Molecular architecture of primate specific neural circuit formation.

The mammalian cortex is a highly evolved brain region, but we still lack a comprehensive understanding of the molecular mechanisms underlying primate-specific neural circuits formation. In this study, we employed spatial transcriptomics to assess gene expression dynamics in the marmoset cortex during development, focusing on key regions and time points. Spatial transcriptomics identified genes that are sexually, spatially, and temporally differentially expressed in the developing marmoset cortex. Our detailed analysis of the visual cortex unveiled dynamic changes in gene expression across layers with distinct projections and functions. Notably, we discovered numerous axon guidance molecules with spatiotemporal expression patterns unique to the developing marmoset prefrontal cortex (PFC), which control PFC neuronal circuits. Among these molecules, PRSS12 (Protease, Serine, 12 (neurotrypsin, motopsin), when ectopically expressed in the mouse prelimbic cortex, caused similar changes in connectivity as observed in the marmoset A32 area. Furthermore, PRSS12 showed similar expression patterns in both marmoset and human PFC during development, suggesting parallels between marmoset and human brain development. The differential expression of axon guidance molecules in the developing PFC, varying by region, likely contributes to the formation of unique circuits observed in primates.

Left-sided hepatic hydrothorax diagnosed by contrast-enhanced ultrasonography with intraperitoneal injection of Levovist.

A 62-year-old Japanese woman was admitted to our hospital with dyspnea. Chest X-ray revealed massive pleural effusion on the left side. Contrast-enhanced ultrasonography using Levovist was performed to confirm the transdiaphragmatic passage of ascitic fluid into the pleural cavity. After injection of Levovist into the peritoneal cavity, an enhanced pulsative flow into the pleural cavity was detected. This is the first report of hepatic hydrothorax diagnosed by contrast-enhanced ultrasonography. This method is safe and useful for the diagnosis of hepatic hydrothorax, and it allows observation of the real-time movement of ascitic fluid from the peritoneal cavity to the pleural space and detection of the site of the peritoneopleural communication.

Human chymase expression in a mice induces mild hypertension with left ventricular hypertrophy.

A number of in vitro studies have suggested potential pathophysiological roles of human (h-) chymase. However, the lack of an appropriate animal model has left the in vivo roles of chymase unclear. To approach this problem, a transgenic mouse (TGM) model carrying the h-chymase gene was established. The h-chymase cDNA transgene was constructed with the chicken beta actin promoter and cytomegalovirus immediate early gene enhancer, and injected into mouse oocytes. Homozygous mice with a high copy number of the h-chymase gene suffered from intrauterine death. In three heterozygous TGM lines, h-chymase transgene expression was detected in entire organs, including the heart, vessels, skin, liver, lung, and brain. The h-chymase immunoreactivity was localized in the extracellular matrices of each organ, especially on the basement membranes of vessels. Aortic and hepatic chymase-dependent angiotensin II formations were significantly higher than those in the wild-type littermates. Three independent TGM lines showed the same phenotypic changes: elevation of blood pressure, left ventricular hypertrophy, emaciation with reduction in the lipid tissue, leukocytosis, and oligotrichia. The angiotensin II subtype 1 (AT1) receptor antagonist valsartan suppressed the elevated blood pressure completely and left ventricular hypertrophy incompletely, but did not affect the other phenotypes. These data suggested that in vivo expression of h-chymase caused mild hypertension (AT1 receptor-dependent) with left ventricular hypertrophy (partially AT1 receptor-dependent), and also chronic inflammatory changes (AT1 receptor-independent).