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The article presents information on the supramolecular chemistry of the cucurbit[n]uril (CB[n]) family. The family expanded dramatically with the discovery of CB[n] homologues CB[5], CB[7], CB[8], and CB[5]@CB[10]). More recently, the disclosure of methods for the direct functionalization of CB[n] and building block strategies for the preparation of CB[n] derivatives and analogues providing CB[n] with solubility in both organic and aqueous solution has further expanded the range of applications to which CB[n] can be applied. The implications of the new iCB[n] for the future of CB[n] research are manifold.

Doping of conjugated polymers (CPs) is a promising strategy to obtain solution‐processable and highly conductive films; however, the improvement in electrical conductivity is limited owing to the relatively poor carrier mobility of CPs. Herein, a CP with excellent molecular doping ability, i.e., poly[2‐([2,2'‐bithiophen]‐5‐yl)‐3,8‐difluoro‐5,10‐bis(5‐octylpentadecyl)‐5,10‐dihydroindolo[3,2‐b]indole] (PIDF‐BT) is wrapped onto the surface of single‐walled carbon nanotubes (SWCNTs). The resulting PIDF‐BT@SWCNT simultaneously achieves excellent solution dispersibility and a high electrical conductivity of over 5000 S cm−1 through AuCl3 doping. The doping mechanism is systematically studied using spectroscopic analysis, and the four‐probe field‐effect transistor based on the doped PIDF‐BT@SWCNT confirms a carrier mobility up to 138 cm2 V−1 s−1. The carrier‐transfer barrier energy is related to the Schottky barrier between the SWCNT and PIDF‐BT, which can be controlled by doping. Finally, when the doped PIDF‐BT@SWCNT is applied to a thermoelectric device, a power factor exceeding 210 μW m−1 K−2 is achieved because of its high electrical conductivity, even if the increased carrier density reduces the Seebeck coefficient.

Cooperative transitions have acquired much attention for low transition barriers, ultrafast kinetics, and structural reversibility but cooperative transitions are rare in molecular crystals and their origin is poorly understood. Here the authors show that reorientation of the alkyl side chains in a 2-dimensional quinoidal terthiophene triggers cooperative behavior, and establish alkyl chain engineering to control the polymorphic behavior.

AbstractThe fungal-like family Saprolegniaceae (Oomycota), also called “water mold,” includes mostly aquatic saprophytes as well as notorious aquatic animal pathogens. Most studies on Saprolegniaceae have been biased toward pathogenic species that are important to aquaculture rather than saprotrophic species, despite the latter’s crucial roles in carbon cycling of freshwater ecosystems. Few attempts have been made to study the diversity and ecology of Saprolegniaceae; thus, their ecological role is not well-known. During a survey of oomycetes between 2016 and 2021, we investigated the diversity and distribution of culturable Saprolegniaceae species in freshwater ecosystems of Korea. In the present study, members of Saprolegniaceae were isolated and identified at species level based on their cultural, morphological, and molecular phylogenetic analyses. Furthermore, substrate preference and seasonal dynamics for each were examined. Most of the species were previously reported as animal pathogens; however, in the present study, they were often isolated from other freshwater substrates, such as plant debris, algae, water, and soil sediment. The relative abundance of Saprolegniaceae was higher in the cold to cool season than that in the warm to hot season of Korea. This study enhances our understanding of the diversity and ecological attributes of Saprolegniaceae in freshwater ecosystems.

Background Early‐stage unilateral moyamoya disease (MMD) is difficult to discriminate from isolated intracranial atherosclerotic stenosis, and identification of contralateral progression may aid in the diagnosis of MMD. The RNF213 (ring finger protein 213) R4810K variant is a strong genetic susceptibility factor for MMD; however, the role of contralateral progression in unilateral MMD is unknown. Methods and Results Patients who had undergone RNF213 R4810K genotyping with suspected unilateral MMD between January 2017 and August 2021 from 2 tertiary university hospitals were retrospectively reviewed. We compared the clinical features and radiographic outcomes of patients with and without this variant. The risk factors of contralateral progression in patients with suspected unilateral MMD were evaluated. The RNF213 R4810K variant was observed in 72 of 123 patients with suspected unilateral MMD, all of which were heterozygous. The allele frequency of the R4810K variant was significantly higher in the suspected unilateral MMD group compared with the historical control group (29.3% versus 1.2%; P

