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Biomedical subjects

S Liu

Publications and source records attributed to S Liu.

At least 163 records · Page 9Linked to original sources
PubMed2001

Intake of vegetables rich in carotenoids and risk of coronary heart disease in men: The Physicians' Health Study.

BACKGROUND: Previous studies of diet and coronary heart disease (CHD) have focused on intake of nutrients rather than whole foods. Because of the findings that dietary fibre, folate and antioxidants may be protective for CHD, increased intake of vegetables has been recommended. However, due to the chemical and physical complexity of vegetables, the effects of individual nutrients may differ if eaten as whole foods. Moreover, little is known about the direct association between vegetable intake and risk of CHD. METHODS: We prospectively evaluated the relation between vegetable intake and CHD risk in the Physicians' Health Study, a randomized trial of aspirin and beta-carotene among 22 071 US male physicians aged 40-84 years in 1982. In this analysis, we included 15 220 men without heart disease, stroke or cancer at baseline who provided information on their vegetable intake at baseline, and in the 2nd, 4th and 6th years of follow-up using a simple semiquantitative food frequency questionnaire including eight vegetables. We confirmed 1148 incident cases of CHD (387 incident cases of myocardial infarction and 761 incident cases of coronary artery bypass grafting or percutaneous transluminal coronary angioplasty) during 12 years of follow-up. RESULTS: After adjusting for age, randomized treatment, body mass index (BMI), smoking, alcohol intake, physical activity, history of diabetes, history of hypertension, history of high cholesterol, and use of multivitamins, men who consumed at least 2.5 servings/day of vegetables had a relative risk (RR) of 0.77 (95% CI : 0.60-0.98) for CHD, compared with men in the lowest category (<1 serving/day). Adjusting for the same covariates in an analysis of the overall trend that considered intake of vegetables as a continuous variable, we found a RR of 0.83 (95% CI : 0.71-0.98) for risk of CHD for each additional serving/day of vegetables. The inverse relation between vegetable intake and CHD risk was more evident among men with a BMI > or =25 (RR = 0.71, 95% CI : 0.51-0.99) or current smokers (RR = 0.40, 95% CI : 0.18-0.86) comparing highest to the lowest categories of intake. CONCLUSIONS: Our results suggest an inverse association between vegetable intake and risk of CHD. These prospective data support current dietary guidelines to increase vegetable intake for the prevention of CHD.

Adult↗
PubMed2001

Time urgency and risk of non-fatal myocardial infarction.

BACKGROUND: Inconsistencies in the literature linking Type A behaviour pattern (TAB) to coronary heart disease (CHD) may be due to differences in the effects of various components of TAB, namely aggressiveness, hostility, ambitiousness, competitive drive, and a chronic sense of time urgency. METHODS: We investigated the association between sense of time urgency/impatience and non-fatal myocardial infarction (MI) in a study of 340 cases and an equal number of age-, sex-, and community-matched controls. RESULTS: A dose-response relation was apparent among subjects who rated themselves higher on the four-item time urgency/impatience scale (P-value for trend <0.001), with a matched odds ratio (OR) for non-fatal MI of 4.45 (95% CI : 2.20-8.99) comparing those with the highest rating to those with the lowest. After further adjustment for family history of premature MI, physical activity, body mass index, occupation, cigarette smoking, total caloric intake, per cent calories from saturated fat, alcohol intake, lipid levels, treated hypertension and diabetes, the dose-response relation remained (P-value for trend = 0.015) and the adjusted OR for MI was 3.99 (95% CI : 1.32-12.0) comparing those with the highest rating to those with the lowest. CONCLUSION: In these data, a sense of time urgency/impatience was associated with a dose-response increase in risk of non-fatal MI, independent of other risk factors. Prospective cohort studies of time urgency/impatience and incident CHD events are needed to confirm or refute these observations from a case-control study.

Adult↗
PubMed2001

Granulocyte-macrophage colony-stimulating factor in a combination gene therapy strategy for head and neck cancer.

