Combined endovascular and video-assisted thoracoscopic procedure for treatment of a ruptured pulmonary arteriovenous fistula: Case report and review of the literature.
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Adult↗
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Mapping clinically relevant plasticity after stroke.
After stroke, patients show a wide range in the degree of recovery. Recovery occurs on the basis of discrete physiologic events. Identifying and measuring these events will be useful for a better understanding of stroke recovery mechanisms. The most extensive experience mapping these events has been with positron emission tomography, functional magnetic resonance imaging, and transcranial magnetic stimulation. This article reviews brain mapping studies that have examined stroke recovery. Serial assessment of patients during recovery raises the need for control studies evaluating the effect of intra-subject variability over time. The clearest insights into the significance of bilateral activation during unilateral movements by the stroke-affected hand will come from studies that include bilateral electromyographic measurements. Most brain imaging studies have focused on patients with very good recovery; further study of patients with a wide range of outcomes is needed. The described brain mapping methods have complementary strengths. Insights into the biological basis of recovery may best be achieved when results are considered together. With the advent of treatments targeting stroke recovery, measurement of post-stroke restorative events may also have value as a surrogate end point in clinical trials.
Animals↗
The recurrence risk of adverse outcome in the second pregnancy in women with rheumatic disease1.
OBJECTIVE: To study recurrence risks of adverse pregnancy outcome in the second pregnancy in women with rheumatic disease. METHODS: In a national population-based cohort study, women with rheumatic disease recorded from 1967 to 1995 in the Medical Birth Registry of Norway were compared with mothers without such diagnoses with regard to recurrence risks of adverse pregnancy outcomes in the second pregnancy. The odds ratios (ORs) of all outcomes were adjusted for maternal age, those of cesarean delivery for time period, and those of preeclampsia for interpregnancy interval. RESULTS: Women with rheumatic disease an dadverse pregnancy outcome in the first pregnancy had a statistically significant higher recurrence risk of the same event in the second pregnancy than women without rheumatic disease (preeclampsia: OR 2.22; 95% confidence interval [CI] 1.18, 4.19) (cesarean delivery: OR 1.52; 95% CI 1.05, 2.21) (preterm birth: OR 1.86; 95% CI 1.12, 3.11). In women with rheumatic disease diagnosed between the first and second births, a significantly increased recurrence risk of low birth weight occurred. Women with rheumatic disease also had a higher occurrence of markers for placental dysfunction (preeclampsia, preterm birth, or small for gestational age) in the second birth after any of these outcomes in the first birth (OR 1.35; 95% CI 1.02, 1.78) (35.1% versus 29.2%). CONCLUSION: The recurrence risk of an adverse outcome in the second pregnancy is increased in any woman, but was even higher in women with a rheumatic disease. These patients should be counseled accordingly, be closely monitored during pregnancy, and have access to appropriate subspecialists.
Adult↗
Cyclosporine A: peak or trough level monitoring in renal transplant recipients?
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Administration, Oral↗
Pharmacokinetic studies of oral and intravenous cyclosporine in prekidney transplant patient.
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Administration, Oral↗
Malignant lymphoma in Nebraska and Guangzhou, China: a comparative study.
Two hundred thirty-four consecutive cases of malignant lymphoma (192 non-Hodgkin's lymphomas and 42 Hodgkin's disease) from Guangzhou, China, and 589 cases (498 non-Hodgkin's lymphomas and 91 Hodgkin's disease) from the University of Nebraska Lymphoma Registry were examined in a retrospective histopathologic analysis and the results compared to those of the National Cancer Institute (NCI) Working Formulation Summary. Aggressive non-Hodgkin's lymphoma was excessive in Guangzhou (82.3 per cent; P less than 0.001) and Nebraska (80.3 per cent; P less than 0.001) when compared with the NCI data (54.2 per cent). The small noncleaved cell, lymphoblastic, and diffuse mixed-cell subtypes were more frequent in China (15.6 per cent each; P less than 0.001), whereas the small lymphocytic, follicular large cell, and immunoblastic subtypes predominated in Nebraska (8 per cent, 8.4 per cent, and 21.8 per cent, respectively; P less than 0.001). The overall median age of onset for non-Hodgkin's lymphoma was 42.0 years in Guangzhou and 63.5 years in Nebraska. Hodgkin's disease represented 18 per cent of the malignant lymphomas in Guangzhou and 15 per cent in Nebraska. The mixed-cellularity type was most common in Guangzhou (52 per cent; P less than 0.001) and the nodular-sclerosing type in Nebraska (56 per cent; P less than 0.010). The low median age and excess of certain aggressive subtypes of non-Hodgkin's disease in Guangzhou suggest a possible viral etiology, whereas the excess of certain subtypes of non-Hodgkin's lymphoma in Nebraska may be related to intense agricultural activity.
