate that: (i) LAD-1 and BP180 are normally expressed in all subtypes of JEB except GABEB, (ii) the majority of GABEB patients show absent or near absent expression of both LAD-1 and BP180 but normal expression of laminin-5, and (iii) a smaller subset of GABEB patients show normal LAD-1 and BP180 expression but express persistent but reduced levels of laminin-5.

Autoantibodies↗

PubMed2026

Epidermolysis Bullosa Classification and Current Approach to Diagnosis.

Epidermolysis bullosa (EB) is a heterogeneous group of rare genodermatoses marked by skin fragility and bullae formation induced by minor trauma. Pathologic variants in at least 21 genes are associated with EB, grouped into four major subtypes based predominantly on the plane of cleavage within the skin. EB simplex is characterized by epidermal bullae formation and is due to gene mutations that affect epidermal proteins, most commonly keratin filaments. Junctional EB is due to gene mutations affecting proteins in the basement membrane zone, causing a split within the lamina lucida of the dermal-epidermal junction. Dystrophic EB is characterized by subepidermal bullae formation and is due to mutations in the gene encoding type VII collagen, which makes up the anchoring fibrils in the papillary dermis. Kindler EB is the rarest subtype and may be associated with cleavage at various levels within the skin due to a mutation in the FERMT1 gene causing defects in kindlin-1, a protein associated with integrins and focal adhesions. Because EB is such a heterogeneous disease, an understanding of genotype-phenotype correlations is necessary to help guide management. Traditionally, the first step in diagnosis was inducing a blister that was biopsied for immunofluorescence mapping. Currently, the gold standard for diagnosis is a blood sample or buccal swab for extraction of genomic DNA via next-generation sequencing, which can identify the exact causative gene. A diagnosis of EB is life altering for patients and families alike. A firm understanding of EB classification and initial diagnostic workup can help dermatologists feel empowered to support and counsel families.

Humans↗

PubMed1982

The language of paranoia.

In order to assess which of three current models is most useful in understanding paranoia, the authors applied computer speech content analysis to 55 patients--24 of whom were in four groups expressing paranoid delusions and 31 of whom were in four groups not expressing such delusions. The results delineated a semantic or verbal profile of paranoid self-presentation. This self-presentation is more identifiable than the effects of any other patient characteristic, even if the delusion is not discussed by the patient. The strength of the statistical evidence supports the model of paranoid delusions as a separate disease rather than as a subtype of schizophrenia or as a trait that exists on a spectrum from normality to pathology.

Adult↗

PubMed1991

Relations among clinical scales in schizophrenia.

OBJECTIVE: Clinical scales have become established as tools to quantify phenomenological features of schizophrenia. The goal of this study was to examine relations among the following: the Brief Psychiatric Rating Scale (BPRS), the Scale for the Assessment of Positive Symptoms, the Scale for the Assessment of Negative Symptoms, and the deficit-nondeficit classification. METHOD: Forty-seven patients with schizophrenia were recruited according to specific inclusion and exclusion criteria. The standardized assessment procedures were administered by a trained psychiatric research team. RESULTS: Examination of the BPRS showed that the patients had highest scores on the thought disorder factor and the symptoms specific to schizophrenia. Classification of patients as having the positive, negative, or mixed type of schizophrenia resulted in a finding of seven with the positive, seven with the negative, and 33 with the mixed type. The division of patients into those with the deficit syndrome (N = 29) and those without (N = 18) was related to symptom specificity and to positive and negative symptoms. Deficit syndrome patients had more symptoms specific to schizophrenia, fewer nonspecific symptoms, and, as expected, greater severity of negative symptoms. Cluster analysis revealed three clusters of patients: those with low negative symptom scores and high scores on specific symptoms (the majority were without the deficit syndrome); those with high scores on negative, positive, and specific symptoms (the majority had the deficit syndrome); and those with lower scores on specific symptoms and high scores on negative and positive symptoms (the majority had the deficit syndrome). CONCLUSIONS: The scales showed some overlap but also seemed to measure complementary aspects of the phenomenology of schizophrenia. Subtypes of patients identified by the combined use of these scales may differ in underlying pathology.

Cluster Analysis↗

PubMed1989

Correlates of positive and negative schizophrenic syndromes in Nigerian patients.

