Non-invasive determination of surface features of banana during ripening.

Ripening of dessert banana (Musa sap.) is associated with changes in colour (green to yellow starting from the cente), softening, and surface features. These have mostly been investigated using distinct technologies. Hence, here changes in surface features were examined with two novel, non-invasive techniques: a luster sensor and a 3D profilometer. The profiler measures the 3D surface characteristics of an area, rather than a single profile line, and corrects data for curvature of the fruit. The luster sensor detected an increase in glossiness from stage 3 (green) to stage F7a (ripe) of ca. 35%, followed by a decrease in glossiness from stage F7a to F7b (overripe). The profilometer provided visual and parametric roughness values (Ra) for ripening. Cavendish bananas showed an increase from 2.5 to 6.6 µm during ripening stage 3 (green) to stage 7b (overripe). Another roughness value, Rz, increased concomitantly from 13.1 µm at stage 3 (green) to 26.9 µm at stage F7b (overripe). The study showed that the centre of the fruit was the best region for surface imaging, because it was the most advanced ripening part of the banana fruit, easily curved, and the region of the fruit can be accessed when a carton was opened. This study shows that it is now possible to monitor the changes in surface glossiness and roughness during the ripening of Cavendish bananas using two novel non-invasive technologies. The compact luster sensor may become a component of a portable probe and manual control of packing units. Differences in the predicted green life can be used to prioritize containers for unloading in the discharge port or to implement quality-based warehouse management strategies. Containers that arrive at banana ripening rooms before their green life ends, can be re-routed, in addition to the present, colour-based ripening scale.

Daily iTBS worsens hand motor training--a combined TMS, fMRI and mirror training study.

INTRODUCTION: Repetitive transcranial magnetic stimulation (rTMS) is used to increase regional excitability to improve motor function in combination with training after neurological diseases or events such as stroke. We investigated whether a daily application of intermittent theta burst stimulation (iTBS; a short-duration rTMS that increases regional excitability) improves the training effect compared with sham stimulation in association with a four-day hand training program using a mirror (mirror training, MT). The right dorsal premotor cortex (dPMC right) was chosen as the target region for iTBS because this region has recently been emphasized as a node within a network related to MT. METHODS: Healthy subjects were randomized into the iTBS group or sham group (control group CG). In the iTBS group, iTBS was applied daily over dPMC right, which was functionally determined in an initial fMRI session prior to starting MT. MT involved 20 min of hand training daily in a mirror over four days. The hand tests, the intracortical excitability and fMRI were evaluated prior to and at the end of MT. RESULTS: The results of the hand training tests of the iTBS group were surprisingly significantly poorer compared with those from the CG group. Both groups showed a different course of excitability in both M1 and a different course of fMRI activation within the supplementary motor area and M1 left. CONCLUSION: We suggest the inter-regional functional balance was affected by daily iTBS over dPMC right. Maybe an inter-regional connectivity within a network is differentially balanced. An excitability increase within an inhibitory-balanced network would therefore disturb the underlying network.

Optical illusion alters M1 excitability after mirror therapy: a TMS study.

The contralesional primary motor cortex (M1) has been suggested to be involved in the motor recovery after mirror therapy, but whether the ipsilesional M1 is influenced by the contralesional M1 via transcallosal interhemispheric inhibition (IHI) is still unclear. The present study investigated the change of IHI as well as the intracortical inhibition and intracortical facilitation of both M1 induced by training in a mirror with the use of transcranial magnetic stimulation (TMS). In this 2 × 2 factorial design (time × group), healthy subjects exercised standardized motor skills with their right hand on four consecutive days. Either a mirror (mirror group) or a board (control group) was positioned between their hands. Before and after training TMS was applied along with training tests of both hands. Tests were the same motor skills exercised daily by both groups. Tests of the untrained left hand improved significantly more in the mirror group than in the control group after training (P = 0.02) and showed a close correlation with an increase of intracortical inhibition of M1(left). IHI did not show any difference between investigation time points and groups. The present study confirms the previous suggestion of the involvement of the "contralesional" left-side (ipsilateral to the hand behind the mirror) M1 after mirror therapy, which is not mediated by IHI. Even with the same motor skill training (both groups performed same motor skills) but with different visual information, different networks are involved in training-induced plasticity.

