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PubMed2006

Effects of group I metabotropic glutamate receptors blockade in experimental models of Parkinson's disease.

The present study was devoted to investigate the effects of the metabotropic glutamate receptor(mGluR)5 antagonist [(2-methyl-1,3-thiazol-4-yl)ethynyl]pyridine (MTEP) and the mGluR1 antagonist, (3-ethyl-2-methyl-quinolin-6-yl)-(4-methoxy-cyclohexyl)-methanone methanesulfonate (EMQMCM), in animal studies indicative of antiparkinsonian-like activity such as haloperidol-induced catalepsy, hypoactivity in open field following haloperidol, and rotation in rats with unilateral 6-hydroxydopamine(OHDA)-induced lesions of the midbrain dopaminergic system (alone and in combination with L-DOPA). Moreover, antidyskinetic activity of different mGluR ligands was evaluated in the rat model of L-DOPA-induced dyskinesia. Both MTEP (5 mg/kg) and EMQMCM (4 mg/kg) slightly inhibited haloperidol (0.5 mg/kg)-induced catalepsy. However, neither substance reversed the hypoactivity produced by haloperidol (0.2 mg/kg). Although MTEP did not produce significant turning, it inhibited contralateral rotations after L-DOPA (at 5 mg/kg) and alleviated L-DOPA-induced dyskinesia (at 2.5 and 5 mg/kg) in 6-OHDA-lesioned rats. In contrast, mGluR1 antagonists EMQMCM and RS-1-aminoindan-1,5-dicarboxylic acid (AIDA) failed to modify L-DOPA-induced dyskinesia. The results of the present study suggest that either subtype of group I of mGluRs may be involved in the pathologically altered circuitry in the basal ganglia. However, the equivocal results do not strongly support the hypothesis that mGluR1 and mGluR5 antagonists may be beneficial in the symptomatic treatment of Parkinson's disease. However, mGluR5 antagonists may prove useful for the symptomatic treatment of L-DOPA-induced dyskinesia.

Analysis of Variance↗

PubMed2006

Liposarcoma of the colon: a case report and review of literature.

Liposarcoma is a malignant mesenchymal tumor frequently located in the retroperitoneum and rarely presents as an isolated lesion in the colon. To our knowledge, only three cases of primary colon liposarcoma have been reported in the world literature to date. In this article, we report a case of liposarcoma of the colon in a 46-year-old man. The patient presented with abdominal pain and a palpable mass. Abdominal ultrasonography and computed tomogram confirmed the presence of a large intra-abdominal fatty tissue mass, but the colon origin of the tumor was revealed only on laparotomy. During surgery, a voluminous (12 cm x 11 cm x 10 cm) lesion situated in the subserosa of the ascending colon was found, and a right hemicolectomy with radical lymph node dissection was performed. The pathological diagnosis of the resected tumor revealed primary colon liposarcoma (myxoid subtype). The postoperative course was uneventful, and the patient remained free of disease for 12 months. No adjuvant therapy was performed. Diagnostic and therapeutic problems related to this type of neoplasm as well as literature reviews are reported. Curative R0 resection remains the main treatment for primary and recurrent liposarcomas.

Colonic Neoplasms↗

PubMed2006

Can MRI reveal phenotypes of multiple sclerosis?

The multicontrast capability of magnetic resonance imaging (MRI) is discussed in its role in the search for phenotypes of multiple sclerosis (MS). Aspects of MRI specificity, putative markers for pathogenetic components of disease and issues of spatial and temporal distribution are discussed. While particular reference is made to MS, the concepts apply to common pathological features of many neurologic diseases and to neurodegenerative disease in general. The assessment and dissociation of disease activity and disease severity, as well as the combination of varied metrics for the purposes of inferential and predictive disease modeling, are explored with respect to biomarkers and clinical outcomes. By virtue of its noninvasive nature and multicontrast capabilities depicting multiple facets of MS pathology, MRI lends itself to the systematic search of pathogenetically distinct subtypes of MS in large populations of patients. In conjunction with clinical, immunological, serological and genetic information, clusters of MS patients with distinct clinical prognosis and diverse response profiles to available and future treatments may be identified.

