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Biomedical subjects

Andrew Baker

Publications and source records attributed to Andrew Baker.

At least 19 recordsLinked to original sources
PubMed2026

The chromosomal genome sequence of the lesser starlet coral, Siderastrea radians (Pallas, 1766) (Scleractinia: Rhizangiidae) and its associated microbial metagenome sequences.

We present a genome assembly from a specimen of Siderastrea radians (lesser starlet coral; Cnidaria; Anthozoa; Scleractinia; Rhizangiidae). The genome sequence has a total length of 807.19 megabases. Most of the assembly (94.17%) is scaffolded into 14 chromosomal pseudomolecules. The mitochondrial genome has also been assembled, with a length of 19.38 kilobases. Gene annotation of this assembly by Ensembl identified 47 051 protein-coding genes. From the metagenome data, we recovered two binned metagenomes assigned to the bacterial phylum Bacteroidota and class Bacteroidia.

Scleractinia↗
PubMed2006

Number of deaths by neurological criteria, and organ and tissue donation rates at three critical care centres in Canada.

PURPOSE: Comparative organ donation rates are expressed per million population and by this measurement, Canada lags behind other countries. These estimates do not account for differing demographics and health patterns of populations which can result in different rates of death by neurological criteria and subsequent donation rates. We sought to measure directly the number of deaths by neurological criteria, the associated donation rates, and the reasons for the differences. METHODS: A prospective evaluation of deaths by neurological and cardiorespiratory criteria in the critical care areas of three major adult Canadian tertiary care centres over a seven month period was undertaken. Patients were assessed for eligibility for organ and tissue donation and ultimate disposition. RESULTS: Annualized rates of death by neurological criteria varied from 2.3%-7.5% (8.6-28 patients) of all deaths. Conversion to actual donors ranged from 20-86%, with family refusal rates accounting for most of this variation. There were only three cases of suspected death by neurological criteria where a complete examination was not performed. CONCLUSIONS: There is substantial geographic variability in the rate of neurological death and actual organ donation rates in these Canadian tertiary care centres. These variations are principally related to regional differences in demographics of brain injury, referral patterns and donation consent rates, rather than lack of identification of potential donors.

Adult↗
PubMed2006

Clinical, biochemical, and electrocardiographic aspects of Trypanosoma cruzi infection in free-ranging golden lion tamarins (Leontopithecus rosalia).

BACKGROUND: Wild golden lion tamarins from the Biological Reserve of Poço das Antas, Rio de Janeiro, Brazil, have high prevalence of Trypanosoma cruzi infection leading us to clinically assess the disease in this endangered species. METHODS: 34 tamarins were sampled for the presence of T. cruzi infection (through serology) and clinical evaluation (electrocardiography, blood counts and biochemical analysis). RESULTS: 32% of the sampled tamarins were T. cruzi positive, 45% of these displayed cardiac abnormalities. Main cardiac abnormality in infected tamarins was T wave low voltage; R wave low voltage and V3S wave high voltage were also found. The tamarins displaying T wave low voltage had high proportion of seric cardiac creatine kinase. Seric mean total protein was significantly higher in infected tamarins. CONCLUSIONS: Sampled tamarins displayed typical signs of T. cruzi infection, similar to experimentally infected primates and human natural infection. Potential risk of T. cruzi infection to this endangered species is discussed.

Aging↗
PubMed2005

Long-term potentiation of evoked presynaptic response at CA3-CA1 synapses by transient oxygen-glucose deprivation in rat brain slices.

Physiological activity-dependent long-term changes in synaptic transmission, as long-term potentiation (LTP) are thought to be the substrate of learning and memory. However, a form of postsynaptic pathological LTP at the CA3-CA1 synapses has been demonstrated following few minutes of anoxia and aglycemia in vitro. The ischemia LTP shared many molecular mechanisms with the physiological LTP, and was believed to be involved in the delayed neuronal death following ischemia. However, the role of the presynaptic component in this regard is not known. Here we show that a short period of oxygen-glucose deprivation can induce a form of LTP (lasting for hours) of the presynaptic response at the CA3-CA1 synapses. This form of LTP is independent of postsynaptic alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors, but Ca(2+) dependent. This presynaptic LTP may represent a presynaptic hyperexcitability of the afferent fibers following ischemia, and responsible for the excitotoxicity to the CA1 neurons (ischemia-induced increases of glutamate release that kills neurons) and the postsynaptic pathological ischemic LTP.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2005

GAL4-GFP enhancer trap lines for genetic manipulation of lateral root development in Arabidopsis thaliana.

Lateral root development occurs throughout the life of the plant and is responsible for the plasticity of the root system. In Arabidopsis thaliana, lateral root founder cells originate from pericycle cells adjacent to xylem poles. In order to study the mechanisms of lateral root development, a population of Arabidopsis GAL4-GFP enhancer trap lines were screened and two lines were isolated with GAL4 expression in root xylem-pole pericycle cells (J0121), i.e. in cells competent to become lateral root founder cells, and in young lateral root primordia (J0192). These two enhancer trap lines are very useful tools with which to study the molecular and cellular bases of lateral root development using targeted gene expression. These lines were used for genetic ablation experiments by targeting the expression of a toxin-encoding gene. Moreover, the molecular bases of the enhancer trap expression pattern were characterized. These results suggest that the lateral-root-specific GAL4 expression pattern in J0192 is due to a strong enhancer in the promoter of the LOB-domain protein gene LBD16.

