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D Patterson

Publications and source records attributed to D Patterson.

At least 163 records · Page 9Linked to original sources

Lactobacillus casei microbiological assay of folic acid derivatives in 96-well microtiter plates.

Microbiological assay is still widely used for estimating folic acid derivatives in serum and other biological samples. We describe here a modification of this procedure involving use of 96-well microtiter plates. This procedure, used with modern, computer-interfaced microtiter-plate readers and data-reduction software, greatly shortens the time and minimizes reagent costs for this assay. Under the conditions of our assay procedures, all folic acid derivatives tested gave equal growth response for Lactobacillus casei. Results for assays of rat liver extracts showed excellent agreement between the standard bioassay and the 96-well procedure.

Animals↗

The human erg gene maps to chromosome 21, band q22: relationship to the 8; 21 translocation of acute myelogenous leukemia.

There is accumulating evidence to support that genes on chromosome 21 play an important role in the development of pathologies associated with leukemia, Down's syndrome, and Alzheimer's disease. We have previously described erg, a human gene related to the ets oncogene. In this study, we have regionally assigned the erg gene to chromosome 21q22.3 by using somatic cell hybrids and in situ hybridization analysis. In light of this chromosome assignment, the relationship of erg to the 21q translocation breakpoint characteristic of acute myelogenous leukemia (AML) was considered. By using a DNA probe that is specific for the erg gene, a panel of rodent-human cell hybrids was analyzed by the Southern technique to study specific chromosome translocations occurring in acute myeloblastic leukemia. The erg gene was found to translocate from chromosome 21 to 8 in the t(8; 21) (q22; q22), a non-random translocation found in patients with acute myelogenous leukemia of the subgroup M2 (AML-M2). The localization of the erg gene to chromosome 21q22 raises the possibility that this gene may be involved in the pathogenesis of AML-M2.

Animals↗

Complete interruption of the aortic arch in a dog.

Complete interruption of the aortic arch was diagnosed by angiocardiography in a dog with exercise intolerance, a cardiac murmur, polycythemia, and cardiomegaly. The defect was accompanied by a patent ductus arteriosus, ventricular septal defect, and subaortic stenosis. The dog was euthanatized, and the clinical diagnosis was documented by gross dissection of the heart. The site of aortic interruption was between the left carotid and left subclavian arteries, which is the most common location in human beings. The similarity with the pathologic findings of interrupted aortic arch in human beings suggests a similar mechanism responsible for the abnormal cardiac morphogenesis. The defect may be confused with other cardiac anomalies that can result in exercise intolerance, polycythemia, and cardiac murmur. This defect is amenable to surgical treatment, which emphasizes the importance of a correct anatomic diagnosis in clinical patients.

Animals↗

Amyloid beta protein gene: cDNA, mRNA distribution, and genetic linkage near the Alzheimer locus.

The amyloid beta protein has been identified as an important component of both cerebrovascular amyloid and amyloid plaques of Alzheimer's disease and Down syndrome. A complementary DNA for the beta protein suggests that it derives from a larger protein expressed in a variety of tissues. Overexpression of the gene in brain tissue from fetuses with Down syndrome (trisomy 21) can be explained by dosage since the locus encoding the beta protein maps to chromosome 21. Regional localization of this gene by both physical and genetic mapping places it in the vicinity of the genetic defect causing the inherited form of Alzheimer's disease.

Alzheimer Disease↗

Confirmation of assignment of the human alpha 1-crystallin gene (CRYA1) to chromosome 21 with regional localization to q22.3.

The crystallins are highly conserved structural proteins universally found in the eye lens of all vertebrate species. In mammals, three immunologically distinct classes are present, alpha-, beta-, and gamma-crystallins, and each class represents a multigene family. The alpha-crystallin gene family consists of alpha 1-crystallin (CRYA1) and alpha 2-crystallin (CRYA2) genes (previously designated alpha A- and alpha B-crystallin, respectively), which show extensive sequence homology. We constructed a synthetic oligonucleotide probe of 25 bases corresponding to a specific region of the human alpha 1-crystallin gene sequence. This 25-mer probe bears little sequence homology to human alpha 2-crystallin gene and does not cross-hybridize to alpha 2-crystallin sequences in Southern blot analysis. Using this unique synthetic probe, we have demonstrated the identity of the alpha 1-crystallin gene in human genomic DNA. In addition, we have also confirmed its chromosomal location on human chromosome 21. Finally, we have regionally localized the gene to q22.3 by using both Southern blot analysis of a panel of cell hybrids containing different parts of human chromosome 21, and in situ hybridization to metaphase chromosomes. The use of synthetic oligonucleotide probes specific for individual genes should be useful in identifying and mapping members of multigene families.

Animals↗

The severity of late skin damage related to fraction size in women treated by radiotherapy after mastectomy.

A retrospective study has been undertaken to test the NSD formula as a predictor of isoeffective schedules in women treated after mastectomy by parasternal radiotherapy using fraction sizes of 2-3 Gy. Forty three women were identified who have been treated on the same orthovoltage unit 8-18 years previously and the severity of overall skin changes and telangiectasia were assessed by three observers using a 4-point categorical scale. At each level of skin damage, radiotherapy schedules delivered using fraction sizes of 250 R or 300 R were associated with lower TDF values than schedules using 225 R fraction. The difference between TDF factors for isoeffective regimes using small (225 R) and large (250 R and 300 R) fraction sizes is highly significant for both overall skin damage and telangiectasia (p = 0.004 by rank sum test). Care should be exercised when using current empirical formulae to calculate regimes isoeffective for late skin damage, even when modest changes in fraction size from 2 to 3 Gy are contemplated.

