Medical student assessments-frequency of radiological images used: a national study.

OBJECTIVES: Assessments are a key part of life for medical students at University. We know there is variation in these assessments across Universities. The aims of this study were to expatiate summative assessments in Scottish Medical Schools and to examine how frequently radiological images feature in them. METHODS: All Scottish medical schools were invited to participate in the study. Data on objective structured clinical examinations (OSCEs; 5 years) and written assessments (3 years) were retrospectively collected for each university and results were collated. Each University was randomly assigned a letter from A to E and anonymised for data presentation. RESULTS: 10,534 multiple choice questions (MCQ) and 1083 OSCE stations were included in this study. There was wide variation in the number, type and timing of assessments across Scottish medical schools. There were highly significant differences in the number of OSCE stations and the number of MCQs set over the study period (p < 0.0001). Radiological images were used on average 0.6 times (range 0-1.1) in each OSCE examination and 2.4 times (range 0.1-3.7) for written assessments. CONCLUSION: In this detailed study, we demonstrated significant differences in medical student assessments across Scottish Universities. Given the importance of Radiology in modern medicine, the frequency and differences in which radiological images were used in assessments across Universities should be addressed. ADVANCES IN KNOWLEDGE: This is the first national longitudinal study to quantify the role of radiological images in summative Medical Student Assessments. Great variability exists in the extent and how (clinical versus written assessments) radiological images are used to assess Scottish medical students. Radiological images are used infrequently in clinical assessments, but are present in every written assessment. These findings could help inform medical schools and academic radiologists as they prepare medical students for the imminent unified medical licensing examination, where Clinical Imaging is a subject with one of the highest number of associated conditions examinable.

Thirty minutes of handgrip exercise potentiates flow-mediated dilatation in response to sustained and transient shear stress stimuli to a similar extent.

NEW FINDINGS: What is the central question of this study? This study sought to determine whether enhancement of brachial artery flow-mediated dilatation (FMD) after acute exposure to a sustained elevation in shear stress is greater when the shear stress stimulus for FMD is also sustained. What is the main finding and its importance? Brachial artery FMD in response to a sustained (handgrip exercise) and transient (reactive hyperaemia) shear stress stimulus was enhanced to a similar extent 10 min after a 30 min handgrip exercise intervention. This suggests that prior exposure to a sustained elevation in shear stress results in a similar acute augmentation of the ability of the endothelium to transduce sustained and transient shear stress stimuli. ABSTRACT: Brief (30 min) exposure of the brachial artery (BA) to a sustained elevation in shear stress has been shown to potentiate subsequent BA flow-mediated dilatation (FMD) in response to a transient shear stress stimulus [reactive hyperaemia (RH) FMD]. It is unknown whether matching the sustained shear stress exposure to a subsequent sustained shear stress stimulus for FMD [via handgrip exercise (SS-FMD)] might enhance the potentiation of FMD. The purpose of the study, therefore, was to assess the impact of a 30 min handgrip exercise intervention-induced elevation in shear stress on subsequent BA SS-FMD versus RH-FMD. Nineteen healthy men (22 ± 3 years) preformed a 30 min rhythmic handgrip exercise intervention on two experimental days. BA-FMD was assessed using either an RH or a 6 min sustained shear stress stimulus created via handgrip exercise (order of visits counterbalanced) at three time points: pre-intervention and 10 and 60 min post-intervention. The FMD was assessed using duplex ultrasound. Shear stress was estimated as shear rate (SR = BA blood velocity/BA diameter). Data are mean ± SD. Both SS and RH-FMD increased from pre-intervention to 10 min post-intervention [SS-FMD (6 min average), from 0.11 ± 0.05 to 0.16 ± 0.08 mm; P = 0.008; Cohen's d = 0.66; and RH-FMD, from 0.25 ± 0.1 to 0.32 ± 0.11 mm; P = 0.013; Cohen's d = 0.68]. The magnitude of enhancement in RH and SS-FMD did not differ (change in RH versus SS-FMD pre- versus 10 min post-intervention, P = 0.344). These findings suggest that exposure to elevated shear stress via 30 min of handgrip exercise potentiates subsequent FMD in response to sustained and transient elevations in shear stress to a similar extent.