OBJECTIVES/HYPOTHESIS: Gene therapy offers a new approach for treatment of head and neck squamous cell carcinoma (HNSCC). This study examined the effectiveness of granulocyte-macrophage colony-stimulating factor (GM-CSF) in combination gene therapy strategy against HNSCC in an orthotopic mouse model. STUDY DESIGN: Experimental animal research. METHODS: Established tumors were treated with recombinant adenovirus constructs containing the genes for murine granulocyte-macrophage colony-stimulating factor (Ad-mGM-CSF), murine interleukin 2(Ad-mIL-2), or herpes simplex virus thymidine kinase (Ad-tk). RESULTS: The combination of Ad-mGM-CSF or Ad-mIL-2 and Ad-tk resulted in significantly greater reduction in tumor size versus other treatment groups or control subjects. There was no statistical significance between the triple combination of Ad-mGM-CSF, Ad-mIL-2, and Ad-tk versus Ad-mIL-2 and Ad-tk at 1 to 2 weeks after treatment. There was no tumor reduction seen from Ad-mGM-CSF alone and no additional benefit seen from Ad-mGM-CSF combinations in long-term follow-up studies. The greatest cytotoxic T-lymphocyte and natural killer cell activity occurred in the combination Ad-mIL-2 and Ad-tk groups with and without Ad-mGM-CSF. CONCLUSION: Results suggest that the additional mGM-CSF did not enhance the immunogenicity of the HNSCC. Optimal activation of T lymphocytes may require additional co-stimulatory molecules to stabilize the interaction of the T lymphocyte and antigen presenting cell. The presence of major histocompatibility complex Class II may increase CD4+ T-cell mediated immunogenicity and augment therapeutic antitumor immune responses in combination with tk, mIL-2, and mGM-CSF.

Adenoviridae↗
PubMed2001

Combination nonviral cytokine gene therapy for head and neck cancer.

OBJECTIVE: To establish the feasibility and efficacy of combination nonviral murine interferon-alpha (mIFN-alpha)and murine interleukin-2 (mIL-2) or murine interleukin-12 (mIL-12) gene therapy for head and neck squamous cell carcinoma in a murine model. STUDY DESIGN: Randomized controlled studies in a murine head and neck cancer model were performed to assess antitumor responses, secondary cytokine expression, and both natural killer (NK) cell and cytolytic T-cell (CTL) activity. METHODS: Tumors were established in the floor of mouth in C3H/HeJ immunocompetent mice. Established tumors were directly injected with polymer-formulated murine interferon-alpha (mIFN-alpha), lipid-formulated mIL-2, and polymer-formulated mIL-12 alone or in combination. Primary and secondary cytokine expression,NK cell activity, and CTL activity were assayed. RESULTS: The use of mIFN-alpha gene therapy in combination with either mIL-2 or mIL-12 resulted in significant antitumor effects as compared with each of the single cytokine and control treatment groups (P = .002). Increased levels of NK cell activity and tumor specific CD8+ cytotoxic T-lymphocyte activity were found in the combination mIFN-alpha and mIL-2 or mIL-12 groups. Augmented immune responses correlated with clinical antitumor effects. CONCLUSIONS: The present study demonstrates that mIL-2 or mIL-12 augments tumor inhibition from mIFN-alpha and increases activation of NK and CD8+ T cells. These data support further investigation of polymer and lipid mediated delivery of cytokine genes for head and neck cancer.

Animals↗
PubMed2001

Regrowth of the rostral spinal axons into the caudal ventral roots through a collagen tube implanted into hemisected adult rat spinal cord.

