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Biomedical subjects

M A Adams

Publications and source records attributed to M A Adams.

At least 55 records · Page 3Linked to original sources

Simultaneous determination by capillary gas chromatography of organic acids, sugars, and sugar alcohols in plant tissue extracts as their trimethylsilyl derivatives.

A capillary gas chromatographic (GC) method for the simultaneous determination of organic acids, sugars, and sugar alcohols extracted from plant tissues is described. Plant leaves were extracted in 5% (w/v) perchloric acid and neutralized extracts were purified using C18 cartridges. Organic acids, sugars, and sugar alcohols in purified extracts were converted to their trimethylsilyl (TMS)/TMS-oxime derivatives prior to separation and detection by capillary GC with flame ionization detection (FID). Derivatization procedures were investigated in detail and the compounds of interest were readily converted to their TMS/TMS-oxime derivatives using hexamethyldisiazane reagent in acetonitrile solvent (1:6 v/v) at 100 degreesC for 60 min. The derivatives were sufficiently volatile and stable. The FID response to derivatized compounds was generally linear in the concentration range 30-300 microg ml-1, with detection limits in the order of 3-76 ng. The proposed method was demonstrated for the determination of organic acids, sugars, and sugar alcohols in leaf extracts of two native Australian plants.

Biochemistry↗

Experimental determination of stress distributions in articular cartilage before and after sustained loading.

OBJECTIVE: To test the hypotheses that stress concentrations exist within articular cartilage, and are intensified by sustained 'creep' loading. DESIGN: Matched-pair comparison of stress distributions in cartilage, in vitro, before and after creep. BACKGROUND: The ability of cartilage to equalize contact stresses between articulating surfaces may be compromised by undulations in the subchondral bone, and by variations in chemical composition. Furthermore, any stress concentrations within cartilage may be affected by creep loading, which-reduces its water content. METHODS: Sixteen specimens of apparently normal cartilage-on-bone, 12 mm x 15 mm, were removed from the femoral condyles and tibial plateaux of patients undergoing total knee replacement. The cartilage was subjected to a nominal compressive stress of 2 MPa by means of a 10 mm-diameter flat impermeable indentor. During the 20 s loading period, a miniature pressure transducer, side-mounted in a 0.9 mm-diameter needle, was pulled through the cartilage in a direction parallel to the surface, while transducer output and position were sampled at 25 Hz. 'Stress profiles' were obtained with the transducer pointing in the 12 o'clock and 3 o'clock directions, and were repeated after creep loading at 1.6 MPa for 2 h. RESULTS: Validation tests indicated that transducer output was proportional to the average compressive stress, but overestimated it by 9-15%. Stresses were greatest under the centre of the indentor, and showed local variations ('concentrations') which were increased in number and size after creep loading. CONCLUSIONS: Measured values of compressive stress incorporate small systematic errors. Nevertheless, the results presented clearly support both hypotheses.

Aged↗

The penis is not protected--in hypertension there are vascular changes in the penis which are similar to those in other vascular beds.

In hypertension, small arteries in a variety of vascular beds undergo structural changes that increase resistance. To assess whether there are differential structural changes in the penis that accompany hypertension, we began with determining structurally-based vascular resistance properties in penile and hindlimb vascular beds of adult spontaneously hypertensive rats (SHR) and Sprague-Dawley (SD) rats. In anesthetized SHR, the penile and hindlimb vasculature were isolated and perfused, maximum dilation was induced, and a flow-pressure assessment and alpha 1-adrenoceptor agonist concentration-response curves were generated. Both the baseline and maximum constrictor responses were similar in the two beds of each strain, and overall the maximum structurally-based vascular resistance in SHR was higher than in SD rats. Our data suggests that the penile vasculature is not protected from the structural changes that take place in the other vascular beds in hypertension. There does not appear to be an underlying functional control mechanism that protects the penile vasculature from structural changes that may have a negative impact on penile blood flow.

Animals↗

Prediction of maximal back muscle strength from indices of body mass and fat-free body mass.

