Environmental pH signals the release of monosaccharides from cell wall in coral symbiotic alga.

Reef-building corals thrive in oligotrophic environments due to their possession of endosymbiotic algae. Confined to the low pH interior of the symbiosome within the cell, the algal symbiont provides the coral host with photosynthetically fixed carbon. However, it remains unknown how carbon is released from the algal symbiont for uptake by the host. Here we show, using cultured symbiotic dinoflagellate, Breviolum sp., that decreases in pH directly accelerates the release of monosaccharides, that is, glucose and galactose, into the ambient environment. Under low pH conditions, the cell surface structures were deformed and genes related to cellulase were significantly upregulated in Breviolum. Importantly, the release of monosaccharides was suppressed by the cellulase inhibitor, glucopyranoside, linking the release of carbon to degradation of the agal cell wall. Our results suggest that the low pH signals the cellulase-mediated release of monosaccharides from the algal cell wall as an environmental response in coral reef ecosystems.

Coral reefs are known as 'treasure troves of biodiversity' because of the enormous variety of different fish, crustaceans and other marine life they support. Colonies of marine animals, known as corals, which are anchored to rocks on the sea bed, form the main structures of a coral reef. Many corals rely on partnerships with microscopic algae known as dinoflagellates for most of their energy needs. The dinoflagellates use sunlight to make sugars and other carbohydrates and they give some of these to the coral. In exchange, the coral provides a home for the dinoflagellates inside its body. The algae live inside special compartments within coral cells known as symbiosomes. These compartments have a lower pH (that is, they are more acidic) than the rest of the coral cell. Previous studies have shown that the algae release sugars into the symbiosome but it remains unclear what triggers this release and whether it only occurs when the algae are in a partnership. Ishii et al. studied a type of dinoflagellate known as Breviolum sp. that had been grown in sea water-like liquid in a laboratory. The experiments found that the alga released two sugar molecules known as glucose and galactose into its surroundings even in the absence of a host coral. Increasing the acidity of the liquid caused the alga to release more sugars and resulted in changes to some of the structures on the surface of its cells. The alga also produced an enzyme, called cellulase, to degrade the wall that normally surrounds the cell of an alga. Treating the alga with a drug that inhibits the activity of cellulase also suppressed the release of sugars from the cells. These findings suggest that when dinoflagellates enter acidic environments, like the guts of marine animals or symbiosomes inside coral cells, the decrease in pH can activate the algal cellulase enzyme, which in turn triggers the release of sugars for the coral. This research will provide a new viewpoint to those interested in how partnerships between animals and algae are sustained in marine environments. It also highlights the importance of the alga cell wall in establishing partnerships with corals. Further work will seek to clarify the precise biological mechanisms involved.

Convergent evolution of nitrogen-adding enzymes in the purine nucleotide biosynthetic pathway, based on structural analysis of adenylosuccinate synthetase (PurA).

Adenylosuccinate synthetase (PurA) is an enzyme responsible for the nitrogen addition to inosine monophosphate (IMP) by aspartate in the purine nucleotide biosynthetic pathway. And after which the fumarate is removed by adenylosuccinate lyase (PurB), leaving an amino group. There are two other enzymes that catalyze aspartate addition reactions similar to PurA, one in the purine nucleotide biosynthetic pathway (SAICAR synthetase, PurC) and the other in the arginine biosynthetic pathway (argininosuccinate sythetase, ArgG). To investigate the origin of these nitrogen-adding enzymes, PurA from Thermus thermophilus HB8 (TtPurA) was purified and crystallized, and crystal structure complexed with IMP was determined with a resolution of 2.10 Å. TtPurA has a homodimeric structure, and at the dimer interface, Arg135 of one subunit interacts with the IMP bound to the other subunit, suggesting that IMP binding contributes to dimer stability. The different conformation of His41 side chain in TtPurA and EcPurA suggests that side chain flipping of the His41 might play an important role in orienting γ-phosphate of GTP close to oxygen at position 6 of IMP, to receive the nucleophilic attack. Moreover, through comparison of the three-dimensional structures and active sites of PurA, PurC, and ArgG, it was suggested that the active sites of PurA and PurC converged to similar structures for performing similar reactions.

