Protective effect of betaine against lead-induced testicular toxicity in male mice.

Lead (Pb) is an environmental toxicant reported to impair male reproductive system. Betaine is a natural product which has promising beneficial effects against oxidative stress. In this experimental study, we evaluated the ameliorative effect of betaine on sperm quality and oxidative stress induced by lead (Pb) in the testis of adult male mice. Sixty male Kunming mice were divided equally into four groups: control group, betaine group (1% in drinking water), lead group (100 mg kg-1  bw-1  day-1 ) and betaine + lead group. In the last group, mice were supplemented with betaine for two weeks prior to the initiation of lead treatment and concurrently during lead treatment for 3 weeks until sacrificed. Our results indicated that in the lead-administrated group, body weights together with sperm count were significantly decreased (p < .05). The numbers of abnormal sperms were found to be higher in lead-treated mice. The activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (Cat) were significantly reduced, while the level of malondialdehyde (MDA) content was increased in the testis tissue following lead treatment. The mRNA levels of antioxidant-related genes (SOD1, GPX1 and CAT) were significantly decreased in the lead group. Betaine enhanced these parameters in betaine + lead group. In testis histology span, Johnson score was decreased (p < .05) in lead group and co-treatment with betaine increased Johnson score significantly in betaine + lead group. These results indicate that betaine improves sperm quality and ameliorate oxidative damage in testis of mice exposed to lead.

SIRT7 Regulates Lipopolysaccharide-Induced Inflammatory Injury by Suppressing the NF-κB Signaling Pathway.

Mastitis has severely affected the cattle industry worldwide and has resulted in decreased dairy production and cattle reproduction. Although prevention and treatment methods have been implemented for decades, cattle mastitis is still an intractable disease. Sirtuin 7 (SIRT7) is an NAD+-dependent deacetylase that is involved in various biological processes, including ribosomal RNA synthesis and protein synthesis, DNA damage response, metabolism, and tumorigenesis. However, whether SIRT7 participates in inflammation remains unknown. Our results revealed that SIRT7 is downregulated in tissue samples from mastitic cattle. Therefore, we isolated dairy cow mammary epithelial cells (DCMECs) from breast tissues and developed an in vitro model of lipopolysaccharide- (LPS-) induced inflammation to examine SIRT7 function and its potential role in inflammation. We showed that SIRT7 was significantly downregulated in LPS-treated DCMECs. SIRT7 knockdown significantly increased the LPS-stimulated production of inflammatory mediators, like reactive oxygen and nitric oxide, and upregulated TAB1 and TLR4. In addition, SIRT7 knockdown significantly increased the phosphorylation of TAK1 and NF-κBp65 in LPS-treated DCMECs. Moreover, SIRT7 knockdown promoted the translocation of NF-κBp-p65 to the cell nucleus and then increased the secretion of inflammatory cytokines (IL-1ß and IL-6). In contrast, SIRT7 overexpression had the opposite effects when compared to SIRT7 knockdown in LPS-treated DCMECs. In addition, SIRT7 overexpression attenuated LPS-induced DCMEC apoptosis. Taken together, our results indicate that SIRT7 can suppress LPS-induced inflammation and apoptosis via the NF-κB signaling pathway. Therefore, SIRT7 may be considered as a potential pharmacological target for clinical mastitis therapy.

Heme oxygenase 1 regulates apoptosis induced by heat stress in bovine ovarian granulosa cells via the ERK1/2 pathway.

