Effect of voriconazole combined with glucocorticoid on nephrotic syndrome in children.

OBJECTIVE: To explore the efficacy of voriconazole combined with glucocorticoid on the nephrotic syndrome in children. PATIENTS AND METHODS: A total of 62 children with nephrotic syndrome were enrolled in this study. They were treated in our hospital from February 2016 to August 2019, including 35 children treated with voriconazole in a control group, and 27 children treated with glucocorticoid combined with voriconazole in a research group. The efficacy was evaluated, and a logistic regression analysis was carried out to find out the risk factors affecting the efficacy. The enzyme-linked immunosorbent assay (ELISA) was used to determine the serum creatinine and urine protein expression before and after treatment. In addition, receiver operating characteristic (ROC) curves were drawn to analyze the predictive value of serum creatinine and urine protein expression. RESULTS: The marked efficacy and total effective rate in the research group were significantly higher than those in the control group, while the non-efficacy in the research group was significantly lower than that in the control group (p<0.05). After treatment, the expression of serum creatinine and urine protein in the research group was significantly lower than that in the control group (p<0.05). The area under the curve (AUC) of urine protein was 0.798. The AUC of serum creatinine was 0.724. Multivariate logistic regression analysis revealed that serum albumin, high edema, infection, serum creatinine, and urine protein were independent risk factors. CONCLUSIONS: Glucocorticoid can improve clinical efficacy. Serum creatinine and urine protein can be adopted as predictive factors for efficacy on children with nephrotic syndrome. Serum albumin, high edema, infection, serum creatinine, and urine protein were independent risk factors for the efficacy on children with nephrotic syndrome.

Lipopolysaccharide-stimulated bone marrow mesenchymal stem cells-derived exosomes inhibit H2O2-induced cardiomyocyte inflammation and oxidative stress via regulating miR-181a-5p/ATF2 axis.

OBJECTIVE: Myocardial infarction (MI) is a cardiovascular disease that seriously endangers human health. Exosomes secreted by stem cells have big potential for the treatment of many diseases. The purpose of this study was to study the therapeutic effects of exosomes derived from lipopolysaccharide (LPS)-stimulated bone marrow mesenchymal stem cells (BMSCs) on MI. PATIENTS AND METHODS: The surface markers of BMSCs were detected by Western blot. After BMSCs were stimulated with LPS for 2 days, the exosomes secreted by BMSCs were extracted and observed by transmission electron microscopy (TEM), and their specific surface markers were detected by Western blot. H9c2 cells were co-cultured with exosomes for 24 hours, and then, treated with H2O2 for 4 hours. Next, H9c2 cells were transfected with miRNA-181a-5p mimic (MIM) or negative control (NC). Inflammation and oxidative stress of H9c2 cells were detected by Western blot, cell staining, reactive oxygen species (ROS) quantification, and SOD activity assay. At last, miR-181a-5p expression in BMSCs, exosomes, and H9c2 cells was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). RESULTS: The results revealed that the expression of miR-181a-5p was increased in LPS-stimulated BMSCs (L-BMSC) and in their secreted exosomes. Besides, the expressions of TNF-α and IL-1ß were decreased, while those of SOD1 and SOD2 were increased in H9c2 cells co-cultured with exosomes secreted by LPS-stimulated BMSCs (L-EXO) and transfected with MIM. Moreover, the fluorescence intensity of IL-1ß immunofluorescence was decreased in H9c2 cells co-cultured with L-EXO or transfected with MIM. The level of ROS was also decreased in H9c2 cells co-cultured with L-EXO or transfected with MIM. Furthermore, miR-181a-5p was found to target ATF2 through target gene prediction databases and Western blot and Dual-Luciferase reporter assays. CONCLUSIONS: LPS stimulation can increase the expression of miR-181a-5p in BMSCs, and miR-181a-5p inhibits myocardial inflammation and oxidative stress by targeting ATF2.

LncRNA SNHG7 promotes development of breast cancer by regulating microRNA-186.