The two-syndrome concept of schizophrenia was investigated in a sample of 70 Nigerian schizophrenic patients. The positive and negative syndromes were studied in relation to demographic, historical, neurological and psychometric measures. The negative syndrome was associated with cognitive impairment, behavioural deterioration and left eye dominance, and also with poor pre-morbid educational achievement and longer length of current stay in hospital. The positive syndrome was unrelated to any of the independent variables. The two syndromes were not significantly related, supporting the view that they represent relatively independent dimensions of pathology. This provides further support for the validity of the Type I-Type II subtyping of schizophrenia in populations of patients from different cultural backgrounds, and suggests that the negative syndrome is related to the presence of neurodevelopmental deficits that possibly antedate the schizophrenic illness.

Adult↗

PubMed1988

Clinicopathologic correlations of cutaneous neuroendocrine Merkel cell carcinoma.

A study of 50 consecutive cases (22 men, 28 women; age range, 39 to 84 years; mean age, 65 years) of cutaneous neuroendocrine Merkel cell carcinoma (CNC), 39 of whom had a mean follow-up of 34 months, revealed that the prognostic significance of the histopathologic subtyping in trabecular, solid, and diffuse variants of CNC was not as important as the pathologic postsurgical staging in localized, regional, and extraregional disease. The overall mortality was 23.5%. None of the 19 patients with localized disease died of CNC, while 11% of the 24 patients with regional disease and all seven patients with extraregional disease at presentation died of CNC. A second primary malignancy was found to be associated with the CNC in 15% of the cases. The clinical course in patients with localized disease was favorable in spite of the high number of local recurrences. Also, the presence of regional metastases was not related to an unfavorable prognosis. In 68% of the cases the disease involved the lower limbs or girdle. In ten cases the overt exophytic presentation of primary CNC was replaced by the presence of tumor masses infiltrating the inguinal soft tissues with or without nodal involvement.

Adult↗

PubMed1991

Results of treatment of malignant germ cell tumors in 93 children: a report from the Childrens Cancer Study Group.

We report treatment results in 93 children entered on study from 1978 to 1984 with malignant germ cell tumors (MGCTs), excluding dysgerminoma and tumors of the testis or brain. The estimated 4-year survival and event-free survival (EFS) for all 93 patients were 54% and 49%, respectively. For 30 children with ovarian tumors, the estimated 4-year survival was 67% and EFS was 63%. For 63 children with nongonadal tumors, survival and EFS were 48% and 42%, respectively. The comparison of EFS between ovarian and nongonadal tumors was significant at P = .03. The treatment plan included a second-look surgical procedure after 18 weeks of chemotherapy. Over half of 36 patients evaluated as having a residual mass present immediately before second-look surgery had no malignant tumor after review of surgical specimens. Age greater than 11 years at diagnosis, incomplete removal of tumor at first surgery, and more than one structure or organ involved at diagnosis increased the risk for adverse event. The histologic subtype of the primary tumor was not related to outcome. Diagnosis was verified by independent pathologic review, and treatment was uniform. Seventeen percent of all registered patients (21 of 127) were excluded because of ineligible pathologic diagnoses; sixty percent (13 of 21) were immature teratomas.

Adolescent↗

PubMed2006

Therapeutic potential of novel selective drugs targeting nicotinic acetylcholine receptors.

The potential therapeutic benefit of nicotinic ligands in a variety of neurodegenerative pathologies involving the CNS has energized research efforts to develop nicotinic acetylcholine receptor (nAChR) subtype-selective ligands (Bencherif and Schmitt, 2005). In particular, there has been a concerted effort to develop nicotinic compounds with selectivity for CNS nAChRs as potential pharmaceutical tools in the management of these disorders. Clinical and experimental data demonstrate a central role for alpha7 and alpha4beta2 nAChRs in cognitive function, sensory processing, mood, and neuroprotection (Bencherif and Schmitt, 2005; Buccafusco et al., 2005). The development of safe alpha7-selective ligands has been hampered by their lack of discrimination with hERG channels and 5-HT3 receptors. We have developed a number of compounds that display nanomolar affinity to the alpha7 and/or the alpha4beta2 receptor. Investigation of alpha7 functional activity showed a full range of activities from antagonists to full agonists without any significant activity at the human 5-HT3 receptor, P450 isozymes, hERG channels, or in the AMES test. Our findings demonstrate that potent and highly selective nAChR ligands can be designed.

Animals↗

PubMed1999

[Cystic renal cell carcinoma diagnosed as a simple cyst preoperatively with incidental renal tumor: a case report].