Defining an orbitofrontal compass: Functional and anatomical heterogeneity across anterior-posterior and medial-lateral axes.

The orbitofrontal cortex (OFC) plays a critical role in the flexible control of behaviors and has been the focus of increasing research interest. However, there have been a number of controversies around the exact theoretical role of the OFC. One potential source of these issues is the comparison of evidence from different studies, particularly across species, which focus on different specific sub-regions within the OFC. Furthermore, there is emerging evidence that there may be functional diversity across the OFC which may account for these theoretical differences. Therefore, in this review we consider evidence supporting functional heterogeneity within the OFC and how it relates to underlying anatomical heterogeneity. We highlight the importance of anatomical and functional distinctions within the traditionally defined OFC subregions across the medial-lateral axis, which are often not differentiated for practical and historical reasons. We then consider emerging evidence of even finer-grained distinctions within these defined subregions along the anterior-posterior axis. These fine-grained anatomical considerations reveal a pattern of dissociable, but often complementary functions within the OFC. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Sex Differences in Risk Preference and c-Fos Expression in Paraventricular Thalamic Nucleus of Rats During Gambling Task.

Different biological requirements between males and females may cause sex differences in decision preference when choosing between taking a risk to get a higher gain or taking a lower but sure gain. Several studies have tested this assumption in rats, however the conclusion remains controversial because the previous real-world like gambling tasks contained a learning component to track a global payoff of probabilistic outcome in addition to risk preference. Therefore, we modified a simple gambling task allowing us to exclude such learning effect, and investigated the sex difference in risk preference of rats and its neural basis. The task required water deprived rats to choose between a risky option which provided four drops of water or no reward at a 50% random chance vs. a sure option which provided predictable amount x (x = 1, 2, 3, 4). The amount and the risk were explicitly instructed so that different choice conditions could be tested trial by trial without re-learning of reward contingency. Although both sexes correctly chose the sure option with the same level of accuracy when the sure option provided the best offer (x = 4), they exhibited different choice performances when two options had the same expected value (x = 2). Males and females both preferred to take risky choices than sure choices (risk seeking), but males were more risk seeking than females. Outcome-history analysis of their choice pattern revealed that females reduced their risk preference after losing risky choices, whereas males did not. Rather, as losses continued, reaction time for subsequent risky choices got shorter in males. Given that significant sex difference features mainly emerged after negative experiences, male and female rats may evaluate an unsuccessful outcome of their decision in different manners. Furthermore, c-Fos expression in the paraventricular nucleus of the thalamus (PV) was higher in the gambling task than for the control task in males while c-fos levels did not differ in females. The present study provides a clear evidence of sex differences in risk preference in rats and suggests that the PV is a candidate region contributing to sex differences in risky decision making.

Dopaminergic and serotonergic modulation of anterior insular and orbitofrontal cortex function in risky decision making.

Systemic manipulations have shown that dopamine and serotonin systems are involved in risky decision making. However, how they work within the regions that implement risky choices remains unclear. The present study investigated the role of dopamine and serotonin in the rat anterior insular cortex (AIC) and orbitofrontal cortex (OFC), which make different contributions to risky decision making. We examined the effects of local injection of the D1 (SCH23390), D2 (eticlopride), 5-HT1A (WAY100635) and 5-HT2A (M100907) receptor antagonists into the AIC or OFC on risk preference in a gambling task. We found that different dopamine and serotonin receptor subtypes in the AIC and OFC differentially influence risky decision making: intra-AIC injection of D2R or 5-HT1AR blockers increased risk preference whereas intra-OFC injection of the 5-HT1AR blocker decreased it. Risk preference was not altered by intra-AIC injection of D1R and 5-HT2AR blockers or by intra-OFC injection of D1R, D2R, and 5-HT2AR blockers. Furthermore, additional analyses revealed that dopamine and serotonin signaling in the AIC have outcome history-dependent effects on risk taking: intra-AIC injection of the D2R blocker increased risk preference particularly after winning in a previous risky choice, whereas intra-AIC injection of the 5-HT1AR blocker increased risk preference after losing.

[Risk taking and the insular cortex].

