Factors associated with quality of life in Chinese people with psoriasis: a cross-sectional study.

BACKGROUND: The ultimate goal of medical care is to eradicate disease and restore normality to a person's life. Quality of life (QOL) is a concern as dermatologists and researchers strive to find better drug treatments. However, there have been few reports on the factors associated with QOL among Chinese people with psoriasis. METHODS: A total of 185 people with psoriasis were surveyed to assess their sociodemographic status, disease-related information, psychosocial status, and QOL. The questionnaires included a sociodemographic questionnaire, the Athens Insomnia Scale, the Hospital Anxiety and Depression Scale, the Perceived Social Support Scale, the Psychosocial Adaptation Questionnaire of Chronic Skin Disease and the Dermatology Life Quality Index. Multiple stepwise regression and path analysis were used to study the factors associated with QOL among Chinese people with psoriasis and to analyse the relationship between them. RESULTS: The results showed that the presence of anxiety/depression, lesion area, sleep disorders, psychosocial adaptation, and sex could jointly predict 62.1% of the variance in QOL among Chinese people with psoriasis. According to previous theories and the literature, a path model was established for five variables. Four internal variables could be effectively explained. The values of the explanatory variables were 62.1% (F(1056) = 61.020, p = 0.000) for QOL, 71.8% (F(2433) = 117.370, p = 0.000) for anxiety/depression, 44.0% (F(660) = 36.935, p = 0.000) for sleep disorders, and 66.9% (F(6886) = 93.556, p = 0.000) for psychosocial adaptation. The path analysis confirmed that 9 paths were consistent with the predicted path, and 3 paths were not confirmed. CONCLUSION: To improve QOL among Chinese people with psoriasis, attention should be given to the presence of anxiety/depression, lesion area, sleep disorders, psychosocial adaptation and sex differences. Therefore, health care programs for psoriasis should include physical, psychological and social aspects.

Loss of C3a and C5a receptors promotes adipocyte browning and attenuates diet-induced obesity via activating inosine/A2aR pathway.

Complement activation is thought to underline the pathologic progression of obesity-related metabolic disorders; however, its role in adaptive thermogenesis has scarcely been explored. Here, we identify complement C3a receptor (C3aR) and C5a receptor (C5aR) as critical switches to control adipocyte browning and energy balance in male mice. Loss of C3aR and C5aR in combination, more than individually, increases cold-induced adipocyte browning and attenuates diet-induced obesity in male mice. Mechanistically, loss of C3aR and C5aR increases regulatory T cell (Treg) accumulation in the subcutaneous white adipose tissue during cold exposure or high-fat diet. Activated Tregs produce adenosine, which is converted to inosine by adipocyte-derived adenosine deaminases. Inosine promotes adipocyte browning in a manner dependent on activating adenosine A2a receptor. These data reveal a regulatory mechanism of complement in controlling adaptive thermogenesis and suggest that targeting the C3aR/C5aR pathways may represent a therapeutic strategy in treating obesity-related metabolic diseases.

Brown Adipocyte ADRB3 Mediates Cardioprotection via Suppressing Exosomal iNOS.

BACKGROUND: The ADRB3 (ß3-adrenergic receptors), which is predominantly expressed in brown adipose tissue (BAT), can activate BAT and improve metabolic health. Previous studies indicate that the endocrine function of BAT is associated with cardiac homeostasis and diseases. Here, we investigate the role of ADRB3 activation-mediated BAT function in cardiac remodeling. METHODS: BKO (brown adipocyte-specific ADRB3 knockout) and littermate control mice were subjected to Ang II (angiotensin II) for 28 days. Exosomes from ADRB3 antagonist SR59230A (SR-exo) or agonist mirabegron (MR-exo) treated brown adipocytes were intravenously injected to Ang II-infused mice. RESULTS: BKO markedly accelerated cardiac hypertrophy and fibrosis compared with control mice after Ang II infusion. In vitro, ADRB3 KO rather than control brown adipocytes aggravated expression of fibrotic genes in cardiac fibroblasts, and this difference was not detected after exosome inhibitor treatment. Consistently, BKO brown adipocyte-derived exosomes accelerated Ang II-induced cardiac fibroblast dysfunction compared with control exosomes. Furthermore, SR-exo significantly aggravated Ang II-induced cardiac remodeling, whereas MR-exo attenuated cardiac dysfunction. Mechanistically, ADRB3 KO or SR59230A treatment in brown adipocytes resulted an increase of iNOS (inducible nitric oxide synthase) in exosomes. Knockdown of iNOS in brown adipocytes reversed SR-exo-aggravated cardiac remodeling. CONCLUSIONS: Our data illustrated a new endocrine pattern of BAT in regulating cardiac remodeling, suggesting that activation of ADRB3 in brown adipocytes offers cardiac protection through suppressing exosomal iNOS.