SHOX gene is expressed in vertebral body growth plates in idiopathic and congenital scoliosis: implications for the etiology of scoliosis in Turner syndrome.

Reduced SHOX gene expression has been demonstrated to be associated with all skeletal abnormalities in Turner syndrome, other than scoliosis (and kyphosis). There is evidence to suggest that Turner syndrome scoliosis is clinically and radiologically similar to idiopathic scoliosis, although the phenotypes are dissimilar. This pilot gene expression study used relative quantitative real-time PCR (qRT-PCR) of the SHOX (short stature on X) gene to determine whether it is expressed in vertebral body growth plates in idiopathic and congenital scoliosis. After vertebral growth plate dissection, tissue was examined histologically and RNA was extracted and its integrity was assessed using a Bio-Spec Mini, NanoDrop ND-1000 spectrophotometer and standard denaturing gel electrophoresis. Following cDNA synthesis, gene-specific optimization in a Corbett RotorGene 6000 real-time cycler was followed by qRT-PCR of vertebral tissue. Histological examination of vertebral samples confirmed that only growth plate was analyzed for gene expression. Cycling and melt curves were resolved in triplicate for all samples. SHOX abundance was demonstrated in congenital and idiopathic scoliosis vertebral body growth plates. SHOX expression was 11-fold greater in idiopathic compared to congenital (n = 3) scoliosis (p = 0.027). This study confirmed that SHOX was expressed in vertebral body growth plates, which implies that its expression may also be associated with the scoliosis (and kyphosis) of Turner syndrome. SHOX expression is reduced in Turner syndrome (short stature). In this study, increased SHOX expression was demonstrated in idiopathic scoliosis (tall stature) and congenital scoliosis.

The vertebral body growth plate in scoliosis: a primary disturbance of growth?

UNLABELLED: STUDY DESIGN AND AIMS: This was an observational pilot study of the vertebral body growth plates in scoliosis involving high-resolution coronal plane magnetic resonance (MR) imaging and histological examination. One aim of this study was to determine whether vertebral body growth plates in scoliosis demonstrated abnormalities on MR imaging. A second aim was to determine if a relationship existed between MR and histological abnormalities in these vertebral body growth plates. METHODS: MR imaging sequences of 18 patients demonstrated the vertebral body growth plates well enough to detect gross abnormalities/deficient areas/zones. Histological examination of ten vertebral body growth plates removed during routine scoliosis surgery was performed. Observational histological comparison with MR images was possible in four cases. RESULTS: Four of the 18 MR images demonstrated spines with normal curvature and normal vertebral body growth plates. In 13 scoliotic spines, convex and concave side growth plate deficiencies were observed most frequently at or near the apex of the curve. One MR image demonstrated a 55 degrees kyphosis and no convex or concave side deficiencies. The degree of vertebral body wedging was independent of the presence of vertebral body growth plate deficiency. Histological abnormalities of the vertebral body growth plates were demonstrated in four with MR imaging abnormalities. CONCLUSION: This study demonstrated MR image abnormalities of scoliotic vertebral body growth plates compared to controls. A qualitative relationship was demonstrated between MR imaging and histological abnormalities. The finding that vertebral body growth plate deficiencies occurred both on the convex and concave sides of the spine, closest to the apical vertebra of the scoliosis curve, implied that they are less likely to be the result of adaptive changes to the physical forces involved in the scoliotic deformity. One explanation is that they represent a primary disturbance of growth.

Idiopathic scoliosis and pineal lesions in Australian children.

PURPOSE: To determine whether treatment of pineal lesions in children is associated with development of idiopathic scoliosis. METHODS: 38 boys and 10 girls with pineal lesions were identified. Their mean age at presentation was 10 years. The pineal pathology varied from cysts and epidermoid to teratoma, germinoma, pineocytoma, and glioblastoma. Treatment ranged from biopsy/extirpation to radiotherapy. RESULTS: 12 patients died. No scoliosis was found in any females or any of the deceased. Two boys had scoliosis: one had a 12-degree right upper thoracic curve with 32-degree kyphosis and the other had a 60-degree right thoracolumbar idiopathic curve, requiring a 2-stage arthrodesis. CONCLUSION: Pineal ablation is not related to the development of idiopathic scoliosis in humans.

