Advantages of unilateral percutaneous kyphoplasty for osteoporotic vertebral compression fractures-a systematic review and meta-analysis.

Data from English randomized controlled trials comparing unilateral versus bilateral PKP for the treatment of OVCFs were retrieved and analyzed, and the results showed that unilateral PKP is a better choice for the treatment of patients with OVCFs, which will provide a reliable clinical rationale for the treatment of OVCFs. PURPOSE: To investigate the advantages of unilateral percutaneous kyphoplasty (PKP) for the treatment of osteoporotic vertebral compression fractures(OVCFs). METHODS: The systematic evaluation program met all program requirements (CRD 42023422383) by successfully passing the PROSPERO International Prospective Systematic Evaluation Registry. Researchers searched the references of English-language randomized controlled trials comparing unilateral and bilateral PKP for the treatment of osteoporotic vertebral compression fractures published between 2010 and 2023 and manually searched for known primary and review articles. The study statistically analyzed data from all the included literature, which primarily included time to surgery, visual pain score(VAS) and Oswestry disability index(ODI) at postoperative follow-up time points, polymethylmethacrylate (PMMA, bone cement) injection dose, cement leakage, radiation dose, and improvement in kyphotic angle. RESULTS: This meta-analysis searched 416 articles published from 2010 to 2023 based on keywords, and 18 articles were finally included in this study. The results of the forest plot showed that unilateral PKP operative time, amount of bone cement used, and radiation dose to the patient were significantly reduced (p < 0.01, p < 0.01, and p < 0.01, respectively), and unilateral and bilateral PKP had comparable cement leakage (p = 0.49, 95% CI = 0.58-1.30), and there was no significant difference in the kyphotic angle between unilateral and bilateral PKP (p = 0.42, 95% CI = - 2.29-0.96). During follow-up, there was no significant difference in pain relief between unilateral and bilateral PKP (p = 0.70, 95% CI = - 0.09-0.06), nor was there a significant difference in ODI (p = 0.27, 95% CI = - 0.35-1.24). CONCLUSIONS: There is no difference in clinical efficacy between unilateral PKP and bilateral PKP, but unilateral PKP has a shorter operative time, a lower incidence of cement leakage, a lower amount of cement, and a lower radiation dose to the patient and operator. Unilateral PKP is a better option for patients with OVCFs.

Communication: crystallite nucleation in supercooled glycerol near the glass transition.

Heterogeneity and solid-like structures found near the glass transition provide a key to a better understanding of supercooled liquids and of the glass transition. However, the formation of solid-like structures and its effect on spatial heterogeneity in supercooled liquids is neither well documented nor well understood. In this work, we reveal the crystalline nature of the solid-like structures in supercooled glycerol by means of neutron scattering. The results indicate that inhomogeneous nucleation happens at temperatures near T(g). Nevertheless, the thermal history of the sample is essential for crystallization. This implies such structures in supercooled liquids strongly depend on thermal history. Our work suggests that different thermal histories may lead to different structures and therefore to different length and time scales of heterogeneity near the glass transition.

Novel biodegradable α-TCP/poly(amino acid) composite artificial lamina following spinal surgery for prevention of intraspinal scar adhesion.

Biodegradable copolymer α-TCP/poly(amino acid) composite artificial lamina was prepared and used in goat cervical vertebra resection repair. Cervical 4 was removed by laminectomy, and a vertebra defect of 27 × 9 mm was made. α-TCP/poly(amino acid) composite artificial lamina was inserted in the test group. The efficiency of the copolymer during repair and reconstruction of the goats' vertebra was tested by using X-ray, CT scanning, and histological and biomechanical measurements. In the 24 weeks following the operation, the artificial lamina refrained from shifting, and no dural adhesion pressure was observed. In contrast, the control group suffered from infiltration of soft tissue in the spinal canal, dural pressure and α-TCP/poly(amino acid) degradation. In conclusion, α-TCP/poly(amino acid) composite artificial lamina can significantly prevent scar tissue from infiltrating the spinal canal.

Haloterrigena daqingensis sp. nov., an extremely haloalkaliphilic archaeon isolated from a saline-alkaline soil.

