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Biomedical subjects

C Calder

Publications and source records attributed to C Calder.

At least 19 recordsLinked to original sources
PubMed2006

Incidence and outcome of idiopathic pneumonia syndrome in pediatric stem cell transplant recipients.

Idiopathic pneumonia syndrome (IPS) is a rare complication following stem cell transplant (SCT) and its incidence among pediatric SCT recipients is not known. To assess the incidence of IPS, we retrospectively reviewed the incidence of IPS at our center. IPS is defined as the presence of multilobar infiltrates by chest radiograph or computed tomography scan, need for supplemental oxygenation with declining pulse oximetry and no identifiable pulmonary infection. Between July 1999 and August 2005, 11 of 93 children who received a fully ablative allogeneic SCT (11.8%) developed IPS. All 11 patients had normal pulmonary evaluation before transplant. IPS developed at a median of 17 days (range 8-42 days) after transplant. Recipients of unrelated donor transplant had increased risk of developing IPS. There was a significant association between acute or hyperacute graft-versus-host disease (GVHD) and IPS (P=0.035). All patients had significant hypoxia and five patients required assisted ventilation. IPS was the cause of death in two patients. Although there was complete resolution of respiratory symptoms in the other nine patients, overall transplant-related mortality was significantly higher among patients with IPS (64 vs 17%, P=0.002). IPS is a relatively common complication in pediatric SCT recipients and acute GVHD is an important associated factor.

Adolescent↗
PubMed2005

Pericardial effusion and cardiac tamponade in pediatric stem cell transplant recipients.

Pericardial effusion and cardiac tamponade is a rarely reported complication following stem cell transplant (SCT). The incidence among pediatric SCT recipients is not well defined. To assess the frequency of clinically significant pericardial effusions, we retrospectively examined clinically significant cardiac effusions at our center. Between January of 1993 and August 2004, clinically significant pericardial effusions were identified in nine of 205 patients (4.4%). The median age at the time of transplant was 9 years (range 0.6-18 years) and seven received an allogeneic transplant. All nine had normal cardiac function prior to transplant. The effusion developed at a median of 30 days (range 18-210 days). All allogeneic recipients had acute or clinically extensive graft-versus-host disease (GVHD) at the time the effusion was diagnosed. Seven patients (78%) required pericardiocentesis or surgical creation of a pericardial window. No patient died as a complication of the effusion or the therapeutic procedures. Clinically significant pericardial effusions are more common than previously reported in pediatric SCT recipients. Acute and chronic GVHD is an associated factor.

Adolescent↗
PubMed2004

Incidence and clinical complications of vancomycin-resistant enterococcus in pediatric stem cell transplant patients.

Vancomycin-resistant enterococcus (VRE) are increasingly important pathogens in stem cell transplant (SCT). In all, 61 pediatric SCT patients had surveillance stool cultures for VRE between July 1999 and November 2002. When VRE was identified, the patients were placed on strict contact isolation. VRE was detected in 15 patients (24.6%). The median age was 3.6 years (range 0.6-18.5 years). Of the 15, 13 (87%) received an allogeneic transplant (six unrelated and seven related). Five of the 15 (33%) colonized patients developed VRE bacteremia. The bacteremia resolved in all five patients after therapy with quinupristin/dalfopristin; three patients required central line removal. Four patients died (38-153 days) post-SCT due to relapse or transplant complication not related to VRE. Of the 11 surviving patients, seven cleared the colonization at a median of 144 days (range 61-198 days) postcolonization. Four patients remain colonized at 68-702 days after the first positive culture. Intestinal colonization with VRE occurred commonly in pediatric SCT patients. Although the morbidity from VRE was not substantial, transplant patients were colonized for prolonged periods. Our results indicate that surveillance for VRE is an effective way to identify colonized patients and may lead to a decrease in transmission to other patients.

Adolescent↗
PubMed2004

Bayesian modeling of multiple lesion onset and growth from interval-censored data.