Cluster Analysis↗

PubMed2005

In vitro characterization of novel NR2B selective NMDA receptor antagonists.

N-Methyl-D-aspartate (NMDA) subunit specific receptor antagonism has potential therapeutic application for multiple CNS pathologies. MERCK 1, MERCK 2, and MERCK 3 are novel NR2B subtype selective NMDA receptor antagonists. The affinity and the kinetic mechanism of inhibition by these antagonists and ifenprodil were investigated using the whole-cell configuration of the patch clamp technique, calcium flux, and radioligand binding on a mouse cell line L(tk-) expressing recombinant human heteromeric NMDA receptors consisting of NR1a/NR2B subunit combinations. The rank order of potency, as determined by electrophysiology, was ifenprodil<MERCK 2<MERCK 1<MERCK 3 with K(D)'s 79+/-8, 2.4+/-1.1, 1.3+/-0.9, and approximately 0.16+/-0.02 nM, respectively. The apparent dissociation rate constants among these compounds differed by as much as 394-fold whereas the apparent association constants varied less than 3-fold. Higher affinities were a result of slower drug dissociation kinetics of receptor unbinding. Maximal inhibition was not voltage-dependent and was not statistically different at saturating concentrations by these compounds. These results provide the first detailed functional analysis of the kinetic mechanism of MERCK 1, MERCK 2, and MERCK 3 inhibition of NMDA receptors.

Animals↗

PubMed2005

Activation of metabotropic glutamate receptor 3 enhances interleukin (IL)-1beta-stimulated release of IL-6 in cultured human astrocytes.

Previous studies have demonstrated that human astrocytes express mRNA and receptor protein for group I and II metabotropic glutamate receptors (mGluRs). Whether these receptors can influence the inflammatory and immune response and can modulate the capacity of astrocytes to produce inflammatory cytokines is still unclear. Inflammatory cytokines can be produced by activated glial cells and play a critical role in several neurological disorders. Astrocyte-enriched human cell cultures growing in a serum-free chemically defined medium were used to study the regulation of IL (interleukin)-1beta and IL-6 in response to mGluR activation. Astrocytes cultured in the absence or in the presence of epidermal growth factor (EGF), did not secrete significant IL-1beta and IL-6, as determined by specific enzyme-linked immunosorbent assay (ELISA). Activation of mGluRs using (S)-3,5-dihydroxyphenylglycine (DHPG; selective group I agonist) or DCG-IV (selective group II agonist) did not affect the production of interleukins under both growth conditions. On exposure to IL-1beta high levels of IL-6 were detected. Activation of mGluR3 with DCG-IV (but not of mGluR5 with DHPG) enhanced, in the presence of IL-1beta, the release of IL-6 in a dose dependent manner in astrocytes cultured under conditions (+EGF) in which the mGluR expression is known to be upregulated. The effect of mGluR3 activation on IL-1beta stimulated release of IL-6 was prevented by selective group II mGluR antagonists. The capacity of mGluR3 to modulate the release of IL-6 in the presence of IL-1beta supports the possible involvement of this receptor subtype in the regulation of the inflammatory and immune response under pathological conditions associated with glial cell activation.

Adult↗

PubMed2001

Systemic infusion of angiotensin II into normal rats activates nuclear factor-kappaB and AP-1 in the kidney: role of AT(1) and AT(2) receptors.

Recent studies have pointed out the implication of angiotensin II (Ang II) in various pathological settings. However, the molecular mechanisms and the AngII receptor (AT) subtypes involved are not fully identified. We investigated whether AngII elicited the in vivo activation of nuclear transcription factors that play important roles in the pathogenesis of renal and vascular injury. Systemic infusion of Ang II into normal rats increased renal nuclear factor (NF)-kappaB and AP-1 binding activity that was associated with inflammatory cell infiltration and tubular damage. Interestingly, infiltrating cells presented activated NF-kappaB complexes, suggesting the involvement of AngII in inflammatory cell activation. When rats were treated with AT(1) or AT(2) receptor antagonists different responses were observed. The AT(1) antagonist diminished NF-kappaB activity in glomerular and tubular cells and abolished AP-1 in renal cells, improved tubular damage and normalized the arterial blood pressure. The AT(2) antagonist diminished mononuclear cell infiltration and NF-kappaB activity in glomerular and inflammatory cells, without any effect on AP-1 and blood pressure. These data suggest that AT(1) mainly mediates tubular injury via AP-1/NF-kappaB, whereas AT(2) receptor participates in the inflammatory cell infiltration in the kidney by NF-kappaB. Our results provide novel information on AngII receptor signaling and support the recent view of Ang II as a proinflammatory modulator.

