• Applied Chemistry for Engineering
• /
• v.23 no.3
• /
• pp.289-292
• /
• 2012

Au electrodes modified with self-assembled monolayers (SAMs) were used to control the work function of source/drain electrodes in triethylsilylethynyl anthradithiophene (TES ADT)-based organic thin film transistors (OTFTs). By using benzothiol (BT) and pentafluorobenzothiol (PFBT) SAMs, the hole injection barrier between Au and the highest occupied molecular orbital (HOMO) of TES ADT was controlled. After a solvent annealing, TES ADT OTFTs with PFBT SAM-treated Au electrodes were found to exhibit high field-effect mobilities of $0.05\;cm^2/Vs$ and on/off current ratios of $10^6$.

• The Korean Journal of Ceramics
• /
• v.2 no.2
• /
• pp.95-101
• /
• 1996

Variations of the leakage current behaviors and interface potential barrier $({\Phi}_B)$ of rf-sputter deposited (Ba, Sr)$TiO_3$ (BST) thin films with thicknesses ranging from 20 nm to 150nm are investigated as a function of the thickness and bias voltages. The top and bottom electrodes are dc-sputter-deposited Pt films. ${\Phi}_B$ critically depends on the BST film deposition temperature, postannealing atmosphere and time after the annealing. The postannealing under $N_2$ atmosphere results in a high interface potential barrier height and low leakage current. Maintaining the BST capacitor in air for a long time reduces the ${\Phi}_B$ from about 2.4 eV to 1.6 eV due to the oxidation. ${\Phi}_B$ is not so dependent on the film thickness in this experimental range. The leakage conduction mechanism is very dependent on the BST film thickness; the 20 nm thick film shows tunneling current, 30 and 40 nm thick films show Shottky emission current.

• The Transactions of the Korean Institute of Electrical Engineers C
• /
• v.48 no.5
• /
• pp.385-390
• /
• 1999

Surface corona discharge characteristics of a dc corona charged ferroelectric pellet barrier have been investigated experimentally. Electric charges stored on the surfaces of the ferroelectric pellets by a dc corona discharge provide partial electric fields on the surfaces of the ferroelectric pellets, which could generate surface corona discharges on the ferroelectric pellets. This system utilizes both the surface discharges on the ferroelectric pellet barrier and the corona discharge between corona tip and mesh electrode. Positive and negative dc voltages were applied to the tip to generate partial discharges, and corona currents were estimated to investigate the buildup charge on ferroelectric pellets as a function of the applied time and the charge relaxation time constants of ferroelectric pellets. As a result, in the case of the negative corona discharge with the ferroelectric pellet barrier, the mean corona current and ozone generation increase greatly, and the surface discharges on the ferroelectric pellets can be fenerated efficiently. It is also found that, charge relaxation time, dielectric constants offerroelectric pellets, polarity of applied voltage and applied time affected to the surface discharges among the ferroelectric pellets.

• Journal of the Korean Institute of Electrical and Electronic Material Engineers
• /
• v.24 no.4
• /
• pp.271-275
• /
• 2011

In this paper, thermal stability of palladium germanide (Pd germanide) is analyzed for high performance Schottky barrier germanium metal oxide semiconductor field effect transistors (SB Ge-MOSFETs). Pd germanide Schottky barrier diodes were fabricated on n-type Ge-on-Si substrates and the formed Pd germanide shows thermal immunity up to $450^{\circ}C$. The barrier height of Pd germanide is also characterized using two methods. It is shown that Pd germanide contact has electron Schottky barrier height of 0.569~0.631 eV and work function of 4.699~4.761 eV, respectively. Pd germanide is promising for the nanoscale Schottky barrier Ge channel MOSFETs.