Heat stress can inhibit follicular development in dairy cows, and thus can affect their reproductive performance. Follicular granulosa cells can synthesize estrogen, that affects the development and differentiation of follicles by apoptosis. Heme oxygenase 1 (HO-1/heat shock protein 32) plays an antiapoptotic and cytoprotective role in various cells during stress-induced apoptosis, but little is known about its definitive function in bovine (ovarian) granulosa cells (bGCs). In our study, the roles and mechanism of HO-1 on the heat stress-induced apoptosis of bGCs were studied. Our results show that the expression of HO-1 was significantly increased under heat stress. Moreover, HO-1 silencing increased apoptosis, whereas its overexpression dampened apoptosis by regulating the expression of Bax/Bcl-2 and the levels of cleaved caspase-3. In addition, HO-1 can also play a cytoprotective role by affecting estrogen levels and decomposing heme to produce biologically active metabolite carbon monoxide (CO). Meanwhile, CO significantly increased the level of HO-1, decreased Bax/Bcl-2 levels, and inhibited the activation of extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway. The apoptosis of ovarian GCs can affect the secretion of estrogen and lead to disorder of the ovarian microenvironment, thus affecting the normal function of the ovary. Our results indicate that HO-1 acts as a cytoprotective enzyme and plays a protective role in heat-induced apoptosis of bGCs. In conclusion, HO-1 and its metabolite CO inhibit the apoptosis of bGCs induced by heat stress through the ERK1/2 pathway. The results of this study provide a valuable clue for improving the fertility of heat stressed cows in summer.

SIRT7 depletion inhibits cell proliferation, migration, and increases drug sensitivity by activating p38MAPK in breast cancer cells.

SIRT7 is a member of the sirtuin family of proteins that are known to be associated with tumor development. However, the functional roles and molecular mechanisms underlying the function of SIRT7 in breast cancer cell survival and tumor development remain unclear. Recent studies demonstrated that SIRT7 is upregulated in breast cancer cells and tissues. In the present study, we systematically explored the roles of SIRT7 in the growth of breast cancer cells and tumors both in vitro and in vivo. Our results showed that SIRT7 plays a major role in facilitating cell survival by promoting cell proliferation and inhibiting apoptosis. SIRT7 depletion significantly inhibited cell invasion and wound healing by blocking cell cycle progression and inducing cell apoptosis. Meanwhile, SIRT7 depletion can increase the sensitivity of breast cancer cells to doxorubicin (DOX). Xenograft model studies showed that stable silencing of SIRT7 inhibited tumor growth and enhanced tumor sensitivity to DOX. Further research revealed that p38MAPK is involved in SIRT7-mediated regulation of breast cancer cell proliferation and tumor growth. Taken together, our results showed that SIRT7 plays a critical role in breast cancer cell survival, migration, and tumor growth, and increased the efficiency of DOX treatment both in vitro and in vivo. Therefore, SIRT7 is a promising therapeutic target in breast cancer treatment.

Long noncoding RNA and mRNA profiling in MDA-MB-231 cells following RNAi-mediated knockdown of SIRT7.

Breast cancer is one of the most common malignant cancers among women and a major clinical obstacle. Although studies have reported the abnormal expression of SIRT7 in breast cancer, whether the function of SIRT7 regulates the expression of long noncoding RNAs (lncRNAs) in breast cancer remains unknown. We aimed to determine the differential expressions of mRNAs and lncRNAs associated with SIRT7 and understand the regulatory mechanism of SIRT7 in breast cancer. RNA sequencing was performed to explore the transcriptome in MDA-MB-231 cells after SIRT7 depletion, and a total of 50,634 different transcripts were identified. In comparison with the negative control, siSIRT7 groups showed 240 differentially expressed mRNAs and 26 differentially expressed lncRNAs. Gene ontology analysis revealed that the differentially expressed mRNAs mainly regulated DNA replication, CXCR chemokine receptor binding, and maturation of large subunit rRNA from tricistronic rRNA transcript, nucleoplasm, mitochondrion, and NAD+ ADP-ribosyltransferase activity. Kyoto Encyclopedia of Genes and Genomes analysis showed that the differentially expressed mRNAs were mainly involved in pathways associated with MAPK signaling pathway, tumor necrosis factor signaling pathway, hepatitis B, and cancer. Moreover, the target genes of the differentially expressed lncRNAs mainly regulated the carboxylic acid metabolic processes and were involved in glycolysis pathway. The mRNA-lncRNA coexpression network comprised 186 mRNAs and 23 lncRNAs. Our results provide essential data regarding differentially expressed lncRNAs and mRNAs after the depletion of SIRT7 in breast cancer cells, which may be useful to elucidate the role of SIRT7 in breast cancer development.

Changes in expression and production of heme oxygenase-1 in rats with acute liver injury induced by lipopolysaccharide.

