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PubMed2006

Deregulation of AP-1 proteins in collagen gel-induced epithelial cell apoptosis mediated by low substratum rigidity.

In this study, we established that collagen gel, but not collagen gel coating, induced apoptosis exclusively in epithelial cell lines, which indicated that low substratum rigidity might trigger cell apoptosis. To confirm this, we used collagen gels with different rigidities due to cross-linking or physical disruption of collagen fibrils caused by sonication. We found that collagen gel-induced apoptosis was inversely correlated with substratum rigidity. Low substratum rigidity collagen gel-induced apoptosis was neither prevented by Bcl-2 overexpression nor preceded by mitochondrial release of cytochrome c. This suggested that the mitochondrial pathway was not involved in low substratum rigidity-induced apoptosis. Low substratum rigidity activated c-Jun N-terminal kinase (JNK) within 4 h, but it also rapidly down-regulated c-Jun within 1 h and triggered persistent aberrant expression of c-Fos for at least 24 h. Either reduced c-Jun expression or c-Fos overexpression induced apoptosis in several epithelial cells. Inhibiting low substratum rigidity-induced JNK activation prevented aberrant c-Fos expression but only partially blocked low substratum rigidity-induced apoptosis. Taking these results together, we conclude that low substratum rigidity collagen gel induced apoptosis in epithelial cells and that deregulated AP-1 proteins mediated that apoptosis, at least in part.

Animals↗
PubMed1980

Does rigidity in structure of muscarinic agonists and antagonists reflect drug specificity?

The present work is an attempt to elucidate: (1) whether highly rigid structural analogs of acetylcholine are still capable of activating the muscarinic receptor; (2) whether such analogs, be they agonists or antagonists, discriminate among the various ACh-mediated functions, thereby providing a tool for the study of a possible receptor heterogeneity; (3) whether structural rigidity is a significant factor in the kinetics of drug-receptor interaction. To this end, we investigated some properties of drugs in the spiro-(1,3-dioxolane-4,3')-quinuclidine system (SDQ) which embodies the muscarinic pharmacophore in a framework of utmost rigidity. Wherever possible, these properties were compared with those of a closely related but more flexible analog. Variation in effect between members of a rigid-flexible pair or among drugs of varying rigidity is considered to reflect varying affinities towards various sites of action. 2-Methyl-spiro-(1,3-dioxolane-4,3')-quinuclidine (AF-30) is a weak but selective muscarinic agonist. It can be viewed as a highly rigid version of 3-acetoxyquinuclidine (3-AcQ) and it can be used as a probe for detection of heterogeneity among muscarinic receptors. AF-30 is equipotent with 3-AcQ in causing tremors (mice), but has 1/17th the activity of 3-AcQ in the guinea-pig ileum, 1/30th in lowering blood pressure (cats) and 1/10th in inducing analgesia (mice). 2-Diphenylmethyl-spiro(1,3-dioxolane-4',3)-quinuclidine (AF-41) and 2.2-diphenyl-spiro-(1,3-dioxolane-4,3')-quinuclidine (AF-32 are potent antagonists and possess KD values in the same range as those of the more flexible congener 3-diphenylacetoxy-quinuclidine (AF-43) and atropine (0.6--2 nM) but with koff = 0.1 msec-1 (AF-41) and koff = 1 msec-1 (AF-43) (carp atrium). Thus, duration of drug action of drug action at the receptor is a function of structural rigidity in the drug molecule, termination of action being fastest with the flexible molecules. Differences in rigidity among various antagonists also find expression in an unequal distribution of potencies in various tests; thus the rigid antagonists differentiate between two central effects in mice, viz., prevention of oxotremorine-induced tremors and fall from the rotating rod by a factor of 1:20 (especially AF-41 versus AF-43), whereas the more flexible antagonists (AF-43, atropine or even 3-quinuclidinyl-benzilate) do not show such as a selectivity. The existence of heterogenous muscarinic receptors can be inferred from data presented. Both theoretical and practical implications are discussed.

Acetylcholine↗
PubMed1997

Monocular discrimination of rigidly and nonrigidly moving objects.

