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This article reports an experiment examining the extent to which younger and older speakers engage in audience design, the process of adapting one’s speech for particular addressees. Through an initial card-matching task, pairs of younger adults and pairs of older adults established common ground for sets of picture cards. Subsequently, the same individuals worked separately on a computer-based picturedescription task that involved a novel partner-cuing paradigm. Younger speakers’ descriptions to the familiar partner were shorter and were initiated more quickly than were descriptions to an unfamiliar partner. In addition, younger speakers’ descriptions to the familiar partner exhibited a higher proportion of lexical overlap with previous descriptions than did descriptions to an unfamiliar partner. Older speakers showed no equivalent evidence for audience design, which may reflect difficulties with retrieving partner-specific information from memory during conversation.

In typical interactions, speakers frequently produce utterances that appear to reflect beliefs about the common ground shared with particular addressees. Horton and Gerrig (2005a) proposed that one important basis for audience design is the manner in which conversational partners serve as cues for the automatic retrieval of associated information from memory. This paper reports the results of two experiments demonstrating the influence of partner-specific memory associations on language production. Following an initial task designed to establish associations between specific words (Experiment 1) or object categories (Experiment 2) and each of two partners, participants named a series of pictures in the context of the same two individuals. Naming latencies were shortest for responses associated with the current partner, and were not significantly correlated with explicit recall of partner-item associations. Such partner-driven memory retrieval may constrain the information accessible to speakers as they produce utterances for particular addressees.

Context Diabetic muscle infarction (DMI) is a rare complication associated with poorly controlled diabetes mellitus. Less than 200 cases have been reported in the literature since it was first described over 45 years ago. There is no clear ‘standard of care’ for managing these patients. Evidence acquisition PubMed searches were conducted for ‘diabetic muscle infarction’ and ‘diabetic myonecrosis’ from database inception through July 2014. All articles identified by these searches were reviewed in detail if the article text was available in English. Evidence synthesis The current literature exists as case reports or small case series, with no prospective or higher-order treatment studies available. Thus, an evidence-based approach to data synthesis was difficult. The available literature is presented objectively with an attempt to describe clinically relevant trends and findings in the diagnosis and management of DMI. Conclusions Early recognition of DMI is key, so appropriate treatment can be initiated. MRI is the radiological study of choice. A combination of bed rest, glycemic control, and non-steroidal anti-inflammatory drug therapy appears to yield the shortest time to symptom resolution and the lowest risk of recurrence.

STUDY DESIGN Multicenter, prospective, consecutive clinical series. OBJECTIVES To establish and validate classification of scoliosis in the adult. SUMMARY OF BACKGROUND DATA Studies of adult scoliosis reveal the impact of radiographic parameters on self-assessed function: lumbar lordosis and frontal plane obliquity of lumbar vertebrae, not Cobb angle, correlate with pain scores. Deformity apex and intervertebral subluxations correlate with disability. METHODS A total of 947 adults with spinal deformity had radiographic analysis: frontal Cobb angle, deformity apex, lumbar lordosis, and intervertebral subluxation. Health assessment included Oswestry Disability Index and Scoliosis Research Society instrument. Deformity apex, lordosis (T12-S1), and intervertebral subluxation were used to classify patients. Outcomes measures and surgical rates were evaluated. RESULTS Mean maximal coronal Cobb was 46 degrees and lumbar lordosis 46 degrees . Mean maximal intervertebral subluxation (frontal plane) was 4.2 mm (sagittal plane, 1.2 mm). In thoracolumbar/lumbar deformities, the loss of lordosis/higher subluxation was associated with lower Scoliosis Research Society pain/function and higher Oswestry Disability Index scores. Across the study group, lower apex combined with lower lordosis led to higher disability. Higher surgical rates with decreasing lumbar lordosis and higher intervertebral subluxation were detected. CONCLUSIONS A clinical impact classification has been established based on radiographic markers of disability. The classification has shown correlation with self-reported disability as well as rates of operative treatment.

