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Biomedical subjects

K A Koch

Publications and source records attributed to K A Koch.

25 records · Page 2Linked to original sources
PubMed1993

tRNA-guanine transglycosylase from Escherichia coli: gross tRNA structural requirements for recognition.

tRNA-guanine transglycosylase (TGT) is the enzyme responsible for the post-transcriptional modification of specific tRNAs (those for Asn, Asp, His, and Tyr) with the hypermodified base, queuine. In Escherichia coli this enzyme catalyzes the exchange of guanine-34 in the anticodon with preQ1, which is subsequently further modified to queuine. There is evidence that such hypermodified tRNA molecules may play a role in the control of cell proliferation and differentiation. In order to perform detailed, in vitro mechanistic studies and to probe the tRNA-enzyme interaction, we have generated unmodified E. coli tRNA(Tyr) and truncated analogues using an in vitro RNA synthesis system suggested by Milligan and Uhlenbeck [Milligan, J. F., & Uhlenbeck, O. C. (1989) Methods Enzymol. 180, 51-62]. From this system we have generated three tRNA analogues totally devoid of any post-transcriptional modifications. In order to compare the unmodified tRNA with the true physiological substrate for TGT, that is, tRNA that contains all modified bases except queuine, we have isolated E. coli tRNA(Tyr) from an overexpressing clone in a TGT-deficient strain of E. coli. We report here that unmodified, full-length tRNA(Tyr) serves as a substrate for TGT with kinetic parameters that are, within experimental error, the same as those for in vivo isolated tRNA(Tyr). This indicates that other post-transcriptional modifications have negligible effects upon TGT recognition of tRNA. A 17-base oligoribonucleotide, corresponding to the anticodon loop and stem, is also a substrate for TGT with only a 20-fold loss in Vmax/KM, versus the full-length tRNA.(ABSTRACT TRUNCATED AT 250 WORDS)

Base Sequence↗
PubMed1993

Effects of the Patient Self-Determination Act on patient knowledge and behavior.

BACKGROUND: In effect since 1991, the Patient Self-Determination Act (PSDA) requires that institutions receiving government insurance payments document that they have informed patients of their right to decide on life-preserving measures. Implementing the PSDA should make discussion of advance directives a routine part of acute care hospital admissions. Yet the proportion of those actually completing advance directives such as living wills remains relatively small. METHODS: A telephone survey questionnaire was administered to patients who were hospitalized before and after the implementation of the PSDA. Survey questions probed patient knowledge about living wills and behavior toward obtaining living wills. RESULTS: Patient knowledge about advance medical directives correlated positively with race (white), income (> or = $10K), and level of education (high school or more). Moreover, a significantly greater number of patients hospitalized after implementation of the PSDA knew about living wills than the number of those hospitalized before the Act's implementation. However, actually obtaining a living will correlated positively with age (> 36 years) alone, and implementation of the PSDA was not related to the number of patients who obtained a living will. CONCLUSIONS: Although the study results show that the measures the hospital in the study used to meet PSDA requirements increased patient awareness of living wills, they failed to increase the number of patients who act on this awareness. This finding indicates that simply informing patients about their right of self-determination is insufficient to meet the intended goals of the legislation.

Adult↗
PubMed1992

Patient Self-Determination Act.

The Patient Self-Determination Act (PSDA) took effect December 1, 1991. As a direct result of the Nancy Cruzan case, this Act is intended to promote awareness and discussion of health-care issues in preparation for medical decisions at the end of life. The mechanism is the federal requirement that any health-care institution which expects to receive Medicare or Medicaid funds must inform patients upon admission of state laws governing self-determination issues. Any discussion among patients, families and their physicians stimulated by the PSDA is healthy. Physicians must be prepared for new questioning by patients about self-determination issues and must be knowledgeable of state laws. They must also defend against bureaucratization of medical decision-making by taking a leadership role in the patient autonomy movement, injecting into the movement an awareness of the rational capacity of medical technology.

Advance Directives↗
PubMed1990

The sugar moiety of bovine S-antigen.

To obtain insight into the glycoprotein nature of S-antigen (S-Ag), we have investigated the affinity of bovine S-Ag for plant lectins, location of the sugar moiety within the molecule, and incorporation of radiolabelled mannose and glucosamine into S-Ag. It was found (i) that only about 10% of purified S-Ag was bound to concanavalin A (Con A) and wheat germ agglutinin (WGA) columns, (ii) that both concanavalin A and wheat germ agglutinin bound chymotryptic peptides derived from the C-terminal half of S-Ag, and (iii) that radiolabelled D-mannose and D-glucosamine were incorporated into S-Ag and the incorporation was inhibited by tunicamycin, an N-glycosylation inhibitor. 14C-Mannose-labelled S-Ag was identified by affinity chromatography on an anti-S-Ag antibody column. These results support the supposition that only a small population of S-Ag is glycosylated (probably in N-glycosylated form), and the sugar moiety is located in the C-terminal half of the molecule.

Animals↗
PubMed1984

Total cerebral ischemia: effect of alterations in arterial PCO2 on cerebral microcirculation.

Radiolabeled 15-microns microspheres were used to examine alterations in regional CBF and cerebrovascular resistance in response to changes in arterial PCO2. Flow measurements were obtained before and 1-3 and 24 h after 12 min of total cerebral ischemia. Striking sensitivity of blood flow in all areas of the central nervous system was shown to changes in arterial PCO2 between 24 and 50 mm Hg during the control nonischemic period. Following 12 min of total cerebral ischemia, cerebrovascular resistance increased, producing a decrease in regional blood flow when the important controlling variables for CBF were held constant. One to 3 h after total cerebral ischemia, the effect of variations in arterial PCO2 on cerebral blood flow was almost completely abolished. Within 24 h after total cerebral ischemia, the sensitivity of CBF to changes in PCO2 was almost completely restored, whereas the secondary severe neurologic deficit remained. Therapeutic interventions following global cerebral ischemia, designed to ameliorate the "no-reflow" phenomenon and minimize residual ischemic neurologic damage, must take into account this marked early post-ischemic reduction in sensitivity to normally potent cerebrovasodilatory influences.

Animals↗
PubMed1984

Effect of thiopental therapy on cerebral blood flow after total cerebral ischemia.

The effect of barbiturate coma upon regional cerebral blood flow (RCBF) and ultimate neurologic outcome was examined after total cerebral ischemia (TCI). TCI was induced in dogs using a relatively noninvasive double-occlusion balloon technique; cardiopulmonary protection was provided during the period of ischemia. RCBF was measured using 15-mu radioactively labeled microspheres. A reproducible pattern of impaired reperfusion of the central nervous system (CNS) was observed in control animals after the restoration of cerebral perfusion pressure after TCI. This pattern was accentuated by the administration of pentothal to induce barbiturate coma. The additional depression in RCBF in those animals receiving pentothal was most prominent in cortical gray matter and brainstem structures at 3 and 6 h after TCI. It was also observed in cortical white matter. No untreated animal surviving TCI achieved a neurologic functional level better than persistent vegetative (decerebrate) survival over 1 wk of observation. Animals receiving 90 mg/kg body weight of pentothal post-TCI demonstrated irreversible cardiogenic shock related to the myocardial depressant effect of the drug. Animals receiving 40 to 60 mg/kg of pentothal post-TCI demonstrated a survival rate similar to that of untreated animals. Although this study did not establish the possible effectiveness of barbiturate coma in improving residual neurologic damage after TCI, the data do demonstrate that any possible effectiveness in this model is not associated with any improvement in the markedly decreased cerebral perfusion after TCI.

Animals↗