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Biomedical subjects

J Cunningham

Publications and source records attributed to J Cunningham.

At least 73 records · Page 4Linked to original sources
PubMed1998

Hospital-acquired blood stream infections in New Zealand.

AIM: To determine the number and rates of hospital-acquired blood stream infections in New Zealand public hospitals. METHOD: From October 1994 to December 1996 each of the 23 Crown Health Enterprises (CHEs) provided the Crown Company Monitoring Advisory Unit with data on the number of episodes of hospital-acquired blood stream infection (HA-BSI) and the number of inpatient admissions. RESULTS: During the 27 month study period, 3049 episodes of HA-BSI occurred in an inpatient population of 1 300 892 giving a national average rate of 0.23%. HA-BSI rates were highest for the six tertiary level, metropolitan CHEs (range 0.19% - 0.56%) in which 79% of all HA-BSIs occurred. CONCLUSION: The HA-BSI rate for New Zealand is within the range that would be expected for a developed country with a comprehensive health service. The variability between CHEs in terms of the clinical services provided and case mix differences invalidates direct comparison of HA-BSI rates. Surveillance for HA-BSI should continue with the collection of data which would allow meaningful comparison of similar tertiary level services.

Bacteremia↗
PubMed1998

The importance of clinical experience in aboriginal communities.

The importance of preparing nurses adequately to meet the health needs of Aboriginal people cannot be understated. Much of the reason for negative attitudes among nurses is a lack of knowledge and understanding of cultural differences. Clinical practice in an Aboriginal community can assist in the development of cross-cultural skills among student nurses. In recent times it has been accepted that nursing curricula in Australia must reflect an understanding and awareness of cultural perspectives, diversity and sensitivity. Exposing students to Aboriginal health workers has been found to result in a positive change in attitude among students (Hayes et al. 1994). Providing clinical experiences in Aboriginal communities can increase students' awareness of Aboriginal health status, the socio-cultural and historical influences involved, and the nurse's role in relation to Aboriginal health. Nurses are a major provider of health care within Aboriginal communities throughout Australia. Culturally diverse clinical placements challenge students to become aware of their own health beliefs, attitudes, and values, which can facilitate bridging cross-cultural gaps with clients and also facilitate the delivery of quality nursing care.

Australia↗
PubMed1998

Selective release of nitric oxide from retinal amacrine and bipolar cells.

PURPOSE: To investigate the cellular origin of nitric oxide released from the rabbit retina in response to physiological stimulation with light. METHODS: The release of nitric oxide from the retina was measured in rabbits anesthetized with urethane. An eye-cup was prepared and was filled with Krebs-Ringer bicarbonate. After washing for 45 minutes, 0.5 ml medium was placed in the eyecup. The medium was replaced every 10 minutes, and nitric oxide in the resultant samples was measured using nitrate reductase and a nitric oxide meter. RESULTS: In the unstimulated dark-adapted retina there was a spontaneous resting release of nitric oxide (1.20 nmol/min). When the retina was stimulated for 10 minutes with flickering light there was an increase in nitric oxide release to almost double the resting release. Stimulation of the retina for 10 minutes with continuous light produced a similar increase in nitric oxide release. The exposure of the retina to L-amino-4-phosphonobutyrate (APB), which specifically blocks transmission between the photoreceptors and the depolarizing bipolar cells, abolished the evoked release of nitric oxide caused by flickering light and continuous light. In contrast, the nonselective excitatory amino acid antagonist cis-2,3-piperidinedicarboxylic acid (PDA) had no effect on the flicker-evoked release of nitric oxide, but it more than halved the release caused by continuous light. A similar differential effect on release was found with glycine, which abolished the nitric oxide release evoked with continuous light but did not affect the flicker-evoked release. The inhibitory effect of glycine was blocked by strychnine. CONCLUSIONS: Nitric oxide was released in the retina by flickering light and by continuous light, but the two types of stimulation cause nitric oxide release from different cells. Because in the rabbit retina nitric oxide synthase occurs mainly in a subpopulation of amacrine cells and a few bipolar cells, our pharmacologic results suggest that continuous light causes nitric oxide release from amacrine cells, whereas flickering light evokes nitric oxide release from bipolar cells.

Aminobutyrates↗
PubMed1997

Reduced expression of mismatch repair genes measured by multiplex reverse transcription-polymerase chain reaction in human gliomas.

