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Biomedical subjects

James P McAllister

Publications and source records attributed to James P McAllister.

16 recordsLinked to original sources
PubMed2007

Effect of surface modification of siliconeon Staphylococcus epidermidis adhesion and colonization.

Cerebrospinal fluid (CSF) shunts for the treatment of hydrocephalus are generally made of silicone rubber. The growth of bacterial colonies on the silicone surface leads to frequent CSF shunt complications. A systematic study of the effect of the surface modification of silicone on Staphylococcus epidermidis adhesion and colonization was performed for different incubation times by means of colony counting and scanning electron microscopy (SEM). Silicone was modified with different biopolymers and silanes, including heparin, hyaluronan, octadecyltrichlorosilane (OTS), and fluoroalkylsilane (FAS) to provide a stable and biocompatible surface with different surface functional groups and degrees of hydrophobicity. The modified silicone surfaces were studied by using contact angle measurements, X-ray photoelectron spectroscopy (XPS), and atomic force microscopy (AFM). After 4 and 8 h of incubation, the FAS- and OTS-coated silicone and the hyaluronan coated OTS/silicone surfaces showed significantly reduced bacterial adhesion and colonization compared to blank silicone by both quantification methods. However, the heparin coated OTS/silicone showed significantly increased bacterial adhesion. These results indicate that the nature of the surface functional group and surface roughness determine the extent of bacterial adhesion and colonization. However, the degree of hydrophobicity of the surface did not appear to play a determining role in bacterial adhesion and colonization.

Bacterial Adhesion↗
PubMed2007

Stability of and inflammatory response to silicon coated with a fluoroalkyl self-assembled monolayer in the central nervous system.

A self-assembled monolayer (SAM) of fluoroalkyl silane (FAS) (CF(3)(CF(2))(5)(CH(2))(2)SiCl(3)) was deposited on the surface of silicon wafers, aiming to enhance its stability and to reduce the inflammatory response in the central nervous system. Following implantation of the FAS SAM coated silicon in rat brains, the FAS SAM coating failed to reduce the inflammatory response of silicon, because it could not prevent the corrosion of the underlying silicon. The corrosion was hindered for the initial 10 days by the FAS SAM coating, but there was nearly no difference when compared to the uncoated silicon when the implantation periods were extended to 28 and 90 days. The FAS SAM coating was completely removed within 28 and 90 days. Meanwhile, on all the extracted uncoated and FAS SAM coated silicon wafers, there were proteinaceous substances deposited on the surfaces, and the amount of the deposits increased with exposure time.

Animals↗
PubMed2006

Effect of surface proteins on Staphylococcus epidermidis adhesion and colonization on silicone.

Shunt infections are one of the most serious complications in shunt implant surgery. Previous studies have suggested that cerebrospinal fluid (CSF) proteins could affect bacterial adhesion and subsequent shunt infection. A systematic study using immobilized protein on the surface of silane-modified silicone was conducted to determine how these modifications influenced Staphylococcus epidermidis adhesion and colonization. A comparison was also made with silicone having physically adsorbed protein. A colony-counting adhesion assay and scanning electron microscopy (SEM) were used to provide quantitative analysis of bacterial adhesion and semi-quantitative analysis of bacterial colonization, respectively. In order to determine the appropriate silanization process for effective protein immobilization, the effect of bovine serum albumin (BSA) immobilized on n-3-(trimethoxysilyl)propyl-ethylenediamine (AEAPS)/silicone, aminopropyltriethoxysilane (APTMS)/silicone, 3-(glycidyloxypropyl)trimethoxysilane (GPTMS)/silicone, and octadecyltrichlorosilane (OTS)/silicone on bacterial adhesion was investigated. Upon identifying that OTS is the most effective silane, different types of proteins, including: BSA, human serum albumin (HSA), gamma-globulin, and fibrinogen were immobilized on OTS/silicone by a photo-immobilization method. Immobilized protein on modified silicone surfaces was found to be stable in saline for 30 days, while physically adsorbed protein showed instability within hours as determined by contact angle measurements and X-ray photoelectron spectroscopy (XPS). For HSA/OTS/silicone, BSA/OTS/silicone, gamma-globulin/OTS/silicone, fibrinogen/OTS/silicon, and physically absorbed BSA on silicone, the contact angles were 78.5 degrees, 80.7 degrees, 78.9 degrees, 81.3 degrees, and 96.5 degrees; and the amount of nitrogen content was found to be 4.6%, 5.0%, 5.6%, 7.2%, and 3.2%, respectively. All protein immobilized on OTS/silicone surfaces significantly reduced bacterial adhesion by around 75% compared to untreated silicone, while physically adsorbed BSA on silicone reduced by only 29.4%, as determined by colony-counting adhesion assay. However, there was no significant difference on bacterial adhesion among the different types of proteins immobilized on OTS/silicone. Minimizing bacterial adhesion and colonization can be attributed to the increased concentration of -NH2 group, and stability and more hydrophilic nature of the protein/OTS/silicone surfaces.