A haloalkaliphilic archaeon, strain JX313(T), was isolated from a saline-alkaline soil from Daqing, Heilongjiang Province, China. Its morphological, physiological and biochemical features and 16S rRNA gene sequence were determined. Colonies of the strain were orange-red and cells were non-motile cocci and Gram-stain-variable. The strain required at least 1.7 M NaCl for growth, with optimal growth occurring in 2.0-2.5 M NaCl. Growth was observed at 20-50°C and pH 8.0-10.5, with optimal growth at 35°C and pH 10.0. The G+C content of its genomic DNA was 59.3 mol%. Phylogenetic analysis of 16S rRNA gene sequences showed that strain JX313(T) is associated with the genera Haloterrigena and Natrinema and is most closely related to Haloterrigena salina XH-65(T) (96.2  % sequence similarity) and Haloterrigena hispanica FP1(T) (96.2 %). DNA-DNA hybridization experiments revealed that the relatedness of strain JX313(T) to type strains of related species of the genus Haloterrigena or Natrinema was less than 50 %. Furthermore, the cellular polar lipids of strain JX313(T), identified as phosphatidylglycerol, phosphatidylglycerol phosphate methyl ester and mannose-2,6-disulfate (1→2)-glucose glycerol diether (S2-DGD), were consistent with the polar lipid characteristics of the genus Haloterrigena. Therefore, phylogenetic analysis, phenotypic assessment and chemotaxonomic data showed that JX313(T) represents a novel species within the genus Haloterrigena, for which the name Haloterrigena daqingensis sp. nov. is proposed. The type strain is JX313(T) (=CGMCC 1.8909(T) =NBRC 105739(T)).

[Effects of gensenoside Rg1 on tau protein phosphorylation induced by okadaic acid in rat brain slices].

OBJECTIVE: To investigate the effects of gensenoside Rg1 on expressions of phosphorylated tau protein (P-tau), protein phosphatase 2A (PP2A) and tau protein in Alzheimer's disease-like tau phosphorylation rat brain slices, and to explore the mechanisms of gensenoside Rg1 in inhibiting tau phosphorylation. METHODS: Brains of 5-week-old Wistar rats were cut into slices which were 400 µm thick. These brain slices were randomly divided into blank control group, untreated group, low-dose ginsenoside Rg1 group, medium-dose ginsenoside Rg1 group and high-dose ginsenoside Rg1 group, with 10 slices in each group. All brain slices were cultured with artificial cerebrospinal fluid (ACSF). And brain slices in the ginsenoside R1 groups were administered with ginsenoside Rg1 (60, 120 and 240 µmol/L respectively) in ACSF for 2 h firstly. After 2-hour culture, okadaic acid (OA) was administered into ACSF of the untreated group and the ginsenoside Rg1 groups separately for 3 h to induce tau phosphorylation to prepare AD models. The concentration of OA in each group was 1 µmol/L. There was no any intervention for the brain slices in the blank control group. Expressions of P-tau, PP2A and tau proteins in the brain slices were determined by immunohistochemical method, and the results were analyzed by image acquisition and analysis system. RESULTS: Compared with the blank control group, the expression of P-tau protein was significantly increased (P<0.01) and the expressions of tau and PP2A proteins were decreased (P<0.01, P<0.05) in the untreated group. Compared with the untreated group, the expression of P-tau was significantly decreased (P<0.01) and the expressions of tau and PP2A proteins were increased (P<0.01, P<0.05) in the ginsenoside Rg1 groups, especially in the high-dose ginsenoside Rg1 group. CONCLUSION: Ginsenoside Rg1 can promote dephosphorylation of P-tau by increasing the expression of PP2A in Alzheimer's disease-like tau phosphorylation rat brain slices, so as to inhibit tau phosphorylation.

[Effects of Naoerkang on expressions of beta-amyloid peptide 1-42 and neprilysin in hippocampus in a rat model of Alzheimer's disease].

