发布求助
文献互助 智能选刊 最新文献

Pediatric pathology & molecular medicine最新文献

筛选
英文 中文
Effects of oral genistein in mice. 口服染料木素对小鼠的影响。
Pediatric pathology & molecular medicine Pub Date : 2003-03-01 DOI: 10.1080/pdp.22.2.131.141
Anita Bhandari, Susan E Crawford, Lijun Huang, William W Reenstra
{"title":"Effects of oral genistein in mice.","authors":"Anita Bhandari,&nbsp;Susan E Crawford,&nbsp;Lijun Huang,&nbsp;William W Reenstra","doi":"10.1080/pdp.22.2.131.141","DOIUrl":"https://doi.org/10.1080/pdp.22.2.131.141","url":null,"abstract":"<p><p>In cell culture systems, genistein, a soy-derived isoflavone with chemopreventive and estrogenic effects, enhances cAMP-dependent activation of the most common cystic fibrosis-causing mutation, deltaF508-CFTR, by as much as 20-fold. DeltaF508-CFTR is present in the apical membrane at far lower levels than wild-type CFTR. If genistein can enhance cyclic AMP-dependent activity in vivo, the presence of deltaF508-CFTR, at even a few percent of wild-type levels, might permit genistein to be of therapeutic benefit to cystic fibrosis patients with this mutation. Before determining if oral genistein would be of benefit in mice with a deltaF508 mutation in the murine CFTR gene, a maximal dose of oral genistein with minimal side effects needed to be established. Accordingly, C57Bl/6 mice pups were randomly weaned onto soy-free diet, AIN-76, containing between 0 and 1.0 g/kg genistein and allowed to feed ad libitum for 3 weeks. Genistein had no significant effects on growth rates of either male or female mice. Histology of the lung, heart, kidney, liver, and intestine revealed no significant genistein-dependent changes in morphology. When mice on a 1.0 g/kg of genistein diet were sacrificed in the morning, the mean level of serum genistein was 1.4+/-0.2 micro moles/L. Serum genistein increased during the daylight hours reaching a maximum of 7.5+/-0.6 micro moles/L in the early evening. Our results demonstrate that dietary genistein is not inhibitory to growth or caloric intake and up to 1.0 g/kg ad libitum genistein causes no significant organ specific abnormalities.</p>","PeriodicalId":82276,"journal":{"name":"Pediatric pathology & molecular medicine","volume":"22 2","pages":"131-41"},"PeriodicalIF":0.0,"publicationDate":"2003-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/pdp.22.2.131.141","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22218997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 16
SIALYL-Tn antigen distribution in Helicobacter pylori chronic gastritis in children: an immunohistochemical study. 儿童幽门螺杆菌慢性胃炎SIALYL-Tn抗原分布:免疫组织化学研究。
Pediatric pathology & molecular medicine Pub Date : 2003-03-01
Marta Cohen, Ricardo Drut, Eduardo Cueto Rúa
{"title":"SIALYL-Tn antigen distribution in Helicobacter pylori chronic gastritis in children: an immunohistochemical study.","authors":"Marta Cohen,&nbsp;Ricardo Drut,&nbsp;Eduardo Cueto Rúa","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Sialyl-Tn antigen (STn) is a mucin-type carbohydrate normally present in goblet cells of small and large bowel. STn expression has been demonstrated to occur in complete and incomplete intestinal metaplasia as well as in many carcinomas but in no normal gastric cell. The aim of our present study was to evaluate the distribution of STn in Helicobacter pylori chronic gastritis (HpCG) of pediatric patients. Eighteen gastric biopsies from 15 children (mean age: 11.5 years) with HpCG, 9 gastric biopsies from 9 children without H. pylori infection, and 1 heterotopic gastric mucosa in Meckel's diverticulum were immunostained using the anti-STn antibody STn1 (18/18), NCL-MUC-1 (7/18), and NCL-MUC-2 (18/18) antibodies. Also, sulfated mucosubstances were investigated with the Alcian Blue-Periodic Acid Schiff (AB-PAS), pH 1.0 stain. Although with different intensity (weak in 5/18, moderate 9/18, and intense 4/18) all cases with HpCG exhibited STn immunoreactivity. The expression of STn was found to be located mainly to the supranuclear region of the epithelial cells at the foveolae and glandular necks, with occasional cells showing diffuse cytoplasmic staining. When reactivity was intense, it was for the most part found in the cells at the neck of the glands. The mucus out of the luminal border above the positive cells was usually also stained. MUC-1 was negative (2/7) or weakly positive (5/7) in a few surface mucous cells. MUC-2 was negative (16/18) or occasionally detected in some foveolar and surface cells (2/18). AB-PAS pH 1.0 revealed the presence of sulfomucins in the cytoplasm of isolated cells of gastric pits and glands of most cases (11/15). None of these findings was observed in the control group. We conclude that STn can be identified in gastric cells of pediatric patients with HpCG and that this does not correlate with other mucosubtances markers. The findings could indicate that minimal intestinal metaplasia takes place in children with HpCG.