PDGF-D activation by macrophage-derived uPA promotes AngII-induced cardiac remodeling in obese mice.

Obesity-induced secretory disorder of adipose tissue-derived factors is important for cardiac damage. However, whether platelet-derived growth factor-D (PDGF-D), a newly identified adipokine, regulates cardiac remodeling in angiotensin II (AngII)-infused obese mice is unclear. Here, we found obesity induced PDGF-D expression in adipose tissue as well as more severe cardiac remodeling compared with control lean mice after AngII infusion. Adipocyte-specific PDGF-D knockout attenuated hypertensive cardiac remodeling in obese mice. Consistently, adipocyte-specific PDGF-D overexpression transgenic mice (PA-Tg) showed exacerbated cardiac remodeling after AngII infusion without high-fat diet treatment. Mechanistic studies indicated that AngII-stimulated macrophages produce urokinase plasminogen activator (uPA) that activates PDGF-D by splicing full-length PDGF-D into the active PDGF-DD. Moreover, bone marrow-specific uPA knockdown decreased active PDGF-DD levels in the heart and improved cardiac remodeling in HFD hypertensive mice. Together, our data provide for the first time a new interaction pattern between macrophage and adipocyte: that macrophage-derived uPA activates adipocyte-secreted PDGF-D, which finally accelerates AngII-induced cardiac remodeling in obese mice.

Patient satisfaction, clinical outcomes and oral health-related quality of life after treatment with traditional and modified protocols for complete dentures.

BACKGROUND/PURPOSE: Conventional complete denture treatment course requires six appointments, but modified protocol only takes four appointments. This study compared the conventional and modified protocol for complete denture fabrication regarding patient satisfaction and clinical outcomes. MATERIALS AND METHODS: A total of 24 patients accepted complete denture treatment. According to complete denture treatment protocol, these patients were divided into the conventional group (group C, n = 12) and the modified group (group M, n = 12). Group C used the conventional protocol and required six appointments. Group M used the one-appointment master impression and jaw relation record technique, and it took four appointments. Data of oral health impact profile-14 (OHIP-14), satisfaction scale and the number of recalls in the first year were collected for the statistical analysis. RESULTS: The mean OHIP-14 scores in group C and group M were 13.79 ±â€¯3.81 and 15.33 ±â€¯5.25, respectively. In terms of satisfaction, the mean scores in group C and group M were 8.33 ±â€¯0.61 points and 8.66 ±â€¯1.13 points, respectively. There were no statistically significant differences between the group C and M in terms of participant ratings for satisfaction and OHIP-14. At the same time, the results indicated that group M significantly reduced the number of postinsertion visits (P < 0.05). CONCLUSION: In terms of OHIP-14 and patients' satisfaction, the modified treatment protocol is comparable to the conventional protocol. Based on the number of recalls in the first year, the modified treatment protocol has a better clinical outcome.

Suppression of Endothelial-to-Mesenchymal Transition by SIRT (Sirtuin) 3 Alleviated the Development of Hypertensive Renal Injury.