OBJECTIVE: To investigate the effects of Naoerkang (NEK), a compound traditional Chinese herbal medicine, on the expressions of beta-amyloid peptide 1-42 (Abeta(1-42)) and neprilysin (NEP) in hippocampal tissues in a rat model of Alzheimer's disease (AD). METHODS: Forty-eight male SD rats were randomly divided into normal control group, untreated group, piracetam group, low-dose NEK group, medium-dose NEK group, and high-dose NEK group, with 8 rats in each group. Five microliters of Abeta(1-42) (2 microg/microL) were injected into CA1 area of hippocampus in rat to establish AD model whereas the normal control rats were injected with same volume of normal saline for comparison. The rats in the NEK groups were treated respectively with high-, medium- and low-dose [60, 30, 15 g/(kg.d)] NEK for 28 days consecutively; piracetam [0.375 g/(kg.d)] was intragastrically administered to rats in the piracetam group; and normal saline was applied in the control and untreated groups. Y-maze test was used for behavioral study to test the learning and memory abilities of rats in different groups. The expressions of Abeta(1-42) and NEP in hippocampus were determined by immunohistochemical method, and the results were analyzed by image acquisition and analysis system. RESULTS: Injection of Abeta(1-42) could induce learning and memory dysfunction and up-regulate Abeta(1-42) expression in hippocampal tissue in rats of the untreated group. Compared with the normal control group, the abilities of learning and memory of rats in the untreated group were significantly decreased (P<0.01) and the expression of Abeta(1-42) was significantly increased (P<0.01) after model establishment. After 28-day administration of NEK and piracetam, the abilities of learning and memory of AD rats in piracetam and low-dose, medium-dose and high-dose NEK groups were significantly improved as compared with the untreated group (P<0.01 or P<0.05); the expression of Abeta(1-42) in hippocampal tissues was decreased (P<0.01 or P<0.05) and the expression of NEP was increased (P<0.01 or P<0.05), especially in the high-dose NEK group. CONCLUSION: NEK can play the role of anti-dementia by increasing the expression of NEP in hippocampal tissues of AD rats so as to reduce the quantity of AAbeta(1-42) and by improving the ability of learning and memory of rats with AD.

[Expression of p38MAPK in the olfactory bulb of rats with Alzheimer's disease].

OBJECTIVE: To identify the changes of expression of p38MAPK in the olfactory bulb (OB) of rats with Alzheimer's Disease (AD) and to explore the functional mechanism of p38MAPK in the pathological changes of AD. METHODS: AD animal model was established by injecting amyloid-beta peptide 25-35 into the lateral cerebral ventricle of rats. The learning and memory abilities of rats were measured by Y-maze experiment. The expressions of p38MAPK in the OBs of rats in the AD group, saline control group, p38MAPK inhibitor group and inhibitor control (con-inhibitor) group were examined by immunohistochemistry. RESULTS: (1) The capabilities of learning and memory of the rats were impaired significantly at day 7 and day 14 after the induction of AD. Significant learning and memory differences were found (P < 0.05) between the AD group and the other groups. (2) The expression of p38MAPK in the OBs of rats was found at day 4 after the induction of AD. The expression increased with time. The AD rats had more positive p38MAPK cells than those in the saline controls (P < 0.05). The expression of phospho-p38MAPK in the rats with AD increased significantly (P < 0.01) compared with those in the saline group. The AD rats treated with p38MAPK inhibitor had less expression of phospho-p38MAPK than those in the AD group and the inhibitor control (P < 0.01). CONCLUSIONS; Abeta25-35 can activate p38MAPK signal transduction pathway. p38MAPK may play a role in the formation of dysosmia in AD. SB203580, a p38MAPK inhibitor, can reduce the neurotoxicity evoked by p38MAPK.

[Progress of research on effects of ginsenoside Rg1 in promoting capability of learning and memory].

It is testified by long-standing traditional Chinese medicine clinical practice that ginseng was effective in treating dementia and promoting capability of learning and memory, for which ginsenoside Rg1 has been proved the main effective ingredient. Recently many researches have been carried out on the mechanism and action links of ginsenoside Rg1, and illustrated that it could exert the anti-dementia and nootropic effects through intervening multiple targets and links, thus to provide a theoretical basis for bettering the clinical use of ginsenoside Rg1.

[The clinical causes of the thoracic ossification of ligamentum flavum].

OBJECTIVE: To assess the different causes of thoracic ossification of the ligamentum flavum (TOLF). METHODS: From July 1989 to November 2005, 142 cases were diagnosed the TOLF, in which 121 were operated. The lesions were classified into three types on the basis of the clinical result: (1) In such primary group (Group 1, 90 cases), without incorporation disease and Ca, P and AKP was all normal; (2) In systemic ossified TOLF group (Group 2, 30 cases), 6 cases ankylosing spondylitis, 3 cases DISH, 10 cases fluorosis, 11 cases OPLL; (3) In local spine disease group (Group 3, 22 cases), 5 cases fracture in spine, 4 cases spine TB, 13 cases posterior marginal intraosseous cartilaginous node. Such clinical feature was analysed, moreover surveyed the thoracic kyphosis angle, upper thoracic kyphosis angle, lower thoracic kyphosis angle and the vertebra body wedge change. The effect was assessed using Epstein Scale. RESULTS: (1) In Group 1, the mainly type was connected type (67/90, 74%). The ossified ligamentum flavum was mainly located at the lower thoracic and thoracic-lumber levels. The local type was less. In Group 2, the mainly type was connected type (21/30, 70%). The local type was none. The lesions figure was the most. In Group 3, the local type was the most (18/22, 82%). (2) In Group 1, the ossified ligamentum flavum was mainly located at the upper and lower thoracic levels (225/486, 47%). In Group 2, mainly located at the whole thoracic, some include cervix and lumber. In Group 3, mainly location was related with the location of primary disease. (3) In group 1, the curve was normal in 81% (73/90) of cases. In Group 2, the curve was abnormal in 87% (26/30) of cases. In Group 3, the curve was normal in the 82% (18/22) of cases. CONCLUSIONS: The TOLF relates with systemic ossify disease, the change of load on the spine, aging and so on. It should be classified according to its causes.