Angiotensin II↗

PubMed1997

Mistaken diagnoses of Hodgkin's disease.

This article reviews the frequency of and general types of diagnostic errors in Hodgkin's disease (HD) over the past several decades, discusses the most common diagnostic errors in the four histologic subtypes of HD today, and describes some of the clinical and pathologic features that may aid in avoiding a mistaken diagnosis of HD.

Diagnostic Errors↗

PubMed1998

Increased basal ganglia iron in striatonigral degeneration: in vivo estimation with magnetic resonance.

BACKGROUND: As many as 20% of individuals with the clinical diagnosis of Parkinson's disease (PD) do not have the characteristic neuropathologic features of PD at post mortem. The striatonigral degeneration (SND) subtype of multiple system atrophy is one of the categories of pathology which may be incorrectly diagnosed as PD on the basis of clinical presentation. SND may be associated with increased iron deposition in the putamen which can be detected with magnetic resonance imaging. METHODS: We have estimated regional brain iron content in a patient with probable SND, using a novel imaging method developed in our laboratory, and have compared the results in this patient to those which we have previously reported in patients with PD and in age-matched controls. RESULTS: We observed that putamenal iron content was increased in our SND patient, beyond the 95% confidence limit for inclusion in the PD group, even when considering clinical severity. In contrast, pallidal and thalamic iron were within the PD range. CONCLUSIONS: The demonstration of increased putamenal iron content may be a useful adjunctive investigative procedure in patients with suspected SND.

Basal Ganglia↗

PubMed2002

Excitatory glycine receptors containing the NR3 family of NMDA receptor subunits.

The N-methyl-D-aspartate subtype of glutamate receptor (NMDAR) serves critical functions in physiological and pathological processes in the central nervous system, including neuronal development, plasticity and neurodegeneration. Conventional heteromeric NMDARs composed of NR1 and NR2A-D subunits require dual agonists, glutamate and glycine, for activation. They are also highly permeable to Ca2+, and exhibit voltage-dependent inhibition by Mg2+. Coexpression of NR3A with NR1 and NR2 subunits modulates NMDAR activity. Here we report the cloning and characterization of the final member of the NMDAR family, NR3B, which shares high sequence homology with NR3A. From in situ and immunocytochemical analyses, NR3B is expressed predominantly in motor neurons, whereas NR3A is more widely distributed. Remarkably, when co-expressed in Xenopus oocytes, NR3A or NR3B co-assembles with NR1 to form excitatory glycine receptors that are unaffected by glutamate or NMDA, and inhibited by D-serine, a co-activator of conventional NMDARs. Moreover, NR1/NR3A or -3B receptors form relatively Ca2+-impermeable cation channels that are resistant to Mg2+, MK-801, memantine and competitive antagonists. In cerebrocortical neurons containing NR3 family members, glycine triggers a burst of firing, and membrane patches manifest glycine-responsive single channels that are suppressible by D-serine. By itself, glycine is normally thought of as an inhibitory neurotransmitter. In contrast, these NR1/NR3A or -3B 'NMDARs' constitute a type of excitatory glycine receptor.

Animals↗

PubMed2001

Pathological gambling: addiction or compulsion?