Quantitative and qualitative investigation of the main flavonoids in heartsease (Viola tricolor L.).

Liquid chromatography coupled to electrospray ionization tandem mass spectrometry (MSn) is used for the analysis of flavonoids in heartsease (Viola tricolor L.). Our data suggested that the two main flavonoid components were violanthin (6-C-glucosyl-8-C-rhamnosyl apigenin) and rutin (3-O-rutinosyl quercetin). The identification of rutin was confirmed by comparing its retention time, UV spectrum, molecular mass, and fragmentation pattern with the reference standard. In this paper, we also report on the quantitative analysis of rutin by high-performance liquid chromatography. According to our results, heartsease herb contained 420+/-1.17 microg/g rutin.

Effects of physiological aging and cerebrovascular risk factors on the hemodynamic response to brain activation: a functional transcranial Doppler study.

The influence of the vascular system on the coupling of cerebral blood flow (CBF) to focal brain activation during aging is incompletely understood. Using functional transcranial Doppler sonography and a hypercapnic challenge as a marker of intact cerebral vasoreactivity, we determined CBF velocity (CBFV) changes in response to a language and arithmetic task in a group of 43 healthy young subjects (mean age 32 +/- 8.6 years), 18 healthy old subjects (mean age 64 +/- 9.8 years) and 29 old subjects with risk factors for an atherosclerosis (mean age 69 +/- 8.4 years). Despite a similar performance during the cognitive tasks the CBFV changes were significantly lower in the group of old subjects with vascular risk factors compared with the healthy young and old subjects. Similarly, the CBFV changes during hypercapnia were significantly lower in the group of old subjects with vascular risk factors compared with the healthy young and old subjects. In contrast, both cognitive tasks and hypercapnia produced comparable CBFV changes in the group of healthy young and old subjects. These results suggest that the hemodynamic response to neuronal activation is unaffected by aging alone, whereas the presence of cardiovascular risk factors significantly diminishes the capability of cerebral vessels to react to vasodilating stimuli.

Overexpression of HSP72 after induction of experimental stroke protects neurons from ischemic damage.

The 72-kD inducible heat shock protein (HSP72) can attenuate cerebral ischemic injury when overexpressed before ischemia onset. Whether HSP72 overexpression is protective when applied after ischemia onset is not known, but would have important clinical implications. Fifty-seven rats underwent middle cerebral artery occlusion for 1 hour. Defective herpes simplex viral (HSV) vectors expressing hsp72 with lacZ as a reporter were delivered 0.5, 2, and 5 hours after ischemia onset into each striatum. Control animals received an identical vector containing only lacZ. Striatal neuron survival at 2 days was improved by 23% and 15% when HSP72 vectors were delayed 0.5 and 2 hours after ischemic onset, respectively ( P < 0.05). However, when delayed by 5 hours, HSP72 overexpression was no longer protective. This is the first demonstration that HSP72 gene transfer even after ischemia onset is neuroprotective. Because expression from these HSV vectors begins 4 to 6 hours after injection, this suggests that the temporal therapeutic window for HSP72 is at least 6 hours after ischemia onset. Future strategies aimed at enhancing HSP72 expression after clinical stroke may be worth pursuing. The authors suggest that in the future HSP72 may be an effective treatment for stroke.

Reversal of early diffusion-weighted magnetic resonance imaging abnormalities does not necessarily reflect tissue salvage in experimental cerebral ischemia.