[The research of bone morphogenetic protein expression, CT value and mature degree of ossification in the thoracic ossification of ligamentum flavum].

OBJECTIVE: To investigate the correlation of pathology, bone morphogentic protein (BMP) expression, CT value with the ossification of thoracic ligamentum flavum (TOLF) to afford the evidence to choose appropriate treatment methods. METHODS: Twenty-three patients aged 35 - 65 years old had TOLF in my hospital as case. Their courses of disease were 2 months to 9 years. The values of blood calcium, blood phosphorus and AKP in them were normal. The 5 peoples aged 21 - 35 years old who presented fracture of thoracic but not the ligamentum flavum ossification were selected as control. We excluded those who have DISH, ankylosing spondylitis, fluorosis and other disease related with TOLF. The lesion locus were scanned and mensurated by CT. The pathology characteristics were classified into immature ossification and mature ossification by general observation, histology examination. BMP were measured by the immunohistochemical (IHC) staining techniques. RESULTS: The CT value was significantly higher in the case group (547.2 +/- 131.4) than controlled group (137.7 +/- 10.6) (t = 6.922, P = 0.000). Further, the CT value in the mature ossification (702.9 +/- 17.7) was significantly higher than the immature (480.5 +/- 180.2) (t = 5.623, P = 0.000). In addition, BMP both expressed negative in the mature ossification and the controlled group, but positive in the immature ossification. BMP expression was significantly different between the immature ossification and the mature (chi2 = 70.000, P = 0.000). CONCLUSIONS: The CT values, pathological types and BMP expression results are similar to evaluate the ossification degrees of ligamentum flavum, and then could be indirectly judged the maturation degrees of TOLF by CT to confirm the treatment methods before operation.

Ginsenoside Rg1 inhibits high-voltage-activated calcium channel currents in hippocampal neurons of beta-amyloid peptide-exposed rat brain slices.

OBJECTIVE: To examine whether ginsenoside Rg1 (Rg1) inhibits the high-voltage-activated calcium currents (ICa,HVA) via mitogen-activated protein kinase (MAPK) in hippocampal neurons in rat brain slices exposed to beta-amyloid peptide 25-35 (Aß25-35). METHODS: An experimental Alzheimer disease (AD) model was prepared by exposure of rat brain slices to Aß25-35 (10 µmol/L). After treatment with Rg1 (20 µmol/L), the ICa,HVA elicited in hippocampal neurons in these rat brain slices upon depolarization from-40 to 40 mV for 200 ms was recorded by a whole-cell patch clamp to analyze the changes in the peak current density, I-V curve, activation-V curve, and inactivation-V curve. RESULTS: Exposure of rat brain slices to Aß led to a significant increase in ICa,HVA, enhancement of the voltage sensitivity of channel activation, and reduction of the voltage sensitivity of channel inactivation in neurons in the hippocampus of rat brain slices. Rg1 treatment significantly inhibited these changes. These effects of Rg1 could be effectively inhibited by the MAPK inhibitor PD98059. CONCLUSION: Rg1 can inhibit Ica,HVA via MAPK in hippocampal neurons in Aß-exposed rat brain slices.

[Observation of the promotion effect taurine on hepatic stellate cell's apoptosis in rat hepatic fibrosis model].