Abstract Background Current diagnostic tests for hereditary spherocytosis (HS) focus on the detection of hemolysis or indirectly assessing defects of membrane protein, whereas direct methods to detect protein defects are complicated and difficult to implement. In the present study, we investigated the patterns of genetic variation associated with HS among patients clinically diagnosed with HS. Methods Multi-gene targeted sequencing of 43 genes (17 RBC membrane protein-encoding genes, 20 RBC enzyme-encoding genes, and six additional genes for the differential diagnosis) was performed using the Illumina HiSeq platform. Results Among 59 patients with HS, 50 (84.7%) had one or more significant variants in a RBC membrane protein-encoding genes. A total of 54 significant variants including 46 novel mutations were detected in six RBC membrane protein-encoding genes, with the highest number of variants found in SPTB (n = 28), and followed by ANK1 (n = 19), SLC4A1 (n = 3), SPTA1 (n = 2), EPB41 (n = 1), and EPB42 (n = 1). Concurrent mutations of genes encoding RBC enzymes (ALDOB, GAPDH, and GSR) were detected in three patients. UGT1A1 mutations were present in 24 patients (40.7%). Positive rate of osmotic fragility test was 86.8% among patients harboring HS-related gene mutations. Conclusions This constitutes the first large-scaled genetic study of Korean patients with HS. We demonstrated that multi-gene target sequencing is sensitive and feasible that can be used as a powerful tool for diagnosing HS. Considering the discrepancies of clinical and molecular diagnoses of HS, our findings suggest that molecular genetic analysis is required for accurate diagnosis of HS.

Background : : von Willebrand disease (VWD) is one of the most common inherited bleeding disorders. However, the number of patients who register to the Korea Hemophilia Foundation (KHF) is much lower than the expected prevalence rate and only few hospitals perform tests for diagnosis autonomously. Thus, we surveyed practical realities of VWD in Yeungnam region. Methods : : Patients with VWD (N=267) who were diagnosed at eleven university hospitals from March 1995 to March 2018 were enrolled in this study. We evaluated the medical records from each hospital retrospectively. Results : : Two hundred and twenty-eight children and 39 adults met the diagnostic criteria for VWD. Seventy-eight (57.4%) patients had the blood type O. Fifty-eight patients were definite type 1 (21.7%), 151 were possible type 1 (56.6%), and the others were type 2. Abnormal laboratory findings were the most common factor for the diagnosis in children. VWF mutations were detected in 17 patients. Patients with a family history showed age of diagnosis of 9 y, which is higher than in those with no family history (6 yr), and also showed a higher rate of significant bleeding (32.1% vs. 14.2%). VWF:RCo and VWF:Ag tests were performed in-hospital at only 1 of 11 hospitals. Twelve of 267 patients were enrolled at the KHF (4.5%). Conclusion : : A high rate of out-sourcing studies may result in inaccurate diagnosis. The registration rate to the KHF is still lower than the prevalence rate. A comprehensive nationwide registration system is necessary in order to identify the actual prevalence rate and promote the diagnosis of VWD in Korea.

Background/Aims Differentiating extraluminal compressions from true subepithelial tumors in the duodenum by endoscopy alone is difficult. Endoscopic ultrasonography (EUS) is one of the most useful diagnostic modalities for this purpose. Extraluminal compression in the duodenum is occasionally observed, but its clinical significance has not been reported. Therefore, the aim of this study was to evaluate the clinical significance of extraluminal compression in the duodenum according to lesion location.Materials and Methods We retrospectively evaluated 22 patients diagnosed as having extraluminal compression in the duodenum based on EUS findings between January 2006 and December 2017. Some patients underwent abdominal computed tomography for accurate diagnosis. Results The location of the extraluminal compression was the duodenal bulb in 10 cases, the superior duodenal angle in 10 cases, and the second portion of the duodenum in 2 cases. Of the 22 cases, 12 were caused by normal structures, including vessels, the right kidney, the gallbladder, and the pancreas, and 10 were caused by pathological lesions, including the hepatic cyst, remnant cystic duct and dilated common bile duct after cholecystectomy; gallstones, gallbladder polyps, remnant cystic duct cancer, and pseudomyxoma peritoneii. The anterior wall of the duodenum was the most frequent location of extraluminal compression. However, the lesions in the anterior wall of the duodenal bulb and superior duodenal angle showed a high frequency of pathologic lesions, including malignancy. Conclusions If the extraluminal compression is found in the anterior wall of the duodenum, EUS is needed because of the high frequency of pathological lesions.