Endothelial-to-mesenchymal transition (EndoMT) has recently emerged as a potentially important contributor in promoting fibrosis in chronic kidney disease. However, little is known about the role and molecular basis of its involvement in hypertensive renal injury. Here, we aim to determine the role of SIRT (sirtuin) 3 on EndoMT in hypertensive renal injury and to explore its underlying mechanisms. We found that SIRT3 expression was significantly reduced in Ang II (angiotensin II)-induced hypertensive model, accompanied with induction of EndoMT and increased reactive oxygen species and renal fibrosis. In SIRT3-/- (SIRT3 knockout) mice subjected to Ang II infusion, renal dysfunction was aggravated with an increased EndoMT and reactive oxygen species level, whereas in SIRT3-TgEC (SIRT3 endothelial cell-specific transgenic) mice, the Ang II-induced renal fibrosis and EndoMT and oxidative stress were ameliorated. With primary mouse glomerular endothelial cells, we confirmed that Ang II treatment initiated EndoMT and decreased catalase expression, which were suppressed by SIRT3 overexpression. Using immunoprecipitation, luciferase, and chromatin immunoprecipitation assay, we demonstrated that SIRT3-mediated deacetylation and nuclear localization of Foxo3a (forkhead box O3a) resulted in activated Foxo3a-dependent catalase expression. Moreover, Foxo3a knockdown abolished SIRT3-mediated suppression of EndoMT. In conclusion, these results established the SIRT3-Foxo3a-catalase pathway as a critical factor in the maintenance of endothelial homeostasis and point to an important role of EndoMT in the vascular pathology of renal fibrosis, which may provide a new therapeutic target to impede the progression of hypertensive renal injury.

Perivascular Adipose Tissue-Derived PDGF-D Contributes to Aortic Aneurysm Formation During Obesity.

Obesity increases the risk of vascular diseases, including aortic aneurysm (AA). Perivascular adipose tissue (PVAT) surrounding arteries are altered during obesity. However, the underlying mechanism of adipose tissue, especially PVAT, in the pathogenesis of AA is still unclear. Here we showed that angiotensin II (AngII) infusion increases the incidence of AA in leptin-deficient obese mice (ob/ob) and high-fat diet-induced obese mice with adventitial inflammation. Furthermore, transcriptome analysis revealed that platelet-derived growth factor-D (PDGF-D) was highly expressed in the PVAT of ob/ob mice. Therefore, we hypothesized that PDGF-D mediates adventitial inflammation, which provides a direct link between PVAT dysfunction and AA formation in AngII-infused obese mice. We found that PDGF-D promotes the proliferation, migration, and inflammatory factors expression in cultured adventitial fibroblasts. In addition, the inhibition of PDGF-D function significantly reduced the incidence of AA in AngII-infused obese mice. More importantly, adipocyte-specific PDGF-D transgenic mice are more susceptible to AA formation after AngII infusion accompanied by exaggerated adventitial inflammatory and fibrotic responses. Collectively, our findings reveal a notable role of PDGF-D in the AA formation during obesity, and modulation of this cytokine might be an exploitable treatment strategy for the condition.

Deficiency of Complement C3a and C5a Receptors Prevents Angiotensin II-Induced Hypertension via Regulatory T Cells.

RATIONALE: Inflammation and immunity play crucial roles in the development of hypertension. Complement activation-mediated innate immune response is involved in the regulation of hypertension and target-organ damage. However, whether complement-mediated T-cell functions could regulate blood pressure elevation in hypertension is still unclear. OBJECTIVE: We aim to determine whether C3aR (complement component 3a receptor) and C5aR (complement component 5a receptor) could regulate blood pressure via modulating regulatory T cells (Tregs). METHODS AND RESULTS: We showed that angiotensin II (Ang II)-induced hypertension resulted in an elevated expression of C3aR and C5aR in Foxp3 (forkhead box P3)+ Tregs. By using C3aR and C5aR DKO (double knockout) mice, we showed that C3aR and C5aR deficiency together strikingly decreased both systolic and diastolic blood pressure in response to Ang II compared with WT (wild type), single C3aR-deficient (C3aR-/-), or C5aR-deficient (C5aR-/-) mice. Flow cytometric analysis showed that Ang II-induced Treg reduction in the kidney and blood was also blocked in DKO mice. Histological analysis indicated that renal and vascular structure remodeling and damage after Ang II treatment were attenuated in DKO mice compared with WT mice. In vitro, Ang II was able to stimulate C3aR and C5aR expression in cultured CD4+CD25+ natural Tregs. CD3 and CD28 antibody stimuli downregulated Foxp3 expression in WT but not DKO Tregs. More important, depletion of Tregs with CD25 antibody abolished the protective effects against Ang II-induced hypertension and target-organ damage in DKO mice. Adoptive transfer of DKO Tregs showed much more profound protective effects against Ang II-induced hypertension than WT Treg transfer. Furthermore, we demonstrated that C5aR expression in Foxp3+ Tregs was higher in hypertensive patients compared with normotensive individuals. CONCLUSIONS: C3aR and C5aR DKO-mediated Treg function prevents Ang II-induced hypertension and target-organ damage. Targeting C3aR and C5aR in Tregs specifically may be an alternative novel approach for hypertension treatment.

