Preexercise meal composition alters plasma large neutral amino acid responses during exercise and recovery

This study was designed to determine metabolic and physical performance responses to ingestion of pre-exercise meals with different macronutrient and fiber profiles. Twelve physically active subjects (6 males and 6 females) were used to investigate the metabolic and physical performance consequences of consuming pre-exercise meals consisting of oat, corn, or wheat cereals. A fasting trial served as the control, and all subjects received each treatment in a Latin-square design. Blood samples were drawn before and 85 min after meal ingestion, during 90 min of cycling exercise (60% VO2peak), after a 6.4 km performance ride, and during 60 min of recovery. Expired air samples were collected to determine nutrient utilization. Resting carbohydrate oxidation rates and plasma insulin concentrations after oat ingestion were less than after wheat, and corn and wheat ingestion, respectively (P < 0.05). During exercise, the change in plasma glucose from pre-exercise was greater after consuming wheat and corn compared with oat (P < 0.05), and it was inversely related to pre-exercise plasma insulin concentration (r = -0.55, P = 0.0001). Plasma free fatty acid concentrations were inversely related to plasma lactate concentrations (r = -0.58, P = 0.0001). Free fatty acid concentrations and fat oxidation were greater in fasting trials than all others, but performance ride times did not differ among treatments. Plasma branched-chain amino acid concentrations resembled their respective meal profiles throughout exercise, the performance ride, and recovery. These results indicate that pre-exercise meal composition can influence glucose homeostasis during early exercise and plasma branched-chain amino acid concentrations over a substantial range of metabolic demands.     

Conformation and activity of mannose- and N-acetylgalactosamine-specific lectins from Vicia villosa seeds

The conformation of two Vicia villosa lectins specific for mannose and N-acetylgalactosamine, respectively, was studied by circular dichroism. Both showed a broad negative CD band around 220 nm and a positive one above 190 nm. CD data analysis indicated that they were rich in beta-sheet. However, they differed in conformational stability against extreme pH, at elevated temperature, and in guanidine hydrochloride and sodium dodecyl sulfate solutions. The unusual feature was that the conformation of N-acetylgalactosamine-specific lectin was virtually unaltered in 6 M guanidine hydrochloride and 7.5 mM surfactant.     

Astrocytic neurotransmitter receptors in situ and in vivo

In the brain, astrocytes are associated intimately with neurons and surround synapses. Due to their close proximity to synaptic clefts, astrocytes are in a prime location for receiving synaptic information from released neurotransmitters. Cultured astrocytes express a wide range of neurotransmitter receptors, but do astrocytes in vivo also express neurotransmitter receptors and, if so, are the receptors activated by synaptically released neurotransmitters? In recent years, considerable efforts has gone into addressing these issues. The experimental results of this effort have been compiled and are presented in this review. Although there are many different receptors which have not been identified on astrocytes in situ, it is clear that astrocytes in situ express a number of different receptors. There is evidence of glutamatergic, GABAergic, adrenergic, purinergic, serotonergic, muscarinic, and peptidergic receptors on protoplasmic, fibrous, or specialized (Bergmann glia, pituicytes, Müller glia) astrocytes in situ and in vivo. These receptors are functionally coupled to changes in membrane potential or to intracellular signaling pathways such as activation of phospholipase C or adenylate cyclase. The expression of neurotransmitter receptors by astrocytes in situ exhibits regional and intraregional heterogeneity and changes during development and in response to injury. There is also evidence that receptors on astrocytes in situ can be activated by neurotransmitter(s) released from synaptic terminals. Given the evidence of extra-synaptic signaling and the expression of neurotransmitter receptors by astrocytes in situ, direct communication between neurons and astrocytes via neurotransmitters could be a widespread form of communication in the brain which may affect many different aspects of brain function, such as glutamate uptake and the modulation of extracellular space.     

Imaging spectrum of thrombo-occlusive vascular disease associated with antiphospholipid antibodies

The association of antiphospholipid antibodies with unexplained thrombo-occlusive vascular disease is well known but often remains unrecognized. The most well-studied clinical manifestation is venous thrombosis, but arterial occlusive disease involving multiple sites is also well documented. Twenty-six cases of thrombo-occlusive disease were observed in 22 patients over a 3-year period. Magnetic resonance imaging and angiography were used to make the diagnoses. None of the patients who underwent angiography or venography developed thrombolytic disease related to the puncture site. This group of patients with antiphospholipid antibody syndrome had a wide distribution of arterial and venous thrombotic disease. Radiologists should consider antiphospholipid antibody syndrome in the differential diagnosis when evaluating thrombo-occlusive vascular disease that is unexpected or occurs without risk factors. Knowledge of antiphospholipid antibody status has important implications for prognosis and therapy.     

