Clinical outcomes following sublaminar-trimming laminoplasty for extensive lumbar canal stenosis

Purpose

Current surgical approaches for treatment of lumbar canal stenosis are often associated with relatively high rates of reoperation and recurrent stenosis. We have developed a new approach for treatment of this condition: sublaminar-trimming laminoplasty. To describe the surgical approach of sublaminar-trimming laminoplasty and to assess associated outcomes.

Methods

Patients with extensive lumbar canal stenosis who received sublaminar-trimming laminoplasty from 2006 to 2008 were considered for inclusion in the study. The surgery comprised aspects of laminotomy and laminectomy. The following were assessed before surgery and 3 years after surgery: leg and back pain by visual analog scale (VAS), extent of disability by Oswestry Disability Index (ODI), severity of back pain by Japanese Orthopedic Association Score for Back Pain (JOA), walking tolerance, and leg numbness. Complications were noted.

Results

A total of 49 patients were included in the study (mean age 65.6 ± 10.6 years). VAS leg and back pain, ODI, and JOA scores significantly changed from before surgery to 3 years after surgery (P < 0.001). Mean changes (95 % confidence interval) were ?6.2 (?6.7, ?5.7), ?4.3 (?4.8, ?3.8), ?21.4 (?23.4, ?19.5), and 13.4 (12.1, 14.7) for leg pain, back pain, ODI, and JOA scores, respectively. Patients experienced significant improvements in walking tolerance and leg numbness (P < 0.001). There were no instances of recurrent stenosis or postoperative spinal instability. Complications included intraoperative dural tear (n = 2), postoperative urinary tract infection (n = 2), and inadequate decompression and junctional stenosis during follow-up (both n = 1).

Conclusion

Sublaminar-trimming laminoplasty shows promise as an effective treatment for extensive lumbar canal stenosis.     

Experimental and Numerical Investigation in Directed Energy Deposition for Component Repair

Directed energy deposition (DED) has been widely used for component repair. In the repair process, the surface defects are machined to a groove or slot and then refilled. The sidewall inclination angle of the groove geometry has been recognized to have a considerable impact on the mechanical properties of repaired parts. The objective of this work was to investigate the feasibility of repairing various V-shaped defects with both experiments and modeling. At first, the repair volume was defined by scanning the defective zone. Then, the repair volume was sliced to generate the repair toolpath. After that, the DED process was used to deposit Ti6Al4V powder on the damaged plates with two different slot geometries. Mechanical properties of the repaired parts were evaluated by microstructure analysis and tensile test. Testing of the repaired parts showed excellent bonding between the deposits and base materials with the triangular slot repair. 3D finite element analysis (FEA) models based on sequentially coupled thermo-mechanical field analysis were developed to simulate the corresponding repair process. Thermal histories of the substrate on the repair sample were measured to calibrate the 3D coupled thermo-mechanical model. The temperature measurements showed very good verification with the predicted temperature results. After that, the validated model was used to predict the residual stresses and distortions in the parts. Predicted deformation and stress results can guide the evaluation of the repair quality.     

Genghis Khan (Gek) as a putative effector for Drosophila Cdc42 and regulator of actin polymerization

The small GTPases Cdc42 and Rac regulate a variety of biological processes, including actin polymerization, cell proliferation, and JNK/mitogen-activated protein kinase activation, conceivably via distinct effectors. Whereas the effector for mitogen-activated protein kinase activation appears to be p65^PAK, the identity of effector(s) for actin polymerization remains unclear. We have found a putative effector for Drosophila Cdc42, Genghis Khan (Gek), which binds to Dcdc42 in a GTP-dependent and effector domain-dependent manner. Gek contains a predicted serine/threonine kinase catalytic domain that is 63% identical to human myotonic dystrophy protein kinase and has protein kinase activities. It also possesses a large coiled-coil domain, a putative phorbol ester binding domain, a pleckstrin homology domain, and a Cdc42 binding consensus sequence that is required for its binding to Dcdc42. To study the in vivo function of gek, we generated mutations in the Drosophila gek locus. Egg chambers homozygous for gek mutations exhibit abnormal accumulation of F-actin and are defective in producing fertilized eggs. These phenotypes can be rescued by a wild-type gek transgene. Our results suggest that this multidomain protein kinase is an effector for the regulation of actin polymerization by Cdc42.     