The bone morphogenetic protein (BMP) and growth and differentiation factor (GDF) signaling pathways have well-established and essential roles within the developing skeleton in coordinating the formation of cartilaginous anlagen. However, the identification of bona fide targets that underlie the action of these signaling molecules in chondrogenesis has remained elusive. We have identified the gene for the retinoic acid (RA) synthesis enzyme Aldh1a2 as a principal target of BMP signaling; prochondrogenic BMPs or GDFs lead to attenuation of Aldh1a2 expression and, consequently, to reduced activation of the retinoid signaling pathway. Consistent with this, antagonism of retinoid signaling phenocopies BMP4 action, whereas RA inhibits the chondrogenic stimulatory activity of BMP4. BMP4 also down-regulates Aldh1a2 expression in organ culture and, consistent with this, Aldh1a2 is actively excluded from the developing cartilage anlagens. Collectively, these findings provide novel insights into BMP action and demonstrate that BMP signaling governs the fate of prechondrogenic mesenchyme, at least in part, through regulation of retinoid signaling.

A novel role for IGF-I in MSC chondrogenesis was determined. IGF-I effects were evaluated in the presence or absence of TGF-β signaling by conditionally inactivating the TGF-β type II receptor. We found that IGF-I had potent chondroinductive actions on MSCs. IGF-I effects were independent from and additive to TGF-β. Introduction: Mesenchymal stem cells (MSCs) can be isolated from adult bone marrow (BM), expanded, and differentiated into several cell types, including chondrocytes. The role of IGF-I in the chondrogenic potential of MSCs is poorly understood. TGF-β induces MSC chondrogenic differentiation, although its actions are not well defined. The aim of our study was to define the biological role of IGF-I on proliferation, chondrogenic condensation, apoptosis, and differentiation of MSCs into chondrocytes, alone or in combination with TGF-β and in the presence or absence of TGF-β signaling. Materials and Methods: Mononuclear adherent stem cells were isolated from mouse BM. Chondrogenic differentiation was induced by culturing high-density MSC pellets in serum- and insulin-free defined medium up to 7 days, with or without IGF-I and/or TGF-β. We measured thymidine incorporation and stained 2-day-old pellets with TUNEL, cleaved caspase-3, peanut-agglutinin, and N-cadherin. Seven-day-old pellets were measured in size, stained for proteoglycan synthesis, and analyzed for the expression of collagen II and Sox-9 by quantitative real time PCR. We obtained MSCs from mice in which green fluorescent protein (GFP) was under the Collagen2 promoter and determined GFP expression by confocal microscopy. We conditionally inactivated the TGF-β type II receptor (TβRII) in MSCs using a cre-lox system, generating TβRII knockout MSCs (RIIKO-MSCs). Results and Conclusions: IGF-I modulated MSC chondrogenesis by stimulating proliferation, regulating cell apoptosis, and inducing expression of chondrocyte markers. IGF-I chondroinductive actions were equally potent to TGF-β1, and the two growth factors had additive effects. Using RIIKO-MSCs, we showed that IGF-I chondrogenic actions are independent from the TGF-β signaling. We found that the extracellular signal-related kinase 1/2 mitogen-activated protein kinase (Erk1/2 MAPK) pathway mediated the TGF-β1 mitogenic response and in part the IGF-I proliferative action. Our data, by showing the role of IGF-I and TGF-β1 in the critical steps of MSC chondrogenesis, provide critical information to optimize the therapeutic use of MSCs in cartilage disorders.

Bone elongation by endochondral ossification occurs through the differentiation cascade of chondrocytes of cartilaginous growth plates. Molecules from the systemic vasculature reach the growth plate from three different directions: epiphyseal, metaphyseal, and via a ring vessel and plexus associated with the perichondrium. This study is an analysis of the real-time dynamics of entrance of fluoresceinated tracers of different molecular weights into the growth plate from the systemic vasculature, and tests the hypothesis that molecular weight is a key variable in the determination of both the directionality and the extent of tracer movement into the growth plate. Multiphoton microscopy was used for direct in vivo imaging of the murine proximal tibial growth plate in anesthetized 4-5-week-old transgenic mice with green fluorescent protein linked to the collagen II promoter. Mice were given an intracardiac injection of either fluorescein (332.3 Da), or fluoresceinated dextrans of 3, 10, 40, 70 kDa, singly or sequentially. For each tracer, directionality and rate of arrival, together with extent of movement within the growth plate, were imaged in real time. For small molecules (up to 10 kDa) vascular access from all three directions was observed and entrance was equally permissive from the metaphyseal and the epiphyseal sides. Within our detection limit (a few per cent of vascular concentration) 40 kDa and larger dextrans did not enter. These results have implications both for understanding systemic and paracrine regulation of growth plate chondrocytic differentiation, as well as variables associated with effective drug delivery to growth plate chondrocytes.

