PubMed Health⌕ Search

Biomedical subjects

H Forster

Publications and source records attributed to H Forster.

At least 19 recordsLinked to original sources

Creep behavior of bone cement: a method for time extrapolation using time-temperature equivalence.

The clinical lifetime of poly(methyl methacrylate) (PMMA) bone cement is considerably longer than the time over which it is convenient to perform creep testing. Consequently, it is desirable to be able to predict the long term creep behavior of bone cement from the results of short term testing. A simple method is described for prediction of long term creep using the principle of time-temperature equivalence in polymers. The use of the method is illustrated using a commercial acrylic bone cement. A creep strain of approximately 0.6% is predicted after 400 days under a constant flexural stress of 2 MPa. The temperature range and stress levels over which it is appropriate to perform testing are described. Finally, the effects of physical aging on the accuracy of the method are discussed and creep data from aged cement are reported.

Journal Article↗

Frictional behaviour of bovine articular cartilage.

The experimentally measured indentation displacement and friction of normal and degraded (treated with chondroitinase AC) bovine articular cartilage plugs against a smooth steel plate were compared with the predictions based on the biphasic theory using the finite element method. It was found that the measured indentation displacement of both cartilage specimens could be predicted from the biphasic theory and the permeability for the degraded cartilage specimen was increased approximately three times. However, the measured friction coefficient was much lower for short period of loading, and the difference in the finite element prediction of friction coefficient between the normal and degraded cartilage specimens was not observed in the experiment. Therefore, it was concluded that both biphasic and other mechanisms were important in controlling the frictional and lubricating characteristics of articular cartilage in mixed and boundary lubrication regimes.

Animals↗

Medical and osteopathic boards' positions on chaperones during gynecologic examinations.

OBJECTIVE: The objective of this study was to determine whether United States medical or osteopathic boards have opinions, position statements, or policies on chaperone use, and whether any state laws regulate chaperone use. METHODS: United States Medical and Osteopathic Boards were surveyed by mail to determine whether policies, opinions, positions, or laws exist regarding use of chaperones during gynecologic examinations. We sent the survey to executives at 67 state boards, identified by a list from The Federation of State Medical Boards. Our main outcome measure was positive response to the survey questions. RESULTS: Of 67 targeted sites, 61 responded (91%). Fourteen sites (23%) reported having informal or unpublished opinions recommending chaperones. Eleven sites (18%) reported having positions related to chaperones that have been published for their physicians. Four sites (6.5%) reported having policies specifically related to chaperone use. Thirty-two sites (52.5%) reported that they do not have opinions, positions, or policies related to chaperone use. No site reported state laws governing chaperone use. CONCLUSION: Response to our survey showed no concensus among state medical boards on the use of chaperones, leaving doctors and patients to decide for themselves whether they want or need chaperones present during gynecologic examinations.

Female↗

The influence of continuous sliding and subsequent surface wear on the friction of articular cartilage.

Reciprocating motion friction tests were conducted upon cartilage-on-metal contacts while subjected to a constant load. Initial friction coefficients were compared with repeat friction coefficients following a sufficient load removal period. The repeat friction coefficients were marginally higher than the initial values and both were primarily dependent on the loading time. It was concluded that while a wear component had been identified, which modestly increased friction coefficients, the overriding parameter influencing friction was loading time. The authors postulate that fluid phase load carriage (being dependent on loading time) within the articular cartilage is largely responsible for low friction coefficients in the mixed and boundary lubrication regimes. This mechanism has been referred to as biphasic lubrication. Both synovial fluid and Ringer's solution were used as lubricants. Over the assessed 120 min loading time friction coefficients rose from 0.005 (for both lubricants) after 5 s to 0.50 and 0.57 for synovial fluid and Ringer's solution respectively. Synovial fluid was found to significantly reduce friction coefficients compared to Ringer's solution over broad ranges of the assessed loading times (p < 0.05). Stylus and non-contacting laser profilometry were successfully employed to provide reliable, quantitative and accurate measures of surface roughness. Laser profilometry before and after a continuous sliding friction test revealed a significant increase in surface roughness from Ra = 0.8 (+/- 0.2) micron to Ra = 2.1 (+/- 0.2) microns, (p < 0.0005); confirming that surface wear was occurring. Scanning electron microscopy (SEM) revealed the typical highly orientated collagen fibres of the superficial tangential zone. Environmental SEM (ESEM) of fully hydrated cartilage specimens provided largely featureless images of the surface which suggested that sample preparation for conventional SEM was detrimental to the authenticity of the cartilage surface appearance using SEM. Two distinct acellular, non-collagenous surface layers were identified using ESEM and transmission electron microscopy (TEM); respectively referred to as the boundary layer and surface lamina. The phospholipid/glycoprotein based boundary layer will provide boundary lubrication during intimate contact of opposing cartilage surfaces. The surface lamina, being a continuum of the proteoglycan interfibrillar matrix, is present to prevent fibrillation of the underlying collagen fibres. Both layers may contribute to the time dependent frictional response of articular cartilage. Although laser profilometry did reveal surface wear which was consistent with a small increase in friction, the primary variable controlling the friction coefficient was the period of loading.

