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Mol Cell Biol. 2000 Dec;20(23):9068-75.
Coupled homologous and nonhomologous repair of a double-strand break preserves genomic integrity in mammalian cells.

Richardson C, Jasin M.

Cell Biology Program, Memorial Sloan-Kettering Cancer Center, and Cornell University Graduate School of Medical Sciences, New York, New York 10021, USA.

DNA double-strand breaks (DSBs) may be caused by normal metabolic processes or exogenous DNA damaging agents and can promote chromosomal rearrangements, including translocations, deletions, or chromosome loss. In mammalian cells, both homologous recombination and nonhomologous end joining (NHEJ) are important DSB repair pathways for the maintenance of genomic stability. Using a mouse embryonic stem cell system, we previously demonstrated that a DSB in one chromosome can be repaired by recombination with a homologous sequence on a heterologous chromosome, without any evidence of genome rearrangements (C. Richardson, M. E. Moynahan, and M. Jasin, Genes Dev., 12:3831-3842, 1998). To determine if genomic integrity would be compromised if homology were constrained, we have now examined interchromosomal recombination between truncated but overlapping gene sequences. Despite these constraints, recombinants were readily recovered when a DSB was introduced into one of the sequences. The overwhelming majority of recombinants showed no evidence of chromosomal rearrangements. Instead, events were initiated by homologous invasion of one chromosome end and completed by NHEJ to the other chromosome end, which remained highly preserved throughout the process. Thus, genomic integrity was maintained by a coupling of homologous and nonhomologous repair pathways. Interestingly, the recombination frequency, although not the structure of the recombinant repair products, was sensitive to the relative orientation of the gene sequences on the interacting chromosomes.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11074004&dopt=Abstract

Mol Med Today. 2000 Nov;6(11):449-51.
Murine, canine and non-human primate models of Krabbe disease.

Wenger DA.

Departments of Neurology, and Biochemistry and Molecular Pharmacology, Jefferson Medical College, 1020 Locust St, Room 394, Philadelphia, PA 19107, USA. david.wengeail.tju.edu

Globoid cell leukodystrophy (GLD) or Krabbe disease is an autosomal recessively inherited neurological disease caused by mutations in the gene coding for the lysosomal enzyme galacto-cerebrosidase (GALC). GALC is responsible for the degradation of specific galactolipids, including several that are important in the production of compact, stable myelin. A failure to adequately degrade galactosylceramide and psychosine (galactosylsphingosine) results in the characteristic pathological findings observed in tissue from humans and animals affected with GLD. These galactosphingolipids are normally synthesized during active myelination, and psychosine accumulates in individuals with very low GALC activity. Psychosine is highly toxic to the myelin-forming oligodendrocytes, causing their death and the paucity of myelin found on autopsy. While most human patients present with symptoms before six months of age and die before 18 months of age, older children and adults can also be diagnosed with GLD[1,2]. The cloning of both the human GALC cDNA and the GALC gene opened the way for the identification of mutations causing GLD in humans and animals and the development of novel strategies to treat this severe and fatal disease[3]. The pheno-typic differences between human patients result from the wide range of mutations identified, as well as additional unknown factors. Treatment of late-onset patients and pre-symptomatic individuals (identified either because prenatal testing was not requested or a fetus predicted to be affected was not aborted) by hemato-poietic stem cell transplantation (HSCT) resulted in a less severe phenotype than was predicted and, in some cases, a significant delay in the onset of symptoms[4]. Attempts to treat this disorder by in utero HSCT have not been successful[5].GLD in dogs

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11074371&dopt=Abstract

Am J Hematol. 2000 Nov;65(3):234-8.
Epstein-Barr virus associated B-cell lymphoma of brain developing in myelodysplastic syndrome with c-kit mutation (Try-557 -->stop).

Kuwahara Y, Hirata A, Miwa H, Munakata S, Ueda S, Kanakura Y, Maruno M, Hongyo T, Nomura T, Aozasa K.

Department of Pathology, Osaka University Medical School, Suita, Japan.

