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Pediatr Surg Int. 2003 Jul;19(5):391-4. Epub 2003 May 21.
ICAM-1 expression is upregulated in reflux nephropathy.

Unemoto K, Chertin B, Shima H, Bi X, Sakai M, Puri P.

Children's Research Centre, Our Lady's Hospital for Sick Children, University College Dublin, Dublin 12, Ireland.

Reflux nephropathy (RN) is a major cause of end-stage renal failure in children and young adults. Intercellular adhesion molecule-1 (ICAM-1), a cell surface glycoprotein, has a role in the regulation of interaction among immune cells. It has been demonstrated that increased levels of tubular ICAM-1 correlate with an extent of tubular damage in diabetic nephropathy. We hypothesized that ICAM-1 local synthesis is altered in reflux nephropathy and therefore designated this study to investigate ICAM-1 expression in RN. The kidney specimens from six patients with severe reflux nephropathy secondary to primary vesicoureteral reflux were obtained at the time of nephrectomy. Control materials included normal kidney specimens obtained from three adult patients during partial nephrectomy for an incidentaloma. Fluorescent immunohistochemistry was carried out using monoclonal antibodies to ICAM-1 utilizing confocal laser scanning microscopy. Reverse transcriptase polymerase chain reaction (RT-PCR) was performed to evaluate the relative amount of ICAM-1. In the control kidneys, there was lack of ICAM-1 immunoreactivity in the interstitium and proximal tubules and moderate immunoreactivity in the glomerulus. In the refluxing kidney there was strong ICAM-1 immunoreactivity in the glomerulus, interstitium and proximal tubules. The RT-PCR showed strong ICAM-1 mRNA expression in the refluxing kidneys and absent or weak ICAM-1 expression in the controls. Our findings of increased expression of ICAM-1 in the severe reflux nephropathy kidney suggests that ICAM-1 may play a role in the pathogenesis of renal parenchymal damage associated with RN.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12759765&dopt=Abstract [PubMed - in process]

Genes Chromosomes Cancer. 2003 Jul;37(3):314-20.
Differentiating pathogenic mutations from polymorphic alterations in the splice sites of BRCA1 and BRCA2.

Claes K, Poppe B, Machackova E, Coene I, Foretova L, De Paepe A, Messiaen L.

Center for Medical Genetics, Ghent University Hospital, Belgium. Kathleen.Claeug.ac.be

About 4% of all BRCA1 and BRCA2 alterations reported to the Breast Information Core database are splice site variants. Only a limited number of them have been studied at the RNA level. By BRCA1 and BRCA2 mutation analysis of breast/ovarian cancer families, we identified two novel and eight previously reported potential splice site mutations, never characterized at the cDNA level before. RT-PCR was performed to determine whether these variants disrupted correct splicing. To ensure efficient detection of transcripts containing premature termination codons, a nonsense-mediated mRNA decay inhibitor was added to the lymphoblastoid cell lines of the patients before RNA extraction. We found that BRCA1 IVS3+3A>C, 4304G>A (in the last codon of exon 12), and IVS19+2delT and BRCA2 IVS6+1G>A, IVS23-2A>G, and IVS24+1G>A lead to aberrant transcripts in lymphocytes. Therefore, they were considered to be true pathogenic mutations, predisposing carriers to cancers of the hereditary breast/ovarian cancer syndrome. BRCA2 IVS24-16T>C is a frequent polymorphism in linkage disequilibrium, with a polymorphic stop codon in exon 27, K3326X. BRCA1 IVS2-14C>T and BRCA2 IVS9-5insT and IVS25+9A>C represent rare variants, not disrupting normal splicing in blood lymphocytes. However, some of the alterations may act differently, qualitatively and/or quantitatively, in breast or ovarian tissues. The data provided in this paper allowed more accurate risk estimation of patients and relatives carrying the mutations described herein and have facilitated genetic counseling. Furthermore, our study is important for a better understanding of splicing mechanisms and revealed new patterns of alternative splicing in BRCA1 and BRCA2. 2003 Wiley-Liss, Inc.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12759930&dopt=Abstract

Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi. 1999 Mar;13(1):71-3.
[Dynamic observation of serological and histological changes of Chinese rhesus monkeys infected by hepatitis G virus]

[Article in Chinese]

Xu J, Ju J, Yang Z.