OBJECTIVE: To elucidate the biological functions of long non-coding RNA (lncRNA) SNHG7 in breast cancer (BC), and its underlying mechanism in the occurrence and progression of BC. PATIENTS AND METHODS: The expression of SNHG7 in 72 pairs of BC tissues and paracancerous tissues was detected by quantitative Real-time polymerase chain reaction (qRT-PCR). Correlation between SNHG7 expressions with pathological indicators of BC patients was analyzed. Similarly, SNHG7 expression in BC cell lines was determined by qRT-PCR as well. After constructing the small inference RNA of SNHG7, cell proliferation, migration and invasion were determined by cell counting kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) and transwell assay. MicroRNA-186 expression in BC tissues and cells was accessed. Dual-luciferase reporter gene assay was conducted to verify the binding condition between SNHG7 and microRNA-186. RESULTS: SNHG7 expression was higher in BC tissues than that of paracancerous tissues. High expression of SNHG7 was positively correlated to tumor stage, lymph node metastasis and distant metastasis, whereas not correlated to age, sex and tumor location of BC. Kaplan-Meier curves revealed that higher expression of SNHG7 is correlated to the worse prognosis of BC patients. SNHG7 was highly expressed in BC cells as well. Knockdown of SNHG7 inhibited proliferative, invasive and migratory abilities of BC cells. QRT-PCR data showed that microRNA-186 is lowly expressed in BC tissues compared with that of paracancerous tissues. MicroRNA-186 was lowly expressed in BC cells as well. Both mRNA and protein levels of microRNA-186 were negatively correlated to SNHG7 in BC tissues. Finally, the dual-luciferase reporter gene assay demonstrated that SNHG7 could be directly targeted by microRNA-186. CONCLUSIONS: SNHG7 is highly expressed in BC, which is correlated to tumor stage, lymph node metastasis and distant metastasis of BC patients. SNHG7 could promote malignant progression of BC by regulating microRNA-186.

Understanding the Unusual Response to High Pressure in KBe2BO3F2.

Strong anisotropic compression with pressure on the remarkable non-linear optical material KBe2BO3F2 has been observed with the linear compression coefficient along the c axis found to be about 40 times larger than that along the a axis. An unusual non-monotonic pressure response was observed for the a lattice parameter. The derived bulk modulus of 31 ± 1 GPa indicates that KBe2BO3F2 is a very soft oxide material yet with stable structure up to 45 GPa. A combination of high-pressure synchrotron powder X-ray diffraction, high-pressure Raman spectroscopy, and Density Functional Theory calculations points to the mechanism for the unusual pressure response being due to the competition between the K-F bond length and K-F-K bond angle and the coupling between the stretching and twisting vibration modes.

Comparison of half- and standard-dose ticagrelor in Chinese patients with NSTE-ACS.

Ticagrelor is a novel direct-acting P2Y12 receptor antagonist used for preventing atherothrombotic events in patients with acute coronary syndromes (ACS). The current recommended dose is 90 mg bid, but a low dose of ticagrelor has not been previously studied in Chinese ACS patients. Therefore, we performed this study to observe the different effects of half- and standard-dose ticagrelor on platelet aggregation in Chinese patients with NSTE-ACS. Sixty-two NSTE-ACS subjects were assigned to half-dose ticagrelor (n = 20), standard-dose ticagrelor (n = 22) and clopidogrel (n = 20) groups. Five days after drug administration, VerifyNow P2Y12 assay was performed to test P2Y12 reaction units (PRU) and inhibition of platelet aggregation (IPA). High-platelet reactivity (HPR) was defined as a PRU > 208. The adverse events, including bleeding events and dyspnoea, were monitored throughout the study. PRU values in the half-dose (44.55 ± 32.88) and standard-dose (39.10 ± 40.02) ticagrelor were dramatically lower than those in the clopidogrel group (189.20 ± 65.22; P < 0.0001). The half-dose (84% ± 10%) and standard-dose (86% ± 13%) ticagrelor both showed greater IPA than clopidogrel (33% ± 20%; P < 0.0001). There were no significant differences in PRU and IPA between the two ticagrelor groups (P = 0.3085 and 0.4028, respectively). HPR rates were significantly lower in the two ticagrelor groups (0% for both) than those in the clopidogrel group (35%). In conclusion, half-dose ticagrelor had a similar inhibitory effect on platelet aggregation as standard-dose ticagrelor in Chinese patients with NSTE-ACS, which was significantly stronger than that of clopidogrel.