Adult↗
Expression of the 67-kD laminin receptor, galectin-1, and galectin-3 in advanced human uterine adenocarcinoma.
Alterations of tumor cell interactions with laminin, a basement membrane glycoprotein, are consistent features of the invasive and metastatic phenotype. Qualitative and quantitative changes in the expression of cell surface laminin-binding proteins have been correlated with the ability of cancer cells to cross basement membranes during the metastatic cascade. Such phenotypic modifications are usually associated with poor prognosis. In this study, the authors examined the possibility that expression of three laminin-binding proteins, the 67-kD laminin receptor (67LR), galectin-1, and galectin-3, is altered in human endometrial cancer in a fashion similar to that reported in other carcinomas, such as breast, colon, and ovarian cancer. Twenty advanced uterine adenocarcinomas were analyzed for expression of these three molecules using immunoperoxidase staining and specific antibodies. The authors found a significant increase in the expression of the 67LR and galectin-1 in cancer cells compared with normal adjacent endometrium (P = .0004 and .0022, respectively). As observed in other carcinomas, a significant down-regulation of galectin-3 expression was found in endometrial cancer cells compared with normal mucosa (P = .02). In the galectin-3 positive tumors, galectin-3 was detected in the cytoplasm and/or nucleus of cancer cells. Interestingly, tumors in which galectin-3 was detected only in the cytoplasm were characterized by deeper invasion of the myometrium than lesions where galectin-3 was found both in nucleus and cytoplasm (P = .02). This study shows an alteration of nonintegrin laminin-binding protein expression in advanced human endometrial cancer. Further studies on larger populations should determine the prognostic value of the detection of these laminin-binding proteins in endometrial carcinoma. Inverse modulation of the 67LR and galectin-3 appears to be a phenotypical feature of invasive carcinoma.
Adenocarcinoma↗
Biochemistry and biology of ARHI (DIRAS3), an imprinted tumor suppressor gene whose expression is lost in ovarian and breast cancers.
ARHI is a maternally imprinted tumor suppressor gene that is downregulated in 60% of ovarian and breast cancers. Loss of ARHI expression is associated with tumor progression in breast cancer and decreased disease-free survival in ovarian cancer. ARHI encodes a 26-kDa protein with 55-62% homology to Ras and Rap. In contrast to Ras, ARHI inhibits growth, motility, and invasion. ARHI contains a unique 34 amino-acid extension at its N-terminus and differs from Ras in residues critical for GTPase activity and for its putative effector function. Deletion of ARHI's unique N-terminal extension markedly reduces its inhibitory effect on cell growth. The gene maps to chromosome 1p31 at a site of LOH in 40% of ovarian and breast cancers. Mutations have not been detected, but the remaining allele is silenced by methylation in approximately 10-15 % of cases. In the remaining cancers, ARHI is downregulated by transcriptional mechanisms that involve E2F1 and E2F4, as well as by the loss of RNA binding proteins that decrease the half-life of ARHI mRNA. Transgenic expression of human ARHI in mice produces small stature, induces ovarian atrophy, and prevents postpartum milk production. Reexpression of ARHI in cancer cells inhibits signaling through Ras/Map and PI3 kinase, upregulates P21(WAF1/CIP1), downregulates cyclin D1, induces JNK, and inhibits signaling through STAT3. Marked overexpression of ARHI with a dual adenoviral vector induces caspase-independent, calpain-dependent apoptosis. When ARHI is expressed from a doxycycline-inducible promoter at more physiological levels, autophagy is induced, rather than apoptosis. Growth of ovarian and breast cancer xenografts is reversibly suppressed by ARHI, but expression of the NTD mutant produced only a limited inhibitory effect on growth of xenografts.
Animals↗
Use of Ras-transformed human ovarian surface epithelial cells as a model for studying ovarian cancer.
The Ras gene family has been implicated in the development of many human epithelial cancers. Mutations in K-ras or its downstream mediator BRAF have been detected in about two thirds of low-grade serous carcinomas and borderline serous tumors; mutations in K-ras are also often present in benign and invasive mucinous ovarian cancers. Although the oncogenic allele H-ras(V12) is present in only approximately 6% of ovarian cancers, physiologically activated H-ras protein is commonly detected in human ovarian cancer, presumably because of an increase in upstream signals from tyrosine kinase growth factor receptors such as Her-2/neu, despite the lack of a Ras mutation. The mechanisms by which ras oncogenes transform human epithelial cells are not clear. The methods described here are what we use to culture human ovarian surface epithelial cells, to immortalize those cells, and to transform the immortalized cells with oncogenic H-ras or K-ras. These Ras-transformed human ovarian surface epithelial cells form tumors in nude mice and recapitulate many features of human ovarian cancer, thus providing an excellent model system for studying the initiation and progression of human ovarian cancer.
