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Biomedical subjects

A Bussey

Publications and source records attributed to A Bussey.

14 recordsLinked to original sources
PubMed1996

Collecting morbidity data in general practice: the Somerset morbidity project.

OBJECTIVE: To collect a valid, complete, continuous, and representative database of morbidity presenting to primary care and to use the data to help commission services on the basis of local need and effectiveness. SETTING: Computerised general practices in Somerset. METHODS: Participating general practices were selected to be representative of the district health authority population for general practice and population characteristics. All conditions presented at face to face consultations were assigned a Read code and episode type and the data were regularly validated. Data were sent by modem from the practices via a third party to the health authority each week. MAIN OUTCOME MEASURES: Proportion of consultations coded and accuracy of coding. RESULTS: 11 practices agreed to participate. Validations for completeness during April 1994 to March 1995 revealed that 96.4% of the records were coded; 94% of the 1090 records validated had appropriate episode types and 87% appropriate Read codes. The results have been used to help formulate the health authority's purchasing plans and have enabled a change in the local contracts for surgery for glue ear. CONCLUSIONS: The project has shown the feasibility of establishing a network of practices recording and reporting the morbidity seen in primary care. Early indications are that the data can be useful in evidence based purchasing.

Adolescent↗
PubMed1994

Comparison of thermoradiosensitization in two human melanoma cell lines and one fibroblast cell line by concurrent mild hyperthermia and low-dose-rate irradiation.

Two human melanoma cell lines, one radioresistant (SK-MEL-3) and one radiosensitive (HT-144), and a normal human fibroblast line (AG1522) were evaluated for thermoradiosensitization of low-dose-rate irradiation by concurrent mild hyperthermia (39-41 degrees C). None of the cell lines expressed chronic thermotolerance during heating at 39-41 degrees C. The SK-MEL-3 cells were the most heat sensitive, while AG1522 and HT-144 cells had the same sensitivity at 39 and 40 degrees C but HT-144 cells were more sensitive at 41 degrees C. All cell lines expressed thermal enhancement of radiosensitivity with heating during irradiation which increased with heating temperature. The SK-MEL-3 cells, which were the most resistant to radiation and demonstrated the greatest repair of sublethal damage (SLD) during low-dose-rate irradiation, had the greatest thermal enhancement of radiosensitivity, while the HT144 cells, which were the most sensitive and expressed little repair of SLD during low-dose-rate irradiation, had the smallest thermal enhancement of radiosensitivity. These data show that concurrent mild hyperthermia during low-dose-rate irradiation may be most efficacious in radiation-resistant tumor cells which express resistance through an enhanced capacity for repair of SLD.

Cell Line↗
PubMed1993

Postirradiation exposure to hypotonic saline shows normal damage processing in radiation-sensitive cell lines.

Three pairs of cell lines (one human and two Chinese hamster ovary (CHO) cell lines) each comprising a cell line with a normal radiation response and a radiation-sensitive mutant, were evaluated for recovery of potentially lethal damage (PLDR) and recovery of sublethal damage (SLDR). In all cases, the normal cell lines (GM1522, human; AA8-4 and K1, CHO) exhibited capacity for PLDR and SLDR was also normal in the two CHO lines. For the mutants (GM3395, human AT; V3 and 5-11, CHO) there was no ability for PLDR and SLDR was also absent in the two CHO cell lines. Postirradiation exposure to hypotonic NaCl solutions resulted in fixation of radiation damage in all the cell lines. This form of damage is repaired if left unperturbed after irradiation. This shows that cells have a large capacity for repair of this form of damage which accounts for much greater changes in survival than those observed in conventional PLDR experiments. These data show that the mutant cell lines retained their capacity to repair the damage which was susceptible to postirradiation fixation by anisotonic salt solutions. In addition, initial (i.e. preirradiation) DNA polymerase activities were measured in the four CHO cell lines; they were not correlated to radiation sensitivity.