OBJECTIVE: A collagen tube was used to guide axonal regrowth from the spinal cord to the periphery to contribute to improvement of paralysis after lower thoracic spinal cord injury. METHODS: The spinal cords of adult male Sprague-Dawley rats were lesioned by removing the left hemicord from T12 to 5 mm below this level and additionally sectioning all left lumbar ventral roots. In experimental animals (n = 9), a collagen tube was inserted into this gap, spanning the rostral hemisected cord to the caudal sectioned lumbar ventral roots (gap, 7 mm). In control animals (n = 6), no treatment was performed. RESULTS: Six months after surgery, the return of some tension and resistance of the paralyzed hindlimb muscles was observed in all experimental rats except the untreated controls. Nine months postoperatively, muscle action potentials were recorded from the target muscles of the experimental animals while electrostimulating the tissue continuity within the collagen tube. Horseradish peroxidase retrograde labeling showed that the neurons in the rostral cord near the implantation site regrew into the reconnected lumbar ventral roots. Histological examination indicated numerous myelinated axons in the reconnected root pathways and newly formed endplates in the target muscles. No axonal regeneration was found in the control rats. CONCLUSION: These results indicate that the rostral spinal axons can regrow into the caudal sectioned and reconnected ventral roots through a collagen tube, thus innervating the denervated peripheral targets in adult rats after spinal cord injury. This surgical repair model also provides a means for testing the use of trophic factors that may further promote axonal regeneration.

Animals↗
PubMed2001

Dietary carbohydrates, physical inactivity, obesity, and the 'metabolic syndrome' as predictors of coronary heart disease.

Several decades of epidemiological and clinical research have identified physical inactivity, excessive calorie consumption, and excess weight as common risk factors for both type 2 diabetes mellitus and coronary heart disease. This trio forms the environmental substrate for a now well-recognized metabolic phenotype called the insulin resistance syndrome. Recent data suggest that a high intake of rapidly absorbed carbohydrates, which is characterized by a high glycemic load (a measure of carbohydrate quality and quantity), may increase the risk of coronary heart disease by aggravating glucose intolerance and dyslipidemia. These data also suggest that individuals who are obese and insulin resistant are particularly prone to the adverse effects of a high dietary glycemic load. In addition, data continue to accumulate suggesting the important beneficial effects of physical activity, even at moderate levels, and weight reduction on improving insulin sensitivity and reducing the risk of coronary heart disease. Future metabolic studies should continue to quantify the physiological impact of different foods on serum glucose and insulin, and such information should routinely be incorporated into large-scale and long-term prospective studies, in which the possible interaction effects between diet and other metabolic determinants such as physical activity and obesity can be examined. Until more definitive data are available, replacing refined grain products and potatoes with minimally processed plant-based foods such as whole grains, fruits, and vegetables, and reducing the intake of high glycemic load beverages may offer a simple strategy for reducing the incidence of coronary heart disease.

Blood Glucose↗
PubMed2001

Differential effects of rexinoids and thiazolidinediones on metabolic gene expression in diabetic rodents.

Both retinoid X receptor (RXR)-selective agonists (rexinoids) and thiazolidinediones (TZDs), PPAR (peroxisome proliferator-activated receptor)-gamma-specific ligands, produce insulin sensitization in diabetic rodents. In vitro studies have demonstrated that TZDs mediate their effects via the RXR/PPAR-gamma complex. To determine whether rexinoids lower hyperglycemia by activating the RXR/PPAR-gamma heterodimer in vivo, we compared the effects of a rexinoid (LG100268) and a TZD (rosiglitazone) on gene expression in white adipose tissue, skeletal muscle, and liver of Zucker diabetic fatty rats (ZDFs). In adipose tissue, rosiglitazone decreased tumor necrosis factor-alpha (TNF-alpha) mRNA and induced glucose transporter 4 (GLUT4), muscle carnitine palmitoyl-transferase (MCPT), stearoyl CoA desaturase (SCD1), and fatty acid translocase (CD36). In contrast, LG100268 increased TNF-alpha and had no effect or suppressed the expression of GLUT4, MCPT, SCD1, and CD36. In liver, the rexinoid increased MCPT, SCD1, and CD36 mRNAs, whereas rosiglitazone induced only a small increase in CD36. In skeletal muscle, rosiglitazone and LG100268 have similar effects; both increased SCD1 and CD36 mRNAs. The differences in the pattern of genes induced by the rexinoids and the TZDs in diabetic animals found in these studies suggests that these compounds may have independent and tissue-specific effects on metabolic control in vivo.

