[Study on the safety and clinical efficacy of osteotomy after halo pelvic traction in severe scoliosis accompanied with split cord malformation].

Objective: To investigate the safety and clinical efficacy of osteotomy after halo pelvic traction in severe scoliosis accompanied with split cord malformation. Methods: The clinical data of 14 patients with severe scoliosis accompanied with split cord malformation admitted to the Department of Spinal Surgery, Guizhou Orthopedic Hospital from August 2015 to August 2019 were retrospectively analyzed.There were 6 males and 8 females, aged (19.8±5.0) years (range:13 to 34 years). All patients received spinal orthopedic surgery after halo pelvic traction for 3 to 7 weeks.The data of traction time, height, Cobb angle in the main curved coronal plane and sagittal plane, lung function and nutritional status of the patient were collected before and after the treatment. Paired t test was used to compare the evaluation indexes. Results: The traction time of the 14 patients was (35.2±8.3)days (range:20 to 49 days), and the height of them increased from (156.7±7.6)cm (range:141 to 166 cm) before traction to (167.0±6.4)cm (range:154 to 177 cm) after traction（t=-10.49，P<0.01）. The Cobb angle on the main curved coronal plane decreased from (117.4±17.2) ° (range: 91°to 176°) before traction to (56.4±8.1) ° (range:44°to 68°) after traction（t=13.90，P<0.01）. The sagittal Cobb angle decreased from (92.5±11.6) ° (range:62°to 132°) before traction to (41.7±7.7) °(range:29°to 51°) after traction（t=12.11，P<0.01）. No complications such as loosening of nailing and infection occurred during traction, and no decrease of nerve function occurred. Nine patients underwent single segment acromial transpedicle osteotomy and five underwent double segment adjacent asymmetric shortening osteotomy. None of the patients underwent longitudinal fracture resection. The lung function and nutritional status were improved after traction and surgery(all P<0.01). Postoperative follow-up was (22.5±9.1)months (range:12 to 36 months). At the last follow-up, the coronal Cobb angle was (56.3±7.1) °, and the sagittal Cobb angle was (37.7±6.5) °, showing no statistically significant difference from the angle after traction(t=0.16,P=0.88; t=2.28,P=0.32). There was no loss of orthopedic angle. None of the patients had internal fixation displacement, loosening or fracture. Conclusion: The treatment of severe scoliosis with accompanied with split cord malformation by halo pelvic traction is safe and effective, which is worthy of further confirmation by large sample study.

[Preliminavy clinical study of the treatment of hemorrhoids by superselective embolization of superior rectal artery].

Objective: To investigate the safety and feasibility of the treatment of hemorrhoids by superselective arterial embolization. Methods: The clinical data of 15 patients with grade Ⅱ to Ⅳ hemorrhoids were collected who were treated by superselective SRA embolization.According to the number and shape of SRA in the vicinity of the dentate line, chosed coils, PVA particles and gelfoam particles, ethanol and bletilla mixture of gelfoam particles for embolization.And intraoperative operations, postoperative complications, follow-up treatment results were observed. Results: The interventional procedures were successfully accomplished in all 15 cases.The operation time was (30±14) min, and the hospital stay was 1-7 (2.0±1.8) days after operation, and the patients recovered to normal life in 12 hours after the operation.Tenesmus (14/15), pain (5/15) and low fever (11/15) can alleviate without special treatment. All patients were follow up (19.0±2.6) months, bleeding symptoms were cured, there's no serious complications. Conclusion: The treatment of hemorrhoids by transcatheter superselective embolization of superior rectal artery is technically safe and feasible.

The role of lymphocyte count in the early diagnosis of surgical site infection following posterior lumbar fusion.

