Ocular leptospirosis in four patients: A diagnostic dilemma.

Leptospirosis is a zoonotic disease that is caused by the pathogenic spirochetes of the genus Leptospira. The infection occurs worldwide and is particularly more common in the tropics. However, it is becoming a neglected reemerging global health disease due to rapid urbanisation. This disease has a wide range of clinical manifestations from flu-like illness to pneumonia, acute kidney injury, etc. But many uncommon clinical findings are being reported as well. In this paper, we report four patients who presented initially with uveitic features who turned out serologically positive for Leptospira after extensive investigations.

Modification of short peptides using epsilon-aminocaproic acid for improved coating efficiency in indirect enzyme-linked immunosorbent assays (ELISA).

The hydrophobicity of short synthetic peptides of 5-10 residues was enhanced for high coating efficiency as antigens in indirect ELISA. To obtain enhanced hydrophobicity, coupling of epsilon-aminocaproic acids to the synthetic peptides was carried out during solid phase peptide synthesis. As a short peptide model, three analogues of a streptavidin binding peptide consisting of 5 amino acid residues were prepared with four epsilon-aminocaproic acid residues. HPLC analysis showed a dramatic increase in hydrophobicity after modification and the modified peptides showed a better adsorption ability than the unmodified peptides in indirect ELISA. The whole process from antigen coating to color development was carried out within 2.5 to 3 h by dissolving the peptide in methyl alcohol and evaporating the solvent in each well of the microplate. As an application of this method, a peptide assumed to function as one of the epitopes of the human 60 kDa Ro/SSA antigen was selected from hydrophilicity, acrophilicity and hydropathy plots. The peptide was synthesized having an epsilon-aminocaproic acid modification at both N and C terminal ends and was tested with 30 sera from patients with systemic lupus erythematosus (SLE), 20 normal sera and a standard anti-Ro/SSA serum. The ELISA results revealed that the method gave a high signal-to-background ratio without altering the specificity of the assay. Moreover, our process was far simpler and more rapid than conventional methods used in indirect ELISA. Thus this method could be useful in the development of techniques for the diagnosis of SLE.

Cholinergic modulation of synaptic transmission and plasticity in entorhinal cortex and hippocampus of the rat.

Effects of cholinergic agents on synaptic transmission and plasticity were examined in entorhinal cortex and hippocampus. Bath application of carbachol (0.25-0.75 microM) induced transient depression of field potential responses in all cases tested (24/24 in layer III of medial entorhinal cortex slices and 24/24 in CA1 of hippocampal slices; 11.0+/-1.9% and 7.8+/-2.5%, respectively) and long-lasting potentiation in some cases (4/24 in entorhinal cortex and 12/24 in hippocampus; 33.7+/-3.7% and 32.1+/-9.9%, respectively, in successful cases). Carbachol (0.5 microM) induced transient depression, but not long-lasting potentiation, of N-methyl-D-aspartate receptor-mediated responses in entorhinal cortex. At 5 microM, carbachol induced transient depression only (55. 9+/-4.7% in entorhinal cortex and 41.4+/-2.9% in hippocampus), which was blocked by atropine. Paired-pulse facilitation was not altered during carbachol-induced potentiation but enhanced during carbachol-induced depression. These results suggest that the underlying mechanisms of carbachol-induced depression and potentiation are decreased transmitter release and selective enhancement of non-N-methyl-D-aspartate receptor-mediated responses, respectively. Long-term potentiation could be induced in the presence of 10 microM atropine by theta burst stimulation. The magnitude was significantly lower (15.2+/-5.2%, n=9) compared with control (37.2+/-6.1%, n=8) in entorhinal cortex, however. These results demonstrate similar, but not identical, cholinergic modulation of synaptic transmission and plasticity in entorhinal cortex and hippocampus.

Long-term synaptic plasticity in deep layer-originated associational projections to superficial layers of rat entorhinal cortex.