In studying rates of occurrence and progression of lesions (or tumors), it is typically not possible to obtain exact onset times for each lesion. Instead, data consist of the number of lesions that reach a detectable size between screening examinations, along with measures of the size/severity of individual lesions at each exam time. This interval-censored data structure makes it difficult to properly adjust for the onset time distribution in assessing covariate effects on rates of lesion progression. This article proposes a joint model for the multiple lesion onset and progression process, motivated by cross-sectional data from a study of uterine leiomyoma tumors. By using a joint model, one can potentially obtain more precise inferences on rates of onset, while also performing onset time-adjusted inferences on lesion severity. Following a Bayesian approach, we propose a data augmentation Markov chain Monte Carlo algorithm for posterior computation.

Adult↗
PubMed2002

A randomised trial of self-management planning for adult patients admitted to hospital with acute asthma.

BACKGROUND: There is still debate over the benefit of self-management programmes for adults with asthma. A brief self-management programme given during a hospital admission for acute asthma was tested to determine whether it would reduce readmission. METHOD: A randomised controlled trial was performed in 280 adult patients with acute asthma admitted over 29 months. Patients on the self-management programme (SMP) received 40-60 minutes of education supporting a written self-management plan. Control patients received standard care (SC). RESULTS: One month after discharge SMP patients were more likely than SC patients to report no daytime wheeze (OR 2.6, 95% CI 1.5 to 5.3), no night disturbance (OR 2.0, 95% CI 1.2 to 3.5), and no activity limitation (OR 1.5, 95% CI 0.9 to 2.7). Over 12 months 17% of SMP patients were re-admitted compared with 27% of SC patients (OR 0.5, 95% CI 0.3 to 1.0). Among first admission patients, OR readmission (SMP v SC) was 0.2 (95% CI 0.1 to 0.7), p<0.01. For patients with a previous admission, OR readmission was 0.8 (95% CI 0.4 to 1.6), p=0.6. SMP patients were more likely than SC patients to be prescribed inhaled steroids at discharge (99% v 92%, p=0.03), oral steroids (98% v 90%, p=0.06), and to have hospital follow up (98% v 84%, p<0.01) but adjustment for these differences did not diminish the effect of the self-management programme. CONCLUSIONS: A brief self-management programme during hospital admission reduced post discharge morbidity and readmission for adult asthma patients. The benefit of the programme may have been greater for patients admitted for the first time. The programme also had a small but significant effect on medical management at discharge.

Acute Disease↗
PubMed2000

Symptoms, quality of life, and health service contact among young adults with mild asthma.

This report assesses Quality of Life (QoL) and its relationship to current symptoms and prospective medical contact among 396 adult patients with asthma. Patients were 16 to 52 yr of age and in the care of family physicians in the northeast of Scotland. All patients had been prescribed asthma medication within the previous 3 mo. Mean %pred FEV(1) was 87.4, mean %pred PEF was 85.1; 41% reported respiratory symptoms every week in the month before interview. Patients completed the SF-36, SF-12, and St. George's Respiratory Questionnaire (SGRQ) scales. Although mean scores on the SF-36 and SF-12 were close to population norms for patients without chronic illness, the presence of any respiratory symptoms in the month before interview was related to significantly lower QoL scores on the SF-36 scales of Physical Functioning, Energy, Mental Health, Pain, and Health Perception: the SF-12 Physical Functioning scale, and the SGRQ Symptoms, Impact and Activities scales. Physician contact for asthma in the 12 mo after interview was significantly related to SF-36, SF-12, and SGRQ scores at time of interview; however, when adjusted for symptoms at time of interview, only the SGRQ scales remained significant predictors of prospective physician contact. We conclude that respiratory symptoms have significant impact on QoL among patients with mild asthma, measured by generic and respiratory QoL scales, but that a specific respiratory scale is better able to discriminate patients who will seek physician care for asthma.