Animals↗
PubMed2006

Effect of cast molded rifampicin/silicone on Staphylococcus epidermidis biofilm formation.

Infection is one of the most common catheter-related complications, especially in shunt systems used to treat hydrocephalus. Staphylococcus epidermidis is directly related to biomaterial infections owing to its ability to form a biofilm on implanted materials. In this study, scanning electron microscopy (SEM) and atomic force microscopy (AFM) were employed to investigate the effect of the antibiotic rifampicin on the colonization and growth of S. epidermidis 35984 on the surface of silicone. A cast molding method was used to load rifampicin into the silicone precursor before it was cured. Bacteria with a diameter of 800-1000 nm and height of 200-500 nm were found to be embedded in the biofilm. Compact multilayer biofilm structures were found on silicone surfaces upon incubation for 4 and 24 h. On the other hand, sparser biofilm structures were observed on rifampicin-loaded surfaces after incubation for the same duration. Deformation of bacteria was observed by AFM. Moreover, different bacterial colony structures on the surfaces of silicone and rifampicin-loaded silicone were observed by AFM and SEM.

Antibiotics, Antitubercular↗
PubMed2006

Immobilization of polysaccharides on a fluorinated silicon surface.

A self-assembled monolayer (SAM) of fluoroalkyl silane (FAS) was deposited on a silicon surface by chemical vapor deposition (CVD) at room temperature under 1.01x10(5)Pa nitrogen. Using this new approach, the quality and reproducibility of the SAM are better than those prepared either in solution or by vapor phase deposition, and the deposition process is simpler. In this modified CVD process, the silane monomers, instead of the oligomeric species, are the primary reactants. Full coverage of the silicon surface by FAS molecules was achieved within 5 min. Heparin and hyaluronan, two naturally occurring biocompatible polysaccharides, were successfully covalently attached on the FAS SAM/Si surface by photo-immobilization. Atomic force microscopy (AFM) revealed the morphologic changes after the immobilization of heparin and hyaluronan, and X-ray photoelectron spectroscopy (XPS) confirmed the change in chemical compositions. Such combination of coatings is expected to enhance the stability and biocompatibility of the base material.

Biocompatible Materials↗
PubMed2006

What we don't (but should) know about hydrocephalus.

In an effort to identify critical gaps in the prevailing knowledge of hydrocephalus, the authors formulated 10 key questions. 1) How do we define hydrocephalus? 2) How is cerebrosinal fluid (CSF) absorbed normally and what are the causes of CSF malabsorption in hydrocephalus? 3) Why do the ventricles dilate in communicating hydrocephalus? 4) What happens to the structure and function of the brain when it is compressed and stretched by the expanding ventricles? 5) What is the role of cerebrovenous pressure in hydrocephalus? 6) What causes normal-pressure hydrocephalus? 7) What causes low-pressure hydrocephalus? 8) What is the pathophysiology of slit ventricle syndrome? 9) What is the pathophysiological basis for neurological impairment in hydrocephalus, and to what extent is it reversible? 10) How is the brain of a child with hydrocephalus different from that of a young or elderly adult? Rigorous answers to these questions should lead to more effective and reliable treatments for this disorder.

Adolescent↗
PubMed2005

Increased astrocyte proliferation in rats after running exercise.

