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排序方式: 共有156条查询结果,搜索用时 15 毫秒
61.
Melanie Steele Nicola L. Jones MD FRCPC PhD Vicky Ng MD FRCPC Binita Kamath MBBChir Yaron Avitzur MD Rose Chami MD Ernest Cutz MD FRCPC Annie Fecteau MDCM MHSc MSc Sylvain Baruchel MD 《Pediatric blood & cancer》2013,60(3):515-517
We report a 2.5‐month‐old infant with bilateral adrenal neuroblastoma, stage 4S(M), with liver metastases and chemotherapy‐induced veno‐occlusive disease leading to cirrhosis requiring liver transplantation. Despite unknown tumour histology and MYCN‐amplification status, we proceeded with liver transplant. This decision was based on clinical suspicion that our patient was MYCN‐negative due to significant tumour regression, and was supported by evidence indicating that MYCN‐amplification is rare in infants with favourable‐stage neuroblastoma. This is the second case report of neuroblastoma requiring liver transplantation; however, in the previously reported case, the diagnosis of neuroblastoma was not established until after transplantation. We discuss this unique case to justify the potential use of life‐saving liver transplants in infants with neuroblastoma. Pediatr Blood Cancer 2013; 60: 515–517. © 2012 Wiley Periodicals, Inc. 相似文献
62.
The pulmonary neuroendocrine (NE) cells, from 16 term infants dying at 1-4 days of age from birth asphyxia, were immuno stained for bombesin-like immunoreactivity by the immunoperoxidase method. The distribution and frequency of bombesin-immunoreactive NE cells were quantified morphometrically and correlated with the presence or absence of brainstem function and persistent fetal circulation (PFC). In infants with loss of brainstem function, the frequency of bombesin immunoreactive NE cells was significantly increased compared to infants with intact brainstem function, i.e. meconium aspiration with PFC. Infants with brainstem injury, with one exception, failed to develop PFC. Pathological changes in the tegmentum of the brainstem, i.e. containing the respiratory center, correlated in nine of 10 cases with loss of brainstem function. These data suggest an inverse relationship between brainstem function, release of bombesin-like peptide from the pulmonary NE cells and the functional state of the pulmonary vasculature. Intact brainstem function appears to be essential for both the release of bombesin-like peptide from the NE cells and for pulmonary vasoconstriction leading to PFC; absence of brainstem function is, on the other hand, associated with failure to release bombesin-like peptide and loss of PFC type reactivity in the pulmonary vasculature. However, it appears unlikely that bombesin itself is a direct mediator of pulmonary vasoconstriction. 相似文献
63.
Lineage development in a patient without goblet, paneth, and enteroendocrine cells: a clue for intestinal epithelial differentiation 总被引:2,自引:0,他引:2
We report a patient who presented with severe enterocolitis and apparent absence of Paneth, goblet, and enteroendocrine lineages from the small bowel and colon. The absorptive enterocyte seemed to be normal morphologically and functionally. Because normal enterocytes were present, we hypothesized that this patient had a developmental block in the differentiation of a common stem cell precursor for Paneth, goblet, and neuroendocrine lineages. By using antibodies to protein markers of each cell line, including some that are expressed early in the differentiation process, we aimed to study lineage development in this patient. From our data, we surmise that there may be a two-step process in lineage commitment. The stem cell may commit to an absorptive cell or a granule-containing cell. The daughter cell that is committed to the granule lineage then further commits to a goblet, enteroendocrine, or Paneth cell lineage. 相似文献
64.