OBJECTIVES: The purpose of this study was to examine, in healthy volunteers, the relationship between back extensor muscle strength and body size. METHODS: The maximal voluntary isometric back extensor strength of 456 volunteers, aged 18-42 yr and with no history of low back pain, was measured in a standing, slightly flexed forward posture. This was then correlated with two indices of body size: body mass and fat-free body mass. RESULTS: Significant linear relationships were observed between back muscle strength and each of the two indices of body size. There was a gender difference in both the slope and the intercept of the regression equations describing the relationships. There was no independent influence of age within the range studied. CONCLUSION: It was possible to establish predictive equations for back extensor strength based on body size which could be used to quantify strength 'deficits', for instance in patients with low back pain, and to prescribe submaximal target forces for use in endurance training and testing.

Adult↗

Short- and long-term enalapril affect renal medullary hemodynamics in the spontaneously hypertensive rat.

Long-term angiotensin-converting enzyme (ACE) inhibition in the spontaneously hypertensive rat (SHR) resets pressure natriuresis and shifts the relationship between renal arterial pressure (RAP) and renal interstitial hydrostatic pressure (RIHP) to lower levels of arterial pressure. These effects persist after withdrawal of treatment. The purpose of this study was to determine the effect of short- and long-term ACE inhibition on medullary blood flow (MBF). Enalapril (25 mg. kg-1. day-1 in drinking water) was given to male SHR from 4 to 14 wk of age. Four weeks after stopping treatment, we measured MBF over a wide range of RAP using laser-Doppler flowmetry in anesthetized rats. Additional rats, either untreated or previously treated for 10 wk, received 3-day enalapril treatment just before the experiment. MAP (mmHg +/- SE) was 178 +/- 6 (n = 8), 134 +/- 6 (n = 8), 138 +/- 5 (n = 9), and 111 +/- 6 mmHg (n = 9) for the untreated, 3 day, 10 wk, and 10 wk + 3 day groups, respectively. Total renal blood flow for the groups receiving 3-day treatment was significantly higher when compared with that in rats with an intact renin-angiotensin system. Three-day treatment had no effect on the relationship between RAP and RIHP, whereas that in rats receiving 10-wk treatment was shifted to lower levels of RAP by approximately 30 mmHg. Both 10-wk and 3-day treatment independently increased the slope of the RAP versus MBF relationship at values of RAP > 100 mmHg. The slopes in perfusion units/mmHg were 0.12 +/- 0.01 (n = 8), 0.26 +/- 0.01 (n = 8), 0.27 +/- 0.01 (n = 9), and 0.30 +/- 0.02 (n = 9) for the untreated, 3 day, 10 wk, and 10 wk + 3 day groups, respectively. These results indicate that the effect of short-term and the persistent effect of long-term enalapril alter renal medullary hemodynamics in a way that may contribute to the resetting of the pressure-natriuresis relationship in treated rats.

Angiotensin-Converting Enzyme Inhibitors↗

Differential regulation of IGF-I, its receptor and GH receptor mRNAs in the right ventricle and caval vein in volume-loaded genetically hypertensive and normotensive rats.

It has been suggested, mainly by in vitro findings, that cardiovascular tissue in the spontaneously hypertensive rat (SHR) should be more prone to proliferate/hypertrophy than that of the Wistar-Kyoto rat (WKY). The present study tests the hypothesis that the tissue of the low-pressure compartment in SHR, being structurally similar to that of the WKY, shows an increased growth response due to activation of the GH-IGF-I system. An aortocaval fistula (ACF) was induced in 64 SHR and WKY male rats and 44 rats served as controls. They were all followed for 1, 2, 4 and 7 days after surgery. In separate groups of SHR (n=4) and WKY (n=3), central venous pressure was measured by telemetry recordings prior to opening of the fistula and for up to 16 h post-surgery. Systolic blood pressure was measured during the week post-surgery. The right ventricular (RV) and the caval vein IGF-I mRNA and RV IGF-I receptor and GH receptor mRNAs were quantitated by means of solution hybridisation assay. In rats with ACF the systolic blood pressure decreased, approximately 29% in SHR and 16% in WKY between 1 and 7 days post-surgery (P<0.05, n=5-6 in each group). SHR with ACF showed a transient elevation in central venous pressure vs WKY. Within the week following fistula induction both strains showed a similar, pronounced increase in RV hypertrophy. SHR with ACF showed a smaller, or even blunted, overall response with respect to activation of the GH-IGF-I system compared with WKY, the latter showing clear-cut elevation of gene expressions. Two days after shunt opening in SHR, RV and caval vein IGF-I mRNA increased by 57% and 108% (P<0.05 for both, n=5-6 in each group) respectively, and these expressions were then turned off, whereas RV GH receptor and IGF-I receptor mRNA expression remained unaffected compared with WKY rats. WKY rats showed on average a later and a greater response of GH-IGF-I system mRNA expression vs SHR. The present in vivo study suggests that the SHR requires less activation of the GH-IGF-I system for creating a given adaptive structural growth response.