To investigate the changes of heme oxygenase-1 (HO-1) expression and production in rats with acute liver injury induced by lipopolysaccharide (LPS), and explore the role of HO-1 in the pathogenesis of liver injury. Liver injury was assessed histologically and the serum level of alanine transaminase (ALT) and aspartate transaminase (AST) were examined. The activity of super oxide dismutase (SOD) and the content of malondialdehyde (MDA) and carbon monoxide (CO) in liver tissues were also examined at the same time. HO-1 mRNA expression was examined at different time points following LPS treatment and the expression of HO-1 protein was determined by immunohistochemical staining. Administration of LPS caused severe hepatic damage, characterized by significant elevation of serum ALT and AST levels and hepatic MDA content as well as a remarkable reduction of liver SOD activity at 24 hr as compared with those in the control group. HO-1 activity was elevated significantly after modeling, showing a time-dependent manner from 6 to 24 hr, while expression of HO-1 protein was increased remarkably from 6 to 24 hr. Endogenous CO concentration in the liver of control rats remained very low but was elevated significantly after LPS treatment (6, 12, 24 hr), which was in accordance with the changes of HO-1. HO-1 activity and protein are increased significantly in rats with acute liver injury induced by LPS, suggesting that HO-1 plays an important role in the pathogenesis of acute hepatic damage.

Heat stress impairs mice granulosa cell function by diminishing steroids production and inducing apoptosis.

Ovarian injury can be induced by heat stress. Mice granulosa cells (GCs) are critical for normal ovarian function and they synthesize a variety of growth factors and steroids for the follicle. Furthermore, the growth, differentiation, and maturate of theca cells and oocyte are dependent upon the synthesis of GCs. Due to the critical biological functions of GCs, we hypothesized that the apoptosis and dysfunction of GCs could also be induced by heat stress. We analyzed GCs apoptosis and evaluated the expression of apoptosis-related genes (caspase-3, Bax, Bcl-2) after heat treatment. Radio immunity assay was used to measure the secretion of 17ß-estradiol (E2) and progesterone (P4). RT-PCR was used to evaluate the expression of steroids-related genes (Star, CYP11A1, CYP19A1). Our data suggested that heat stress inhibited GCs proliferation, induced GCs apoptosis, decreased E2 and P4 secretion, reduced the steroids-related genes mRNA expression. Besides, our results indicated that heat treatment-induced apoptosis of GCs through the mitochondrial pathway, which involved caspase-3 and Bax. The reduction in steroids secretion and mRNA expression of Star, CYP11A1, and CYP19A1 might also play a role in heat-induced GCs apoptosis and ovarian injury.

Percutaneous Kyphoplasty for Kummell Disease with Severe Spinal Canal Stenosis.

BACKGROUND: Percutaneous kyphoplasty (PKP) has been proven as an effective, minimally invasive procedure for the treatment of Kummell's disease in the early stages. However, a risk of cement leakage and further neurological damage remains during and after PKP, especially in chronic osteoporotic stage III Kummell's disease with severe spinal canal stenosis. OBJECTIVE: To evaluate the feasibility and efficacy of PKP for the treatment of chronic osteoporotic stage III Kummell's disease with severe spinal canal stenosis. STUDY DESIGN: A retrospective evaluation of postoperative radiographs. SETTING: Pain management clinic. METHODS: A retrospective study was performed on 9 patients with 11 levels managed with PKP for chronic osteoporotic stage III Kummell's disease with severe spinal canal stenosis. Clinical and radiological outcomes were assessed. RESULTS: Substantial pain relief was attained in all the patients. Both visual analogue scale (VAS) and Oswestry Disability Index (ODI) scores improved significantly from pre- to post-operation (P < 0.05), and remained unchanged at every follow-up. No neurological deterioration was found. Postoperatively, the anterior and midline vertebral body heights were significantly corrected (P < 0.05), and were sustained at the final follow-up. Similar results were seen in the correction of kyphotic angle. Neither cement leakage into the spinal canal nor further dislodging of the posterior vertebral fragments occurred. Two cases experienced subsequent fractures with one having a second PKP and the other being treated conservatively. LIMITATIONS: Retrospective study of 9 cases with 11 levels due partly to the rarity of the disorder. CONCLUSIONS: PKP is an effective, minimally invasive procedure for the treatment of chronic osteoporotic stage III Kummell's disease with severe spinal stenosis, leading to a significant relief of symptoms and improvement of functional status. INSTITUTIONAL REVIEW: This study was approved by the Institutional Review Board.

