Effect of pepper extracts on the viability kinetics, topography and Quantitative NanoMechanics (QNM) of Campylobacter jejuni evaluated with AFM.

Campylobacter jejuni is a pathogen bacterium that causes foodborne gastroenteritis in humans. However, phenolic compounds extracted from natural sources such as capsicum pepper plant (Capsicum annuum L. var. aviculare) could inhibit the growth of C. jejuni. Therefore, different extracts were prepared using ultrasonic extraction (USE), conventional extraction (CE) and thermosonic extraction (TSE). C. jejuni was then exposed to chili extracts to examine the antimicrobial effect and their growth/death bacterial kinetics were studied using different mathematical models. Atomic force microscopy was applied to investigate the microstructural and nanomechanical changes in the bacteria. Extracts obtained by TSE had the highest phenolic content (4.59 ± 0.03 mg/g of chili fresh weight [FW]) in comparison to USE (4.12 ± 0.05 mg/g of chili FW) and CE (4.28 ± 0.07 mg/g of chili FW). The inactivation of C. jejuni was more efficient when thermosonic extract was used. The Gompertz model was the most suitable mathematical model to describe the inactivation kinetics of C. jejuni. Roughness and nanomechanical analysis performed by atomic force microscopy (AFM) provided evidence that the chili extracts had significant effects on morphology, surface, and the reduced Young's modulus of C. jejuni. The novelty of this work was integrating growth/death bacterial kinetics of C. jejuni using different mathematical models and chili extracts, and its relationship with the morphological, topographic and nanomechanical changes estimated by AFM.

Activity profile in multiple sclerosis: an integrative approach. A preliminary report.

In order to define an activity profile in patients with multiple sclerosis (MS), T-cell subpopulations and proliferative responses to myelin basic protein (MBP) associated with anti-MBP antibodies, nitrotyrosine levels in serum and cerebrospinal fluid (CSF), and serum CD40L (sCD154) were simultaneously assessed in 29 consecutive and untreated MS patients. When compared to controls, patients in secondary progressive stable (SP/I), or in full remission (RR/I) stages, individuals with secondary progressive active disease (SPIA) or in acute relapse (RR/A) showed a significant decrease of CD4/CD45RA+ T cells associated with an increase of absolute numbers of CD4/45R0+ T cells (p < 0.001). In addition, in vitro-specific T-cell proliferative responses against MBP (SP/A, RR/A, SP/I: p < 0.001 versus controls) in association with augmented sCD154 serum levels (SP/A, RR/A, versus controls p < 0.001) and a significant increase of both CSF and serum levels of anti-MBP antibodies and nitrotyrosine levels (p < 0.001) were also found. Thus, the simultaneous evaluation of antibody and cell-mediated immunopathological parameters, along with the effector mediators of inflammation such as the nitric oxide products, offers a new integrative approach to characterize markers of clinical activity in MS patients, which may be used at the moment of the initial diagnosis and during an apparent recurrences of the disease to monitor therapeutic protocols and to determine whether immune-based nerve destruction mechanisms are still operating in patients with few clinical findings.

Clonidine reduces elevated cerebrospinal fluid catecholamine levels in patients with essential hypertension.

Cerebrospinal fluid (CSF) catecholamines were measured in normotensive patients and in patients with mild to moderate essential hypertension. CSF-norepinephrine (NE) concentrations were 50% lower in the normotensive individuals (127 +/- 28 vs. 240 +/- 23 pg/ml) (P less than 0.01). In hypertensive patients, CSF-NE was inversely related to age (r = -0.68; P less than 0.01) and directly related to plasma NE (r = 0.61; P less than 0.05). Clonidine (450 mcg/day for 2 weeks) significantly reduced CSF-NE (-40%) in hypertensive patients. In addition, it decreased blood pressure, plasma and urinary NE. Urinary VMA was not affected by clonidine. No correlation was observed between clonidine effects on BP and on plasma or CSF catecholamines. This study indicates that patients with essential hypertension have elevated levels of CSF-NE which are reduced after treatment with clonidine. The elevation of CSF-NE suggests that central (spinal?) noradrenergic activity may be increased in patients with mild to moderate essential hypertension, and that can be reduced by treatment with clonidine.

Cerebrospinal fluid and plasma dopamine-beta-hydroxylase activity in human hypertension.

Cerebrospinal fluid (CSF) and plasma dopamine-beta-hydroxylase (DBH) activity was measured in 22 normotensive (NT), 31 essential hypertensive (EH), and 11 renal hypertensive (RH) patients. Although no differences were observed in their plasma DBH, the mean CSF-DBH activity and specific activity of EH were significantly lower than those of NT and RH patients. Very low CSF-DBH (less than 0.15 units/ml of CFS or less than 0.5 units/mg of CSF protein) was found only in EH (26% of EH). Of the 31 EH patients, 19(60%) had CSF-DHB activities lower than 0.5 units/ml, whereas only 5 of 22 NT (23%) and no RH fell within this range. Nevertheless, 20% of EH, 55% of NT, and 40% of RH patients had CSF-DBH activities above the mean value for NT (less than 0.9 units/ml). NT subjects with very low plasma DBH (less than 50 units/ml) had CSF-DBH activities that fell within normal range. With the exception of these subjects, the specific activity of CSF-DBH was always lower than that of the plasma enzyme. The concentration of albumin, alpha 1, beta, and gamma globulins was measured in plasma and CSF obtained from the last five NT, four EH, and two RH patients. A positive linear relationship was obtained when the log of the plasma/CSF concentration ratio for these proteins was plotted against their molecular weight. Similar slopes and intercepts were obtained for these patients, suggesting that no major differences seem to exist in their blood-brain-barrier permeability to proteins. The results suggest that measurements of CSF-DBH could be of help in the differential diagnosis of human hypertension and in the neurochemical characterization of EH. If CSF-DBH reflects central noradrenergic activity, its reduction might indicate the existence of a central catecholaminergic defect in a subgroup of EH patients.