Adipose Tissue↗
PubMed2001

Immunomodulatory effects of anti-CD4 antibody in host resistance against infections and tumors in human CD4 transgenic mice.

Anti-CD4 antibodies, which cause CD4(+) T-cell depletion, have been shown to increase susceptibility to infections in mice. Thus, development of anti-CD4 antibodies for clinical use raises potential concerns about suppression of host defense mechanisms against pathogens and tumors. The anti-human CD4 antibody keliximab, which binds only human and chimpanzee CD4, has been evaluated in host defense models using murine CD4 knockout-human CD4 transgenic (HuCD4/Tg) mice. In these mice, depletion of CD4(+) T cells by keliximab was associated with inhibition of anti-Pneumocystis carinii and anti-Candida albicans antibody responses and rendered HuCD4/Tg mice susceptible to P. carinii, a CD4-dependent pathogen, but did not compromise host defense against C. albicans infection. Treatment of HuCD4/Tg mice with corticosteroids impaired host immune responses and decreased survival for both infections. Resistance to experimental B16 melanoma metastases was not affected by treatment with keliximab, in contrast to an increase in tumor colonization caused by anti-T cell Thy1.2 and anti-asialo GM-1 antibodies. These data suggest an immunomodulatory rather than an overt immunosuppressive activity of keliximab. This was further demonstrated by the differential effect of keliximab on type 1 and type 2 cytokine expression in splenocytes stimulated ex vivo. Keliximab caused an initial up-regulation of interleukin-2 (IL-2) and gamma interferon, followed by transient down-regulation of IL-4 and IL-10. Taken together, the effects of keliximab in HuCD4/Tg mice suggest that in addition to depleting circulating CD4(+) T lymphocytes, keliximab has the capability of modulating the function of the remaining cells without causing general immunosuppression. Therefore, keliximab therapy may be beneficial in controlling certain autoimmune diseases.

Animals↗
PubMed2001

Identification of a cellular protein that interacts and synergizes with the RTA (ORF50) protein of Kaposi's sarcoma-associated herpesvirus in transcriptional activation.

Lytic reactivation of Kaposi's sarcoma-associated herpesvirus (KSHV), or human herpesvirus 8, from latency requires transcriptional transactivation by the viral protein RTA encoded by the ORF50 gene. Very little is known about how RTA functions and the cellular factors that may be involved in its transactivation function. Using the yeast two-hybrid system, we have identified a human cellular protein that can interact with KSHV RTA. The cellular protein, referred to as the human hypothetical protein MGC2663 by GenBank, is encoded by human chromosome 19. This protein is 554 amino acids (aa) in size and displays sequence similarity with members of the Krueppel-associated box-zinc finger proteins (KRAB-ZFPs). MGC2663 expression could be detected in all primate cell lines tested, and its expression level was neither stimulated nor inhibited by RTA. MGC2663 specifically synergizes with RTA to activate viral transcription, and overexpression of MGC2663 in the presence of RTA further enhances RTA transactivation of several viral promoters that were identified as targets for RTA. Coimmunoprecipitation and pull-down assays further demonstrated that MGC2663 interacts with RTA both in vivo and in vitro, and the N-terminal 273 aa of KSHV RTA and the potential zinc finger domain of MGC2663 are required for their interaction. Our results indicate that this novel human cellular protein, MGC2663, named K-RBP (KSHV RTA binding protein) due to its RTA binding feature, specifically interacts with the KSHV RTA protein and functions as a cellular RTA cofactor to activate viral gene expression. Though its normal cellular function needs to be further studied, K-RBP may play a significant role in mediating RTA transactivation in vivo.

Binding Sites↗
PubMed2001

Redistribution and abnormal activity of phospholipase A(2) isoenzymes in postinfarct congestive heart failure.

