Synthesis of Two- and Three-Dimensional Carbon-Based Materials and Their Applications

Department of Energy EngineeringDue to abundant carbon reserves (15th most element in the earth???s crust) and light weight advantage, carbon based materials have been studied to replace rare and expansive inorganic materials in energy materials. Since the discovery of graphene, two dimensional structure, in 2004, two dimensional carbon materials have attracted the attention of researchers from around the globe. Keeping in view the importance of carbon materials, we first produced edge-selective functionalized graphene (EFG) for the production of large-area uniform graphene film for transparent and flexible electrode and transistor by top-down method from graphite to graphene. The resultant graphene films show ambipolar transport properties with sheet resistances of 0.52-3.11 k??/sq at 63-90% optical transmittance. EFG allows solution processing methods for the scalable production of electrically conductive, optically transparent, and mechanically robust flexible graphene films for use in practice. Secondary, we designed and synthesized two dimensional benzimidazole based network polymer for counter electrode in dye-sensitized solar cell (DSSC) to replace platinum. We confirm the effect of thermal annealing and additives of iron from T-HPBI for electrocatalytic activity from the symmetrical dummy cell with two identical electrodes. Furthermore, we also designed and synthesized three-dimensional polymer through solid-state reaction without catalyst at low-temperature for solid sorbent for CO2 capture. The reaction is triggered by metastable crystal lattice energy below its crystal melting temperature. The driving force for the reaction is systematically studied with single-crystal X-ray diffraction and differential scanning calorimetry.ope

A case of anemia caused by combined vitamin B12 and iron deficiency manifesting as short stature and delayed puberty

Anemia caused by vitamin B12 deficiency resulting from inadequate dietary intake is rare in children in the modern era because of improvements in nutritional status. However, such anemia can be caused by decreased ingestion or impaired absorption and/or utilization of vitamin B12. We report the case of an 18-year-old man with short stature, prepubertal sexual maturation, exertional dyspnea, and severe anemia with a hemoglobin level of 3.3 g/dL. He had a history of small bowel resection from 50 cm below the Treitz ligament to 5 cm above the ileocecal valve necessitated by midgut volvulus in the neonatal period. Laboratory tests showed deficiencies of both vitamin B12 and iron. A bone marrow examination revealed dyserythropoiesis and low levels of hemosiderin particles, and a cytogenetic study disclosed a normal karyotype. After treatment with parenteral vitamin B12 and elemental iron, both anemia and growth showed gradual improvement. This is a rare case that presented with short stature and delayed puberty caused by nutritional deficiency anemia in Korea

Discovery of new epigenomics-based biomarkers and the early diagnosis of neurodegenerative diseases

Treatment options for many neurodegenerative diseases are limited due to the lack of early diagnostic procedures that allow timely delivery of therapeutic agents to affected neurons prior to cell death. While notable advances have been made in neurodegenerative disease biomarkers, whether or not the biomarkers discovered to date are useful for early diagnosis remains an open question. Additionally, the reliability of these biomarkers has been disappointing, due in part to the large dissimilarities between the tissues traditionally used to source biomarkers and primarily diseased neurons. In this article, we review the potential viability of atypical epigenetic and/or consequent transcriptional alterations (ETAs) as biomarkers of early-stage neurodegenerative disease, and present our perspectives on the discovery and practical use of such biomarkers in patient-derived neural samples using single-cell level analyses, thereby greatly enhancing the reliability of biomarker application. © 2020 The Authors1

Stimulation of the Migration and Expansion of Adult Mouse Neural Stem Cells by the FPR2-Specific Peptide WKYMVm

Neural stem cells (NSCs) are multipotent cells capable of self-renewal and differentiation into different nervous system cells. Mouse NSCs (mNSCs) are useful tools for studying neurogenesis and the therapeutic applications of neurodegenerative diseases in mammals. Formyl peptide receptor 2 (FPR2), expressed in the central nervous system and brain, is involved in the migration and differentiation of murine embryonic-derived NSCs. In this study, we explored the effect of FPR2 activation in adult mNSCs using the synthetic peptide Trp-Lys-Tyr-Met-Val-D-Met-NH2 (WKYMVm), an agonist of FPR2. After isolation of NSCs from the subventricular zone of the adult mouse brain, they were cultured in two culture systems—neurospheres or adherent monolayers—to demonstrate the expression of NSC markers and phenotypes. Under different conditions, mNSCs differentiated into neurons and glial cells such as astrocytes, microglia, and oligodendrocytes. Treatment with WKYMVm stimulated the chemotactic migration of mNSCs. Moreover, WKYMVm-treated mNSCs were found to promote proliferation; this result was confirmed by the expansion of mNSCs in Matrigel and the increase in the number of Ki67-positive cells. Incubation of mNSCs with WKYMVm in a supplement-free medium enhanced the survival rate of the mNSCs. Together, these results suggest that WKYMVm-induced activation of FPR2 stimulates cellular responses in adult NSCs. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.1

Percutaneous radiofrequency ablation for hepatic tumors: factors affecting baseline impedance

