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Biomedical subjects

C R Baker

Publications and source records attributed to C R Baker.

At least 19 recordsLinked to original sources
PubMed2003

Cognitive behavioural therapy as a potential treatment for vasovagal/neurocardiogenic syncope--a pilot study.

Vasovagal syncope (VVS) is an exaggerated tendency to the common faint that affects any age group. Conventional treatment is non-specific and involves strategies to increase blood pressure. Patients with VVS are often unable to work or complete education due to actual, or fear of, syncopal symptoms. Here we present a series of nine patients with VVS whose symptoms had proved resistant to conventional treatments where intervention with cognitive behavioural therapy (CBT) led to significant reductions in reported syncopal episodes and consultations at our unit. All subjects post-intervention were able to return to work or schooling. CBT is an effective treatment in those with difficult to manage VVS. Randomized controlled trials are needed.

Adolescent↗
PubMed2002

Arterial elastic properties and cardiovascular risk/event.

Cardiovascular disease is a major cause of morbidity and mortality in the western world. There is convincing evidence that the elastic properties, particularly of large arteries, are impaired in the presence of cardiovascular disease and risk factors such as cigarette smoking, hypertension, diabetes and ageing. Evidence is also emerging that treatment of these risk factors is associated with an improvement in the elastic properties, mirrored by a reduction in the cardiovascular risk and events. The main problems associated with arterial elasticity are the multiple definitions and methods of measurement and the problem of obtaining reliable nearby blood pressure measurement. Nevertheless, duplex estimation appears to be a non-invasive, accurate and reliable method of defining these properties. This method is broadly used as a research tool, but there is a good case for its use in clinical practice, particularly in the screening of patients at risk of cardiovascular events.

Age Factors↗
PubMed2002

Absorbed dose behind eye shields during kilovoltage photon radiotherapy.

The absorbed dose at the position of the lens of the eye under lead or tungsten eye shields during kilovoltage photon radiotherapy is critically dependent not so much on the thickness of the eye shield itself as on the size of the treatment field and the diameter of the shield used. Whilst dose from primary photons is easily attenuated to relatively insignificant levels by a few millimetres of lead or tungsten, scattered photons from outside the shielded area can provide over 25% of the prescribed dose. Since backscatter factors do not increase monotonically with photon energy, it is not safe to assume that the highest photon energy used will provide the highest dose. A simple method to estimate the dose under an eye shield based on tabulated backscatter factors is shown. Measurements under commercially available eye shields were made to verify the expression and to determine the attenuation of primary photons. Predicted and measured absorbed dose under the eye shields were found to agree to within 1% of the prescribed dose. The relative dose due to primary photons beneath the eye shields was found to be less than 0.1% and 0.5 (+/-0.1)% for the 150 kV and 260 kV beams, respectively. This is considerably less than the dose from backscattered radiation.

Eye Protective Devices↗
PubMed2001

How much surplus capacity is required to maintain low waiting times?

Random fluctuations in demand make it impossible to see all patients in a very short time scale unless capacity exceeds the mean demand. We describe a model to estimate the capacity levels required as a function of mean demand. Random fluctuations were assumed to follow a Poisson distribution. A Monte Carlo analysis was used to model variations in length of waiting times. To see patients without a waiting list the capacity must exceed mean demand by an amount proportional to the square root of the mean; if capacity equals mean demand, then actual demand will exceed capacity almost half the time. The smaller the mean demand, the greater the percentage increase in capacity that is required. Thus, subdivision of numbers, for subspecialization or fast-tracking, demands greater overall capacity. When multiple serial steps are required, each step must have spare capacity if a waiting list is to be avoided. When capacity is only slightly greater than mean demand, random fluctuations mean that targets can be met for long stretches of time, but these are interspersed with periods when the waiting list rises substantially. Allowing a small waiting time (2-4 weeks) considerably reduces the excess capacity required. Targets such as the 2-week wait for cancer referrals can be achieved only if resource levels are set to give considerably more patient slots per week than mean demand. The level of spare capacity required depends on the level of demand and the maximum waiting time permitted. Without surplus capacity, waiting targets cannot be met. To meet the 2-week waiting target, capacity must exceed mean demand by two patient slots per week for 99% success, or by one slot per week for 90% success.

Efficiency, Organizational↗
PubMed2000

Specificity of a new lipid mediator produced by testicular and peritoneal macrophages on steroidogenesis.

