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Background/Aims Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by fat accumulation in the liver. MASLD encompasses both steatosis and MASH. Since MASH can lead to cirrhosis and liver cancer, steatosis and MASH must be distinguished during patient treatment. Here, we investigate the genomes, epigenomes, and transcriptomes of MASLD patients to identify signature gene set for more accurate tracking of MASLD progression. Methods Biopsy-tissue and blood samples from patients with 134 MASLD, comprising 60 steatosis and 74 MASH patients were performed omics analysis. SVM learning algorithm were used to calculate most predictive features. Linear regression was applied to find signature gene set that distinguish the stage of MASLD and to validate their application into independent cohort of MASLD. Results After performing WGS, WES, WGBS, and total RNA-seq on 134 biopsy samples from confirmed MASLD patients, we provided 1,955 MASLD-associated features, out of 3,176 somatic variant callings, 58 DMRs, and 1,393 DEGs that track MASLD progression. Then, we used a SVM learning algorithm to analyze the data and select the most predictive features. Using linear regression, we identified a signature gene set capable of differentiating the various stages of MASLD and verified it in different independent cohorts of MASLD and a liver cancer cohort. Conclusions We identified a signature gene set (i.e., CAPG, HYAL3, WIPI1, TREM2, SPP1, and RNASE6) with strong potential as a panel of diagnostic genes of MASLD-associated disease.

Motion planning for mobile manipulators is challenging because of their high degrees of freedom. The most effective approach for the motion planning of a mobile manipulator is to consider the different characteristics of a mobile robot and a manipulator while planning and controlling each system separately. In a previous study, different characteristics were considered using virtual impedance. This method involves forming a virtual impedance relationship between the two subsystems, enabling the mobile robot to track the movement of the manipulator. However, this study had certain limitations. Firstly, this method is not applicable to non-holonomic mobile robots. Secondly, obstacle avoidance methods for mobile robots are not considered. To address these limitations, our study proposes a novel concept for our motion planner that is called the virtual impedance energy field (VIEF), which refers to the work and change in total energy. We solved the first limitation of the previous study by transforming the virtual impedance force into the VIEF. Moreover, by integrating an obstacle field with the VIEF and using it as a local costmap, the second limitation was addressed. To validate the performance of our motion planner, we conducted simulations in environments comprising obstacles, with straight and curved trajectories of the end-effector. We then analyzed the pose change graph of the mobile robot and end-effector, pose error of the end-effector, and velocity of the mobile robot. We therefore confirmed that the manipulator successfully followed the desired trajectory, while the mobile robot maintained a distance from the end-effector and avoided obstacles.

The effects of aging on the healing capacity of maxillofacial bone defects have not been studied. The aim of this study was to evaluate the effects of aging on the regeneration of round bony defects in the mandible. We created a round-shaped bony defect in the mandibular angle area in rats of different ages (2-[2 M], 10-[10 M], and 20-month-old [20 M]) and evaluated new bone regeneration in these groups. Changes in bone turnover markers such as alkaline phosphatase, procollagen type I N-terminal propeptide (PINP), cross-linked C-telopeptide of type I collagen, and tartrate-resistant acid phosphatase 5B (TRAP5b) were investigated. The bone volume/total volume and bone mineral density of the 20 M group were significantly higher than those of the 2 M group (p = 0.029, 0.019). A low level of the bone formation marker PINP was observed in the 20 M group, and a high level of the bone resorption marker TRAP5b was observed in the 10 M and 20 M groups. Micro-computed tomography (µ-CT) results showed that older rats had significantly higher bone formation than younger rats, with lower serum levels of PINP and higher levels of TRAP5b. The local environment of the old rat bone defects, surrounded by thickened bone, may have affected the results of our study. In conclusion, old rats showed greater new bone regeneration and healing capacity for round mandibular bone defects. This result was related to the fact that the bone defects in the 20 M rat group provided more favorable conditions for new bone regeneration.