BACKGROUND AND PURPOSE: Diffusion-weighted MRI (DWI) can detect early ischemic changes and is sometimes used as a surrogate neurological end point in clinical trials. Recent experimental stroke studies have shown that with brief periods of ischemia, some DWI lesions transiently reverse, only to recur later. This study examined the histological condition of the tissue during the period of DWI reversal. METHODS: Rats underwent 30 minutes of middle cerebral artery occlusion followed by reperfusion. DWI images were obtained during ischemia and 3 to 5 hours, 1 day, and 7 days later. MRI scans were compared with histology (5 hours, n=5; 7 days, n=5) with the use of neuronal (microtubule-associated protein 2 [MAP2]) and astrocytic (glial fibrillary acidic protein [GFAP]) markers and heat-shock protein 72 (HSP72). RESULTS: DWI abnormalities reversed 3 to 5 hours after ischemia onset but recurred at 1 day. Four animals showed complete reversal of the initial DWI hyperintensity, and 6 showed partial reversal. When the 5-hour DWI was completely normal, there was significant loss of MAP2 immunoreactivity, comprising approximately 30% of the initial DWI lesion. However, GFAP staining revealed morphologically normal astrocytes. HSP72 immunoreactivity at 5 hours was extensive and corresponded to the initial DWI lesion. CONCLUSIONS: After brief ischemic periods, normalization of the DWI does not necessarily imply that the tissue is normal. Neurons already exhibit evidence of structural damage and stress. Normal GFAP staining suggests that other nonneuronal cell populations may partially compensate for altered fluid balances at the time of DWI reversal despite the presence of neuronal injury. These observations suggest that caution is warranted when relying solely on DWI for assessment of ischemic damage.

MRI of subacute hemorrhagic transformation in the rat suture occlusion model.

In this study we investigated the utility of different MRI techniques for the detection and predictability of hemorrhagic transformation (HT) in a rat model of transient focal cerebral ischemia. Hemorrhagic infarction was reliably identified with gradient-echo sequences and developed between 2 and 7 days following the insult. None of the investigated early MRI features of the ischemic lesions (including the apparent diffusion coefficient and post-reperfusion blood-brain barrier damage) was a good predictor of HT severity at 7 days. This indicates that subacute HT at 2-7 days occurs independently of the severity of acute tissue and BBB damage.

On competency, consent and emotional duress: a case study.

This case study examines the matters of competency and informed consent in the case of a patient whose express-but potentially misguided-wishes conflict with medical opinion and the desires of the family. It considers the roles played by emotional, physical and circumstantial factors and attempts to reach a solution which is both consistent with medical ethics and feasible in a clinical setting. Also contains a brief review of Health Care Ethics in Canada, a Canadian bioethics textbook edited by Francois Baylis et al.

Serial MRI after transient focal cerebral ischemia in rats: dynamics of tissue injury, blood-brain barrier damage, and edema formation.

BACKGROUND AND PURPOSE: With the advent of thrombolytic therapy for acute stroke, reperfusion-associated mechanisms of tissue injury have assumed greater importance. In this experimental study, we used several MRI techniques to monitor the dynamics of secondary ischemic damage, blood-brain barrier (BBB) disturbances, and the development of vasogenic edema during the reperfusion phase after focal cerebral ischemia in rats. METHODS: Nineteen Sprague-Dawley rats were subjected to transient middle cerebral artery occlusion of 30 minutes, 60 minutes, or 2.5 hours with the suture occlusion model. MRI, including diffusion-weighted imaging (DWI), T2-weighted imaging, perfusion-weighted imaging, and T1-weighted imaging, was performed 5 to 15 minutes before reperfusion, as well as 0.5, 1.5, and 2.5 hours and 1, 2, and 7 days after withdrawal of the suture. Final infarct size was determined histologically at 7 days. RESULTS: In the 30-minute ischemia group (and partially also after 60 minutes), DWI abnormalities reversed transiently during the early reperfusion period but recurred after 1 day, probably due to secondary ischemic damage. After 2.5 hours of ischemia, DWI abnormalities no longer reversed, and signal intensity on both DWI and T2-weighted images increased rapidly in the previously ischemic region due to BBB damage (enhancement on postcontrast T1-weighted images) and edema formation. Early BBB damage during reperfusion was found to be predictive of relatively pronounced edema at subacute time points and was probably related to the increased mortality rates in this experimental group (3 of 7). CONCLUSIONS: Reperfusion after short periods of ischemia (30 to 60 minutes) appears to be mainly complicated by secondary ischemic damage as shown by the delayed recurrence of the DWI lesions, whereas BBB damage associated with vasogenic edema becomes a dominant factor with longer occlusion times (2.5 hours).

