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At least 1,387 records · Page 77Linked to original sources

PubMed2005

Oculomotor nerve schwannoma mimicking ophthalmoplegic migraine.

Ophthalmoplegic migraine (OM) is a rare variant of migraine characterized by recurrent attacks of severe headache followed by oculomotor nerve palsy. The recent revision of the International Headache Classification has reclassified OM from a subtype of migraine, defined as a functional headache, to the neuralgia category. We describe a case of an 11-year-old girl with pathologically confirmed oculomotor nerve schwannoma who had been suffering from symptoms mimicking OM. For five years, she has been under treatment for OM, an initial diagnosis which was corroborated by brain magnetic resonance imaging (MRI). Usually, most OM attacks occur during one period in a lifetime and remit completely. In contrast, however, her attacks became more frequent and were not controlled by medication. After surgery, the frequency of OM attacks was reduced. From this experience, we hypothesize that optic nerve tumor is one condition that can mimic OM, without apparent signs suggestive of intracranial mass. To our knowledge, this is the first report to describe a pathologically confirmed case of oculomotor nerve schwannoma mimicking OM.

Child↗

PubMed1988

Studies on subtype "d" biliary atresia.

Nine cases of specific type (subtype d) biliary atresia were experienced at the Tohoku University Hospital and were classified into three groups on the basis of their clinical and pathological findings. Group 1 cases were defined as cases showing obstruction on the side of the hepatic duct and cystic dilatation, communicating with the gallbladder, in the common bile duct. Group 2 cases were those showing dilatation similar to Group 1, but measuring less than 20 mm, the dilated part being covered with thick connective tissue. Group 3 cases were those showing isolated dilatation in the common hepatic duct or the common bile duct and having no communication with the gallbladder. The postoperative course was good in Group 1 patients, while jaundice was prolonged in Group 2 patients. In Group 3, jaundice disappeared in one patient who died later, while the other patient showed recurrence of slight jaundice.

Bile Ducts↗

PubMed2003

Host prostaglandin E(2)-EP3 signaling regulates tumor-associated angiogenesis and tumor growth.

Nonsteroidal antiinflammatories are known to suppress incidence and progression of malignancies including colorectal cancers. However, the precise mechanism of this action remains unknown. Using prostaglandin (PG) receptor knockout mice, we have evaluated a role of PGs in tumor-associated angiogenesis and tumor growth, and identified PG receptors involved. Sarcoma-180 cells implanted in wild-type (WT) mice formed a tumor with extensive angiogenesis, which was greatly suppressed by specific inhibitors for cyclooxygenase (COX)-2 but not for COX-1. Angiogenesis in sponge implantation model, which can mimic tumor-stromal angiogenesis, was markedly suppressed in mice lacking EP3 (EP3(-/-)) with reduced expression of vascular endothelial growth factor (VEGF) around the sponge implants. Further, implanted tumor growth (sarcoma-180, Lewis lung carcinoma) was markedly suppressed in EP3(-/-), in which tumor-associated angiogenesis was also reduced. Immunohistochemical analysis revealed that major VEGF-expressing cells in the stroma were CD3/Mac-1 double-negative fibroblasts, and that VEGF-expression in the stroma was markedly reduced in EP3(-/-), compared with WT. Application of an EP3 receptor antagonist inhibited tumor growth and angiogenesis in WT, but not in EP3(-/-). These results demonstrate significance of host stromal PGE(2)-EP3 receptor signaling in tumor development and angiogenesis. An EP3 receptor antagonist may be a candidate of chemopreventive agents effective for malignant tumors.

Animals↗

PubMed2006

Kidney-specific gene targeting: insight into thiazolidinedione-induced fluid retention.

Conditional gene targeting technique, which is based on the use of Cre-loxP or Flp/FRT systems, has been increasingly used to study gene function of a particular cell type in vivo. The introduction of this technique to the kidney field is relatively recent but has already provided important insights into physiological or pathological functions of a number of genes in the kidney. This technique has recently been used to inactivate the peroxisome proliferator-activated receptor subtype gamma in the collecting duct, which leads to remarkable blockade of body weight gains and plasma volume expansion associated with thiazolidinediones. This finding not only helps understand pharmacology of the novel class of antidiabetic drugs, but also uncovers an important role of peroxisome proliferator-activated receptor subtype gamma in regulation of distal nephron fluid reabsorption. The present review represents an example for the use of the modern technique to address complex clinical problems. It is anticipated that over next few years this technique will be used by an increasing number of investigators for studying gene function in the kidney.