With depth cameras and LiDAR improving and generating more data, their applications in 3D point clouds are growing rapidly. However, the vast amount of generated data increases the computational load and results in a shortage of storage space. Therefore, a preprocessing step to reduce the number of points is required before using the 3D point cloud. This study proposes region of interest (ROI) determination methods that sequentially construct circular and rectangular ROIs along the target trajectory of the robot to extract only crucial data for the target task. These two ROI determination methods have two benefits. First, they maintain the resolution of the raw data; second, they create two ROIs that match perfectly regardless of the complexity of the trajectory. To verify the high performance of these two ROI determination methods, we conducted simulations and experiments using various data; artificial frames, keyframes, and sequential frames. As a result, when the distance between the center points was small, 25% of the diameter or height of the circular and rectangular ROIs, the classification evaluation results were closer to 1 and the processing speed was faster than the raw data acquisition rate. However, we confirm that there is a trade-off relationship between the classification results and the processing time according to the distance parameter. In addition, through the qualitative comparison with the previous study, the long cuboid ROI determination method, we identified the limitations of the previous study and the advantages of the two proposed ROI determination methods.

Cancer stem-like cells (CSCs) have been suggested to be responsible for chemoresistance and tumor recurrence owing to their self-renewal capacity and differentiation potential. Although WEE1 is a strong candidate target for anticancer therapies, its role in ovarian CSCs is yet to be elucidated. Here, we show that WEE1 plays a key role in regulating CSC properties and tumor resistance to carboplatin via a microRNA-dependent mechanism. We found that WEE1 expression is upregulated in ovarian cancer spheroids because of the decreased expression of miR-424 and miR-503, which directly target WEE1. The overexpression of miR-424/503 suppressed CSC activity by inhibiting WEE1 expression, but this effect was reversed on the restoration of WEE1 expression. Furthermore, we demonstrated that NANOG modulates the miR-424/503-WEE1 axis that regulates the properties of CSCs. We also demonstrated the pharmacological restoration of the NANOG-miR-424/503-WEE1 axis and attenuation of ovarian CSC characteristics in response to atorvastatin treatment. Lastly, miR-424/503-mediated WEE1 inhibition re-sensitized chemoresistant ovarian cancer cells to carboplatin. Additionally, combined treatment with atorvastatin and carboplatin synergistically reduced tumor growth, chemoresistance, and peritoneal seeding in the intraperitoneal mouse models of ovarian cancer. We identified a novel NANOG-miR-424/503-WEE1 pathway for regulating ovarian CSCs, which has potential therapeutic utility in ovarian cancer treatment.

Autophagy has a dual role in the maintenance of cancer stem cells (CSCs), but the precise relationship between autophagy and cancer stemness requires further investigation. In this study, it was found that luminal and triple‐negative breast cancers require distinct therapeutic approaches because of their different amounts of autophagy flux. We identified that autophagy flux was inhibited in triple‐negative breast cancer (TNBC) CSCs. Moreover, miRNA‐181a (miR‐181a) expression is upregulated in both TNBC CSCs and patient tissues. Autophagy‐related 5 (ATG5) and autophagy‐related 2B (ATG2B) participate in the early formation of autophagosomes and were revealed as targets of miR‐181a. Inhibition of miR‐181a expression led to attenuation of TNBC stemness and an increase in autophagy flux. Furthermore, treatment with curcumin led to attenuation of cancer stemness in TNBC CSCs; the expression of ATG5 and ATG2B was enhanced and there was an increase of autophagy flux. These results indicated that ATG5 and ATG2B are involved in the suppression of cancer stemness in TNBC. In summary, autophagy inhibits cancer stemness through the miR‐181a‐regulated mechanism in TNBC. Promoting tumor‐suppressive autophagy using curcumin may be a potential method for the treatment of TNBC.

Abstract Although postoperative delirium is a common complication in older patients, few papers have described risk factors after of spinal surgery. The purpose of this study was to analyze various perioperative risk factors for delirium after spinal surgery in older patients. This study was performed on retrospective data collection with prospective design. We analyzed 138 patients over 65 years of age who underwent spinal surgery. Preoperative factors were cognitive function (Mini-Mental State Examination-Korean (MMSE-K) and the Korean version of the Delirium Rating Scale-Revised-98 (K-DRS 98)), age, sex, type of admission, American Society of Anesthesiologist classification, metabolic equivalents, laboratory findings, visual analog scale, and Oswestry Disability Index. Intraoperative factors were operation time, blood loss, and type of procedure. Postoperative factors were blood transfusion and type of postoperative pain control. Postoperative delirium developed in 25 patients (18.16%). Patients were divided into two groups: Group with delirium (group A) and group without delirium (group B). MMSE-K scores in Group A were significantly lower than in Group B (p

