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Biomedical subjects

J Hedges

Publications and source records attributed to J Hedges.

13 recordsLinked to original sources
PubMed2001

A longitudinal field trial of the effect of biotin on lameness in dairy cows.

A longitudinal prospective intervention study investigated the effect of biotin supplementation on the incidence (new cases per day) of visible lameness in milking cows and heifers on five commercial farms in Gloucestershire, United Kingdom. The trial lasted from June 1997 to April 1999. Each farm participated in the trial for 18 mo. Within each herd the cows were randomly allocated to either receive a supplement of 20 mg of biotin per day or not. All cows were run as one herd on each farm. When a lame cow was identified, the farmer called one of six veterinarians to examine and treat the affected animal; findings were recorded on a standard form. A veterinarian also carried out a bimonthly locomotion assessment to ensure that all lame cows were diagnosed. There were a total of 900 cows, 1120 cow years, in the trial. The overall incidence rate of lameness (per 100 cows per year) was 68.9, with a range of 31.6 to 111.5 per farm. The incidence rates of the four most frequently reported causes of lameness were sole ulcer, 13.8; white line separation, 12.7; digital dermatitis, 12.0; and interdigital necrobacillosis, 7.1 per 100 cows per year. There was a significant difference in the incidence rate of these four lesions between supplemented and unsupplemented cows on two of the five farms, with a significant decrease in lameness in the cows supplemented with biotin. When all the farms were pooled, the risk of lameness caused by white line separation in cattle supplemented with biotin was approximately halved (Cox proportional hazard survival analysis hazard ratio = 0.57).

Animals↗
PubMed1999

Cyclooxygenase-2 inhibition by rofecoxib reverses naturally occurring fever in humans.

Cyclooxygenase (COX) exists as constitutive (COX-1) and inducible (COX-2) isoforms. Nonsteroidal antiinflammatory drugs (NSAIDs) such as ibuprofen and diclofenac inhibit both COX-1 and COX-2. The role of COX-2 in the genesis of fever in monkeys and humans was examined with use of the specific COX-2 inhibitor rofecoxib. Rofecoxib was administered to monkeys made febrile by 6 microg/kg intravenous lipopolysaccharide. Induced pyrexia was followed by oral rofecoxib (1 or 3 mg/kg), diclofenac (3 mg/kg), or vehicle. Rofecoxib and diclofenac rapidly reversed the elevated temperature (P < .05 versus vehicle for 3 mg/kg rofecoxib and diclofenac at 70 to 90 minutes after dosing). A single-dose, parallel-group, double-blind randomized trial was conducted in 94 patients with fever caused by a viral-type illness. Mean baseline temperature was similar for all groups (-38.5 degrees C). Patients received oral doses of 12.5 mg rofecoxib, 25 mg rofecoxib, 400 mg ibuprofen, or placebo and the mean +/- SE change in oral temperature at 4 hours after dosing was -0.97 degrees C +/- 0.11 degrees C, -1.19 degrees C +/- 0.09 degrees C, -1.20 degrees C +/- 0.11 degrees C, and 0.01 C +/- 0.17 C, respectively (P < .001 for active treatments versus placebo). Specific inhibition of COX-2 by rofecoxib results in antipyretic activity in monkeys and humans comparable to dual COX-1/COX-2 inhibitors such as diclofenac or ibuprofen. The data support the hypothesis that it is the COX-2 isoform that is primarily involved in the genesis of fever in humans.

Administration, Oral↗
PubMed1996

Appropriate helicopter transport of urban trauma patients.

OBJECTIVE: Inappropriate use of helicopter transport of trauma patients in urban areas increases costs, risk of injury, and unavailability for appropriate flights. We evaluated the effect of an emergency medical service (EMS) system audit of helicopter trauma scene flights (TSFs) on appropriateness of TSFs. METHODS AND DESIGN: Retrospective cohort. SETTING: Defined urban area with two Level I trauma hospitals. PARTICIPANTS: Consecutive TSFs 2 years before (PRE) and 2 years after (POST) audit. INTERVENTION: EMS system audit established criteria for appropriate TSFs. MAIN RESULTS: The total number of trauma system entries were similar for the two periods: PRE (1989) = 2862; POST (1990 and 1991) = 2787 and 2772. The total number of TSFs decreased after audit (PRE = 122; POST = 50). The proportion of inappropriate (INAPPRO)/total TSFs did not change (62% vs. 66%; chi 2 = 0.04; p = 0.85). There was no difference between appropriate (APPRO) and INAPPRO TSFs for mean vital signs, mechanism of injury, Trauma and Injury Severity Score (TRISS) and Injury Severity Score (ISS), mean length of stay, and proportion of survivors. Scene and transport time intervals were similar. For both PRE and POST periods, 26 APPRO patients (45%) were admitted to non-intensive care unit wards. CONCLUSIONS: An EMS system audit with general awareness of audit criteria decreased the total number of TSFs and hence the number of INAPPRO TSFs in this urban trauma system population. However, the proportion of TSFs that were considered INAPPRO did not change. Criteria for urban TSFs should be based on markers of critical physiologic patient status matched to unique care that the helicopter personnel can provide (e.g., advanced airway management).