Metal ion levels in patients with stainless steel spinal instrumentation.

STUDY DESIGN: Case-control study. OBJECTIVES: To determine whether metal ion concentrations are elevated in patients with spinal instrumentation. SUMMARY OF BACKGROUND DATA: Studies have shown that serum and urinary levels of component metal ions are abnormally elevated in patients with total joint arthroplasties. Little is known of metal ion release and concentrations in patients with spinal instrumentation. METHODS: The study group consisted of patients who had undergone spinal instrumentation for various spinal disorders with a variety of stainless steel implants, 5 to 25 years previously. A group of volunteers without metal implants were controls. All subjects were tested for serum nickel, blood chromium, and random urine chromium/creatinine ratio estimation. RESULTS: The study group consisted of 32 patients with retained implants and 12 patients whose implants had been removed. There were 26 unmatched controls. There was no difference in serum nickel and blood chromium levels between all 3 groups. The mean urinary chromium/creatinine ratio for patients with implants and those with implants removed was significantly greater than controls (P < 0.001). The difference between study subgroups was not significant (P = 0.16). Of several patient and instrumentation variables, only the number of couplings approached significance for correlation with the urine chromium excretion (P = 0.07). CONCLUSION: Spinal implants do not raise the levels of serum nickel and blood chromium. There is evidence that metal ions are released from spinal implants and excreted in urine. The excretion of chromium in patients with spinal implants was significantly greater than normal controls although lower where the implants have been removed. The findings are consistent with low-grade release of ions from implants with rapid clearance, thus maintaining normal serum levels. Levels of metal ions in the body fluids probably do not reach a level that causes late side-effect; hence, routine removal of the implants cannot be recommended.

Cyclic nucleotide signalling: a molecular approach to drug discovery for Alzheimer's disease.

The EPAC (exchange protein directly activated by cAMP) proteins are GEFs (guanine nucleotide-exchange factors) that activate Rap GTPases upon binding to cAMP. The involvement of these proteins in a number of diseases, neurodegenerative, inflammatory and metabolic, has started to show how they may prove to be important targets for therapeutic intervention. We first became interested in EPAC when we discovered that the expression levels of both EPAC1 and EPAC2 were altered in those regions of the brain associated with Alzheimer's disease [McPhee, Breslin, Kewney, MacKenzie, Cooreman, Gibson and Hammond (2004) International Patent number WO 2004/096199 A2]. It was known that compounds could be designed to be selective for EPAC over PKA (protein kinase A); however, these compounds were all based around the core structure of cAMP. We decided to screen a small compound library (10000 compounds) to investigate the possibility of developing a compound series outside of the cAMP structure. We subsequently developed a novel, high-throughput screen based on the displacement of [3H]cAMP from the EPAC cAMP-binding site and identified small molecule hits from the Scottish Biomedical Lead Generation Library. These compounds selectively bind to the cAMP-binding sites of EPAC1 and EPAC2 and are structurally dissimilar to cAMP. They have similar affinities for both EPAC1 and EPAC2 and have a high degree of specificity for EPAC over PKA. We believe that these compounds provide a valuable starting point for a drug optimization programme.

Nocardia farcinica spinal osteomyelitis.

STUDY DESIGN: A case of disseminated Nocardia farcinica infection with spine involvement is reported. OBJECTIVE: To describe the first case of Nocardia farcinica spinal osteomyelitis, and to propose spine instrumentation with debridement and multiple antibiotics for treatment of nocardia spinal osteomyelitis. SUMMARY OF BACKGROUND DATA: Only 11 cases involving Nocardia asteroides spinal osteomyelitis have been reported over the past 40 years. These case reports describe various presentations and treatments of nocardia spinal osteomyelitis. METHODS: A 54-year-old nonambulant, paraparetic man was admitted to the authors' hospital with acutely increased low back pain, fever, and signs of dementia. A disseminated Nocardia farcinica infection including spinal osteomyelitis at T11, T12, L1, L2, and L4; epidural abscess T10-L4, L5-S1 discitis, empyemas, cerebral abscess, and bilateral psoas abscess was noted. RESULTS: Antibiotic therapy, multiple debridements, and posterior instrumentation were performed to palliate the Nocardia farcinica infection. At a recent 3-year follow-up assessment, the patient was independent and ambulant. He had been off antibiotics for 5 months. CONCLUSIONS: Previous case reports of nocardia spinal osteomyelitis describe treatment with antibiotics, debridements, and arthrodesis with autologous bone graft. Prolonged recumbency ensued. In the reported case, a combination of antibiotics, debridements, arthrodesis, and posterior instrumentation for immediate stabilization of the spine resulted in a favorable outcome at 3 years.