Transbronchial biopsy is clinically useful in classifying patients with interstitial pneumonia associated with polymyositis and dermatomyositis

Background and objective: The histological type of intraluminal fibrosis is an important prognostic factor for interstitial pneumonia. We therefore examined whether transbronchial lung biopsy (TBLB) specimens are useful for predicting the clinical course and prognosis of patients with interstitial pneumonia associated with polymyositis and dermatomyositis (PM/DM), with particular attention to the different types of intraluminal fibrosis. Methods: Twenty‐five cases of interstitial pneumonia associated with PM/DM were classified according to the pattern of intraluminal fibrosis as assessed by TBLB, and the clinical course and response to treatment were compared. Interstitial fibrosis was evaluated by sequential thin‐section CT scans. Results: In 19 of 25 (76%) cases, there was sufficient intraluminal fibrosis to perform an evaluation. Intraluminal fibrosis was classified as bud (polyp) type or mural incorporation type (either alone or mixed with bud type). The bud type was seen in five cases and these improved following treatment with corticosteroids only. The mural incorporation type was seen in 14 cases. In 11 of these 14 cases, progressive long‐term fibrosis developed and four cases were fatal, in spite of corticosteroid and immunosuppressive therapy. The response to drugs (P < 0.01) and survival (P < 0.05) were significantly greater in patients with bud‐type than mural incorporation‐type intraluminal fibrosis. Conclusions: Classification of the pattern of intraluminal fibrosis as assessed by TBLB is useful for predicting the response to treatment, clinical course and prognosis of interstitial pneumonia associated with PM/DM.     

Changes in body surface potential distributions induced by isoproterenol and Na channel blockers in patients with the Brugada syndrome

BACKGROUND: The characteristics of unique ECG findings in the Brugada syndrome have not been well explained. METHODS: To clarify their characteristics and mechanisms, body surface maps (BSM) were recorded from patients with the Brugada syndrome (13 cases; a mean age of 48 years) before and after administration of isoproterenol (ISP) or Na channel blockers (12 cases). RESULTS: ST elevation in V1-V3 was decreased by 0.1 mV or more after ISP infusion in 8 of 11 cases and elevated after Na channel blockers in 8 of 12. In ventricular activation time (VAT) isochronal map, delayed conduction was noted on upper anterior chest in 11 and on anterior left chest in two. Delayed conduction areas were decreased by ISP and expanded by Na channel blockers. QRST isointegral map showed normal findings in baseline with minimal changes after ISP or Na channel blockers. Activation recovery interval (ARI) isochronal map showed prolonged area on upper anterior chest in baseline, being reduced by ISP and expanded by Na channel blockers. ARI dispersion (ARI-d), defined as difference between the maximum and minimum value of ARI, was larger in Brugada patients than that of normal subjects in baseline, and decreased after ISP and increased after Na channel blockers. CONCLUSION: ST elevation in the Brugada syndrome is primarily caused by abnormality in depolarization rather than in repolarization. BSM can provide better information to clarify a mechanism of ECG changes adding its diagnostic value for this unique syndrome.     

Evidence that the nucleotide exchange and hydrolysis cycle of G proteins causes acute desensitization of G-protein gated inward rectifier K+ channels

The G-protein gated inward rectifier K⁺ channel (GIRK) is activated in vivo by the Gβγ subunits liberated upon G_i-coupled receptor activation. We have recapitulated the acute desensitization of receptor-activated GIRK currents in heterologous systems and shown that it is a membrane-delimited process. Its kinetics depends on the guanine nucleotide species available and could be accounted for by the nucleotide exchange and hydrolysis cycle of G proteins. Indeed, acute desensitization is abolished by nonhydrolyzable GTP analogues. Whereas regulators of G-protein signaling (RGS) proteins by their GTPase-activating protein activities are regarded as negative regulators, a positive regulatory function of RGS4 is uncovered in our study; the opposing effects allow RGS4 to potentiate acute desensitization without compromising GIRK activation.