Superficial layers of the entorhinal cortex (EC) relay the majority of cortical input projections to the hippocampus, whereas deep layers of the EC mediate a large portion of hippocampal output projections back to other cortical areas, suggesting a functional segregation between superficial and deep layers of the EC as input and output structures of the hippocampus, respectively. However, deep layers of the EC send associational projections to superficial layers, suggesting a potential interaction between neocortical input and hippocampus-processed output in superficial layers. This possibility was investigated by examining whether deep to superficial EC projections support long-term synaptic plasticity, and whether they interact with other pathways in superficial layers in rat medial EC slice preparations. Synaptic responses of the deep-to-superficial layer projections were verified based on field potential profiles, paired-pulse facilitation, physical separation between superficial and deep layers, and pharmacological manipulation. Long-term potentiation (LTP) was reliably induced in the deep-to-superficial layer projections by burst stimulations that emulated theta or sharp wave electroencephalogram (EEG),and it was blocked by an N-methyl-d-aspartate receptor antagonist (D-2-amino-5-phosphonopentanoic acid) and a calcium channel blocker (nifedipine). Prolonged low frequency stimulation induced long-term depression. A weak stimulation of deep layers, which induced a small degree of LTP by itself, generated a much larger degree of LTP when paired with a strong stimulation of superficial layers, indicating that the deep-to-superficial layer projections cooperate with other pathways in the superficial EC to enhance synaptic weights. Our results suggest that neocortical input and hippocampal output information are integrated in superficial layers of the EC.

Cholinergic modulation of synaptic physiology in deep layer entorhinal cortex of the rat.

We have recently shown that cholinergic effects on synaptic transmission and plasticity in the superficial (II/III) layers of the rat medial entorhinal cortex (EC) are similar, but not identical, to those in the hippocampus (Yun et al. [2000] Neuroscience 97:671-676). Because the superficial and deep layers of the EC preferentially convey afferent and efferent hippocampal projections, respectively, it is of interest to compare cholinergic effects between the two regions. We therefore investigated the physiological effects of cholinergic agents in the layer V of medial EC slices under experimental conditions identical to those in the previous study. Bath application of carbachol (0.5 microM) induced transient depression of field potential responses in all cases tested (30 of 30; 18.5% +/- 2.3%) and rarely induced long-lasting potentiation (only 3 of 30; 20.4% +/- 3.2% in successful cases). At 5 microM, carbachol induced transient depression only (20 of 20, 48.9% +/- 2.8%), which was blocked by atropine (10 microM). Paired-pulse facilitation was enhanced during carbachol-induced depression, suggesting presynaptic action of carbachol. Long-term potentiation (LTP) could be induced in the presence of 10 microM atropine by theta burst stimulation, but its magnitude was significantly lower (9.1% +/- 4.7%, n = 15) compared to LTP in control slices (22.4% +/- 3.9%, n = 20). These results, combined with our previous findings, demonstrate remarkably similar cholinergic modulation of synaptic transmission and plasticity across the superficial and deep layers of EC.

Ginsenoside Rb1 and Rg1 improve spatial learning and increase hippocampal synaptophysin level in mice.

We investigated the cognition enhancing effects of ginsenoside Rb1 and Rg1. Mice were trained in a Morris water maze following injection (i.p.) of Rb1 (1 mg/kg) or Rg1 (1 mg/kg) for 4 days. Both Rb1- and Rg1-injected mice showed enhanced spatial learning compared to control animals. The hippocampus, but not the frontal cortex, of treated mice contained higher density of a synaptic marker protein, synaptophysin, compared to control mice. Electrophysiological recordings in hippocampal slices revealed that Rb1 or Rg1 injection did not change the magnitude of paired-pulse facilitation or long-term potentiation. Our results suggest that Rb1 and Rg1 enhance spatial learning ability by increasing hippocampal synaptic density without changing plasticity of individual synapses.