OBJECTIVE: This study aimed to explore the early diagnostic value of lymphocyte count in the early diagnosis of surgical site infection (SSI) following posterior lumbar fusion. PATIENTS AND METHODS: In this study, we retrospectively analyzed the data from a total of 37 patients with lumbar SSI from Guizhou  Province Orthopaedic Hospital and Nanyang Central Hospital, 2008.1-2018.11, and 104 patients without SSI. We analyzed the C-reactive protein (CRP) level, white blood cell count (WBC) and differential count before instrumented lumbar fusion at 3 and 7 days postoperatively. The significance of the differences was evaluated by one-way ANOVA, followed by Fisher's test. The parameters mentioned above were analyzed on postoperative days 3 and 7 using the receiver operating characteristic curve and the area under the curve (AUC). Furthermore, the analyses were conducted by SPSS 22.0 software. RESULTS: The lymphocyte count in the SSI group on postoperative day 3 was significantly lower than that in the no-SSI group after surgery (p=0.000). According to the ROC curve analysis of related parameters on postoperative day 3, the AUC value of lymphocytes (0.840) was significantly larger than the AUC value of C-reactive protein (0.749). CONCLUSIONS: The lymphocyte count and C-reactive protein level on postoperative day 3 are reliable predictors of infection.

Dictyostelium discoideum lipids modulate cell-cell cohesion and cyclic AMP signaling.

During Dictyostelium discoideum development, cell-cell communication is mediated through cyclic AMP (cAMP)-induced cAMP synthesis and secretion (cAMP signaling) and cell-cell contact. Cell-cell contact elicits cAMP secretion and modulates the magnitude of a subsequent cAMP signaling response (D. R. Fontana and P. L. Price, Differentiation 41:184-192, 1989), demonstrating that cell-cell contact and cAMP signaling are not independent events. To identify components involved in the contact-mediated modulation of cAMP signaling, amoebal membranes were added to aggregation-competent amoebae in suspension. The membranes from aggregation-competent amoebae inhibited cAMP signaling at all concentrations tested, while the membranes from vegetative amoebae exhibited a concentration-dependent enhancement or inhibition of cAMP signaling. Membrane lipids inhibited cAMP signaling at all concentrations tested. The lipids abolished cAMP signaling by blocking cAMP-induced adenylyl cyclase activation. The membrane lipids also inhibited amoeba-amoeba cohesion at concentrations comparable to those which inhibited cAMP signaling. The phospholipids and neutral lipids decreased cohesion and inhibited the cAMP signaling response. The glycolipid/sulfolipid fraction enhanced cohesion and cAMP signaling. Caffeine, a known inhibitor of cAMP-induced adenylyl cyclase activation, inhibited amoeba-amoeba cohesion. These studies demonstrate that endogenous lipids are capable of modulating amoeba-amoeba cohesion and cAMP-induced activation of the adenylyl cyclase. These results suggest that cohesion may modulate cAMP-induced adenylyl cyclase activation. Because the complete elimination of cohesion is accompanied by the complete elimination of cAMP signaling, these results further suggest that cohesion may be necessary for cAMP-induced adenylyl cyclase activation in D. discoideum.

Simultaneous multicompartment intracellular Ca2+ measurements in the perfused heart using 19F NMR spectroscopy.

Although Ca2+ transport regulation at subcellular organelles is of great interest, only limited methodology has been available for measuring organellar [Ca2+] levels. The present study employs the 19F NMR resonance frequency of 4F-BAPTA to measure free [Ca2+]. In 4F-BAPTA loaded perfused rabbit hearts, two 19F NMR resonances were clearly observed. The frequency of one was consistent with cytosolic [Ca2+] levels. Responses to agents that after sarcoplasmic reticulum function identified the other resonance as originating from that organelle. The experiments demonstrate the utility of NMR shift indicator methodology in obtaining simultaneous multi-compartment intracellular [Ca2+] measurements and in enabling organellar [Ca2+] measurements to be made from within intact living tissue.

Nuclear magnetic resonance studies of cationic and energetic alterations with oxidant stress in the perfused heart. Modulation with pyruvate and lactate.

