Biomedical subjects

David M Jackson

Publications and source records attributed to David M Jackson.

7 recordsLinked to original sources

PubMed2007

Creating a successful school-based mobile dental program.

BACKGROUND: Dental disease is one of the leading causes of school absenteeism for children. This article describes the creation and evolution of the St. David's Dental Program, a mobile school-based dental program for children. METHODS: The dental program is a collaboration of community partners in Central Texas that provides free dental care to low-income children in schools without relying on reimbursements or government funding. RESULTS: Since 1998, the program has provided 132,791 screenings for oral health treatment needs and 38,634 encounters for sealants or treatment. In 2005, the program provided $2.1 million worth of services at a cost of $1.2 million (not including donated services). Factors important to the program's success included sustained funding for general operating costs; well-compensated clinicians to deliver care and experienced human service workers to manage program operations; the devotion of resources to maximize consent form return rates; and the development of strong relationships with school district and individual school staff. CONCLUSIONS: By removing cost, time, transportation, and bureaucratic barriers, the program was able to reach more children than fixed-site clinics. The program was a merging of private and public health dentistries. This model can be useful to other communities in light of the unmet need for dental care and tighter federal, state, and local government budgets.

Adolescent↗

PubMed2006

Back pain in whitewater rafting guides.

OBJECTIVE: The purpose of this study was to quantify rates of back pain among whitewater rafting guides and to look for correlations between the presence of back pain and specific activities associated with guiding. The secondary objective was to provide suggestions for outfitters according to the results of this study, which may be of assistance to their guide staff. METHODS: A mail-out-mail-back survey was sent to 2510 rafting guides working in Washington, Oregon, Idaho, Utah, Colorado, and the Grand Canyon during the summer of 2004 to quantify whitewater raft guiding characteristics and incidence of back pain. RESULTS: Of the 390 surveys returned, 77.4% of guides reported back pain while guiding and 20.8% had back pain lasting longer than 1 week at the time of the survey. Stacking 5 or more inflated boats for transport was correlated with the presence of pain (chi(2) = 8.4, v = 1, P < .01), and loading and unloading rafts while guests are waiting was correlated with back pain lasting longer than 1 week (chi(2) = 8.1, v = 1, P < .01). CONCLUSIONS: The rates of back pain among, and activities of, whitewater rafting guides were reported. Rates of back pain among whitewater rafting guides who returned our survey appear similar to the general population. Although determining a particular cause of pain is difficult, the typical injury seems to be relatively minor in scope.

Adolescent↗

PubMed2005

Clomethiazole: mechanisms underlying lasting neuroprotection following hypoxia-ischemia.

Damage after hypoxia-ischemia (HI) is observed in both cortical and subcortical regions. In this study, we employed a "Levine" rat model of HI (left carotid ligation + 1 h global hypoxia on PND-26) and used histological and electrophysiological paradigms to assess the long-term neuroprotective properties of clomethiazole (CMZ; a GABA(A) receptor modulator). Key enzymes involved in inflammation, namely nitric oxide synthase (NOS) and arginase, were also examined to assess potential CMZ mechanisms not involving GABA-R activation. Assessments were carried out 3 and 90 days post-HI. Extensive CNS lesions were evident after HI ipsilaterally at both short- and long-term intervals. CMZ significantly decreased the lesion size at 3 and 90 days (P<0.01; P<0.05). Evoked field potential analyses were used to assess hippocampal CA1 neuronal activity ex vivo. Electrophysiological measurements contralateral to the occlusion revealed impaired neuronal function after HI relative to short- and long-term controls (P<0.001, 3 and 14 days; P<0.01, 90 days), with CMZ treatment providing near complete protection (P<0.001 at 3 and 14 days; P<0.01 at 90 days). Both NOS and arginase activities were significantly increased at 3 days (P<0.01), with arginase remaining elevated at 90 days post-HI (P<0.05) ipsilaterally. CMZ suppressed the HI-induced increase in iNOS and arginase activities (P<0.001; P<0.05). These data provide evidence of long-term functional neuroprotection by CMZ in a model of HI. We further conclude that under conditions of HI, functional deficits are not restricted to the ipsilateral hemisphere and are due, at least in part, to changes in the activity of NOS and arginase.

Animals↗

PubMed2004

Neuroprotective effects of spermine following hypoxic-ischemic-induced brain damage: a mechanistic study.