The aim in this study was to investigate whether physical exercise could induce astroglial proliferation in the frontoparietal cortex and dorsolateral striatum where extensive angiogenesis had been found after exercise in previous studies. Adult male Sprague Dawley rats (n=48) were used in four experimental groups. Animals were exercised 30 min each day on a treadmill on which repetitive locomotor movement was required, for 0 (n=12), 3 (n=12) or 6 (n=12) weeks, as well as 3-week exercise plus 3-week rest (n=12). Brain tissues of the exercised and non-exercised rats were processed for glial fibrillary acidic protein (GFAP) immunocytochemistry (n=6 x 4) and Western blotting (n=6 x 4) to evaluate regional astrocyte proliferation in the frontoparietal cortex and dorsolateral striatum. By using GFAP immunocytochemistry and stereological methods, we compared the density of astrocytes in the animals with or without exercise. In comparison to non-exercised animals, a significant (p<0.01) increase in the number of astrocytes was observed in both cortex and striatum of rats exercised for 3 or 6 weeks. Our data also indicated that astrocytic density continued to increase up to 6 weeks either with an additional 3 weeks of exercise (p<0.01) or 3 weeks of rest (p<0.01). In addition, Western blotting analysis showed an obvious increase in GFAP protein from cortex and striatum of exercised animals. Astrocytosis after exercise, coupled with angiogenesis, is thought to provide strength to the neurovascular unit (a construct consisting of microvascular endothelium, astroglia, neurons and the extracellular matrix). Strengthening of this unit by exercise may protect blood-brain-barrier function following brain injury, such as that occurring after stroke.

Animals↗
PubMed2005

Evaluation of polymer and self-assembled monolayer-coated silicone surfaces to reduce neural cell growth.

The development of silicone catheters has improved the treatment of hydrocephalus. Unfortunately, the functionality of the catheters used for the treatment of hydrocephalus is compromised by cell obstruction. In this study silicone surfaces coated with biopolymers (heparin and hyaluronan) and self-assembled monolayers (SAM) (octadecyltrichlorosilane-OTS and fluoroalkylsilane-FAS) were employed to investigate the effect of these coatings on astrocyte and choroid plexus cell growth in vitro. Compared to unmodified silicone, FAS surfaces significantly reduced (p<0.05) astrocyte proliferation, heparin (p<0.001) and hyaluronan (p<0.001) surfaces significantly increased astrocyte growth, while no significant difference was observed on OTS surfaces. A similar trend was observed for choroid plexus cell growth on heparin (p<0.05) and hyaluronan (p<0.05) coatings, however, no significant reduction in cell growth was observed on FAS- or OTS-coated surfaces compared to silicone. Low cell growth may be attributed to hydrophobicity of the surfaces (FAS 112.2+/-2.6 degrees , OTS 102.2+/-1.3 degrees). Contact angle measurements confirmed the stability of the hydrophobic and hydrophilic properties of all the coatings on the silicone surfaces for 30 days. Surface roughness did not play an important role on cell growth. Silicone shunts coated with SAMs may be suitable for future clinical applications to improve the treatment of hydrocephalus.

Animals↗
PubMed2005

The value of C-reactive protein in the management of shunt infections.

OBJECT: Shunt infections and their management remain a clinically important problem in patients with hydrocephalus. The authors evaluated, in comparison with traditional parameters, C-reactive protein (CRP) in blood/serum (S-CRP) and in cerebrospinal fluid (CSF; C-CRP) for its power to identify and treat patients with infected shunts. METHODS: On 84 different occasions, CSF and blood samples from 59 children suspected of having shunt/CSF infections were obtained and evaluated. An infection was proven by a CSF culture in 35 of 84 evaluations. Values for S-CRP in infected individuals were higher than in noninfected ones (91.8 +/- 70.2 mg/L compared with 16.1 +/- 28.3 mg/L, p < 0.0001). The sensitivity of S-CRP testing was 97.1%, the specificity 73.5%, the negative predictive value 97.3%, and the receiver operating characteristic area 91.6%. The probability of shunt/CSF infection--provided that the S-CRP level was greater than 7 mg/L--rose from 41.7% (prevalence) to a posttest level of 72.3%. Specificity and posttest probability were 87.8 and 87.2%, respectively, if cases with other concurrent infections were excluded. The probability of missing a CSF/shunt infection at an S-CRP lower than 7 mg/L was 2.7%. All other diagnostic parameters did not yield useful test results. The rate of reinfection was elevated in patients in whom S-CRP levels were greater than 7 mg/L at the time of shunt reimplantation. CONCLUSIONS: Analysis of these data suggests that the S-CRP level should be included in the first-line workup of patients with suspected shunt/CSF infection. It seems justified to avoid performing a shunt tap if S-CRP levels are less than 7 mg/L. A larger multicenter trial is necessary to confirm these promising diagnostic results and to deliver hard data concerning whether or not a normalized S-CRP level is a reliable indicator of successful antibiotic therapy and whether a shunt can be safely reimplanted.