Animals↗

Renal interstitial hydrostatic pressure and urinary sodium excretion in rats with angiotensin-converting enzyme inhibitor-induced papillary atrophy.

The importance of angiotensin type-1 (AT1) receptor stimulation during renal development has recently been established in both pharmacological and knockout models. We have previously reported irreversible and progressive papillary atrophy and a reduced baseline renal interstitial hydrostatic pressure (RIHP) after neonatal angiotensin-converting enzyme (ACE) inhibition. The aim of the present study was to investigate the consequences of these abnormalities on urinary sodium excretion during acute extracellular sodium loading. Rats were treated neonatally with enalapril (10 mg kg-1 day-1) or saline control from days 3 to 23 after birth. Urinary sodium excretion was assessed in relation to mean arterial pressure (MAP) and RIHP responses in adult anaesthetised rats during moderate (1.5 and 3 % body weight) and severe (9 % body weight) saline-induced volume expansion. Control rats responded to the moderate volume expansion by increasing MAP by 16 +/- 6 % and RIHP by 40 +/- 23 %, respectively. In neonatally enalapril-treated rats, however, MAP and RIHP remained unchanged and were associated with a smaller increase in sodium excretion (44 +/- 11 % of the total amount infused versus 71 +/- 16 % for controls, P < 0.05). In contrast, severe volume expansion resulted in marked pressure rises in both the enalapril-treated group (36 +/- 12 and 112 +/- 48 % of baseline for MAP and RIHP, respectively) and the control group (34 +/- 21 and 130 +/- 34 % of baseline for MAP and RIHP, respectively). Moreover, the increases in MAP and RIHP were associated with complete excretion of the severe sodium challenge within 60 min in both treatment groups. We conclude that a RIHP response appears to be a prerequisite for adequate urinary sodium excretion in this model of papillary atrophy. Hence, an intact renal medulla is not mandatory in the renal handling of sodium during extracellular loading.

Angiotensin-Converting Enzyme Inhibitors↗

Simultaneous analysis of amino and organic acids in extracts of plant leaves as tert-butyldimethylsilyl derivatives by capillary gas chromatography.

The simultaneous determination of amino and organic acids in plant tissue extracts using capillary gas chromatography is described. Plant leaves were extracted in 5% (w/v) perchloric acid and neutralized extracts were purified using C18 cartridges. The amino and organic acids in purified extracts were then converted to tert-butyldimethylsilyl (TBDMS) derivatives prior to separation and detection by capillary gas chromatography (GC) with flame ionization detection. Conditions required for optimal derivatization were investigated. Amino and organic acids were readily converted to their TBDMS derivatives using N-methyl-N-tert-butyldimethylsilyltrifluoroacetamide in dimethylformamide solvent 1:6 (v/v) with an average recovery of 90% and a reproducibility of about 5%. The characteristic [M-57] and [M-159] fragment ion of the TBDMS derivatives was confirmed using GC-MS. The proposed method was demonstrated by the determination of amino and organic acids in extracts of Acacia and Eucalyptus leaves, where detection limits were 1-20 ng.