The postischemic generation of oxygen-derived free radicals may contribute to myocardial reperfusion injury by affecting sarcolemmal ion transport. Recent evidence indicates that exposure to reactive oxygen intermediates induces rapid increases in myocardial cytosolic free Ca2+ (Ca2+i). The mechanism is undetermined but may involve disturbances in Na+ homeostasis. We tested this hypothesis by interleaving 23Na and 31P nuclear magnetic resonance (NMR) measurements of Na+i and high-energy phosphates in glucose-perfused rat hearts exposed to hydroxyl radicals generated from H2O2 and Fe3+. In separate experiments, K+i and Ca2+i were measured with 39K and 19F NMR, respectively. The hearts rapidly exhibited contracture. Threefold Na+i increases and substantial K+i depletion were observed. Glycolytic inhibition was indicated by rapid sugar phosphate accumulation and cellular energy depletion. Notably, however, severe functional and energetic deterioration and substantial elevation of Ca2+i occurred before substantial Na+i accumulation or K+i depletion was observed. Further experiments investigated the ability of pyruvate to scavenge H2O2 and to protect the myocardium from oxidant stress. Pyruvate (1 or 2.5 mmol/L) dramatically attenuated functional and energetic alterations and alterations in Na+i and K+i, whereas acetate (2.5 mmol/L) offered no protection. Unlike pyruvate, lactate (5 mmol/L) has little or no capacity to scavenge H2O2 but has similar protective effects. In conclusion, pyruvate effectively protects against H2O2/Fe3+, largely by direct H2O2 scavenging. Protection with lactate may involve intracellular pyruvate augmentation. Without exogenous pyruvate or lactate, myocardial Na+ homeostasis can be substantially altered by oxidant stress, possibly via cellular energy depletion. Excess Na+i accumulation may, in turn, hasten metabolic and functional deterioration, but a causal link with the initial alterations in function or Ca2+i was not supported.

23Na and 31P nuclear magnetic resonance studies of ischemia-induced ventricular fibrillation. Alterations of intracellular Na+ and cellular energy.

To clarify the role of Na+i, pHi, and high-energy phosphate (HEP) levels in the initiation and maintenance of ischemia-induced ventricular fibrillation (VF), interleaved 23Na and 31P nuclear magnetic resonance spectra were collected on perfused rat hearts during low-flow ischemia (51 minutes, 1.2 mL/g wet wt). When untreated, 50% of the hearts from normal (sham) rats and 89% of the hypertrophied hearts from aorticbanded (band) rats (P < .01 versus sham) exhibited VF. Phosphocreatine content was significantly higher in sham than band hearts during control perfusion (53.3 +/- 1.6 versus 39.8 +/- 2.0 mumol/g dry wt). Before VF at 20 minutes of ischemia, Na+i accumulation was greater in hearts that eventually developed VF than in hearts that did not develop VF for both band and sham groups (144% versus 128% of control in sham; P < .005) and was the strongest metabolic predictor of VF; ATP depletion was also greater for VF hearts in the sham group. Infusion of the Na(+)-H+ exchange inhibitor 5-(N,N-hexamethylene)-amiloride prevented VF in sham and band hearts; reduced Na+i accumulation but similar HEP depletion were observed compared with VF hearts before the onset of VF. Rapid changes in Na+i, pHi, and HEP began with VF, resulting in intracellular Na+i overload (approximately 300% of control) and increased HEP depletion. A delayed postischemic functional recovery occurred in VF hearts, which correlated temporally with the recovery of Na+i. In conclusion, alterations in Na+i were associated with spontaneous VF transitions, consistent with involvement of excess Na+i accumulation in VF initiation and maintenance and with previously reported alterations in Ca2+i with VF.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of K(atp)channel activation on myocardial cationic and energetic status during ischemia and reperfusion: role in cardioprotection.