Identification and bioinformatics analysis of microRNAs associated with stress and immune response in serum of heat-stressed and normal Holstein cows.

MicroRNAs (miRNAs) are small single-stranded non-coding RNAs that have an important regulatory function in animal growth and developmental processes. However, the differential expression of miRNA and the role of these miRNAs in heat-stressed Holstein cows are still unknown. In this study, the profile of differentially expressed miRNAs and the target genes analysis in the serum of heat-stressed and normal Holstein cows were investigated by a Solexa deep-sequencing approach and bioinformatics. The data identified 52 differentially expressed miRNAs in 486 known miRNAs which were changed significantly between heat-stressed and normal Holstein cows (fold change >2, P < 0.001). Target genes analysis showed that at least 7 miRNAs (miR-19a, miR-19b, miR-146a, miR-30a-5p, miR-345-3p, miR-199a-3p, and miR-1246) were involved in the response to stress, oxidative stress, development of the immune system, and immune response among the identified 52 differentially expressed miRNAs. Five miRNAs (miR-27b, miR-181a, miR-181b, miR-26a, and miR-146b) were involved in stress and immune responses and the expression of five miRNAs was striking (P < 0.001). In addition, RT-qPCR and deep-sequencing methods showed that 8 miRNAs among the 12 selected miRNAs (miR-19a, miR-19b, miR-27b, miR-30a-5p, miR-181a, miR-181b, miR-345-3p, and miR-1246) were highly expressed in the serum of heat-stressed Holstein cows. GO and KEGG pathway analysis showed that these differentially expressed miRNAs were involved in a pathway that may differentially regulate the expression of stress response and immune response genes. Our study provides an overview of miRNAs expression profile and the interaction between miRNAs and their target genes, which will lead to further understanding of the important roles of miRNAs in heat-stressed Holstein cows.

Effects of heat stress on antioxidant defense system, inflammatory injury, and heat shock proteins of Muscovy and Pekin ducks: evidence for differential thermal sensitivities.

Rising temperatures are severely affecting the mortality, laying performance, and meat quality of duck. Our aim was to investigate the effect of acute heat stress on the expression of heat shock proteins (HSPs: HSP90, 70, 60, 40, and 10) and inflammatory factors (nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2)) and antioxidant enzyme activity (superoxide dismutase (SOD), malondialdehybe (MDA), catalase (CAT), total antioxidant capacity (T-AOC)) in livers of ducks and to compare the thermal tolerance of Pekin and Muscovy ducks exposed to acute heat stress. Ducks were exposed to heat at 39 ± 0.5 °C for 1 h and then returned to 20 °C for 1 h followed by a 3-h recovery period. The liver and other tissues were collected from each individual for analysis. The mRNA levels of HSPs (70, 60, and 40) increased in both species, except for HSP10, which was upregulated in Muscovy ducks and had no difference in Pekin ducks after heat stress. Simultaneously, the mRNA level of HSP90 decreased in the stress group in both species. Morphological analysis indicated that heat stress induced tissue injury in both species, and the liver of Pekin ducks was severely damaged. The activities of several antioxidant enzymes increased in Muscovy duck liver, but decreased in Pekin duck. The mRNA levels of inflammatory factors were increased after heat stress in both duck species. These results suggested that heat stress could influence HSPs, inflammatory factors expression, and the activities of antioxidant enzymes. Moreover, the differential response to heat stress indicated that the Muscovy duck has a better thermal tolerance than does the Pekin duck.

Upregulation of heat shock protein 32 with hemin alleviates acute heat-induced hepatic injury in mice.