Valerie Speirs Elizabeth Bienkowski Veronica Wong Ernest Cutz 《Anatomical record (Hoboken, N.J. : 2007)》1993,236(1):53-69
Pulmonary neuroendocrine cells (PNEC) are numerous in the fetus where they have been implicated to have a role in fetal lung development. We assessed the effects of putative growth factors, gastrin releasing peptide (GRP), cholecystokinin (CCK), gastrin (GN), serotonin (5-HT), and epidermal growth factor (EGF), some of which are produced by PNEC, either alone or in combination, on cultured fetal rabbit PNEC from 20, 24, and 28 day fetuses. GRP increased the total protein of the cultures over a 7 day period in an age-dependent manner, with greatest effect in cultures from the 24 day fetus, no effect with the 28 day fetus, and an inhibitory effect on 20 day cultures. This was accompanied by an increase in PNEC, which could be blocked by treatment of the cultures with a monoclonal antibody to GRP (2A11). There was no increase in 3H-thymidine labeling of PNEC in GRP treated cultures but an increase in numbers of cells partially stained for 5-HT, suggesting the induction of a precursor cell. Other growth factors had neither an inhibitory nor a stimulatory effect either alone or in combination with GRP. Preliminary studies with 125I-GRP receptor localization suggests that the GRP receptor is mostly expressed on pulmonary fibroblasts, and less on epithelial cells, so that the role for GRP in fetal lung development, at least in the rabbit, is probably indirect, acting via a paracrine mechanism. © 1993 Wiley-Liss, Inc. 相似文献
65.
M Rabinovitch T Bothwell B N Hayakawa W G Williams G A Trusler R D Rowe P M Olley E Cutz 《Laboratory investigation; a journal of technical methods and pathology》1986,55(6):632-653
Scanning electron microscopy and transmission electron microscopy were applied to lung biopsy specimens from patients with congenital heart defects, and pulmonary artery endothelium was analyzed for alterations in surface characteristics and intracytoplasmic composition which might reflect abnormal function. The patients were divided into four groups distinguished by increasing severity of pulmonary vascular changes on light microscopy graded both morphometrically and by the Heath-Edwards classification; group 1, normal vasculature or only abnormal extension of muscle into peripheral arteries; group 2, medial hypertrophy; group 3, medial hypertrophy +/- decreased artery number + intimal hyperplasia; group 4, decreased artery number + occlusive intimal hyperplasia. On scanning electron microscopy, the pulmonary artery endothelial surface in group 1 patients was "crinkled" or "corduroy-like", i.e., composed of narrow, even ridges; in groups 2 and 3, it was "cable-like", i.e., comprised of deep intertwined ridges; in group 4 it was "chenille" in texture, i.e., high ridges alternated with low, uneven, and twisted ones. There was significant increased density of surface microvilli in groups 2 and 3 patients when compared to groups 1 and 4 (p less than 0.05 for each comparison). On transmission electron microscopy pulmonary artery endothelial cells in groups 2 and 3 patients were also characterized by a significant increase in the volume density of rough endoplasmic reticulum (p less than 0.01) and microfilament bundles (p less than 0.05). The coarse endothelial surface characteristics associated with pulmonary vascular changes may result in abnormal interaction with blood elements and release of vasoactive substances. The increased microvilli, rough endoplasmic reticulum, and microfilament bundles in patients with moderate but not advanced arterial changes suggest a phase where increased endothelial metabolic function and alterations in the cytoskeleton may also contribute to heightened pulmonary vascular reactivity. 相似文献
66.
Alona Zer Jean Claude Cutz Harman Sekhon David M. Hwang Christina Sit Manjula Maganti Mike Sung Matthew Binnie Anthony Brade Tae Bong Chung Suzanne Kamel-Reid Narinder Paul Ming S. Tsao Tom Waddell Gilda da Cunha Santos Milan Patel Ron F. Carter Natasha B. Leighl 《Journal of thoracic oncology》2018,13(7):1004-1011
Background
Molecular testing in advanced lung cancer is standard in guiding treatment selection. However, population-wide implementation of testing remains a challenge. We developed a knowledge translation intervention to improve understanding among diagnostic specialists about molecular testing and appropriate diagnostic sampling in lung cancer.Methods
Specialty-specific education programs were developed from existing literature and input from Canadian leaders in lung pathology, respirology, interventional radiology, thoracic surgery, radiation oncology, and medical oncology. The programs, including key messages, review of current data, existing guidelines, group discussion, and participant feedback, were administered at provincial and national specialty meetings. Participant knowledge was assessed before and after the intervention by using anonymous questionnaires. Molecular (EGFR) testing rates in Ontario were also evaluated before and after the intervention period.Results
Ten programs were administered to diagnostic specialists, including respirologists, pathologists, thoracic surgeons, radiologists, radiation oncologists, and medical oncologists, with completion of 255 preintervention and 219 postintervention surveys. At baseline, 30% were unsure of tissue handling methods for molecular testing, 20% chose an incorrect technique, and half were unfamiliar with how to initiate testing. After intervention, specialist knowledge improved regarding tissue handling and appropriate fixation techniques and uncertainty decreased from 30% to 2% (p < 0.001). A 12% increase (relative increase 57%) in molecular (EGFR) testing requests in Ontario was observed over the intervention period (p = 0.0032).Conclusions
Significant knowledge gaps exist among diagnostic specialists regarding molecular testing and targeted therapy in lung cancer. This initiative significantly improved understanding of the importance and methods of successful molecular testing and correlated with increased testing rates. 相似文献67.