Cartilage oligomeric matrix protein (COMP) is a secreted glycoprotein found in the extracellular matrices of skeletal tissues. Mutations associated with two human skeletal dysplasias, pseudoachondroplasia and multiple epiphyseal dysplasia, disturb COMP secretion leading to intracellular accumulation of mutant COMP, especially in chondrocytes. Here we show that the manifestation of this secretory defect is dramatically influenced by the signal peptide that targets COMP for secretion. The comparison of wild type and mutant COMP secretion directed by the COMP or BM40 signal peptide in HEK-293 cells and rat chondrosarcoma cells revealed that the BM40 signal peptide substantially enhances secretion of mutant COMP that accumulates in endoplasmic reticulum-like structures when targeted by its own signal peptide. Additionally, we demonstrate that mutant COMP forms mixed pentamers with wild type COMP. Our findings suggest that the secretory defect in pseudoachondroplasia and multiple epiphyseal dysplasia is not specific for chondrocytes, nor does it require interaction of mutant COMP with other matrix proteins prior to transport from the cell. They also imply a previously unappreciated role for the signal peptide in the regulation of protein secretion beyond targeting to the endoplasmic reticulum.

Study design Prospective analysis of a consecutive cohort of adult spinal deformity patients queried over a 12-month period. Objectives To assess the SRS-22 instrument compared with the SF-12 and Oswestry. Summary of background data Very few reports in the literature have applied the SRS-22 to adult spinal deformity patients. Methods Consecutive adult spinal deformity patients were applied the SRS-22, SF-12, and Oswestry. Four analyses were done: 1) floor/ceiling effect; 2) Pearson's correlation coefficients between the SRS-22, SF-12, and Oswestry; 3) Cronbach's alpha analysis for internal consistency within the SRS-22; and 4) test/retest. Results Floor/ceiling range for the SRS-22 compared favorably with the SF-12 and Oswestry. The Pearson's coefficients correlating the two questionnaires relative to the SRS-22 were > 0.7. The Cronbach's alpha within each domain for the SRS-22 were > 0.7, except for pain (0.67). Test/retest correlation coefficients ranged from 0.84 to 0.95 for the subscales. Conclusions The SRS-22 is a disease-specific instrument with the capacity to demonstrate change in health status more effectively than the SF-12 and in more domains than the Oswestry. The SRS-22 showed high criterion validity with the SF-12 and Oswestry based on Pearson's coefficients. High Cronbach's alpha scores suggested a high internal consistency within each domain of the SRS-22, except for pain (0.67). Test/retest reliability was excellent.

The Sarbanes-Oxley Act (Act) significantly changed the expected corporate behavior of public companies. The Act governs the relationship between corporate organizations and their in-house or outside counsel. Under Section 307 of the Act, the Securities and Exchange Commission initially proposed expansive rules regarding counsel's duties. After comments and criticism from much of the bar, a final, narrower, version of rules under Section 307 (Final Rule) was adopted. The Final Rule contains alternative reporting procedures, attorney responsibilities, and sanctions for violations. In addition to the Act, the American Bar Association's (ABA) Task Force on Corporate Responsibility(Task Force), which was itself a reaction to Enron, reported on the importance of counsel's role in a corporate setting (Cheek Report). The ABA adopted amendments to its Model Rules of Professional Conduct (Model Rules) 1.6 and 1.13 as proposed in the Cheek Report. The Final Rule and amended Model Rules together suggest that attorneys may owe duties beyond those owed to their clients.