Animals↗

Arginine vasopressin interacts with thromboxane in hydronephrosis.

The influence of hydronephrosis (6-10 wk) on the renal vascular response to arginine vasopressin (AVP) was assessed, using isolated perfused normal and hydronephrotic rat kidneys. In normal kidneys, AVP (0.3 nM) reduced renal perfusate flow (RPF) by 55 +/- 7% (P < 0.01). AVP-induced decrements in RPF were reversed partially by diltiazem (10 microM) and completely by 10 nM of an AVP (V1)-receptor antagonist (AVPX). In hydronephrotic kidneys, AVP reduced RPF by 81 +/- 2% (P < 0.01) and constricted afferent (AA) and efferent arterioles (EA) by 33 +/- 3 (P < 0.01) and 33 +/- 5% (P < 0.01), respectively. The addition of diltiazem altered neither RPF nor vessel diameters. Administration of AVPX recovered RPF, AA, and EA diameters. When hydronephrotic kidneys were pretreated with thromboxane (Tx) inhibitors, AVP reduced RPF by 62 +/- 5% (P < 0.01) and constricted AAs and EAs by 26 +/- 2 (P < 0.01) and 17 +/- 3% (P < 0.05), respectively. Under Tx blockade, diltiazem partially reversed the AVP-induced reduction in RPF and restored the decrements in AA diameter. Subsequent addition of AVPX returned RPF and EA diameter. Our data indicate that AVP elicits substantial renal microvascular constriction and suggest that AVP stimulates Tx production in hydronephrotic kidneys, thereby altering renal vascular responsiveness to this peptide.

Animals↗

The influence of loading time and lubricant on the friction of articular cartilage.

Friction of cartilage on metal, metal on cartilage and cartilage on cartilage contact configurations, within a mixed lubrication regime, was measured using synovial fluid, Ringer's solution or with no lubricant present. The main test variable was the period of stationary loading which ranged from 5 s to 45 min, prior to sliding and consequently measuring friction. The coefficient of friction rose gradually with increasing stationary loading time, up to a value of approximately 0.3 at 45 min for all the contact configurations. Following the re-application of load, after short periods of load removal, friction was also found to drop sharply. The flow of liquid in the biphasic cartilage and load carriage by the fluid phase was highlighted as being an important factor in reducing friction within the mixed or boundary lubrication regime. Movement of the contact zone over the cartilage counterface ensured very low friction as the slider moved over fully hydrated cartilage. For the cartilage--cartilage contacts synovial fluid significantly reduced friction compared to Ringer's solution. This was attributed to an effective boundary lubrication action, which was not as effective for the cartilage--metal contacts.

Animals↗

A quantitative assessment of renal blood flow autoregulation in experimental diabetes.

Several approaches have been utilized to describe renal blood flow (RBF) autoregulation in normal and pathological conditions. When describing the relation between RBF and stepwise decrements in renal perfusion pressure (RPP), these methods have several limitations, including: the necessity for predetermining a pressure 'break-point', and establishing constraints on changes in flow. To circumvent these limitations, we successfully utilized a third order polynomial, the cubical parabola, to characterize the autoregulatory responses in untreated streptozotocin (STZ) diabetic and control rats. The nonlinear relationship occurring between RBF and RPP was estimated from individual observations using the equation RBF = a + b x 10(-6) (RPP-c)3. Variables a and c represent RBF and RPP at the inflection point of the curve, respectively; variable b represents the rate of fall of RBF as RPP decreases (shape factor). Variable c was significantly lower in the diabetic group than in the control group whereas variable b was greater in the diabetic group. RBF (a) did not differ between the two groups. In conclusion, we determined that the range of RBF autoregulation in untreated diabetic rats is reset to a lower RPP. Furthermore, the curve below the inflection point declines more rapidly in diabetic rats than in controls. We propose that the equation described herein constitutes a promising and reproducible method for describing RBF autoregulation in vivo.

Animals↗

Effects of changing the pattern of sickness absence referrals in a local authority.

