PubMed · 2147251
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K Mourad, H Johanet, L Guibert, G Benhamou, H Charleux. 1990-10-20. [Appendicitis caused by gold].. https://pubmed.ncbi.nlm.nih.gov/2147251/
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Cultured astrocytes do not succumb to hypoxia/zero glucose for up to 24 h, yet astrocyte death following injury can occur within 1 h. It was previously demonstrated that astrocyte loss can occur quickly when the gaseous and interstitial ionic changes of transient brain ischemia are simulated: After a 20-40-min exposure to hypoxic, acidic, ion-shifted Ringer (HAIR), most cells died within 30 min after return to normal saline (i.e., "reperfusion"). Astrocyte death required external Ca2+ and was blocked by KB-R7943, an inhibitor of reversed Na+-Ca2+ exchange, suggesting that injury was triggered by a rise in [Ca2+]i. In the present study, we confirmed the elevation of [Ca2+]i during reperfusion and studied the role of Na+-Ca2+ and Na+-H+ exchange in this process. Upon reperfusion, elevation of [Ca2+]i was detectable by Fura-2 and was blocked by KB-R7943. The low-affinity Ca2+ indicator Fura-FF indicated a mean [Ca2+]i rise to 4.8+/-0.4 microM. Loading astrocytes with Fura-2 provided significant protection from injury, presumably due to the high affinity of the dye for Ca2+. Injury was prevented by the Na+-H+ exchange inhibitors ethyl isopropyl amiloride or HOE-694, and the rise of [Ca2+]i at the onset of reperfusion was blocked by HOE-694. Acidic reperfusion media was also protective. These data are consistent with Na+ loading via Na+-H+ exchange, fostering reversal of Na+-Ca2+ exchange and cytotoxic elevation of [Ca2+]i. The results indicate that mechanisms involved in pH regulation may play a role in the fate of astrocytes following acute CNS injuries.
Acute hepatitis C is known to respond better to interferon therapy than chronic hepatitis C. The reason for this difference remains unclear. The present study was undertaken to examine HCV quasispecies in blood from patients with acute hepatitis C caused by accidental exposure to blood-borne pathogens and in blood from the source patients. Three patients who developed hepatitis C (recipient patients; R-Pt.) and two patients who served as a source of HCV infection (source patients; S-Pt.) were the subjects of this study. The number of quasispecies and the genetic diversity in hypervariable region-1 (HVR-1) were examined on the basis of fluorescence single-strand conformation polymorphism and sequence analysis (FSSA). On the day of the accident, the number of quasispecies and genetic diversity were 13 and 36 in S-Pt.1 and 6 and 20 in S-Pt.3, respectively. At the time of diagnosis of acute hepatitis, the number of quasispecies and nucleotide diversity were 2 and 2 in R-Pt.1, 2 and 0 in R-Pt.2, and 4 and 0 in R-Pt.3, respectively. Immediately before the start of treatment, the number of quasispecies and genetic diversity were 4 and 4 in R-Pt.1, 2 and 0 in R-Pt.2, and 3 and 0 in R-Pt.3., respectively. In three R-Pts, interferon therapy resulted in eradication of HCV. These findings indicate that in the early stage of HCV infection, only a portion of HCV transmitted from S-Pts to R-Pts can proliferate. The low number of quasispecies of HCV appears to be one of the reasons why acute hepatitis responds well to interferon therapy.
An 82-year-old man developed severe, acute, predominantly motor polyneuropathy, signs of autonomic involvement, and skin changes following aminolevulinic acid (ALA) administration. The compound was used as a prodrug for photodynamic therapy of Barrett's esophagitis. Changes were observed in various parameters of the heme pathway. The case reported represents a rare response to ALA treatment, resembling an acute attack of hepatic porphyria with neurological features.