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N J O'Connor

Publications and source records attributed to N J O'Connor.

7 recordsLinked to original sources
PubMed2000

Blind deconvolution of 3D transmitted light brightfield micrographs.

The blind deconvolution algorithm for 3D transmitted light brightfield (TLB) microscopy, published previously [Holmes et al. Handbook of Biological Confocal Microscopy (1995)], is summarized with example images. The main emphasis of this paper is to discuss more thoroughly the importance and usefulness of this method and to provide more detailed evidence, some being quantitative, of its necessity. Samples of horseradish peroxidase (HRP)-stained pyramidal neurones were prepared and evaluated for the ability to see fine structures clearly, including the dendrites and spines. It is demonstrated that the appearance of fine spine structure, and means of identifying spine categories, is made possible by using blind deconvolution. A comparison of images of the same sample from reflected light confocal microscopy, which is the conventional light microscopic way of viewing the 3D structure of these HRP-stained samples, shows that the blind deconvolution method is far superior for clearly showing the structure with less distortion and better resolution of the spines. The main significance of this research is that it is now possible to obtain clear images of 3D structure by light microscopy of absorbing stains. This is important because the TLB microscope is probably the most widely used modality in the life-science laboratory, yet, until now, there has been no reliable means for it to provide visualization of 3D structure clearly. The main importance of the blind deconvolution approach is that it obviates the need to measure the point spread function of the optical system, so that it now becomes realistic to provide a 3D light microscopic deconvolution method that can be pervasively used by microscopists.

Algorithms↗
PubMed1996

Effect of coronary artery diameter in patients undergoing coronary bypass surgery. Northern New England Cardiovascular Disease Study Group.

BACKGROUND: Coronary artery diameter is known to be inversely associated with perioperative mortality related to coronary artery bypass grafting (CABG). This association is believed to be responsible for increased risk among women and smaller people. However, the associations between sex, body size, and coronary size have not been carefully examined because direct information about coronary size is rarely available. Also, whether sex has an independent effect on vessel size is largely unknown. METHODS AND RESULTS: Height, weight, sex, age, status at hospital discharge, and luminal diameter of the midleft anterior descending coronary artery (mid-LAD) were recorded prospectively in 1325 patients undergoing CABG. Small vessel size was associated with substantially increased risk of in-hospital mortality (15.8% for 1.0-mm vessels, 4.6% for 1.5- to 2.0-mm vessels, and 1.5% for 2.5- to 3.5-mm vessels, P[trend] < .001). Vessel size was strongly related to both sex and measures of body size. In multiple linear regression analysis, vessel size was positively correlated with body surface area (P[trend] < .01), body mass index (P[trend] = .004), height (P[trend] = .001), and weight (P[trend] = .001). After controlling for differences in age and body size, sex remained an important predictor of coronary size. Within each quartile of each body-size measure, mid-LAD diameter in men was greater than that in women (mean difference [range], 0.14 to 0.23 mm). CONCLUSIONS: Small mid-LAD diameter is associated with substantially increased risk of in-hospital mortality with CABG. Although body size is correlated with mid-LAD diameter, women have smaller coronary arteries than men after controlling for differences in body size. These findings further support the hypothesis that smaller coronary arteries explain higher perioperative mortality with CABG in women and smaller people.

Body Constitution↗
PubMed1996

The effect of peripheral vascular disease on long-term mortality after coronary artery bypass surgery. Northern New England Cardiovascular Disease Study Group.

OBJECTIVE: To examine the effect of peripheral vascular disease (PVD) on long-term mortality after successful myocardial revascularization. METHODS: We performed a regional cohort study of 2871 consecutive patients discharged alive after coronary artery bypass graft surgery at five tertiary care centers in Maine, New Hampshire, and Vermont between 1987 and 1989. Data reflecting patient characteristics, heart disease severity, and comorbidity were collected prospectively; the presence of clinical and subclinical indicators of PVD was determined by medical record review; and vital status was determined using the National Death Index (mean follow-up, 4.4 years). RESULTS: Five-year mortality following coronary artery bypass graft surgery was substantially higher in the 755 patients with indicators of PVD (20%; 95% confidence interval [CI], 17% to 23%) than in the 2116 patients without PVD (8%, 95% CI, 7 to 9; P<.001). The crude hazard ratio of long-term mortality associated with PVD was 2.77 (95% CI, 2.19 to 3.50; P<.001). After adjusting for their higher comorbidity scores, more advanced cardiac disease, and age, mortality rates in patients with PVD remained twice as high as those in patients without PVD (adjusted hazard ratio, 2.01; 95% CI, 1.57 to 2.58; P<.001). Long-term mortality was increased in patients with any of the indicators of PVD. Patients with multilevel PVD had especially high late mortality rates (adjusted hazard ratio, 2.46; 95% CI, 1.64 to 3.68; P<.001). CONCLUSIONS: Even after successful myocardial revascularization, patients with PVD remain at substantially increased risk for long-term mortality. The presence of clinical or subclinical PVD is important when predicting both short- and long-term outcomes in patients considering coronary artery bypass graft surgery.