Animals↗
Nitric oxide radical scavenging of flavonoids.
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Animals↗
Overexpression of kallikrein 10 in epithelial ovarian carcinomas.
OBJECTIVE: We wanted to identify genes up-regulated in ovarian tumors that might serve as early markers for ovarian cancer. One promising focus is the family of genes that encode secreted proteases, which play essential roles in tumor invasion and metastasis. Kallikrein 10 (KLK10) is a member of the kallikrein family of serine proteases which include 15 proteins, including the prostate-specific antigen (PSA), also known as hK3. We investigated whether KLK10 and its related protein, hK10, might serve as equally accurate markers for ovarian carcinoma. METHODS: Transcriptional profiling was performed using RNA isolated from normal ovarian epithelium, ovarian cancer cell lines, and primary ovarian tumors. Microarray data were confirmed by Northern blot analysis of 66 ovarian tumor samples and 6 ovarian cancer cell lines. In situ hybridization and Western blot analysis confirmed the Northern blot findings. RESULTS: KLK10 was more highly expressed by primary ovarian tumors than by NOE. Thirty-two of 35 primary serous ovarian carcinoma samples (91.4%) expressed higher levels of KLK10 than NOE did. Eleven of 15 nonserous epithelial ovarian carcinoma samples (73.3%) and 8 of 11 primary peritoneal carcinoma samples (72.7%) also expressed KLK10. Overall, 84.8% of all epithelial ovarian and peritoneal carcinoma tumor samples showed elevated expression of KLK10. Similarly, Western blot analysis demonstrated that levels of the KLK10-related protein, designated hK10, are elevated in primary ovarian tissue lysates, but the protein is undetectable in immortalized ovarian epithelium. Finally, in situ hybridization established that KLK10 mRNA is much more highly expressed by tumor tissue than by normal epithelium and stromal tissues. CONCLUSIONS: Our data support recent immunoassay findings of elevated levels of hK10 in the tumor tissue and serum of ovarian cancer patients. Thus, it is likely that KLK10 and other kallikreins will serve as useful diagnostic and prognostic markers in patients with ovarian carcinoma.
Biomarkers, Tumor↗
Effects of MK801 and neuroleptics on prepulse inhibition: re-examination in two strains of rats.
Disruption of prepulse inhibition (PPI) induced by NMDA receptor antagonists, such as MK801, has been used as an animal model of positive and negative symptoms of schizophrenia. Previous studies suggested that atypical, but not typical, neuroleptics can selectively restore MK801-induced PPI disruption and that such selectivity may depend on strain differences. The present study re-examined PPI disruption by systemic MK801 in Wistar (WS) and Sprague-Dawley (SD) strains, and addressed the issue whether clozapine (atypical), compared to haloperidol (typical), effectively antagonizes MK801-induced PPI disruption. In addition, we tested the effects of bilateral microinfusion of MK801 into the ventral hippocampus in WS. Systemic MK801 disrupted PPI in both strains. Neither clozapine nor haloperidol antagonized MK801-induced PPI in either strain. Our clozapine data do not agree with previous reports of clozapine's ability to antagonize MK801-induced PPI disruption. Similar to previous results with SD, MK801 infusion into the ventral hippocampus failed to affect PPI in WS. In our view, the selective ability of atypical neuroleptics to restore PPI disruption by NMDA antagonists, and to serve as a tool for identifying possible atypical neuroleptics, requires further examination. PPI disruption with systemic MK801 may be due to the blockade of NMDA receptors in multiple brain sites.
Animals↗
Prepulse inhibition in rats with temporary inhibition/inactivation of ventral or dorsal hippocampus.