Mitochondrial division inhibitor Mdivi-1 ameliorates angiotensin II-induced endothelial dysfunction.

Mitochondrial fission can occur via activation of dynamin-related protein 1 (Drp1), which participates in the mitochondrial membrane scission process. The present study was designed to investigate the effect of angiotensin II (AngII) on mitochondrial fission and fusion in human umbilical vascular endothelial cells (HUVECs). And we further inquire into whether Mdivi-1, a newly identified pharmacological inhibitor of Drp1, can prevent endothelial dysfunction induced by AngII. The HUVECs were treated with AngII alone or in combination with Mdivi-1. Western blot was used to detect protein expressions of Drp1, endothelial nitric oxide synthase (eNOS) and apoptosis-related enzymes. MitoTracker Red and JC-1 dye were used to detect mitochondrial morphology and membrane potential, respectively. DCFH-DA probe was used to access intracellular reactive oxygen species (ROS) generation. Transwell assay was used to evaluate cell migration. Annexin V/PI staining was used to assess cellular apoptosis. The results showed that, in cultured HUVECs, AngII (1 × 10-7 mol/L, 12 h) treatment significantly upregulated the expression of Drp1 followed by increased apoptosis and decreased eNOS expression. The treatment of AngII resulted in a change in mitochondrial morphology from elongated to uniformly punctate organelles, which was accompanied by decreased mitochondrial membrane potential. Furthermore, Mdivi-1 significantly protected against AngII-induced endothelial dysfunction, as shown by increased mitochondrial membrane potential and eNOS expression, reduced ROS level, decreased apoptosis and migration ability. Taking together, our data suggest that inhibition of Drp1 with Mdivi-1 can restore AngII-induced endothelial dysfunction.

Synthesis of Demissidine and Solanidine.

Demissidine and solanidine, two steroidal alkaloids, are synthesized in eight steps from tigogenin acetate and diosgenin acetate, respectively, which involve the replacement of three C-O bonds with C-N bonds. Key transformations include a cascade ring-switching process of furostan-26-acid, an epimerization of C25, an intramolecular Schmidt reaction, and an imine reduction/intramolecular aminolysis process.

Downregulation of dynamin-related protein 1 contributes to impaired autophagic flux and angiogenic function in senescent endothelial cells.

OBJECTIVE: Recent studies have shown that altered mitochondrial dynamics impairs the function in senescent endothelial cells (ECs). However, the underlying molecular mechanism remains to be elucidated. Herein, we investigated the role and underlying mechanism of mitochondrial fission protein dynamin-related protein 1 (DRP1) in vascular aging. APPROACH AND RESULTS: We found that DRP1 expression is decreased in senescent ECs, accompanied with long interconnected mitochondria and impaired angiogenic function. In addition, there was marked increase of autophagosomes but not of autolysosomes (assessed as punctate dual fluorescent mCherry-GFP (green fluorescent protein) tandem-tagged light chain 3 expression) in senescent ECs, indicating impaired autophagic flux. DRP1 knockdown or pharmacological inhibition in young ECs resulted in elongated mitochondria, suppressed autophagic flux, premature senescence, and impaired angiogenic function. In contrast, adenoviral-mediated overexpression of DRP1 in senescent ECs restored autophagic flux and improved angiogenic function. EC senescence was associated with the increase of mitochondrial reactive oxygen species and antioxidant N-acetyl-cysteine restored autophagosome clearance and improved angiogenic function. Consistently, en face staining of old rat thoracic aorta revealed a decrease of DRP1 expression and increase of autophagosomes accumulation. Furthermore, in vivo knockdown of Drp1 in common carotid arteries significantly impaired the autophagosome clearance. Importantly, downregulation of Drp1 directly abrogated microvessels outgrowth from ex vivo aortic rings. CONCLUSIONS: These results suggest that loss of DRP1 during senescence exacerbates ECs dysfunction by increasing mitochondrial reactive oxygen species and subsequently inhibiting autophagic flux.