Heat shock protein 32 (HSP32) is a stress response protein that can be induced by heat stress in the liver, and its induction can act as an important cellular defence mechanism against heat-induced liver injury. To investigate the functional role of HSP32 in protecting liver tissue against heat stress in mice and the mechanism by which it achieves this protective effect, HSP32 expression and carbon monoxide (CO) contents in a model of mice subjected to acute, transient heat exposure were examined. Furthermore, functional and histological parameters of liver damage and the possible involvement of oxidative stress to induce oxidative deterioration of liver functions and caspase-3 expression were also investigated in this study. We found that heat treatment of mice produced severe hepatic injury, whereas upregulation of HSP32 with hemin pretreatment prevented mice from liver damage. In contrast, addition of Sn-protoporphyrin (SnPP) to inhibit HSP32 expression completely reversed its hepatoprotective effect. It is concluded that upregulation of HSP32 by hemin could alleviate acute heat-induced hepatocellular damage in mice, and its by-product CO seems to play a more important role in hepatoprotective mechanism.

Heat shock protein 32/heme oxygenase-1 protects mouse Sertoli cells from hyperthermia-induced apoptosis by CO activation of sGC signalling pathways.

Heat shock protein 32 (Hsp32)/heme oxygenase-1 (HO-1) may be a key enzyme for the protection of cells against stress. Its anti-apoptotic effect has been attributed to its product, carbon monoxide (CO), in many types of cells. However, whether its anti-apoptotic mechanism plays a role in Sertoli cells (SCs) is not yet clear. We hypothesise that Hsp32/HO-1 and CO generated from it provide survival advantages in SCs by preventing apoptosis under heat exposure. After treatment of cultured SCs with hyperthermia and/or Hsp32/HO-1 activater hemin, apoptosis was measured valuated by annexin V-FITC and caspase-3 activation. We have also analysed the Hsp32/HO-1-derived CO content of cultured media and cyclic guanosine monophosphate (cGMP) production by enzyme-linked immunosorbent assay (ELISA). Hyperthermia induced SCs apoptosis, while preincubation with hemin suppressed SC hyperthermia-induced apoptosis. Hyperthermia and/or hemin increase Hsp32/HO-1 gene expression and the production of CO, which, in turn, stimulates the generation of cGMP. The results suggest that Hsp32/HO-1 is a protective factor in heat-stressed SCs, and that CO generated from Hsp32/HO-1 is involved in the anti-apoptotic pathway.

High expression of survivin in sacral chordoma.

Chordoma is a rare and invasive malignant tumor which primarily relies on surgical treatments. Anticipation of its recurrence and patient survival longevity has been a critical issue of the treatments. This retrospective study examined the survivin expression of sacral chordoma in 30 patients undergoing surgery in our hospital from January 2000 to July 2010, and compared it with chordoma recurrence. Survivin expression was 70 % positive in 30 patients. The positive expression of survivin with recurrence was significantly higher than that without recurrence (p = 0.017) and was inversely related to the continuous disease-free survival time (p < 0.001). Survivin expression was associated with recurrence. The correlation suggested that the survivin expression could be used as an independent predictor of recurrence and could be a potential bio-target gene of angiogenesis in sacral chordoma.

Upregulation of heat shock protein 32 in Sertoli cells alleviates the impairments caused by heat shock-induced apoptosis in mouse testis.

Heat stress results in apoptosis in testicular germ cells. A small heat shock protein (hsp), hsp32, is induced by heat stress in the testis, but little is known about its definitive function in physiological processes. To clarify the underlying role of hsp32, hsp32 expression and related signals in the heat shock pathway were analysed in mouse testes and Sertoli cells after heat stress in vivo and in vitro; meanwhile, expression of hsp32 was silenced only in the Sertoli cells using three different small interfering RNAs (siRNAs) to further verify the functional role of hsp32 in Sertoli cells, and hsp32-derived carbon monoxide (CO) contents in cultured media were analysed to clarify whether hsp32-derived CO involve in the apoptosis regulation mechanisms. The results from the in vivo experiment showed that the high expression levels of hsp32 (P < 0.05) were observed whether chronic, moderate or acute, transient heat exposure. The in vitro experiment showed that acute, transient heat exposure resulted in increases in Sertoli cells apoptosis (P < 0.01), the expression of hsp32 and caspase-3 activity; hsp32-siRNA knockdown of hsp32 expression resulted in upregulated apoptosis (P < 0.01) and caspase-3 activity (P < 0.01) in the Sertoli cells and hyperthermia increases CO (P < 0.01) release by Sertoli cells. The results suggested that upregulating hsp32 in Sertoli cells inhibits caspase-3 activity and alleviates heat-induced impairments in mouse testis; hsp32-derived CO may involve in the regulation mechanism.

