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Biomedical subjects

M Potter

Publications and source records attributed to M Potter.

At least 145 records · Page 8Linked to original sources
PubMed1990

gamma-Glutamylglutamine identified in plasma and cerebrospinal fluid from hyperammonaemic patients.

gamma-Glutamylglutamine has been identified in plasma and cerebrospinal fluid. Preparative high voltage electrophoresis was used to isolate the compound from two to three ml of sample. Analysis of archival material from eight patients with urea cycle disorders showed that plasma gamma-glutamylglutamine was 20-214 mumol/l when the plasma glutamine was greater than 1,000 mumol/l and that the relationship was strongly positive (P less than 0.0005). Plasma gamma-glutamylglutamine concentration was also raised in one patient with secondary hyperammonaemia, but not in three other cases, one of whom had a plasma glutamine of 10,000 mumol/l. Cerebrospinal fluid from the last patient contained 97 mumol/l of gamma-glutamylglutamine. Samples of cerebrospinal fluid from two patients with urea cycle disorders were available and the gamma-glutamylglutamine levels were 203 and 313 mumol/l. gamma-Glutamylglutamine and 5-oxoproline concentrations were not significantly increased in urine from any of these patients.

Ammonia↗
PubMed1990

DNA repair in the c-myc locus.

We have studied DNA repair after UV damage in the murine c-myc locus. It appears that a region in B cells upstream of the murine c-myc gene is repaired with a different efficiency in plasmacytoma-resistant DBA/2N mice than in plasmacytoma-susceptible BALB/cAn mice. The region just upstream of c-myc is inefficiently repaired in B lymphoblasts derived from BALB/cAn mice. In contrast, this same region of c-myc is efficiently repaired in B lymphoblasts derived from DBA/2N mice. DNA fragments located in the coding region of c-myc and in another gene, dihydrofolate reductase (DHFR), are repaired with equal efficiency in cells from these two strains of mice. It is possible that repair efficiency of the 5' flank of c-myc may be involved in tumor susceptibility of the mouse strain.

Animals↗
PubMed1990

A murine plasmacytoma with a variant (15;16)(D2/3;B1) translocation that involves the c-myc and lambda light chain gene-carrying chromosomes.

A murine plasmacytoma (MPC) with a reciprocal translocation between chromosomes 15 and 16 with breakpoints in 15D2/3 and 16B1 is reported. The breakpoint on chromosome 15 is identical to the breakpoint in the MPC-associated typical (12;15) and kappa variant (6;15) translocation. Therefore it probably involves the c-myc gene as well. Unlike the Burkitt lymphoma (BL) system, a lambda/myc variant translocation has not been described in the MPC system. Chromosome 16 is known to carry the lambda gene. Therefore, the 15;16 translocation probably represents the "missing" lambda/myc variant in MPC, suggesting that the lambda gene is localized at 16B1.

Animals↗
PubMed1990

A genetic map of mouse chromosome 1 near the Lsh-Ity-Bcg disease resistance locus.

Isozyme and restriction fragment length polymorphism (RFLP) analyses of backcross progeny, recombinant inbred strains, and congenic strains of mice positioned eight genetic markers with respect to the Lsh-Ity-Bcg disease resistance locus. Allelic isoforms of Idh-1 and Pep-3 and RFLPs detected by Southern hybridization for Myl-1, Cryg, Vil, Achrg, bcl-2, and Ren-1,2, between BALB/cAnPt and DBA/2NPt mice, were utilized to examine the cosegregation of these markers with the Lsh-Ity-Bcg resistance phenotype in 103 backcross progeny. An additional 47 backcross progeny from a cross between C57BL/10ScSn and B10.L-Lshr/s mice were examined for the cosegregation of Myl-1 and Vil RFLPs with Lsh phenotypic differences. Similarly, BXD recombinant inbred strains were typed for RFLPs upon hybridization with Vil and Achrg. Recombination frequencies generated in the different test systems were statistically similar, and villin (Vil) was identified as the molecular marker closest (1.7 +/- 0.8 cM) to the Lsh-Ity-Bcg locus. Two other DNA sequences, nebulin (Neb) and an anonymous DNA fragment (D2S3), which map to a region of human chromosome 2q that is homologous to proximal mouse chromosome 1, were not closely linked to the Lsh-Ity-Bcg locus. This multipoint linkage analysis of chromosome 1 surrounding the Lsh-Ity-Bcg locus provides a basis for the eventual isolation of the disease gene.

Animals↗
PubMed1990

Neoplastic development in B-lymphocytes.