Clinical characteristics of somatic mutations in Chinese patients with aldosterone-producing adenoma.

Recent studies have shown that somatic mutations in the KCNJ5, ATP1A1, ATP2B3, and CACNA1D genes are associated with the pathogenesis of aldosterone-producing adenoma. Clinical profile and biochemical characteristics of the mutations in Chinese patients with aldosterone-producing adenoma remain unclear. In this study, we performed DNA sequencing in 168 Chinese patients with aldosterone-producing adenoma and found 129 somatic mutations in KCNJ5, 4 in ATP1A1, 1 in ATP2B3, and 1 in CACNA1D. KCNJ5 mutations were more prevalent in female patients and were associated with larger adenomas, higher aldosterone excretion, and lower minimal serum K(+) concentration. More interestingly, we identified a novel somatic KCNJ5 mutation (c.445-446insGAA, p.T148-T149insR) that could enhance CYP11B2 mRNA upregulation and aldosterone release. This mutation could also cause membrane depolarization and intercellular Ca(2+) increase. In conclusion, somatic KCNJ5 mutations are conspicuously more popular than mutations of other genes in aldosterone-producing adenomas of Chinese patients. The T148-T149insR mutation in KCNJ5 may influence K(+) channel selectivity and autonomous aldosterone production.

[Retrospective study of complication of interspinous implants for degenerative lumbar disease].

OBJECTIVE: To summarize and analyze the complications of interspinous implants for degenerative lumbar disease. METHODS: From September 2007 to September 2011, 177 cases with degenerative lumbar diseases were treated with interspinous implants. There were 99 male patients and 78 female patients, the average age was 44.5 years (26 - 71 years). According to the application interspinous dynamic stabilization system type were divided into the Wallis group (136 cases) and Coflex group (41 cases). The clinical results were assessed by visual analog scale (VAS) of pain on lumbar and lower limbers, lumbar Japanese Orthopedic Association (JOA) score and Prolo functional score. The radiological results including segmental lodosis and segement movement degree were assessed by lumbar X ray and dynamic X ray. Summarize and analyze the complications both during operation and post operation. Quantitative datas were compared by paried-samples t test and complication rate was compared by χ(2) test. RESULTS: There were 168 cases had completed follow-up and the average time was 34.7 months (3 - 50 months). In the final follow-up, lumbar pain VAS, lower limber pain VAS, lumbar JOA score and Prolo functional score were better than pre-operation (t = 10.7, 7.9, 13.4 and 8.8, P < 0.01). Segment lodosis angles was 14° ± 4° which was less than pre-operation 19° ± 4° (t = 9.4, P < 0.01).Segment movement degree was larger in Coflex group (12.6° ± 3.1°) than in Wallis group (9.7° ± 2.7°) (t = 8.6, P < 0.05). Complication rate was 10.7% (18/168), which of Wallis group was 6.2% (8/130) and Coflex group was 26.3% (10/38) (χ(2) = 12.5, P < 0.01). In Wallis group, there were 3 cases with dura tear and cerebrospinal fluid leakage, 1 case with nerve root injury and foot drop, 2 cases with spacer breakage when implantation and change the implants and 2 cases with recurrence of lumbar disc herniation. In Coflex group, there was 1 case with dura tear and cerebrospinal fluid leakage, 2 cases with mild displacement post operation, 1 case with debridement for aseptic wound exudates, 1 case with implant removal for breakage 1 week post operation, 4 cases with recurrence of lumbar disc herniation and 1 case with lumbar disc herniation 6 months post operation of lumbar stenosis. CONCLUSIONS: The application of interspinous implants for degenerative lumbar diseases is effective and relative safe, but would suffer from the risk of complications.

