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Surgical outcomes for functional vestibulocochlear diseases vary, and the influencing factors are not fully understood. The role of a rhomboid lip (RL) and choroid plexus (CP) in microvascular decompression (MVD) of the vestibulocochlear nerve has not been studied. This study aims to evaluate the surgical efficacy of MVD for vestibulocochlear diseases, with and without addressing the RL and CP, to enhance our understanding of their etiology. A total of 15 patients who underwent MVD for the vestibulocochlear nerve between 2013 and 2022 were retrospectively identified and followed up. The patients were classified into 4 categories: vestibular paroxysmia (VP), benign positional paroxysmal vertigo (BPPV), and Meniere disease (MD). The fourth was a "tinnitus" group. The relief of symptoms, recurrence, satisfaction after surgery, available relevant imaging studies, and intraoperative observation data were evaluated. Following MVD, 6 of the 7 patients in the VP group, the 1 patient in the BPPV group, and 1 of 2 patients in the MD group were completely relieved of vertigo. The seventh VP patient showed significant improvement. The 5 patients in the "tinnitus" group remained unchanged. Retrospectively, 4 patients from the VP, BPPV, and MD groups who underwent RL incision and CP excision were also free of vertigo, although vascular compression was not confirmed in these cases. MVD is generally considered a useful treatment for VP and could also be effective in managing recurrent vertigo caused by BPPV and MD. Our results highlight the potential role of an abnormal RL and CP in the development of vertigo symptoms. Patients presenting with "tinnitus" require further investigation and might not be suitable for MVD. [ABSTRACT FROM AUTHOR]

Activation of hepatic stellate cells (HSCs) is a critical step in the development of liver fibrosis. During activation, HSCs lose their lipid droplets (LDs) containing triacylglycerols (TAGs), cholesteryl esters, and retinyl esters (REs). We previously provided evidence for the presence of two distinct LD pools, a preexisting and a dynamic LD pool. Here we investigate the mechanisms of neutral lipid metabolism in the preexisting LD pool. To investigate the involvement of lysosomal degradation of neutral lipids, we studied the effect of lalistat, a specific lysosomal acid lipase (LAL/Lipa) inhibitor on LD degradation in HSCs during activation in vitro. The LAL inhibitor increased the levels of TAG, cholesteryl ester, and RE in both rat and mouse HSCs. Lalistat was less potent in inhibiting the degradation of newly synthesized TAG species as compared with a more general lipase inhibitor orlistat. Lalistat also induced the presence of RE-containing LDs in an acidic compartment. However, targeted deletion of the Lipa gene in mice decreased the liver levels of RE, most likely as the result of a gradual disappearance of HSCs in livers of Lipa-/- mice. Lalistat partially inhibited the induction of activation marker α-smooth muscle actin (α-SMA) in rat and mouse HSCs. Our data suggest that LAL/Lipa is involved in the degradation of a specific preexisting pool of LDs and that inhibition of this pathway attenuates HSC activation. [ABSTRACT FROM AUTHOR]

Hepatic stellate cell (HSC) activation is a critical step in the development of chronic liver disease. We previously observed that the levels of triacylglycerol (TAG) species containing long polyunsaturated fatty acids (PUFAs) are increased in in vitro activated HSCs. Here we investigated the cause and consequences of the rise in PUFA-TAGs by profiling enzymes involved in PUFA incorporation. We report that acyl CoA synthetase (ACSL) type 4, which has a preference for PUFAs, is the only upregulated ACSL family member in activated HSCs. Inhibition of the activity of ACSL4 by siRNA-mediated knockdown or addition of rosiglitazone specifically inhibited the incorporation of deuterated arachidonic acid (AA-d8) into TAG in HSCs. In agreement with this, ACSL4 was found to be partially localized around lipid droplets (LDs) in HSCs. Inhibition of ACSL4 also prevented the large increase in PUFA-TAGs in HSCs upon activation and to a lesser extent the increase of arachidonate-containing phosphatidylcholine species. Inhibition of ACSL4 by rosiglitazone was associated with an inhibition of HSC activation and prostaglandin secretion. Our combined data show that upregulation of ACSL4 is responsible for the increase in PUFA-TAG species during activation of HSCs, which may serve to protect cells against a shortage of PUFAs required for eicosanoid secretion. [ABSTRACT FROM AUTHOR]

• Three levels of smartness are distinguished for smart city projects, consisting of decisional intelligence, perceptual intelligence, and computational intelligence. • Four organizational conditions of governments that influence the smartness levels are established, including financial capacity, human resources, information-sharing, and leadership. • Three configurations of organizational conditions are found to match the highest level of smartness, decisional intelligence. • The combination of strong financial capacity and facilitative leadership is a necessary condition to achieve the highest level of smartness. Nowadays, an increasing amount of literature acknowledges that smart cities' core aspect is not technology per se but how organizational characteristics and capabilities influence the technology enactment. However, the extant studies primarily focus on business-led smart city projects. Little attention is paid to the causal relations between organizational conditions and technology enactment in government-led projects. Therefore, there is a research gap concerning what conditions of governmental organizations, singly or jointly, drive technology enactment in smart city projects. To fill the gap, this article establishes three increasing levels of smartness and formulates four government conditions. Based on this conceptual framework, this article explores different configurations of organizational conditions that lead to varying levels of smartness. It uses the Qualitative Comparative Analysis (QCA) method to study 11 smart city projects in Hangzhou, China. The results generate three configurations of organizational conditions that lead to decisional intelligence, indicating that multiple pathways exist to achieve the highest level of smartness. These configurations often emphasize the significant role of human resource pressure in driving decisional intelligence. But no single condition is necessary because when human resource pressure is absent, strong financial capacity, good information-sharing, and facilitative leadership can work together as a substitution. [Display omitted] [ABSTRACT FROM AUTHOR]

• Source to estuary surveys revealed specific pollution and dam effects on river GHGs. • Pollution effects on riverine CO 2 , CH 4 , and N 2 O vary with source size and location. • Cascade weirs boost CH 4 production, offsetting CO 2 sinks in eutrophic river-estuary. • δ13C indicates wastewater-derived GHGs and temperature-enhanced CH 4 oxidation. • Basin-specific perturbations warn generalizing eutrophic river-estuary as C sinks. Large uncertainties exist regarding the combined effects of pollution and impoundment on riverine greenhouse gas (GHG) emissions. It has also been debated whether river eutrophication can transform downstream estuaries into carbon sinks. To assess human impacts on the riverine and estuarine distributions of CO 2 , CH 4 , and N 2 O, two source-to-estuary surveys along three impounded rivers in Korea were combined with multiple samplings at five or six estuarine sites. The basin-wide surveys revealed predominant pollution effects generating localized hotspots of riverine GHGs along metropolitan areas. The localized pollution effect was pronounced in the lower Han River and estuary adjacent to Seoul, while the highest GHG levels in the upper Yeongsan traversing Gwangju were not carried over into the faraway estuary. CH 4 levels were elevated across the eutrophic middle Nakdong reaches regulated by eight cascade weirs in contrast to undersaturated CO 2 indicating enhanced phytoplankton production. The levels of all three GHGs tended to be higher in the Han estuary across seasons. Higher summer-time δ13C-CH 4 values at some Nakdong and Yeongsan estuarine sites implied that temperature-enhanced CH 4 production may have been dampened by increased CH 4 oxidation. Our results suggest that the location and magnitude of pollution sources and impoundments control basin-specific longitudinal GHG distributions and estuarine carryover effects, warning against simple generalizations of eutrophic rivers and estuaries as carbon sinks. [Display omitted] [ABSTRACT FROM AUTHOR]