68.
69.
Ernest Cutz Donald G Perrin Jie Pan Elisabeth A Haas Henry F Krous 《Pediatric and developmental pathology》2007,10(2):106-116
Pulmonary neuroendocrine cells (PNEC), including neuroepithelial bodies (NEB), are amine- and peptide (for example, bombesin)-producing cells that function as hypoxia/hypercapnia-sensitive chemoreceptors that could be involved in the pathophysiology of sudden infant death syndrome (SIDS). We assessed morphometrically the frequency and size of PNEC/NEB in lungs of infants who died of SIDS (n = 21) and compared them to an equal number PNEC/NEB in lungs of age-matched control infants who died of accidental death or homicide, with all cases obtained from the San Diego SIDS/SUDC Research Project database. As a marker for PNEC/NEB we used an antibody against chromogranin A (CGA), and computer-assisted morphometric analysis was employed to determine the relative frequency of PNEC per airway epithelial area (% immunostained area, %IMS), the size of NEB, the number of nuclei/NEB, and the size of the NEB cells. The lungs of SIDS infants showed significantly greater %IMS of airway epithelium (2.72 +/- 0.28 [standard error of the mean, SEM] versus 1.88 +/- 0.24; P < 0.05) and larger NEB (1557 +/- 153 microm(2) versus 1151 +/- 106 microm(2); P < 0.05) compared to control infants. The size of NEB cells was also significantly increased in SIDS cases compared to the controls (180 +/- 6.39 microm(2) versus 157 +/- 8.0 microm(2); P < 0.05), indicating the presence of hypertrophy in addition to hyperplasia. Our findings support previous studies demonstrating hyperplasia of PNEC/NEB in lungs of infants who died of SIDS. These changes could be secondary to chronic hypoxia and/or could be attributable to maturational delay. Morphometric assessment and/or measurement of the secretory products of these cells (for example, CGA, bombesin) could provide a potential biological marker for SIDS. 相似文献
70.
Karen Choong J.T.R. Clarke E. Cutz R.J. Pollit S.E. Olpin 《Pediatric and developmental pathology》2001,4(6):573-579
Carnitine-acylcarnitine translocase (CACT) deficiency is an inherited defect of the co-transport of free and esterified carnitine
across the inner mitochondrial membrane. We report a case of CACT deficiency in a newborn who died at 72 h of age from severe,
intractable cardiac tachyarrhythmia, despite an improvement in his neurological and biochemical status. Postmortem examination
showed marked steatosis of myocardium, liver, and kidney. In addition, electron microscopic studies showed virtually complete
elimination of mitochondria from cardiomyocytes. It appears that the correction of the acute metabolic derangements in this
condition may not prevent rapid progression to death, suggesting that the rhythm disturbances in CACT deficiency result from
prior and ongoing accumulation of toxic metabolites, rather than from an acute metabolic derangement. Furthermore, we speculate
that the choice of anti-arrhythmic agent in this patient may paradoxically have contributed to his death.
Received March 14, 2001; accepted June 22, 2001. 相似文献