We measured thresholds for the monocular discrimination of rigidly and nonrigidly moving objects defined by motion parallax. The retinal projections of rigidly moving objects are subject to certain constraints. By applying smooth 2-D transformations to the projections of rigidly moving objects, we created stimuli in which these constraints were affected. Thresholds for (generic) nonrigid transformations that in theory can be detected from rigid ones by processing pairs of views depended not only on the extent to which the rigidity constraints were affected, but also on the structure and the movement of the simulated object. Nonrigid transformations under which every three successive views had a rigid interpretation were not discriminable from rigid transformations, except in cases where the distortions were very large. Under the rigidity assumption, this would mean that a large class of nonrigidly moving objects is erroneously perceived as rigidly moving.

Adult↗
PubMed2002

Rigidity of thought and behavior: 100 years of research.

Rigidity is one of the oldest psychological constructs, with systematic research dating back to the late 19th century. The authors review this research in an attempt to clarify the construct of rigidity and to investigate its correlates. Rigidity is described as a multidimensional construct encompassing the tendency to form and perseverate in the use of mental and behavioral sets. A series of meta-analyses was performed based on three measures of behavioral rigidity: the Einstellung Water-Jar Task, the Wisconsin Card Sorting Task, and the motor-cognitive dimension of the Test of Behavioral Rigidity. The results indicated that rigidity is curvilinearly related to age, positively related to authoritarianism (particularly under stressful situations), and negatively related to intelligence; that men are more rigid than women; that obsessive-compulsiveness is positively related to rigidity; and that schizophrenics are more rigid than nonschizophrenic siblings and normal controls. Unresolved issues and gaps in the research are discussed.

Adult↗
PubMed1996

The treatment of loss of penile rigidity associated with Peyronie's disease.

Patients with Peyronie's Disease on occasion present with loss of rigid erections. A full evaluation is required to determine the presence or absence of arterial insufficiency or corporal veno-occlusive dysfunction. Treatment for these patients include intracavernosal pharmacotherapy, a vacuum/constrictor device, venous ligation surgery or a penile prosthesis. Whatever the therapeutic approach, the angulation produced by the Peyronie's plaque must be taken into account. Patients with Peyronie's Disease will present to their physicians with a variety of clinical scenarios. They may merely be concerned with the presence of an asymptomatic penile plaque and will simply require reassurance. More typically, however, penile curvature, pain, and/or difficulty with sexual relations will prompt the desire for medical advice. Treatment of penile pain which usually abates with time and attempts at non surgically treating the Peyronies plaque will not be discussed in this paper. Patients with penile plaque and curvature present in three distinct ways: a. penile rigidity preserved and the ability to continue sexual relations; b, penile rigidity preserved and the inability to continue with sexual relations because of significant angulation; c. the inability to have rigid erections. The patient who is able to continue sexual relations with preserved penile rigidity and the lack of significant penile angulation requires no treatment. However, the patient who has lost his ability to have sexual relations because of significant angulation is a candidate for penile straightening surgery (e.g. graft) (1, 11). It is the last group of patients. Namely those who are not able to maintain penile rigidity because of their Peyronie's Disease that will be addressed in this paper. Patients who present with impotence (i.e. loss of penile rigidity) and Peyronie's disease should be evaluated in a similar manner as patients who present with erectile dysfunction and do not have Peyronie's Disease. The standard approach would therefore include a detailed medical and sexual history, a measurement of penile arterial pressure or flow to determine adequate arterial inflow (5,8), a measurement of penile sensation (10) to determine if an underlying neurological problem is present and lastly an evaluation of the veno-occlusive mechanism (12,17). In addition, the presence of penile curvature and plaque may cause significant and disturbing psychological manifestations and it is advisable that these patients undergo a psychological interview to determine the presence or absence of psychiatric influences. Obviously, many older patients with Peyronie's Disease may suffer concomitant arterial insufficiency leading to loss of rigidity and impotence. An evaluation of arterial input into the penis by penile Doppler studies, duplex ultrasound, or cavernosal occlusion pressures is required to determine the presence of arterial insufficiency. Patients who are found to have significant decreases in arterial flow and/or pressure would therefore become candidates for either self-injection with vasoactive agents or a vacuum constrictor device. It is our feeling in general that these nonsurgical therapies should be tried prior to considering the implantation of a penile prosthesis in any patient who presents with erectile dysfunction. It should be noted, however, that many patients with Peyronie's Disease who present with loss of penile rigidity will have an underlying veno-occlusive dysfunction secondary to the plaque itself. Normally, venules draining the corpora are passively compressed between the expanding corporal tissue and the tunica albugince (6). When a Peyronie's plaque is present compliance of the underlying corporal smooth musculature may be decreased thus preventing venous compression. In a recent evaluation of 92 patients who presented in this manner 87% were noted to have veno-occlusive dysfunction as determined by dynamic cavernosometry and cavernosography (3)...

