Effects of recombinant sCRl on the immune inflammatory reaction in acute spinal cord injury tissue of rats

OBJECTIVE: To determine the effects of recombinant soluble complement receptor type I (sCR1) on the immune inflammatory reaction in acute spinal cord injury tissue of rats and its protective effects. METHODS: SD rat models of acute spinal cord injury were prepared by modified Allen's method. The motor function of the rat lower extremities in sCR1 group and normal saline (NS) group was evaluated by the tiltboard experiment at 12 h, 1 d, 3 d, 7 d, and 14 d. The neutrophil infiltration and C3c positive expression were observed. The myeloperoxidase activity was assessed in the injury tissue at 12 h, 1 d, 3 d, 7 d, and 14 d after injury in the two groups. RESULTS: The motor function of rat in sCR1 group at 3 d, 7 d, and 14 d was obviously better than that in NS group (P<0.01, P<0.01, P<0.01). C3c positive expression in sCR1 group at each time point after injury was obviously less than that in NS group (P<0.01). The myeloperoxidase activity in sCR1 group at each time point after injury was obviously less than that in NS group (P<0.01). CONCLUSIONS: Recombinant soluble complement receptor type I (sCR1) can lessen the immune inflammatory reaction in acute spinal cord injury tissue and relieve secondary spinal cord injury by inhibiting the activation of the complement system.     

Effects of recombinant sCR1 on the immune inflammatory reaction in acute spinal cord injury tissue of rats

cutespinalcordinjuryisaseverekindoftrauma.Thesecondaryinjurymechanismhasbeentoocomplextobetotallyunderstoodtillnow .Studieshaveshownthattheimmuneinflammatoryreactionparticipatesinsecondaryspinalcordinjuryasanimportantpathologicalprocessinearlyinjury .Itwa…     

The classification and treatment of antibody-mediated renal allograft injury: Where do we stand?

Since the acceptance of the detection of C4d in allografts as a reliable tool to mark a humoral alloresponse, de novo antibody-induced graft injury has attracted much attention. Antibodies and B cells are the new frontier in transplantation. At this juncture carefully designed studies are critical in order to gain solid diagnostic, therapeutic, and prognostic knowledge about the role of antibodies in graft injury and to avoid any confusion and misconception. One prerequisite is the strict adherence to refined classification systems of renal transplant rejection that carefully split and categorize different phenotypes of humoral mediated graft damage and ideally also include information on anti-donor antibody specificity and titers. Sun and colleagues follow this concept and provide evidence that mixed cellular and antibody-mediated graft rejection can respond favorably to intensified immunosuppression with tacrolimus and mycophenolate mofetil. What will the future bring to treat rejection episodes with a dominant, co-dominant, or minor antibody response?     

Repair of spinal cord injuries: where are we,where are we going?

Repairing the spinal cord has for a long time been a 'holy grail' for neuroscientists. No achievement in neuroscience is more difficult to achieve, and none would have the same impact amongst the medical profession and the public. Yet no patient has yet benefited from a regeneration therapy. At last sufficient progress has been made in the basic science of axon regeneration that treatments that would partially repair a spinal injury are imminent. A full repair of spinal injury still remains elusive. This review summarises progress to date, and suggests ways in which progress towards treatment of spinal injury patients might be made.     

Monocyte chemoattractant protein-1 level in serum of patients with acute spinal cord injury

Spinalcordinjury(SCI)withinthefirstfewhours,isfrequentlycomplicatedbyinflammatorymechanisms,includingtheinfluxofmonocyte/macrophagesaswellastheactivationofresidentspinalmicrogliaandastrocytes.Numerousstudieshave suggestedthattheinitialinfiltrationofthe hematogenouscellsmaybeduetothesecretionof cytokinesandchemokinesintheinjuredcentral nervoussystem(CNS),amongwhichmonocyte chemoattractantprotein1(MCP1),amemberofβfamilychemokines,isthemostwellrecognized.Studiesconductedinmanylaboratorieshave…     

Experimental study on spinal cord injury treated by embryonic spinal cord transplantation and greater omental transposition

Objective: To observe the clinical efficacy of the embryonic spinal cellular transplantation and greater omentaltranspesition for treatment of the spinal cord injury in 24 mongrel dogs. Methods: 24 adult mongrel dogs, weighing 10 ～ 13kg, without male and female limit, were employed in this experimental study and randomly divided into 4 groups:①simple injury group(group A) ;②greater omental transposition group (group B) ;③embryonic spinal cellular transplantation group (group C) ;④em-bryonic spinal cellular transplantation and greater omental transposition group (group D). Each group consisted of 6 dogs. SEP(somatosensory evoked potential) and MEP (motor evoked potential) of the spinal cord were examed prior to the spinal cord injuryand 2 months after the treatment to observe the changes of the animals‘ behavior. All dogs were killed 2 months after surgery andthe spinal cord sections were obtained from TI2 to LI level for pathological analysis and observation under the electron microscope.Re.lilts: There was an obvious difference in the spinal sematosensory evoked potential and the motor evoked potential between thegroup D.and the other three groups (group A, B, and C). Recovery of the behavior was noted. The spinal cells had survived fortwo months following the transplantation. Conclusion: Transplantation of the embryonic spinal cell and greater omentum for treat-ment of the spinal cord injury in dogs can gain a better outcome than the other groups in behavior and spinal somatosensory andmotor evoked potential, but the further study is still essential to confirm its clinical efficacy.     

