Biomedical subjects

Peter Brink

Publications and source records attributed to Peter Brink.

6 recordsLinked to original sources

PubMed2006

Factors associated with pressure ulcers in palliative home care.

BACKGROUND: Studies have identified factors associated with pressure ulcers in many health care settings including acute care, complex continuing care, long-term care, and home care. OBJECTIVE: The purpose of this study was to identify factors associated with pressure ulcers among palliative home care clients. Identifying associations specific to each setting is important for ulcer prevention and has implications for clients overall well-being and quality of life. METHODS: The study included all palliative home care clients diagnosed with terminal cancer from one palliative home care agency in Ontario. Information on health was gathered using the interRAI instrument for palliative care. RESULTS: The study found male gender, the inability to lie flat because of shortness of breath, catheter, or ostomy care, and a reduced ability to perform activities of daily living to be associated with pressure ulcers. SIGNIFICANCE OF RESULTS: In some instances, treatment and prevention of pressure ulcers is the primary goal of care. However, pressure ulcers are also suggestive of deterioration and considered as a part of the disease trajectory. Sometimes the primary goal of care of treatment and prevention is displaced by a greater need for comfort.

Female↗

PubMed2005

Risk of new clinical fractures within 2 years following a fracture.

INTRODUCTION: Clinical fractures are associated with an increased relative risk of future fractures, but the absolute risk and timing of new clinical fractures immediately after a clinical fracture have not been reported extensively. The study objective was to determine the absolute risk of subsequent clinical fractures within 2 years after a clinical fracture. METHODS: We analyzed clinical fracture data from a university hospital recruiting all fractures in the area between January 1999 and December 2001. Subjects were 2,419 male and female patients aged 50 years and older, with a total of 2,575 fractures. There were 139 patients with more than one simultaneous fracture. Mean age was 66 years for males and 72 for females. RESULTS: The cumulative incidence of patients with new clinical fractures over 2 years was 10.8% (262/2,419). In the 262 patients with subsequent fractures, we observed a higher mean age, more females and more often multiple baseline fractures compared with the 2,157 patients without subsequent fractures. Kaplan-Meier analysis indicated that age, gender and having multiple baseline fractures contributed significantly to cumulative new fracture incidence. Cox regression showed that these variables independently contributed to a higher subsequent fracture incidence. New fracture incidence was higher with increasing age ( p <0.001; hazard ratio [HR] 1.2 per decade; confidence interval [CI] 1.1-1.3). Females had a new fracture incidence of 12.2% compared with 7.4% in males ( p =0.015; HR 1.5; CI 1.1-2.0). Patients with multiple baseline fractures had a new fracture incidence of 17.3% compared with 10.4% for subjects with one baseline fracture ( p =0.006; HR 1.8; CI 1.2-2.7). Of all clinical fractures occurring within 2 years after a clinical fracture, 60% occurred during the first year and 40% during the second year ( p =0.005). The absolute risk to develop an incident clinical fracture within 2 years after any clinical fracture was 10.8%. Increased age, female gender and the presence of multiple simultaneous fractures at baseline each independently increased the risk of incident fracture. Significantly more fractures occurred in the first year following the index fracture than in the second year. CONCLUSION: Altogether, these data support the need for early prevention of future fracture among individuals with a fracture after age 50, using interventions which have been shown to have a rapid anti-fracture benefit.

Age Distribution↗

PubMed2004

Recreating the biological pacemaker.

In recent years, several groups have reported a variety of strategies for developing biological pacemakers whose ultimate function would be to supplement/replace electronic pacemakers. Strategies have included gene therapy using naked plasmids or viral vectors and cell therapy for which both adult human mesenchymal stem cells (hMSCs) and human embryonic stem cells have been employed. This article reviews the various approaches and summarizes our own research in which the pacemaker gene, HCN2, is administered via viral vector or in an hMSC platform to produce pacemaker function in the intact canine heart.

Adenoviridae↗

PubMed2002

Gap junction uncoupling protects the heart against ischemia.