Animals↗

PubMed2003

Cancer-associated immunodeficiency and dendritic cell abnormalities mediated by the prostaglandin EP2 receptor.

Prostaglandin E(2) (PGE(2)), a major COX metabolite, plays important roles in several facets of tumor biology. We characterized the contribution of the PGE(2) EP2 receptor to cancer-associated immune deficiency using EP2(-/-) mice. EP2(-/-) mice exhibited significantly attenuated tumor growth and longer survival times when challenged with MC26 or Lewis lung carcinoma cell lines as compared with their wild-type littermates. While no differences in T cell function were observed, PGE(2) suppressed differentiation of DCs from wild-type bone marrow progenitors, whereas EP2-null cells were refractory to this effect. Stimulation of cells in mixed lymphocyte reactions by wild-type DCs was suppressed by treatment with PGE(2), while EP2(-/-)-derived DCs were resistant to this effect. In vivo, DCs, CD4(+), and CD8(+) T cells were significantly more abundant in draining lymph nodes of tumor-bearing EP2(-/-) mice than in tumor-bearing wild-type mice, and a significant antitumor cytotoxic T lymphocyte response could be observed only in the EP2(-/-) animals. Our data demonstrate an important role for the EP2 receptor in PGE(2)-induced inhibition of DC differentiation and function and the diminished antitumor cellular immune responses in vivo.

Animals↗

PubMed1997

Differential expression of the fibroblast growth factor receptor (FGFR) multigene family in normal human adult tissues.

This report describes a systematic analysis of the expression of the fibroblast growth factor receptor (FGFR) multigene family (FGFR1, FGFR2, FGFR3, and FGFR4) in archival serial sections of normal human adult tissues representing the major organ systems, using immunohistochemical techniques. Polyclonal antisera specific for FGFR1, FGFR2, FGFR3, and FGFR4 and a three-stage immunoperoxidase technique were employed to determine the cellular distribution of these receptors at the protein level. The expression profiles for the tissue-specific cellular localization of the FGFR multigene family demonstrated wide-spread and striking differential patterns of expression of individual receptors in the epithelia and mesenchyme of multiple tissues (stomach, salivary glands, pancreas, thymus, ureter, and cornea) and co-expression of FGFR1-4 in the same cell types of other tissues. The wide-spread expression of FGFR1-4 in multiple organ systems suggests an important functional role in normal tissue homeostasis. Differences in the spatial patterns of FGFR gene expression may generate functional diversity in response to FGF-1 and FGF-2, both of which bind with equally high affinity to more than one receptor subtype. In vivo, this may lead to functional differences that are crucial for the regulation of normal physiological processes and are responsible for the pathological mechanisms that orchestrate various disease processes.

Adult↗

PubMed1989

Numbers of host "helper" T cells and proliferating cells predict survival in diffuse small-cell lymphomas.

Diffuse small-cell lymphomas of B-lineage comprise a group of immunophenotypically related lymphoid malignancies that display variable clinical aggressiveness. We compared a variety of clinical, pathologic, and immunologic characteristics of 64 B-lineage diffuse small-cell lymphomas to patient survival in an effort to define prognostically relevant subtypes of these neoplasms. Neither clinical parameters nor histological subclassification correlated with patient outcome. In contrast, three immunologic features of these lymphomas showed a statistically significant relationship with actuarial survival. Neoplasms that manifested greater than or equal to 25% Ki-67+ cells (proliferation-associated antigen), less than 25% Leu 4+ cells (pan-T antigen), or less than 15% Leu 3+ cells (helper/inducer T-subset antigen) were associated with significantly decreased patient survival as compared to neoplasms with the reverse phenotype (P = .02, P = .003, P = .0005, respectively). Leu 3 findings were of particular importance in initial biopsies (P = .0007), while the Ki-67 findings were significant regardless of time of biopsy (P = .01 for biopsies at diagnosis and P = .004 for other biopsies). These data indicate that immunologic analysis can demonstrate subsets of diffuse small-cell lymphoma with different biologic potential, and suggest that such analysis be included in the routine work-up of patients with this type of neoplasm.