Ketamine-induced ventricular structural, sympathetic and electrophysiological remodelling: pathological consequences and protective effects of metoprolol.

BACKGROUND AND PURPOSE: Growing evidence suggests that long-term abuse of ketamine does harm the heart and increases the risk of sudden death. The present study was performed to explore the cardiotoxicity of ketamine and the protective effects of metoprolol. EXPERIMENTAL APPROACH: Rats and rabbits were divided into control, ketamine, metoprolol alone and ketamine plus metoprolol groups. Ketamine (40 mg·kg(-1) ·day(-1), i.p.) and metoprolol (20 mg·kg(-1) ·day(-1), p.o.) were administered continuously for 12 weeks in rats and 8 weeks in rabbits. Cardiac function, electrophysiological disturbances, cardiac collagen, cardiomyocte apoptosis and the remodelling-related proteins were evaluated. KEY RESULTS: Rabbits treated with ketamine showed decreased left ventricular ejection fraction, slowed ventricular conduction velocity and increased susceptibility to ventricular arrhythmia. Metoprolol prevented these pathophysiological alterations. In ketamine-treated rats, cardiac collagen volume fraction and apoptotic cell number were higher than those of control animals; these effects were prevented by co-administration of metoprolol. Consistently, the expressions of poly (ADP-ribose) polymerases-1, apoptosis-inducing factor and NF-κB-light-chain-enhancer of activated B cells were all increased after ketamine treatment and sharply reduced after metoprolol administration. Moreover, ketamine enhanced sympathetic sprouting, manifested as increased growth-associated protein 43 and tyrosine TH expression. These effects of ketamine were prevented by metoprolol. CONCLUSIONS AND IMPLICATIONS: Chronic treatment with ketamine caused significant ventricular myocardial apoptosis, fibrosis and sympathetic sprouting, which altered the electrophysiological properties of the heart and increased its susceptibility to malignant arrhythmia that may lead to sudden cardiac death. Metoprolol prevented the cardiotoxicity of ketamine, indicating a promising new therapeutic strategy.

Bioaccumulation of nickel from aqueous solutions by genetically engineered Escherichia coli.

This study constructed a genetically engineered Escherichia coli JM109 which simultaneously expressed nickel transport system and metallothionein to remove and recover Ni(2+) from aqueous solution. Bioaccumulation process was rapid and followed linearized Langmuir isotherm. A more than six-fold increase of Ni(2+) binding capacity was obtained by genetically engineered E. coli cells compared with original host E. coli cells. A pH assay showed genetically engineered E. coli cells accumulated Ni(2+) effectively over a broad range of pH (4-10). The presence of 1000 mg/L Na(+) and Ca(2+), or 50mg/L Cd(2+) or Pb(2+) did not have a significant effect on Ni(2+) bioaccumulation, while Mg(2+), Hg(2+) and Cu(2+) posed a severe adverse influence on Ni(2+) uptake by genetically engineered E. coli. Furthermore, genetically engineered E. coli cells did not require extra nutrients for Ni(2+) bioaccumulation.

Traumatic spondylolisthesis of the axis: 42 cases.