Adolescent↗
PubMed1995

Neuroprotective properties of lifarizine compared with those of other agents in a mouse model of focal cerebral ischaemia.

1. Changes in the peripheral type benzodiazepine binding site density following middle cerebral artery occlusion in the mouse, have been used as a marker of neuronal damage. These sites can be identified using the selective ligand [3H]-PK 11195 located on non neuronal cells, macrophages and astroglia, within the CNS. Glial cell proliferation and macrophage invasion is an unvoidable sequelae to cerebral ischaemic injury, secondary to neuronal loss. Following occlusion of the left middle cerebral artery (left MCA) a reproducible lesion was found in the parietal cortex within 7 days which gave rise to a significant increase in [3H]-PK 11195 binding. 2. Treatment of animals with the sodium channel blocker, lifarizine, significantly reduced the ischaemia-induced increase in [3H]-PK 11195 binding when given either 30 min pre-ischaemia and three times daily for 7 days at 0.5 mg kg-1, i.p. (P < 0.01) or delayed until 15 min post-ischaemia and three times daily for 7 days at 0.5 mg kg-1, i.p. (P < 0.001). Lifarizine was an effective neuroprotective agent in this model of focal ischaemia in the mouse. 3. Lifarizine also showed a dose-related protection against the ischaemia-induced increase in [3H]-PK 11195 binding with significant protection at doses of 0.1 mg kg-1, i.p. (P < 0.05), 0.25 mg kg-1, i.p. (P < 0.01) or 0.5 mg kg-1, i.p. (P < 0.01) 15 min post-ischaemia and b.i.d. for 7 days. No significant change is seen in the Kd for [3H]-PK 11195. The first dose could be delayed for up to 4 h after cerebralartery cauterization and protection was maintained.4. Phenytoin (28 mg kg-1, i.v. 15 min and 24 h post-ischaemia) was also neuroprotective in this model(P<0.01). This agent is thought to interact with voltage-dependent sodium channels to effect its anticonvulsantactions and this mechanism may also underlie its neuroprotective actions in focal cerebralischaemia.5. Agents with other mechanisms of action were also shown to have significant neuroprotection in this model. The non-competitive NMDA antagonist, MK 801, showed significant neuroprotection in the model when given at 0.5 mg kg-1, i.p. 30 min pre-ischaemia with t.i.d. dosing for 7 days (P< 0.001). The dihydropyridine calcium antagonist, nimodipine was not protective when given using the same dosing protocol as MK 801, 0.5 mg kg-1 30 min pre-occlusion and three times daily for 7 days but showed significant protection when given at 0.05 mg kg-1 15 min post-ischaemia and three times daily for 7days. The lipid peroxidation inhibitor, tirilazad (single dose 1 mg kg-1, i.v.) showed significant neuroprotection when given 5 min post-ischaemia but not when the first dose was delayed for 4 h.

Animals↗
PubMed1995

Reduction by lifarizine of the neuronal damage induced by cerebral ischaemia in rodents.

