Late-onset non-islet cell tumor hypoglycemia: A case report.

BACKGROUND: Hypoglycemia due to non-insulin-producing tumors is referred to as non-islet cell tumor hypoglycemia (NICTH). As NICTH is a rare lesion, the natural course of NICTH is not well understood. We report a case of NICTH that was observed 30 years before the onset of hypoglycemia. CASE SUMMARY: A 50-year-old man was diagnosed with an abnormal right chest shadow during a routine X-ray examination, but no further examination was undertaken because the lesion appeared benign. Thirty years after the tumor discovery, the patient was admitted to the hospital with symptoms of severe hypoglycemia, which was diagnosed as NICTH based on a complete examination. The tumor was resected and found to be a solitary fibrous mass (15.6 cm × 13.7 cm × 10.4 cm); thereafter, the patient's blood glucose levels normalized and he completely recovered. CONCLUSION: NICTH can have an acute onset, even if the tumor has been present and asymptomatic over a long time period.

Inflammation-induced reversible switch of the neuron-specific enolase promoter from Purkinje neurons to Bergmann glia.

Neuron-specific enolase (NSE) is a glycolytic isoenzyme found in mature neurons and cells of neuronal origin. Injecting adeno-associated virus serotype 9 (AAV9) vectors carrying the NSE promoter into the cerebellar cortex is likely to cause the specific transduction of neuronal cells, such as Purkinje cells (PCs) and interneurons, but not Bergmann glia (BG). However, we found BG-predominant transduction without PC transduction along a traumatic needle tract for viral injection. The enhancement of neuroinflammation by the co-application of lipopolysaccharide (LPS) with AAV9 significantly expanded the BG-predominant area concurrently with the potentiated microglial activation. The BG-predominant transduction was gradually replaced by the PC-predominant transduction as the neuroinflammation dissipated. Experiments using glioma cell cultures revealed significant activation of the NSE promoter due to glucose deprivation, suggesting that intracellularly stored glycogen is metabolized through the glycolytic pathway for energy. Activation of the glycolytic enzyme promoter in BG concurrently with inactivation in PC may have pathophysiological significance for the production of lactate in activated BG and the utilization of lactate, which is provided by the BG-PC lactate shuttle, as a primary energy resource in injured PCs.

Syntrophic degradation of proteinaceous materials by the thermophilic strains Coprothermobacter proteolyticus and Methanothermobacter thermautotrophicus.

Protein is a major component of organic solid wastes, and therefore, it is necessary to further elucidate thermophilic protein degradation process. The effects of hydrogenotrophic methanogens on protein degradation were investigated using the proteolytic bacterial strain CT-1 that was isolated from a methanogenic thermophilic (55°C) packed-bed reactor degrading artificial garbage slurry. Strain CT-1 was closely related to Coprothermobacter proteolyticus, which is frequently found in methanogenic reactors degrading organic solid wastes. Strain CT-1 was cultivated in the absence or presence of Methanothermobacter thermautotrophicus by using 3 kinds of proteinaceous substrates. Degradation rates of casein, gelatin, and bovine serum albumin were higher in co-cultures than in monocultures. Strain CT-1 showed faster growth in co-cultures than in monocultures. M. thermautotrophicus comprised 5.5-6.0% of the total cells in co-culture. Increased production of ammonia and acetate was observed in co-cultures than in monocultures, suggesting that addition of M. thermautotrophicus increases the products of protein degradation. Hydrogen produced in the monocultures was converted to methane in co-cultures. These results suggest that thermophilic proteolytic bacteria find it favorable to syntrophically degrade protein in a methanogenic environment, and that it is important to retain hydrogen-scavenging methanogens within the reactor.