Arabidopsis↗
PubMed2005

Loss or inhibition of uPA or MMP-9 attenuates LV remodeling and dysfunction after acute pressure overload in mice.

Left ventricular (LV) hypertrophy is a natural response of the heart to increased pressure loading, but accompanying fibrosis and dilatation may result in irreversible life-threatening heart failure. Matrix metalloproteinases (MMPs) have been invoked in various cardiac diseases, however, direct genetic evidence for a role of the plasminogen activator (PA) and MMP systems in pressure overload-induced LV hypertrophy and in heart failure is lacking. Therefore, the consequences of transverse aortic banding (TAB) were analyzed in mice lacking tissue-type PA (t-PA(-/-)), urokinase-type PA (u-PA(-/-)), or gelatinase-B (MMP-9(-/-)), and in wild-type (WT) mice after adenoviral gene transfer of the PA-inhibitor PAI-1 or the MMP-inhibitor TIMP-1. TAB elevated LV pressure comparably in all genotypes. In WT and t-PA(-/-) mice, cardiomyocyte hypertrophy was associated with myocardial fibrosis, LV dilatation and dysfunction, and pump failure after 7 weeks. In contrast, in u-PA(-/-) mice or in WT mice after PAI-1- and TIMP-1-gene transfer, cardiomyocyte hypertrophy was moderate and only minimally associated with cardiac fibrosis and LV dilatation, resulting in better preservation of pump function. Deficiency of MMP-9 had an intermediate effect. These findings suggest that the use of u-PA- or MMP-inhibitors might preserve cardiac pump function in LV pressure overloading.

Animals↗
PubMed2004

Differential alterations in the expression and activity of matrix metalloproteinases 2 and 9 after transient cerebral ischemia in mice.

Abnormal expression and activity of matrix metalloproteinases (MMPs) may contribute to the pathophysiology of cerebral disease such as ischemic injury. In this study, we compared the cellular localization, expression, and activity of MMP-2 and -9 in relation to the evolution of neuronal damage 24 and 72 h after transient global ischemia. In response to ischemia, there was a generalized increase in cellular MMP-2 immunoreactivity at 24-h reperfusion (in neurons, glia and vessels) whereas at 72-h reperfusion the increase in MMP-2 was predominantly in glia. These glial alterations contributed to a significant increase in pro MMP-2 levels in ischemic regions (P < 0.01) as measured by zymography. In contrast, MMP-9 was predominantly upregulated in neurons and this was significantly different to shams at 24- and 72-h reperfusion after ischemia (P < 0.05). Notably, a dramatic increase in proteolytic activity in neurons was observed 24 h after ischemia and this response was absent at 72 h post-ischemia. The present data are supportive of a role for MMPs in contributing to neuronal injury after ischemia.

Animals↗
PubMed2004

Presynaptic excitability as a potential target for the treatment of the traumatic cerebellum.

Using an extracellular recording method, we have previously shown a hyperexcitability of the presynaptic response in fluid percussion injury (FPI) in rats. In this study, we demonstrated that treatment with cis-ACBD, a glutamate reuptake inhibitor, depressed the presynaptic potential (PSP) in naive/sham controls, while it potentiated the PSP in FPI rats. On the contrary, (RS)-APICA, a selective group II metabotropic glutamate receptor antagonist, potentiated PSP in controls, but depressed PSP in FPI rats. These results indicate that an alteration of the normal function of metabotropic glutamate receptors and glutamate reuptake system or an altered reactivity of presynaptic fibers was induced by FPI. This alteration may contribute to the reported loss of Purkinje cells after FPI. PSP may be used as a potential tool for evaluating treatments of FPI or as a potential target for the prevention of Purkinje cell death.

Animals↗
PubMed2003

MMP-2 and MMP-9 synergize in promoting choroidal neovascularization.

Matrix metalloproteinase 2 (MMP-2) and MMP-9 are increased in human choroidal neovascularization (CNV) occurring during the exudative most aggressive form of age-related macular degeneration (AMD), but their precise role and potential interactions remain unclear. To address the question of MMP-2 and MMP-9 functions, mice deficient in the expression of MMP-2 (MMP-2 KO), MMP-9 (MMP-9 KO), and both MMP-2 and MMP-9 (MMP-2,9 KO) with their corresponding wild-type mice (WT) underwent CNV induction by laser-induced rupture of the Bruch's membrane. Both the incidence and the severity of CNV were strongly attenuated in double deficient compared with single gene deficient mice or corresponding WT controls. The reduced neovascularization was accompanied by fibrinogen/fibrin accumulation. Furthermore, overexpression of the endogenous MMP inhibitors TIMP-1 or TIMP-2 (delivered by adenoviral vectors) in WT mice or daily injection of a synthetic and gelatinase selective MMP inhibitor (Ro 26-2853) significantly decreased the pathological reaction. These findings suggest that MMP-2 and MMP-9 may cooperate in the development of AMD and that their selective inhibition represents an alternative strategy for the treatment of choroidal neovascularization.