The novel long PDE4A10 cyclic AMP phosphodiesterase shows a pattern of expression within brain that is distinct from the long PDE4A5 and short PDE4A1 isoforms.

In situ hybridisation methods were used to map the distribution of the novel long PDE4A10 isoform in the brain. PDE4A10 distribution was compared to that of the long PDE4A5 isoform and the short PDE4A1 isoform using probes specific for unique sequences within each of these isoforms. Coronal sections of the brain, taken at the level of the olfactory bulb, prefrontal cortex, striatum, thalamus, hippocampus and cerebellum, were analysed. Strongest expression of PDE4A isoforms was found in the olfactory bulb granular layer with high signals also in the piriform cortex, the dentate gyrus and the CA1 and CA2 pyramidal cells. For the two long forms, level general staining was noted throughout the striatum, thalamus and hippocampus but no signal was evident in the cerebellum. The long PDE4A10 and PDE4A5 isoforms localised to essentially the same regions throughout the brain, although PDE4A10 was uniquely expressed in the major island of Calleja. A signal for the short PDE4A1 isoform was found in regions in which the two long isoforms were both expressed, with the exception of the medial nucleus of the amygdala where weak signals for PDE4A5 and PDE4A10 were detected but PDE4A1 was absent. Uniquely, strong signals for PDE4A1 were detected in the glomerular layer of the olfactory bulb, the CA3 pyramidal cell region and the cerebellum; areas where signals for the two long forms were not evident. PDE4A transcripts for both PDE4A5 and PDE4A10 were not apparent in the brain stem and those for PDE4A1 were low. PDE4A isoforms are present in several key areas of the brain and therefore present valid targets for therapeutic interventions. Whilst the two long PDE4A isoforms show a remarkably similar distribution, in at least three regions there is clear segregation between their pattern of expression and that of the PDE4A1 short form. This identifies differential regulation of the expression of PDE4A long and short isoforms. We suggest that specific PDE4A isoforms may have distinct functional roles in the brain, indicating that PDE4A isoform-selective inhibitors may have specific therapeutic and pharmacologic properties.

Adenosine 3',5'-cyclic monophosphate (cAMP)-dependent inhibition of IL-5 from human T lymphocytes is not mediated by the cAMP-dependent protein kinase A.

IL-5 is implicated in the pathogenesis of asthma and is predominantly released from T lymphocytes of the Th2 phenotype. In anti-CD3 plus anti-CD28-stimulated PBMC, albuterol, isoproterenol, rolipram, PGE2, forskolin, cholera toxin, and the cAMP analog, 8-bromoadenosine cAMP (8-Br-cAMP) all inhibited the release of IL-5 and lymphocyte proliferation. Although all of the above compounds share the ability to increase intracellular cAMP levels and activate protein kinase (PK) A, the PKA inhibitor H-89 failed to ablate the inhibition of IL-5 production mediated by 8-Br-cAMP, rolipram, forskolin, or PGE2. Similarly, H-89 had no effect on the cAMP-mediated inhibition of lymphocyte proliferation. Significantly, these observations occurred at a concentration of H-89 (3 microM) that inhibited both PKA activity and CREB phosphorylation in intact cells. Additional studies showed that the PKA inhibitors H-8, 8-(4-chlorophenylthio) adenosine-3',5'-cyclic monophosphorothioate Rp isomer, and a myristolated PKA inhibitor peptide also failed to block the 8-Br-cAMP-mediated inhibition of IL-5 release from PBMC. Likewise, a role for PKG was considered unlikely because both activators and inhibitors of this enzyme had no effect on IL-5 release. Western blotting identified Rap1, a downstream target of the cAMP-binding proteins, exchange protein directly activated by cAMP/cAMP-guanine nucleotide exchange factors 1 and 2, in PBMC. However, Rap1 activation assays revealed that this pathway is also unlikely to be involved in the cAMP-mediated inhibition of IL-5. Taken together, these results indicate that cAMP-elevating agents inhibit IL-5 release from PBMC by a novel cAMP-dependent mechanism that does not involve the activation of PKA.