The high costs of sickness absence in North Tyneside Metropolitan Borough Council prompted a review of the system of referral of cases of long-term sickness absence to their occupational health service for opinion about fitness to work. Earlier and more consistent referral of these employees produced reductions in average lengths of sickness absence. Time off before medical retirement was reduced from 72 weeks to 53 weeks, and time off before returning to work was reduced from 40 weeks to 25 weeks. Exact figures of the financial savings could not be calculated, but the estimated saving was 760,000 pounds in the first year. Although the occupational health service was not responsible for the whole of this saving, it played an important role in the exercise. It was concluded that earlier referral of employees with long-term sickness absence enabled decisions about returning to work to be made sooner, thus saving large amounts of money.

Absenteeism↗

Protein kinase C and calcium channel activation as determinants of renal vasoconstriction by angiotensin II and endothelin.

The mechanisms mediating renal microvascular constriction induced by angiotensin II (Ang II) and endothelin (ET) have not been fully established. In the present study, we have determined the effects of isradipine, a dihydropyridine calcium antagonist, on Ang II- or ET-induced constriction of afferent arterioles (AAs) and efferent arterioles (EAs) using the isolated perfused hydronephrotic kidney. Ang II (0.3 nmol/L) and ET (0.3 nmol/L) constricted AAs by 36 +/- 2% and 29 +/- 3%, respectively. Isradipine reversed AA constriction induced by both peptides. However, Ang II-induced AA constriction was more sensitive to isradipine than ET-induced constriction (half-maximal inhibitory concentration [IC50], 1.2 +/- 0.2 nmol/L [n = 12] versus 170 +/- 65 nmol/L [n = 19]; P < .01). The sensitivity of Ang II-induced AA constriction to isradipine was identical to that of KCI-induced AA constriction (IC50, 4.2 +/- 0.9 nmol/L; n = 12). Pretreatment with staurosporine (50 nmol/L), a protein kinase C inhibitor, enhanced the sensitivity of ET-induced AA constriction to isradipine (4.3 +/- 1.7 nmol/L, n = 14), rendering it identical to that of KCl-induced AA constriction. Ang II and ET decreased EA diameter by 26 +/- 2% (n = 12) and 12 +/- 2% (n = 8), respectively. In contrast to AA constriction, EA constriction induced by both peptides was relatively refractory to isradipine.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaloids↗

Characterization of the renal microvascular actions of a new dopaminergic (DA1) agonist, YM435.

The renal vasculature is known to possess receptors for dopamine. The effects of dopamine and its mimetics on renal hemodynamics, however, have not been fully determined. In the present study, we have characterized the actions of the dopaminergic (DA1) agonist, YM435, on renal microvascular constriction induced by two dissimilar peptide vasoconstrictors, angiotensin II (AII) and endothelin (ET), in the isolated perfused hydronephrotic rat kidney. AII (0.3 nM) constricted afferent (AA) and efferent arterioles (EA) by 30 +/- 2% and 28 +/- 4%, respectively. ET (0.3 nM) preferentially constricted AA (37 +/- 2%) more than EA (18 +/- 2%). The subsequent administration of YM435 reversed the constrictor effects of AII or ET on both AA and EA in a dose-dependent manner. Although YM435 reversed AA and EA vasoconstriction induced by each peptide, the half-maximal inhibitory concentration for YM435 of ET-induced constriction exceeded that of AII (P < .001). Our findings constitute the first demonstration that YM435 is a potent vasodilator in the setting of either AII- or ET-induced AA and EA constriction. These results indicate that DA1 agonists reverse renal microvascular constriction mediated by AII and/or ET, and suggest that both AA and EA constitute the renal microvascular sites of action for DA1 agonists.

Angiotensin II↗

Attenuation of endothelin effects by a chloride channel inhibitor, indanyloxyacetic acid.

