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Biomedical subjects

B Phipps

Publications and source records attributed to B Phipps.

12 recordsLinked to original sources

Fifteen years follow up with the St. Jude Medical Biocor porcine bioprosthesis.

BACKGROUND AND AIM OF STUDY: The study aim was to review the 15-year results of aortic (AVR) and mitral (MVR) valve replacement with the St. Jude Medical Biocor porcine prosthesis, in order to investigate long-term survival and valve-related complications. METHODS: Between January 1983 and January 1998, a total of 1,187 patients underwent either AVR (n = 1,029; mean age 69 years) or MVR (n = 158; mean age 63 years). Follow up (99.7% complete) was monitored in 1998, and all data were analyzed with regard to actuarial valve failure rates. Long-term echocardiographic data were obtained. RESULTS: Cumulative follow up time was 5,049 patient-years (pt-yr) for AVR patients, and 845 pt-yr for MVR patients. Actuarial survival rate at 15 years was 41 +/- 3%, and freedom from valve-related death was 94 +/- 1% for the AVR group; corresponding values for the MVR group were 25 +/- 11% and 84 +/- 6%. The occurrence of structural valve deterioration (SVD) varied with age; older patients were less affected. Freedom from SVD was 76 +/- 7% and 92 +/- 4% for AVR and MVR patients, respectively. Thromboembolism (TE) occurred mainly among the oldest patients, and was most prevalent among those with MVR. Actuarial freedom from TE was 82 +/- 5% after AVR and 75 +/- 7% after MVR. Prosthetic valve endocarditis (PVE) was rare, but caused the only reoperative mortality. Freedom from PVE was 95 +/- 2% after AVR and 93 +/- 3% after MVR. CONCLUSION: Although the optimal valve substitute remains to be found, this long-term study of a third-generation bioprosthesis showed a low incidence of valve-related complications, especially of valve deterioration. This type of bioprosthesis appears to be more durable than valves of previous generations.

Actuarial Analysis↗

Corticotropin-releasing factor--immunolabeled fibers in brain regions with localized kainate neurotoxicity.

Rats treated with the neuroepileptic drug, kainic acid, exhibit a specific regional pattern of neurodegeneration 24 h following onset of acute limbic status epilepticus. At 24 h post-seizure, the areas undergoing neurodegeneration also exhibit substantial amounts of the neuropeptide corticotropin-releasing factor (CRF) which is not present under normal conditions. In experimental brains, CRF is localized immunocytochemically to cells and densely labeled fibers in areas with neurodegeneration. Networks of CRF fibers closely surround moribund neurons staining intensely for acid fuchsin. Acid fuchsin, an acidophilic dye, is used routinely as a marker for irreversible neuronal injury, and acid fuchsin-positive neurons are identified in specific areas affected by kainic neurotoxicity. Evidence exists in the literature that CRF functions in brain as a excitatory neurotransmitter/neuromodulator. Under certain pathological conditions (i.e., seizures, brain trauma, ischemia), it has been postulated that CRF could act as an neurotoxic agent. This study provides anatomical evidence that CRF may function following seizures as an neurotoxin because of the close proximity of CRF-labeled fibers to degenerating neurons.

Animals↗

Reproducible fentanyl doses delivered intermittently at different time intervals from an electrotransport system.

The electrotransport transdermal fentanyl system (ET [fentanyl]), uses a small electrical current to enhance delivery of fentanyl to systemic circulation. Intermittent doses can be administered by periodic application of the current. The purpose of this study was to compare the effects of the frequency of intermittent drug delivery by ET (fentanyl) and compare the drug delivery to systemic circulation by ET (fentanyl) with intravenous administration. The topical safety was also determined for the ET (fentanyl) system. Nine adult male volunteers completed this three-treatment, randomized, 24-h, crossover study. ET (fentanyl) treatments with 200 microA direct current applied for 30 min at frequent (hourly) or infrequent (4-hourly) intervals over a 24-h period were compared. Also, the drug delivery to systemic circulation from ET (fentanyl) was compared with intravenous fentanyl 75 microg infused over 30 min every 4 h over a 24-hour period. The mean serum fentanyl concentration achieved with the hourly ET (fentanyl) regimen was higher than that for the 4-hourly ET (fentanyl) regimen as expected from the higher frequency of drug doses. The amount of fentanyl delivered estimated per dose from the ET (fentanyl) system using the iv fentanyl treatment as the reference was similar for the two ET regimens throughout the dosing period. This indicates consistent drug delivery regardless of the frequency of ET dosing. The majority of subjects reported either no, or barely perceptible, erythema 24 h after removal of the system.

Administration, Cutaneous↗

Increased corticotropin-releasing factor immunoreactivity in select brain sites following kainate elicited seizures.