Molecular cloning, genomic positioning, promoter identification, and characterization of the novel cyclic amp-specific phosphodiesterase PDE4A10.

We describe the cloning and expression of HSPDE4A10, a novel long form splice variant of the human cAMP phosphodiesterase PDE4A gene. The 825 amino acid HSPDE4A10 contains a unique N terminus of 46 amino acids encoded by a unique 5' exon. Exon-1(4A10) lies approximately 11 kilobase pairs (kb) downstream of exon-1(4A4) and approximately 13.5 kb upstream of the PDE4A common exon 2. We identify a rat PDE4A10 ortholog and reveal a murine ortholog by nucleotide sequence database searching. PDE4A10 transcripts were detected in various human cell lines and tissues. The 5' sequence flanking exon-1(4A10) exhibited promoter activity with the minimal functional promoter region being highly conserved in the corresponding mouse genomic sequence. Transient expression of the engineered human PDE4A10 open reading frame in COS7 cells allowed detection of a 121-kDa protein in both soluble and particulate fractions. PDE4A10 was localized primarily to the perinuclear region of COS7 cells. Soluble and particulate forms exhibited similar K(m) values for cAMP hydrolysis (3-4 microM) and IC(50) values for inhibition by rolipram (50 nM) but the V(max) value of the soluble form was approximately 3-fold greater than that of the particulate form. At 55 degrees C, soluble HSPDE4A10 was more thermostable (T(0.5) = 11 min) than the particulate enzyme (T(0.5) = 5 min). HSPDE4A10 and HSPDE4A4B are shown here to be similar in size and exhibit similar maximal activities but differ with respect to sensitivity to inhibition by rolipram, thermostability, interaction with the SRC homology 3 domain of LYN, an SRC family tyrosyl kinase, and subcellular localization. We suggest that the unique N-terminal regions of PDE4A isoforms confer distinct properties upon them.

Palliative care nurses' perceptions of good and bad deaths and care expectations: a qualitative analysis.

Individuals who are involved with the death of a person with a terminal illness will often classify the death as either 'good' or 'bad'. Families and healthcare practitioners assess many factors when determining their 'success' or 'failure' in assisting someone in the terminal phase. Palliative care nurses are particularly vulnerable to self-assessments about care of the dying, because death is a daily occurrence. Feelings of failure, unmet expectations and feeling of regret about not being able to prevent a traumatic death may be a source of stress for palliative care nurse and may affect their abilities to function effectively. This article reports the findings of a study involving interviews with 20 palliative care nurses to determine their perceptions of a good and bad death. The study also examined the expectations they hold of themselves and that they believe others hold of them in helping patients to attain a good death. Clinical implications are discussed based on these findings.

Sub-family selective actions in the ability of Erk2 MAP kinase to phosphorylate and regulate the activity of PDE4 cyclic AMP-specific phosphodiesterases.

Expressed in intact cells and in vitro, PDE4B and PDE4C isoenzymes of cyclic nucleotide phosphodiesterase (PDE), in common with PDE4D isoenzymes, are shown to provide substrates for C-terminal catalytic unit phosphorylation by the extracellular signal-regulated kinase Erk2 (p42(MAPK)). In contrast, PDE4A isoenzymes do not provide substrates for C-terminal catalytic unit phosphorylation by Erk2. Mutant PDE4 enzymes were generated to show that Erk2 phosphorylation occurs at a single, cognate serine residue located within the C-terminal portion of the PDE4 catalytic unit. PDE4 long-form isoenzymes were markedly inhibited by Erk2 phosphorylation. The short-form PDE4B2 isoenzyme was activated by Erk2 phosphorylation. These functional changes in PDE activity were mimicked by mutation of the target serine for Erk2 phosphorylation to the negatively charged amino acid, aspartic acid. Epidermal growth factor (EGF) challenge caused diametrically opposed changes in cyclic AMP levels in COS1 cells transfected to express the long PDE4B1 isoenzyme compared to cells expressing the short PDE4B2 isoenzyme. We suggest that PDE4 enzymes may provide a pivotal point for integrating cyclic AMP and Erk signal transduction in cells with 4 genes encoding enzymes that are either insensitive to Erk2 action or may either be activated or inhibited. This indicates that PDE4 isoenzymes have distinct functional roles, giving credence to the notion that distinct therapeutic benefits may accrue using either PDE4 subfamily or isoenzyme-selective inhibitors.