A 54-year-old man visited our hospital with right incidentally-found renal tumor detected by ultrasonography. Computed tomography, magnetic resonance imaging and angiography showed a small tumor, 1.5 cm in size, at the upper portion and a simple cyst, 4 cm in size, at the lower pole of the right kidney. We enucleated the small tumor and aspirated the cyst with outer part resection of the cyst wall. Pathological findings of the tumor showed renal cell carcinoma, alveolar type, common type, clear cell subtype, G1, pT1, INF-alpha. Microscopic appearance of the excised cyst wall also revealed sheets of renal cell carcinoma inside the wall. Therefore, two weeks after the first operation, we performed right radical nephrectomy. The resected specimen had severe inflammation without any evidence of residual tumor. Eight months after the nephrectomy, no recurrence has occurred.

Carcinoma, Renal Cell↗

PubMed1991

[The clinico-morphological characteristics of thyroid cancer in a region of endemic goiter].

The study deals with the results of clinico-morphologic analysis of thyroid cancer in 351 patients who have been operated on in the Carpathian Mountain [correction of Prikarpatsky] region endemic for goiter over the period of 25 years. Certain peculiarities of thyroid cancer were established: relatively high occurrence of the disease, specific ratio of basic histologic subtypes, high frequency of early stage cases and regular concomitance of cancer with other thyroid pathologies. The importance of further studies into the epidemiology of thyroid cancer is emphasized.

Adenocarcinoma, Follicular↗

PubMed1997

[A case of chromophobe cell renal carcinoma].

We report a case of chromophobe cell renal carcinoma. A 59-year-old female was admitted to our hospital with asymptomatic gross hematuria. Abdominal computerized tomography showed an approximately 4 cm. minimally enhancing mass in the left kidney. Angiography revealed a hypovascular tumor in the left kidney. Under the diagnosis of renal cell carcinoma, left radical nephrectomy was performed. The cut surface of the tumor was beige in color with few foci of hemorrhage and necrosis. Microscopically, the tumor was composed of the cells with voluminous reticulated cytoplasm stained lightly with routine hematoxylin and eosin. Hale's colloidal iron staining demonstrated a positive cytoplasmic reaction. Pathological diagnosis was chromophobe cell renal carcinoma. Chromophobe cell renal carcinoma is a recently established subtype of renal cell carcinoma, which has rarely been reported in Japan.

Carcinoma, Renal Cell↗

PubMed1999

NCL-CD10-270: a new monoclonal antibody recognizing CD10 in paraffin-embedded tissue.

CD10 (CALLA) antigen is expressed in a wide variety of epithelial and nonepithelial tissues, but its most significant application is in the diagnosis and classification of certain types of malignant lymphoma and leukemia. CD10 is expressed in a high percentage of cases of acute lymphoblastic leukemia (ALL), follicular lymphoma, Burkitt's lymphoma, and some hematopoietic tumors. Although the antigen is not lineage specific, CD10 expression is widely used to define subgroups within B-ALL and is a useful tool for detecting the presence of leukemic blasts in the bloodstream. Currently available monoclonal antibodies to CD10 have been found to be effective only in fresh-frozen tissue and for techniques such as flow cytometry. We have used a recombinant protein corresponding to the whole of CD10 to generate a monoclonal antibody that is effective in paraffin-embedded tissue sections. We have used this antibody to assay for the presence of CD10 on a range of normal and pathological tissues. Strong staining was seen in lymphoid germinal centers, renal tubules, glomeruli, syncytiotrophoblast, hepatic parenchymal canaliculi, B-lineage ALL, follicle center cell lymphoma, and a proportion of cases of large-B-cell lymphoma. We believe that this antibody will be of value in the characterization of malignant lymphoma, in particular the differential diagnosis of small-B-cell lymphoma and subtyping of lymphoblastic leukemia, as well as the investigation of the significance of expression of CD10 in other normal and pathological tissues.

Animals↗

PubMedDate not supplied

Pathological changes in frontal cortex from biopsy to autopsy in Alzheimer's disease.

We evaluated the change in density of total senile plaques, plaque subtypes, and neurofibrillary tangles, from biopsy to autopsy in left frontal cortical sections from four patients with clinically typical Alzheimer's disease (AD). Comparisons were made on sections stained with modified Bielschowsky and Thioflavin S. In two cases, comparisons were also made on tissue stained with a monoclonal Alz-50 antibody and an antiserum to A beta (beta-amyloid protein). Despite a marked decline in mental status over several years of follow-up clinical evaluations, there was no consistent significant change in numerical density of plaques or tangles among the four cases. However, we did find fewer primitive plaques in the autopsy specimens. These results from longitudinally evaluated persons with typical AD suggest that although plaques and tangles may serve as adequate markers of the presence of AD, their numerical density within a single neocortical region may not reflect dementia severity. This conclusion supports the results of recent cross-sectional studies on the progression of pathology among persons with AD.