Interbody cages are used as an adjunct to anterior lumbar interbody fusion, but exposure and insertion of two cages can be difficult. A biomechanical study was performed to compare the stability and exposed surface for fusion obtained with interbody reconstruction using two traditional cylindrical cages (18-mm diameter) vs. a single expanded mega-cage (24-mm diameter). A single-cage technique could result in safer exposure, shorter operating time, and less cost.nondestructive testing of L5-S1 motion segments with cages compared the two configurations, and direct measure of the size of the fusion bed was made.16 human cadaveric lumbar motion segments.significant differences in motion segment stiffness and cancellous surface areas were compared using a Wilcoxon rank sum test. Motion segments were biomechanically tested intact, and then tested again after insertion of two interbody cages (n=8) or a single mega-cage (n=8). Nondestructive biomechanical loading was performed consisting of: (1) compression (maximum load 900 N); (2) Flexion, extension, left and right lateral bending (maximum moment 18 Nm); and (3) left and right torsion (maximum moment 10 Nm). From the load-deformation curves obtained, stiffness values were calculated to compare the two-cage and the single mega-cage reconstructions. After testing, the specimens were disarticulated and the surface area of the endplate bed created in the cancellous bone (of both vertebrae) was measured to compare the potential vascular surface for osteogenesis with both constructs.The averages of the normalized values of stiffness were significantly greater for the two-cage group as compared to the mega-cage group in flexion only (1.08 vs. 0.74, p0.05). For extension, torsion and lateral bending there was no significant difference in stiffness. In compression the two-cage group was stiffer, although not significantly (0.92 vs. 0.68, p0.07). The average cancellous bed surface area was slightly greater for the single-cage reconstruction (1,208 mm(2) vs. 1,155 mm(2)), although this difference was not significant.The stiffness with a single anterior mega-cage was significantly lower in flexion compared with two standard cages. However, in all other modes of testing the constructs were statistically equivalent, although neither construct was significantly stiffer than the intact specimen. Additionally, the single mega-cage provides an equivalent cancellous bed for fusion as compared to dual cages. While this study is not sufficient to recommend human application, these results and our previous experience with the successful in vivo use of a single cage in rhesus monkeys [4] suggest that the single expanded anterior cage may be an acceptable concept although subsidence risk needs further investigation. The potential advantages of a single mega-cage (safer for the foramen, safer for the vessels, more consistent decortication and possibly cheaper) further suggest that examination should be given to this method as an approach to anterior interbody reconstruction in selected patients.

Hypochondroplasia (MIM 146000) is an autosomal dominant skeletal dysplasia with skeletal features similar to but milder than those seen in achondroplasia. Within the past year, the achondroplasia locus has been mapped to 4p 16.3 (refs 5-7) and mutations in the fibroblast growth factor receptor 3 (FGFR3) gene have been identified in patients with the disorder. More than 95% of 242 cases reported so far are accounted for by a single Gly380Arg mutation. McKusick et al. proposed that achondroplasia and hypochondroplasia are allelic based on the similarities in phenotype between the two disorders and the identification of a severely dwarfed individual whose father had achondroplasia and whose mother had hypochondroplasia. There is also genetic linkage evidence that hypochondroplasia and achondroplasia map to the same locus. We therefore began a systematic screening of FGFR3 to detect mutations in patients with hypochondroplasia. We now report a single FGFR3 mutation found in 8 out of 14 unrelated patients with hypochondroplasia. This mutation causes a C to A transversion at nucleotide 1620, resulting in an Asn540Lys substitution in the proximal tyrosine kinase domain.

Manipulation of the mouse genome through mis-expressing, knocking out, and introducing mutations into genes of interest has provided important insights into the genetic pathways responsible for human skeletal development. These pathways contribute to the sequential phases of skeletal morphogenesis that include patterning, condensation, and overt organogenesis of the membranous and endochondral embryonic skeletons and to subsequent linear growth. Disturbances in these pathways account for many developmental syndromes and disorders of the human skeleton. Recurrent themes include establishment of interlocking regulatory circuits involving growth factors, receptors, signalling pathways, and transcription factors that control cellular programmes such as migration, adhesion, proliferation, differentiation, and apoptosis, and use of common molecules for different purposes. Technical advances suggest that genetic engineering in mice will continue to be highly instructive in the field of skeletal biology.

