Comparison of IgM-MGUS and IgG-MGUS polyneuropathy

Objective – To compare the clinical and electrodiagnostic features and response to treatment in patients with IgM-MGUS and IgG-MGUS associated polyneuropathy. Material and methods – Retrospective review of 34 consecutive patients with MGUS associated neuropathy evaluated over 5 years. Results – There were 19 patients with IgM-MGUS and 15 with IgG-MGUS. There were no differences in age, duration of symptoms, or distribution of motor and sensory symptoms or signs. IgM-MGUS patients had prolonged distal latencies of the median and ulnar motor potentials, greater slowing of the peroneal nerve conduction velocity and more often absent ulnar sensory potentials. Half of the patients in both groups improved following immunotherapy. Conclusion – IgM-MGUS patients had more severe dernyelination on the nerve conduction studies, but there were no clinical features that differentiated the 2 groups. IgM and IgG-MGUS patients improved with plasma exchange and other immune therapies. Anti-MAG antibodies failed to distinguish a subgroup of patients with IgM-MGUS neuropathy     

Pulmonary MnSOD is nitrated following hepatic ischemia-reperfusion

BACKGROUND: Ischemia-reperfusion (I/R) of remote organs is a common cause of lung injury. We observed that lung injury after partial hepatic I/R in mice coincides with the appearance of 3-nitrotyrosine (NT) in the lung tissue, a marker of peroxynitrite involvement and oxidant stress. Peroxynitrite can cause mitochondrial dysfunction by inactivation of manganese superoxide dismutase (MnSOD), the major antioxidant enzyme in mitochondria. Our aims were to examine whether pulmonary MnSOD is a target of nitration following hepatic I/R and whether nitrated MnSOD (N-MnSOD) correlates with acute lung injury. METHODS: Five 20-25-g male C57BL/6 mice underwent laparotomy, and atraumatic occlusion of the portal and arterial blood supply to the upper three lobes of the liver for 90 min. This warm ischemic period was followed by 4 h of reperfusion, and the animals were then euthanized. Lung injury was assessed by LDH and protein levels in bronchoalveolar lavage (BAL) fluid. Pulmonary MnSOD activity in pulmonary homogenates was measured by the cytochrome c reduction method. The presence of N-MnSOD was determined by immunoprecipitation (IP) and Western Blot analysis. Controls (N = 5) underwent sham operation. RESULTS: Elevated plasma transaminases confirmed hepatic injury. Lung injury was demonstrated by elevation in BAL protein and LDH levels (495.7 (48.4) versus 644.9 (37.3) [p < 0.05] and 56.5 (11.8) versus 345.2 (80) [p < 0.01], respectively). Immunoprecipitation and Western blot demonstrated N-MnSOD in the lung tissue of I/R animals but not controls. MnSOD activity decreased following I/R (8.1 (0.7) versus 10.8 (0.3) [p < 0.05]). CONCLUSIONS: Pulmonary MnSOD is both nitrated and inactivated following hepatic I/R and is associated with acute lung injury. These findings suggest that MnSOD incapacitance may contribute to I/R-induced lung injury and provide a therapeutic target in attenuating multisystem injury following hepatic I/R.     

Small bowel ischaemia-reperfusion increases plasma concentrations of oxidised proteins in rats.

OBJECTIVES: To find out whether plasma concentrations of protein carbonyl (a specific marker of oxidative damage of proteins) are increased during intestinal ischaemia-reperfusion and whether they are correlated with von Willebrand's factor (vWF, a marker of endothelial injury) or myeloperoxidase (a marker of neutrophil activation). DESIGN: Randomised experimental study. SETTING: University department of surgery, New Zealand. ANIMALS: Thirty anaesthetised adult Wistar rats. INTERVENTIONS: The sham operated group (n = 10) had laparotomy and isolation of the superior mesenteric artery without clamping. The ischaemia-reperfusion group (IR, n = 10) had the superior mesenteric artery clamped for 1 hour and reperfusion for 15 minutes. The control group (n = 10) had direct puncture of the heart to sample blood. MAIN OUTCOME MEASURES: Plasma concentrations of protein carbonyl, vWF, and myeloperoxidase. RESULTS: Plasma protein carbonyl concentrations were significantly higher in the IR group than in the sham group (p < 0.02, Mann-Whitney test, median (range) 0.187 (0.141-0.242) compared with 0.144 (0.121-0.185) nmol/mg) and in the control group (p < 0.01, Mann-Whitney test, median (range) 0.187 (0.141-0.242) compared with 0.136 (0.108-0.175) nmol/mg). There was a significant correlation between protein carbonyl and vWF concentrations (r = 0.54, F = 10.9, p < 0.003, linear regression) but not with those of myeloperoxidase. CONCLUSION: Intestinal ischaemia-reperfusion caused an increase in the plasma protein carbonyl concentration, which is possibly produced by endothelial cells.     