Adult↗

PubMed1992

"Central" and "peripheral" benzodiazepine receptors: opposite changes in human epileptogenic tissue.

We measured the density of two benzodiazepine (BZ) receptor subtypes in neurosurgically obtained hippocampal tissue from the seizure focus of patients with temporal lobe epilepsy (TLE) showing mesial temporal sclerosis, the most common pathologic finding in TLE. We performed quantitative in vitro receptor autoradiography with [125I]Ro 16-0154, a probe for the central-type BZ receptor and with [3H]PK 11195, a probe for the peripheral-type BZ receptor. In comparison with autopsy and neurosurgical control groups, patients with mesial temporal sclerosis had regionally selective decreased central-type and increased peripheral-type BZ receptors. These changes paralleled regional losses of neurons and proliferation of glia. Decreases of the inhibitory central-type BZ receptor may be a component of the enhanced excitability of the seizure focus and also may allow localization of the focus by in vivo neuroreceptor imaging. Single photon emission computed tomography (SPECT) imaging of two TLE patients with [123I]Ro 16-0154 suggests that this technique may provide a more sensitive means of localizing the seizure focus than current imaging methods relying on changes in blood flow or glucose metabolism.

Adult↗

PubMed1996

Delayed emergence of a parkinsonian disorder in 38% of 29 older men initially diagnosed with idiopathic rapid eye movement sleep behaviour disorder.

We report longitudinal data on a group of 29 male patients 50 years of age or older who were initially diagnosed as having idiopathic REM sleep behavior disorder (RBD) after extensive polysomnographic and neurologic evaluations. Thirty-eight percent (11/29) were eventually diagnosed as having a parkinsonian disorder (presumably Parkinson's disease) at a mean interval of 3.7 +/- 1.4 (SD) years after the diagnosis of RBD+, and at a mean interval of 12.7 +/- 7.3 years after the onset of RBD. To date, only 7% (2/29) of patients have developed any other neurologic disorder. At the time of RBD diagnosis, data from the RBD group with eventual Parkinson's disease (n = 11) and the current idiopathic RBD group (n = 16) were indistinguishable, with two exceptions: the RBD-Parkinson's disease group had a significantly elevated hourly index of periodic limb movements of non-REM sleep and an elevated REM sleep percentage. RBD was fully or substantially controlled with nightly clonazepam treatment in 89% (24/27) of patients in both groups. Thus, RBD can be the heralding manifestation of Parkinson's disease in a substantial subgroup of older male RBD patients. However, a number of presumed Parkinson's disease patients may eventually be diagnosed with multiple system atrophy (striatonigral degeneration subtype). Our findings indicate the importance of serial neurologic evaluations after RBD is diagnosed and implicate the pedunculopontine nucleus as a likely site of pathology in combined RBD-Parkinson's disease, based on experimental and theoretical considerations rather than on autopsy data.

Brain↗

PubMed2001

Neuropathology of Pick's disease.

The author reviews the gross, microscopic, and biochemical pathology associated with classic Pick's disease, as defined by Constantinidis' Type A Pick's disease. This is contrasted with other Pick's disease subtypes, including Constantinidis' Type B (corticobasal degeneration) and Type C (dementia lacking distinctive histology).

Atrophy↗

PubMed2001

Transdifferentiation in neoplastic development and its pathological implication.

Transdifferentiation is a process in which a cell committed to a particular specialization changes to another quite distinct type. It occurs during embryological development and some pathological processes, and causes the tumor cells to express a phenotype different from that of their normal progenitors. Neoplastic transdifferentiation involves pathogenesis of cancer subtype, transition between neoplastic epithelia and neuroendocrine cell, transition between neoplastic epithelia and mesenchyme, as well as transition between non-neuroectodermal and neuroectodermal cells. We propose that differentiation disturbance of cancer cells should include not only lower-, un-, or de-differentiation, but also transdifferentiation. Tumor cell transdifferentiation results from genetic instabilities. In some type of neoplastic transition, the initiation may be induced by extracellular matrix and growth factors.

Animals↗

PubMed2004

Ion channels in drug discovery and development.