Regulation of fertilization in male rats by CatSper2 knockdown.

Interest in ion channels as drug targets for contraception has grown with the realization that certain ion channel subunits are located exclusively in sperm. Selective knockdown of ion channel subunits can lead to infertility without ill effects, and selective inhibitors and/or openers of these ion channels could interfere with sperm function. In this study, in vivo electroporation (EP) and rete testis microinjection-mediated plasmid DNA were adopted to silence CatSper2 expression, which is essential in sperm hyperactivation. The results showed that high transfection efficiency and expression were achieved by plasmid DNA that was directly injected into the rete testis. As a result of the expression of CatSper2 being blocked, the treatment group showed significantly lower (P<0.05) hyperactivation rate, fertilization rate in vitro, migration motility in viscoelastic solution and intracellular Ca(2+) peak. The low hyperactivation and fertilization rates lasted for 60 days. Meanwhile, analysis of the sperm survival rate and testis histology indicated that in vivo EP had no significant effect on the function of the testis, spermatogenesis or sperm activity. The present study demonstrated that it was feasible to achieve male contraception by silencing the expression of CatSper2, the key protein involved in sperm hyperactivation.

The Signaling Mechanism of TGF-ß1 Induced Bovine Mammary Epithelial Cell Apoptosis.

The present study showed that Transforming growth factor beta 1 (TGF-ß1) can induce apoptosis of bovine mammary epithelial cells. This apoptosis was also observed with phosphorylation of Smad2/3 within 0.5-2 h. Afterwards the signal transferred into the nucleus. Moreover, intracellular free Ca(2+) concentration was significantly elevated as well as Caspase-3 activated and DNA lysised, thereby inducing the programmed cell death. This signaling pathway of TGF-ß1 was blocked by SB-431542 (10(-2) µM) via inhibiting ALK-5 kinase activity, which thus reversed the anti-proliferation and apoptosis effect of TGF-ß1 in mammary epithelial cells. These results indicated that TGF-ß1 induced apoptosis of bovine mammary epithelial cells through the ALK-5-Smad2/3 pathway, which plays an important role in inhibiting survival of mammary epithelial cells. Moreover, intracellular Ca(2+) also played a critical role in TGF-ß1-induced cell apoptosis.

[The effect of genetic polymorphism of the exon 2 of the beta-lactoglobulin gene on the milk composition in Chinese Holstein].

OBJECTIVE: In order to study the effect of the polymorphism at the exon2 region of the (3-LG allele gene on milk composition and yield. METHODS: The single-strand conformation polymorphism method (PCR-SSCP) was used to analyze for polymorphism the exon2 region of the 3-LG gene (NCBI accession number: DQ489319) in Chinese Holstein. RESULTS: Eight SSCP patterns were detected in the fragments: ab, abc, abd, abe, abcd, abce, abde and abcde, and the patterns frequencies as follows: 0.14, 0.10, 0.27, 0.23, 0.05, 0.04, 0.11 and 0.06 (P < 0.05); Six single nucleotide polymorphism (SNP) were detected in this study: sitel C>T, site2 T>C, site3 C>T, site4 C>C, site5 C> A, site6 A>T or C, and the polymorphism infonnation content (PIC) of these SNPs were in median or high polymorphism (PIC > 0.25). CONCLUSION: These SNPs at the exon2 region of the beta-LG gene were remarkably and affected milk performance traits (milk yield, protein and fat contents) in Chinese Holstein.

Combination of skull traction with posterior C1-2 fusion for old C1-2 dislocations.

