Significant Increase In Force Research Articles

Biomechanical evaluation of a low anterior wall fracture: correlation with the CT subchondral arc.

To measure the effect of a simulated low anterior wall fracture of the acetabulum on load transmission in the hip joint. We measured the contact areas and pressure between the acetabulum and the femoral head of cadaveric pelves in three different conditions: intact, with an operatively created fracture of the anterior wall, and after anatomic reduction and internal fixation of the fracture. Hips were loaded in simulated single-limb stance. Pressure and area measurements were made with Fuji pressure-sensitive film. Seven hip joints in seven whole pelves were tested. Anterior wall fractures were anatomically reduced and fixed. Contact area, load, and mean and maximum pressures were measured. Anterior wall fractures in our specimens entered the hip joint an average of 9.7 millimeters from the vertex of the acetabulum, corresponding to a 45-degree roof arc measurement. Peripheral loading seen in the intact acetabulum was disrupted after fracture. The loading pattern was not restored to preinjury levels with anatomic reduction and fixation. There was no significant change in the contact area (p = 0.43), force (p = 0.06), or mean (p = 0.57) or maximum (p = 0.20) pressures in the superior aspect of the acetabulum after creation of the anterior wall fracture. These results differ from those of previous studies with posterior wall acetabulum fractures, where significant increases in force and mean and maximum pressures were noted in the superior acetabulum after fracture. The lack of significant increases in superior acetabular pressures is discussed in relation to the mean computed tomographic subchondral arc of approximately ten millimeters in our specimens.

PHYSICOCHEMICAL CHANGES IN STARCH DURING DEEP-FAT FRYING OF A MOLDED CORN STARCH PATTY

Corn starch patties with an initial moisture content of 46.5 % (wet basis) were fried in oil at 165C. The results indicated that oil content in the patty ranged from 10.6 to 12.5% in the crust region, and 1.5 to 3.9% in the core region. Starch gelatinization was significantly dependent on frying time and location of starch in the patty. Both, water absorption and water solubility indices of starch increased with frying time, with the starch contained in the crust exhibiting much higher water absorption ability and water solubility than that contained in the core region. Measurements of 'blue value' (the intensity of blue color of starch solution upon addition of iodide ion) and the absorbance spectra of starch samples indicated that amylose-lipid complexes were present in the fried materials. The degree of starch complexation was 10.9 to 13.2% in the crust and 0.3 to 6. 6% in the core region. The puncture force on the surface of food fried for no more than 5 min was close to that in the food center, although a significant increase in force was required for the crust region during the later stages of frying.

Effect of angiotensin-(1-7) on reperfusion arrhythmias in isolated rat hearts.

There is increasing evidence that angiotensin-(1-7)(Ang-(1-7)) is an endogenous biologically active component of the renin-angiotensin system(RAS). In the present study, we investigated the effects of Ang-(1-7) on reperfusion arrhythmias in isolated rat hearts. Isolated rat hearts were perfused with two different media, i.e., Krebs-Ringer (2.52 mM CaCl2) and low-Ca2+ Krebs-Ringer (1.12 mM CaCl2). In hearts perfused with Krebs-Ringer, Ang-(1-7) produced a concentration-dependent (27-210 nM) reduction in coronary flow (25% reduction at highest concentration), while only slight and variable changes in contraction force and heart rate were observed. Under the same conditions, angiotensin II (Ang II; 27 and 70 nM) produced a significant reduction in coronary flow (39% and 48%, respectively) associated with a significant increase in force. A decrease in heart rate was also observed. In low-Ca2+ Krebs-Ringer solution, perfusion with Ang-(1-7) or Ang II at 27 nM concentration produced similar changes in coronary flow, contraction force and heart rate. In isolated hearts perfused with normal Krebs-Ringer, Ang-(1-7) produced a significant enhancement of reperfusion arrhythmias revealed by an increase in the incidence and duration of ventricular tachycardia and ventricular fibrillation (more than 30-min duration). The facilitation of reperfusion arrhythmias by Ang-(1-7) was associated with an increase in the magnitude of the decreased force usually observed during the postischemic period. The effects of Ang-(1-7) were abolished in isolated rat hearts perfused with low-Ca2+ Krebs-Ringer. The effect of Ang II (27 nM) was similar but less pronounced than that of Ang-(1-7) at the same concentration. These results indicate that the heart is a site of action for Ang-(1-7) and suggest that this heptapeptide may be involved in the mediation of the cardiac effects of the RAS.

Halothane reduces force and intracellular Ca2+ in airway smooth muscle independently of cyclic nucleotides.

Halothane relaxes airway smooth muscle in part by a direct effect on the smooth muscle cell. The purpose of this study was to investigate the possible role of cyclic nucleotides in this direct effect. Strips of canine tracheal smooth muscle in vitro were contracted with acetylcholine (ACh) and then exposed to 0.7-2.6% halothane. Isometric force and the intracellular concentrations of adenosine cyclic 3',5'-monophosphate ([cAMP]i) guanosine cyclic 3',5'-monophosphate ([cGMP]i), and free calcium ([Ca2+]i, using the fluorescent Ca(2+)-sensitive dye fura 2) were measured. ACh caused significant increases in force, [cAMP]i, [cGMP]i, and [Ca2+]i. Subsequent exposure of the strips to halothane caused an additional increase in [cAMP]i, decreases in force and [Ca2+]i, and no effect on [cGMP]i. The additional increase in [cAMP]i was similar to that produced by a concentration of isoproterenol (0.03 microM) that caused equipotent relaxation. Indomethacin abolished the increase in [cAMP]i produced by ACh and abolished the additional increase in [cAMP]i produced by halothane. In contrast, indomethacin had no effect on the decreases in force and [Ca2+]i. These findings suggest that in canine tracheal smooth muscle contracted with ACh 1) halothane increases [cAMP]i by a cyclooxygenase-dependent mechanism and 2) the increase in [cAMP]i produced by halothane is not responsible for the relaxation or the decrease in [Ca2+]i.

