Sensitivity study of an ultrasound coupled transrectal electrical impedance tomography system for prostate imaging.

In 2009, prostate cancer ranked as the most common cancer and the second most fatal cancer in men in the United States. Unfortunately, the current clinical diagnostic methods (e.g. prostate-specific antigen (PSA), digital rectal examination, endorectal MRI, transrectal ultrasound, biopsy) used for detecting and staging prostate cancer are limited. It has been shown that cancerous prostate tissue has significantly different electrical properties when compared to benign tissues. Based on these electrical property findings, a transrectal electrical impedance tomography (TREIT) system is proposed as a novel prostate imaging modality. The TREIT system comprises an array of electrodes interfaced with a clinical transrectal ultrasound (TRUS) probe. We evaluate this imaging system through a series of phantom imaging experiments to assess the system's ability to image high and low contrast objects at various positions. We found that the TREIT system can easily discern high contrast inclusions of 1 cm in diameter at distances centered at two times the radius of the TREIT probe away from the probe surface. Furthermore, this technology's ability to detect low contrast inclusions suggests that it has the potential to successfully detect prostate cancer.

An apparatus and method to characterize causes of positional plagiocephaly.

Positional plagiocephaly (misshapen head in infants) has increased dramatically in the United States since the beginning of the Back to Sleep program in 1992. In order to understand the increase due to repositioning from prone to supine position for sleep, we developed a home-based monitoring system to discern state of sleep and re-positioning frequency in infants. The portable system allows real-time logging of sleep position and patterns by a simplified sleep algorithm and association of sleep head position and movement which are time-stamped for correlation. Preliminary correlatory results suggest that plagiocephalic infants experience greater periods of rapid-eye-movement (REM) sleep than controls and show more narrow range of motion during sleep.

A provocative test to determine brain compliance in the management of patients with hydrocephalus.

Non-invasive techniques to explore intracranial compliance and pressure have been extensively explored in recent years. Previous techniques have used expensive technologies to make these measurements, often with difficulty. We present a novel, inexpensive method and algorithm to observe trends in intracranial compliance measurement targeted towards the treatment and management of hydrocephalus. The technique uses two photo-plethysmographic sensors to record arterial pulse perfusion, a common tilt table apparatus to methodically and artificially increase intracranial pressure, and a digital signal processing algorithm to determine phase difference between the waveforms. A secondary phase-difference disease signature approach is also hypothesized.

A signal analysis algorithm for determining brain compliance non-invasively.

Patients with increased intracranial pressure (ICP) caused by hydrocephalus or brain injury have poor brain compliance or increased brain stiffness. The condition is commonly treated by a surgical diversion of cerebrospinal fluid (CSF) through placement of a ventriculoperitoneal (VP) shunt. These inserted devices frequently fail and require replacement. Assessment of failed devices typically requires an invasive surgical procedure to implant an ICP sensor. Brain compliance can be determined non-invasively by comparing the intracranial pressure (ICP) waveform to the digital artery waveform. The ICP waveform is derived from a piezo sensor snugged into the external ear canal and worn as a headset. The digital artery waveform is derived from a stand pulse oximeter. Digital signal processing performed on sampled data from these two sensors shows a time-lag or phase relationship between the two waves which widens with worsening brain stiffness or compliance. An algorithm is presented that shows how these signals can be used to compute brain compliance. An instrument designed to calculate real-time brain compliance to aid healthcare professionals is described.

Effects of hormone replacement therapy on ambulatory blood pressure and vascular responses in normotensive women.

The effects of chronic oestrogen replacement therapy (ERT) (conjugated equine oestrogen 0.625 mg/day) and combined oestrogen and progestogen replacement therapy (HRT) (ERT plus continuous medroxyprogesterone acetate 5 mg/day) on 24-h ambulatory blood pressure recordings, forearm vascular resistance (FVR) and FVR responses to noradrenaline, angiotensin II, acetylcholine and nitroprusside were studied in 17 normotensive postmenopausal women in a 3-month randomized, double-blind, placebo-controlled crossover trial with 1 month of therapy in each treatment arm. During the last few days of each 1-month treatment period, the subjects underwent 24-h ambulatory blood pressure recordings and measurements of FVR responses. ERT and HRT reduced mean 24-h diastolic blood pressure by 4 and 5 mmHg, systolic blood pressure by 6 and 9 mmHg and mean 24-h heart rate by 5 and 3 beats/min, respectively for ERT and HRT (p < 0.05). Basal FVR was reduced by approximately 18% by ERT and HRT, but FVR responses to noradrenaline, angiotensin II, acetylcholine and nitroprusside were unaffected. ERT and HRT therapy for 1 month lowers blood pressure and basal FVR, but does not appear to influence FVR responses to acetylcholine, nitroprusside, noradrenaline and angiotensin II.