Erectile Dysfunction↗
PubMed1998

The diagnostic relevance of red cell rigidity.

Red cell rigidity is an important hemorheological parameter determining the passage of erythrocyte through narrow capillaries and the reduction of blood viscosity under high shear rates. The changes in red cell rigidity in various diseases of altered blood flow - hypertension (HT), diabetes mellitus (DM), myocardial infarction (MI) and cerebrovascular accidents (CVA), using equal sample sizes of 25 each, have been analysed in this paper. One of the essential elements of red cell rigidity is the structural and functional properties of erythrocyte membrane which, in turn, is determined by the membrane biochemistry. Since cholesterol-rich erythrocytes have increased rigidity, the serum cholesterol and triglycerides levels have been monitored in order to detect the extent to which they affect red cell rigidity. No significant change in red cell rigidity have been found in CVA. RBC rigidity is found to be significantly increased in the other diseases. Significant increase in triglyceride levels have been found in all the diseases studied. Cholesterol levels were significantly increased in all diseases except CVA. Hence, increased cholesterol levels have been found to consistently cause a simultaneous increase in RBC rigidity. Triglycerides levels, on the other hand, have not shown a consistent change with changes in RBC rigidity, but have been shown to be a more sensitive marker for early detection of diseased status.

Blood Viscosity↗
PubMed2001

Rigidity decreases resting tremor intensity in Parkinson's disease: A [(123)I]beta-CIT SPECT study in early, nonmedicated patients.

Tremor is one of the clinical hallmarks of Parkinson's disease (PD). Although it is accepted that other classic symptoms of PD such as rigidity and bradykinesia result from a degeneration of the nigrostriatal system and subsequent reduction in striatal dopamine, the pathophysiology of resting tremor remains unclear. The majority of recent single photon emission computed tomography (SPECT) and positron emission tomography (PET) studies, using various radioligands, demonstrated significant correlation between striatal radioligand bindings and the degree of parkinsonian symptoms such as rigidity and bradykinesia, but not tremor. We investigate the relationship between the degeneration of the nigrostriatal pathway and the appearance of resting tremor, taking into account the possible interference of rigidity with the resting tremor. Thirty early and drug-naïve PD patients were examined. Tremor and rigidity of the arms were assessed using UPDRS, and the power of tremor was estimated using spectral analysis of tremor peaks. [(123)I]beta-CIT SPECT was used to assess degeneration of the dopaminergic system in PD patients. A comparison between asymmetry indices showed that in terms of both tremor and rigidity, the most affected arm corresponded significantly with the contralateral striatum, having the largest reduction in radioligand binding. Furthermore, tremor power accounted for a significant part of variance in the contralateral striatum, suggesting a relationship between this PD symptom and the degeneration of the dopaminergic system. Further, the degree of tremor was reduced with increasing rigidity. However, correcting for the influence of rigidity, the significant contribution of tremor in the variance in the contralateral striatal [(123)I]beta-CIT binding disappeared. When the confounding influence of rigidity is taken into account, no significant direct relationship between dopaminergic degeneration and the degree of tremor could be found. Other pathophysiological mechanisms should be similarly investigated in order to further our understanding of the origin of resting tremor in PD.

Adult↗
PubMed1997

Measurement of rigidity in Parkinson's disease.