Spontaneous intramural hematoma is a rare complication of oral anticoagulants, and its incidence is expected to increase because of the increasing number of elderly patients undergoing anticoagulant therapy. Clinical manifestations of spontaneous intramural hematoma vary from mild abdominal pain to intestinal obstruction or acute abdomen. Early diagnosis is important because most patients can be treated successfully without surgery. The role of endoscopy in the diagnosis of intramural hematoma is not well established because almost all cases are diagnosed non-invasively with computed tomography scans. However, confirmation of the intramural hematoma through direct visualization of the involved bowel mucosa is helpful, if the imaging diagnosis is uncertain. We report a case of anticoagulant-induced spontaneous intramural hematoma, which was diagnosed using endoscopy, with relevant literature review.

Curcumin, a compound found in Indian yellow curry, is known to possess various biological activities, including anti-oxidant, anti-inflammatory, and anti-cancer activities. Cur2004- 8 is a synthetic curcumin derivative having symmetrical bis-alkynyl pyridines that shows a strong anti-angiogenic activity. In the present study, we examined the effect of dietary supplementation with Cur2004-8 on response to environmental stresses and aging using Caenorhabditis elegans as a model system. Dietary intervention with Cur2004-8 significantly increased resistance of C. elegans to oxidative stress. Its anti-oxidative-stress effect was greater than curcumin. However, response of C. elegans to heat stress or ultraviolet irradiation was not significantly affected by Cur2004-8. Next, we examined the effect of Cur2004-8 on aging. Cur2004-8 significantly extended both mean and maximum lifespan, accompanying a shift in time-course distribution of progeny production. Age-related decline in motility was also delayed by supplementation with Cur2004-8. In addition, Cur2004- 8 prevented amyloid-beta-induced toxicity in Alzheimer's disease model animals which required a forkhead box (FOXO) transcription factor DAF-16. Dietary supplementation with Cur2004-8 also reversed the increase of mortality observed in worms treated with high-glucose-diet. These results suggest that Cur2004-8 has higher anti-oxidant and antiaging activities than curcumin. It can be used for the development of novel anti-aging product. [ABSTRACT FROM AUTHOR]

PAK1 (RAC/CDC42-activated kinase 1) is the major oncogenic/ageing kinase, and its dysfunction extends the healthy lifespan of C. elegans by activating HSP16 gene. 15K is a highly cell-permeable 1,2,3-triazolyl ester of ketorolac that down-regulates both PAK1 and its down-stream COX-2 in R- and S-forms, respectively. 15K is 500-5,000 times more potent than ketorolac, an old pain-killer, inhibiting the growth of cancer cell lines with IC50 ranging 5-24 nM. Scores of natural and synthetic PAK1-blockers have been shown to extend the lifespan of small animals such as C. elegans, but none of them has been effective at nM levels. Thus, we examined in vivo effect of 15K at nM levels on the survival rate of C. elegans with or without heat-shock. Like the PAK1-deficient mutant, 15K (at 50 nM)-treated worm significantly lives longer, is far more heat-resistant and less productive (fertile) than the non-treated counterpart, with an increased expression of HSP16 gene. 15K has been proven to be among the most potent anti-cancerous and longevity-promoting PAK1-blockers, and therefore has a potential to treat a variety of solid tumours without severe side effect. [ABSTRACT FROM AUTHOR]

In the brain, aquaporin-1 (AQP-1), a water channel for high osmotic water permeability, is mainly expressed in the apical membrane of the ventricular choroid plexus and regulates formation of cerebrospinal fluid (CSF). Although the physiology of AQP-1 has been the subject of several publications, much less is known about the trans-acting factors involved in the control of AQP-1 gene expression. Here we report that TTF-1, a homeodomain-containing transcriptional regulator, is coexpressed with AQP-1 in the rat brain choroid plexus and enhances AQP-1 gene transcription by binding to conserved core TTF-1-binding motifs in the 5′-flanking region of the AQP-1 gene. Intracerebroventricular administration of an antisense TTF-1 oligode-oxynucleotide significantly decreased AQP-1 synthesis and reduced CSF formation. In addition, blockade of TTF-1 synthesis increased survival of the animals following acute water intoxication-induced brain edema. These results suggest that TTF-1 is physiologically involved in the transcriptional control of AQP-1, which is required for CSF formation. [ABSTRACT FROM AUTHOR]