PurposeWe aimed to evaluate factors that affect baseline impedance of percutaneous radiofrequency ablation.MethodsIn this retrospective study, we analyzed 51 patients with 55 hepatic tumors from November 2015 until April 2018. We measured the baseline impedance nine times with three adjustable tip sizes (2 cm, 2.5 cm, 3 cm) and three different pad locations (two pads attached on the thigh, four on the thigh, two on the back). The first roll-off time was measured with two grounding pads attached on the back. Body mass index, cirrhotic or non-cirrhotic liver parenchyma, previous procedure, tumor location, artificial ascites, active tip size, and the pad location were evaluated as potential factors affecting baseline impedance using the Mann–Whitney U test, t-test and analysis of variance test.ResultsComplete radiofrequency ablation was achieved in 51 patients. Body mass index (p = 0.897), cirrhotic or non-cirrhotic liver parenchyma (p = 0.767), previous procedure (p = 0.957), tumor location (p = 0.906), and artificial ascites (p = 0.882) did not significantly affect baseline impedance. Grounding pads located on the back showed the lowest baseline impedance (p < 0.001). Increase in active tip size showed gradual decrease in baseline impedance (p = 0.016).ConclusionThe factors affecting baseline impedance were the pad location and the tip size. Positioning pads on the back lowers the baseline impedance and can shorten the first roll-off time, ultimately resulting in reduced total ablation time

Successful Hemostasis with Recombinant Activated Factor VII in a Patient with Massive Hepatic Subcapsular Hematoma

Recombinant activated coagulation factor VII (rFVIIa) is known to be effective in the management of acquired deficiencies of factor VII and platelet function defects. But recently, rFVIIa has been successfully used to treat ongoing bleeding in disseminated intravascular coagulopathy (DIC) condition. The patient reported here was suspected to be suffering from toxic hepatitis on admission. After percutaneous liver biopsy, bleeding occurred and did not stop even after right hepatic artery embolization. The patient developed a severe hemorrhage that resulted in hypovolemic shock, hemoperitoneum, and a massive subcapsular hematoma. The patient then developed DIC due to massive transfusion, as well as acute liver necrosis. The patient was given 400 μg/kg of rFVIIa. Recombinant factor VIIa was administered in an attempt to control the bleeding. This stabilized the hemoglobin levels of the patient. The patient gradually recovered in 4 months. In conclusion, this case suggests that rFVIIa can be successfully used for the hemostasis of uncontrolled bleeding in DIC

MMP9 Processing of HSPB1 Regulates Tumor Progression

Matrix metalloproteinases regulate pathophysiological events by processing matrix proteins and secreted proteins. Previously, we demonstrated that soluble heat shock protein B1 (HSPB1) is released primarily from endothelial cells (ECs) and regulates angiogenesis via direct interaction with vascular endothelial growth factor (VEGF). Here we report that MMP9 can cleave HSPB1 and release anti-angiogenic fragments, which play a key role in tumorprogression. We mapped the cleavage sites and explored their physiological relevance during these processing events. HSPB1 cleavage by MMP9 inhibited VEGF-induced ECs activation and the C-terminal HSPB1 fragment exhibited more interaction with VEGF than did full-length HSPB1. HSPB1 cleavage occurs during B16F10 lung progression in wild-type mice. Also, intact HSPB1 was more detected on tumor endothelium of MMP9 null mice than wild type mice. Finally, we confirmed that secretion of C-terminal HSPB1 fragment was significantly inhibited lung and liver tumor progression of B16F10 melanoma cells and lung tumor progression of CT26 colon carcinoma cells, compared to full-length HSPB1. These data suggest that in vivo MMP9-mediated processing of HSPB1 acts to regulate VEGF-induced ECs activation for tumor progression, releasing anti-angiogenic HSPB1 fragments. Moreover, these findings potentially explain an anti-target effect for the failure of MMP inhibitors in clinical trials, suggesting that MMP inhibitors may have pro-tumorigenic effects by reducing HSPB1 fragmentation

Successful switching from insulin to sulfonylurea in a 3-month-old infant with diabetes due to p.G53D mutation in

Permanent neonatal diabetes mellitus is most commonly caused by mutations in the ATP-sensitive potassium channel (KATP) subunits. Prompt initiation of sulfonylurea treatment can improve glycemic control in children with KCNJ11 mutation. In this report, we present a case of permanent neonatal diabetes caused by a mutation in the KCNJ11 gene that was successfully treated via early switching of insulin to sulfonylurea treatment. A 53-day-old female infant presented with diabetic ketoacidosis. Insulin was administered for the ketoacidosis and blood glucose regulation. At 3 months of age, using genomic DNA extracted from peripheral lymphocytes, direct sequencing of KCNJ11 identified a heterozygous mutation of c.158G>A (p.G53D) and confirmed the diagnosis of permanent neonatal diabetes mellitus. Subsequently, treatment with sulfonylurea was initiated, and the insulin dose was gradually tapered. At 4 months of age, insulin therapy was discontinued, and sulfonylurea (glimepiride, 0.75 mg/kg) was administered alone. At 6 months after initiation of administration of sulfonylurea monotherapy, blood glucose control was stable, and no hypoglycemic events or developmental delays were reported. C-peptide levels increased during treatment with sulfonylurea. Early switching to sulfonylurea in infants with permanent diabetes mellitus owing to a KCNJ11 mutation could successfully help regulate glycemic control, which suggests the need for early genetic testing in patients presenting with diabetes before 6 months of age