Institute of Liver Disease, 81 St Hospital of PLA, Nanjing 210002.

OBJECTIVE: To study the genesis, development and pathogenesis of hepatitis G. METHODS: The Chinese Rhesus monkeys were intravenously injected with the serum from a hepatitis G patient only with HGV RNA positive. The dynamic changes of serum and liver tissues of the animals were observed before and after infection. Also the immunohistochemical study were done with monocolonal antibody against NS5 gene antigen of HGV. One male monkey was dissected and the internal organs were taken for histological examination 18 months after infection. RESULTS: Serum ALT and AST became increasing 30 days after infection and showed abnormal continuously for 9 months. Spotty and focal necrosis and piecemeal necrosis were found in liver tissue from 2 to 18 months after infection. Positive staining of HGV antigen was present in cytoplasm of liver cells by immunohistochemistry. Histological observation showed that the internal organs were normal except the liver tissue in which the damages were similar with that in hepatitis. CONCLUSION: The successful infection of Chinese Rhesus monkey by serum from hepatitis G patient can used as a good animal model for the study of hepatitis G.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12759960&dopt=Abstract [PubMed - in process]

Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi. 1999 Mar;13(1):80-2.
[The pathogenicity of HFRS patient's soft palate mucosa to suckling mice]

[Article in Chinese]

Zhang L, Zhang L, Wang S.

First Military Medical University, Guangzhou 510515.

OBJECTIVE: To explore the pathogenic mechanism of hemorrhagic fever with renal syndrome(HFRS). METHODS: 2-3 days old inbred Balb/C suckling mice were inoculated intracerebrally with tissue suspension of soft palate petechia of HFRS patients and the HFRS virus RNA was tested in brain, lung and kidney tissues of sucking mice by nested PCR. RESULTS: Some of the mice developed acute disease and died. The autopsy analysis indicated that these mice showed pathological changes in microvascular system and parenchymatous tissues. HFRS virus RNA was detected in their brains, lungs and kidney tissues. CONCLUSIONS: These results indicate that HFRS virus exists in the tissue of petechial hemorrhagic spots on soft palate petechia of HFRS patients.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12759963&dopt=Abstract [PubMed - in process]

Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi. 1999 Dec;13(4):355-7.
[Preliminary study on relationship between different viral pathogenesis and disease prognosis in patients with severe viral hepatitis]

[Article in Chinese]

Lian Y, Wu W, Shi Y.

Institute of Infectious Diseases, Guangzhou 8th People's Hospital, Guangzhou 510060.

OBJECTIVE: To study the relationship between different viral pathogenesis and disease prognosis in severe viral hepatitis. METHODS: Different viral pathogenesis of 87 dead and live cases with severe viral hepatitis were compared. RESULTS: Total mortality of 87 patients with severe hepatitis was 74.71% (65/87), total prevalence of HBV infection alone in these patients was 41.38% (36/87). The detection rates of HBV infection alone and superinfection of different hepatitis viruses in 68 patients with chronic severe hepatitis (CSH) were 41.18% (28/68) and 58.82% (40/68) respectively. The prevalences of superinfection of HBV and HEV or HAV and superinfection of HBV and CMV in patients with CSH were 27.94% (19/68) and 10.29 (7/68) respectively. The mortality of superinfection of HBV and CMV (85.71%) was the highest, followed by HBV infection alone (77.78%). In addition, the prevalence and mortality of HBV infection alone in 19 patients with acute or subacute severe hepatitis was the highest. CONCLUSION: HBV, HEV or HAV infection alone was the main viral pathogenesis of severe hepatitis. Superinfection of different viruses in patients with CSH was the most common viral infection type. An unpromising prognosis of superinfection of HBV and CMV in CSH is noted.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12759976&dopt=Abstract [PubMed - in process]

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