</p>","PeriodicalId":82276,"journal":{"name":"Pediatric pathology & molecular medicine","volume":"22 2","pages":"117-29"},"PeriodicalIF":0.0,"publicationDate":"2003-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22219000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
DNA content and proliferative activity in pediatric genitourinary rhabdomyosarcoma. 小儿泌尿生殖系统横纹肌肉瘤的DNA含量和增殖活性。
Pediatric pathology & molecular medicine Pub Date : 2003-03-01
Pilar San Miguel-Fraile, Rosario Carrillo-Gijón, Jose Luis Rodríguez-Peralto, José Antonio Ortiz-Rey, Carlos Alvarez-Alvarez, Ana de la Fuente-Buceta
{"title":"DNA content and proliferative activity in pediatric genitourinary rhabdomyosarcoma.","authors":"Pilar San Miguel-Fraile,&nbsp;Rosario Carrillo-Gijón,&nbsp;Jose Luis Rodríguez-Peralto,&nbsp;José Antonio Ortiz-Rey,&nbsp;Carlos Alvarez-Alvarez,&nbsp;Ana de la Fuente-Buceta","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Most of the studies have reported that cases of pediatric rhabdomyosarcoma (RMS) with hyperdiploid DNA and low cellular proliferative activity have better outcomes. The aim of our study was to evaluate the possible clinical relevance of DNA ploidy and proliferative activity in childhood genitourinary RMS. Twelve childhood genitourinary RMS cases were reexamined histologically and correlated with clinical features and patient survival. DNA analysis was performed on cytospin single-cell preparations obtained from the paraffin-embedded tissue blocks. MIB-1 was the proliferative marker used on paraffin sections. All patients were male with a mean age at diagnosis of 65 months. There were 5 tumors on the bladder, 5 on the pàratesticular region, and 2 on the prostate. All cases were treated with multimodality therapy using the protocols proposed by the International Society of Pediatric Oncology. The following subtypes of RMS were recognized: embryonal (n=6), spindle cell (n=4), and botryoid (n=2). DNA hyperdiploid was detected in 11 tumors (92%) and high MIB-1 index (>19%) in 4 cases (33%). Now, 10 patients are alive without evidence of disease and 2 patients are alive with evidence of disease. Our data suggested that childhood RMS of the genitourinary tract are preponderantly DNA hyperdiploid and have low cellular proliferative activity. It is also interesting that 83% of our genitourinary pediatric RMS patients are alive. As consequence of this study, we propose that DNA content and proliferative activity is a useful method to supplement findings in children with RMS.</p>","PeriodicalId":82276,"journal":{"name":"Pediatric pathology & molecular medicine","volume":"22 2","pages":"143-52"},"PeriodicalIF":0.0,"publicationDate":"2003-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22218998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Late onset ornithine transcarbamylase deficiency: a case report. 迟发性鸟氨酸转氨基甲酰基酶缺乏症1例。
Pediatric pathology & molecular medicine Pub Date : 2003-03-01 DOI: 10.1080/pdp.22.2.153.157
Smaragdi Fessatou, Anastasia Garoufi, Helen Tsapra, George Maropoulos, Helen Michelakakis, Kleopatra Schulpis
{"title":"Late onset ornithine transcarbamylase deficiency: a case report.","authors":"Smaragdi Fessatou,&nbsp;Anastasia Garoufi,&nbsp;Helen Tsapra,&nbsp;George Maropoulos,&nbsp;Helen Michelakakis,&nbsp;Kleopatra Schulpis","doi":"10.1080/pdp.22.2.153.157","DOIUrl":"https://doi.org/10.1080/pdp.22.2.153.157","url":null,"abstract":"<p><p>Ornithine transcarbamylase deficiency, an X-linked disorder, is the most common inherited urea cycle defect. Previous reports have documented the existence of several different mutations that can, partly at least, explain the phenotypic variability of the disorder. We describe the only male with T343K mutation, which also is present in his mother. We underline the disorientation of the beginning of clinical presentation; the patient became ill when fruits were added to his diet.</p>","PeriodicalId":82276,"journal":{"name":"Pediatric pathology & molecular medicine","volume":"22 2","pages":"153-7"},"PeriodicalIF":0.0,"publicationDate":"2003-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/pdp.22.2.153.157","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22218999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