Prepulse inhibition (PPI) of the acoustic startle response is a measure of sensorimotor gating and is decreased in neuropsychiatric diseases, including schizophrenia. Hippocampal involvement in PPI has been the subject of several studies, in particular, as aberrant hippocampal activity has been associated with schizophrenia. In rats, chemical stimulation of the ventral hippocampus reduced PPI, while normal PPI was found following hippocampal lesions, suggesting that ventral hippocampal overactivity is detrimental for PPI, but that normal hippocampal activity does not contribute substantially to PPI. In the present study, we investigated the importance of hippocampal activity for PPI by examining PPI in Wistar rats with temporarily decreased hippocampal activity, aiming to avoid compensatory processes that may occur with permanent lesions. Bilateral ventral or dorsal hippocampal infusions of the gamma-aminobutyric acid A (GABA(A)) receptor agonist muscimol (1 microg/side) or the sodium-channel blocker tetrodotoxin (TTX, 10 ng/side) reduced PPI. This reduction is probably neuroleptic-resistant since haloperidol and clozapine did not antagonize the muscimol-induced decreases in PPI. PPI reduction by muscimol inhibition or TTX inactivation of the dorsal or ventral hippocampus indicates that hippocampal activity contributes to sensorimotor gating, suggesting intact PPI after permanent hippocampal lesions to reflect compensatory processes. The data are discussed with respect to hippocampal dysfunction in schizophrenia.
Animals↗
Bioavailability and metabolism.
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Animals↗
Streptolysin S and necrotising infections produced by group G streptococcus.
BACKGROUND: We encountered three patients with severe necrotising soft tissue infections due to beta-haemolytic group G streptococcus. Due to strong clinical similarities with invasive infections produced by group A streptococcus, we investigated a potential link of shared beta-haemolytic phenotype to disease pathogenesis. METHODS: Hybridisation, DNA sequencing, targeted mutagenesis, and complementation studies were used to establish the genetic basis for group G streptococcus beta-haemolytic activity. The requirement of group G streptococcus beta-haemolysin in producing necrotising infection was examined in mice. FINDINGS: Each patient had an underlying medical condition. beta-haemolytic group G streptococcus was the sole microbial isolate from debrided necrotic tissue. The group G streptococcus chromosome contained a homologue of the nine-gene group A streptococcus sag operon encoding the beta-haemolysin streptolysin S (SLS). Targeted mutagenesis of the putative SLS structural gene sagA in group G streptococcus eliminated beta-haemolytic activity. Mice injected subcutaneously with wild-type group A streptococcus or group G streptococcus developed an inflammatory lesion with high bacterial counts, marked neutrophil infiltration, and histopathological evidence of diffuse tissue necrosis. These changes were not found in mice injected with the isogenic group A streptococcus or group G streptococcus SLS-negative mutants. INTERPRETATION: In patients with underlying medical conditions, beta-haemolytic group G streptococcus can produce necrotising soft tissue infections resembling those produced by group A streptococcus. The beta-haemolytic phenotype of group G streptococcus is produced by the exotoxin SLS, encoded by a functional homologue of the nine-gene group A streptococcus sag operon. SLS expression contributes to the pathogenesis of streptococcal necrotising soft tissue infection.
Animals↗
Autologous bone-marrow transplantation in CALLA-positive acute lymphoblastic leukemia after in-vitro treatment with J5 monoclonal antibody and complement.
A monoclonal antibody (J5) specific for the common acute-lymphoblastic-leukaemia antigen (CALLA) was used for in-vitro pre-treatment of bone-marrow before autologous transplantation in four patients with CALLA-positive acute lymphoblastic leukaemia (ALL) in relapse, who did not have HLA-compatible donors. After remission induction and intensification, bone-marrow cells were harvested, treated with J5 antibody and rabbit complement, and cryopreserved in liquid nitrogen. Patients received ablative chemotherapy and total-body irradiation before reinfusion of autologous J5-treated bone marrow. The transplantation protocol was well tolerated, and engraftment of normal myeloid cells occurred in all for patients. Two patients have continued in unmaintained remission with complete haematopoietic reconstitution for more than 1 year after autologous transplantation.
Antibodies, Monoclonal↗
Anti-B1 monoclonal antibody and complement treatment in autologous bone-marrow transplantation for relapsed B-cell non-Hodgkin's lymphoma.
Eight patients with relapsed B-cell non-Hodgkin's lymphoma were treated with intensive chemoradiotherapy and reconstituted with autologous bone marrow rendered free of tumour cells by the B-cell-specific monoclonal antibody anti-B1 and complement. Before the autologous marrow transplantation patients were induced with chemotherapy, radiotherapy, or both, into a minimum disease state with less than 5% bone-marrow involvement with tumour. All patients treated achieved a complete clinical response and had stable haematological engraftment by 8 weeks. No significant acute or chronic toxic effects have occurred. B cells could be detected by 2 months after transplantation and normal immunoglobulin levels were achieved by 6 months. Six of eight patients are disease free in unmaintained remission more than 20, 19, 10, 8, 5, and 3 months after transplantation.
Adult↗