Cardiac sarcolemmal (SL) cis-unsaturated fatty acid sensitive phospholipase D (cis-UFA PLD) is modulated by SL Ca(2+)-independent phospholipase A(2) (iPLA(2)) activity via intramembrane release of cis-UFA. As PLD-derived phosphatidic acid influences intracellular Ca(2+) concentration and contractile performance of the cardiomyocyte, changes in iPLA(2) activity may contribute to abnormal function of the failing heart. We examined PLA(2) immunoprotein expression and activity in the SL and cytosol from noninfarcted left ventricular (LV) tissue of rats in an overt stage of congestive heart failure (CHF). Hemodynamic assessment of CHF animals showed an increase of the LV end-diastolic pressure with loss of contractile function. In normal hearts, immunoblot analysis revealed the presence of cytosolic PLA(2) (cPLA(2)) and secretory PLA(2) (sPLA(2)) in the cytosol, with cPLA(2) and iPLA(2) in the SL. Intracellular PLA(2) activity was predominantly Ca(2+) independent, with minimal sPLA(2) activity. CHF increased cPLA(2) immunoprotein and PLA(2) activity in the cytosol and decreased SL iPLA(2) and cPLA(2) immunoprotein and SL PLA(2) activity. sPLA(2) activity and abundance decreased in the cytosol and increased in SL in CHF. The results show that intrinsic to the pathophysiology of post-myocardial infarction CHF are abnormalities of SL PLA(2) isoenzymes, suggesting that PLA(2)-mediated bioprocesses are altered in CHF.

Animals↗
PubMed2001

Analysis of recombinant Phex: an endopeptidase in search of a substrate.

X-linked hypophosphatemia (XLH) is caused by inactivating mutations of Phex, a phosphate-regulating endopeptidase. Further advances in our knowledge of the pathogenesis of XLH require identification of the biological function of Phex and its physiologically relevant substrates. We evaluated several potential substrates using mouse recombinant wild-type Phex proteins (rPhex-WT) and inactive mutant Phex proteins (rPhex-3'M) lacking the COOH-terminal catalytic domain as controls. By Western blot analysis, we demonstrated that Phex is a membrane-bound 100-kDa glycosylated monomer. Neither casein, a substrate for the related endopeptidase thermolysin, human stanniocalcin 1 (hSTC-1), an osteoblast-derived phosphate-regulating factor, nor FGF-23 peptide (amino acid 172-186), comprising the region mutated in autosomal dominant hypophosphatemia, was cleaved by rPhex-WT. In addition, membranes expressing rPhex-WT, rPhex-3'M, and the empty vector hydrolyzed parathyroid hormone-(1-34), indicating the lack of Phex-specific cleavage of parathyroid hormone. In contrast, rPhex-WT did display an EDTA-dependent cleavage of the neutral endopeptidase substrate [Leu]enkephalin. Further studies with wild-type and mutant rPhex proteins should permit the identification of physiologically relevant substrates involved in the pathogenesis of XLH.

Amino Acid Sequence↗
PubMed2001

Pre- and postsynaptic inhibition by nociceptin in guinea pig small intestinal myenteric plexus in vitro.

Actions of nociceptin on electrical and synaptic behavior of morphologically and neurochemically identified neurons in the guinea pig duodenal myenteric plexus were studied with conventional techniques. Nociceptin hyperpolarized the membrane potential in 104 of 121 AH-type and 28 of 51 S-type neurons with an EC(50) of 11.9 +/- 1.2 nM. Increased K(+) conductance accounted for the hyperpolarizing responses that were blocked by pertussis toxin and unaffected by naloxone. The selective opioid receptor-like (ORL)(1) receptor antagonist [Phe(1)-psi(CH(2)-NH)-Gly(2)]nociceptin(1--13)-NH(2) suppressed the nociceptin-evoked responses while behaving like a partial agonist. The nonselective ORL(1) antagonist naloxone benzoylhydrazone competitively suppressed nociceptin actions with a pA(2) value of 5.8. Nociceptin acted at presynaptic inhibitory receptors to suppress fast excitatory nicotinic postsynaptic potentials in 25 of 30 neurons (EC(50) = 22.5 +/- 4.4 nM) and slow synaptic excitation in 38 of 45 neurons (EC(50) = 15.1 +/- 1.6 nM). Presynaptic inhibitory action of nociceptin was unaffected by naloxone and was antagonized by [Phe(1)-psi(CH(2)-NH)-Gly(2)]nociceptin(1--13)-NH(2) or naloxone benzoylhydrazone. The results suggest that nociceptin acts both pre- and postsynaptically by activating an ORL(1) receptor that is distinct from typical naloxone-sensitive opioid receptors.