In this research, a multi-slit prompt-gamma camera was developed to locate the distal dose falloff of the proton beam spots in spot scanning proton therapy. To see the performance of the developed camera, therapeutic proton beams were delivered to a solid plate phantom and then the prompt gammas from the phantom were measured using the camera. Our results show that the camera locates the 90% distal dose falloff (= d90%), within about 2–3 mm of error for the spots which are composed 3.8 × 108 protons or more. The measured location of d90% is not very sensitive to the irradiation depth of the proton beam (i.e., the depth of proton beam from the phantom surface toward which the camera is located). Considering the number of protons per spot for the most distal spots in typical treatment cases (i.e., 2 Gy dose divided in 2 fields), the camera can locate d90% only for a fraction of the spots depending on the treatment cases. However, the information of those spots is still valuable in that, in the multi-slit prompt-gamma camera, the distal dose falloff of the spots is located solely based on prompt gamma measurement, i.e., not referring to Monte Carlo simulation. Keywords: Proton therapy, Prompt gamma, Beam range verification, Distal dose falloff

Abstract Background X-linked spondyloepiphyseal dysplasia tarda (SEDT-XL) is a skeletal disorder characterized by defective structures of vertebral bodies and/or of epiphyses of the long bones, resulting in moderately short stature and early joint degeneration. TRAPPC2 gene, which is important for collagen secretion, has been reported as causative for SEDT-XL. Case presentation Here, we report two variants of TRAPPC2 gene of SEDT-XL patients, a missense variant of start codon, c.1A > T, and a deletion variant, c.40delG. To understand molecular consequence of the variants, we establish an in vitro gene expression assay system and demonstrate that both mutated genes are transcribed, but are not properly translated, indicative of the pathogenic nature of those TRAPPC2 variants. Conclusions In the current study, we provide additional experimental data showing that loss-of-function TRAPPC2 variants are probably causative for SEDT-XL phenotype. These findings further contribute to the understanding the clinical picture related to TRAPPC2 gene.

The mechanical-collimation imaging is the most mature technology in prompt gamma (PG) imaging which is considered the most promising technology for beam range verification in proton therapy. The purpose of the present study is to compare the performances of two mechanical-collimation PG cameras, knife-edge (KE) camera and multi-slit (MS) camera. For this, the PG cameras were modeled by Geant4 Monte Carlo code, and the performances of the cameras were compared for imaginary point and line sources and for proton beams incident on a cylindrical PMMA phantom. From the simulation results, the KE camera was found to show higher counting efficiency than the MS camera, being able to estimate the beam range even for 107 protons. Our results, however, confirmed that in order to estimate the beam range correctly, the KE camera should be aligned, at least approximately, to the location of the proton beam range. The MS camera was found to show lower efficiency, being able to estimate the beam range correctly only when the number of the protons is at least 108. For enough number of protons, however, the MS camera estimated the beam range correctly, errors being less than 1.2 mm, regardless of the location of the camera. Keywords: Proton therapy, Beam range verification, Prompt gamma, Knife-edge camera, Multi-slit camera

Background: Polycystic kidney disease (PKD) involves renal cysts arising from proliferating tubular cells. Autophagy has been recently suggested as a potential therapeutic target in PKD, and mammalian target of rapamycin (mTOR) is a key negative regulator of autophagy. However, the effect of autophagy regulation on cystogenesis has not been elucidated in PKD mice. Methods: Clinical validation was performed using GEO datasets and autosomal dominant polycystic kidney disease (ADPKD) patient samples. Newly established PKD and LC3 transgenic mice were used for in vivo verifications, and additional tests were performed in vitro and in vivo using multiple autophagy drugs. Findings: Neither autophagy stimulation nor LC3 overexpression alleviated PKD. Furthermore, we observed the inhibitory effect of an autophagy inhibitor on cysts, indicating its possible therapeutic use in a specific group of patients with ADPKD. Interpretation: Our findings provide a novel insight into the pathogenesis related to autophagy in PKD, suggesting that drugs related to autophagy regulation should be considered with caution for treating PKD. Funding Sources: This work was supported by grants from the Bio & Medical Technology Development Program; the Collaborative Genome Program for Fostering New Post-Genome Industry of the NRF; the Basic Science Program.

Autophagy is a catabolic process required for maintaining intracellular energy homeostasis. It eliminates harmful proteins and recycles functional macromolecules back into the cell via cargo breakdown. Autophagy is generally suppressed under fed conditions and induced by serum starvation; therefore, it is considered to be a nutrient-sensing mechanism. Cilia, finger-like organelles harboring multiple receptors along their surface, are energy-sensing structures that are also triggered by serum deprivation. Herein, we verified the effect of autophagy alterations on cilia assembly and the specific underlying mechanisms. Autophagy flux altered either by drugs or autophagy-targeting siRNAs strongly inhibited ciliogenesis, and this inhibition was affected by p62, an autophagy regulator, via Pten/Dvl2/AurKA signaling.