PATHOLOGY OF THE UMBILICAL CORD IN ADRENAL FUSION SYNDROME 肾上腺融合综合征脐带病理
Pediatric pathology & molecular medicine Pub Date : 2003-01-01 DOI: 10.1080/pdp.22.3.243.246
Ricardo Drut, MD, CCPM, Rosa Mónica Drut, MD, CCPM
{"title":"PATHOLOGY OF THE UMBILICAL CORD IN ADRENAL FUSION SYNDROME","authors":"Ricardo Drut, MD, CCPM, Rosa Mónica Drut, MD, CCPM","doi":"10.1080/pdp.22.3.243.246","DOIUrl":"https://doi.org/10.1080/pdp.22.3.243.246","url":null,"abstract":"We report the placental findings of a newborn with multiple anomalies that include small and fused adrenal glands, meningomyelocele, lobar holoprosencephaly, cerebellar hypoplasia, short pancreas, and small spleen, fitting with the features of the so-called adrenal fusion syndrome. The placenta was small and presented a short, undercoiled and segmentally uncoiled umbilical cord with a short constriction in the middle of its length. We speculate that adrenal fusion syndrome and abnormal spleen lobulation and short pancreas may represent part of the same complex and probably related to the one including midline anomalies and defects of laterality formation in which horseshoe (fused) adrenal gland also may be found. Undercoiled umbilical cord might represent the placental component of this malformation complex. We also underline the value in identifying abnormalities of the umbilical cord to establish the cause of death.","PeriodicalId":82276,"journal":{"name":"Pediatric pathology & molecular medicine","volume":"22 1","pages":"243 - 246"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/pdp.22.3.243.246","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"60772859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
AN UNUSUAL RENAL MALIGNANCY OF CHILDHOOD: UNILATERAL TERATOID WILMS'S TUMOR 罕见的儿童肾脏恶性肿瘤:单侧畸胎瘤
Pediatric pathology & molecular medicine Pub Date : 2003-01-01 DOI: 10.1080/pdp.22.5.435.441
N. Bakshi, I. Mansoor, N. K. Venkataramu, S. Katariya
{"title":"AN UNUSUAL RENAL MALIGNANCY OF CHILDHOOD: UNILATERAL TERATOID WILMS'S TUMOR","authors":"N. Bakshi, I. Mansoor, N. K. Venkataramu, S. Katariya","doi":"10.1080/pdp.22.5.435.441","DOIUrl":"https://doi.org/10.1080/pdp.22.5.435.441","url":null,"abstract":"Teratoid Wilms's tumor is a rare histologic variant of the classical Wilms's tumor, containing predominantly heterolougus tissues (adipose, glial, muscle, cartilage, or bone). We report an unusual variant of such tumor, which simulated renal teratoma because of abundant fat within the tumor. The child underwent radical excision; postoperatively, he was treated with chemotherapy, and now the child is well at 36 months after surgery. The behavior of this kind of tumor usually is not aggressive, and the outcome is good. Surgery should be the treatment of choice, because the efficacy of chemotherapy and radiotherapy is probably reduced by the high amount of differentiated and mature tissue that characterizes this neoplasm. Radiologic imaging and pathological features of this rare entity are described.","PeriodicalId":82276,"journal":{"name":"Pediatric pathology & molecular medicine","volume":"22 1","pages":"435 - 441"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/pdp.22.5.435.441","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"60773550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 17
PATHOLOGY TEACH AND TELL: CENTRAL NERVOUS SYSTEM ATYPICAL TERATOID/RHABDOID TUMOR 病理教诉:中枢神经系统非典型畸胎瘤/横纹肌样瘤
Pediatric pathology & molecular medicine Pub Date : 2003-01-01 DOI: 10.1080/pdp.22.5.443.447
Z. Avcı, İ. Safa Kaya, A. Selman Doğukan, O. Aydin, O. Ismailoglu
{"title":"PATHOLOGY TEACH AND TELL: CENTRAL NERVOUS SYSTEM ATYPICAL TERATOID/RHABDOID TUMOR","authors":"Z. Avcı, İ. Safa Kaya, A. Selman Doğukan, O. Aydin, O. Ismailoglu","doi":"10.1080/pdp.22.5.443.447","DOIUrl":"https://doi.org/10.1080/pdp.22.5.443.447","url":null,"abstract":"Atypical teratoid/rhabdoid tumor (AT/RT) is extremely malignant, highly aggressive primitive central nervous systemneoplasm of infancy with very poor prognosis. Histologically, AT/RT is defined as a polymorphous neoplasm often featuring rhabdoid, PNET, mesenchymal, and epithelial components. We report the clinical history, radioligical, and pathological findings in a child affected bycentral nervous system AT/RT.","PeriodicalId":82276,"journal":{"name":"Pediatric pathology & molecular medicine","volume":"22 1","pages":"443 - 447"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/pdp.22.5.443.447","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"60773565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 7