Microsatellite instability (MIN) is frequently observed in hereditary nonpolyposis colon cancer and in other sporadic cancers including gliomas. Abnormalities in at least one of five mismatch repair (MMR) genes are implicated in the development of cancers in hereditary nonpolyposis colon cancer and the associated MIN. Using a newly developed multiplex reverse transcription-PCR assay, we evaluated the expression of the five known human MMR genes (hMSH2, hMLH1, hPMS1, hPMS2, and GTBP) in human gliomas by measuring simultaneously the relative levels of the transcripts. The beta-actin gene was used as an internal control for RNA degradation and DNA contamination and as a reference for quantifying the levels of their transcripts. Of the 33 gliomas examined, 42% (14) had low expression of hMSH2 (at least 4-5-fold lower than normal mean), 21% (7) had low expression of hMLH1, and 18% (6) had low expression of hPMS1 compared with the expression in the lymphocytes from 13 normal individuals. Furthermore, six of the 33 (18%) tumor samples had decreased expression of more than one MMR gene. Two of these six patients with multiple gene abnormalities had second primary cancers, and an additional patient had multifocal gliomas. Further molecular analysis of available DNA samples indicated that one of five of those tumors with aberrant expression of MMR genes had MIN, as compared with none of five tumors with normal expression. These data suggest that reduced expression of MMR genes is frequent in human gliomas and that aberrant expression of more than one MMR gene may be associated with increased risk of second primary malignancies in glioma patients.

Adaptor Proteins, Signal Transducing↗
PubMed1997

Human cationic amino acid transporter gene hCAT-2 is assigned to 8p22 but is not the causative gene in lysinuric protein intolerance.

Lysinuric protein intolerance (LPI) is a recessively inherited amino acid disorder characterized by defective efflux of cationic amino acids at the basolateral membrane of the intestinal and renal tubular epithelium. Recently, cDNAs encoding the related proteins hCAT-2A and hCAT-2B have been cloned. These two carrier proteins are most likely to product of the same gene, hCAT-2. Using the hCAT-2B cDNA, we assigned the hCAT-2 gene to chromosome 8p22. Furthermore, by linkage analysis in Finnish LPI families, we ruled out that hCAT-2B is involved in LPI disease.

Amino Acid Metabolism, Inborn Errors↗
PubMed1997

Peer mentorship in clinical education: outcomes of a pilot programme for first year students.

Identifying effective strategies for promoting learning in the clinical setting continues to pose challenges for nurse educators. The aim of the present paper is to examine the potential that peer mentorship may have in helping nursing students to improve clinical learning outcomes. An example of a peer mentorship programme for nursing students undertaking their first clinical practicum is described, and preliminary findings from an evaluation of this pilot programme are presented. The results suggest that peer mentorship may be of some benefit to students, particularly in relation to reducing anxiety and improving confidence with clinical practice experiences, and is therefore a strategy which is worthy of further investigation.

Clinical Competence↗
PubMed1997

Pancreatic sphincter hypertension increases the risk of post-ERCP pancreatitis.

BACKGROUND AND STUDY AIMS: The reason for the increased risk of pancreatitis after endoscopic retrograde cholangiopancreatography (ERCP) in patients with sphincter of Oddi dysfunction is not known. This study sought to determine whether pancreatic sphincter hypertension might explain some of the increased risk. PATIENTS AND METHODS: The incidence of pancreatitis was determined from a cohort of patients who underwent pancreatic sphincter manometry. Additional data collected included: pancreatic and biliary sphincter manometry results, distal bile duct diameter, chronic pancreatitis grade by pancreatography, and endoscopic treatments. RESULTS: Ten of 32 patients (31%) with pancreatic sphincter hypertension developed post-ERCP pancreatitis, compared to one of 33 (3%) with normal pancreatic manometry (P = 0.002). Patients with pancreatic sphincter hypertension were more likely to undergo endoscopic treatments (88%) compared to those with normal manometry (27%) (P = 0.001). The distal bile duct diameter was significantly smaller (4.5 +/- 0.5 mm) in patients who developed post-ERCP pancreatitis than in those who did not (6.2 +/- 0.3) (P = 0.025). Patients with small distal bile duct diameters (< 5 mm) were three times more likely to develop post-ERCP pancreatitis than those with larger ducts (relative risk [RR] 3.1, 95% confidence interval [CI] 0.9, 10.7). Patients with pancreatic sphincter hypertension were ten times more likely to develop post-ERCP pancreatitis than those with normal pancreatic manometry (RR 10.3, 95% CI 1.5, 76.0). In patients with a small bile duct size, pancreatic sphincter hypertension substantially increased the risk compared to those with normal manometry (RR 18.1, 95% CI 1.1, 287.6). CONCLUSIONS: Pancreatic sphincter hypertension greatly increases the risk of post-ERCP pancreatitis in patients undergoing treatment or evaluation, or both, for sphincter of Oddi dysfunction.

Acute Disease↗
PubMed1997

Reduced calcium dialysate in CAPD patients: efficacy and limitations.