Clinical assessment of rigidity in parkinsonian patients is largely qualitative. The reliability and validity of the assessments are sometimes in doubt. Several "engineering" methods of quantifying rigidity have been described, but none has been adopted into general clinical practice. A possible reason is that these methods differ in crucial aspects from the clinical exam. We therefore tackled the problem by monitoring the clinical exam itself, using small sensors to measure the forces and displacements applied. Limb impedance (Z) was computed using parameter identification methods and compared to raters' verbalized ratings of rigidity based on a 5-point scale: the Unified Parkinson's Disease Rating System. The qualitative and quantitative estimates of impedance covaried over a fourfold range, depending on the forces imposed and the subject's motor set. Raters differed by up to 1 full point in their mean qualitative ratings and sometimes disagreed on whether levodopa reduced rigidity. This was not due to any significant differences in the overall range of rigidity they evoked, but rather to the way they scored this range [the ratio of mean rating to mean impedance (R/Z) varied between raters and subjects]. On the other hand, the R/Z ratio was reproducible over separate sets of ratings and may therefore serve to convert measured impedance into a standardized rating. Our results indicate that the current clinical exam may be too abbreviated to detect the sometimes quite small reductions in rigidity after levodopa. We conclude that a device that conveniently quantifies the clinical assessment of rigidity is now available and will lead to more standardized protocols for rating rigidity in the near future.

Antiparkinson Agents↗
PubMed1995

A role for CNS alpha-2 adrenergic receptors in opiate-induced muscle rigidity in the rat.

A number of potential neurochemical mediators of opiate-induced muscle rigidity have been proposed based on the results of systemic drug studies and on knowledge of the brain sites implicated in opiate rigidity. The effects of i.c.v. pretreatment with selected opioidergic, alpha adrenergic and serotonergic drugs on muscle rigidity induced with systemic injection of the potent opiate agonist alfentanil (ALF) were investigated in spontaneously ventilating rats. The opiate antagonist methylnaloxonium (MN; 0.2-14 nmol), alpha-2 adrenergic agonists dexmedetomidine (DEX; 0.4-42 nmol) or 2-(2,6-diethylphenylamino)-2-imidazoline hydrochloride (ST91; 4-400 nmol), alpha-1 adrenergic antagonist prazosin (PRZ; 7-70 nmol) or serotonergic antagonist ketanserin (KET; 18-550 nmol) were injected i.c.v. (10 microliters) and ALF (500 micrograms/kg s.c.) was administered 10 min later. S.c. electrodes were used to record gastrocnemius electromyographic activity. Both MN and DEX dose-dependently and potently antagonized ALF-induced rigidity. ST91 produced shorter-lived, less profound, antagonism of ALF rigidity. PRZ, at the highest dose tested, produced a delayed and modest reduction in ALF rigidity. A large, non-selective, dose of KET incompletely attenuated ALF rigidity. These results lend support to the hypothesis that central opioid and alpha-2 adrenergic receptors mediate opiate-induced muscle rigidity in the rat.

Adrenergic alpha-Agonists↗
PubMed1982

Effect of lesioning dopamine, noradrenaline and 5-hydroxytryptamine pathways on tremorine-induced tremor and rigidity.

The effects of lesioning monoamine pathways in the rat brain on tremorine-induced hind-limb tremor and rigidity were studied. Nigro-striatal and mesolimbic dopamine (DA) neurones were lesioned unilaterally by injecting 6-hydroxydopamine (6-OHDA) into the median forebrain bundle. Tremor was reduced in the contralateral leg and rigidity was prevented in the ipsilateral leg. Injection of 6-OHDA into the nucleus accumbens affected tremor but not rigidity. In general, nigral DA neurones may influence rigidity whilst mesolimbic DA neurones affect tremor. A unilateral locus coeruleus electrolesion which destroys noradrenaline (NA) fibres reduced both tremor and rigidity. A median raphe electrolytic lesion affecting 5-hydroxytryptamine (5-HT) neurones had no effect on tremor and rigidity, whereas lesioning the dorsal raphe electrolytically or by injecting 5,6-dihydroxytryptamine prevented rigidity without affecting tremor. Electrical stimulation of the dorsal raphe increased transiently the hindlimb tone of normal rats. The findings demonstrate that the monoamines, especially 5-HT, are differently involved in the mechanisms of tremor and rigidity produced by tremorine.