[Mid-term follow-up and analysis of the failure cases of interspinous implants for degenerative lumbar diseases].

OBJECTIVE: To assess the indications,efficacy and safety of application of interspinous implants for degenerative lumbar diseases by mid-term follow-up and analysis of the failure cases. METHODS: In our study, 52 cases of degenerative lumbar diseases treated with interspinous implants From September 2007 to September 2008 were divided into Wallis group (25 cases) and Coflex group (27 cases). The clinical results were assessed by lumbar pain visual analog score (VAS) and lower limber pain VAS, lumbar Japanese Orthopedic Association (JOA) score and Prolo functional score; the radiological results including implant positon, segmental lodosis and segment movement degree were assessed by lumbar X ray post-operation compared with pre-operation. For cases of discogenic low back pain, lumbar disc changes were assessed by lumbar MRI 12 months post operation. RESULTS: Fifty-two cases had complete follow-up and the average time was 30.4 months. In the final follow up, lumbar pain VAS,lower limber pain VAS,lumbar JOA score and Prolo functional score of Wallis group were (2.5 ± 1.7),(2.7 ± 1.4),(23.4 ± 3.1)and(8.9 ± 1.4), which were better than pre-operation (5.3 ± 3.0),(7.4 ± 2.6),(13.5 ± 4.6)and(4.5 ± 2.6 ),lumbar pain VAS P=0.027, all others P<0.001 ;lumbar pain VAS,lower limber pain VAS,lumbar JOA score and Prolo functional score of Coflex group were (2.6 ± 2.9),(3.8 ± 1.9),(21.2 ± 3.5)and(8.5 ± 1.8),which were better than pre-operation (5.5 ± 3.2),(7.1 ± 2.8), (13.1 ± 4.8)and(4.2 ± 2.5), lumbar pain VAS P=0.036, all others P<0.001;in the final follow up,lower limber pain VAS of Wallis group was (2.7 ± 1.4), which was better than (3.8 ± 1.9) of Coflex group(P=0.039);in the final follow up, Segment lodosis angles of Wallis group was 14.3° ± 3.9°, which was larger than 13.2° ± 3.5° of Coflex group (P=0.028); Segment movement degree of Wallis group was 9.6° ± 2.8°, which was smaller than 12.8°±3.0°of Coflex group (P=0.019).In Coflex group,four cases of lumbar disc herniation relapsed and three cases received second operation. One case with lumbar stenosis suffered from lumbar disc herniation of the same segments and received second revision operation. CONCLUSION: Treatments with interspinous implants for the degenerative lumbar diseases are effective, but we should pay attention to the indication and apply them for lumbar disc herniation with caution.

[Prevention for venous thromboembolism prophylaxis after spinal surgery].

OBJECTIVE: To investigate the efficacy and safety of venous thrombus embolism (VTE) prophylaxis according to risk stratifications after spinal surgery. METHODS: From June 2008 to June 2009, we separated 298 spinal patients who had different VTE risk factors into low-, medium- and high-risk groups for 22 cases, 48 cases and 228 cases respectively. Physical prevention measures such as thigh-length thromboembolic deterrent stockings (TEDS) and pneumatic sequential compression device (PSCD) were used in low- and medium-risk groups. In high-risk groups, low molecular weight heparin(LMWH) was applied in addition to physical prevention measures. Lower limb vascular doppler ultrasonography was used to monitor thrombosis pre- and postoperatively. Simultaneously the occurrences of epidural or wound hematoma, mucosal bleeding, thrombocytopenia caused by low molecular heparin and nerve damage caused by extradural hemorrhage were monitored. RESULTS: Among the 298 cases of patients with spinal surgery, DVT occurred in 23 cases, the incidence of DVT was 7.7%. There were 0, 2 and 21 patients with positive findings of deep vein thrombosis on duplex ultrasonograph respectively in low-, medium- and high-risk groups. There was no case of PE. All DVT was thrombosis in calf which was distal to the knee. There was no clinical symptom of VTE. The DVT needed no therapy. The vein with thrombosis was recanalized 3 months after operation. No case caught epidural or wound hematoma, mucosal bleeding, thrombocytopenia caused by low molecular heparin or nerve damage caused by extradural hemorrhage. CONCLUSION: Individual VTE prophylaxis was taken according to risk stratifications. No VTE of clinical value or no complications from prophylaxis happened. So our prophylaxis is effective and safe. But more prospective, case-control studies are needed to assess the efficacy and safety of VTE prophylaxis.