Silica-lipid hybrid microcapsules: influence of lipid and emulsifier type on in vitro performance

This study reports on the physicochemical characterisation and in vitro investigations of macro-porous silica-lipid hybrid (SLH) microcapsules when formulated using various lipids: long-chain triglycerides (LCT), medium-chain triglycerides (MCT), medium-chain mono-, diglycerides (MCMDG); and emulsifiers: anionic lecithin and cationic oleylamine. For the lipophilic compound coumarin 102 (logP=4.09), a complete and immediate in vitro release was attained for the SLH microcapsules under simulated intestinal sink conditions. The in vitro digestion study of various types of SLH microcapsules demonstrates: (i) reduced variability and enhanced lipid digestibility for the MCMDG-based microcapsules (i.e. 90-100% lipolysis) in comparison with an equivalent lipid solution and emulsion (50-90% lipolysis); and (ii) more controllable digestion kinetics for the LCT-based microcapsules which produce a lipolysis rate higher than that of a lipid solution but lower than that of a lipid emulsion. The drug phase partition results show approximately 5- to 17-fold increase in the drug solubilisation degree resulting from the digestion of MCT and MCMDG-based microcapsules (116 μg/mL), and LCT-based microcapsules (416 μg/mL) in comparison with the blank micellar medium (24 μg/mL). In conclusion, the SLH microcapsules could be tailored to manipulate the digestion patterns of both medium- and long-chain lipids in order to maximise the drug solubilisation capacity.     

Characterization and behavior of anesthetic bioactive textile complex in vitro condition

In this study, a bioactive complex containing nonwoven textile material (polypropilene (PP)/viscose), chitosan hydrogel, and lidocaine hydrochloride, was designed. The purpose of such biomedical textile was in the treatment of painful sites. Mercury intrusion porosimetry was used in order to estimate the influence of medical impregnation on porous structure of nonwoven material. It was estimated that more than 97% of pores in untreated nonwoven sample were larger than 15 μm. Anesthetic treatment of nonwoven reduced total pore volume of ultramacropores and macropores, while total pore volume of mesopores slightly increased. Lidocaine hydrochloride release from the anesthetic/chitosan hydrogel/nonwoven complex was measured in vitro by Franz diffusion cell technique. Mathematical model was developed to estimate the release of the lidocaine from obtained bioactive textile material. The diffusive transport of lidocaine hydrochloride through three connected layers, i.e., polymer hydrogel, membrane, and solution is modeled based on Fick's second law. Taking all the relevant conditions, regarding this experiment, into consideration, the coefficient of lidocaine diffusion through the polymer hydrogel, as well as the concentration ratio parameter were determined by the mathematical model.     

Acquired Blaschko Dermatitis-seventh case

The February edition of Dermatology Online Journal 2002;7(1):8, contained an article entitled Acquired Blaschko Dermatitis.[1] A 64 year old patient with erythematous patches and papules in a reticulate pattern on the left upper extremity and on the left side of the chest, abdomen, back and buttock was described. Three months later, in the Department of Dermatology, Health Center Krusevac, we examined a 65 year old woman with similar lesions, distributed in a linear pattern on her right lower limb, following the lines of Blaschko.     

Decay accelerating factor (CD55) protects neuronal cells from chemical hypoxia-induced injury

Background  

Activated complement system is known to mediate neuroinflammation and neurodegeneration following exposure to hypoxic-ischemic insults. Therefore, inhibition of the complement activation cascade may represent a potential therapeutic strategy for the management of ischemic brain injury. Decay-accelerating factor (DAF, also known as CD55) inhibits complement activation by suppressing the function of C3/C5 convertases, thereby limiting local generation or deposition of C3a/C5a and membrane attack complex (MAC or C5b-9) production. The present study investigates the ability of DAF to protect primary cultured neuronal cells subjected to sodium cyanide (NaCN)-induced hypoxia from degeneration and apoptosis.