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Summary We conducted a prospective comparative study of the effect of teriparatide therapy for preventing vertebral-failure-type PJK after reconstructive surgery for adult spinal deformity. Prophylactic teriparatide improved the volumetric bone mineral density and fine bone structure of the vertebra above the upper-instrumented vertebra and reduced the incidence of vertebral-failure-type PJK. Introduction Proximal junctional kyphosis (PJK) is a complication after corrective surgery for spinal deformity. This study sought to determine whether teriparatide (TP) is an effective prophylactic against PJK type 2 (vertebral fracture) in surgically treated patients with adult spinal deformity (ASD). Methods Forty-three patients who started TP therapy immediately after surgery and 33 patients who did not receive TP were enrolled in this prospective case series. These patients were female, over 50, surgically treated for ASD, and followed for at least 2 years. Preoperative and postoperative standing whole-spine X-rays and dual-energy X-ray absorptiometry scans, and multidetector CT images obtained before and 6 months after surgery were used to analyze the bone strength in the vertebra above the upper-instrumented vertebra (UIV+1). Results Mean age was 67.9 years. After 6 months of treatment, mean hip-bone mineral density (BMD) increased from 0.721 to 0.771 g/cm 2 in the TP group and decreased from 0.759 to 0.729 g/cm 2 in the control group. This percent BMD change between groups was significant ( p  < 0.05). The volumetric BMD (326 to 366 mg/cm 3 ) and bone mineral content (BMC) (553 to 622 mg) at UIV+1 were also significantly increased in TP group. The bone volume/tissue volume ratio increased from 46 to 54 % in the TP group, and the trabecular bone thickness and number increased by 14 and 5 %, respectively. At the 2-year follow-up, the PJK type 2 incidence was significantly lower in the TP group (4.6 %) than in the control group (15.2 %; p  = .02). Conclusions Prophylactic TP treatment improved the volumetric BMD and fine bone structure at UIV+1 and reduced the PJK-type 2 incidence.

Study design: A cross-sectional study. Objectives: Neuropathic pain (NP) after spinal cord injury (SCI) tends to be hard to treat, and its heterogeneous properties make it difficult to identify and characterize. This study was conducted to assess the characteristics of SCI-related NP in detail. Setting: A single hospital for SCI rehabilitation. Methods: This study included 72 patients who were seen at our hospital in 2012 and 2013 and who had sustained SCI at least 3 months before enrollment. The patients completed the Neuropathic Pain Symptom Inventory (NPSI) and the Short Form (SF)-36 Health Inventory. The NPSI score was analyzed for correlations with clinical presentations of SCI and SF-36 subitems. Results: Paresthesia/dysesthesia was the most common subtype of NP after SCI. With regard to location, below-level superficial NP was significantly more intense than at-level pain. Patients who underwent surgery showed significantly less evoked pain compared with patients with non-surgery. Patients reported significantly more severe pain if >1 year had elapsed after the SCI. Patients with an American Spinal Injury Association Impairment Scale grade of B for completeness of injury reported more intense NP than those with other grades. Among the SF-36 subitems, NP correlated significantly with bodily pain, general health and mental health. Conclusion: NP in SCI patients was significantly associated with the location of pain, the time period since the injury, surgery and quality-of-life factors. A more detailed understanding of the characteristics of NP may contribute to better strategies for relieving the pain associated with SCI.

Mutant mitochondrial DNA with large-scale deletions (Δ-mtDNA) has been frequently observed in patients with chronic progressive external ophthalmoplegia (CPEO), a subgroup of the mitochondrial encephalomyopathies. To exclude involvement of the nuclear genome in expression of the mitochondrial dysfunction characteristic of CPEO, we introduced the mtDNA of a CPEO patient into clonal mtDNA-less HeLa cells and isolated cybrid clones. Quantitation of Δ-mtDNA in the cybrids revealed that Δ-mtDNA was selectively propagated with higher levels of Δ-mtDNA correlating with slower cellular growth rate. In these cybrid clones, translational complementation of the missing tRNAs occurred only when Δ-mtDNA was <60% of the total mtDNA, whereas accumulation of Δ-mtDNA to >60% resulted in progressive inhibition of overall mitochondrial translation as well as reduction of cytochrome c oxidase activity throughout the organelle population. Because these cybrids shared the same nuclear background as HeLa cells, these results suggest that large-scale deletion mutations of mtDNA alone are sufficient for the mitochondrial dysfunction characteristic of CPEO.