Renal scarring in spinal cord injury: a progressive process?

STUDY DESIGN: A retrospective analysis. OBJECTIVES: To examine the natural history of renal scarring in the spinal cord injured population.Setting:United Kingdom. METHODS: All spinal cord injured patients with renal scars at our establishment were considered eligible. A total of 27 patients with renal scars were identified. No patient had renal scarring at presentation on radiological imaging. All patients had annual renal imaging with a mean follow up period of 19.1 years. The presence of new scars was considered as evidence of progression. RESULTS: In all, 59% of kidneys developed renal scars with a mean time interval between spinal injury and renal scar development of 13 years. Of these kidneys with scars, only 15.6% demonstrated progression of the scarring process. There were no deaths due to renal causes. CONCLUSION: The aetiology of renal scarring is multifactorial. The findings of this study suggest that renal scarring in the spinal cord injured population is predominantly a nonprogressive process once a scar has developed. This is in concordance with the belief that renal scarring in the paediatric population with vesicoureteric reflux is also a stable, nonprogressive process.     

Can cell therapy heal a spinal cord injury?

STUDY DESIGN: Literature survey. OBJECTIVES: To summarize and discuss current possibilities and success rates for the treatment of spinal cord injury in animal models. SETTINGS: University of Antwerp, Belgium. METHODS: We searched Pubmed for publications from 1997 onwards. Seven older papers were used for completion of data. RESULTS: Despite major progress in pharmacological and surgical approaches, a spinal cord injury still remains a very complex medical and psychological challenge, both for the patients and their relatives, as well as for the involved physicians, with currently no existing curative therapy. For a future efficient treatment, one has to consider and combine four main approaches: (1) tissue or cell transplantation, (2) providing growth-stimulating factors (neurotrophic factors), (3) blocking factors which inhibit neural regeneration and (4) modulation of inflammatory response following spinal cord injury. CONCLUSIONS: Although different treatment options have proven to be successful in animal models, they also provide a realistic view on a complex therapeutical approach, which needs to be further investigated in many carefully designed animal studies before human applications can be considered.     

Antioxidation of quercetin against spinal cord injury in rats

Objective : To observe the effect of quercetin on experimental spinal cord injury (SCI) in rats. Methods: Sixty Sprague-Dawley rats were randomly divided into four groups : Group A only for laminectomy, Group B for laminectomy with SCI, Group C for SCI and intraperitoneal injection with a bolus of 200 mg/kg quercetin and Group D for SCI and intraperitoneal injection of saline. SCI model was made by using modified Aliens method on T12. Six rats of each group were killed at 4 h after injury and the levels of free iron and malondialdehyde ( MDA) of the involved spinal cord segments were measured by bleomycin and thiobarbituric acid (TBA) assays separately. The recovery of hind limb function was assessed by Modified Tarlov 's scale and inclined plane method at 7 d,14 d and 21 d after SCI. The histological changes of the damaged spinal cord were also examined at 7 d after SCI. Results: After SCI, the levels of free iron and MDA were significantly increased in Groups B and D, while not in Group C. The Modified Tarlov 's score and the inclined plane angles were significantly decreased in Groups B, C and D. The histological findings were not improved. Conclusions: After SCI, quercetin can reduce the level of lipid peroxidation, but not improve recovery of function.     

Biomarkers of acute kidney injury: can we replace serum creatinine?

Acute kidney injury (AKI) is frequent in hospitalized critically ill patients and mortality associated with AKI is largely unchanged over many decades. The new nomenclature, AKI, reflects the entire spectrum of acute renal failure, recognizing that an acute decline in kidney function can be secondary to an injury that causes functional or structural changes in the kidneys [Mehta et al. 2007]. An abrupt change in serum creatinine level has been the primary method for diagnosing AKI for nearly 60 years despite its well recognized limitations [Addis et al. 1947, Barrett and Addis 1947, Fisher and Wilhelmi 1937, Star 1998]. These limitations are mainly related to the delayed diagnosis of AKI associated with delayed rise in serum creatinine and the lack of specificity and sensitivity associated with small changes in serum creatinine. It is believed that these limitations associated with diagnosis of AKI have prevented progress by interfering with the design of clinical trials for newer therapies. It is now widely believed that the availability of accurate and objective early biomarkers of AKI will stimulate progress in the development of early interventions in AKI. Recognition of this concept has led to a surge in preclinical, translational and clinical research for discovery and validation of biomarkers in AKI. In this review we will discuss the role of biomarkers in AKI and the promising biomarkers on the horizon.