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Eur J Hum Genet. 2002 Jun;10(6):375-80.
Locus for susceptibility for familial capillary malformation ('port-wine stain') maps to 5q.

Eerola I, Boon LM, Watanabe S, Grynberg H, Mulliken JB, Vikkula M.

Laboratory of Human Molecular Genetics, Christian de Duve Institute of Cellular Pathology & Universite catholique de Louvain, Brussels, Belgium.

Capillary malformation (CM; 'port-wine stain'), is a common vascular malformation affecting cutaneous capillary vessels in 0.3% of newborns. Increased incidence of lesions in first-degree relatives of these patients and several reported familial cases suggest that genetic factors may play a role in the pathogenesis of CM. We report the first genome-wide linkage analysis of familial CM. In the non-parametric linkage analysis, strong evidence of linkage (peak Z-score 6.72, P-value 0.000136) was obtained in an interval of 69 cM between markers D5S407 and D5S2098, corresponding to 5q11-5q23. Parametric linkage analysis gave a maximum combined HLOD score of 4.84 (alpha-value 0.67) at marker D5S2044 on 5q15, and analysis using only the linked families, defined a smaller, statistically significant locus CMC1 of 23 cM (peak LOD score 7.22) between markers D5S1962 and D5S652 corresponding to 5q13-5q15. Interesting candidate genes implicated in vascular and neural development, such as MEF2C, RASA1, and THBS4, are in this locus.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12080389&dopt=Abstract

Rev Neurol. 2002 Apr 16-30;34(8):724-9.
[Implication of the neuropeptides methionine enkephalin, neurotensin and somatostatin of the caudal trigeminal nucleus in the experimental migraine]

[Article in Spanish]

Samsam M, Covenas R, Yajeya J, Ahangari R, Narvaez JA, Montes-Gonzalo MC, Gonzalez-Baron S.

Laboratorio de Neuroanatomia de los Sistemas Peptidergicos, Instituto de Neurociencias de Castilla y Leon (INCYL), Facultad de Medicina, Salamanca, Espana.

INTRODUCTION: Primary peptidergic sensory neurons of the trigeminal ganglion that innervate the cerebral dura have been involved in the pathogenesis of headache, including the migraine. In addition, it is known that nociceptive central processes of the trigeminal neurons terminate in the caudal trigeminal nucleus. Moreover, the electrical stimulation of the trigeminal ganglion has been used as an experimental model in order to study the vascular headache, including the migraine. AIM: To study whether there is or not a decrease of the immunoreactivity for methionine enkephalin, somatostatin and neurotensin in the caudal trigeminal nucleus after electrical stimulation of the trigeminal ganglion. MATERIAL AND METHODS: The trigeminal ganglia of Wistar albino rats of both sexes were electrically stimulated (frequency, 5 Hz; duration, 5 ms; intensity, 0,8 1.4 mA) and unilaterally for five minutes. Sections of the medulla oblongata containing the caudal trigeminal nucleus were obtained and processed for immunocytochemistry, in which specific antibodies were used against methionine enkephalin, neurotensin and somatostatin 28. RESULTS: In stimulated animals, we observed a decrease in the immunoreactivity for the three neuropeptides studied in the stimulated (ipsilateral) side, in comparison with the not stimulated side (contralateral). In control animals (not stimulated) the degree of the immunoreactivity was the same on both sides. CONCLUSIONS: 1. The decrease of the immunoreactivity in the ipsilateral side (stimulated) suggests that methionine enkephalin, neurotensin and somatostatin 28 are released in the caudal trigeminal nucleus after electrical stimulation of the trigeminal ganglion; 2. Methionine enkephalin and somatostatin 28 could act in the caudal trigeminal nucleus as inhibitors (with antinociceptive action) of another released exciters neuropeptides (with nociceptive action); and 3. These data will allow in the future to try new therapeutic strategies (e.g., the inhibition of the receptors implicated.), in order to alleviate certain headaches.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12080490&dopt=Abstract

Am J Hum Genet. 2002 Dec;71(6):1395-412. Epub 2002 Nov 26.
The founder mutation MSH2*1906G-->C is an important cause of hereditary nonpolyposis colorectal cancer in the Ashkenazi Jewish population.

Foulkes WD, Thiffault I, Gruber SB, Horwitz M, Hamel N, Lee C, Shia J, Markowitz A, Figer A, Friedman E, Farber D, Greenwood CM, Bonner JD, Nafa K, Walsh T, Marcus V, Tomsho L, Gebert J, Macrae FA, Gaff CL, Paillerets BB, Gregersen PK, Weitzel JN, Gordon PH, MacNamara E, King MC, Hampel H, De La Chapelle A, Boyd J, Offit K, Rennert G, Chong G, Ellis NA.