Adult↗
PubMed1990

Time-management study of trauma resuscitation.

A prospective time-management analysis of trauma resuscitation (TR) of 431 patients arriving at a university trauma center documents timing and organization. Severity of injury, patient age, and potential airway injury were significant factors increasing the duration of TR up to a certain time (36 minutes). Moderately injured patients required less time (under 25 minutes). Patients needing emergent operations spent a minimal amount of time (20 minutes) in TR. Potential injuries involving the airway or cervical spine, or shock, added minutes. A review of the timing and organization of TR suggests the need for improvement in airway assessment and management. Patients with certain mechanisms of injury and elderly patients with blunt injuries required additional time in TR. With surgery faculty supervision and senior resident attendance, the month of resident experience had no effect on TR times. A timely and organized TR is critical to trauma care. TR times should be documented for quality assurance and ongoing review.

Adolescent↗
PubMed1988

Effects of dichloroacetate following canine asphyxial arrest.

Sodium dichloroacetate (DCA) has been shown to lower elevated serum lactate levels produced by hypoxia, exercise, and phenformin. We conducted a study to investigate the effect of DCA treatment on lactic acidosis following resuscitation from asphyxial cardiac arrest. Conditioned dogs were anesthetized with pentobarbital (30 mg/kg), endotracheally intubated, and mechanically ventilated to maintain an arterial pCO2 of 30 to 40 mm Hg. Asphyxial cardiac arrest was produced by endotracheal tube occlusion for six to eight minutes. After five minutes of cardiac arrest, the endotracheal tube was unclamped and closed-chest CPR was begun. Six animals received DCA 100 mg/kg IV push after one minute of CPR. Control animals (n = 6) received an equal volume of saline. CPR was continued until the return of a spontaneous pulse, when mechanical ventilation was resumed. Arterial and venous blood gases, glucose, and lactate levels were obtained at baseline and 15, 30, 45, 60, 90, and 120 minutes after resuscitation. Mean arterial blood pressure, pulse, and glucose, and venous and arterial blood gases were similar in both groups throughout the study. By 45 minutes after resuscitation, the DCA-treated group showed a significantly faster rate of decline in lactate levels that continued to the final sampling period. By 90 minutes, arterial lactate in DCA animals was not significantly different from baseline (pre-arrest) values. DCA given during cardiac arrest will cause a more rapid normalization of arterial lactate after successful resuscitation. Further studies are needed to evaluate the effects of lowered lactic acid on survival and neurological outcome following cardiac arrest.

Acetates↗
PubMed1987

Mechanisms of ischemic cerebral injury.

Normal compensatory mechanisms protect the central nervous system (CNS) from moderate hypoxia and ischemia; however, after more severe ischemia progressive brain hypoperfusion ensues and irreversible damage occurs. Ischemic brain injury remains greatly significant clinically and elucidating the determinants of ischemic neuronal injury and death continues to challenge researchers. Although altered perfusion and decreased energy charge may contribute to the production of irreversible damage, the distribution of lesions seen after insult does not correspond with the degree of ischemic blood flow impairment, nor can neuronal energy deprivation explain the cell damage. Other factors, such as derangements in astrocyte function, calcium homeostasis, free radical metabolism, acid-base regulation and excitatory neurotransmitters also probably mediate ischemic neuronal death. Continued investigation to establish the cellular pathophysiology of cerebral ischemia can guide rational research and therapeutic strategies.

Acid-Base Equilibrium↗
PubMed1986

The likelihood ratio. An improved measure for reporting and evaluating diagnostic test results.

The principles and use of likelihood ratios are presented as an aid to the reporting and interpretation of diagnostic data. Likelihood ratios can be determined for multiple levels of test results and provide a readily comprehensible and convenient measure for computing the posttest probability of disease. Unlike sensitivity and specificity, they convey an immediate and direct description of a test's ability to revise the initial probability of disease upward or downward. By incorporating all the raw data, the use of likelihood ratios can improve the assessment of the clinical utility of test results. Their application to the diagnostic performance of serum creatine kinase concentrations in predicting patients with suspected myocardial infarction is discussed.

Creatine Kinase↗
PubMed1978

The trauma room.

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Equipment and Supplies, Hospital↗
PubMedDate not supplied

Community clinics.

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Community Health Centers↗