Animals↗
PubMed2006

Development of GABA-sensitive spasticity and rigidity in rats after transient spinal cord ischemia: a qualitative and quantitative electrophysiological and histopathological study.

Transient spinal cord ischemia may lead to a progressive degeneration of spinal interneurons and subsequently to increased hind limb motor tone. In the present work we sought to characterize the rigidity and spasticity components of this altered motor function by: i) tonic electromyographic activity measured in gastrocnemius muscle before and after ischemia, ii) measurement of muscle resistance during the period of ankle flexion and corresponding changes in electromyographic activity, iii) changes in Hoffmann reflex, and, iv) motor evoked potentials. In addition the effect of intrathecal treatment with baclofen (GABAB receptor agonist; 1 microg), nipecotic acid (GABA uptake inhibitor; 300 microg) and dorsal L2-L5 rhizotomy on spasticity and rigidity was studied. Finally, the changes in spinal choline acetyltransferase (ChAT) and vesicular glutamate transporter 2 and 1 (VGLUT2 and VGLUT1) expression were characterized using immunofluorescence and confocal microscopy. At 3-7 days after ischemia an increase in tonic electromyographic activity with a variable degree of rigidity was seen. In animals with modest rigidity a velocity-dependent increase in muscle resistance and corresponding appearance in electromyographic activity (consistent with the presence of spasticity) was measured during ankle rotation (4-612 degrees /s rotation). Measurement of the H-reflex revealed a significant increase in Hmax/Mmax ratio and a significant loss of rate-dependent inhibition. In the same animals a potent increase in motor evoked potential amplitudes was measured and this change correlated positively with the increased H-reflex responses. Spasticity and rigidity were consistently present for a minimum of 3 months after ischemia. Intrathecal treatment with baclofen (GABA B receptor agonist) and nipecotic acid (GABA uptake inhibitor) provided a significant suppression of spasticity, rigidity, H-reflex or motor evoked potentials. Dorsal L2-L5 rhizotomy significantly decreased muscle resistance but had no effect on increased amplitudes of motor evoked potentials. Confocal analysis of spinal cord sections at 8 weeks-12 months after ischemia revealed a continuing presence of ChAT positive alpha-motoneurons, Ia afferents and VGLUT2 and VGLUT1-positive terminals but a selective loss of small presumably inhibitory interneurons between laminae V-VII. These data demonstrate that brief transient spinal cord ischemia in rat leads to a consistent development of spasticity and rigidity. The lack of significant suppressive effect of dorsal L2-L5 rhizotomy on motor evoked potentials response indicates that descending motor input into alpha-motoneurons is independent on Ia afferent couplings and can independently contribute to increased alpha-motoneuronal excitability. The pharmacology of this effect emphasizes the potent role of GABAergic type B receptors in regulating both the spasticity and rigidity.

Acetyltransferases↗
PubMed1996

Quantifying rigidity with a new computerized elbow device.

A new computerized method is described for measuring parkinsonian rigidity with an elbow device. We present data from 127 subjects (103 controls and 24 parkinsonian patients) to show the clinical utility of the method. The instrumental quantification of rigidity correlates highly with clinical ratings of parkinsonian rigidity. The test-retest repeatability was excellent. In parkinsonian patients versus normal controls, significantly higher values of measured rigidity were observed. Moreover, activation procedure significantly increases rigidity only in parkinsonian patients. Activated rigidity in control subjects is lower than basal values. The procedure was sensitive to increased rigidity in parkinsonian patients during 3 days' drug holiday. Contrary to previous reports, levodopa therapy reduced both basal and activated rigidity in parkinsonian patients. This method is relatively simple and takes only 15 min to complete.

Adult↗
PubMed1998

Muscle thick filaments are rigid coupled tubules, not flexible ropes.