Fourty-two patients (34 males and 8 female) with traumatic spondylolisthesis of the axis were studied in a retrospective review There were 20 stable and 22 unstable fractures. The 22 unstable fractures were treated surgically: 16 anterior interbody fusion (10 non-plated and 6 plated), 4 pedicle screw fixation for osteosynthesis of the fractured pedicles, and 2 posterior wire fixation for flexion and axial load injury. For all non-surgical cases, head halter tractions for 1 to 8 weeks was prescribed and a cervical orthosis was worn for an additional 6 to 18 weeks. The surgical cases underwent 5 to 7 days of preoperative and 1 to 4 weeks of post-operative head halter traction. In all cases pedicle fractures united after 13 weeks on average in group treated conservatively, 12 weeks (11 to 13 weeks) in the posterior wiring group, 8 weeks (7 to 9 weeks) in the group in which pedicle screws were used, and 11 weeks (9 to 15 weeks) in the anterior fusion group (13 weeks in non-plated, and 8 weeks in plated). There were no differences in patterns of anterior fusion between those in the non-plated and plated groups. There were no non-unions of fractured pedicles and there was no late instability of the C2-C3 or neurological complications. In 2 cases in the posterior surgery group, there was mild nuchal discomfort and some rigidity for a short while postoperatively. Final outcomes were good in all cases.

Determination of thirteen common elements in food samples by inductively coupled plasma atomic emission spectrometry: comparison of five digestion methods.

Five sample digestion procedures were evaluated for the determination of Al, B, Ca, Cu, Fe, K, Mg, Mn, Na, P, S, Sr, and Zn in food samples by inductively coupled plasma atomic emission spectrometry. The 5 procedures include dry ashing at 500 degrees C, wet digestion with HNO3-HClO4, microwave digestion with HNO3, microwave digestion with HNO3-H2O2, and microwave digestion with HNO3-H2O2-HF. For microwave digestion with HNO3-H2O2-HF, silicon (IV) oxide was used to eliminate the excess HF, making it possible to determine total Al, B, and other common elements accurately and simultaneously. Seven National Institute of Standards and Technology standard reference materials (SRMs) were analyzed to compare the recovery of 13 elements with above digestion procedures. The results demonstrated that the microwave digestion procedure with HNO3-H2O2-HF yielded the best recoveries for all 13 elements in the selected SRMs. The determined concentrations of most elements were close for all 3 microwave digestion procedures with the exception of Al in oyster tissue, bovine liver, and spinach. Notably, the wet digestion with HNO3-HClO4 is the simplest and the most effective procedure for the selected elements except Al and B. Although there are several concerns with the dry ashing procedure, it might be a preferable procedure for those analyses where only nonvolatile elements are to be determined and the concentrations of the elements are low.

Signaling pathways for tumor necrosis factor-alpha and interleukin-6 expression in human macrophages exposed to titanium-alloy particulate debris in vitro.