There is considerable debate about the appropriate conceptualization of pathological gambling and its place in psychiatric nosology. The authors examined the existing research on different areas of pathological gambling to find evidence for a particular model of this disorder. There are 2 dominant models of pathological gambling: as a nonpharmacologic addiction and as an obsessive-compulsive spectrum disorder. The data available from different areas seem to converge in suggesting that pathological gambling has characteristics that are similar to those of substance abuse, and less close to those of obsessive-compulsive disorder, although those conceptualizations are not mutually exclusive. An alternative model of pathological gambling is that it constitutes a heterogeneous disorder with some subtypes resembling obsessive-compulsive disorder, and other subtypes being closer to substance abuse disorders. Improved understanding of the conceptualization of this disorder may help improve the quality of the treatments available.

Gambling↗

PubMed1999

Screen detected breast cancer in an Asian population: pathological findings of the Singapore breast screening project.

We document the pathological characteristics of 135 cancers detected in 132 predominantly Chinese women in the Singapore breast screening project. Thirty-four (25%) screen detected tumours were in situ ductal cancers; 98 (73%) invasive, while three (2%) women with malignant fine needle aspirate smears refused further treatment. The median size of in situ cancers was 10 mm; the majority (56%) demonstrated a comedo pattern. Of the invasive tumours which had a median size of 15 mm, three (3%) were microinvasive, 75 (77%) infiltrative ductal, three (3%) invasive lobular, and the remaining 17 (17%) special types or others. Histologic grading revealed 23 (24%) grade I, 52 (53%) grade II, 19 (19%) grade III and four (4%) ungraded cases. Sixty-three (65%) of the invasive cancers were node negative, while 64% of all screen detected malignancies were Stages 0 (in situ) or I. From the pathological perspective, problems of borderline lesions, microinvasion, grade assessment and histological subtyping have to be addressed.

Journal Article↗

PubMed1981

Territorial behavior of schizophrenics. A phylogenetic approach.

Utilizing Tinbergen's concept of increasing phenotypic adjustability on the evolutionary scale leading to man and the ethological concept of territoriality, five Territorial Behavior Scales were designed to reflect increasing levels of adaptive behavior in humans. Twenty recently admitted schizophrenics were studied in an active therapeutic milieu during 2 drug-free weeks, followed by 14 weeks of neuroleptic treatment. Four trained raters scored each patient weekly from 0 to 3 on each scale. Ward nursing staff independently rated social behavior and obtained measures reflecting psychomotor activation and autonomic arousal. Two major types of maladaptive behaviors were identified. The first, involving a breakdown of the ability to make any territorial distinctions in structuring social relationships, correlated directly with psychomotor activation as well as autonomic arousal and was a labile, i.e., treatment-responsive, behavior. The second, involving restrictive territoriality in which the individual occupies physical space to the exclusion of social interactions with others, was unrelated to autonomic arousal but correlated inversely with psychomotor activation and was a stable, i.e., treatment-resistant, behavior. Restrictive territoriality most characterized the total group throughout the study. Adaptive territorial behaviors expected in healthy humans were rare. Following treatment, hebephrenics showed the least favorable overall territorial profile. Untreated catatonics showed the highest levels of undifferentiated or chaotic territorial behavior, but with treatment their profile approached that of the paranoids, who were the least impaired. The data support the concept that two distinct pathological processes are involved in schizophrenia and that the three diagnostic subtypes of this syndrome are meaningful clinicopathological entities.

Adult↗

PubMed2003

Mixed papillary transitional cell carcinoma and adenocarcinoma of the uterine cervix: a clinicopathologic study of three cases.

Although tumors consisting of a combination of transitional cell carcinoma (TCC) and adenocarcinoma have been described in the endometrium, they have not been documented in the uterine cervix to our knowledge. Three such cervical cases are reported in this article. Three patients, whose ages ranged from 40 to 61 years, presented with vaginal bleeding and malignant cells on routine Papanicolaou smears. The initial diagnoses based on a biopsy specimen were poorly differentiated squamous cell carcinoma in two patients and adenocarcinoma with a solid component in the third patient. All patients underwent radical hysterectomy. The hysterectomy specimens each contained a polypoid endocervical mass with minimal invasion of the cervical stroma. On microscopic examination, each tumor consisted of a component of papillary TCC admixed with an adenocarcinoma of endometrioid type. Both carcinomatous components were immunoreactive for cytokeratin (CK) 7 but not CK20. The three patients were alive and disease-free from 10 months to 4 years postoperatively. Recognition of this unusual variant of cervical carcinoma is important to delineate its clinical and pathologic features and establish prognostic differences, if any, from other histologic subtypes of cervical carcinoma. Papillary TCC mixed with adenocarcinoma broadens the morphologic spectrum of transitional cell neoplasms of the uterine cervix.