We have recently proposed that the actions of endothelin (ET) are in part mediated by opening of chloride channels (K. Iijima, L. Lin, A. Nasjletti, and M. S. Goligorsky. Am. J. Physiol. 260 (Cell Physiol. 29: C982-C992, 1991). In the present study the ability of a chloride channel inhibitor, an indanyloxyacetic acid (IAA-94), to block ET-induced effects was examined in cultured vascular smooth muscle cells (VSMC) by spectrofluorometry and direct videomicroscopic visualization of the renal microcirculation in isolated perfused hydronephrotic kidneys (IPHK). A fluorescein isothiocyanate (FITC)-labeled IAA-94 analogue showed specific binding to VSMC. IAA-94 (30 microM) neither affected basal cytosolic calcium concentration ([Ca2+]i) in VSMC nor peak response to ET, but it significantly curtailed sustained elevation of [Ca2+]i (half-time recovery was 147 +/- 23 vs. 248 +/- 33 s in control, P less than 0.05). IAA-94 blunted ET-induced membrane depolarization from 24.5 +/- 3.3 to 8.0 +/- 1.8 mV. In IPHK, ET constricted afferent arterioles (AA) by 29 +/- 2% (18.7 +/- 0.8 to 13.2 +/- 0.6 microns, P less than 0.001). Isradipine reversed this ET-induced vasoconstriction. Pretreatment with IAA-94 did not alter AA diameter, but markedly attenuated ET-induced AA constriction (reduction of AA diameters by only 9 +/- 2%, P less than 0.001). The subsequent addition of isradipine (0.1-1 microM) did not further dilate AA. Our data indicate that IAA-94 markedly attenuates AA vasoconstriction elicited by ET and suggest that ET-induced opening of chloride channels, membrane depolarization, and subsequent activation of voltage-dependent calcium channels contribute to the vasoconstrictor mechanisms of this peptide.

Animals↗

Impaired myogenic responsiveness of renal microvessels in Dahl salt-sensitive rats.

The mechanisms mediating abnormal renal autoregulation in Dahl salt-sensitive (DS) rats have not been fully defined. In the present study, we assessed myogenic responsiveness of interlobular arteries (ILAs), afferent arterioles (AAs), and efferent arterioles in isolated perfused hydronephrotic Dahl rat kidneys. Dahl rats were divided into four groups according to strain (Dahl salt-resistant [DR] or DS rats) and dietary sodium manipulation (rats fed low or high salt diets). Systolic blood pressure was elevated only in DS rats fed the high salt diet (202 +/- 4 mm Hg, p less than 0.05). Myogenic responses were obtained by stepwise elevation of renal arterial pressure. Vessel diameters were determined by computer-assisted videomicroscopy. Preglomerular microvessels of DS and DR rats responded differently to changes in renal arterial pressure. AAs and ILAs manifested diminished myogenic responsiveness to increasing renal arterial pressure in DS rats compared with DR rats (p less than 0.05). Both AAs and ILAs in DS rats manifested a higher threshold pressure for eliciting myogenic responses and a decrease in maximal pressure-induced vasoconstriction. The sensitivity of the AA myogenic response to nifedipine was enhanced in DS rats compared with DR rats (p less than 0.05). For rats fed the high salt diet, preglomerular vessels exhibited reduced myogenic responsiveness in both strains. In contrast to preglomerular microvessels, efferent arterioles from all four groups of rats failed to exhibit pressure-induced vasoconstriction. Our data suggest that diminished myogenic responsiveness of AAs and ILAs in DS rats contributes to impaired renal autoregulation in this strain.

Animals↗

Impaired myogenic responsiveness of the afferent arteriole in streptozotocin-induced diabetic rats: role of eicosanoid derangements.

Evidence suggests that diabetes is associated with an impairment of renal autoregulation. It has previously been demonstrated that pressure-induced (myogenic) afferent arteriolar vasoconstriction is well preserved in the isolated perfused hydronephrotic kidney. In this study, pressure-induced afferent arteriolar vasoconstriction was examined in kidneys from streptozotocin-induced diabetic rats. Vessel diameters were measured by videomicroscopy as renal arterial pressure was elevated from 80 to 180 mm Hg. In normal kidneys, the afferent arteriole vasoconstricted progressively as renal arterial pressure was increased (-24 +/- 2% decrement in diameter at 180 mm Hg; N = 35; P less than 0.001). In contrast, afferent arterioles of diabetic kidneys exhibited a greatly attenuated response to pressure (i.e., -3 +/- 2% change at 180 mm Hg; N = 60). In vitro treatment with 100 microM ibuprofen completely restored myogenic vasoconstriction (-21 +/- 2% change at 180 mm Hg), but did not alter myogenic responses of control (i.e., nondiabetic) kidneys. The control of hyperglycemia by insulin treatment resulted in a partial preservation of myogenic vasoconstriction (i.e., -11 +/- 3% change at 180 mm Hg), which was further restored by the administration of a low dose (10 microM) of ibuprofen (-21 +/- 1% change at 180 mm Hg). These observations indicate that diabetes is associated with an impaired responsiveness of the afferent arteriole to pressure that is mediated by an alteration in eicosanoid metabolism. This deranged renal microcirculatory response to pressure may represent a functional impairment of the diabetic kidney that may contribute to the progression of diabetic nephropathy.

Acetylcholine↗