BACKGROUND: Loosening of the implant after total joint arthroplasty remains a serious problem. The activation of macrophages by wear debris from implants, mediated by the release of cytokines that elicit bone resorption, may lead to loosening. The purpose of the present study was to elucidate the mechanisms of macrophage activation by titanium particles from the components of implants and to identify the signaling pathways involved in particle-mediated release of cytokines. METHODS: Macrophages were isolated from mononuclear leukocytes obtained from healthy human donors and were exposed to titanium-alloy particles that had been obtained from periprosthetic membranes collected at revision total joint arthroplasties and then enzymatically prepared. The experimental protocols included examination of the effects of the inhibition of phagocytosis and the binding of antibodies to macrophage complement receptors on particle-induced macrophage activation. The release of the proinflammatory cytokines TNF-alpha (tumor necrosis factor-alpha) and IL-6 (interleukin-6) was used to assess macrophage activation. The signaling pathways involved in the induction of cytokine release were analyzed by identification of phosphorylated proteins with use of the Western blot technique and by translocation of the transcription factors nuclear factor-kappa B (NF-kappaB) and nuclear factor-interleukin-6 (NF-IL-6) into the nuclear protein fraction with use of electrophoretic mobility shift assays. The role of serine/threonine and tyrosine kinase pathways in the activation of nuclear factors and the release of cytokines was examined with use of selective pharmacological agents. RESULTS: Exposure of macrophages to titanium-alloy particles in vitro for forty-eight hours resulted in a fortyfold increase in the release of TNF-alpha and a sevenfold increase in the release of IL-6 (p<0.01). Phagocytosis of particles occurred in approximately 73 percent of the macrophages within one hour of exposure. Pretreatment of the macrophages with cytochalasin B reduced phagocytosis by 95 percent but did not reduce the release of TNF-alpha or IL-6. Thus, phagocytosis of particles was not necessary for induction of the release of TNF-alpha or IL-6 in the cultured macrophages. Ligation of the macrophage CD11b/CD18 receptors by integrin-specific antibodies also increased the release of TNF-alpha and IL-6. Antibodies to CD11b/ CD18 receptors (macrophage Mac-1 receptors) reduced phagocytosis of particles by 50 percent (p<0.05). (The CD11b/CD18 macrophage receptor is the macrophage receptor for the complement component CR3bi. The CD11b/CD18 macrophage receptor can also bind to ICAM-1 and ICAM-2. CD is the abbreviation for cluster of differentiation, and ICAM is the abbreviation for intercellular adhesion molecule.) Inhibition of phagocytosis was not accompanied by a decrease in the release of TNF-alpha and IL-6. Blocking RNA synthesis with actinomycin D or preventing protein synthesis with cycloheximide abolished or decreased particle-induced release of TNF-alpha and IL-6 from the macrophages. Macrophage release of TNF-alpha and IL-6 in response to particles coincided with increased tyrosine phosphorylation and mitogen-activated protein kinase activation. Inhibition of tyrosine and serine/threonine kinase activity decreased the particle-induced release of cytokines. Exposure of macrophages to either titanium-alloy particles or to antibodies to the receptor proteins CD11b and CD18 for thirty minutes activated the transcription factors NF-kappaB and NF-IL-6. Inhibition of particle phagocytosis did not block activation of the transcription factors. However, inhibition of tyrosine and serine/threonine kinase activity decreased the activation of NF-kappaB and NF-IL-6. CONCLUSIONS: These data suggest that particle induced macrophage release of TNF-alpha and IL-6 does not require phagocytosis but is dependent on tyrosine and serine/threonine kinase activity culminating in activation of

Induction of macrophage C-C chemokine expression by titanium alloy and bone cement particles.

Particulate wear debris is associated with periprosthetic inflammation and loosening in total joint arthroplasty. We tested the effects of titanium alloy (Ti-alloy) and PMMA particles on monocyte/macrophage expression of the C-C chemokines, monocyte chemoattractant protein-1 (MCP-1), monocyte inflammatory protein-1 alpha (MIP-1alpha), and regulated upon activation normal T expressed and secreted protein (RANTES). Periprosthetic granulomatous tissue was analysed for expression of macrophage chemokines by immunohistochemistry. Chemokine expression in human monocytes/macrophages exposed to Ti-alloy and PMMA particles in vitro was determined by RT-PCR, ELISA and monocyte migration. We observed MCP-1 and MIP-1alpha expression in all tissue samples from failed arthroplasties. Ti-alloy and PMMA particles increased expression of MCP-1 and MIP-1alpha in macrophages in vitro in a dose- and time-dependent manner whereas RANTES was not detected. mRNA signal levels for MCP-1 and MIP-1alpha were also observed in cells after exposure to particles. Monocyte migration was stimulated by culture medium collected from macrophages exposed to Ti-alloy and PMMA particles. Antibodies to MCP-1 and MIP-1alpha inhibited chemotactic activity of the culture medium samples. Release of C-C chemokines by macrophages in response to wear particles may contribute to chronic inflammation at the bone-implant interface in total joint arthroplasty.

Interleukin-4 inhibits granulocyte-macrophage colony-stimulating factor, interleukin-6, and tumor necrosis factor-alpha expression by human monocytes in response to polymethylmethacrylate particle challenge in vitro.