Adenocarcinoma↗

PubMed2005

Lymphangioma-like Kaposi sarcoma.

BACKGROUND: Lymphangioma-like Kaposi's sarcoma (LLKS) is a rare morphologic expression of Kaposi's sarcoma (KS) that occurs in virtually all of the well-recognized clinical subtypes of the disease and has the potential to mimic other pathologic processes. In this study, we present the clinical and pathological features of four patients with LLKS. METHODS: Four cases of LLKS were retrieved from the dermatopathology files of our institution. All four tumours were tested immunohistochemically with anti-human herpesvirus-8 (HHV-8) latent nuclear antigen-1 (LNA-1) and anti-CD34 antibodies. RESULTS: Clinically, each patient presented with violaceous patches, papules or plaques; one patient presented with bullous lesions. All of the LLKS biopsy specimens revealed areas with characteristic light microscopic features of KS. Lymphangioma-like foci consisted of ectatic, irregularly shaped vascular spaces lined by mildly atypical endothelial cells. All tumour cells, including those associated with LLKS foci, showed a strong and diffuse reactivity for anti-HHV-8 LNA-1 and anti-CD34. KS progressed slowly in two patients with adequate follow-up. CONCLUSIONS: As LLKS can mimic other disease processes, the correct diagnosis relies heavily on the recognition of salient clinical and histological features of conventional KS, including a strong immunohistochemical expression of HHV-8-associated LNA-1 in lesional cells.

Adult↗

PubMedDate not supplied

Hepatoid carcinoma of the ovary: immunohistochemical finding of one case and literature review.

Hepatoid carcinoma is a rare ovarian tumor and is thought to be a histopathologic subtype different from hepatoid type yolk sac tumor based on its pathologic features. A 63-year-old woman who had postmenopausal bleeding and lower abdominal pain was found to have right ovarian mass on pelvic examination and computed tomography. She had high serum levels of alpha fetoprotein (AFP) and CA125. Histologically, the tumor resembled hepatocellular carcinoma by architectural and cytologic features. Immunohistochemically tumor cells were immunoreactive for AFP, alpha 1 antitrypsin, and carcinoembryonic antigens.

Carcinoma, Hepatocellular↗

PubMed2002

Corticotropin-releasing hormone signaling in synovial tissue vascular endothelium is mediated through the cAMP/CREB pathway.

Modulation of locally produced corticotropin-releasing hormone (CRH) is a component of the cytokine network in human inflammatory arthritis. CRH signaling, through the CRH-receptor subtype R1alpha, may play a role in both vascular changes and pathologic mechanisms associated with joint inflammation. Furthermore, the peripheral actions of CRH may be mediated in part through the NURR subfamily of nuclear orphan receptors. The aim of this study was to establish the signaling mechanisms through which CRH receptor-mediated responses contribute to gene regulation in inflamed synovial vasculature. Immunohistochemical analysis of serial rheumatoid arthritis (RA) tissue sections demonstrates CRH and NURR1 expression in the synovial lining layer, subsynovial lining layer, and the vascular endothelium. The identical pattern of immunolocalization confirms that NURR1 is produced at the same synovial sites shown to produce CRH. The distribution of specific NURR1 staining on the synovial vasculature parallels that observed for CRH-R1 expression. Using primary synovial tissue endothelial cells, we demonstrate that CRH induces specific CREB-1 and ATF-2 binding to the NURR1 promoter. We further provide evidence that CRH signaling can be mimicked by activation of cAMP/PKA/CREB using forskolin in primary human microvascular endothelial cells. These data indicate that the CRH receptor-dependent inflammatory response in synovial tissue endothelium is mediated through the cAMP/CREB signaling pathway.