1. The objective of this study was to evaluate the broad neurocytoprotective potential of the novel sodium-calcium ion channel modulator, lifarizine (RS-87476), in two rodent 72 h survival models of forebrain ischaemia. 2. Under fluothane anaesthesia, rats were subjected to 10 min four vessel occlusion and gerbils to either (i) 5 or (ii) 10 min bilateral carotid artery occlusion. 3. Rats were dosed parenterally solely post-ischaemia (reperfusion) in a series of five studies covering a range of intra-arterial/intraperitoneal (i.a./i.p.) combination doses from 2/10, 5/20, 20/100, 50/200 and 100/500 micrograms kg-1, where the initial loading dose was injected i.a. at 5 min. An i.p. dose was given at 15 min and repeated twice daily. In a sixth study, treatment at 50/200 micrograms kg-1 was deferred for 1 h. 4. Gerbils were treated (i) 15 min pre-ischaemia with either (a) 250, (b) 500 micrograms kg-1 i.p., or (c) 5 mg kg-1 by gavage (p.o.) for 3 days then at 1 h pre-ischaemia. Animals treated as (ii) received 500 micrograms kg-1 i.p. 15 min pre-ischaemia. The above doses were repeated twice daily for 3 days post-ischaemia for the respective groups. 5. In rats, the protective effect of lifarizine was regionally and cumulatively assessed in six brain regions (anterior and posterior neocortex, hippocampal CA1 subfield, thalamus, striatum, cerebellar Purkinje cells-brain stem) at each dose level. Cumulative (total) means +/-s.e.mean neurohistopathological scores(0-4) of 1.16+/-0.09 (n=5), 1.02+/-0.10 (n=5), 0.93+/-0.06 (n=6), 0.79+/-0.09 (n=9) and 0.45+/-0.16(n = 7), respectively, were obtained for the above treatment groups compared to the control (2.01 +/- 0.17,n = 16) group (P<0.0035). The score for the 1 h deferred treatment group was also significant at 0.77 +/- 0.10, n =5 (P< 0.0035). The normal group without ischaemia showed a score of 0.52 +/- 0.09 (n = 6).6. In gerbils, (i) percentage delayed neuronal death (DND) of hippocampal pyramidal cells in the CA1subfield was prevented at 250 (a) and 500 microg kg-' i.p. (b) (27.2+/- 14.6, n=6 and 26.9+/- 10.4%, n= 10 respectively, P<0.02) compared to controls (78.3+/-8.5%, n= 12) and by 5 mg kg-1 p.o. (c) (2.9+/-0.8%,n =l1, P <0.002). Mean +/- s.e.mean total brain scores (0-4) for each of 4 different features denoting cerebral 'oedema' were lower for normal brains (1.60 +/-0.34, n =6) and reduced in animals dosed at 250(a) (3.00+/-0.79, n=6) and 500 microg kg-1 i.p. (b) (3.75 0.36, n= 10) compared to controls (6.58+/-1.00,n = 12) (P< 0.02 -0.03). There was a linear relationship (r = 0.97) between the 'oedema' scores and percentage CA1 DND. Percentage CA1 DND in response to 10 min ischaemia (ii) was reduced(53.0+/-21.0%, n=6, P<0.05) compared to controls (100.0+/-0.0%, n=7).7 The significant neuroprotection shown by lifarizine in rodents substantiates findings in other species.These observations, together with its effect on ion channels and efficacy at extremely low doses offers novelty and suggests a broad spectrum of activity in ischaemia.

Animals↗
PubMed1994

Ewing's sarcoma of the retropharynx.

Ewing's sarcoma arising in the head and neck region is very rare. A case arising from C2 in a young child is presented. The unusual presentation, differential diagnosis and pathological features are discussed.

Bone Neoplasms↗
PubMed1993

The effect of lifarizine (RS-87476), a novel sodium and calcium channel modulator, on ischaemic dopamine depletion in the corpus striatum of the gerbil.

1. Unilateral ligation of the right common carotid artery in the anaesthetized gerbil for 3 h caused a 62.7% decrease in ipsilateral dopamine in the corpus striatum from 1.40 (+/- 0.13, n = 27) micrograms g-1 in the non-ischaemic hemisphere to 0.47 (+/- 0.07, n = 27) micrograms g-1 in the ischaemic hemisphere (all results are expressed as mean +/- s.e. mean). In sham-operated animals there were no differences in the dopamine levels (1.31 +/- 0.14 micrograms g-1, n = 11, left; 1.27 +/- 0.13 micrograms g-1, n = 11 in the right hemisphere). Animals with intact communicating arteries in the circulus arteriosus were excluded. 2. Lifarizine (RS-87476; 250, 500, but not 50, micrograms kg-1, i.p.) protected against this dopamine depletion showing only a 9.2% decrease at 250 micrograms kg-1, i.p. (P < 0.01) and no decrease at 500 micrograms kg-1, i.p. (P < 0.01). 3. Nicardipine (250 micrograms kg-1, p.o.) was effective when administered chronically once daily for 10 days (26.6% decrease, P < 0.05) but not when administered acutely at 50 micrograms kg-1, i.p.