The outcome of total joint arthroplasty is determined by biological events at the bone-implant interface. Macrophages phagocytose implant or wear debris at the interface and release proinflammatory mediators such as interleukins 1 and 6, tumor necrosis factor-alpha, and prostaglandin E2. These mediators are thought to contribute to the resorption of periprosthetic bone. Previous studies of tissues harvested from the bone-implant interface of failed orthopaedic implants demonstrated a possible role for two other cytokines, granulocyte-macrophage colony-stimulating factor and interleukin-4. The present study examined the effects of in vitro challenge with polymethylmethacrylate particles on the expression of granulocyte-macrophage colony-stimulating factor by primary human monocytes/macrophages and the role of interleukin-4 in regulating this expression. The polymethylmethacrylate particles caused a dose-dependent release of granulocyte-macrophage colony-stimulating factor at 48 hours. This release was accompanied by increased expression of interleukins 6 and 1beta and tumor necrosis factor-alpha. Release of the lysosomal enzyme hexosaminidase also increased in response to the particles. Interleukin-4 inhibited the expression of granulocyte-macrophage colony-stimulating factor, interleukin-6, and tumor necrosis factor-alpha at 48 hours in a dose-dependent manner. The data presented in this study confirm the hypothesis that interleukin-4 downregulates particle-induced activation of macrophages, as demonstrated by the decreased release of proinflammatory mediators.

Induction of matrix metalloproteinase expression in human macrophages by orthopaedic particulate debris in vitro.

We exposed human macrophages isolated from the peripheral blood of healthy donors to metal and bone-cement particles from 0.2 to 10 microm in size. Zymography showed that macrophages exposed to titanium alloy and polymethylmethacrylate (PMMA) particles released a 92- and 72-kDa gelatinase in a dose- and time-dependent manner. Western immunoblotting confirmed that the 92- and 72-kDa gelatinolytic activities corresponded to matrix metalloproteinase-9 and matrix metalloproteinase-2 (MMP-9, MMP-2), respectively. Western immunoblotting also indicated that titanium alloy and PMMA particles increased the release of MMP-1. Northern blotting showed elevated mRNA signal levels for MMP-1, MMP-2, and MMP-9 after exposure to both types of particle. Collagenolytic activity also increased in the macrophage culture medium in response to both types of particle. Our findings support the hypothesis that macrophages release MMPs in proportion to the amount of particulate debris within periprosthetic tissues.

Effects of serum protein opsonization on cytokine release by titanium-alloy particles.

This study tested whether macrophages respond differently to retrieved titanium-alloy particles than they do to machined titanium-alloy particles and assessed whether pretreatment of machined titanium-alloy particles with human serum would influence macrophage activation and cytokine release in vitro. Human monocyte/macrophages were isolated from normal healthy donors and exposed to increasing concentrations of machined and retrieved titanium-alloy particles. The profile of cytokine release was determined by commercially available ELISA kits. Machined titanium-alloy particles were opsonized with human serum and added to macrophage cultures. Serum protein binding was confirmed by SDS-PAGE analysis. The results showed that machined titanium-alloy particles and retrieved titanium-alloy particles stimulate a similar level of cytokine release when tested at comparable concentrations. Opsonization of the machined particles with human serum increased the macrophage release of cytokines in the first 12 h after exposure compared to nonopsonized particles. At 24 h, the opsonized particles stimulated significantly higher levels of cytokine release, but only at the greatest particle concentrations. This study demonstrates that machined titanium alloy induces a metabolic response in macrophages similar to that of titanium-alloy particles retrieved from failed total hip arthroplasty. In addition, these data show that serum protein binding to orthopedic biomaterial debris alters the macrophage reaction to the particles.

Epidemiologic survey on organophosphate-induced delayed polyneuropathy (OPIDP) among patients recovered from Methamidophos poisoning.