• Journal of Ginseng Research
• /
• v.46 no.1
• /
• pp.115-125
• /
• 2022

Background: Ginsenosides (GS) have potential value as cosmetic additives for prevention of skin photoaging. However, their protective mechanisms against skin barrier damage and their active monomeric constituents are unknown. Methods: GS monomer types and their relative proportions were identified. A UVB-irradiated BALB/c hairless mouse model was used to assess protective effects of GS components on skin epidermal thickness and transepidermal water loss (TEWL). Skin barrier function, reflected by filaggrin (FLG), involucrin (IVL), claudin-1 (Cldn-1), and aquaporin 3 (AQP3) levels and MAPK phosphorylation patterns, were analyzed in UVB-irradiated hairless mice or HaCaT cells. Results: Total GS monomeric content detected by UPLC was 85.45% and was largely attributed to 17 main monomers that included Re (16.73%), Rd (13.36%), and Rg1 (13.38%). In hairless mice, GS ameliorated UVB-induced epidermal barrier dysfunction manifesting as increased epidermal thickness, increased TEWL, and decreased stratum corneum water content without weight change. Furthermore, GS treatment of UVB-irradiated mice restored protein expression levels and epidermal tissue distributions of FLG, IVL, Cldn-1, and AQP3, with consistent mRNA and protein expression results obtained in UVB-irradiated HaCaT cells (except for unchanging Cldn-1 expression). Mechanistically, GS inhibited JNK, p38, and ERK phosphorylation in UVB-irradiated HaCaT cells, with a mixture of Rg2, Rg3, Rk3, F2, Rd, and Rb3 providing the same protective MAPK pathway inhibition-associated upregulation of IVL and AQP3 expression as provided by intact GS treatment. Conclusion: GS protection against UVB-irradiated skin barrier damage depends on activities of six ginsenoside monomeric constituents that inhibit the MAPK signaling pathway.

• Journal of Microbiology and Biotechnology
• /
• v.32 no.7
• /
• pp.825-834
• /
• 2022

Inflammatory bowel disease (IBD) is a global disease that is in increasing incidence. The gut, which contains the largest amount of lymphoid tissue in the human body, as well as a wide range of nervous system components, is integral in ensuring intestinal homeostasis and function. By interacting with gut microbiota, immune cells, and the enteric nervous system, the intestinal barrier, which is a solid barrier, protects the intestinal tract from the external environment, thereby maintaining homeostasis throughout the body. Destruction of the intestinal barrier is referred to as developing a "leaky gut," which causes a series of changes relating to the occurrence of IBD. Changes in the interactions between the intestinal barrier and gut microbiota are particularly crucial in the development of IBD. Exploring the leaky gut and its interaction with the gut microbiota, immune cells, and the neuroimmune system may help further explain the pathogenesis of IBD and provide potential therapeutic methods for future use.

• Journal of Veterinary Clinics
• /
• v.25 no.5
• /
• pp.330-339
• /
• 2008

Ceramide, cholesterol and free fatty acids are the major intercellular lipids, maintaining the integrity of the skin barrier. However, the roles of these lipids in canine skin barrier function are little known. The aim of this study was to evaluate the repairing effects of 2% ceramide (CER), 2% cholesterol (CHO), 2% linoleic acid (LIN) and 2% intercellular lipid mixture (ILM) on damaged canine skin barrier by 1.25% sodium lauryl sulphate (SLS). Transepidermal water loss (TEWL), skin hydration, skin pH and skin thickness were assessed. Histological profiles and transmission electron microscopic (TEM) profiles were assessed on day 12. SLS effectively induced the canine skin barrier damage. TEWL was significantly decreased by topical application of CER and ILM in SLS and vehicle-treated skin on day 8 and 12, respectively (p < 0.05, p < 0.0 I). By end of the experiment all lipids significantly decreased the TEWL as compared with SLS and vehicle control, but CER and ILM more significantly decreased the TEWL than UN and CHO, respectively (p < 0.01). Skin hydration was significantly increased by CER and ILM during experimental periods (p < 0.01). Skin pH was significantly decreased by CER, LIN and ILM. In histological profiles, the thickness of the stratum corneum (SC) was significantly increased by the SC lipids as compared with vehicle and SLS (p < 0.01). Especially, CER and ILM showed more prominent improvement of barrier recovery. In TEM of the SC, SLS induced exfoliations of corneodesmosomes in the SC, and CER and ILM effectively protected exfoliations of corneodesmosomes on SLS-damaged canine skin. These results indicated that topical application of CER and ILM dramatically improved damaged-skin barrier function by SLS. Also, it was considered that the use of CER or ILM was recommended for the management of skin barrier dysfunction by irritant and inflammatory skin disorders such as atopic dermatitis.

• Journal of the Society of Cosmetic Scientists of Korea
• /
• v.29 no.2 s.43
• /
• pp.205-232
• /
• 2003