[Retrospective study of combined application of interspinous process fixation system and rigid fixation system for degenerative lumbar diseases].

OBJECTIVE: To assess the efficacy and safety of combined application of interspinous process fixation system and rigid fixation system for degenerative lumbar diseases. METHODS: From September 2007 to September 2008, 16 cases with degenerative lumbar diseases were treated with combined application of interspinous process fixation system and rigid fixation system. The clinical results were assessed by VAS of pain of lumbar and lower limbs, lumbar JOA score and Prolo functional score. The radiological results including implant position (interspinous process, pedicle screws and plates), spinous process fracture, segmental range of motion (the non-fusion fixation segment, and the intermediate segments between fused and non-fused segments) which were assessed by lumbar static and dynamic X rays. RESULTS: All 16 cases obtained an average follow-up of 17.6 months. At final follow up, lumbar VAS, lower limbers VAS, lumbar JOA score and Prolo functional score were significant improved than those of pre-operation (lumbar VAS: 1.9 +/- 1.4 vs. 4.5 +/- 3.1; lower limbs VAS: 1.7 +/- 1.2 vs. 6.3 +/- 2.9; lumbar JOA score: 22.8 +/- 3.3 vs. 12.5 +/- 4.7; Prolo functional score: 8.3 +/- 1.2 vs. 4.0 +/- 2.3). Range of motion of the non-fusion fixation segment was (9.8 +/- 4.2) degrees and that of the intermediate segments between fused and non-fused segments was (13.2 +/- 3.5) degrees . CONCLUSIONS: Combined application of interspinous process fixation system and rigid fixation system for degenerative lumbar diseases provides a new idea to avoid the multi-segment fusion fixation and pertinent potential problems. Short-term clinical results are successful.

[Retrospective study of application of interspinous implants for degenerative lumbar diseases].

OBJECTIVE: To assess the indications, efficacy and safety of applying interspinous implants for degenerative lumbar diseases. METHODS: From September 2007 to September 2008, 68 cases with degenerative lumbar diseases were treated with interspinous implants. The clinical outcome was assessed by VAS of pain in back and lower extremities, lumbar JOA score and Prolo functional score; the radiological results including implant position, segmental lodosis and segment movement degree were assessed by lumbar X ray including dynamic post-operative versus pre-operative X ray. RESULTS: Sixty-four cases had a complete follow-up and the average time was 11.4 months. At the final follow up, lumbar VAS 1.7 +/- 1.5, lower extremity VAS 1.3 +/- 1.0, lumbar JOA score 23.5 +/- 3.1 and Prolo functional score 8.6 +/- 1.4. They were better than those at pre-operation (1.7 +/- 1.5, 1.3 +/- 1.0, 23.5 +/- 3.1, 8.6 +/- 1.4). Segment lodosis angle (15.4 +/- 4.2) degrees was less than (19.6 +/- 4.7) degrees at pre-operation; segment movement degree was (10.3 +/- 4.5) degrees . Two cases with lumbar disc herniation relapsed and received a second operation. CONCLUSION: The application of interspinous implants for degenerative lumbar diseases is still in its infancy and the selection of indication is very important. Its efficacy and safety have been confirmed by a short follow-up.