Study DesignRetrospective case series of surgically treated adolescent scoliosis patients.ObjectivesTo assess the radiographic changes of cervical kyphosis and identify the possible factors affecting postoperative sagittal cervical kyphosis in surgically treated patients with adolescent idiopathic scoliosis.Summary of Background DataCervical kyphosis is a well-recognized phenomenon in patients with adolescent idiopathic scoliosis. Despite recent reports, the prevalence, radiographic changes, and possible factors affecting postoperative sagittal cervical kyphosis are controversial.Materials and MethodsA retrospective review of a single-center database was performed on 133 consecutive patients with adolescent idiopathic scoliosis treated with long instrumented (more than 5 levels) spine fusion (minimum, 2 years; mean, 3.3 years; range, 2 to 5.5 years). A total of 89 patients met all of the inclusion criteria. Preoperative and postoperative radiographic measurements and patient demographics were investigated.ResultsPostoperative cervical kyphosis was observed in 46 patients. Cobb angle decreased from 48.1° ± 13.1° to 15.4° ± 11.1° at the final follow-up. Cervical kyphosis significantly decreased from 5.5° ± 8.9° preoperatively to −1.5° ± 8.9° at the final follow-up. No difference was observed for T2–T5, T5–T12, lumbar lordosis, sacral slope, pelvic incidence, pelvic tilt, and sagittal vertical axis during the follow-up. Notably, T2 sagittal tilt was significantly increased from preoperatively to the final follow-up. Pearson correlation coefficient test showed a strong correlation between postoperative cervical lordosis and T2 sagittal tilt (r = 0.73; p <.001).ConclusionsDespite the significant increase of cervical lordosis, 85% of patients still have a kyphotic or less lordotic cervical spine. The strong positive association between cervical lordosis and T2 sagittal tilt suggests that the sagittal cervical alignment of adolescent idiopathic scoliosis patients is closely related to the global sagittal spine balance rather than thoracic kyphosis.

The in-vivo effect of vitamin K(2) on bone metabolism was investigated by histochemical and morphometric methods, using an animal model of osteoporosis. Eighteen female Wistar rats were divided into three groups. Rats in group A had sham ovariectomies, group B were ovariectomized, and group C were ovariectomized and received vitamin K(2), at 10 mg/kg per day, injected subcutaneously. The lumbar vertebral bones were evaluated 8 weeks after the operation by a modified tetrachrome method after decalcification. Mineralized bone areas, osteoid, and defectively mineralized bone areas in group B were markedly decreased compared with findings in group A, but these features in group C were not severely decreased. There was no significant difference in total bone areas and total bone volumes among the three groups. Accordingly, it appeared that vitamin K(2) had an effect in reducing mineralized bone loss after the ovariectomy. In conclusion, vitamin K(2) is thought to be beneficial for the properties of bone microarchitecture in the condition of osteoporosis.

: To elucidate the pathogenesis of chronic compartment syndrome, we examined pathological changes in the soleus (red) and extensor digitorum longus (EDL; white) muscles in Japanese white rabbits after repeated compression with a pneumatic tourniquet. Repeated tourniquet compression via cuff inflation was carried out on the rabbits, calves daily, for 2h, then stopped for 30min, and then applied for another 2h. The contralateral hindlimb, which was not compressed, served as a control. Animals were allocated to 15 groups, with pressures of 40, 80, and 120mmHg for periods of 1 day, 3 days, 1 week, 2 weeks, and 4 weeks. Skeletal muscle specimens in each group were studied by histopathological and histochemical (ATPase) methods. After compression for 1 day, regardless of pressure, and compression for 3 days in the 40-mmHg pressure group, edematous changes in regions with mild inflammation and increases in fiber diameter were observed in the muscles. After compression for 3 days in the 80- and 120-mmHg pressure groups, and after 1, 2, or 4 weeks in the 40-mmHg pressure group, a few necrotic fibers and scattered fibers with some mononuclear cell infiltrates indicative of early-stage necrosis were detected. In the groups with 80 or 120mmHg pressure for 1, 2, or 4 weeks, muscle fibers exhibited marked degenerative changes, which were more pronounced in the 120-mmHg group than in the 80-mmHg group. The pathological changes were more pronounced in the soleus than in the EDL muscles, indicating that these two muscles differed in sensitivity to repeated compression. Additionally, average muscle wet weight and average fiber diameter for both types of muscle were increased in the 1-day and 3-day compression groups and decreased in the 1-week, 2- week, and 4-week compression groups. These findings clearly differ from those of previously reported single-compression experiments. Our findings indicate that repeated compression may cause serious muscle degeneration, particularly in red muscles.