Adult↗

Treatment of chronic closed head injury with psychostimulant drugs: a controlled case study and an appropriate evaluation procedure.

The psychostimulant drugs methylphenidate (MPH) and dextroamphetamine (DEA) have proven efficacy in clinical populations whose primary symptoms include disorders of attention, impulse control, and locomotor hyperactivity. These medications have also been shown to influence in a positive manner cognitive functioning, particularly in the areas of sustained attention and memory. In light of these facts, the psychostimulants MPH and DEA were administered in separate trials to a young man who suffered from similar symptoms secondary to a chronic closed head injury. The medication trials were double-blind, placebo-controlled, dose-response studies. Cognitive functions, particularly memory and attention, improved in the active drug conditions. In addition, there was a consistent, positive drug effect across behavioral assessments. This case study emphasizes the importance of studying psychostimulant effects in patients with neuropsychological and behavioral sequelae of closed head injury; it also presents an appropriate methodology for evaluating psychostimulant effects in a clinical research setting.

Adult↗

A somatic cell hybrid with a single human chromosome 22 corrects the defect in the CHO mutant (Ade-I) lacking adenylosuccinase activity.

Adenine-requiring Chinese hamster ovary (CHO-K1) auxotrophs of the complementation group Ade-I were hybridized with various human cells, and hybrids were isolated under selective conditions in which retention of the complementing gene on the human chromosome is necessary for survival. Ade-I cells are deficient in adenylosuccinase activity. This enzyme carries out two independent, but similar, steps of purine biosynthesis: the removal of a fumarate from succinylaminoimidazole carboxamide ribotide to produce aminoimidazole carboxamide ribotide and the removal of fumarate from adenylosuccinate to produce AMP. These are the 9th and 13th steps of adenylate biosynthesis, respectively. Analysis of hybrids by cytogenetics and by Southern blot techniques using chromosome 22-specific DNA probes, one of which encodes an antigen expressed in human fetal brain, indicated that human chromosome 22 was 100% concordant for growth without adenine. One hybrid subclone, isolated after two successive rounds of subcloning, was found to be capable of growth without adenine; the only human chromosome present was 22. In addition, segregants that had lost the ability to grow in adenine-free media had also lost human chromosome 22. These results suggest that the human gene for adenylosuccinase resides on chromosome 22.

Adenylosuccinate Lyase↗

[Therapy of patients with myeloid leukemia with small doses of cytosine arabinoside].

A total of 45 patients were given cytosar and daunorubicin therapy at small doses. Of them 23 patients were with acute nonlymphoblastic leukemia, 12--with hemopoietic dysplasia, and 10--with chronic myeloid leukemia. Cytosar was injected subcutaneously every 12 h at a dose of 10 mg/m2 for 10-25 days, daunorubicin was injected intravenously by drop infusion at a dose of 5 mg/m2. Clinicohematological remission was obtained in 13 patients, clinicohematological improvement in 16. Thus, a positive effect was achieved in 29 patients (64%). The authors provided some data on the influence of small doses of cytosar and daunorubicin on cell maturation in vitro.

Adolescent↗

Legal aspects of athletic injuries to the head and cervical spine.

The author discusses the history of athletic litigation, some reasons for its proliferation, and the effects of such litigation on schools, equipment manufacturers, and others involved with athletics. Some suggestions are offered for minimizing the risk of becoming a defendant in a lawsuit.

Athletic Injuries↗

Hu-ets-1 and Hu-ets-2 genes are transposed in acute leukemias with (4;11) and (8;21) translocations.

Human probes identifying the cellular homologs of the v-ets gene, Hu-ets-1 and Hu-ets-2, and two panels of rodent-human cell hybrids were used to study specific translocations occurring in acute leukemias. The human ets-1 gene was found to translocate from chromosome 11 to 4 in the t(4;11)(q21;23), a translocation characteristic of a subtype of leukemia that represents the expansion of a myeloid/lymphoid precursor cell. Similarly, the human ets-2 gene was found to translocate from chromosome 21 to chromosome 8 in the t(8;21)(q22;q22), a nonrandom translocation commonly found in patients with acute myeloid leukemia with morphology M2 (AML-M2). Both translocations are associated with expression different from the expression in normal lymphoid cells of ets genes, raising the possibility that these genes play a role in the pathogenesis of these leukemias.

Animals↗

Regional assignment of human liver-type 6-phosphofructokinase to chromosome 21q22.3 by using somatic cell hybrids and a monoclonal anti-L antibody.

The three structural loci encoding human phosphofructokinase, a key regulatory enzyme of glycolysis, are located on separate chromosomes. The gene coding for the liver-type subunit PFKL has previously been assigned to chromosome 21. We have used a subunit- and human-specific monoclonal antibody to liver PFK to detect the expression of human PFKL in hamster X human hybrid cell lines. A cell line carrying an 8;21 translocation which contains all of chromosome 21 except the band 21q22.3 was negative for the expression of PFKL whereas cell lines carrying the reciprocal 8;21 translocation were positive. In addition, a cell line with a ring chromosome 21 containing a breakpoint which excluded the distal part of the q22.3 band was negative for expression of PFKL. These results indicate that human PFKL is located on chromosome 21q22.3.

Animals↗