Do readers encode the perceptual perspectives of characters during narrative comprehension? To address this question, we conducted two experiments using stories that sometimes described situations in which certain information was occluded from the protagonists' views. We generated two related hypotheses concerning the potential impact of occlusion events on text representations. One, the event boundary hypothesis, suggested that any salient narrative event would reduce the accessibility of prior story information. The second, the perceptual availability hypothesis, suggested that accessibility would decrease most for information no longer visible to story protagonists. In Experiment 1, the participants were slowest to respond to verification questions that asked about occluded information. In Experiment 2, we demonstrated that this effect did not extend to other, nonoccluded information. These results suggest that readers encode text information from the perceptual perspective of story protagonists. This is consistent with recent perceptual symbol views of language comprehension.

Chondrogenesis results from the condensation of mesenchymal chondroprogenitor cells (MCC) that proliferate and differentiate into chondrocytes. We have previously shown that IGF binding protein (IGFBP)-3 has an IGF-independent antiproliferative effect in MCC. The current study evaluates the IGF-independent apoptotic effect of IGFBP-3 on MCC to modulate chondrocyte differentiation. We employed the RCJ3.1C5.18 chondrogenic cell line, which in culture progresses from MCC to differentiated chondrocytes; cells do not express IGFs or IGFBP-3. We also used IGFBP-3 mutants with decreased (I56 substituted to G56; L80 and L81 to G80G81) or abolished binding for IGFs (I56, L80, and L81 to G56G80G81). MCC transfected with IGFBP-3 detached, changed their phenotype, and underwent apoptosis. A maximal IGFBP-3 apoptotic effect was observed 24 h after transfection (463 ± 73% of controls; P < 0.001). Remarkably, IGFBP-3 mutants had similar effects, demonstrating that the IGFBP-3 apoptotic action was clearly IGF independent. In addition, treatment with IGFBP-3 in serum-free conditions resulted in a significant increase of apoptosis (173 ± 23% of controls; P < 0.05). Moreover, this apoptotic effect was selective for MCC, resulting in a selective reduction of chondrocytic nodules and a significant decrease in type II collagen expression and proteoglycan synthesis. In summary, we have identified a novel IGF-independent role for IGFBP-3 in the modulation of chondrocyte differentiation.

The efficient processing of olfactory information is crucial for many aspects of life in animals, including behavior in insects. While much is known about the organization of the insect olfactory system, comparatively little is understood about the molecules that support its function. To further elucidate the molecular basis of olfaction, we explored the role of the calcium-binding chaperone calreticulin in the behavioral response of Drosophila to aversive odorants. We show that avoidance of naturally aversive odorants is impaired in flies harboring mutations in Calreticulin. Calreticulin mutants have broad defects in odor avoidance without abnormalities in antennal responses to odorants, alterations in central nervous system structure, or deficits in overall locomotor abilities. Interestingly, Calreticulin mutants exhibit defects in behavioral responses to odorants at low strength, whereas responses to higher odorant concentrations are preserved in these animals. Our studies indicate that calreticulin plays a key role in olfactory system function, possibly by establishing its overall sensitivity to odorants.

Mice were generated by pronuclear injection of a type II collagen transgene harboring an Arg789Cys (R789C) mutation that has been found in patients with spondyloepiphyseal dysplasia (SED). Expression was directed to cartilage by the murine Col2a1 promoter to examine the consequences of mutations involving the Y-position of the collagen helix Gly-X-Y triplet on skeletogenesis. The transgenic mice had very short limbs, short trunk, short snout, and cleft palate; they died at birth. Their growth plates were disorganized and collagen fibrils were sparse in cartilage matrix. When the transgene was expressed in RCS cells, there was no evidence that R789C-bearing collagen chains were incorporated into stable collagen molecules. Molecular modeling of the mutation raised the possibility that it destabilizes the collagen triple helix. Together our results suggest that Y-position mutations, such as R789C, can act in a dominant negative manner to destabilize collagen molecules during assembly, reducing their availability to form fibrils, the deficiency of which profoundly disturbs the template functions of cartilage during skeletogenesis.