Understanding the structures of thick filaments and their relation to muscle contraction has been an important problem in muscle biology. The flexural rigidity of natural thick filaments isolated from Caenorhabditis elegans as determined by statistical analysis of their electron microscopic images shows that they are considerably more rigid (persistence length=263 microm) than similarly analyzed synthetic actin filaments (6 microm) or duplex DNA (0.05 microm), which are known to be helical ropes. Indeed, cores of C. elegans thick filaments, having only 11% of the mass per unit length of intact thick filaments, are quite rigid (85 microm) compared with the thick filaments. Cores comprise the backbones of the thick filaments and are composed of tubules containing seven subfilaments cross-linked by non-myosin proteins. Microtubules reconstituted from tubulin and microtubule-associated proteins are nearly as rigid (55 microm) as the cores. We propose a model of coupled tubules as the structural basis for the observed rigidity of natural thick filaments and other linear structures such as microtubules. A similar model was recently presented for microtubules [Felgner et al., 1997]. This coupled tubule model may also explain the differences in flexural rigidity between natural rabbit skeletal muscle thick filaments (27 microm) or synthetic thick filaments reconstituted from myosin and myosin binding protein C (36 microm) and those reconstituted from purified myosin (9 microm). The more flexible myosin structures may be helical ropes like F-actin or DNA, whereas the more rigid muscle or synthetic thick filaments which contain myosin and myosin binding protein C may be constructed of subfilaments coupled into tubules as in C. elegans cores. The observed thick filament rigidity is necessary for the incompressibility and lack of flexure observed with thick filaments in contracting skeletal muscle.

Animals↗
PubMed1996

Helix rigidity of DNA: the meroduplex as an experimental paradigm.

The intrinsic rigidity of the DNA helix is generally believed to arise primarily from vertical base-stacking interactions; however, relatively little experimental information exists regarding the relationship between the thermodynamic stability of base-stacking interactions and the mechanical rigidity imparted by such interactions. To address this issue, the solution conformations of complexes formed between adenine (A) or N-6-methyladenine (meA) monomer and deoxythymidylate (dTn) polymers of varying length (n = 40, 60, 81, and 110) have been examined. Such complexes are known to exist as extended, chiral structures in which the purine monomers exist as extensively stacked arrays. Thus, one can in principle examine the structural consequences of base-pair stack formation in the absence of any change in stoichiometric (phosphate) charge. The current approach has utilized the method of transient electric birefringence (TEB), which is highly sensitive to changes in nucleic acid conformation. Addition of millimolar concentrations of either A or meA to the dTn species leads to the formation of relatively rigid, chiral complexes whose dimensions are strictly limited by the length of the polymer strand. For adenine, the principal species appears to be [A] approximately n/2-dTn in which the polymer strand doubles back to form the two continuous strands of the complex (merotriplex). The addition of a methyl group to the N-6 position of adenine (meA) results in a shift to a meroduplex form, [meA] approximately n-dTn, with an intrinsic rigidity that is nearly identical to the rigidity of the corresponding duplex, dAn-dTn, despite the fact that the stoichiometric charge of the meroduplex is only one-half of that of the full duplex. The current results thus support a model in which helix rigidity is primarily due to the intrinsic resistance to deformation of base-stacking interactions; the deformation energies, as with the stacking energies themselves, are expected to be quite sequence-dependent. Phosphate-phosphate (repulsive) interactions, whose contributions are both salt-dependent and relatively sequence-independent, appear to play a secondary role in establishing helix rigidity. In particular, the DNA helix is likely to possess substantial rigidity in the absence of phosphate interactions. Thus, proteins whose interactions with DNA lead to substantial bending of the helix axis may facilitate such distortions through solvation of bases in addition to partial charge neutralization.

Adenine↗
PubMed2005

Evaluation of surgical performance with standard rigid and flexible-tip laparoscopes.