The regulation of hepatic glucose metabolism is important in glucose homeostasis, and liver glucokinase (LGK) plays a central role in this process. Hepatic glucokinase expression is known to be regulated by insulin. Recently it has been suggested that sterol regulatory element binding protein-1c (SREBP-1c) mediates the action of insulin on LGK transcription; however, the precise mechanism is not, to date, well known. In the present study, we identified two functional SREBP-1c response elements, SREa and SREb, in the rat LGK promoter. SREBP-1c could bind to these SREs and activate the LGK promoter, and insulin activated the LGK promotet in Alexander cells. The physical interaction between the protein and SREs of the LGK promoter in vivo was also confirmed. Insulin selectively increased SREBP-1c and LGK expression in primary hepatocytes. Adenoviral expression of SREBP-1c stimulated LGK expression, and the dominant negative mutant of SREBP-1c blocked the increased gene expression of LGK by insulin and SREBP-1c. A chromatin immunoprecipitation assay using primary hepatocytes showed increased binding of SREBP-1 to SREs of the LGK promoter by insulin. [ABSTRACT FROM AUTHOR]

Small heterodimer partner (SHP; NROB2) is an un- usual orphan nuclear receptor that lacks a conventional DNA-binding domain and acts as a modulator of transcriptional activities of a number of nuclear receptors. Herein, we report that the human SHP promoter (hSHP) is activated by sterol regulatory element-binding protein-1 (SREBP-1), which regulates the expression of various genes involved in cholesterol and fatty acid synthesis. Overexpression of SREBP-1 activated the human but not mouse SHP promoter, although SREBP-2 had little effect on the SHP promoter in CV-1 cells. Serial deletion reporter assays revealed that SREBP-l-responsive region is located within the sequences from -243 to -120 bp in the hSHP promoter. DNase I footprinting, gel shift assays, and chromatin immunoprecipitation assays demonstrated that SREBP-1 binds directly to the hSHP promoter. Site-directed mutagenesis made it clear that the hSHP promoter activation by SREBP-1 is mostly mediated by the SRE1 (-186 to -195 bp) in the hSHP promoter, which is not conserved in the mouse SHP promoter. Moreover, adenovirus-mediated overexpression of SREBP-lc/ADD-1 induced SHP mRNA expression and repressed CYP7A1 expression in HepG2 cells. Fi- nally, we found that a four-nucleotide deletion (- 195CT- GAdel) in the hSHP promoter, which is reported to be associated with altered body weight and insulin secretion in human, coincides with the SRE1. This mutation strongly decreased both basal and SREBP-1 dependent activities of the hSHP promoter, because of the reduced binding of SREBP-1 to the mutated SRE1. Overall, our results demonstrate a differential regulation of human and mouse SHP promoters by SREBP-1. We propose a possible role of SREBP-1 in the species differential regulation of cholesterol and bile acid homeostasis via a novel mechanism of up-regulation of the hSHP gene expression. [ABSTRACT FROM AUTHOR]

In recent years, it has become increasingly evident that angiotensins synthesized in the brain contribute to regulating body fluid homeostasis. Although angiotensinogen, the unique angiotensin precursor, is produced in the brain, the factors that regulate its gene expression remain unknown. We recently found that TTF-1, a homeodomain-containing transcription factor essential for the development of the fetal diencephalon, is postnatally expressed in discrete areas of the hypothalamus. We now report that the subfornical organ, an important site of angiotensinogen synthesis, is an extrahypothalamic site of TTF-1 expression. Double in situ hybridization histochemistry demonstrated the presence of TTF-1 mRNA in angiotensinogen-producing cells of the rat subfornical organ. RNase protection assays showed that TTF-1 and angiotensinogen mRNA levels are simultaneously increased in the subfornical organ by water deprivation. The angiotensinogen promoter contains seven presumptive TTF-1 binding motifs, four of which are recognized by the TTF-1 homeodomain. In the C6 glioma cell line, TTF-1 transactivates the angiotensinogen promoter in a dose-dependent manner. This transactivation is abolished by deletion of the TTF-1 binding motif at -125. Intracranial administration of an antisense TTF-1 oligodeoxynucleotide decreased angiotensinogen mRNA in the snbfornical organ and dramatically reduced the animal's water intake while increasing urine excretion. Moreover, plasma arginine vasopressin content was decreased by the same treatment. These results demonstrate a novel role for TTF-1 in the regulation of body fluid homeostasis, exerted via the transactivational control of angiotensinogen synthesis in the subfornical organ. [ABSTRACT FROM AUTHOR]