The role of cation and cellular energy homeostasis in ATP-sensitive K(+)(K(ATP)) channel-induced cardioprotection is poorly understood. To evaluate this, rapidly interleaved(23)Na and(31)P NMR spectra were acquired from isolated rat hearts exposed to direct K(ATP)channel activation from nicorandil or pinacidil. Nicorandil attenuated ATP depletion and intracellular Na(+)(Na(+)(i)) accumulation, delayed the progression of acidosis during zero-flow ischemia and prevented ischemic contracture. The K(ATP)channel inhibitor 5-hydroxydecanoate abolished these effects. Pinacidil did not alter Na(+)(i)accumulation, ATP depletion or pH during ischemia under the conditions employed. Both agonists greatly improved the post-ischemic functional recovery. Both agonists also dramatically improved the rate and extent of the reperfusion recoveries of Na(+)(i), PCr and ATP. The Na(+)(i)and PCr reperfusion recovery rates were tightly correlated, suggesting a causal relationship. Separate atomic absorption tissue Ca(2+)measurements revealed a marked reperfusion Ca(2+)uptake, which was reduced two-fold by pinacidil. In conclusion, these results clearly indicate that while K(ATP)channel-induced metabolic alterations can vary, the functional cardioprotection resulting from this form of pharmacological preconditioning does not require attenuation of acidosis, cellular energy depletion, or Na(+)(i)accumulation during ischemia. Rather than preservation of cationic/energetic status during ischemia, the cardioprotective processes may involve a preserved capability for its rapid restoration during reperfusion. The enhanced reperfusion Na(+)(i)recovery may be enabled by the improved reperfusion cellular energy state. This accelerated Na(+)(i)recovery could play an important cardioprotective role via a potential causal relationship with the reduction of reperfusion tissue Ca(2+)uptake and resultant reperfusion injury.

NMR measurements of Na+ and cellular energy in ischemic rat heart: role of Na(+)-H+ exchange.

Interleaved 23Na- and 31P-nuclear magnetic resonance (NMR) spectra were continuously collected on perfused rat hearts subjected to low-flow ischemia (30 min, 10% flow) or zero-flow ischemia (21 min) followed by reperfusion. During untreated low-flow and zero-flow ischemia, intracellular Na+ (Nai+) increased by 53 +/- 11 (+/- SE) and 78 +/- 8%, respectively, and remained elevated for zero-flow hearts. However, during both low- and zero-flow ischemia, Nai+ did not increase in hearts treated with the Na(+)-H+ exchange inhibitor, 5-(N-ethyl-N-isopropyl)amiloride (EIPA). The pH decreases during ischemia were unchanged. EIPA treatment reduced ATP depletion during ischemia. During reperfusion from zero-flow ischemia, EIPA-treated hearts displayed more rapid and extensive recoveries of phosphocreatine and ATP. Recovery of left ventricular developed pressure was improved for zero-flow hearts treated with EIPA during the ischemic period exclusively (104 +/- 13%) compared with untreated hearts (36 +/- 21%). These data indicate that Na(+)-H+ exchange is an important mechanism for Nai+ accumulation, but not for pH regulation, during myocardial ischemia. Additionally, Nai+ homeostasis plays an important role in the postischemic recovery of cellular energy and ventricular function.

Limit on the electron neutrino magnetic moment from the kuo-sheng reactor neutrino experiment.

A search of neutrino magnetic moment was carried out at the Kuo-Sheng Nuclear Power Station at a distance of 28 m from the 2.9 GW reactor core. With a high purity germanium detector of mass 1.06 kg surrounded by scintillating NaI(Tl) and CsI(Tl) crystals as anti-Compton detectors, a detection threshold of 5 keV and a background level of 1 kg(-1) keV(-1) day(-1) at 12-60 keV were achieved. Based on 4712 and 1250 h of reactor ON and OFF data, respectively, the limit on the neutrino magnetic moment of mu(nu;(e))<1.3x10(-10)mu(B) at 90% confidence level was derived. An indirect bound of the nu;(e) radiative lifetime of m(3)(nu)tau(nu)>2.8x10(18) eV(3) s can be inferred.