The polyamines (spermine, putrescine, and spermidine) can have neurotoxic or neuroprotective properties in models of neurodegeneration. However, assessment in a model of hypoxia-ischemia (HI) has not been defined. Furthermore, the putative mechanisms of neuroprotection have not been elucidated. Therefore, the present study examined the effects of the polyamines in a rat pup model of HI and determined effects on key enzymes involved in inflammation, namely, nitric oxide synthase (NOS) and arginase. In addition, effects on mitochondrial function were investigated. The polyamines or saline were administered i.p. at 10mg/kg/day for 6 days post-HI. Histological assessment 7 days post-HI revealed that only spermine significantly (P<0.01) reduced infarct size from 46.14 +/- 10.4 mm3 (HI + saline) to 4.9 +/- 2.7 mm3. NOS activity was significantly increased following spermine treatment in the left (ligated) hemisphere compared with nonintervention controls (P<0.01) and HI + saline (P<0.05). In contrast, spermine decreased arginase activity compared with HI + saline but was still significantly elevated in comparison to nonintervention controls (P<0.01). Assessment of mitochondrial function in the HI + saline group, revealed significant and extensive damage to complex-I (P<0.01) and IV (P<0.001) and loss of citrate synthase activity (P<0.05). No effect on complex II-III was observed. Spermine treatment significantly prevented all these effects. This study has therefore confirmed the neuroprotective effects of spermine in vivo. However, for the first time, we have shown that this effect may, in part, be due to increased NOS activity and preservation of mitochondrial function.

Animals↗

PubMed2004

Oxygen free radical traps for the treatment of ischemia-associated organ injury.

Ischemia and reperfusion can induce an excess of free radicals that cannot be mopped-up by the body's endogenous defense mechanisms. This can lead to a breakdown in protein, lipid and DNA molecules, resulting in potentially irreversible organ damage. Radical traps are currently under development for the prevention of major damage in tissues such as the brain (after a stroke-like episode) and heart (after ischemia and reperfusion). While clinical studies are scant, many compounds have been developed and tested in the laboratory. Most radical traps are effective in a variety of preclinical models and one particular class, the nitrones (which includes NXY-059), has been studied intensively as potential neuroprotectants in acute ischemic stroke. NXY-059 is currently undergoing phase III clinical trials and will be the first compound to test the concept that radical traps may be effective and safe neuroprotectants in acute ischemic stroke.

Animals↗

PubMed2003

Neuroprotective effects of nitrone radical scavenger S-PBN on reperfusion nerve injury in rats.

The nitrone-based free radical scavengers have potent neuroprotective activities in models of stroke in which oxidative stress plays a key role in its development. We examined the effects of S-PBN (sodium 4-[(tert-butylimino) methyl]benzene-3-sulfonate N-oxide), a spin trap nitrone, on reperfusion injury in rat peripheral nerves. Immediately after the onset of 4-h ischaemia in rat right hindlimb, S-PBN was administered via mini-osmotic pumps, containing 2 ml of S-PBN (1.2 M), inserted subcutaneously. S-PBN, in addition, was given by a single injection (50 mg/kg BW, i.p.). Mean plasma concentrations of S-PBN were significantly greater in S-PBN-treated rats than in controls after 24, 48 and 72 h of reperfusion. Pump and dosing solution analysis indicated that the rats received between 82 and 99% of the target S-PBN concentration. Morphology in sciatic, tibial and peroneal nerves was assessed after 4 h of ischaemia followed by 72 h and 7 days of reperfusion. After 72 h of reperfusion, saline-treated control rats showed endoneurial oedema at the thigh level and diffuse axonal degeneration of myelinated nerve fibres distally. S-PBN-treated nerves were normal or revealed less severe abnormalities in myelinated fibres after 72 h and 7 days of reperfusion, when compared with those in saline-treated control nerves. Morphometrically, the frequency of abnormal myelinated fibres at calf levels was significantly less in S-PBN-treated nerves than in controls. In conclusion, post-ischaemic administration of S-PBN exhibits substantial neuroprotective properties in ischemia/reperfusion nerve injury.

Animals↗

PubMed2003

Nitrones as neuroprotective agents in cerebral ischemia, with particular reference to NXY-059.

Stroke is a major clinical problem, and acute pharmacological intervention with neuroprotective agents has so far been unsuccessful. Recently, there has been considerable interest in the potential therapeutic benefit of nitrone-derived free radical trapping agents as neuroprotective agents. Nitrone compounds have been shown to be beneficial in animal models of various diseases, and the prototypic compound alpha-phenyl-N-tert-butylnitrone (PBN) has been extensively demonstrated to be neuroprotective in rat models of transient and permanent focal ischemia. The nitrone radical trapping agent disodium 2,4-disulfophenyl-N-tert-butylnitrone (NXY-059) has also been shown to be neuroprotective in these models. Furthermore, it has recently been shown to improve neurological function and reduce infarct volume in a primate model of permanent focal ischemia even when given 4 hr postocclusion. While radical trapping activity is demonstrable with NXY-059 and other nitrone compounds such as PBN, this activity is weak. Arguments for and against ascribing radical trapping as the therapeutic mechanism of action are discussed. This compound is well tolerated in human stroke patients and can be administered to produce plasma concentrations exceeding those effective in animal models; crucially, at the same time, it has also been shown to be effective in animal models. NXY-059 may thus be the first compound to be examined in stroke patients using drug exposure and time to treatment that have been shown to be effective in animal models of stroke.

Aged↗