An excellent meeting on ion channels in drug discovery and development was organised by the Strategic Research Institute. Recent progress in the molecular and cellular biology of ion channels, their localisation and their physio-pathological roles, was presented by a selected number of academic researchers. The status of development, by pharmaceutical companies, of drugs targeting specific ion channel subtypes (e.g., AMPA receptors, nicotinic receptors, GABA(A) receptors, K(+) channels, transient receptor potential channels) and with different modalities (agonists versus potentiators) was reviewed. More comparative data on the emerging ion channel screening technologies are now available and were shared in a number of presentations. Finally, cardiac ion channel liability, in the context of drug discovery and development, was thoroughly discussed.

Animals↗

PubMed2005

A stochastic two-dimensional model of intercellular Ca2+ wave spread in glia.

We describe a two-dimensional stochastic model of intercellular Ca(2+) wave (ICW) spread in glia that includes contributions of external stimuli, ionotropic and metabotropic P2 receptors, exo- and ecto-nucleotidases, second messengers, and gap junctions. In this model, an initial stimulus evokes ATP and UTP release from a single cell. Agonists diffuse and are degraded both in bulk solution and at cell surfaces. Ca(2+) elevation in individual cells is determined by bound agonist concentrations s and by number and features of P2 receptors summed with that generated by IP(3) diffusing through gap junction channels. Variability of ICWs is provided by randomly distributing a predetermined density of cells in a rectangular grid and by randomly selecting within intervals values characterizing the extracellular compartment, individual cells, and interconnections with neighboring cells. Variability intervals were obtained from experiments on astrocytoma cells transfected to express individual P2 receptors and/or the gap junction protein connexin43. The simulation program (available as Supplementary Material) permits individual alteration of ICW components, allowing comparison of simulations with data from cells expressing connexin43 and/or various P2 receptor subtypes. Such modeling is expected to be useful for testing phenomenological hypotheses and in understanding consequences of alteration of system components under experimental or pathological conditions.

Adenosine Triphosphate↗

PubMed2000

Immune deficiency in mouse models for inherited peripheral neuropathies leads to improved myelin maintenance.

The adhesive cell surface molecule P(0) is the most abundant glycoprotein in peripheral nerve myelin and fulfills pivotal functions during myelin formation and maintenance. Mutations in the corresponding gene cause hereditary demyelinating neuropathies. In mice heterozygously deficient in P(0) (P(0)(+/-) mice), an established animal model for a subtype of hereditary neuropathies, T-lymphocytes are present in the demyelinating nerves. To monitor the possible involvement of the immune system in myelin pathology, we cross-bred P(0)(+/-) mice with null mutants for the recombination activating gene 1 (RAG-1) or with mice deficient in the T-cell receptor alpha-subunit. We found that in P(0)(+/-) mice myelin degeneration and impairment of nerve conduction properties is less severe when the immune system is deficient. Moreover, isolated T-lymphocytes from P(0)(+/-) mice show enhanced reactivity to myelin components of the peripheral nerve, such as P(0), P(2), and myelin basic protein. We hypothesize that autoreactive immune cells can significantly foster the demyelinating phenotype of mice with a primarily genetically based peripheral neuropathy.

Animals↗

PubMed2000

Radiologic features of pediatric thalamic and hypothalamic tumors.

A variety of histologic subtypes of tumor may affect the thalamus and the hypothalamus in the pediatric population. These tumors have radiologic features that are useful in predicting pathology. We discuss the radiologic findings of childhood thalamic and hypothalamic tumors and provide imaging examples.

Adolescent↗

PubMed2002

Cyclooxygenase 2- and prostaglandin E(2) receptor EP(2)-dependent angiogenesis in Apc(Delta716) mouse intestinal polyps.