Acacia↗

Repetitive lifting tasks fatigue the back muscles and increase the bending moment acting on the lumbar spine.

During manual handling, the back muscles protect the spine from excessive flexion, but in doing so impose a high compressive force on it. Epidemiological links between back pain and repetitive lifting suggest that fatigued muscles may adversely affect the balance between bending and compression. Fifteen volunteers lifted and lowered a 10 kg weight from floor to waist height 100 times. Throughout this task, the bending moment acting on the osteoligamentous lumbar spine was estimated from continuous measurements of lumbar flexion, obtained using the 3-Space Isotrak. Spinal compression was estimated from the electromyographic (EMG) activity of the erector spinae muscles, recorded from skin-surface electrodes at the levels of T10 and L3. EMG signals were calibrated against force when subjects pulled up on a load cell, and correction factors were applied to account for changes in muscle length and contraction velocity. Fatigue in the erector spinae muscles was quantified by comparing the frequency content of their EMG signal during static contractions performed before, and immediately after, the 100 lifts. Results showed that peak lumbar flexion increased during the 100 lifts from 83.3 +/- 14.8% to 90.4 +/- 14.3%, resulting in a 36% increase in estimated peak bending moment acting on the lumbar spine (P = 0.008). Peak spinal compression fell by 11% (p = 0.007). The median frequency of the EMG signal at L3 decreased by 5.5% following the 100 lifts (p = 0.042) confirming that the erector spinae were fatigued, but measures of fatigue showed no significant correlation with increased bending. We conclude that repetitive lifting induces measurable fatigue in the erector spinae muscles, and substantially increases the bending moment acting on the lumbar spine.

Adult↗

Inhibited expression of insulin-like growth factor I mRNA and attenuated cardiac hypertrophy in volume overloaded hearts treated with difluoromethylornithine.

The present study examined whether the previously reported hypertrophy and increased expression of insulin-like growth factor I (IGF-I) mRNA in the volume-overloaded right ventricle was dependent on an intact production of polyamines. Volume overload was created in normotensive Wistar rats by means of an aorto-caval fistula. Difluoromethylornithine (DFMO) 2%, which is a specific, irreversible blocker of ornithine decarboxylase, was administered in the drinking water to intervention groups and one sham group, respectively, 24 h prior to surgery and for up to 26 days. DFMO blocked transiently the early over-expression of right ventricular IGF-I mRNA and attenuated the rapid development of both right and left ventricular hypertrophy during volume overload. Expression of IGF-I mRNA in the right ventricle in the early phase of volume overload appears to be dependent on activation of ornithine decarboxylase, whereas other pathways are involved in the later phase of cardiac structural adaptation. Thus, these findings link together early and late growth responses potentially important for compensatory cardiac hypertrophy.

Angiotensin II↗

When is a lifting movement too asymmetric to identify low-back loading by 2-D analysis?

In ergonomics research, two-dimensional (2-D) biomechanical models are often used to study the mechanical loading of the low back in lifting movements. When lifting movements are asymmetric, errors of unknown size may be introduced in a 2-D analysis. In the current study, an estimation of these errors was made by comparing the outcome of a 2-D analysis to the results of a recently developed and validated 3-D model. Four subjects made two repetitions of five lifting movements, differing in the amount of asymmetry. The results showed a significant underestimation of the peak torque by 20, 36 and 61% when the initial position of a box was rotated 30, 60 and 90 degrees with respect to the sagittal plane of the subject. The main cause of this underestimation was a pelvic twist, resulting in an erroneous projection of a pelvic marker on to the sagittal plane due to pelvic twist. It is suggested that from 30 degrees box rotation a 2-D analysis may easily lead to wrong conclusions when it is used to study asymmetric lifting.

Adult↗

Long-term reduction of renal interstitial hydrostatic pressure after neonatal renin-angiotensin system inhibition in the rat.