Alzheimer Disease↗

PubMed2005

Cognitive differences in dementia patients with autopsy-verified AD, Lewy body pathology, or both.

OBJECTIVE: To examine the neuropsychological profile of dementia patients from a community-based autopsy sample of dementia, comparing Alzheimer disease (AD), Lewy body pathology (LBP) alone, and LBP with coexistent AD (AD/LBP). METHODS: The authors reviewed 135 subjects from a community-based study of dementia for whom autopsy and brain tissue was available. Diagnostic groups were determined according to standard neuropathologic methods and criteria, and the presence of LBs was determined using alpha-synuclein immunostaining. Neuropathologically defined diagnostic groups of AD, AD/LBP, and LBP were examined for differences on neuropsychological test performance at the time of initial study enrollment. RESULTS: There were 48 patients with AD alone, 65 with LB and AD pathology (AD/LBP), and 22 with LBP alone (LBP alone). There were no significant differences between groups demographically or on performance of enrollment Mini-Mental State Examination (MMSE) or Dementia Rating Scale (DRS). AD patients performed worse than the LBP patients on memory measures (Fuld Object Memory Evaluation Delayed Recall, Wechsler Memory Scale Logical Memory Immediate and Delayed Recall; p < 0.05) and a naming task (Consortium to Establish a Registry for Alzheimer's Disease Naming; p < 0.05). LBP patients were more impaired than AD patients on executive function (Trail Making Test Part B; p < 0.05) and attention tasks (Wechsler Adult Intelligence Scale-Revised Digit Span; p < 0.05). Decline in MMSE and DRS scores over time were greatest in the patients with AD/LBP. CONCLUSIONS: In a community-based sample of older, medically complicated patients with dementia, there are neuropsychological differences between dementia subtypes at the time of diagnosis. In particular, patients with Alzheimer disease (AD) alone and AD/Lewy body pathology (LBP) had more severe memory impairment than patients with LBP. LBP alone was associated with more severe executive dysfunction. Patients with AD/LBP had the most rapid rate of cognitive decline.

Age of Onset↗

PubMed2003

Increased prevalence of platelet glycoprotein IIb/IIIa PLA2 allele in ischaemic stroke associated with large vessel pathology.

INTRODUCTION: Platelet glycoprotein IIb/IIIa is a membrane receptor with a central function in the platelet adhesion and ultimately in the thrombus formation. Two major variants of the gene encoding the IIIa subunit, called PLA1 (A1) and PLA2 (A2), have been identified in the general population. There are indications that the A2 allele can also be associated with acute thrombosis or stroke. The purpose of this study was to study the distribution of the A2 allele in different vascular subtypes of stroke disease. MATERIALS AND METHODS: A total of 638 consecutive patients were analyzed and classified as having large vessel pathology (n=168) or a small vessel infarct (n=210). Localization of the vascular occlusions was deducted from analysis of the magnetic resonance imaging (MRI) scan results in stroke patients. The remainder patients were listed into a mixed vascular pathology group (n=167). Patients with other or poorly characterized stroke etiology were excluded from the study (n=93). RESULTS: In the small vessel and mixed vascular pathology groups, the PLA2 allele frequency was similar to that in the controls. By contrast, PLA2 allele frequency was approximately two-fold higher in patients with large vessel pathology (23.3%) than in the stroke-free control subjects (11.7%, p<0.0005). Multivariate logistic regression analysis of data confirmed this association with an odds ratio (OR) of 2.9 (95% confidence interval [CI]: 1.6-4.9, p<0.0005). CONCLUSIONS: These data suggest that the PLA2 allele is more frequent in brain infarcts associated with large-vessel occlusion.

Adult↗

PubMed2001

Synergism between vascular endothelial growth factor and placental growth factor contributes to angiogenesis and plasma extravasation in pathological conditions.