Use of an activation-specific probe to show that Rap1A and Rap1B display different sensitivities to activation by forskolin in rat1 cells.

Rap1A and Rap1B are small GTPases of the Ras superfamily whose activation can be measured using a probe that interacts specifically with the GTP-bound forms of Rap1A and Rap1B. Using this procedure we demonstrate that the cyclic AMP-elevating agent forskolin activates both Rap1A and Rap1B in Rat1 cells. Whilst the protein kinase A inhibitor H89 ablated the ability of forskolin to cause cAMP response element binding protein (CREB) phosphorylation in Rat1 cells, it did not affect the ability of forskolin to activate either Rap1A and Rap1B. Forskolin differentially activated Rap1A and Rap1B isoforms in a time- and dose-dependent manner. The cAMP-specific type 4 family phosphodiesterase inhibitor rolipram potentiated the rate of activation of both Rap1A and Rap1B by forskolin challenge of Rat1 cells. Challenge of Rat1 cells with rolipram alone was able to elicit the phosphorylation of CREB but not activation of either Rap1A or Rap1B.

ERK2 mitogen-activated protein kinase binding, phosphorylation, and regulation of the PDE4D cAMP-specific phosphodiesterases. The involvement of COOH-terminal docking sites and NH2-terminal UCR regions.

The cAMP-specific phosphodiesterase family 4, subfamily D, isoform 3 (PDE4D3) is shown to have FQF and KIM docking sites for extracellular signal-regulated kinase 2 (ERK2) (p42(MAPK)). These straddle the target residue, Ser(579), for ERK2 phosphorylation of PDE4D3. Mutation of either or both of these docking sites prevented ERK2 from being co-immunoprecipitated with PDE4D3, ablated the ability of epidermal growth factor to inhibit PDE4D3 through ERK2 action in transfected COS cells, and attenuated the ability of ERK2 to phosphorylate PDE4D3 in vitro. The two conserved NH(2)-terminal blocks of sequence, called upstream conserved regions 1 and 2 (UCR1 and UCR2), that characterize PDE4 long isoforms, are proposed to amplify the small, inherent inhibitory effect that ERK2 phosphorylation exerts on the PDE4D catalytic unit. In contrast to this, the lone intact UCR2 region found in PDE4D1 directs COOH-terminal ERK2 phosphorylation to cause the activation of this short isoform. From the analysis of PDE4D3 truncates, it is suggested that UCR1 and UCR2 provide a regulatory signal integration module that serves to orchestrate the functional consequences of ERK2 phosphorylation. The PDE4D gene thus encodes a series of isoenzymes that are either inhibited or activated by ERK2 phosphorylation and thereby offers the potential for ERK2 activation either to increase or decrease cAMP levels in cellular compartments.

Association with the SRC family tyrosyl kinase LYN triggers a conformational change in the catalytic region of human cAMP-specific phosphodiesterase HSPDE4A4B. Consequences for rolipram inhibition.