Animals↗
PubMed1988

Comparative protective effects of nicardipine, flunarizine, lidoflazine and nimodipine against ischaemic injury in the hippocampus of the Mongolian gerbil.

1. Morphological changes characterizing delayed neuronal death (DND) of selectively vulnerable CA1 pyramidal cells in the hippocampus of the Mongolian gerbil brain occurred 72 h after transient (5 min) bilateral occlusion of the common carotid arteries. 2. Different groups of animals were treated 15 min before carotid artery occlusion and twice daily during the 72 h post-ischaemia period with either saline alone, nicardipine, flunarizine, lidoflazine or nimodipine at doses of 500 micrograms kg-1 intraperitoneally. 3. At 72 h the animals were killed and their brains examined histologically. Absolute cell counts were made from 5 sites distributed linearly throughout the hippocampal CA1 subfield in each hemisphere to determine the percentage DND in each group. Normal brains and those of sham-operated animals were included in the study for comparison. 4. Features of DND were distributed evenly throughout the CA1 subfield in both hemispheres in all groups of gerbils. Nicardipine, lidoflazine and flunarizine, but not nimodipine, were protective. This protection extended linearly throughout the hippocampus without altering the pattern of neuronal damage. 5. Compared to saline-treated (78.3 +/- 2.9% DND) and nimodipine-treated (76.5 +/- 3.4% DND) gerbils, the overall protection afforded by nicardipine (41.8 +/- 3.8% DND) was statistically significant. The effects of lidoflazine (53.6 +/- 7.1%) and flunarizine (55.8 +/- 3.9% DND) were of borderline significance. 6. Abnormal neurones appeared in normal and sham-operated brains to the extent of 4.5 +/- 1.0% and 4.6 +/- 0.4%, respectively. Such changes can be attributed to fixation artefacts. 7. The results demonstrate that overall protection is conferred on ischaemic hippocampal CA1 neurones by nicardipine and to a lesser extent by flunarizine and lidoflazine, but not by nimodipine.

Animals↗
PubMed1985

Nicardipine in models of myocardial infarction.

In a dog model of partial myocardial ischaemia, superimposed ST segment elevations in epicardial ECGs were inhibited by nicardipine over a cumulative i.v. dose range of 1-20 micrograms kg-1. Over the cumulative i.v. dose range of 0.5-166.5 micrograms kg-1, nicardipine had little overall effect on gross cardiac conduction, at spontaneous heart rate. Dogs that received oral 1-2 mg kg-1 nicardipine daily for 16 weeks and then survived 1 week occlusion of the left anterior descending coronary artery (LAD) developed a superior coronary collateral circulation compared with untreated animals. Nicardipine given by three different dosing schedules to baboons markedly limited myocardial infarction over a 6 h period of LAD occlusion. Compared with a group of completely untreated dogs, there was protection of the myocardium in the animals given nicardipine that survived 3 months occlusion of the LAD.

Animals↗
PubMed1984

Peripheral nerve morphometry in stroke patients.

Sural nerve biopsy specimens from affected and non-affected limbs of stroke patients were examined morphometrically. Two principle abnormalities of peripheral nerve were found in hemiparetic and hemiplegic limbs. First, the frequency of abnormal teased nerve fibers was significantly increased with abnormal internodes frequently "clustered" and showing a 50% or more reduction in myelin thickness. Second, the mean diameter of myelinated nerve fibers was reduced. These results suggest a primary atrophy of peripheral nerve fibers in the affected limbs of stroke patients with secondary demyelination. Possible aetiological factors include disuse, transynaptic degeneration, ischemia, pressure effect, and decreased axoplasmic flow. It would seem that the structural integrity of peripheral nerve is frequently compromised following a cerebral lesion.

Adult↗