The differentiation of B-cells, unlike other hematopoietic cells that develop in a single burst, occurs in interrupted steps. As a consequence there are different types of B-cells that are distinguished by their level of development. Accordingly there are a variety of different kinds of B-cell tumors. The most common proto-oncogene that is mutated in B-cell tumors is c-myc. In mammalian systems c-myc is mutated by chromosomal rearrangements with immunoglobulin-gene-bearing chromosomes. The c-myc gene may be directly rearranged in some translocations but in a number of others the breaksites are only near the c-myc locus. The mechanism of dysregulation of myc transcription in the latter is currently being investigated. Probably the most striking finding is the number of different B-cell tumor-forming systems in different species in which one or more of the characteristic 'myc' chromosomal translocations occur. In humans these occur in eBL, sBL and AIDS-associated lymphomas. B-cell lymphomas. Dysregulation of c-myc is a major phenotype in many (but not all) B-cell tumors and further does not appear to be sufficient to establish an autonomously growing B-cell. Surprisingly the nature of the additional changes has not been determined in B-cell tumor systems. It is known though that when certain other oncogenes are passively introduced into cells with dysregulated c-myc genes autonomously growing phenotypes do emerge. The oncogenes known to cooperate with a dysregulated myc (e.g. Ha-ras, raf-1 and v-abl) are thought to code for proteins that participate in growth-factor-induced signal transductions.

Animals↗
PubMed1990

Platelet concentrates irradiated with ultraviolet light retain satisfactory in vitro storage characteristics and in vivo survival.

We have previously reported that platelet concentrates (PC) may be irradiated with ultraviolet light (UVL) in a cryostorage pack such that mixed lymphocyte reactions (MLR) are abolished whilst satisfactory platelet function is retained during subsequent storage using Fenwal PL-1240 containers. We have now studied both platelet structure and function after irradiation in DuPont Stericell bags which are both UV-permeable and biocompatible. The irradiation dosage was 3000 Joules/m2 of UVL at a mean wavelength of 310 nm; a dose previously shown to abolish MLR. No detriment to platelet function was observed when compared to control as measured by aggregation responses to adenosine diphosphate (ADP), collagen and ristocetin, hypotonic shock response and pH during 5 d of storage. Lactate levels were significantly higher (P less than 0.01) and glucose levels lower (P less than 0.01) in UV-treated PC, although in the majority the lactate level did not exceed 20 mmol/l. Betathromboglobulin and platelet factor 4 levels were higher during storage in the UV group, the latter reaching significance (P less than 0.05). When whole platelets and platelet membranes were stained with Coomassie blue or Periodic Acid-Schiff's reagent after electrophoresis in polyacrylamide gels no obvious alterations to major membrane constituents were observed on days 1 and 5 of storage. Paired in vivo autologous studies in healthy volunteers using 111Indium-labelling were performed at the end of 5 d of storage. The UV-treated platelets gave satisfactory and equivalent results for recovery, half life and survival when compared to controls. We conclude that PC irradiated with UVL and stored for 5 d in DuPont Stericell containers appear suitable for transfusion and may prove to be nonimmunogenic. Further in vivo studies of haemostatic efficacy and recipient alloimmunization are now warranted.

Blood Platelets↗
PubMed1990

Mentally disordered homeless offenders--diversion from custody.

The homeless mentally ill petty offender is a familiar sight in the Inner London Magistrates' courts and presents a considerable problem regarding appropriate placement. This paper describes a new psychiatric service which transfers the focus of assessment of such offenders from the prison to the magistrates' courts. The service commenced in February 1989 and centres on two Inner London magistrates' courts, Bow Street and Marlborough Street. It provides a psychiatric assessment of the homeless mentally ill petty offender at the earliest possible opportunity following arrest, with the intention of diverting them from custody. This paper discusses the advantages of this scheme compared with prison-based assessments, and describes its success in diverting defendants from custody without necessarily resorting to hospital admission.

Adult↗
PubMed1990

Military dependent medical care during World War II.

Dependent medical care at Army expense or at Army facilities during World War II was offered only on an emergency basis and at the discretion of the facility commanding officer. This had been the practice since 1884 when such care was specifically authorized by Congressional appropriation. Mobilization in 1898 and 1917 had brought a large number of state militiamen or inductees into the army--men who could leave their families behind. When mobilization began again in 1940, it was thought that a similar procedure would be followed. Events, however, overwhelmed the system as commanders of Army bases faced large numbers of young, pregnant wives who had followed their husbands. This had happened, in part, because of the dislocations of the Great Depression and, in part, because the wives of military inductees hoped to find work close to where their husbands were stationed. Although dependent medical care was not increased in proportion to the numbers of new dependents brought in by the war mobilization, medical care was provided for the four lower grades under the Emergency Maternity and Infant Care section of the Social Security Act of 1935. Subsequent to World War II and the experience of the Korean War, Congress saw it fit to specifically authorize medical care for dependents of military personnel as part of the soldiers' terms of employment, as a device to stimulate retention in service of both soldiers and doctors. In 1956 the United States Congress established the right at law of military dependents to medical care as specified in the Dependents' Medical Care Act.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1990

v-myc and v-raf act synergistically to induce B-cell tumors in pristane-primed adult BALBC mice.