Animals↗
PubMed2001

Cloning and characterization of the proximal murine Phex promoter.

Phex is an endopetidase that regulates systemic phosphate homeostasis. We investigated Phex gene transcription by cloning and performing functional analysis of the 2736 bp of the 5' flanking region of the mouse Phex gene containing its promoter. We identified a transcription start site, a consensus TATA-box, and multiple potential cis-acting regulator elements. To determine whether the promoter directs cell-type restricted Phex expression, we transfected full-length and 5'-deleted Phex luciferase reporter constructs into various cell lines. Phex-expressing C5.18 chondrocytes displayed the highest activity of the transfected Phex promoter constructs compared with non-Phex-expressing COS-7 cells, whereas promoter activity was intermediate in ROS 17/2.8 osteoblasts and maturation stage-dependent in MC3T3-E1 osteoblasts. Analysis of sequential 5'-deletion mutants of the Phex promoter in ROS 17/2.8 cells revealed bimodal activity, suggesting that both positive and negative cis-acting regions may be present. The chondrogenic factor SOX9 markedly stimulated Phex promoter activity, whereas Cbfa1, PTH, and 1,25(OH)(2)D(3) had no effect. Our findings are consistent with the predominant expression of Phex in bone and cartilage. Additional studies will be needed to confirm the regulatory regions in the Phex promoter that function in a cell-restricted manner.

5' Untranslated Regions↗
PubMed2001

Changes in stillbirth and infant mortality associated with increases in preterm birth among twins.

OBJECTIVE: To examine whether the recent substantial increase in preterm birth among twins has been associated with changes in fetal and infant mortality. DESIGN: Cohort study based on information in the linked live birth, stillbirth, and mortality databases of Statistics Canada. SETTING: Ten of 12 provinces and territories in Canada. PARTICIPANTS: All twin live births and stillbirths between 1985 and 1996, along with information on deaths during infancy (1985-1997). MAIN OUTCOME MEASURE: Fetal and infant mortality rates. RESULTS: The rate of preterm birth among twin live births increased significantly by 17% (95% confidence interval: 14%-20%) from 42.5% between 1985 and 1987 to 49.6% between 1994 and 1996. Overall, stillbirth rates among twins declined from 22.4 per 1000 total births in 1985 to 1987 to 18.8 per 1000 total births in 1994 to 1996. Among twin fetuses >/=34 weeks' gestation, stillbirth rates decreased from 9.5 per 1000 in 1985 to 1987 to 5.4 per 1000 fetuses at risk in 1994 to 1996. Infant mortality rates among twin live births declined substantially in all categories of gestational age above 24 weeks except for live births at 32 to 33 and 34 to 36 weeks' gestation. CONCLUSIONS: The recent increase in preterm birth among twins was associated with a substantial reduction in stillbirth rates at and near term gestation. Infant mortality rates declined concurrently, although the absence of a significant decrease in infant mortality among twin live births at 32 to 33 and 34 to 36 weeks' gestational age needs additional scrutiny.

Canada↗
PubMed2001

Resonance Rayleigh method for the determination of proteins with Orange G.