Glomus tumors are rare neoplasms that characteristically occur in subungual regions, but may also be found in other regions of the body. The clinical diagnosis of this tumor may be difficult if the tumor is located in an extradigital site. Most extradigital glomus tumors form in superficial locations. Herein, we present the case of a 34-year-old woman who experienced chronic knee pain with pinpoint tenderness resulting from a deep-seated periosteal glomus tumor of the distal femur. Extradigital glomus tumors should be considered in the differential diagnosis when characteristic clinical features and imaging findings indicative of glomus tumors are present, even if the tumor is located within deep tissues.

Osteoid osteomas are benign bone-forming lesions that usually present in adolescence. In patients with severe pain and those not responding to medication, surgical treatment should be considered. Medulloscopy is a standard arthroscopic technique for visualizing the intramedullary canal of the tibia. Herein, we report two patients with intramedullary osteoid osteomas in the posterior area of the tibia, which were successfully treated using medulloscopy. Hence, medulloscopy is an effective minimally invasive method in patients with intramedullary osteoid osteomas in the posterior tibial area.

Study DesignRadiographic review of healthy volunteers.PurposeTo determine the ideal sitting positions by measuring changes in lumbar lordosis (LL) and pelvic parameters (PPs) in various positions.Overview of LiteratureProlonged sitting is generally accepted as an important risk factor for low back pain (LBP). It is now recognized that spinopelvic alignment is important for maintaining an energy-efficient posture.MethodsLateral spine radiographs of thrirty healthy volunteers (male participants) were taken in standing and five sitting positions. Radiographic measurement of LL and PPs was performed in each position. Statistical analysis was performed to identify a correlation between changes in the LL and PPs in each positions.ResultsLL in standing was 48.5°±8.7°. Sitting significantly decreased LL and segmental angle when compared with standing (p

Anorectal melanoma is a rare neoplasm that accounts for less than 1-4% of anorectal malignant tumors. The main therapeutic modality for anorectal melanoma is surgical treatment, with abdominoperineal resection or wide local excision being the most common approaches. A 77-year-old male with a history of cerebral infarction and hypertension presented with anal bleeding. Here, we report a case of anorectal melanoma treated by endoscopic mucosal resection with adjuvant interferon therapy rather than surgical resection. The patient has been disease-free for 5 years after endoscopic treatment.

Purpose: To find out the factors suggesting lumbar segmental instability in patients with degenerative spondylolisthesis (DS) on conventional magnetic resonance imaging (MRI). Methods: Ninety-four patients with DS who underwent decompression surgery with or without fusion were selected. Patient demographics and findings on simple radiographs and MRI were analyzed. We divided patients into two groups by the presence of lumbar instability on simple standing plain radiographs and measured degeneration status of intervertebral discs and facet joints and distance of facet fluid signal on T2 axial MRI on each groups. The data were analyzed to find out the correlation between facet fluid signal and lumbar instability. Results: Sixty-three patients were confirmed to have lumbar instability (unstable group (UG), 67%), while 31 patients (stable group (SG), 33%) did not have instability on simple radiographs. The mean age was slightly older in SG ( p < 0.05) and SG patients’ degeneration status of intervertebral discs and facet joints was advanced than UG patients. Fifty-five of 63 patients had high signal intensity on T2-weighted MR images in the UG, but only 4 of 31 patients had high signal intensity in the SG ( p < 0.001) and UG patients have more larger facet joint distance than SG patients ( p < 0.001). Conclusion: High signal in facet joints on T2 MR images can be a useful factor suggestive of lumbar instability. Thus, the identification of fluid signal in the facet joints on MRI should raise the suspicion for lumbar instability and prompt additional evaluations such as with stress radiographs.