In a variety of systems, evidence is accumulating which suggests that neoplastic transformation requires the action of two or more genes such as mutated or over-expressed proto-oncogenes. To determine whether the cytoplasmic serine/threonine kinase oncogene raf could complement a deregulated myc gene and induce tumors in adult mice, BALBC mice were primed with an intraperitoneal (ip.) injection of mineral oil (pristane) and then given an ip. injection of a retroviral construct, J1, J2 or J5, which expresses either v-raf (J1), v-myc (J5) or both (J2). The J1 virus induced no tumors in 150 days in 38 mice, except for 5 helper virus-associated T-cell lymphomas. Under identical conditions the J5 virus, which expresses only v-myc, induced exclusively monocytic neoplasms in 93% of 15 mice. The J2 virus expresses both v-myc and v-raf and caused equal numbers of monocytic and B cell tumors in 66% of 30 mice. Under these conditions, it appears that v-raf expression acts synergistically with v-myc to induce the transformation of B cells, which neither oncogene could do alone. The J3 virus, which originally contained a complete v-myc and an inactivated v-raf, can induce tumors of later stage B cells (plasmacytomas, Potter et al., 1987). Recent studies of virus recovered from these plasmacytomas (called the J3V1 virus, Troppmair et al., 1989) show that the J3 virus has undergone deletions which have reactivated v-raf in a mutated form. Only J3V1, not J3, induced tumors in vivo. Our data presented here corroborate Troppmair et al. and extend Potter et al. (1987) which reported that J3 (presumably J3V1) induced 10% myeloid tumors and 90% plasmacytomas. In light of the discovery, our J2 and J3 data indicate that in combination with the same form of v-myc, different forms of v-raf induce different spectra of tumors.

Animals↗
PubMed1989

An altered v-raf is required in addition to v-myc in J3V1 virus for acceleration of murine plasmacytomagenesis.

We have isolated and molecularly cloned a highly pathogenic virus variant, J3V1, from murine plasmacytomas induced by a combination of pristane and the weakly transforming recombinant retrovirus J3. J3 virus is a derivative of the v-raf/v-myc-carrying J2 virus that was generated by a frameshifting deletion inactivating v-raf in J2. J3V1 contains an additional deletion of 334 base paris in gag, which restores the correct reading frame for v-raf and results in the expression of a p57 gag-raf fusion protein. Reactivation of v-raf in J3 is required for efficient plasmacytoma acceleration in pristane-conditioned BALB/cAn mice.

Amino Acid Sequence↗
PubMed1989

Recent and future molecular genetic research into schizophrenia.

The difficulties anticipated in the application of molecular genetics to schizophrenia research have not prevented the first successful localization of a susceptibility gene for a subtype of schizophrenia. It is argued that this approach is the most useful of the possible molecular genetic strategies because it leads both to enhanced clinical genetic investigation and to further recombinant DNA research to clone and sequence schizophrenia susceptibility mutations. Future recombinant DNA research can now use long-range mapping and cloning techniques such as the chromosome walking/jumping approach and the strategy of cloning brain-specific cDNAs from brain mRNA. The identification of carriers for high-risk studies and the genetic validation of diagnosis appear to be the most promising clinical developments. Prenatal counseling will only become widely feasible when much more is known about the extent of heterogeneity of linkage in schizophrenia.

Chromosomes, Human, Pair 5↗
PubMed1988

Localization of a susceptibility locus for schizophrenia on chromosome 5.

Schizophrenia is a common disorder with a life time prevalence of approximately 1 per cent. The illness often develops in young adults, who were previously normal, and is characterized by a constellation of symptoms including hallucinations and delusions (psychotic symptoms) and symptoms such as severely inappropriate emotional responses, a disorder of thinking and concentration, erratic behaviour as well as social and occupational deterioration. A considerable proportion of the variance in the liability to develop schizophrenia may be genetic, but segregation analysis, to establish a mode of transmission, has not produced a consistent result. One of these studies was carried out in Iceland and made use of the large family size and extensive geneaological information present in that country. Here we demonstrate genetic linkage of two DNA polymorphisms on the long arm of human chromosome 5 to schizophrenia in seven British and Icelandic families with multiple affected members. The results indicate the existence of a gene locus with a dominant schizophrenia-susceptibility allele. Inheritance of the allele in the families studied suggests that it may also predispose to psychiatric conditions such as schizophrenia spectrum disorders and a variety of other disorders. This report provides the first strong evidence for the involvement of a single gene in the causation of schizophrenia.

Chromosomes, Human, Pair 5↗