Active Transport, Cell Nucleus↗

PubMed2003

[Prostate histopathology of NIH category IV prostatitis detected by sextant prostate needle biopsy from the patients with high prostatic specific antigen].

Asymptomatic prostatitis is classified as category IV in NIH classification of prostatitis syndrome (1999). No report concerning this category has been present. We investigated this category histopathologically and clinically, in order to clarify the histopathological distribution and its correlation to the clinical features, in this study. Among 785 patients who were suspected prostate cancer because of their high prostatic specific antigen (PSA) values and to have a sextant prostate needle biopsy was performed between January, 1996 and December, 2000, 88 patients (11.2%) were diagnosed as NIH category IV prostatitis (asymptomatic prostatitis). We observed all pathological specimens stained with Hematoxylin-Eosine, and classified them into subtypes according to the classification criteria for prostatitis defined by True et al. (1999). We also investigated the relationship between histopathological distribution and clinical features such as PSA values, PSA density, the incidence of pyuria or bacteriuria. In the histopathological study, grade distributions were 12.5% (11/88) in mild, 71.6% (63/88) in moderate, and 15.9% (14/88) in severe. Location distributions were 2.3% (2/88) in glandular, 68.2% (60/88) in periglandular, and 29.5% (26/88) in stromal. No relationship between these subtypes and clinical features was recognized statistically. However, 7 patients (7.95%) were diagnosed as prostate cancers, later. Pyuria was found in 29.1% (23/79). Bacteriuria was present in 14.3% (11/77). Isolated bacteria were 4 strains of Enterococcus faccalis, 2 strains of each of Pseudomonas aeruginosa and Staphylococcus aureus, and one strain of each of Escherichia coli, Klebsiella oxytoca, Enterobacter cloacae, Enterobacter aerogenes, Staphylococcus haemolyticus, and Staphylococcus epidermidis. Gram positive rod, and Candida sp. No relationship between these subtypes and bacterial species was recognized. These results indicated that the incidence of NIII category IV prostatits was not low without correlation to any clinical features. However, we should pay attention to the presence of prostate cancer, because a small number of the patients were diagnosed as prostate cancer, later.

Aged↗

PubMed2026

Lineage-associated differences in adenine methylation patterns of mammalian-associated Campylobacter fetus isolates: a possible role for epigenetic factors in host tropism and pathogenesis.

Mammalian Campylobacter fetus (CF) is divided into two subspecies, C. fetus fetus (CFF) and C. fetus venerealis (CFV), the latter being bovine-adapted and responsible for the notifiable disease bovine genital campylobacteriosis (BGC). Differentiation between CF subspecies has traditionally been undertaken by a few biochemical tests, but these are complicated by the existence of a biotype, C. fetus venerealis intermedius (CFVi), which shares attributes of both CFF and CFV. Molecular methods targeting specific genes have gained acceptance for more accurate subtype identification and align well with whole-genome analysis. However, limited genomic diversity between subtypes has confounded efforts to understand the genetic basis for differential host tropism and pathogenesis of these organisms. A previous study of a small cohort of C. fetus isolates suggested that dam gene coding variations might correlate with CF subtype. Accordingly, this study examines a cohort of 331 C. fetus genomes, representative of all seven phylogenetic groups for their complement of adenine methylases and the genomic motifs they target in representative isolates. All CF isolates retained a cfeM1 gene, the presence of which correlates with RAATTY methylation, while seven other adenine methylase genes exhibited distinct cladal distributions. Notably, a cjeM1 gene appears to target the CCAN7TAG/CTAN7TGG motif in CFV and CFVi isolates only. Given the increasing recognition of the impact of adenine methylation on bacterial-host interactions, further exploration of the role of adenine methylation in C. fetus pathogenesis could reveal mechanisms contributing to BGC and thus aid in its eradication.IMPORTANCECampylobacter fetus remains an important zoonotic pathogen, for which a better understanding of its host tropism and pathogenesis is sought. However, the limited genomic variation observed between subtypes has to date confounded efforts in this regard. This study suggests that an alternative approach that examines epigenetic differences between subtypes, specifically adenine methylation patterns, may reveal mechanisms critical to the pathologies of these organisms.

Animals↗