BACKGROUND: Neonatal inhibition of the renin angiotensin system (RAS) causes a decreased urinary concentrating ability, papillary atrophy, and tubulointerstitial inflammation long term. As a consequence of these morphological changes, we surmised that renal blood flow and renal interstitial hydrostatic pressure (RIHP) may be altered during and shortly after cessation of neonatal angiotensin-converting enzyme (ACE) inhibition, and that tentative changes of these variables would persist long after treatment withdrawal. METHODS: Rats were given daily intraperitoneal injections of the ACE inhibitor, enalapril (10 mg/kg) or saline from days 3 to 23 postpartum, and the relationship between renal perfusion pressure (PP) and RIHP was investigated in 6- and 13-week-old anaesthetized rats. RESULTS: Neonatal ACE inhibition did not affect baseline RIHP short term, whereas RIHP was reduced at 13 weeks of age versus controls (11.6+/-1.6 vs 18.5+/-1.0 mmHg, P<0.05). Changes in RIHP correlated positively to changes in renal PP, independent of treatment and age (slope averaged 0.11+/-0.03). Ongoing ACE inhibition until 6 weeks of age neither affected baseline RIHP nor altered the reactivity to changes in perfusion pressure. Mild renal histopathological abnormalities were present already 3 weeks after cessation of treatment and were aggravated significantly in the 13-week-old rats, showing a complete loss of the papillary parenchyma. CONCLUSION: The reduced baseline RIHP in adult rats seemed to constitute a functional correlate to the major papillary atrophy. However, RIHP responses to changes in renal perfusion pressure was maintained, possibly indicating a compensatory effect of the remaining vasa recta and/or peritubular capillary network. Taken together, lack of neonatal angiotensin II type-1 (AT1) receptor stimulation induces not only irreversible abnormalities of the renal architecture, but causes alteration of intrarenal haemodynamics, such as a reduced RIHP, which may have implications for the regulation of pressure-natriuresis.

Angiotensin-Converting Enzyme Inhibitors↗

The compressive strength of articular cartilage.

Articular cartilage provides the smooth bearing surfaces in freely moving (synovial) joints. Its mechanical properties are important because structural failure of cartilage is closely associated with joint disorders, including osteoarthritis. Some mechanical properties of cartilage are well characterized, but little is known about its compressive strength. A technique for measuring cartilage compressive strength is evaluated, and an overview of experiments which relate strength to stiffness and tissue hydration is given. Specimens of bovine articular cartilage-on-bone, approximately 15 mm square, were loaded on a hydraulic materials testing machine using flat impermeable indentors. Linear-ramp loading/unloading cycles of 1 s duration, and of increasing severity, were applied until failure was evident on force-displacement graphs. Some specimens were tested following a 30 min period of creep loading. Inkstaining and histology were used to locate the site of initial damage to each specimen. Specimen failure occurred first in the cartilage surface layer at a nominal applied stress of 14-59 MPa (mean 35.7 MPa). Mechanical properties were little affected by specimen or indentor size, provided both remained within defined limits, and compressive strength could be measured to an accuracy of approximately +/- 5 per cent. Compressive stiffness was a significant predictor of strength, but only if it was measured at high levels of stress. Strength increased following creep-induced water loss, and initial mechanical damage could propagate under moderate cyclic loading. This technique for measuring cartilage compressive strength has potential for investigating the causes of cartilage failure in vivo.

Animals↗

Sustained loading increases the compressive strength of articular cartilage.

INTRODUCTION: When synovial joints are subjected to sustained or repetitive loading, fluid is driven from the articular cartilage so that it is less able to equalise compressive stress between opposing joint surfaces. We test the hypothesis that sustained loading reduces the compressive strength of cartilage-on-bone. METHODS: Forty specimens of articular cartilage-on-bone, approximately 15 mm square, were removed from the patella groove of mature bovine knees. Specimens were loaded on a materials testing machine using a 5 mm-diameter plane-ended indentor. Controlled loading/unloading cycles of 1s duration, and of increasing severity, were applied until failure was evident on the force-deformation graphs. Half of the specimens were 'creep loaded' for 30 at 2 MPa before their strength was assessed. After testing, damage was investigate using ink staining of the cartilage surface, and histology. RESULTS: Sustained loading reduced cartilage thickness by 45% and creep-loaded specimens were 21% stronger (P = 0.01). Most specimens appeared to fail by fissuring of the cartilage surface zone. CONCLUSION: Sustained loading strengthens cartilage by expelling water from it, reducing the tendency of the surface zone to rupture in the manner of an over-inflated car tyre.