Neoplastic disease and deletion 22q11.2: a multicentric study and report of two cases. 肿瘤疾病和22q11.2缺失:一项多中心研究和两例报告。
Pediatric pathology & molecular medicine Pub Date : 2003-01-01 DOI: 10.1080/15227950307713
A. Scattone, G. Caruso, A. Marzullo, D. Piscitelli, M. Gentile, L. Bonadonna, G. Balducci, M. Digilio, A. Jenkner, F. Camassei, R. Boldrini, P. Nazzaro, L. Pollice, G. Serio
{"title":"Neoplastic disease and deletion 22q11.2: a multicentric study and report of two cases.","authors":"A. Scattone, G. Caruso, A. Marzullo, D. Piscitelli, M. Gentile, L. Bonadonna, G. Balducci, M. Digilio, A. Jenkner, F. Camassei, R. Boldrini, P. Nazzaro, L. Pollice, G. Serio","doi":"10.1080/15227950307713","DOIUrl":"https://doi.org/10.1080/15227950307713","url":null,"abstract":"Deletion 22q11.2 is a chromosomal abnormality detected in young patients with clinical manifestations of the DiGeorge/velocardiofacial syndrome. Conotruncal heart defects are also associated with del22q11.2. An association of these cardiac malformations with neoplasias has been observed. Our series includes two cases of malignancies, a hepatoblastoma and a renal-cell carcinoma, arising in children with complex cardiac malformations. The aim of the study was to determine if the deletion at 22q11.2 was present and could be responsible for both pathological processes. Del22q11.2 was identified in both cases. Comparative genomic hybridization revealed terminal gains on chromosomes 1q and Xq and terminal loss on 1p in the hepatoblastoma, and gains in 1p, 12q, 16p, 20q, 22q, and whole chromosome 19 and loss of Xq in the renal-cell carcinoma. Our results confirm a common genetic basis for cardiac malformations, and del22q11.2 presents a risk factor for the development of pediatric tumours.","PeriodicalId":82276,"journal":{"name":"Pediatric pathology & molecular medicine","volume":"41 1","pages":"323-41"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"59824795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 10
PATHOLOGIC QUIZ CASE: MISSED ABORTION AT 6 WEEKS GESTATION 病理测验病例:妊娠6周漏流产
Pediatric pathology & molecular medicine Pub Date : 2003-01-01 DOI: 10.1080/PDP.22.6.495.496
Terry Fox, E. Gilbert-Barness
{"title":"PATHOLOGIC QUIZ CASE: MISSED ABORTION AT 6 WEEKS GESTATION","authors":"Terry Fox, E. Gilbert-Barness","doi":"10.1080/PDP.22.6.495.496","DOIUrl":"https://doi.org/10.1080/PDP.22.6.495.496","url":null,"abstract":"","PeriodicalId":82276,"journal":{"name":"Pediatric pathology & molecular medicine","volume":"22 1","pages":"495 - 496"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"60773623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Recent progress in the molecular genetics of sclerosing bone dysplasias. 硬化性骨发育不良分子遗传学研究进展。
Pediatric pathology & molecular medicine Pub Date : 2003-01-01
Wim Van Hul
{"title":"Recent progress in the molecular genetics of sclerosing bone dysplasias.","authors":"Wim Van Hul","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Bone mineral density is a quantitative trait influenced by both genetic and environmental factors. Epidemiological and twin studies have shown heritability for the variance of bone density of up to 80%. The role of genetic factors in bone homeostasis also is clearly illustrated by the existence of an extended group of genetic conditions associated with an abnormal bone density. These conditions are mainly monogenic in that they are caused by mutations in one gene. Recent developments in molecular genetics and genomics have resulted in a dramatically increased power to identify such disease-causing genes. The group of conditions with increased bone density has been poorly studied and understood at the molecular genetic level but recently for some of them, major breakthroughs have been made. These findings will make the molecular analysis of such patients an additional tool in diagnostics and in genetic counseling.</p>","PeriodicalId":82276,"journal":{"name":"Pediatric pathology & molecular medicine","volume":"22 1","pages":"11-22"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22333799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
首页 上一页 下一页 尾页
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整，为了账户安全，请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们：info@booksci.cn Book学术提供免费学术资源搜索服务，方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号：604180095
Book学术官方微信
小红书