We have developed a noninvasive confocal fluorescence spectrometer to measure in vivo fluorescence spectra in mice. Our motivation is the study of the healing process of wounded cartilage in the murine model. The spectrometer measures the expression of green fluorescent protein (GFP) which is linked to the promoter of type II collagen as a marker for the expression of the chondrocyte phenotype. The confocal system uses an argon ion laser (488 nm) to excite fluorescence in a confocal volume about 200 um below the skin surface in the cartilage of the xyphoid process. In vitro studies showed how the refractive mismatch at the surface boundary and the light scattering of the tissue affect the depth and size of the confocal volume. A thin fluorescent layer was detected through a 130 um tissue phantom (murine skin) by moving the confocal volume axially through the phantom. The presence of skin increased the axial full width at half maximum of the confocal response from 7 um to 72 um. In conclusion, we achieve a low-spatial-resolution confocal spectrometer, which yields a fluorescence spectrum that maximizes the GFP fluorescence of cartilage and minimizes the skin autofluorescence.

In an effort to identify putative transcription factors involved in chondrocyte differentiation during human endochondral bone formation, a human fetal cartilage-specific cDNA library was screened with a degenerate oligonucleotide probe corresponding to a conserved stretch of eight amino acids from the zinc finger region of the Drosophila Kruppel gene family of DNA-binding proteins. Using this strategy, we have identified a novel zinc finger gene ZFP-37. ZFP-37 corresponds to a putative transcription factor containing 12 tandemly repeated zinc finger motifs and a Kruppel-associated box (KRAB) domain. The KRAB domain has been reported to function as a transcriptional repressor and is located in the amino terminus, while the zinc finger repeats are positioned at the carboxy-terminal end of ZFP-37. Gene mapping with a somatic cell hybrid panel and fluorescence in situ hybridization (FISH) localized ZFP-37 to human Chr 9q32. The gene is expressed at low level as a 3.2-kb mRNA in several tissues including fetal human cartilage. Sequence comparison revealed that ZFP-37 may represent the human homolog of the mouse gene Zfp-37. The map location and expression pattern suggest ZFP-37 as a candidate gene for a craniofacial-limb malformation, Nager syndrome (acrofacial dysostosis).

The biochemical consequences of a type II procollagen mutation that contained a Gly574Ser amino acid substitution were analyzed in a transgenic mouse strain. The mutation correlated with one previously characterized in a patient with the lethal human chondrodysplasia, hypochondrogensis [horton et al., 1992], and resulted in a similar shortlimbed phenotype. There were fewer collagen fibrils present in the transgenic cartilage and reduced immunofluorescence of cartilage matrix using a type II collagen antibody. Pepsin-extracted collagen from transgenic mouse embryocartilage was analyzed electrophoretically and indicated less type II as well as type XI collagen compared to their wild-type littermates. A pulse-chase experiment was performed to evaluate the biosynthesis and fate of type II collagen. Chondrocytes isolated from transgenic tissue synthesized fewer stable molecules, resulting in decreased secretion of the procollagen chains. By amino acid sequence analysis of the type II collagen peptides from cartilage of transgenic mouse embryos, serine was not detected at residue 574, the site mutated in the transgene. Based on sequence data, we believe that the molecules incorporated into collagen fibrils of the extracellular matrix, while fewer in number, were composed of normal α1(II) chains.

Considerable progress has been made in delineating the molecular genetic basis of the human chondrodysplasias. Two genes emerge as harboring mutations found in patients with the most common disorders. Mutations in the type II collagen gene account for most spondyloepiphyseal dysplasia and spondyloepiphyseal dysplasia-like clinical disorders, whereas mutations in the fibroblast growth factor receptor 3 gene are responsible for achondroplasia, thanatophoric dysplasia, and hypochondroplasia. A substantial portion of remaining patients have mutations of the genes encoding cartilage oligomeric matrix protein or diastrophic dysplasia sulfate transporter.