In pH 0.6 - 2.0 HCl-sodium acetate buffer solution, proteins react with an acidic monoazo dye such as Orange G, Methyl Orange, Methyl Red and Orange IV to form a combination product. This results in a significant enhancement of resonance Rayleigh scattering (RRS) and a new RRS spectrum appears. Owing to the fact that Orange G-protein system is the most sensitive, it was taken as an example to study. The RRS spectral characteristics of its combination product and the optimum condition for the reaction were investigated. The intensity of RRS is directly proportional to the concentration of protein in the range of 0 - 5.0 microg/mL. The method has high sensitivity; its detection limits are 2.6 ng/mL for BSA, 3.4 ng/mL for HAS and 7.1 ng/mL for alpha-chymotrypsin, respectively. A new method for the determination of trace amounts of proteins on the basis of RRS spectra has been developed.

Algorithms↗
PubMed2001

Use of a collagen-based sealant to prevent in vivo epidural adhesions in an adult rat laminectomy model.

OBJECT: The authors investigated the effect of a collagen-based sealant, Gel Amidon Oxydé (GAO), in the prevention of epidural scar adhesions in an adult rat model of laminectomy. METHODS: Seventy-two adult Sprague-Dawley rats underwent an L5-6 laminectomy, after which the dura mater and the left L-4 and L-5 nerve roots were exposed. In the 36 animals that received GAO, the sealant was applied over the dura and around the nerve roots, and it was used to fill the laminectomy cavity before it polymerized. In 36 control animals, the same surgical treatment was performed, but the rats did not receive GAO. During the early postoperative period, a significant decrease in the occurrence of epidural hematoma was found in the GAO-treated rats. In contrast to findings in control rats, a thin white connective tissue layer was found between the dura and surrounding muscles after GAO had degraded and been absorbed. One month posttreatment, no epidural scar adhesion was found between the tissue layer and the dura in the GAO-treated animals. Three months postoperatively, both gross inspection and histological examination further confirmed that formation of epidural adhesions was significantly inhibited in the rats treated with GAO. No special inflammatory reaction was observed, and the healing of skin and muscle lesions was not affected by either treatment. CONCLUSIONS: The data obtained in this study suggest that the GAO collagen-based sealant may be an effective biomaterial to prevent epidural adhesions in vivo after laminectomy.

Animals↗
PubMed2001

Innervation of the caudal denervated ventral roots and their target muscles by the rostral spinal motoneurons after implanting a nerve autograft in spinal cord-injured adult marmosets.

OBJECT: The authors conducted a study to determine the effects of using a nerve autograft (NAG) to promote and guide axonal regrowth from the rostral spinal cord to the caudal lumbar ventral nerve roots to restore hindlimb motor function in adult marmosets after lower thoracic cord injury. METHODS: Nine animals underwent a left-sided hemisection of the spinal cord at T-12 via left-sided T9-L3 hemilaminectomy, with section of all ipsilateral lumbrosacral ventral nerve roots. In the experimental group (five animals), an NAG obtained from the right peroneal nerve was anastomosed with the sectioned and electrophysiologically selected lumbar ventral roots (left L-3 and L-4) controlling the left quadriceps muscle and then implanted into the left ventrolateral T-10 cord. In the control group (four animals), the sectioned/selected lumbar ventral roots were only ligated. After surgery, all marmosets immediately suffered from complete paralysis of their left hindlimb. Five months later, some clinical signs of reinnervation such as tension and resistance began to appear in the paralyzed quadriceps of all experimental animals that received autografts. Nine months postoperatively, three of the five experimental marmosets could maintain their lesioned hindlimb in hip flexion. Muscle action potentials and motor evoked potentials were recorded from the target quadriceps in all experimental marmosets, but these potentials were absent in the control animals. Horseradish peroxidase retrograde labeling from the distal sectioned/reconnected lumbar ventral roots traced 234+/-178 labeled neurons in the ipsilateral T8-10 ventral horn, mainly close to the NAG tip. Histological analysis showed numerous regenerating axons in this denervated/reconnected nerve root pathway, as well as newly formed motor endplates in the denervated/reinnervated quadriceps. No axonal regeneration was detected in the control animals. CONCLUSIONS: These data indicate that the rostral spinal neurons can regrow into the caudal ventral roots through an NAG, thereby innervating the target muscle in adult marmosets after spinal cord injury.

Animals↗