Macrophage-derived factor (MDF) is a lipophilic factor produced by rat testicular and peritoneal macrophages that maximally stimulates testosterone production by rat Leydig cells through a steroidogenic acute regulatory protein independent mechanism. The purpose of the present study was to determine whether MDF is also produced by human macrophages, and/or if it acts on human steroidogenic cells. We also studied the tissue-specific functions of MDF by determining if it also acts on steroidogenic cells of the ovary and adrenal glands and, if so, does it require new protein synthesis. It was found that MDF was produced by human peritoneal macrophages, and was capable of stimulating human steroidogenic cells. In terms of tissue specificity, it was found that primary cultures of rat adrenocortical cells respond to MDF with increased secretion of aldosterone and corticosterone, as did rat granulosa cells by producing progesterone. MDF acted in the presence of cycloheximide, indicating that it does not require new protein synthesis. These results indicate that MDF may have significant therapeutic potential and provide a basis for future studies concerning its physiological role in humans. These results further suggest that MDF is not only involved in paracrine regulation of Leydig cells, but also has the potential for the local regulation of steroidogenesis in both granulosa and adrenal cortical cells.

Adrenal Glands↗
PubMed1999

Bradykinin metabolism in perfused rat kidney.

The purpose of this study was to assess the capacity of perfused rat kidney to inactivate bradykinin (BK), and to compare the BK degrading capacity of rat kidney with the BK degrading capacities of rat lung, liver, and skeletal muscle, which was approximated by perfusion of rat hind limbs. Radioactively labeled BK, with the Pro2 and Pro3 residues having been tritiated, in an asanguinous salt solution was perfused through the kidney of the rat, over a concentration range of .0028-33 microM. Rat kidney had a large capacity to degrade BK and the system did not appear to approach saturation until perfusate BK concentrations reached 24 microM. A least-squares linear regression analysis and extrapolation to zero concentration was used to obtain values for amounts of BK degraded and BK fragments formed. The amount of BK cleaved was 99.9% of the administered dose. The major tritiated BK fragments formed, and the amount of each expressed as a percentage of the amount of BK degraded during transrenal passage, were the amino acid proline derived from the Pro2 and/or Pro3 residues of BK (Pro2,3), 60%; Pro-Pro (BK 2-3), 12%; Arg-Pro-Pro-Gly-Phe (BK 1-5), 14%; and Arg-Pro-Pro-Gly-Phe-Ser-Pro (BK 1-7), 14%. The formation of BK 2-3 is indicative of initial aminopeptidase-P cleavage of BK to yield Arg, and des-Arg1-BK. Thus in rat kidney the aminopeptidase-P pathway is the major route for BK degradation, as is the case in rat liver.

Animals↗
PubMed1999

Breast cancer treatment.

Nurse practitioners must be aware of the standard treatments for breast cancer whether they are referring a symptomatic patient to a breast cancer specialist, are involved in the actual treatment process, or are providing ongoing care for patients after completion of therapy. This article reviews the major treatments for breast cancer including surgery, radiation, and chemotherapy, with greater emphasis on treatment of early-stage disease.

Antineoplastic Agents↗
PubMed1998

Bradykinin metabolism in rat hind limbs.

The purpose of this study was to assess the capacity of perfused rat hind limbs, the majority of which is skeletal muscle, to inactivate bradykinin (BK), and to compare the BK degrading capacity of rat hind limbs with the BK degrading capacities of rat lung and liver. BK, with tritiated Pro2 and Pro3 residues, in an asanguinous salt solution was perfused for a single passage through skeletal muscle and other tissues in the hind legs of the rat over a concentration range of .0029 to 49.3 microM. Rat hind limbs had a large capacity to degrade BK and the system did not approach saturation, even at 49.3 microM. A least-squares linear regression analysis and extrapolation to zero concentration was used to obtain values for amounts of BK degraded and BK fragments formed. The amount of BK cleaved was 95% of the administered dose. The major BK fragments formed, and the amount of each expressed as a percentage of the amount of BK degraded were Pro-Pro (BK 2-3), 8.6%; Arg-Pro-Pro-Gly-Phe (BK 1-5), 82%; and Arg-Pro-Pro-Gly-Phe-Ser-Pro (BK 1-7), 6%. The BK 1-5 yield was reduced from 82% to one-fourth of that by angiotensin converting enzyme (ACE) inhibitors. BK 2-3 formation is indicative of initial aminopeptidase-P cleavage of BK to yield Arg, and des-Arg1-BK. ACE inhibitor sensitive formation of BK 1-5 is indicative of initial kininase-II, also known as ACE, cleavage of BK. Thus in rat hind limbs, the ACE pathway is the preponderant mechanism for BK degradation, which is in contrast to our previously published reports that in rat liver the amino-peptidase-P pathway predominates, and that in rat lung both the aminopeptidase-P pathway and the ACE pathway exhibit nearly equal capacities to degrade BK.

Animals↗
PubMed1997

Reconstruction of 6 MV photon spectra from measured transmission including maximum energy estimation.