Animals↗
PubMed2003

A novel function for tissue inhibitor of metalloproteinases-3 (TIMP3): inhibition of angiogenesis by blockage of VEGF binding to VEGF receptor-2.

Tissue inhibitor of metalloproteinases-3 (TIMP3) is one of four members of a family of proteins that were originally classified according to their ability to inhibit matrix metalloproteinases (MMP). TIMP3, which encodes a potent angiogenesis inhibitor, is mutated in Sorsby fundus dystrophy, a macular degenerative disease with submacular choroidal neovascularization. In this study we demonstrate the ability of TIMP3 to inhibit vascular endothelial factor (VEGF)-mediated angiogenesis and identify the potential mechanism by which this occurs: TIMP3 blocks the binding of VEGF to VEGF receptor-2 and inhibits downstream signaling and angiogenesis. This property seems to be independent of its MMP-inhibitory activity, indicating a new function for this molecule.

Cell Division↗
PubMed2003

Long-term outcome of MacIntosh reconstruction of chronic anterior cruciate ligament insufficiency using fascia lata.

The purpose of this study was to assess the long-term outcome of the MacIntosh lateral-substitution over-the-top anterior cruciate ligament (ACL) reconstruction in 82 patients (84 knees) at an average follow-up of 9.8 years. In this retrospective cohort study patients were evaluated with subjective questionnaires and by clinical and radiographic examination. Using the Lysholm score, 17 knees were rated excellent, 35 good, 19 fair, and 13 poor. The pivot shift test was negative in 74 patients. Altogether, 30 knee radiographs were evaluated. The mean Hospital for Special Surgery ACL radiographic score was 20.9. There was a non-significant association between the radiographic score and the Lysholm score and between a worsening radiographic score and increasing time from injury. The MacIntosh lateral-substitution over-the-top ACL reconstruction shows results comparable to those of previously reported long-term studies. Although endoscopically assisted intraarticular reconstructions with faster rehabilitation protocols have now become popular, this procedure may be considered in patients needing an intra- and extraarticular reconstruction in whom cosmesis is not an issue.

Adolescent↗
PubMed2002

Presynaptic hyperexcitability at cerebellar synapses in traumatic injury rat.

Neurotransmission in rat cerebellum following fluid percussion injury (FPI) was studied by extracellular recording method. An increased amplitude of population spikes from presynaptic mossy fibers was detected at 3 days after FPI. However, there were no differences at 1 h, 1 day, 1 week or 2 weeks after FPI compared to nai;ve controls. An enhanced amplitude of the population spikes, as well as the after hyperpolarization component from presynaptic response of the parallel fibers, was seen in the groups at 3 days and 1 week post FPI, but not in other groups. These results indicate a presynaptic hyperexcitation was induced by FPI within a specific time window. This hyperexcitability may contribute to the reported loss of Purkinje cells after FPI.

Animals↗
PubMed2002

The non-steroidal anti-inflammatory drug niflumic acid inhibits Candida albicans growth.

The non-steroidal anti-inflammatory drug niflumic acid was found to inhibit growth of the yeast form of Candida albicans. Niflumic acid inhibited respiratory oxygen uptake and it is hypothesised that this was achieved by cytosolic acidification and block of glycolysis. Inhibitory concentrations are compatible with current practice of topical application.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMedDate not supplied

Continuous jugular venous oximetry in the neurointensive care unit--a brief review.

PURPOSE: To describe the technique of continuous jugular venous oxygen saturation (SjVO(2)) monitoring and review its applications in the neurointensive care unit (NICU), with special reference to the management of raised intracranial pressure (ICP) following severe acute brain injury. SOURCE: This narrative review is based on a selection of current literature on SjVO(2) monitoring in conjunction with local experience using this technique. PRINCIPAL FINDINGS: Despite limitations, the use of SjVO(2) monitoring has the potential to impact on patient care in the NICU. The placement of the catheter is relatively simple. Studies have confirmed that abnormalities in cerebral venous oxygen saturation are associated with adverse outcome following traumatic brain injury. There is evidence that SjVO(2) may be a useful adjunct to ICP monitoring of patients with intracranial hypertension. Furthermore, managing cerebral extraction of oxygen in conjunction with cerebral perfusion pressure may result in an improved outcome. Further research in this area is needed. Other indications for SjVO(2) monitoring include subarachnoid hemorrhage, cardiopulmonary bypass and following ischemic stroke. CONCLUSION: In the past, the management of severe acute brain injury was targeted at ICP and perfusion pressure with little consideration for the metabolic requirements of the injured brain. SjVO(2) monitoring is another tool the intensivist can use to obtain information about the global oxygen requirements of the injured brain on a continuous basis. Whether this will impact on care in the long term remains to be seen.

Brain Injuries↗