Between January 2003 and December 2009, 23 patients who had suffered old C1-2 dislocations, were surgically treated in our orthopedics department. Fifteen patients underwent direct posterior C1-2 fusion following pre-operative reduction by skull traction. In eight patients, reduction was achieved only by skull traction under general anesthesia, facilitated by manual hyperextension of the cervical spine and maintained by simultaneous posterior C1-2 fusion. Intra-operative traction was monitored using C-arm fluoroscopy and cortical somatosensory-evoked potentials. Posterior C1-2 fixation was achieved in nine patients using C1-2 laminar hooks and in 14 patients using C1 laminar hooks with C2 pedicle screws. During the follow-up of 5 to 72 months (mean: 42.8 months), solid bony fusion was accomplished in all patients. Using Di Lorenzo's grades and Japanese Orthopedics Association scores, there was significant improvement (p<0.05). The cervical medullary angle exhibited a significant improvement of 31.7°, from 121.6° to 153.3° (p<0.05). There were no complications, including dural tears, spinal cord damage, vertebral artery damage, or breakage or loosening of implants.

Risk factors for postoperative wound infections of sacral chordoma after surgical excision.

STUDY DESIGN: A retrospective study, analyzing the risk factors for postoperative wound infections of the sacral chordoma after surgical excision. OBJECTIVE: To determine the preoperative, intraoperative, and patient characteristics that contribute to an increased risk of postoperative wound infection in patients undergoing sacral chordoma resection. SUMMARY OF BACKGROUND DATA: Postoperative wound infection after spinal operations is a dreaded complication. The risk factors have been investigated earlier, but the patients with sacral chordoma may be distinct. METHODS: Between January 1992 and December 2007, 45 patients with sacral chordomas were treated with surgical resection. Data regarding preoperative and intraoperative risk factors for postoperative wound infection were evaluated using univariate analysis and multivariable conditional logistic regression. Odds ratios with 95% confidence intervals and P values were calculated. RESULTS: Of the 45 patients with sacral chordoma, 16 (35.6%) acquired postoperative wound infection. Significant risk factors associated with postoperative wound infection in the univariate analysis included the following: albumin <3.0, previous surgery, operating time, instrumentation, and surgical team. Albumin<3.0, operating time >6 hours, and previous surgery were statistically significant in the multivariable model. CONCLUSIONS: Patients undergoing sacral tumor surgery may be at greater risk for developing wound complications. In this study, it seems that albumin<3.0, operating time >6 hours, and previous surgery may predict those patients that were more prone to developing postoperative wound infection. Using a single surgical team and no instrumentation seems to provide protection against postoperative wound infection in this patient population.

Expression of vascular endothelial growth factor and matrix metalloproteinase-9 in sacral chordoma.

Sacral chordoma is a vessel-rich and infiltrative tumor, but the fundamental knowledge of its biological behavior remains unknown. This study was designed to investigate the expression levels and contributions of vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9) in the angiogenesis and recurrence of sacral chordoma and their correlations. An immunohistochemical method was used to investigate the expression of VEGF, MMP-9, and microvascular density (MVD) in 36 patients with sacral chordoma. Their differences in expressions were statistically analyzed and their correlations with angiogenesis and recurrence were evaluated. The mean MVD of sacral chordomas was significantly higher than that of the adjacent normal tissues (P = 0.033). Immunoreactivity for VEGF and MMP-9 was significantly higher in sacral chordoma tissues than in adjacent normal tissues (P = 0.008, P = 0.005). The mean MVD of VEGF and MMP-9 were statistically higher in positive group than in negative group (P = 0.015, P = 0.004), respectively . Moreover, a significant correlation was found between the VEGF and MMP-9 (P = 0.002). The log-rank test revealed that continuous disease-free survival time (CDFS) was significantly shorter in the MMP-9-positive group than in the MMP-9-negative group (P = 0.019), but the difference in the VEGF-positive group and the VEGF-negative group was not statistically significant (P = 0.938). Our data suggest that VEGF and MMP-9 might act with a synergistic effect and can positively regulate the angiogenesis in sacral chordoma. Positive expression of MMP-9 might indicate the local recurrence of sacral chordoma. The result suggests that some specific drugs which inhibit VEGF, MMP-9, or their receptors may have a good therapeutic effect for sacral chordoma.