As Methamidophos (MAF) is currently responsible for half of the pesticide intoxications and fatality cases in China, the need to assess the frequency and the characteristics of the OPIDP among the victims who recovered from MAF poisoning is obvious. One-hundred and four subjects suffering from MAF intoxication were selected according to their medical records in the local rural hospitals in the Mu-du suburb of Su-Zhou, and the Shi-Qiu suburb of Nanjing. Face-to-face interviews were performed during home visits to all selected subjects, with the only exception of 4 patients. In those cases, information was provided by their kin relatives. Fourteen cases of delayed polyneuropathy (OPIDP) were identified: all patients who suffered from OP poisoning and had OPIDP showed a typical clinical course. The overall incidence of OPIDP was surprisingly high: 13.5%. The risk of OPIDP was associated with the severity of the intoxication. No association was found between OPIDP incidence and sex, age or treatment with dexametholone during the acute phase of the disease (RR = 0.98, p = 0.79). All 14 cases of OPIDP recovered in one and a half year without any permanent disability.

Pott's Paraplegia--67 cases.

Sixty-seven patients were treated for Pott's paraplegia: 58 were adults and 9 were children. Sixty-four patients had active disease, and 3 had healed disease. All patients had triple chemotherapy with or without decompression surgery. Thirteen patients, including 9 children, were treated conservatively, whereas 54 patients who met the selection criteria for surgery were treated surgically. Fifty-two patients had anterior radical decompression surgery, and for 14 of them, anterior surgery was preceded by posterior instrumental stabilization surgery. Two patients with healed disease had posterior decompressive corpectomy. There was functional recovery in 60 (89.6%) patients, including 13 who had active disease that was treated conservatively. In 47 of the 54 surgically treated patients there was neurologic recovery, and 2 of these recovered incompletely with some residual spasticity. In the remaining 7 patients, there was no recovery. It took 2 to 6 months for recovery for the patients with conservative treatment, whereas it took <2 months for the patients with anterior decompression. The patients who had the combined 2-stage procedure could be mobilized earlier after neurologic recovery than could the patients having the anterior radical surgery and the conservatively treated patients. It was proven that paraplegia of active disease can be treated successfully by conservative or surgical means and that paraplegia caused by healing of fibrosis in the severely deformed spine was difficult to treat successfully, even with radical surgery.

Habitual voluntary dislocation of the hip in a child. A case report.

A child, 5 years of age, with habitual voluntary dislocation of the hip is reported. He was treated by an intertrochanteric osteotomy and made a satisfactory recovery.

Posterior instrumentation and anterior interbody fusion for tuberculous kyphosis of dorsal and lumbar spines.

STUDY DESIGN: Thirty-nine adults and five children with active spinal tuberculosis and resulting kyphosis of the dorsal and lumbar spine who had combined posterior instrumentation and anterior interbody fusion were observed to determine whether the corrected spinal deformity could be maintained until solid fusion. OBJECTIVE: To evaluate the effectiveness of the combined two-stage procedure for treating kyphosis due to active spinal tuberculosis. SUMMARY OF BACKGROUND DATA: Until 1970, with all methods of treatment, kyphosis due to active spinal tuberculosis tended to increase during therapy. Most of the patients treated with these methods were not happy with this residual kyphosis, even though their disease was arrested or cured. Kyphosis became their main concern regarding further treatment. METHODS: A combined two-stage procedure, under the cover of 18 months of triple chemotherapy, was used for all patients. For posterior stabilization, the Harrington distraction system, Rush nails or Steinmann pins and wires, and Texas Scottish Rite Hospital instrumentation were used. The diagnosis of successful interbody fusion was made if there was no loss of correction, no graft resorption or graft bed resorption, and if there was visible graft remodeling, such as trabeculation between the graft beds and graft and the graft hypertrophy. RESULTS: In the 39 adults, average preoperative, immediate postoperative, and last follow-up kyphosis angles were 37 degrees, 16 degrees, and 18 degrees, respectively. In four children, the average preoperative, immediate postoperative, and last follow-up kyphosis angles were 55 degrees, 28 degrees, and 31 degrees, respectively. The loss of correction did not exceed 3 degrees. For one-segment spondylodesis, the average fusion times were 4 months in adults and 3.5 months in children. For a two-segment fusion, the average fusion times were 6 months in adults and 6.3 months in children. CONCLUSION: Posterior instrumental stabilization and anterior interbody fusion were found helpful in arresting the disease early, providing early fusion, preventing progression of kyphosis, and correcting the kyphosis.