Study Design. A prospective analysis of the clinical outcome of a consecutive series of patients treated with posterior lumbar arthrodesis. Preoperative data were collected retrospectively by chart review. Objectives. To measure by independent review the clinical outcome of posterolateral intertransverse fusion as a treatment for discogenic low back pain in a highly selected group of patients. Summary of Background Data. Although numerous studies have reported on the surgical management of degenerative disc disease, they have been difficult to interpret because they lack patient-oriented outcome assessment and objective pain measurement criteria, independent review, and include patients with diagnoses other than degenerative disc disease. Methods. Between 1991 and February 1993 all patients seen by a single surgeon, evaluated with magnetic resonance imaging and discography, and treated with posterolateral lumbar fusion were reviewed by independent investigation. Outcome was assessed in the areas of radiographic fusion, pain, function, and patient satisfaction. Results. Twenty-three patients (12 women, 11 men; 100% follow-up an average of 47 months after surgery [range, 24-84 months]) met the inclusion criteria. Overall, 39%, had a good or excellent result, 13% fair, and 48% poor. Nine of 10 patients receiving worker's compensation had a poor result; four of five patients with radiographic pseudarthrosis had a poor result. Statistically significant improvement in the visual analogue scale was noted in the good and excellent group (P=0.0001) and the fair group (P=0.002) with no change in the poor group. Patients out of work more than 3 months before surgery tended to have poor results. Overall, 56% of patients were extremely satisfied with the result of their surgery. Conclusion. Posterolateral intertransverse fusion can be used to successfully manage chronic discogenic back pain. However, patient selection remains a challenge, and successful outcome appears to be limited in the subset of patients receiving worker's compensation and those chronically disabled. Prospective and randomized study with objective pain criteria, independent review, and patient-oriented outcome is recommended.

This report documents the Ground Vehicle System Integration (GVSI) and Design Optimization Model GVSI is a top-level analysis tool designed to support engineering tradeoff studies and vehicle design optimization efforts. The model uses simplified functional and parametric relationships to evaluate system performance issues. GVSI's primary function is to illustrate the dependence of various system and subsystem functions; the goal is to provide a better understanding how a change in the performance of one subsystem affects the rest of the vehicle.

What role does common ground play in the production of utterances? We outline and test two models. One model assumes that common ground is involved in initial utterance planning, while the other model assumes that it only plays a role in monitoring. To compare these models, we focus on common ground as evidenced in physical co-presence. We had speakers describe objects for listeners in a modified version of the referential communication task. While descriptions under no time constraints appeared to incorporate common ground with the listener, common ground was not used when the speakers were under time pressure. These results suggest that speakers do not engage in audience design in the initial planning of utterances; instead, they monitor those plans for violations of common ground.

Study Design. The technique of hole preparation and the placement or orientation of anterior transvertebral screws in relation to the endplates were the subjects of two experiments. Objectives. Experiment 1-to determine if anterior transvertebral body screws have higher pull-out strengths after unicortical predrilling compared with a bicortical predrilling ; Experiment 2-to determine the effect of the screw's orientation in the vertebral body on its resistance to loosening. Summary of Background Data. There are a variety of surgical techniques for using anterior transvertebral screws in the vertebral body without any clear guidelines as to which techniques optimize the strength of fixation. Methods. In Experiment 1, 31 cadaveric vertebral bodies were tested for pull-out strength of transvertebral body screws placed after unicortical predrilling compared with bicortical predrilling. In Experiment 2, 48 cadaveric vertebral bodies were tested with transvertebral screws inserted using four different screw orientations. Results. There is no statistically significant difference in pull-out strength of anterior transvertebral body screws inserted after unicortical compared with bicortical predrilling (Experiment 1). The resistance to loosening is greatest when transvertebral screws are oriented in the superior oblique position (Experiment 2). Conclusions. Experiment 1-preparation of the far cortex by predrilling is not necessary. Experiment 2-transvertebral screws should be obliquely oriented so that the forces applied to the screws are resisted by both of the endplates.