Increased macula densa cyclooxygenase-2 (COX-2) is observed in diabetic rats and may contribute to hyperfiltration states. However, the signals mediating increased COX-2 expression in diabetic rats remain undetermined. We recently found that non-proteolytic activation of prorenin by site-specific binding proteins, such as prorenin receptor, plays a pivotal role in the development of diabetic nephropathy. The present study was designed to determine the contribution of prorenin receptor to renal cortical COX-2 expression. The COX-2 mRNA and protein levels of six 4-week-old male wild-type rats and six human prorenin receptor gene-transgenic (hProRenRcTg) rats were measured by real-time polymerase chain reaction methods, Western blotting, and immunohistochemistry, and compared. There were no differences between the two groups in arterial pressure measured by telemetry, urinary sodium excretion, or renal levels of rat prorenin receptor mRNA. The renal cortical COX-2 mRNA levels of the hProRenRcTg rats were significantly higher than those of the wild-type rats, and the renal cortical COX-2 protein levels were also higher in hProRenRcTg rats than in the wild-type rats. Immunohistochemical analysis revealed that COX-2 immunostaining was predominantly present in the macula densa cells, and significantly more COX-2-positive cells were present in the hProRenRcTg rats than in the wild-type rats. In addition, COX-2 inhibition with NS398 significantly decreased renal cortical blood flow in the hProRenRcTg rats but not in the wild-type rats. These results strongly suggest that human prorenin receptor directly or indirectly contributes to the regulation of renal cortical COX-2 expression.

The present study was performed to compare the long-term effects of 24-h ambulatory blood pressure (BP) control with amlodipine versus valsartan on vascular damage in untreated hypertensive patients. Amlodipine and valsartan have benefits on cardiovascular mortality and morbidity in hypertensive patients. Although ambulatory BP is associated with severity of target-organ damage in hypertensive patients, beneficial effects of ambulatory BP control with amlodipine versus valsartan on vascular damage have not been compared. Pulse wave velocity (PWV), intima–media thickness (IMT) of the carotid arteries, urinary albumin excretion (UAE) and 24-h ambulatory BP were determined in 100 untreated hypertensive patients before and 12 months after the start of antihypertensive therapy with amlodipine or valsartan. Amlodipine and valsartan decreased ambulatory BP similarly, but the variability of 24-h and daytime ambulatory systolic BP was significantly reduced by amlodipine but not by valsartan. The reduced variability of ambulatory systolic BP caused by amlodipine significantly contributed to the improvement of PWV, although both drugs decreased PWV similarly. Carotid IMT was unaffected by treatment with either drug. Valsartan significantly decreased UAE independently of its depressor effect, but amlodipine had no effect on UAE. These results suggest that the 24-h control of ambulatory BP with amlodipine had functionally improved the stiffened arteries of hypertensive patients by the end of 12 months of treatment, in part through reducing BP variability, whereas ambulatory BP control with valsartan decreased the arterial stiffness to the same degree as amlodipine without affecting BP variability maybe through some pleiotropic effects.

Study design: This is a retrospective study. Objectives: The objectives of this study were to categorize unexpected postural changes (UPCs) during gait training in paraplegic patients with wearable gait-assist robots, to reveal the incidence of the UPC and its time-dependent changes during initial gait training period and to investigate neurological level-specific differences. Setting: This study was conducted in Fujita Health University, Aichi, Japan. Methods: We investigated five patients (46.2±14.6 years; lesion level: T6:3, T12:2). All patients had previously achieved gait with wearable robot and walker at supervision level. The UPCs were counted for 2 years and classified according to their type. The time-course data were calculated from the incidence of UPCs for 10 days from initial gait training with the walker. The neurological level-specific differences were investigated between T6 and T12 injuries. Results: Eighty-five UPCs were observed and classified into three categories: anterior breakdown, posterior breakdown (PBD) and mal-timing. The average rate over the entire period was 0.96±0.62 (incidents/h/subject). PBD, which was defined as hyperflexion of both hip joints, occurred with the highest frequency (0.64±0.64 incidents/h/subject). During initial gait training, there was a gradual decrease in the occurrence of UPC. For neurological level-specific differences, UPCs were observed more frequently in T6 injuries (1.36±0.35 incidents/h/subject) compared with T12 injuries (0.36±0.31 incidents/h/subject). Conclusion: PBDs might be the result of near collisions between the trunk of the user and the walker, which make it difficult for the users to move their trunk over an anterior stance limb. Training that is focused upon well-timed forward movements of the walker might be required to avoid the occurrence of this common UPC.