The modulatory cholinergic system in goldfish tectum may be necessary for retinotopic sharpening

The cholinergic circuit within the tectum and the cholinergic input from the nucleus isthmi mediate a presynaptic augmentation of retinotectal transmitter release via nicotinic receptors. In this study, the cholinergic systems were either eliminated using the cholinergic neurotoxin AF64A or blocked using nicotinic antagonists to test for effects on the activity-driven sharpening of the regenerating retinotectal projection. The effectiveness of the AF64A was verified by recording field potentials elicited by optic tract stimulation and by immunohistochemical staining for choline acetyltransferase (ChAT). At 1 week after intracranial (IC) injection of AF64A (12 to 144 nmoles) into the fluid above the tectum, field potentials showed a selective dose-dependent decrement of the cholinergic polysynaptic component with no effect on the amplitude of the glutamatergic monosynaptic component. The decrement was only partially recovered in recordings at 2 and 6 weeks. In normal fish, the ChAT antibody stains a population of periventricular neurons, their apical dendrites, and a dense plexus within the optic terminal lamina that consists of their local axons and fine dendrites and of input fibers from the nucleus isthmi. One week after IC AF64A injection (48-72 nmoles), most immunostaining in superficial tectum was lost but most neuronal somas in the deep tectum could still be seen, and staining in the tegmentum below the tectum was completely intact. At 2 weeks and later, the staining of neuronal somata largely recovered, but staining of the superficial plexus did not. AF64A treatment at 18 days after nerve crush, when regenerating retinal fibers are beginning to form synapses, prevented retinotopic sharpening of the projection. Recordings showed a rough retinotopic map on the tectum but the multiunit receptive fields (MURFs) at each tectal point averaged 34 deg vs. 11 deg in vehicle-injected control regenerates. AF64A treatment before nerve crush also blocked sharpening, ruling out a direct effect on retinal growth cones or retinal fibers, as AF64A rapidly decomposes, whereas its effect on the cholinergic fibers is long-lasting. IC injection or minipump infusion of the nicotine antagonists alpha-bungarotoxin (alpha BTX), neuronal bungarotoxin (nBTX), and pancuronium during regeneration also prevented sharpening (MURFs averaging 29.4 deg, 33.0 deg, and 31.4 deg, respectively). Control Ringer's solution infusions or injections over the same period (19-37 days postcrush) had no effect on regenerated MURF size (11.7 deg). The results show that the cholinergic innervation, which modulates transmitter release, is required for activity-driven retinotopic sharpening, thought to be triggered by NMDA receptor activation.     

Arthroplasty implant biomaterial particle associated macrophages differentiate into lacunar bone resorbing cells

OBJECTIVE: To study the pathogenesis of aseptic loosening: in particular, to determine whether macrophages responding to particles of biomaterials commonly used in arthroplasty surgery for arthritis are capable of differentiating into osteoclastic bone resorbing cells, and the cellular and hormonal conditions required for this to occur. METHODS: Biomaterial particles (polymethylmethacrylate, high density polyethylene, titanium, chromium-cobalt, stainless steel) were implanted subcutaneously into mice. Macrophages were isolated from the foreign body granulomas that resulted, cultured on bone slices and coverslips, and assessed for both cytochemical and functional evidence of osteoclast differentiation. RESULTS: Tartrate resistant acid phosphatase (TRAP) negative macrophages isolated from granulomas containing particles of all types of biomaterial composition were capable of differentiating into TRAP positive cells capable of extensive lacunar bone resorption (assessed by scanning electron microscopy). The presence of both UMR106 rat osteoblast-like cells and 1,25-dihydroxy vitamin D3 was necessary for this to occur. CONCLUSION: All implant materials produce wear particles that are the focus of a heavy foreign body macrophage response in the fibrous membrane between a loose implant component and the host bone undergoing resorption. These findings underline the importance of biomaterial wear particle generation and the macrophage response to different types of biomaterial wear particles in the pathogenesis of aseptic loosening.     

Histomorphometric study in children with idiopathic nephrotic syndrome

There is agreement on the clinical diagnostic criteria for acute inflammatory demyelinating polyneuropathy (AIDP/GBS) however, there is lack of consensus for detection of demyelination. In order to critically evaluate the prevailing criteria, sixty-six patients who fulfilled NINCDS criteria and had typical features of GBS were studied for electrophysiological abnormalities of peripheral nerves by using standard methods (median, common peroneal, sural and ulnar) between 1 to 12 weeks after the onset of symptoms. The commonest abnormality on motor nerve conduction study was prolonged distal latency (75%-83%) followed by reduction in CMAP amplitude (63%-82%), decreased velocity (48%-62%), conduction block (17%-39%) and f-wave abnormalities (37.8%-59%). Sensory conduction abnormalities were detected in over 20% of median, 25% of ulnar and 33% of sural nerves. All the patients had abnormality of at least two motor conduction parameters in one nerve when values beyond 2 SD of the mean were considered abnormal and over 70% of patients had three abnormalities in two nerves or two abnormalities in three nerves. Comparison with the prevailing criteria for demyelination revealed that the number of patients fulfilling them varied widely: Albers et al. (1985): 74.2%, Albers et al. (1989): 40.9% and Cornblath: 30.3%. We believe that the current criteria for detection of demyelination in acute neuropathy are too strict, underestimate the underlying pathology in GBS and need reassessment.