The cAMP-specific phosphodiesterase (PDE) HSPDE 4A4B(pde46) selectively bound SH3 domains of SRC family tyrosyl kinases. Such an interaction profoundly changed the inhibition of PDE4 activity caused by the PDE4-selective inhibitor rolipram and mimicked the enhanced rolipram inhibition seen for particulate, compared with cytosolic pde46 expressed in COS7 cells. Particulate pde46 co-localized with LYN kinase in COS7 cells. The unique N-terminal and LR2 regions of pde46 contained the sites for SH3 binding. Altered rolipram inhibition was triggered by SH3 domain interaction with the LR2 region. Purified LYN SH3 and human PDE4A LR2 could be co-immunoprecipitated, indicating a direct interaction. Protein kinase A-phosphorylated pde46 remained able to bind LYN SH3. pde46 was found to be associated with SRC kinase in the cytosol of COS1 cells, leading to aberrant kinetics of rolipram inhibition. It is suggested that pde46 may be associated with SRC family tyrosyl kinases in intact cells and that the ensuing SH3 domain interaction with the LR2 region of pde46 alters the conformation of the PDE catalytic unit, as detected by altered rolipram inhibition. Interaction between pde46 and SRC family tyrosyl kinases highlights a potentially novel regulatory system and point of signaling system cross-talk.

Outcomes following treatment of metastatic spine tumors.

Fifty seven consecutive patients with metastatic spine tumors were assessed for their suitability for operative treatment or radiotherapy and/or chemotherapy using a modified version of the Nihon University scoring system. Using this scoring system 29 patients underwent surgery and 28 received radiotherapy/chemotherapy. The outcomes were assessed to determine if a modified scoring had any effect on patient survival. No statistical difference was found between the two groups, though a trend was noted--the group receiving surgery had a mean survival of 30 weeks compared to a mean survival of 16 weeks found in the non-surgical group.

The surgical management of degenerative lumbar scoliosis. Posterior instrumentation alone versus two stage surgery.

Twenty-one patients who underwent surgery for degenerative scoliosis were retrospectively reviewed. Eleven patients underwent staged anterior and posterior surgery. Ten patients had a single posterior procedure. Posterior instrumentation to the sacrum was done in all cases. Average length of follow-up was 3.8 years (range: 2 to 7 years). All patients were assessed by the Oswestry Disability Questionnaire and Low-Back Outcome Score. Additional questions included analogue scales for pain and quality of life, and self-rating of the outcome of treatment. Nine patients that had two stage surgery and 4 patients that had single posterior surgery considered their outcome to be good or excellent (p = 0.13). This correlated with better functional tolerance, specifically sleep, lifting, sitting, and social life. Although pain intensity was the same for both groups, only the staged group reported significant reduction in analgesic intake. Significant correction in scoliosis and the lumbosacral fractional curve was noted only following staged surgery. A solid spinal fusion determined a satisfactory outcome irrespective of the method of treatment. Staged anterior and posterior surgery for degenerative lumbar scoliosis resulted in a better fusion rate, greater correction of deformity, and more improvement in function than did posterior surgery alone.

Factors influencing wound healing after surgery for metastatic disease of the spine.

STUDY DESIGN: The study group consisted of 53 patients who underwent 75 operations for spine metastases. Patient and tumor demographic factors, preoperative nutritional status, and perioperative adjunctive therapy were retrospectively reviewed. OBJECTIVE: To determine the risk factors for wound breakdown and infection in patients undergoing surgery for spinal metastases. SUMMARY OF BACKGROUND DATA: Spinal fusion using spine implants may be associated with an infection rate of 5% or more. Surgery for spine metastases is associated with an infection rate of more than 10%. Factors other than the type of surgery performed may account for the greater infection rate. METHODS: Data were obtained by reviewing patient records. Age, sex, and neurologic status of the patient; tumor type and site; and surgical details were noted. Adjunctive treatment with corticosteroids and radiotherapy was recorded. Nutritional status was evaluated by determining serum protein and serum albumin concentrations and by total lymphocyte count. RESULTS: Wound breakdown and infection occurred in 15 of 75 wounds. No patient or tumor demographic factors other than intraoperative blood loss (P < 0.1) were statistically associated with infection. The correlation between preoperative protein deficiency (P < 0.01) or perioperative corticosteroid administration (P < 0.10) and wound infection was significant. There was no statistical correlation between lymphocyte count or perioperative radiotherapy and wound infection. CONCLUSIONS: The results indicate that preoperative protein depletion and perioperative administration of corticosteroids are risk factors for wound infection in patients undergoing surgery for spine metastases. Perioperative correction of nutritional depletion and cessation of steroid therapy may reduce wound complications.