Risk taking can lead to ruin, but sometimes, it can also provide great success. How does our brain make a decision on whether to take a risk or to play it safe? Recent studies have revealed the neural basis of risky decision making. In this review, we focus on the role of the anterior insular cortex (AIC) in risky decision making. Although human imaging studies have shown activations of the AIC in various gambling tasks, the causal involvement of the AIC in risky decision making was still unclear. Recently, we demonstrated a causality of the AIC in risky decision making by using a pharmacological approach in behaving rats-temporary inactivation of the AIC decreased the risk preference in gambling tasks, whereas temporary inactivation of the adjacent orbitofrontal cortex (OFC) increased the risk preference. The latter finding is consistent with a previous finding that patients with damage to the OFC take abnormally risky decisions in the Iowa gambling task. On the basis of these observations, we hypothesize that the intact AIC promotes risk-seeking behavior, and that the AIC and OFC are crucial for balancing the opposing motives of whether to take a risk or avoid it. However, the functional relationship between the AIC and OFC remains unclear. Future combinations of inactivation and electrophysiological studies may promote further understanding of risky decision making.

Inactivating anterior insular cortex reduces risk taking.

We often have to make risky decisions between alternatives with outcomes that can be better or worse than the outcomes of safer alternatives. Although previous studies have implicated various brain regions in risky decision making, it remains unknown which regions are crucial for balancing whether to take a risk or play it safe. Here, we focused on the anterior insular cortex (AIC), the causal involvement of which in risky decision making is still unclear, although human imaging studies have reported AIC activation in various gambling tasks. We investigated the effects of temporarily inactivating the AIC on rats' risk preference in two types of gambling tasks, one in which risk arose in reward amount and one in which it arose in reward delay. As a control within the same subjects, we inactivated the adjacent orbitofrontal cortex (OFC), which is well known to affect risk preference. In both gambling tasks, AIC inactivation decreased risk preference whereas OFC inactivation increased it. In risk-free control situations, AIC and OFC inactivations did not affect decision making. These results suggest that the AIC is causally involved in risky decision making and promotes risk taking. The AIC and OFC may be crucial for the opposing motives of whether to take a risk or avoid it.

Refractory diverticular colitis with progressive ulcerative colitis-like changes extending to the rectum.

A 68-year-old man visited our department because of diarrhea and bloody stools. Colonoscopy revealed diverticula scattered in the sigmoid colon with localized mucosal edema and reddening. The mucosa became somewhat rough 9 months later, and had an erosive, ulcerative colitis (UC)-like appearance after a further 6 months, with these changes extending to the rectum. These findings led to a diagnosis of diverticular colitis (DC) with UC-like changes. The condition was refractory to treatment including drug therapy and was thus surgically treated. No cases of DC have been reported in Japan, and a refractory case of DC with progressive UC-like changes extending to the rectum is rare even in Europe and the USA.

Case of inflammatory fibroid polyp of the esophagogastric junction.

Upper gastrointestinal endoscopy of a 25-year-old man with heartburn revealed an elevated lesion in the esophagogastric junction (EGJ). Piecemeal endoscopic mucosal resection (EMR) followed by histopathological examination led to a diagnosis of inflammatory fibroid polyp (IFP). After EMR, the heartburn persisted despite giving a proton pump inhibitor (PPI), and the residual lesion gradually enlarged and a transverse mucosal break developed on the esophageal side of it. However, the combined administration of the PPI and an H2 receptor antagonist reduced the heartburn, and led to endoscopic regression of the lesion and disappearance of the transverse mucosal break. IFP of the esophagogastric junction is extremely rare, and this case is interesting in that potent inhibition of gastric acid secretion resulted in the regression of the lesion.

[A case of Cronkhite-Canada syndrome in which contrast radiologic examinations of the digestive tract were performed at the time of development of the clinical symptoms].

We encountered a case of Cronkhite-Canada syndrome in which contrast radiologic examinations of the upper and lower digestive tract were performed immediately before and after the development of the clinical symptoms. These contrast radiologic images showed mainly mucosal coarseness and no polyposis of the stomach and colon. The endoscopy, performed 3 months later from the development of the clinical symptoms, revealed polyposis of the stomach and colon. So we recognized that the clinical symptoms developed before appearance of the polyposis of the digestive tract and the polyposis progressed rapidly.