Study Design. Two separate experiments (A and B), each involving six human cadaveric torsos with intact rib cages and sternums, were done to determine the effect of two different sequences of surgical releases (at T8-T9) on thoracic spinal motion. Objectives. Experiment A was designed to test the effects of three releases in sequence from anterior to posterior, analogous to a two-stage operative treatment with anterior and posterior releases. Experiment B, which involved three releases, was desgined to determine 1) if unilateral posterior total facetectomy alone allowed a significant increase in motion and 2) if rib head resection without discectomy allowed a significant increase in motion. Summary of Background Data. In the surgical treatment of thoracic spinal deformity, surgical release is often done to impart additional flexibility to the spine. Available releases include discectomy, rib head resection, and facetectomy. There is little work to date on the relative importance of the disc, rib head, and facet joint in the stability of the thoracic spine. Methods. In experiment A and experiment B, the cadaveric torsos were mounted on a custom-made loading frame. Mechanical testing (using weights, pulleys, and digital goniometers) was done after each surgical release to measure the extent of angular rotation in the coronal plane (right lateral bending and left lateral bending) and in the sagittal plane (flexion and extension). Results. The combination of rib head resection and radical discectomy provided the greatest increase in thoracic spinal motion. Standard discectomy alone did not allow a significant increase in motion. Rib head resection without discectomy did not allow a significant increase in motion. Unilateral posterior total facet excision did not allow a significant increase in motion. Conclusions. These experiments indicate that the combination of rib head resection and radical discectomy may be the optimal thoracic spinal release

A number of gene loci have recently been shown to harbor mutations that cause human chondrodysplasias. They encode proteins that occupy cartilage matrix, such as types II, IX, X and XI collagens and COMP, that transduce signals in the growth plate, i.e., FGFR3 and PTHrP receptor, that influence the transport and metabolism of sulfate ions in relevant cells, e.g., DTDST and arylsulfatase E, and that regulate transcription of other genes, such as SOX9. Mutations at two loci, COL2A1 and FGFR3, account for most patients with chondrodysplasias--those with spondyloepiphyseal dysplasia and the achondroplasia classes of disorders, respectively. Mutations in the former tend to be dispersed throughout the gene and in other functionally related genes, whereas mutations in the latter are restricted to a few codons that seem to be very mutable.

The bone-screw interface is critical in the use of spinal instrumentation. The purpose of these experiments described here was twofold. First, to determine whether a correlation existed between torque generated during screw insertion and the pullout strength. Second, to determine how differing surgical methods of screw hole preparation influenced torque of insertion and screw pullout strength. A series of experiments were carried out in which screws were inserted into synthetic bone (experiment 1) and into calf vertebrae (experiment 2). The method of screw hole preparation (i.e., diameter of entrance hole and pilot hole) was varied while the resulting torque of insertion and the pullout strength of the screw was measured in each case. A torque screwdriver was used to measure the torque of insertion of the screws. Screw pullout strength was measured using a materials testing machine. Two important results emerged from these experiments. First, a higher torque of insertion correlated with a higher screw pullout force. This correlation may be useful intraoperatively in evaluating fixation. Second, torque of insertion and pullout force were more influenced by cortex over-drill diameter than pilot hole diameter. These experiments show the importance of the dorsal cortex in pedicle screw fixation.

Despite the proven ability of color to enhance scientific and technical communication, many designers and their teachers strongly avoid chromatic color. They can overcome their reluctance and use color effectively if they understand how color works, respect the limitations of color, and apply it in ways compatible with communications objectives and human perception.© (1993) COPYRIGHT SPIE--The International Society for Optical Engineering. Downloading of the abstract is permitted for personal use only.

A general method for making optical media by a continuous roll process has been developed. The process can accommodate a variety of optical structures, although it has been optimized for those with smaller form factors and thin cover sheets. A test disk was used to demonstrate process capabilities and evaluate media made by this method.

A pilot study was carried out to examine the safety and efficacy of recombinant human growth hormone for growth-promoting therapy of achondroplasia. The data suggest that the agent in doses used to treat non-GH-deficient forms of short stature (0.3 mg/kg/wk) modestly increases overall height velocity in some children with achondroplasia. The effect was seen mainly in children with the lowest growth velocities prior to treatment. No untoward effects were noted. Several questions were raised that require further study.