Aged↗
PubMed1995

Psychosocial risk factors and nonfatal myocardial infarction.

BACKGROUND: Numerous psychosocial factors have been hypothesized to play a role in coronary heart disease. However, existing studies have yielded inconsistent results. METHODS AND RESULTS: The relations between type A personality as well as suppressed versus expressed anger and risk of nonfatal myocardial infarction (MI) were studied in 340 patients and 340 age-, sex-, and community-matched control subjects. Subjects were interviewed at home to assess behavioral and medical cardiovascular risk factors, and fasting blood samples were obtained. Type A personality was associated with nonfatal MI in crude matched-pair analysis (OR, 1.57; 95% CI, 1.12 to 2.20; P = .008). Adjusting for known cardiovascular risk factors (including treated hypertension, body mass index, treated diabetes, family history of premature MI, physical activity, smoking, alcohol, total calories per day, and saturated fat) did not substantially change the magnitude of the point estimate, although the finding was no longer statistically significant (OR, 1.43; 95% CI, 0.97 to 2.09; P = .069). Further adjustment for lipids, including total cholesterol, total HDL, its subfractions (HDL2, HDL3), LDL, VLDL, and triglycerides, markedly attenuated the association (OR, 1.12; 95% CI, 0.66 to 1.90; P = .687), an effect due almost entirely to HDL cholesterol. Suppressed anger was positively but not statistically significantly associated with increased risk of MI in crude matched-pair analysis (OR, 1.33; 95% CI, 0.98 to 1.81; P = .065), in analysis adjusted for behavioral and medical cardiovascular risk factors (OR, 1.26; 95% CI, 0.89 to 1.78; P = .193), or after adjustment for lipids (OR, 1.11; 95% CI, 0.67 to 1.82; P = .695). CONCLUSIONS: These findings suggest a possible association of type A but not suppressed anger with risk of nonfatal MI that may be mediated by alterations in HDL cholesterol level. If decreases in HDL are not in the same causal pathway, then the apparent association between type A personality and risk of MI is due to confounding, principally by HDL.

Anger↗
PubMed1987

Alpha, beta and gamma T-cell receptor genes: rearrangements correlate with haematological phenotype in T cell leukaemias.

We have studied the arrangement of the alpha, beta and gamma T cell receptor (TCR) genes in 27 patients with T cell lymphoproliferative disorders. Nine patients had acute lymphoblastic leukaemia (T-ALL), nine patients had prolymphocytic leukaemia (PLL), six patients presented with a T-CLL/T-lymphocytosis syndrome, two patients had Sezary syndrome (SS) and one patient had HTLV-I positive T-cell leukaemia/lymphoma (ATLL). alpha TCR gene rearrangement could be demonstrated by the use of three available probes in only one case. By contrast, both beta and gamma TCR gene rearrangement could be demonstrated by Southern blot analysis of DNA samples digested with appropriate restriction enzymes in the majority of cases. In general, when rearrangements were present they involved both alleles. The proportion of rearranged chromosomes was lower in T-ALL than in other forms of T-cell leukaemia and it was lower in cases with the CD4-/CD8+ phenotype than in those with a CD4+/CD8- phenotype. In three out of 34 cases of B-cell leukaemia the TCR beta-gene but not the TCR gamma-gene was rearranged, just as in two out of 26 cases of T-cell leukaemia the immunoglobulin (Ig) heavy chain but not the light chain genes were rearranged. These data suggest that development of the machinery required for gene rearrangement may precede commitment to B or T cell lineage. The use of this technique is especially useful for the classification of cases of ALL in which the cells are negative with respect to most current phenotypic markers and in cases of T cell lymphocytosis in which the finding of a gene rearrangement identifies a monoclonal cell population.

Adolescent↗