BACKGROUND: The increasing use of 'reduced calcium' dialysate in CAPD patients treated with calcium-based phosphate binders has raised concerns that this could lead to negative calcium balance, worsening hyperparathyroidism, and osteopenia. METHODS: The present study was conducted to examine the possibilities (a) that 1.25 mM calcium dialysate leads to negative calcium balance and worsening hyperparathyroidism, and (b) that conversely 1.25 mM calcium dialysate is still too high for some patients. We studied 22 patients who, after a 2-month run in using 1.75 mM calcium dialysate and aluminium hydroxide binders, entered a 3-month phase of 1.25 mM calcium dialysate with continuation of aluminium hydroxide as the sole phosphate binder. The patients then entered a final 9-month phase in which dialysate calcium remained at 1.25 mM and calcium carbonate was substituted for aluminium hydroxide and progressively titrated to achieve optimum phosphate control. RESULTS: During the initial 3-month period, parathyroid hormone increased from 259, range 11-1149 to 405, range 16-1318 pg/ml (P = 0.0001) and ionized calcium decreased from 1.17 +/- 0.06 to 1.11 +/- 0.08 mM (P = 0.0004). The subsequent 9-month phase was associated with return of parathyroid hormone to baseline levels. Further dialysate calcium reduction to 0.6 mM was implemented in the four patients who became hypercalcaemic. CONCLUSION: This study has clearly shown that reduction of dialysate calcium to 1.25 mM can be harmful to CAPD patients if oral calcium availability is inadequate. It has also shown that dialysate calcium at 1.25 mM is a compromise, with increased risk of hyperparathyroidism if calcium intake is too low and, conversely, risk of hypercalcaemia and unacceptable increases of the Ca x Pi product in a minority of patients. At these extremes there is a need for a high-calcium dialysate (1.75 mM) and a very low-calcium dialysate (0.6 mM or less), to optimize management.

Adult↗
PubMed1997

Nitric oxide enhancement of cholinergic amacrine activity by inhibition of glycine release.

PURPOSE: To investigate a possible interaction between cholinergic and nitrergic amacrine cells in the rabbit retina. METHODS: The activity of cholinergic amacrine cells was estimated by measuring the light-evoked release of [3H]-acetylcholine (ACh) from the retina of rabbits anesthetized with urethane. An eyecup was prepared and filled with Krebs-Ringer bicarbonate solution, containing [3H]-choline. After washing with fresh medium containing physostigmine, 0.5 ml of medium was placed in the eyecup. The medium was replaced every 5 minutes, and the radioactivity in the resultant samples was measured. In some experiments the release of [3H]-ACh and glycine was measured using isolated retinas. RESULTS: Local application of the nitric oxide (NO) donors, S-nitroso-N-acetyl-DL-penicillamine and sodium nitroprusside strikingly enhanced the light-evoked release of [3H]-ACh. In contrast, inhibition of nitric oxide synthase with L-nitromonomethylarginine (LNMMA) or N-nitro-L-arginine (LNA) greatly reduced the light-evoked release of [3H]-ACh. In that the response of cholinergic amacrine cells is damped by an inhibitory feedback circuit involving glycinergic amacrine cells, the effect of strychnine on the inhibitory action of LNMMA was examined, Strychnine abolished the inhibitory effect of LNMMA on the light-evoked release of [3H]-ACh, suggesting that endogenous NO normally has an inhibitory effect on glycinergic amacrine cells. This idea was supported by experiments using isolated retinas, in which sodium nitroprusside and S-nitroso-N-acetyl-DL-penicillamine inhibited the potassium-evoked release of glycine but enhanced the release of [3H]-ACh. CONCLUSIONS: Endogenous NO is released in the retina and acts indirectly to facilitate the light-evoked response of cholinergic amacrine cells.

Acetylcholine↗
PubMed1997

Efficacy of imidacloprid for removal and control of fleas (Ctenocephalides felis) on dogs.

OBJECTIVE: To evaluate efficacy of a 9.1% (w/w) imidacloprid solution, applied topically, to remove fleas from dogs and the duration of residual flea control when dogs were exposed to continuing flea infestation. ANIMALS: 32 adult mixed-breed dogs. PROCEDURE: Dogs were allocated to 4 groups of 8 dogs each; dogs of 3 groups received a single dose of imidacloprid, and those of the fourth group received excipient. Each dog was infested with 100 adult fleas on study days -3, -1, 6, 13, 20, 27, and 33. Treatments were applied on day 0. Each dog was examined for live fleas on days -2, 1, 7, 14, 21, 28, and 34. Posttreatment efficacy was determined by comparing the mean number of live fleas remaining on the treated dogs with the mean number of live fleas remaining on the control dogs. RESULTS: All 3 imidacloprid dosages provided flea control > or = 96.9% one day after treatment. Maximal efficacy of all 3 dosages (99.1 to 100%) was observed at 7 days after treatment. Flea control with 3.75 mg of imidacloprid/kg of body weight ranged from 94.4 to 96.9% for days 14 to 28 and decreased to 91.6% by 34 days after treatment. Flea control with 7.5 and 10.0 mg of imidacloprid/kg was 97.8 to 100% through day 28. At day 34, dosages of 7.5 and 10.0 mg of imidacloprid/kg were 97.6 and 96.9% efficacious, respectively. CONCLUSION: 7.5 or 10.0 mg of imidacloprid/kg are equivalent and superior to 3.75 mg/kg for flea control over the course of a 34 day posttreatment period. CLINICAL RELEVANCE: Monthly imidacloprid application of 7.5 to 10 mg/kg will rapidly kill existing and reinfesting flea infestations on dogs and break the flea life cycle by killing adult fleas before egg production begins.