Adolescent↗
PubMed2004

Exercise preconditioning ameliorates inflammatory injury in ischemic rats during reperfusion.

There is evidence that physical activity is associated with decreased brain injury resulting from transient middle cerebral artery (MCA) occlusion. We investigated whether exercise could reduce stroke-induced brain inflammatory injury and its associated mediators. Sprague Dawley rats (3 months old) were subjected to 30 min exercise on a treadmill each day for 1-3 weeks. Stroke, in exercised and non-exercised animals, was then induced by a 2-h MCA occlusion followed by 48 h of reperfusion using an intraluminal filament. Endothelial expression of the intercellular adhesion molecule 1 (ICAM-1) and leukocyte infiltration were determined by immunocytochemistry. Expressions of tumor necrosis factor-alpha (TNF-alpha) and ICAM-1 mRNA were detected using a real-time reverse transcriptase-polymerase chain reaction in ischemic rats with or without exercise, and in non-ischemic control rats following exercise. Expression of TNF-alpha increased after exercise for 2 and 3 weeks. The overexpression of TNF-alpha was not further elevated in 3-week exercised rats subjected to a transient MCA occlusion and 6 or 12 h of reperfusion, as compared to that in non-exercised rats. Furthermore, ICAM-1 mRNA expression remained at significantly (P<0.01) low levels in exercised animals during ischemia/reperfusion. Pre-ischemic exercise significantly (P<0.01) reduced numbers of ICAM-1-positive vessels and infiltrating leukocytes in the frontoparietal cortex and dorsolateral striatum in ischemic rats after 48 h of reperfusion. Exercised ischemic rats demonstrated an 11+/-7% infarct volume of contralateral hemisphere as compared to a 52+/-3% volume in non-exercised ischemic rats. The data suggests that exercise inhibits inflammatory injury (i.e., decreased expression of inflammatory mediators and reduced accumulation of leukocytes) during reperfusion, leading to reduced brain damage. Chronically increased expression of TNF-alpha during exercise prevent the same downstream inflammatory events as does acutely elevated TNF-alpha after ischemia/reperfusion.

Analysis of Variance↗
PubMed2004

Long-term neuroprotection induced by regional brain cooling with saline infusion into ischemic territory in rats: a behavioral analysis.

The neuroprotective effect of hypothermia has long been recognized. Our recent studies have demonstrated the significant therapeutic value of local brain cooling in the ischemic territory prior to reperfusion in stroke, with reduced infarction and inflammatory responses up to 48 hours of reperfusion. The goal of this study was to determine if local brain cooling, produced by infusion of cold saline, could induce long-term functional improvement after stroke. A hollow filament was used to block the middle cerebral artery (MCA) for 3 hours, and then to locally infuse the ischemic territory with 6 ml cold saline (20 degrees C) for 10 minutes prior to reperfusion. This brain cooling infusion induced a significant (p < 0.01) decrease in neurologic deficits and significantly (p < 0.01) improved motor behavior in ischemic rats after 14 days of reperfusion, compared with ischemic rats without local cold saline infusion. This improvement continued for up to 28 days after reperfusion. No significant difference in motor performance was observed between the brain cooling infusion and normal control groups. Significant (p < 0.01) reductions in infarct volume were also evident. In conclusion, a local cerebral hypothermia induced by local saline infusion prior to reperfusion produced a long-term functional recovery after ischemic stroke. A therapeutic procedure, which combines prereperfusion infusion into an ischemic region with coincident cerebral hypothermia and perhaps subsequent recanalization of an occluded intracranial vessel, may improve the outcome for stroke patients.

Animals↗
PubMed2004

Local saline infusion into ischemic territory induces regional brain cooling and neuroprotection in rats with transient middle cerebral artery occlusion.