Department of Medicine, Sir Mortimer B Davis-Jewish General Hospital, Montreal, Quebec, Canada, H3G 1A4. william.foulkecgill.ca

Hereditary nonpolyposis colorectal cancer (HNPCC) is caused by mutations in the mismatch-repair genes. We report here the identification and characterization of a founder mutation in MSH2 in the Ashkenazi Jewish population. We identified a nucleotide substitution, MSH2*1906G-->C, which results in a substitution of proline for alanine at codon 636 in the MSH2 protein. This allele was identified in 15 unrelated Ashkenazi Jewish families with HNPCC, most of which meet the Amsterdam criteria. Genotype analysis of 18 polymorphic loci within and flanking MSH2 suggested a single origin for the mutation. All colorectal cancers tested showed microsatellite instability and absence of MSH2 protein, by immunohistochemical analysis. In an analysis of a population-based incident series of 686 Ashkenazi Jews from Israel who have colorectal cancer, we identified 3 (0.44%) mutation carriers. Persons with a family history of colorectal or endometrial cancer were more likely to carry the mutation than were those without such a family history (P=.042), and those with colorectal cancer who carried the mutation were, on average, younger than affected individuals who did not carry it (P=.033). The mutation was not detected in either 566 unaffected Ashkenazi Jews from Israel or 1,022 control individuals from New York. In hospital-based series, the 1906C allele was identified in 5/463 Ashkenazi Jews with colorectal cancer, in 2/197 with endometrial cancer, and in 0/83 with ovarian cancer. When families identified by family history and in case series are included, 25 apparently unrelated Ashkenazi Jewish families have been found to harbor this mutation. Although this pathogenic mutation is not frequent in the Ashkenazi Jewish population (accounting for 2%-3% of colorectal cancer in those whose age at diagnosis is <60 years), it is highly penetrant and accounts for approximately one-third of HNPCC in Ashkenazi Jewish families that fulfill the Amsterdam criteria.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12454801&dopt=Abstract

Hunan Yi Ke Da Xue Xue Bao. 1999;24(4):381-3.
[Study on the relationship between plasma endothelin nitric oxide concentration and renal hypertension and renal function]

[Article in Chinese]

Zhou Q, Sun M, Zhou H.

Department of Internal Medicine, Xiangya Hospital, Hunan Medical University, Changsha 410008.

OBJECTIVE: To investigate the relationship between plasma endothelin(ET), nitric oxide(NO) levels and, renal hypertension and renal function. METHODS: The plasma concentration of ET-1 was detected by immunofluorescence assay. The plasma concentration of NO was detected by biochemistry assay. RESULTS: 1. In renal disease patients, plasma concentration ET-1 was markedly elevated, and plasma concentration of NO was decreased, compared with the healthy subjects(P < 0.01). 2. Plasma concentration of ET-1 was markedly increased and plasma concentration of NO was decreased in the patients with renal hypertension. 3. Plasma level of ET-1 was higher, and plasma level of NO was lower in the patients with renal function damage than that of those without renal function damage. 4. BP, BUN and Scr were positively correlated with plasma ET-1, but they were negatively correlated with plasma concentration of NO. CONCLUSION: Plasma ET-1 and NO may play an important role in pathogenesis of renal hypertension; the change of their levels may be related to the progress of these renal diseases.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12080656&dopt=Abstract

Hunan Yi Ke Da Xue Xue Bao. 1999;24(5):418-20.
[Detection of bcr/abl gene expression on bone marrow cell colonies in chronic myelogenous leukemia by reverse transcriptase-polymerase chain reaction]

[Article in Chinese]

Luo Z, Chen H, Luo S, Tang L, Wang J.

Research Center of Molecular Biology, Hunan Medical University, Changsha 410078.

The t(9;22) (q34;q11) between abl and bcr genes plays a pivotal role in the diagnosis and pathogenesis of chronic myelogenous leukemia(CML). To explore the bcr/abl fusion mRNA expression on hematopoietic precursors, reverse transcriptase-polymerase chain reaction(RT-PCR) was applied to detect bcr/abl mRNA expression on bone marrow cell colonies. Meanwhile, bcr/abl mRNA expressions on 14- or 28-day colonies using HPP-CFC and CFU-GM semisolid agar culture assay were also determined in 4 cases of confirmed Ph-positive CML by karyotyping analysis. The results showed that the bcr/abl mRNA expressions on 14-day colonies and some 14- or 28-day colonies detected singly were positive at presentation by RT-PCR, in agreement with results by karyotype analysis. Thus, a sensitive and powerful technique was offered for studying gene expression on hematopoietic precursors, diagnosis and therapeutic monitoring of CML. Furthermore, this can be used as an ideal method for revealing molecular mechanisms of pathogenesis of CML and screening anti-CML drugs.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12080671&dopt=Abstract

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