Photon spectra from a nominally 6 MV beam under standard clinical conditions and at higher and lower beam qualities have been derived from narrow-beam transmission measurements using a previously published three-parameter reconstruction model. Estimates of the maximum photon energy present in each spectrum were derived using a reduced number of model parameters. An estimate of the maximum contribution of background, or room, scatter to transmission measurements has been made for this study and is shown to be negligible in terms of the quality index and percentage depth-dose of the derived spectra. Percentage depth-dose data for standard beam conditions derived from the reconstructed spectrum were found to agree with direct measurements to within approximately 1% for depths of up to 25 cm in water. Quality indices expressed in terms of TPR10(20) for all spectra were found to agree with directly measured values to within 1%. The experimental procedure and reconstruction model are therefore shown to produce photon spectra whose derived quality indices and percentage depth-dose values agree with direct measurement to within expected experimental uncertainty.

Biophysical Phenomena↗
PubMed1996

Bradykinin metabolism in the liver and lung of the rat.

Bradykinin (BK) in an asanguinous salt solution was perfused through intact rat liver. The perfusate was delivered through the portal vein and was collected from the inferior vena cava. BK concentrations varied from 0.0030 to 38.0 microm. The liver had a large capacity to degrade BK and the system did not approach saturation until perfusate BK concentrations reached 60 microm. The quantitatively predominant BK fragments formed and the amount of each formed, expressed as a percentage of the BK degraded during a single transhepatic passage, were Pro-Pro, 74%; Arg-Pro-Pro-Gly-Phe, 15%; and Arg-Pro-Pro-Gly-Phe-Ser-Pro, 7%; the first is indicative of initial aminopeptidase-P cleavage of BK to yield Arg and des-Arg1-BK and the latter two are indicative of initial angiotension converting enzyme (ACE) cleavage of BK. On the other hand, while the perfused rat lung also had a large capacity to degrade BK, the quantitatively predominant BK fragments formed and the amount of each formed, again expressed as a percentage of BK metabolized during a single transpulmonary passage, were Pro-Pro, 47%; Arg-Pro-Pro-Gly-Phe, 35%; and Arg-Pro-Pro-Gly-Phe-Ser-Pro, 7%. Thus in rat liver the aminopeptidase-P pathway is the major route for BK degradation, whereas in rat lung the aminopeptidase-P and the ACE pathways exhibit nearly equal capacities to degrade BK.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Reflective learning: a teaching strategy for critical thinking.

Most nurse educators claim that ability to critique one's clinical practice is a skill which must be acquired if nursing students are to continue to learn and develop as practitioners after they have graduated. This skill is of particular relevance for nurses who will be working independently in the community. The author reviews recent literature on critical thinking and reflective learning and identifies the results of one baccalaureate nursing school's use of reflective journals.

Clinical Competence↗
PubMed1995

Reconstruction of megavoltage photon spectra by attenuation analysis.

A simple analytical model for reconstructing photon spectra from the indirect measurement of transmission or depth-dose curves is presented, based on the Schiff expression for forward-directed bremsstrahlung differential in photon energy with added inherent filtration. Calculated transmission curves for 21 simulated and measured bremsstrahlung spectra with maximum photon energies in the range 4 to 30 MeV covering a broad range of filtration conditions were used to assess the model's ability to represent megavoltage spectra. Input data were reproduced to within 0.1 per cent in all cases, which is the same order of magnitude as the uncertainty involved in its calculation. Inclusion of a fourth parameter in the model is shown to allow the effective maximum photon energy present in the spectrum to be derived to an accuracy of approximately 3 per cent.

Humans↗
PubMed1992

Case-mix groups for VA hospital-based home care.

The purpose of this study is to group hospital-based home care (HBHC) patients homogeneously by their characteristics with respect to cost of care to develop alternative case mix methods for management and reimbursement (allocation) purposes. Six Veterans Affairs (VA) HBHC programs in Fiscal Year (FY) 1986 that maximized patient, program, and regional variation were selected, all of which agreed to participate. All HBHC patients active in each program on October 1, 1987, in addition to all new admissions through September 30, 1988 (FY88), comprised the sample of 874 unique patients. Statistical methods include the use of classification and regression trees (CART software: Statistical Software; Lafayette, CA), analysis of variance, and multiple linear regression techniques. The resulting algorithm is a three-factor model that explains 20% of the cost variance (R2 = 20%, with a cross validation R2 of 12%). Similar classifications such as the RUG-II, which is utilized for VA nursing home and intermediate care, the VA outpatient resource allocation model, and the RUG-HHC, utilized in some states for reimbursing home health care in the private sector, explained less of the cost variance and, therefore, are less adequate for VA home care resource allocation.

Aftercare↗
PubMed1992

Kinin metabolism in the perfused ventilated rat lung. II: Influence of ventilation, perfusion, and perfusate composition variation on bradykinin metabolism in uninjured lung.