Single- and multiple-dose-response relationships of beta-carotene in cystic fibrosis.

Concentrations of carotenoids are low in patients with cystic fibrosis (CF) and are associated with essential fatty acid deficiency and increased markers of inflammation. We conducted single- and multiple-dose studies of beta-carotene supplementation in patients with CF. Dose-proportional increases in beta-carotene concentrations were found, although clearance was independent of dose. Large doses of beta-carotene were necessary to achieve normal plasma levels.

Lack of effects of beta-carotene on lipids and sex steroid hormones in hyperlipidemics.

Beta-carotene in doses of up to 300 mg daily raises high-density lipoprotein cholesterol levels within 2 to 4 weeks in healthy subjects. The authors, in this study, investigate the short-term effects of high-dose beta-carotene upon serum lipids, lipoproteins, and selected sex steroid hormones in 59 adult patients with Type IIa or IIb hyperlipidemia and 36 healthy subjects. Volunteers took beta-carotene (300 mg) or wheat germ oil capsules daily for 30 days. Lipids were measured on days 1, 14, 21, and 30. Beta-carotene, retinol, free and total testosterone, and estradiol levels were measured on days 1 and 30. Total high-density lipoprotein cholesterol levels increased 10% (p < 0.01) over baseline in all groups by day 14 but returned to baseline by day 30. Total cholesterol, low-density lipoprotein cholesterol, and triglyceride levels transiently increased between days 14 and 21 by up to 9%, 8%, and 20%, respectively, only in the patients with hyperlipidemia treated with beta-carotene, but returned to baseline on day 30. Apolipoproteins A and B were unchanged. Despite 20-fold increases of plasma beta-carotene levels there, were no reports of carotenodermia and no alteration in sex steroid hormones, retinol levels, hepatic transaminases, or persistent changes in serum lipids that were attributable to beta-carotene.

A voltage-dependent and a voltage-independent potassium channel in brown adipocytes of the rat.

Single-channel recordings of a voltage-dependent potassium channel in brown adipocytes of the rat confirm recordings of macroscopic currents. Single-channel conductance (gamma) is 8 pS at 20 degrees C in KF solution inside vs. a modified Ringer's solution outside. With KCl solution outside, gamma is 17 pS for outward currents and 21 pS for inward currents. The majority of the channels inactivate with a time constant around 200 ms; deactivation occurs within milliseconds. The channel is blocked by tetraethylammonium (TEA) with an inhibiting constant of 1.8 mM. The type of block is fast. Selectivity sequence for monovalent cations is K+ > Rb+ >> NH4+ >> Li+ > or = Na+ approximately Cs+. Cs+ at the outside causes a voltage-dependent block of inward currents. This channel is remarkably similar to the delayed rectifier of the F-type in the node of Ranvier. Occasionally, an additional K+ channel was found. This channel is voltage-insensitive, not blocked by 10 mM TEA, and has not been recorded in brown adipocytes before. Physiological relevance of this channel could be the steady-state membrane potential.

Carotenoid levels in normal children and in children with cystic fibrosis.

The carotenoids are potent antioxidants with the ability to quench singlet oxygen and other toxic oxygen species. We studied 17 patients with cystic fibrosis (CF) and 10 normal children to assess plasma levels of four carotenoids, beta-carotene, alpha-carotene, lutein, and lycopene, by high-performance liquid chromatography. We found significantly lower plasma levels of specific carotenoids in children with CF than in normal control subjects. The standardization of carotenoid levels for total cholesterol did not significantly attenuate these differences. No differences in total carotene intake were apparent between the groups. Carotenoid levels did not correlate with fat absorption or measures of adiposity in children with CF. Additionally, levels of selected carotenoids correlated negatively with serum IgG levels, an indirect measure of inflammation. The differences in plasma carotenoid levels between children with CF and normal children may be due to rapid turnover of carotenoids, perhaps through quenching of toxic oxygen species in inflammatory states of CF. Studies assessing supplementation of these antioxidants should be considered.

Laryngospasm after administration of gadopentetate dimeglumine.