Ursolic acid (UA) and Oleanolic acid (ONA), known as urson, micromerol and malol, are pentacyclic triterpenoid compounds which naturally occur in a large number of vegetarian foods, medicinal herbs, and plants. They may occur in their free acid form or as aglycones for triterpenoid saponins, which are comprised of a triterpenoid aglycone, linked to one or more sugar moieties. Therefore UA and ONA are similar in pharmacological activity. Lately scientific research, which led to the identification of UA and ONA, revealed that several pharmacological effects, such as antitumor, hepato-protective, anti-inflammatory, anticarcinogenic, antimicrobial, and anti-hyperlipidemic could be attributed to UA and ONA. Here, we introduced the effect of UA and ONA on acutely barrier disrupted and normal hairless mouse skin. To evaluate the effects of UA and ONA on epidermal permeability barrier recovery, both flanks of 8-12 week-old hairless mice were topically treated with either 0.01-0.1 mg/ml UA or 0.1-1 mg/ml ONA after tape stripping, and TEWL (Transepidermal water loss) was measured . The recovery rate increased in those UA or ONA treated groups (0.1 mg/ml UA and 0.5 mg/ml ONA) at 6 h more than $20\%$ compared to vehicle treated group (p<0.05). Here, we introduced the effects of UA and ONA on acute barrier disruption and normal epidermal permeability barrier function. For verifying the effects of UA and ONA on normal epidermal barrier, hydration and TEWL were measured for 1 and 3 weeks after UA and ONA applications (2mg/ml per day). We also investigated the features of epidermis and dermis using electron microscopy (EM) and light microscopy (LM). Both samples increased hydration compared to vehicle group from f week without TEWL alteration (p<0.005). EM examination using RuO4 and OsO4 fixation revealed that secretion and numbers of lamellar bodies and complete formation of lipid bilayers were most prominent $(ONA{\geq}UA>Vehicle)$. LM finding showed that thickness of stratum corneum (SC) was slightly increased and especially epidermal thickening and flattening was observed (UA>ONA>Veh). We also observed that UA and ONA stimulate epidermal keratinocyte differentiation via $PPAR\;\alpha$. Protein expression of involucrin, loricrin, and filaggrin increased at least 2 and 3 fold in HaCaT cells treated with either $ONA\;(10{\mu}M)$ or UA $(10{\mu}M)$ for 24h respectively. This result suggested that the UA and ONA can improve epidermal permeability barrier function and induce the epidermal keratinocyte differentiation via $PPAR\;{\alpha}$. Using Masson-trichrome and elastic fiber staining, we observed collagen thickening and elastic fiber elongation by UA and ONA treatments. In vitro results of collagen and elastin synthesis and elastase inhibitory activity measurements were also confirmed in vivo findings. These data suggested that the effects of UA and ONA related to not only epidermal permeability barrier functions but also dermal collagen and elastic fiber synthesis. Taken together, UA and ONA can be relevant candidates to improve epidermal and dermal functions and pertinent agents for cosmeseutical applications.

• Journal of the Society of Cosmetic Scientists of Korea
• /
• v.46 no.1
• /
• pp.73-80
• /
• 2020

Psychological stress can affect the physiological condition of the skin and cause various cutaneous disorders. The stress hormone cortisol is secreted by various skin cells such as fibroblasts, keratinocytes, and melanocytes. Tight junctions (TJs) are cell-cell junctions that form a barrier in the stratum granulosum of mammalian skin. TJs can also affect other skin barriers and are affected by chemical, microbial, or immunological barriers. Stress can cause damage to the skin barrier. Interestingly, to our knowledge, there has not been any research demonstrating the involvement of TJs in this process. In this study, cortisol was used to treat keratinocytes to determine its role in regulating TJs. We found that cortisol damaged skin barrier function by regulating the gene expression and structure of TJ components. Cortisol also inhibited the development of the granular layer in a skin equivalent model. These results suggest that cortisol affects the skin barrier function by the regulation of TJs.

• BMB Reports
• /
• v.39 no.4
• /
• pp.339-345
• /
• 2006

The blood-neural barrier (BNB), including blood-brain barrier (BBB) and blood-retinal barrier (BRB), is an endothelial barrier constructed by an extensive network of endothelial cells, astrocytes and neurons to form functional 'neurovascular units', which has an important role in maintaining a precisely regulated microenvironment for reliable neuronal activity. Although failure of the BNB may be a precipitating event or a consequence, the breakdown of BNB is closely related with the development and progression of CNS diseases. Therefore, BNB is most essential in the regulation of microenvironment of the CNS. The BNB is a selective diffusion barrier characterized by tight junctions between endothelial cells, lack of fenestrations, and specific BNB transporters. The BNB have been shown to be astrocyte dependent, for it is formed by the CNS capillary endothelial cells, surrounded by astrocytic end-foot processes. Given the anatomical associations with endothelial cells, it could be supposed that astrocytes play a role in the development, maintenance, and breakdown of the BNB. Therefore, astrocytes-endothelial cells interaction influences the BNB in both physiological and pathological conditions. If we better understand mutual interactions between astrocytes and endothelial cells, in the near future, we could provide a critical solution to the BNB problems and create new opportunities for future success of treating CNS diseases. Here, we focused astrocyte-endothelial cell interaction in the formation and function of the BNB.