Bradykinin metabolism by peptidases of the pulmonary endothelium has been investigated in the previously uninjured, ventilated, and asanguinously perfused rat lung. The influence of short-duration (up to 20 min) abnormal ventilation and perfusion conditions on bradykinin metabolism was assessed. Neither variation of the oxygen concentration (0 to 45%) nor omission of carbon dioxide in the ventilatory gas altered bradykinin metabolism significantly. Tidal volume variation did not alter bradykinin metabolism, and exclusion of one lung from the perfusion circuit reduced the capacity to degrade bradykinin proportionately. Acidification of the perfusion medium to pH 5 did not alter bradykinin metabolism. Acetylsalicylic acid in the perfusate protected the lung from an otherwise irreversible pressure increase associated with high-dose bradykinin perfusion. Endotoxin and hydrogen peroxide in the perfusate did not alter bradykinin metabolism. However, ammonia in the ventilatory gas caused immediate pulmonary edema, diminished lung capacity to metabolize bradykinin and altered the pattern of bradykinin metabolic products. The pulmonary endothelium itself, in the absence of blood, maintains its capacity to metabolize bradykinin under an extraordinary range of conditions.

Amino Acid Sequence↗
PubMed1991

Kinin metabolism in the perfused ventilated rat lung. I: Bradykinin metabolism in a system modeling the normal, uninjured lung.

Bradykinin (BK) in an asanguinous salt solution was perfused through intact rat lung. BK concentration varied from 0.0015 to 89 microM. Below 17 microM, the amount degraded was greater than or equal to 90% of the dose. The BK fragment distributions expressed as a percentage of the BK dose degraded were constant. The BK fragments formed and percentage yields were Pro-Pro (2-3) 49%, Arg-Pro-Pro-Gly-Phe (1-5) 32%, Pro-Pro-Gly-Phe-Ser-Pro (2-7) 6%, Arg-Pro-Pro-Gly-Phe-Ser-Pro (1-7) 6%, Arg-Pro-Pro (1-3) 3% and residual BK 4%. Above 17 microM, the amount of BK degraded was not proportional to the dose. Captopril and enalaprilat inhibited BK degradation, and their maximum inhibitions were about 50% and 30%, respectively. The percentage yield of the 1-5 fragment was greatly reduced by both inhibitors, but the percentage yields of the 2-3 and 1-8 fragments were moderately increased. It was concluded that (1) the intact rat lung itself has a very large capacity to degrade BK in the range of 2 mumoles/min/kg body weight; (2) two major and several minor enzyme pathways exist to degrade BK; (3) the relative contributions of these pathways to overall BK degradation remain essentially constant over a bradykinin concentration range from 0.0015 to 17 microM; (4) ACE/kininase-II catalyzed hydrolysis is one of the major pathways but is not the single major route for BK degradation; and (5) the other major BK degradation pathway involves enzymes cleaving the Arg1-Pro2 and Pro3-Gly4 bonds of BK.

Amino Acid Sequence↗
PubMed1989

Human lung membrane-bound neutral metallo-endopeptidase-catalyzed hydrolysis of bradykinin.

Human lung membrane-bound neutral metallo-endopeptidase (NME; EC 3.4.24.11) has been purified; this enzyme occurred in two forms, NME-I and NME-II. The total NME activity was purified 2,143-fold with the final specific activities for NME-I and NME-II being 750 and 1,124, respectively. The two NME forms were resolved in the final purification step involving ion exchange; in all earlier steps including gel filtration and affinity chromatography (phenyl sepharose) both forms behaved similarly and eluted simultaneously. NME-I and NME-II both had a Mr value of 97,000, and neither form dissociated into subunits. Catalytic actions of NME-I and NME-II upon bradykinin were identical; the Gly4-Phe5 and Pro7-Phe8 bonds of bradykinin were cleaved with the final hydrolytic products for each enzyme being the tetrapeptide, Arg-Pro-Pro-Gly, the tripeptide, Phe-Ser-Pro, and the dipeptide, Phe-Arg. The intermediate products were the heptapeptide, Arg-Pro-Pro-Gly-Phe-Ser-Pro, and the pentapeptide, Phe-Ser-Pro-Phe-Arg. Neither NME-I nor NME-II were inhibited by the angiotensin-converting enzyme inhibitor, captopril. Both enzymes were inhibited by phosphoramidon, dithiothreitol and EDTA. Other peptidase inhibitors and heavy metals were not effective NME inhibitors. Both NME-I and NME-II cleaved angiotensin-I at the Pro7-Phe8 bond, and substance-P at the Glu6-Phe7 bond, with the latter being much slower than the former.

Amino Acid Sequence↗