The effects of hormone replacement therapy on plasma lipids in type II diabetes.

OBJECTIVES: The effects of hormone replacement therapy on cardiovascular risk factors in postmenopausal women with non-insulin dependent diabetes mellitus (type II diabetes) is uncertain. METHODS: The effects of estrogen replacement therapy (ERT, conjugated equine estrogen0.625mg orally daily), combined estrogen and continuous progestogen therapy (HRT, 0.625 mg of conjugated equine estrogens plus medroxyprogesterone acetate 5 mg daily) or placebo was compared in 20 postmenopausal type II diabetic women and 20 normal postmenopausal women in a double blind, randomised, crossover study. Patients receiving insulin were excluded from the study and all lipid modifying drugs were ceased at least 4 weeks prior to randomisation. Other medication including oral hypoglycaemics was kept constant for the duration of the study. RESULTS: Women with type II diabetes were a similar age (58.7+/-1.3 years) to the non-diabetic women (59.6+/-1.6 years) but they had a significantly greater body mass index, a higher incidence of treated hypertension, higher fasting plasma glucose levels, higher triglycerides and lower HDL cholesterol levels than non-diabetic women. ERT reduced total cholesterol and LDL cholesterol by a similar extent (8.9-12.3%) in normal and type II diabetic women and increased HDL cholesterol to a similar extent in both groups (11.0 and 8.9% respectively). ERT did not significantly alter fasting triglyceride levels in either group. The addition of medroxyprogesterone acetate 5 mg daily abolished the increase in HDL cholesterol associated with ERT in both groups but did not significantly affect any of the other lipid measurements. ERT and HRT did not significantly alter fasting insulin levels nor alter fasting glucose levels in either non-diabetic women or women with type II diabetes. CONCLUSIONS: ERT and HRT have similar effects on lipids in women with type II diabetes and non-diabetic women after 1 month of therapy.

Effects of glibenclamide on blood pressure and cardiovascular responsiveness in non-insulin dependent diabetes mellitus.

OBJECTIVE: To compare the effects of chronic glibenclamide therapy and placebo on blood pressure and cardiovascular responsiveness in patients with non-insulin-dependent diabetes. DESIGN AND METHODS: Fourteen patients with non-insulin-dependent diabetes mellitus, seven of whom were receiving angiotensin converting enzyme inhibitor therapy, received glibenclamide or placebo for 1 month in a double-blind, randomized crossover study. At the end of each treatment period patients attended for studies of forearm vascular responsiveness to intra-brachial arterial infusions of angiotensin II, acetylcholine, sodium nitroprusside and noradrenaline, responses of blood pressure to intravenous infusions of noradrenaline and angiotensin II and 24 h ambulatory blood pressure monitoring. RESULTS: Administration of glibenclamide produced significantly better glycaemic control than placebo (fasting blood glucose level 8.5 +/- 2.4 versus 13.5 +/- 4.5 mmol/l, P < 0.001) and plasma insulin levels were significantly higher during glibenclamide treatment than they were with placebo (12.9 +/- 4.4 versus 9.2 +/- 4.1 mU/l, P < 0.05). Body weights at the ends of the glibenclamide treatment and placebo phases were similar (92.1 +/- 14.3 versus 91.1 +/- 14.3 kg, P = 0.085). Night-time systolic blood pressures were significantly higher during glibenclamide treatment than they were with placebo (128 +/- 17 versus 118 +/- 10 mmHg, P < 0.05) due to there being a smaller day-night difference in systolic blood pressure during glibenclamide treatment that appeared to occur mainly in patients receiving angiotensin converting enzyme inhibitors. Responses of diastolic blood pressure to intravenous infusion of angiotensin II and forearm vascular responses to intra-brachial arterial infusion of angiotensin II were significantly greater during glibenclamide treatment than they were with placebo (P < 0.05). However, the enhancement of forearm vascular responses during glibenclamide treatment appeared to be restricted to patients receiving angiotensin converting enzyme inhibitors. Responses of blood pressure to intravenous infusion of noradrenaline and forearm vascular responses to infusions of noradrenaline, acetylcholine and nitroprusside did not differ between glibenclamide treatment and placebo; neither did basal forearm vascular resistance. CONCLUSIONS: Glibenclamide therapy is associated with greater responses of blood pressure and forearm vascular responses to infusion of angiotensin and higher nocturnal blood pressures. This effect appears to be influenced by concomitant angiotensin converting enzyme inhibition.