BACKGROUND: Many stimuli can successfully protect the heart against ischemia. We investigated whether gap junction uncoupling before ischemia was myoprotective. We also studied the function of the adenosine triphosphate-dependent potassium channel, which has been implicated in the mechanism of pharmacologic preconditioning, with respect to gap junction physiology. METHODS: Twenty-eight rabbit hearts were placed on a Langendorff perfusion apparatus. Five were given a 5-minute infusion of 1 mmol/L heptanol (a gap junction uncoupler), 5 were given 10 micromol/L 2,3-butanedione monoxime (an electromechanical uncoupler), and 6 were given no drug. The left anterior descending coronary artery was then occluded for 1 hour and reperfused for 2 hours. Six hearts received 10 micromol/L glybenclamide before heptanol to evaluate the role of the adenosine triphosphate-dependent potassium channel. Six hearts underwent ischemic preconditioning with 2 cycles of 5 minutes of global ischemia and reperfusion. Action-potential duration of the ischemic zone, left ventricular developed pressure, and coronary flow were measured continuously. Infarct size was determined at the end of reperfusion. RESULTS: Heptanol significantly reduced infarct size (from 46% +/- 2% to 22% +/- 5%, P <.01), an effect that was not prevented by glybenclamide. Butanedione monoxime decreased developed pressure but did not significantly reduce infarct size (46% +/- 5% vs 46% +/- 2%, P = not significant). There were no differences among groups with regard to developed pressure or action-potential duration. CONCLUSION: Directly blocking gap junctions preconditions the heart. This protection is not a direct result of a decrease in developed pressure before a prolonged ischemic period nor is it achieved through a mechanism involving the adenosine triphosphate-dependent potassium channel.

Action Potentials↗

PubMed2002

Differences in stimulus induced calcium increases in lacrimal gland acinar cells from normal and NZB/NZW F1 female mice.

PURPOSE: To compare the changes in intracellular free calcium in response to both cholinergic and adrenergic agonists in cells isolated from exorbital lacrimal glands of NZB/NZW F1 female mice (NZB/W) and normal Swiss Webster mice (SW). METHODS: We have loaded cells with Fura-2 and measured total intracellular calcium using ratiomicrofluorometric methods. Isolated cells were also patch-clamped using perforated patch. RESULTS: In all cells, both carbachol (CCh) and phenylephrine (PE) increased intracellular calcium. The calcium increase to both CCh and PE was less in cells from NZB/W animals than in cells from SW animals. In cells from young animals, the baseline calcium levels were the same, but in cells from older (6 months) NZB/W animals, the baseline levels of calcium were 50% higher than those seen in SW animals. CONCLUSION: These data suggest that cells from the NZB/W mice have different calcium dynamics, which could contribute to their compromised fluid secretion.

Adrenergic alpha-Agonists↗

PubMed2002

Paradoxical overexpression and translocation of connexin43 in homocysteine-treated endothelial cells.

Hyperhomocysteinemia is an established cause of defective vasorelaxation. Gene expression screening of human umbilical vein endothelial cells (HUVEC) treated with homocysteine (Hcy) revealed that connexin43 (Cx43) was upregulated. Expression of Cx43 was increased more than twofold in Hcy-treated HUVEC. Gap junctional communication (Lucifer yellow and whole cell patch clamp) was not enhanced in Hcy-treated HUVEC. HUVEC expressing chimeric Cx43-green fluorescent protein exhibited it at cell-cell contacts in control but showed redistribution to the intracellular compartment(s) in Hcy-treated cells. Confocal microscopy of HUVEC stained with anti-Cx43, mitochondrial, and endoplasmic reticulum fluorescent markers showed the localization of Cx43 to the plasma membrane of control cells and its colocalization with the mitochondrial marker in Hcy-treated HUVEC. Studies of isolated mitochondria confirmed overexpression of Cx43 in the mitochondria of Hcy-treated HUVEC. Microdissected renal interlobar arteries, which normally exhibit endothelium-derived hyperpolarizing factor-induced vasorelaxation, showed reduced nitric oxide synthase- and cyclooxygenase-independent vasorelaxation to acetylcholine after pretreatment with Hcy. In summary, Hcy-induced upregulation of Cx43 transcript and protein expression are associated with unaltered intercellular communication, redistribution of Cx43 in HUVEC, and reduced nitric oxide- and prostanoid-independent vascular responses to acetylcholine in Hcy-treated arteries.

Acetylcholine↗