OBJECTIVE: To observe the effect of taurine on hepatic stellate cell's apoptosis induced by carbon tetrachloride (CCl4) in rats and to study its protective mechanisms. METHODS: CCl4-induced rat hepatic fibrosis was treated by taurine. Serum alanine aminotransferase (ALT), plasma protein, hyaluronic acid (HA), procollagen III (PC III), hepatic microsomal drug-metabolizing enzyme and anti-transforming growth factor beta1 (TGF-beta1) were determined. In addition, hepatic stellate cell's apoptosis and the pathological changes of liver tissue were observed under light microscope. RESULTS: The activity of serum ALT and the levels of serum HA, PC III were markedly reduced by taurine treatment. The hepatic cytochrome P450 (Cyt. P450) and cytochrome b5 (Cytb5) contents were increased by the same treatment. In addition, taurine could significantly inhibit the expression of TGF-beta1, promote the hepatic stellate cell's apoptosis, and relieve hepatic fibrosis. CONCLUSION: Taurine fulfills a role in promoting hepatic stellate cell's apoptosis in the case of hepatic fibrosis, it mitigates the liver injury, decreases the expression of TGF-beta1, and relieves hepatic fibrosis.

Scavenging effect of Naoerkang on amyloid beta-peptide deposition in the hippocampus in a rat model of Alzheimer's disease.

OBJECTIVE: To observe the effect of a Chinese medicine compound, Naoerkang (NEK), on amyloid-beta peptide (1-42; Aß(1-42)) and matrix metalloproteinase-9 (MMP-9) expressions in the hippocampus of Alzheimer's disease (AD) model rats. METHODS: A total of 48 male Sprague Dawley (SD) rats were randomly divided into normal control, untreated, and piracetam groups, and low-dose, medium-dose, and high-dose NEK groups, with 8 rats in each group. The 5-µL aggregated Aß(1-42) (2 µg/µL) were injected into both CA1 areas of the hippocampus in the rats to establish an AD model, whereas the normal control was treated with the same dose of normal saline. The rats in the NEK groups were treated with a high, medium, or low dose of NEK [60 g/(kg·d), 30 g/(kg·d), and 15 g/(kg·d)], respectively, intragastrically for 28 days; piracetam (0.375 g/kg, intragastrically) was consecutively administered in the piracetam group; and normal saline was applied in the normal control and untreated groups. A Y-maze test was used for behavioral study to test the learning and memory abilities. Aß(1-42) and MMP-9 expressions in the hippocampus was determined immunohistochemically, and the results were analyzed by image acquisition and an analysis system. RESULTS: Aggregated Aß(1-42) induced obvious learning and memory dysfunction, as well as up-regulation of Aß(1-42) expression in the hippocampus. Compared with those in the normal control group, the learning and memory abilities of rats in the untreated group significantly decreased (P<0.01), and the expression of Aß(1-42) was significantly increased (P<0.01). Twenty-eight days after different treatments, compared with those in the untreated group, the learning and memory abilities of AD model rats in the piracetam, low-dose, medium-dose and high-dose NEK groups were significantly improved (P<0.01 or P<0.05), and the expression of Aß(1-42) in the hippocampus decreased (P<0.01 or P<0.05), and MMP-9 increased (P<0.01 or P<0.05), especially in the high-dose NEK group. CONCLUSION: NEK might play a role of anti-dementia by increasing the expression of MMP-9 in the hippocampus of AD model rats, resulting in the reduction of the quantity of Aß(1-42) and improvement in learning and memory ability in AD model rats.

[Expression of p38MAPK in the hippocampal CA1 region of rats with Abeta25-35-induced Alzheimer disease].

OBJECTIVE: To investigate the changes of p38MAPK expression in a rat model of Alzheimer disease (AD). METHODS: Seventy-two adult SD rats were randomized equally into 4 groups, and a single-dose injection of Abeta25-35 (dementia group), normal saline (saline group), SB203580 (inhibitor group), or DMSO (inhibitor control group) was administered into the lateral cerebral ventricle. Y-maze tast was performed to evaluate the behavioral changes of the rats after the injections, and on days 4, 7 and 14 after the injection, p38MAPK expression in the hippocampal CA1 area was measured by means of immunohistochemistry. RESULTS: On days 7 and 14 following Abeta25-35 injection, the training times, error number and total reaction time were significantly higher in dementia group than in saline group (P<0.05), but all these indices were significantly lowered in the inhibitor group as compared with the dementia group (P<0.05). Immunohistochemistry revealed obvious p38 expression in the dementia group 4 days after Abeta25-35 injection, which increased significantly with the passage of time (P<0.01). The gray scale in the inhibitor group was significantly higher than that in the dementia group (P<0.01). CONCLUSION: p38MAPK activation in the hippocampal CA1 area is an event that persists during the entire course of Abeta25-35-induced AD in rats, and the inhibitor SB203580 prevents p38MAPK expression and improves the learning and memory abilities of the rats.