Few serious adverse reactions associated with the use of gadopentetate dimeglumine in magnetic resonance imaging have been reported. The present case involves an 8-year-old girl who developed laryngospasm after administration of gadopentetate dimeglumine.

Inflammatory host responses in sepsis.

Although microbes and their associated toxins initiate sepsis, it is the subsequent host inflammatory response that defines most of what we characterize as clinical sepsis. This article considers the various cellular as well as humoral mediators involved in this response in addition to the complex networking that may result in both augmentation and modulation of the inflammatory response in sepsis.

Effects of fish oil and endorphins on the cold pressor test in hypertension.

The effects of fish oil and naloxone on blood pressure, catecholamines, and endorphins during the cold pressor test were evaluated in a randomized, double-blind, placebo-controlled, two-way crossover trial of normotensive and medication-free hypertensive men (n = 13 each). Subjects were given 5 gm omega-3 fatty acids per day or placebo for 30 days with a 1-month washout between interventions. The cold pressor test (hand in ice water for 5 minutes) was done at the end of the treatment periods. Intravenous naloxone (10 mg) or placebo was given before the cold pressor test. Fish oil-treated, normotensive, or hypertensive groups had similar changes in blood pressure, plasma catecholamine levels, and beta-endorphins during the cold pressor test, but naloxone treatment was associated with fivefold and tenfold increases in plasma epinephrine and cortisol levels, respectively. Naloxone may modulate sympathomedullary discharge through blockade of endorphin activity. It is unlikely that endorphins are involved in the blood pressure increase during the cold pressor test or that fish oil alters this response.

Beta-carotene's effects on serum lipoproteins and immunologic indices in humans.

Doses of beta-carotene for cancer-prevention trials have been chosen based on epidemiologic data. Mechanisms of the putative antineoplastic effects by beta-carotene are unknown but may involve modulation of the immune system. We measured plasma carotenoid concentrations and selected immunologic indices at baseline and at 2 and 4 wk in 50 healthy humans (5 groups of 10 each) ingesting 0, 15, 45, 180, or 300 mg beta-carotene/d for 1 mo in this randomized placebo-controlled, open-label, parallel study. Plasma beta-carotene concentrations were markedly increased by 2 wk and were correlated with dose. Beta-carotene concentrations plateaued between 2 and 4 wk except for the 300-mg group. Thus, we developed a dose-concentration curve to optimize beta-carotene-dose selection to achieve target plasma concentrations. We were unable to identify any effects of beta-carotene ingestion on the immunologic indices studied, but modest increases in high-density-lipoprotein cholesterol were observed in all beta-carotene-treated groups.

Fish oil produces an atherogenic lipid profile in hypertensive men.

The effects of fish oil supplements on plasma and platelet membrane lipids, lipoproteins, sex steroid hormones, glucose, insulin, platelet aggregation, and blood pressure in normal subjects (n = 13) and patients with essential hypertension (n = 13) were studied in this randomized, double-blind, placebo-controlled, two-way crossover study. Treatments consisted of 30 days of 5 g of n-3 fatty acids (ten 1-g capsules of fish oil daily) or placebo capsules (ten wheat germ oil capsules daily) with a one-month washout in between each crossover. Serum lipids and lipoproteins were measured before dosing and every two weeks during the study. Sex steroid hormones, glucose, insulin, and fatty acid composition in platelet membrane phospholipids were measured before dosing and at the end of each crossover. During treatment with fish oil, only the hypertensive had increases in total cholesterol (8%, p less than 0.026), LDL cholesterol (19%, p less than 0.006) and apolipoprotein B (18%, p less than 0.026). Serum androgens (total and free testosterone) were 30% lower in hypertensives than normotensives before any dosing, but were unchanged with placebo or fish oil capsules in either group. Plasma glucose, insulin, platelet aggregation, and the incorporation of n-3 fatty acids into platelet membrane phospholipid subfractions were similar in both normotensive and hypertensive men. Blood pressure was not affected by fish oil treatment in either group of men. These results provide evidence that fish oil may adversely affect serum lipids to yield an atherogenic lipid profile in hypertensive men.