The first case of B-cell lymphoma of brain in a patient with myelodysplastic syndrome (MDS) was reported. A 68-year-old man was admitted because of anemia, fever, and thrombocytopenia and was diagnosed as having MDS (refractory anemia with excess of blasts) on the basis of the findings of bone marrow aspiration and chromosomal analysis. The patient was followed up without chemotherapy, but a brain tumor appeared after 3 years. Histologic and immunohistologic examinations revealed diffuse large B-cell lymphoma. Mutations of the c-kit proto-oncogene (stem cell factor receptor) and the p53 tumor-suppressor gene were examined in the MDS lesion and malignant lymphoma (ML) by the polymerase chain reaction-single-strand conformational polymorphism (PCR-SSCP) method followed by direct sequencing. The p53 mutation was not found in either MDS or ML, but a nonsense mutation (Try-557 --> stop) in exon 11 of the c-kit, which might lead to dysfunction of tyrosine kinase activity, was detected in MDS. This is the first report of c-kit mutation in MDS. Epstein-Barr virus (EBV) genome was demonstrated in the nucleus of brain ML cells by in situ hybridization with EBV-encoded RNA-1 probe. Immunohistochemistry showed that the tumor cells expressed latent infection gene products, including EBV nuclear antigen-2 and latent membrane protein-1. This pattern of latent gene expression was Lat III, which is usually found in malignant lymphomas developing in immunocompromised hosts. These findings suggest that a profound pancytopenia in MDS resulted in an immunodeficient condition, after which EBV-positive B-cell lymphoma of brain developed.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11074541&dopt=Abstract

Am J Hematol. 2000 Dec;65(4):307-9.
Mast cell disease associated with acute myeloid leukemia: detection of a new c-kit mutation Asp816His.

Pullarkat VA, Pullarkat ST, Calverley DC, Brynes RK.

Division of Hematology, University of Southern California School of Medicine, Los Angeles, California 90033-0804, USA. vinodpullarkaol.net

Mast cell disease (MCD), a proliferation of mast cells (MC), is occasionally associated with hematologic malignancies. Neoplastic MC have activating c-kit mutations. c-kit is a receptor tyrosine kinase required for the development, proliferation, and survival of MC. Interaction of c-kit with its ligand stem cell factor induces dimerization, receptor phosphorylation, and signal transduction. The most common c-kit mutation detected in neoplastic MCD is Asp816Val, which results in ligand-independent autophosphorylation of the receptor leading to MC proliferation. We describe the rare occurrence of MCD associated with acute myeloid leukemia, report a novel c-kit mutation Asp816 His, and discuss the pathogenesis of MCD associated with hematologic malignancies. 2000 Wiley-Liss, Inc.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11074560&dopt=Abstract

J Womens Health Gend Based Med. 2000 Oct;9(8):831-41.
Of clones, stem cells, and children: issues and challenges in human research ethics.

Meslin EM.

National Bioethics Advisory Commission (USA), Bethesda, Maryland 20892-7979, USA.

In the past 3 years, five scientific stories captivated the media and public attention: a sheep, Dolly, was cloned in Scotland; two scientific teams in the United States reported that they had isolated human stem cells; Jesse Gelsinger, an 18-year-old patient, died in a gene transfer experiment at the University of Pennsylvania; Vanderbilt University reported that it is providing fetal surgery for meningomyelocele; and researchers announced that a herd of previously cloned cows appears to be genetically younger than had been expected. These reports illustrate important issues in the ongoing discussion about research on children; indeed some of them challenge the breadth of the definition of research on children. This article, originally presented at an International Symposium sponsored by UNESCO on Bioethics and the Rights of the Child, describes how the National Bioethics Advisory Commission (NBAC) addressed two of these subjects-cloning and stem cell research-and identifies five challenges that science and society must address in the face of such emerging research technologies.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11074949&dopt=Abstract

The most ostensive feature that distinguishes us human from chimps and other primates is the lack of bodily hair. During evolutionary process, we have lost the majority of hair. Hair is no longer an essential part of our body, just like appendix. What little hair we still have on our scalp and a few other bodily parts is still regarded as significant for reasons other than biological necessity. Hair loss is naturally accompanied by aging process, although the extent of hair loss and the timing of onset vary widely among individuals. Thus, loss of hair and baldness is considered as a symbol of maturity or old age. Like winkles and other signs of aging, hair loss is not welcome by most people, because we don't welcome aging, and being perceived as an aging person. However, it is alopecia, or premature hair loss that especially concerns certain people.

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