To investigate angiogenesis during intestinal polyp development, we determined the microvessel density (MVD) in polyps of Apc knockout (Apc(Delta716)) mice, a model for human familial adenomatous polyposis. We scored MVD also in several compound mutants carrying Apc(Delta716), namely, mice with an additional mutation in Smad4, in which the polyps progress into invasive adenocarcinomas; mice with a cyclooxygenase (COX)-2 gene (Ptgs2) mutation, in which adenoma growth is suppressed; and mice with prostaglandin E(2) EP receptor gene mutations. In both simple Apc(Delta716) and compound Apc(Delta716) Smad4 mutants, MVD increased in a polyp size-dependent manner only in the polyps expanded beyond a threshold of about 1 mm in diameter. These results indicate that tumor angiogenesis is stimulated only after tumors grow to a certain size, and this angiogenic switch is common to both benign adenomas and malignant adenocarcinomas. In Apc(Delta716) polyposis attenuated by the COX-2 gene mutation, in contrast, MVD did not increase even in polyps larger than 1 mm. The same phenomenon was observed in the compound mutant mice with Apc(Delta716) and the EP(2) receptor gene mutations, but not in other EP compound mutants. We also immunohistochemically studied COX-2 and angiogenic factors, vascular endothelial growth factor and basic fibroblast growth factor. Interestingly, expression of these proteins was also increased in polyps larger than 1 mm. These results suggest that, in both benign and malignant mouse intestinal tumors, stromal expression of COX-2 results in elevated prostaglandin E(2) levels that stimulate cell surface receptor EP(2), followed by induction of vascular endothelial growth factor that causes tumor angiogenesis.

Adenocarcinoma↗

PubMed2001

[Cytopathology--current trends].

Modern imaging techniques help to detect minute tumours, even in remote locations of the body. This increases the demand to sample cellular material by minimal invasive procedures, such as fine needle aspiration (FNA). For optimal treatment, tumour cells should be characterized for prognostically relevant features. Primary and metastatic neoplasms, and individual disseminated cells of solid tumours are targets for FNA and exfoliative cytology. Recognition and typing of tumour cells is aided by immunochemistry and PCR based molecular studies. Especially immunostaining requires laboratory procedures adapted to cytology samples. Screening for precancerous lesions, highly successful in cervical cancer prevention, extends into areas such as bladder and lung cancer in selected patient groups. Cell image analysis, especially for DNA ploidy, and chromosomal FISH of interphase cells can have predictive value enhancing the information derived from the purely morphologic assessment. Prognostic tumour cell markers are studied using immunochemistry and PCR on cytological material. Cytology has to foster translational research and test the results from molecular cytogenetics, including comparative genomic hybridisation (CGH) and cDNA microarray techniques on dissociated solid tumour cells. Newly identified genetic abnormalities can be evaluated for their functional relevance and may correlate with distinct structural alterations of the tumour cells. Proper training, dedication to diagnostic cytologic work and molecular studies, and sufficient staffing will enable cytology to get the most for the patient out of limited cell material. This approach helps to distinguish genetically defined tumour subtypes by recognizing properties of the cell gestalt.

Biopsy, Needle↗

PubMed2003

Effects of leukocyte depletion filters on matrix metalloproteinase activation in an extracorporeal circulation circuit.

Matrix metalloproteinases (MMPs) are a family of endopeptidases that function to remodel tissue during both normal physiology and pathology. Research performed by the Medical University of South Carolina found an increased release of several MMP species during cardiopulmonary bypass (CPB), including the subtype MMP-9, but whether and to what degree the extracorporeal circulation circuit (ECC) induces the release of MMPs has yet to be determined. Human bank whole blood scheduled for discard was obtained and exposed to an ECC. The first set of studies (N = 8) was performed with a loop circuit using a standard arterial line filter. A leukoreduction filter was incorporated during the first 30 min of the pump run for the second set of trials; the leukoreduction filter was then bypassed and a standard arterial filter used for the remaining 60 minutes on pump (N = 8). Blood samples were drawn at four time points for analysis (baseline, 30, 60, and 90 min). Data were analyzed using repeated measures analysis of variance with between-subjects factors, and a p value of less than .1 was considered statistically significant. The MMP-9 level increased by 130.44% at 90 min on pump in the standard arterial filter group and decreased by 34.62% at 90 min on pump in the leukoreduction group. There was a significant difference between the baseline MMP-9 level and the MMP-9 concentrations at 30, 60, and 90 min for both groups (p = .0348); there was a significant difference in MMP-9 levels between the two filter groups (p = .0611). The present study found a significant increase in MMP-9 levels when blood was exposed to an ECC with a standard arterial filter. The use of a leukoreduction filter significantly reduced MMP-9 concentrations as compared to baseline levels in this study. Leukocyte depletion filtration may serve to benefit CPB patients by attenuating the inflammatory response and disrupting pathways that govern such mediators as the MMPs.

Enzyme Activation↗