The literature has focused on the localization, regulation and function of corticotropin-releasing factor (CRF) expressing neurons localized in the paraventricular nucleus (PVN) of hypothalamus. However, less information is available on the expression, regulation, and function of CRF at extrahypothalamic sites. The current study examined the induction of CRF in extrahypothalamic brain sites following generalized clonic seizures induced by kainic acid. At 24 h post seizure onset, there was a marked increase of CRF immunolabeled perikarya in select brain areas, which contained little, if any, CRF in control brains. This CRF-like labeling was observed in olfactory structures such as the main olfactory bulb (internal granular layer), anterior olfactory nucleus, and deep layers of piriform cortex. Other sites of increased CRF-like immunoreactivity included the tenia tecta, inner layers of cingulate cortex, lateral septum, dorsal endopiriform nucleus, fundus striatum, and nucleus of the lateral olfactory tract. Additionally, CRF-like labeling was atypically increased in the amygdala (lateral and basolateral amygdaloid nuclei) and hippocampal formation (pyramidal cells of regions CA1/CA3 and polymorph cells within the dentate hilus). An association between the increased CRF immunoreactivity and neuropathological processes, characteristic of this seizure model, is hypothesized and discussed.

Animals↗

Effects of generalized convulsive seizures on corticotropin-releasing factor neuronal systems.

Most stressors generate a set of endocrine and neural adaptations that form a stress response. The corticotropin-releasing factor neurons of the paraventricular nucleus of hypothalamus integrate endocrine and neural inputs, and cause a cascade of events with resultant increased levels of pituitary adrenocorticotropic hormone and adrenal hormones. Although activation of the hypothalamic-pituitary-adrenal axis is associated with a large variety of stressors, the effects of seizures on hypothalamic corticotropin-releasing factor neurons are essentially unknown. The goal of the present study was to elucidate the effects of generalized convulsive seizures on distinct and separate corticotropin-releasing factor cell populations in brain. Seizure-activated neurons were identified immunocytochemically through their expression of the Fos protein. Seizures were induced by intraperitoneal injection of kainic acid. In the paraventricular nucleus, the vast majority of corticotropin-releasing factor-like parvocellular neurons also expressed Fos-like protein following seizure elicitation. This response was specific to corticotropin-releasing factor neurons of the paraventricular nucleus, as corticotropin-releasing factor neurons in central nucleus of the amygdala or bed nucleus of the stria terminalis did not simultaneously localize Fos following seizures.

Animals↗

Corticotropin-releasing factor induction in rat piriform cortex following kainate-elicited seizures.

There is a substantial increase in number of cells labeled for corticotropin-releasing factor-like immunoreactivity in specific extrahypothalamic brain regions, particularly the piriform cortex, in rats allowed to survive 24 h following generalized clonic seizures. Seizures were elicited by kainic acid. Vehicle treated control animals had only a few cells labeled for corticotropin-releasing factor-like immunoreactivity at these brain sites. These areas of corticotropin-releasing factor-like induction appear to be localized to brain regions known to be vulnerable to kainate neurotoxicity and cell destruction.

Animals↗

Thrombophilia and lipid profile in post-menopausal women using a new transdermal oestradiol patch.

OBJECTIVE: To assess the changes, over a 6-month period, in serum lipoproteins, apoproteins and coagulation factors, induced in post-menopausal women treated by a new transdermal oestradiol patch. METHODS: Fifty-three hysterectomised, healthy, post-menopausal women were treated by a new transdermal patch designed to deliver 50 micrograms of 17 beta oestradiol per day (Gynaderm, Shire Developments). One patch was applied twice weekly. RESULTS: Forty-two patients completed the study. There was no significant change in the level of total cholesterol, triglycerides, HDL or LDL. There was a significant rise in the level of ApoAI after 3 months on therapy but this was not sustained after 6 months; there was also a significant drop in the level of ApoAII after 6 months on treatment. The changes in ApoB and Lp(a) were not statistically significant. There was a significant drop in the level of antithrombin III and of protein S, and a significant rise in factor VII. The drop in the level of fibrinogen and of protein C were not statistically significant. CONCLUSION: The transdermal route of oestradiol administration causes minimal changes in lipoprotein metabolism. The statistically significant changes in the thrombophilia profile parallel those observed with oral HRT, but, similarly, may not reflect clinical significance. The potential of transdermal oestrogens as cardioprotective agents is yet to be determined.

Administration, Cutaneous↗

Unexplained severe pulmonary hypertension in the older age group.

Two cases of unexplained severe pulmonary hypertension were seen in the older age group. Although classified as primary pulmonary hypertension, the clinical course of these patients was very unusual because of their age and relatively long duration of diseases. The long period of follow-up allowed assessment of both the difficulties of making a definite diagnosis of primary pulmonary hypertension in the older age group and the noninvasive methods which were particularly helpful. Making the diagnosis of primary pulmonary hypertension in the older age group is important because there are now drugs which can ameliorate the severity of pulmonary hypertension.

Aged↗