BACKGROUND: Flexible-tip laparoscopes have recently been introduced into clinical practice, with the goal of improving surgeon performance during complex laparoscopic procedures. We used objective and subjective performance parameters to compare standard rigid 0 degrees and 30 degrees lens laparoscopes two flexible-tip laparoscopes in an in vitro model. METHODS: Twenty-nine subjects with varied levels of surgical experience performed complex laparoscopic tasks in three different models simulating (a) prostate dissection from the rectum, (b) cystic duct clipping, and (c) distal posterior rectum dissection. Each task was performed using two Storz rigid laparoscopes (0 degrees and 30 degrees) and two flexible-tip laparoscopes, the Olympus LTF-V3 and the Fujinon EL2-TF310. The sequence of application of the two flexible-tip laparoscopes was randomized. In each case, an experienced laparoscopic camera driver controlled the field of vision. Time to complete each task, operative precision, and subjective surgeon rating scores were compared. Statistical analysis was performed with analysis of variance (ANOVA) and a two-sided fisher's exact test. RESULTS: In all three models, the flexible laparoscopes offered no advantage in terms of procedure time, surgical precision, or subjective surgeon rating score when compared with the 30 degrees lens rigid laparoscope. The 30 degrees rigid lens laparoscope and the two flexible-tip laparoscopes were superior to the 0 degrees lens rigid laparoscope for all parameters evaluated, with the exception of subjective rating in the cystic duct model and procedure time in the colorectal model. CONCLUSION: In this in vitro experimental model, the flexible-tip laparoscopes found to have no advantage over the standard rigid 30 degrees lens laparoscope. These models were validated, as the 0 degrees lens rigid laparoscope was surpassed by the 30 degrees lens rigid laparoscope and the flexible-tip laparoscopes. Both flexible-tip laparoscopes produced similar results and excellent image quality, but some experience is required before their smooth application can be achieved.

Adult↗
PubMedDate not supplied

Does rigid instrumentation increase the fusion rate in one-level anterior cervical discectomy and fusion?

BACKGROUND CONTEXT: Although plate fixation enhances the fusion rate in multilevel anterior cervical discectomy and fusion (ACDF), debate exists regarding the efficacy of nonplating to rigid plate fixation in one-level ACDF. PURPOSE: To determine the efficacy of nonplating to rigid plate fixation in regards to fusion rate and clinical outcome in patients undergoing one-level ACDF with autograft. STUDY DESIGN: A review of 69 consecutive patients who underwent one-level ACDF with autograft and with or without rigid anterior cervical plate fixation. PATIENT SAMPLE: Sixty-nine patients who underwent one-level ACDF (mean age, 45 years) were evaluated for radiographic evidence of fusion (mean, 14 months) and for clinical outcome. All patients received tricortical iliac crest autografts. Disc space distraction was 2 mm, the grafts were inserted with the cortical surface positioned anteriorly, and each graft was countersunk 2 mm from the anterior vertebral border. Thirty-eight patients underwent nonplated ACDF and 31 patients underwent plated ACDF. Eighteen Orion (Sofamor-Danek, Memphis, TN), eight Atlantis (Sofamor-Danek) and five PEAK polyaxial (Depuy-Acromed, Rayham, MA) anterior cervical plating systems were used. Rigid plate fixation was used in all patients with instrumentation. Postoperatively, hard collars were worn 6 to 8 weeks in nonplated patients and soft collars were worn for 3 to 4 weeks in plated patients. Twenty-four patients were smokers (54.2% nonplating; 45.8% plating) and work-related injuries entailed 23 patients (47.8% nonplating; 52.2% plating). OUTCOME MEASURES: Fusion was assessed based on last follow-up of lateral neutral, flexion and extension radiographs. Radiographs were evaluated blindly to assess fusion and instrumentation integrity between nonplated and plated patients. Clinical outcomes were assessed with the Cervical Spine Outcomes Questionnaire and also assessed on last follow-up as excellent, good, fair or poor based on Odom's criteria. METHODS: Fusion rate and postoperative clinical outcome were assessed in 69 patients who underwent one-level ACDF with autograft and with or without rigid anterior plate fixation. Additional risk factors were also analyzed. Statistical significance was established at p<.05. RESULTS: Sixty-six patients (95.7%) achieved a solid fusion (100% nonplated; 90.3% plated). Nonunions occurred in three patients (1 smoker; 2 nonsmokers) with Orion instrumentation. Slight screw penetration into the involved and uninvolved interbody spaces occurred in one patient who was a nonsmoker and did not achieve fusion. One superficial cervical wound infection was noted in a nonplated patient. No other intraoperative or postoperative complications were noted. No statistically significant difference was noted between nonplating to rigid plating upon fusion rate (p>.05). All nonunions occurred at the C5-C6 level. Mean estimated intraoperative blood loss was significantly greater in plated patients (p=.043). Revision surgery involved 9.7% of the plated patients, whereas none of the nonplated patients required reoperation. Postoperative clinical outcome was assessed in all patients (mean, 21 months). Excellent results were noted in 18.8%, good results in 72.5% and fair results in 8.7% of the patients. Nonunion patients reported satisfactory clinical outcome. No statistical significance was noted between clinical outcome of fused and nonfused patients, the presence of a work-related injury and the use of plating (p>.05). Demographics and history of smoking were not factors influencing fusion or clinical outcome in this series (p>.05). The effect on fusion by various plate types could not be discerned from this study. CONCLUSION: A 100% and 90.3% fusion rate was obtained for one-level nonplated and plated ACDF procedures with autograft, respectively. The effects of smoking or level of fusion could not be discerned from these one-level cases. Excellent and good clinical outcome results were obtained for 91.3%. Nonplating or rigid plate fixation for ACDF in properly selected patients to treat radiculopathy with or without myelopathy has a high fusion rate and yields a satisfactory clinical outcome. Although controversy exists as to the efficacy of rigid plate fixation in one-level ACDF, solid bone fusion can be adequately obtained without plate fixation and instrumentation-related complications can be avoided. In line with the literature, plate fixation should be reserved for patients unwilling or unable to wear a hard orthosis postoperatively for an extended period of time or for those patients who seek a quicker return to normal activities. Proper patient selection, meticulous operative technique and postoperative care is essential to promote optimal graft-host incorporation.