Animals↗

Could sudden increases in physical activity cause degeneration of intervertebral discs?

Epidemiological studies link high repetitive loading of the lower back with degeneration of intervertebral discs, and experiments on cadaver spines confirm that repetitive mechanical loading can disrupt the lumbar discs in a manner characteristic of "degeneration". But why do living discs not just strengthen in response to this stimulus, as other musculo-skeletal tissues do? Our hypothesis proposes that the low metabolic rate of lumbar discs (the largest avascular structures in the body) prevents them from keeping pace with adaptive remodelling changes in adjacent tissues, so that large and abrupt increases in a person's level of physical activity may leave the lumbar discs the weak link in a strengthening and heavily loaded spine. Recent laboratory investigations support the hypothesis, but clinical evidence is required to relate recent disc degeneration with recent increases in physical activity, and so test the hypothesis.

Fatigue↗

Acquired immunodeficiency syndrome dementia complex.

Acquired immunodeficiency syndrome (AIDS) has become an epidemic in the United States. AIDS dementia complex (ADC) is a neurological dysfunction which has been indicated in 25-90% of AIDS patients, 30-40% of HIV-infected patients, and may be the only presenting manifestation of AIDS. Researchers have investigated many aspects of ADC including clinical features, etiology, epidemiology and prevalence, diagnosis (psychological parameters and laboratory investigations such as CSF, EEG, CT, MRI, PET, and ERP), assessment, neurological features (including neuropsychiatric and neuropsychological measures, and neuropathology), prognosis, and treatment. The research is controversial, complex, and contradictory. A discussion of the many areas of ADC and many hypotheses will be included.

AIDS Dementia Complex↗

Vascular control mechanisms in penile erection: phylogeny and the inevitability of multiple and overlapping systems.

A co-ordinated series of vascular events underlie the generation of a penile erection. The control and regulation of this simple event is, in fact, a complex of interactions occurring at multiple levels. Many of these individual pathways and responses have been studied extensively. The understanding of the necessity of the integration between the individual pathways into a complex of series and parallel coupled mechanisms provides a rationale for the development of a framework of multiple and overlapping systems. This paper sets out some of the principles of integrated and balanced control of vasodilation and vasoconstriction in the penis. In addition, the role of growth induction and regression and the importance of time as a factor in studying penile structure and function is discussed.

Animals↗

A therapeutic taxonomy of treatments for erectile dysfunction: an evolutionary imperative.

AIM OF THE STUDY: A functional classification of treatments for erectile dysfunction is important but none exists at present. Advances in the understanding of the mechanisms of drug action and of the mechanisms of penile erection suggest that there is now a rational basis for a therapeutic classification, with the expectation that a logical diagnostic classification will follow. METHODS: The currently available treatments for erectile function and the known relevant basic science were reviewed and assessed. From this, and analysis of classification systems in other fields, a classification was proposed and evaluated with respect to existing treatments. RESULTS: The treatments for erectile dysfunction were classified into five major classes by their mode of action: (I) Central Initiators, (II) Peripheral Initiators, (III) Central Conditioners, (IV) Peripheral Conditioners and (V) Other. Drugs in these classes are further subdivided by the routes of administration and the mechanisms of specificity. CONCLUSIONS: It is possible to analyze all known treatments using this classification. The principles of this scheme should be sufficiently clear as to enable knowledgeable specialists to arrive at similar conclusions about a drug. The classification proposed is general enough such that most new drugs should fall within a class. However, it should be modified if necessary, if new therapeutic agents can not be appropriately classified. It is our conclusion that with such endeavours the specialty itself and national regulatory bodies will find it easier to define and control how to apply new drugs, how to evaluate new drugs, and how to establish reasonable equivalences among agents and in whom these drugs and devices should be used.

Erectile Dysfunction↗