The effects of frustration induced by discontinuation of reinforcement on force of response and magnitude of the skin conductance response

If frustration is an aversive emotion in humans, then the behavioral increment in vigor of response following discontinuation of a positively reinforced force-contingent leverpress (frustration effect) might reasonably be expected to be accompanied by a gross physiological response such as an increase in skin conductance. The present study tested this hypothesis by means of a double-lever force-contingent reinforcement apparatus in which subjects received a small monetary reward if they pressed the first lever (reward lever) with an amount of force that was greater than 1.5 kg but less than 3.0 kg. Presses on the second lever, designated as a reset lever required for reactivation of the reinforcement mechanism and subsequent presses on the reward lever, were never reinforced, but force of response was measured. Following this procedure, any changes in force on the reset lever could not be attributed to associative strategies gained through familiarity with the reward lever. The results indicated a significant increase in force on the reset lever (frustration effect) following discontinuation of reinforcement on the reward lever (first extinction trial) accompanied by a significant increase in the skin conductance response, evidence that suggests that frustration is an emotion with a physiological basis as well as a behavioral effect. Increases in force of response on the reset lever and correlated increases in the magnitude of the skin conductance response were inversely related to the time of delay between the reward leverpress and the reset leverpress.

Beneficial effects of training on developing dystrophic muscle.

The objective of this study was to determine whether increased contractile activity is beneficial or detrimental to developing dystrophic muscle. Hamsters (20-days-old) were gradually introduced to running at a speed of 14 m/min at 10% grade for 2 (T2) or 4 (T4) h/d for 4 weeks, 5 d/wk. Histological and fiber type properties were determined in the soleus (SOL), plantaris (PL), and extensor digitorum longus and contractile properties in SOL and PL from 5 animals/group, including 5 controls. Experimental animals had normal body and muscle mass. Training for 2 h/d had little effect on SOL contractile properties, whereas 4 h/d resulted in significant increases in force, percentage of type I fibers, and type I hypertrophy. Force also increased in PL. Muscle necrosis was reduced in SOL (T2 and T4) and unchanged in PL. In conclusion, endurance training generally had a beneficial or, at least, no detrimental effect on developing dystrophic muscles.

Involvement of the protein kinase C system in calcium-force relationships in ferret aorta.

1. Intracellular Ca2+-force relationships were investigated in ferret aortic smooth muscle by the simultaneous measurement of aequorin luminescence and isometric force. Complete calcium-force curves were constructed by plotting calibrated aequorin luminescence versus force, while intracellular [Ca2+] was made to change by increasing degrees of K+ depolarization or decreasing extracellular [Ca2+]. 2. The steady state calcium-force curve in response to K+ depolarization exhibited maximal force generation at an intracellular [Ca2+] of approximately 4 x 10(-7) M. Further increases in intracellular [Ca2+] did not yield additional increments in force. 3. Protein kinase C activation with the phorbol ester, 12-deoxyphorbol-13-isobutyrate 20 acetate (DPBA) produced contractions accompanied by no detectable increases in aequorin luminescence. DPBA significantly shifted the control [Ca2+]-force relationship leftward to lower intracellular [Ca2+] with an increase in the magnitude of maximal generated force. 4. In aorta maximally precontracted by K+ depolarization, the addition of DPBA resulted in a significant increase in force in the absence of further increases in intracellular [Ca2+]. Conversely, in muscles maximally precontracted with DPBA, responses to K+ depolarization resulted in subsequent increases in force in the presence of simultaneous sustained increases in intracellular [Ca2+]. 5. The relatively specific protein kinase C antagonist H-7 caused a significant decrease in intrinsic myogenic tone in the absence of any statistically significant decrease in intracellular [Ca2+]. 6. These results suggest that protein kinase C may be an important regulator of vascular smooth muscle contractility by: (1) providing a mechanism by which the apparent [Ca2+] sensitivity of the contractile apparatus during agonist-induced contractions is increased, and (2) maintaining intrinsic myogenic tone by a mechanism the [Ca2+] requirement of which is satisfied by the resting [Ca2+]i.

Human muscle strength training: the effects of three different regimens and the nature of the resultant changes.

1. Increases in strength and size of the quadriceps muscle have been compared during 12 weeks of either isometric or dynamic strength training. 2. Isometric training of one leg resulted in a significant increase in force (35 +/- 19%, mean +/- S.D., n = 6) with no change in the contralateral untrained control leg. 3. Quadriceps cross-sectional area was measured from mid-thigh X-ray computerized tomography (c.t.) scans before and after training. The increase in area (5 +/- 4.6%, mean +/- S.D., n = 6) was smaller than, and not correlated with, the increase in strength. 4. The possibility that the stimulus for gain in strength is the high force developed in the muscle was examined by comparing two training regimes, one where the muscle shortened (concentric) and the other where the muscle was stretched (eccentric) during the training exercise. Forces generated during eccentric training were 45% higher than during concentric training. 5. Similar changes in strength and muscle cross-sectional area were found after the two forms of exercise. Eccentric exercise increased isometric force by 11 +/- 3.6% (mean +/- S.D., n = 6), and concentric training by 15 +/- 8.0% (mean +/- S.D., n = 6). In both cases there was an approximate 5% increase in cross-sectional area. 6. It is concluded that as a result of strength training the main change in the first 12 weeks is an increase in the force generated per unit cross-sectional area of muscle. The stimulus for this is unknown but comparison of the effects of eccentric and concentric training suggest it is unlikely to be solely mechanical stress or metabolic fluxes in the muscle.