Administration, Topical↗
PubMed1996

Premature mortality in aboriginal adults in the Northern Territory, 1979-1991.

OBJECTIVE: To identify important causes of premature mortality among Aboriginal adults in the Northern Territory (NT), 1979-1991. METHODS: All deaths of NT Aboriginal residents aged 15-64 years which occurred in the NT between 1979 and 1991 and which were recorded by the Registry of Births, Deaths and Marriages were included. Standardised mortality ratios (SMRs) were used to compare the number of deaths observed among Aboriginals in the NT to those expected, based on overall Australian rates. Years of potential life lost before age 65 (YPLL65) were estimated for specific causes of death. RESULTS: Aboriginal women (overall SMR, 5.5) and Aboriginal men (SMR, 4.7) experienced a high burden of excess mortality from almost every cause of death. This excess increased over time, especially for Aboriginal women. Among Aboriginal men, the most important causes of premature death were motor vehicle accidents (11% of excess deaths and 17% of YPLL65), ischaemic heart disease (10% of excess deaths and 10% of YPLL65), pneumonia and influenza (8% of excess deaths and 6% of YPLL65), and homicide (7% of excess deaths and 8% of YPLL65). For Aboriginal women, the most important causes included homicide (7% of excess deaths and 11% of YPLL65), chronic obstructive pulmonary disease (10% of excess deaths and 5% of YPLL65), rheumatic heart disease (7% of excess deaths and 8% of YPLL65), and ischaemic heart disease (6% of excess deaths and 5% of YPLL65). CONCLUSIONS: The wide variety of causes of excess mortality will require an equally wide variety of solutions, both medical and non-medical, and a long term commitment will be necessary to achieve reductions in premature mortality among NT Aboriginal adults.

Adolescent↗
PubMed1996

Mutagen sensitivity and risk of gliomas: a case-control analysis.

Although the risk factors contributing to the etiology of brain tumors remain largely unknown, this pilot study suggests that genetically determined sensitivity to environmental carcinogens may play a role in the pathogenesis of these tumors. In this study, we examined short-term lymphocyte cultures from 45 adult malignant glioma patients and 117 age-, sex-, and ethnicity-matched healthy controls for mutagen-induced chromatid breaks and evaluated their family history of cancer, smoking, and demographic variables to ascertain the association between mutagen sensitivity and risk of brain tumors. The mutagen selected was gamma-radiation. The mean number of induced breaks/cell was 0.72 (SD=0.45) for the cases and 0.45 (SD = 0.35) for the controls (P < 0.0001). Using the median number of induced breaks/cell in the controls as the breakpoint for defining mutagen sensitivity, we observed an unadjusted odds ratio of 5.36 (95% confidence interval = 2.12-13.69) for mutagen sensitivity and brain tumor risk and an adjusted odds ratio of 5.79 (2.26-14.83), when we controlled for epidemiological risk factors including smoking, race, income, and education. Although a larger study is needed to confirm this intriguing result, these preliminary findings suggest that increased sensitivity to radiation is an independent risk factor for gliomas.

Adult↗
PubMed1996

Mutation detection by highly sensitive methods indicates that p53 gene mutations in breast cancer can have important prognostic value.

Human cancer cells with a mutated p53 tumor-suppressor gene have a selective growth advantage and may exhibit resistance to ionizing radiation and certain chemotherapeutic agents. To examine the prognostic value of mutations in the p53 gene, a cohort of 90 Midwestern Caucasian breast cancer patients were analyzed with methodology that detects virtually 100% of all mutations. The presence of a p53 gene mutation was by far the single most predictive indicator for recurrence and death (relative risks of 4.7 and 23.2, respectively). Direct detection of p53 mutations had substantially greater prognostic value than immunohistochemical detection of p53 overexpression. Analysis of p53 gene mutations may permit identification of a subset of breast cancer patients who, despite lack of conventional indicators of poor prognosis, are at high risk of early recurrence and death.

Alternative Splicing↗