Vascular endothelial growth factor (VEGF) stimulates angiogenesis by activating VEGF receptor-2 (VEGFR-2). The role of its homolog, placental growth factor (PlGF), remains unknown. Both VEGF and PlGF bind to VEGF receptor-1 (VEGFR-1), but it is unknown whether VEGFR-1, which exists as a soluble or a membrane-bound type, is an inert decoy or a signaling receptor for PlGF during angiogenesis. Here, we report that embryonic angiogenesis in mice was not affected by deficiency of PlGF (Pgf-/-). VEGF-B, another ligand of VEGFR-1, did not rescue development in Pgf-/- mice. However, loss of PlGF impaired angiogenesis, plasma extravasation and collateral growth during ischemia, inflammation, wound healing and cancer. Transplantation of wild-type bone marrow rescued the impaired angiogenesis and collateral growth in Pgf-/- mice, indicating that PlGF might have contributed to vessel growth in the adult by mobilizing bone-marrow-derived cells. The synergism between PlGF and VEGF was specific, as PlGF deficiency impaired the response to VEGF, but not to bFGF or histamine. VEGFR-1 was activated by PlGF, given that anti-VEGFR-1 antibodies and a Src-kinase inhibitor blocked the endothelial response to PlGF or VEGF/PlGF. By upregulating PlGF and the signaling subtype of VEGFR-1, endothelial cells amplify their responsiveness to VEGF during the 'angiogenic switch' in many pathological disorders.

Animals↗

PubMed2006

Cyclooxygenase inhibition in early onset of tumor growth and related angiogenesis evaluated in EP1 and EP3 knockout tumor-bearing mice.

It is well established that prostanoids are essential for local inflammation including cell proliferation and apoptosis. Accordingly, prostaglandin E2 (PGE(2)) is a critical factor in wound healing, tumor invasiveness and progression. Therefore, the aim of the present work was to evaluate effects by PGE(2) on tumor vascular density at early onset of tumor growth where hypoxia is limited. Wild-type mice (C57Bl, C3H/HeN) bearing either MCG-101 tumors or a malignant melanoma (K1735-M2) with either high or insignificant PGE(2) production and subsequently different in sensitivity to cyclooxygenase (COX) inhibition were used. Tumor angiogenesis was estimated by intravital microscopy and immune histochemical analysis in wild type and EP(1) or EP(3) subtype receptor knockout mice (C57Bl). Both MCG-101 and K1735-M2 tumor cells stimulated early outgrowth of tumor vessels in proportion to intrinsic growth rate of tumor cells. Indomethacin had no effects on tumor growth or tumor related vascular area in K1735-M2 bearing mice. By contrast, indomethacin decreased tumor cell proliferation and increased apoptosis in MCG-101 tumors with subsequent adaptation in tumor vascular density. Effects of indomethacin on early growth of MCG-101 tumors were not related to tumor content of bFGF protein, while our earlier studies on long-term tumor growth have shown decreased mRNA levels of bFGF during indomethacin treatment. Early onset of tumor growth was significantly promoted in EP(3)- but not in EP(1)-knockouts, although long-term tumor growth is attenuated in EP(1)-knockouts as reported elsewhere. Our results demonstrate that tumor production of PGE(2) promotes primarily net growth of tumor cells with subsequent adaptations in development of the tumor vasculature. Therefore, it is likely that angiogenesis is not a limiting step at the early onset of tumor growth.

Animals↗

PubMed2001

Characterization of group X phospholipase A(2) as the major enzyme secreted by human keratinocytes and its regulation by the phorbol ester TPA.

HaCaT as well as human primary keratinocytes constitutively expressed mRNA of the human secreted phospholipase A(2) subtype groups X, V, IIA, and IID. A similar expression pattern was also found in human skin biopsies. Protein analysis showed that under serum-free conditions only group X secreted phospholipase A(2) is secreted into cell culture supernatants of HaCaT as well as human primary keratinocytes, whereas the other secreted phospholipases A(2) were not detectable at protein level. HaCaT keratinocytes constitutively released secreted phospholipase A(2) activity into the cell culture supernatant, being reflected by a constant release of fatty acids. The phorbol ester 12-O-tetradecanoylphorbol-13-acetate, which is a potent inducer of inflammation in skin, drastically reduced the mRNA level of group X secreted phospholipase A(2) and other secreted phospholipase A(2) subtypes as well as secreted phospholipase A(2) activity in cell culture supernatants. This suggests that inhibition of secreted phospholipase A(2) expression and activity as well as of fatty acid release by 12-O-tetradecanoylphorbol-13-acetate treatment might be a critical step impairing the integrity of the epidermis during phorbol-ester-induced pathologic processes in skin. The results show that group X secreted phospholipase A(2) represents the major secreted phospholipase A(2) subtype in human keratinocytes and thus may indicate a physiologic role for this enzyme in epidermis in vivo.

Blotting, Western↗