Animals↗
PubMed1991

The direct measurement of protein kinase C (PKC) activity in isolated membranes using a selective peptide substrate.

A protein kinase C (PKC)-selective peptide substrate was used to develop a method for measuring PKC activity directly and quantitatively in isolated cell membranes without prior detergent extraction and reconstitution of the enzyme with phosphatidylserine and TPA in the presence of excess Ca2+. This simple and rapid method can reliably measure changes in membrane-associated PKC activity induced by various bioactive compounds such as hormones and growth factors. Also, this method, which measures PKC activity in its native membrane-associated state, has the advantage of being able to distinguish between active and inactive PKC associated with cell membranes.

Amino Acid Sequence↗
PubMedDate not supplied

Thermal radiosensitization by 41 degrees C hyperthermia during low dose-rate irradiation in human normal and tumour cell lines.

Three human cell lines (glioma, melanoma and fibroblast) were evaluated for responses to low dose-rate irradiation (LDRI) (0.88 and 0.41 cGy per min) alone or with concurrent heating (41 degrees C) during irradiation. In order to avoid cell cycle redistribution cells were held in plateau phase. The results show that the lowest LDRI gave maximum sparing in the glioma and the fibroblast cell lines while both dose rates achieved approximately the same effect in the melanoma line. The melanoma line was the most heat sensitive and showed the greatest thermal enhancement ratio (TER). For all cell lines TER was greatest at the lowest dose-rate, and in the melanoma the heat plus LDRI curve gave lower survival than the high dose-rate irradiation survival curves. These data show that concurrent mild hyperthermia combined with LDRI used in brachytherapy can enhance the effectiveness of clinical brachytherapy treatments. In addition, this effect was largest in the most resistant cell line indicating the potential for using this combination to overcome radioresistance in brachytherapy.

Brachytherapy↗
PubMedDate not supplied

Cell killing, DNA polymerase inactivation and radiosensitization to low dose rate irradiation by mild hyperthermia in four human cell lines.

Four human cell lines (one fibroblast, two melanoma and one glioma) were evaluated for their responses to hyperthermia and thermalradiosensitization. For mild hyperthermia (40-42 degrees C), there was little to no chronic thermotolerance development during protracted heating for up to 72 h. In addition, there was no significant thermotolerance for polymerase inactivation during mild hyperthermia. For high temperature hyperthermia, polymerase beta was more thermal sensitive than aphidicolin sensitive polymerase alpha + delta + epsilon, (termed polymerase alpha) but during mild hyperthermia ther relative sensitivities were reversed. Polymerase beta was resistant to mild hyperthermia and polymerase alpha was very sensitive. Within each cell line there was a correlation between polymerase alpha inactivation and the degree of radiosensitization (TER) and amongst the cell lines the most radiation resistant cell line had less polymerase alpha inactivation than the most sensitive cell line for similar values of TER's. These data indicate that, amongst the cell lines, radiosensitivity and polymerase alpha sensitivity may influence TER and that for a given cell line, or possibly tumour, polymerase alpha inactivation may have potential as an indicator to determine TER for mild hyperthermia treatments in radiosensitization to low dose rates.

Cell Death↗
PubMedDate not supplied

Evaluation of cisplatin response in three radiation resistant and three radiation sensitive cell lines.

The cisplatin response was studied in three radiation sensitive mutant cell lines each paired with normally responding or radiation resistant cell lines of parental or similar origin. The radiation sensitive cell lines V3 (CHO), AT5BI (human fibroblast) and HT144 (melanoma) also showed reduced or lack of ability to repair sublethal radiation damage. Also, V3 did not repair radiation induced DNA double strand breaks and AT5BI was excision repair deficient. None of these cell lines show any cross sensitivity to cisplatin treatment. Instead the response was more like the paired normally radiation responding cell lines, except for AT5BI which showed cisplatin resistance. Thus the mechanisms causing radiation sensitivity in the three cell lines are not involved in cisplatin sensitivity.

Animals↗