Adult↗
PubMed1994

Nocturnal penile tumescence and rigidity in men without complaints of erectile dysfunction using a new quantitative analysis software.

Nocturnal penile tumescence and rigidity data were collected during 3 successive nights of home monitoring from 44 men screened for normal sexual functioning. The subjects were well distributed during the interval with an age of 31 to 81 years. Penile brachial indexes, biothesiometry measures and testosterone levels were evaluated. Two new time-intensity measures of tumescence (tumescence activity units) and rigidity (rigidity activity units) were used to summarize erectile activity. A high correlation (r > 0.84, p < 0.001) was found between these summary parameters. It was observed that at least 2 nights of monitoring were required to characterize a subject adequately because some men had single nights with no measurable erectile activity. There were low correlations among penile brachial index, biothesiometry and testosterone outcomes, and nocturnal penile tumescence and rigidity measurements. There was a decrease in measurements of tip rigidity with increasing subject age (r = -0.238, p < 0.05) and an increase in tip rigidity associated with penile girth during erectile events (r = 0.505, p < 0.001). Cumulative distributions of rigidity and tumescence activity units were developed to permit a simple, direct comparison of other nocturnal penile tumescence and rigidity findings to results in the study population.

Adult↗
PubMed1986

Evaluation of erectile dysfunction with continuous monitoring of penile rigidity.

Measurement of nocturnal penile tumescence or circumferential expansion is a valuable method for the diagnosis of erectile impotence. However, only a few investigations have been made of penile rigidity during tumescence with a single isolated measurement. A new method of continuous and simultaneous recording of nocturnal penile rigidity and circumferential expansion (tumescence) was used in 105 patients with erectile impotence. The method provided several findings concerning nocturnal penile erection. Circumferential expansion was not always accompanied by penile rigidity. A dissociation of rigidity between the tip and base of the penis was observed in some patients. Shortened episodes and low amplitude of rigidity also were seen. Of 11 patients with psychogenic impotence diagnosed by conventional methods 3 (27.3 per cent) showed abnormal nocturnal rigidity and 8 of 94 (8.5 per cent) with organic impotence diagnosed by conventional methods showed normal nocturnal rigidity. Because of its ambulatory character the continuous measurement of nocturnal penile rigidity is of value in defining features of nocturnal penile erection and differentiating psychogenic from organic impotence.

Erectile Dysfunction↗