OBJECTIVE: The neuroprotective effect of hypothermia has long been recognized. Use of hypothermia for stroke therapy, which is currently being induced by whole-body surface cooling, has been limited primarily because of management problems and severe side effects (e.g., pneumonia). The goal of this study was to determine whether local infusion of saline into ischemic territory could induce regional brain cooling and neuroprotection. METHODS: A novel procedure was used to block the middle cerebral artery of rats for 3 hours with a hollow filament and locally infuse the middle cerebral artery-supplied territory with 6 ml cold saline (20 degrees C) for 10 minutes before reperfusion. RESULTS: The cold saline infusion rapidly and significantly reduced temperature in cerebral cortex from 37.2 +/- 0.1 to 33.4 +/- 0.4 degrees C and in striatum from 37.5 +/- 0.2 to 33.9 +/- 0.4 degrees C. The significant hypothermia remained for up to 60 minutes after reperfusion. Significant (P < 0.01) reductions in infarct volume (approximately 90%) were evident after 48 hours of reperfusion. In ischemic rats that received the same amount of cold saline systemically through a femoral artery, a mild hypothermia was induced only in the cerebral cortex (35.3 +/- 0.2 degrees C) and returned to normal within 5 minutes. No significant reductions in infarct volume were observed in this group or in the ischemic group with local warm saline infusion or without infusion. Furthermore, brain-cooling infusion significantly (P < 0.01) improved motor behavior in ischemic rats after 14 days of reperfusion. This improvement continued for up to 28 days after reperfusion. CONCLUSION: Local prereperfusion infusion effectively induced hypothermia and ameliorated brain injury from stroke. Clinically, this procedure could be used in acute stroke treatment, possibly in combination with intra-arterial thrombolysis or mechanical disruption of clot by means of a microcatheter.

Animals↗
PubMed2003

Reduced inflammatory mediator expression by pre-reperfusion infusion into ischemic territory in rats: a real-time polymerase chain reaction analysis.

The aim in this study was to investigate if our new experimental model for stroke therapy, flushing the ischemic territory with saline prior to reperfusion, could reduce overexpression of inflammatory mediators during reperfusion. Stroke in Sprague-Dawley rats (n=24) was induced by a 2-h middle cerebral artery occlusion using a novel intraluminal hollow filament. Prior to reperfusion, 12 of the ischemic rats received 6 ml isotonic saline at 37 degrees C infused into the ischemic area through the filament. Expression of interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule 1 (ICAM-1) mRNA was analyzed by real-time reverse transcriptase-polymerase chain reaction (real-time RT-PCR). A significant overexpression (9-26 fold) of the genes encoding TNF-alpha, IL-1beta and ICAM-1 in ischemic rats was found during early reperfusion without flushing at 6 and 12 h. This increase was significantly reduced at both 6 and 12 h post-reperfusion as a result of saline flushing.

Animals↗
PubMed2003

Regional brain cooling induced by vascular saline infusion into ischemic territory reduces brain inflammation in stroke.

The neuroprotective effect of hypothermia has long been recognized. Use of hypothermia for stroke therapy, which is currently being induced by whole body surface cooling, has been largely limited because of management problems and severe side effects (i.e., pneumonia). Our recent studies have demonstrated the significant therapeutic value of local brain cooling in the ischemic territory prior to reperfusion in stroke. The goal of this study was to determine if cerebral local cooling infusion could reduce stroke-mediated brain injury by inhibiting inflammatory responses. A hollow filament was used to block the middle cerebral artery (MCA) for 3 hours, and then to locally infuse the ischemic territory with 6 ml cold saline (20 degrees C) for 10 min prior to 48-h reperfusion. This cold saline infusion significantly ( P<0.01) reduced temperature of the MCA supplied territory (in cerebral cortex from 37.2+/-0.1 degrees C to 33.4+/-0.4 degrees C, in striatum from 37.5+/-0.2 degrees C to 33.9+/-0.4 degrees C), with the hypothermia remaining for at least 45 min after reperfusion. Consequently, significant ( P<0.01) reductions in endothelial expression of intracellular adhesion molecule-1 (ICAM-1), the key step for inflammatory progress, as well as leukocyte infiltration, were evident in both cortex and striatum after reperfusion. As a control, ischemic rats received the same amount of cold saline systemically through a femoral artery. A mild hypothermia was induced in the cerebral cortex (35.3+/-0.2 degrees C) but not in the striatum (36.8+/-0.2 degrees C). The reduced cortical temperature returned to normal within 5 min. Brain temperature in ischemic rats perfused locally with saline at 37 degrees C remained normal. Intensive expression of ICAM-1 and accumulation of leukocytes was observed in ischemic control groups without brain cooling infusion. In conclusion, brain hypothermia induced by local pre-reperfusion infusion ameliorated brain inflammation from stroke.

Analysis of Variance↗