In this retrospective cross-sectional study, we quantitatively analyzed the tomographic features in the neural tissues around the optic disc in patients with diabetic retinopathy with and without panretinal photocoagulation. We analyzed 206 eyes, comprising 33 normal eyes in subjects without diabetes (group I), 30 eyes without diabetic retinopathy (group II), 66 eyes with non-proliferative diabetic retinopathy (group III), 45 eyes with panretinal photocoagulation (group IV), and 32 eyes with normal tension glaucoma (group V). Sequential images acquired using swept-source optical coherence tomography in three-dimensional mode were used to measure peripapillary retinal nerve fiber layer thickness, neuro-retinal rim thickness, anterior lamina cribrosa depth, prelaminar thickness, and thickness of the lamina cribrosa. The peripapillary retinal nerve fiber layer thickness and lamina cribrosa thickness were significantly thinner in group IV than in group III (p = 0.019 and p < 0.001). However, there was no significant difference in rim thickness, anterior lamina cribrosa depth, or prelaminar thickness between groups III and IV (p = 0.307, p = 0.877, and p = 0.212). Multivariate analysis revealed that time since panretinal photocoagulation and thickness of the lamina cribrosa had a significant effect on peripapillary retinal nerve fiber layer thickness (p < 0.001 and p = 0.014). In group IV, there was a negative correlation between time elapsed since panretinal photocoagulation and peripapillary retinal nerve fiber layer thickness, rim thickness, and thickness of the lamina cribrosa (r = -0.765, r = -0.490, and r = -0.419), but no correlation with prelaminar thickness or anterior lamina cribrosa depth (r = 0.104 and r = -0.171). Panretinal photocoagulation may be related to thinning of the peripapillary retinal nerve fiber layer, rim thickness, and lamina cribrosa, but not prelaminar thickness or anterior lamina cribrosa depth. These features are different from the peripapillary features of eyes with typical normal tension glaucoma.

Receptor for advanced glycation endproducts (RAGE) is a multi-ligand receptor that is able to bind several different ligands, including advanced glycation endproducts, high-mobility group protein (B)1 (HMGB1), S-100 calcium-binding protein, amyloid-β-protein, Mac-1, and phosphatidylserine. Its interaction is engaged in critical cellular processes, such as inflammation, proliferation, apoptosis, autophagy, and migration, and dysregulation of RAGE and its ligands leads to the development of numerous human diseases. In this review, we summarize the signaling pathways regulated by RAGE and its ligands identified up to date and demonstrate the effects of hyper-activation of RAGE signals on human diseases, focused mainly on renal disorders. Finally, we propose that RAGE and its ligands are the potential targets for the diagnosis, monitoring, and treatment of numerous renal diseases.

We examined the ways in which fenobam could promote not onlythe transduction of PEP-1-FK506BP into cells and tissues but alsothe neuroprotective effect of PEP-1-FK506BP against ischemicdamage. Fenobam strongly enhanced the protective effect ofPEP-1-FK506BP against H2O2-induced toxicity and DNAfragmentation in C6 cells. In addition, combinational treatment offenobam with PEP-1-FK506BP significantly inhibited the activationof Akt and MAPK induced by H2O2, compared to treatment withPEP-1-FK506BP alone. Interestingly, our results showed thatfenobam significantly increased the transduction of PEP-1-FK506BPinto both C6 cells and the hippocampus of gerbil brains.Subsequently, a transient ischemic gerbil model studydemonstrated that fenobam pretreatment led to the increasedneuroprotection of PEP-1-FK506BP in the CA1 region of thehippocampus. Therefore, these results suggest that fenobam can bea useful agent to enhance the transduction of therapeuticPEP-1-fusion proteins into cells and tissues, thereby promoting theirneuroprotective effects. [BMB Reports 2013; 46(11): 561-566]

microRNAs (miRNAs) are small non-coding RNAs that regulategene expression by targeting the 3’-untranslated region of multipletarget genes. Pathogenesis results from defects in several genesets; therefore, disease progression could be prevented usingmiRNAs targeting multiple genes. Moreover, recent studiessuggest that miRNAs reflect the stage of the specific disease, suchas carcinogenesis. Cystic diseases, including polycystic kidneydisease, polycystic liver disease, pancreatic cystic disease, andovarian cystic disease, have common processes of cyst formationin the specific organ. Specifically, epithelial cells initiate abnormalcell proliferation and apoptosis as a result of alterations to keygenes. Cysts are caused by fluid accumulation in the lumen.However, the molecular mechanisms underlying cyst formationand progression remain unclear. This review aims to introduce thekey miRNAs related to cyst formation, and we suggest thatmiRNAs could be useful biomarkers and potential therapeutictargets in several cystic diseases. [BMB Reports 2013; 46(7):338-345]

Polycystic kidney disease (PKD) is a common hereditarydisorder which is characterized by fluid-filled cysts in thekidney. Mutation in either PKD1, encoding polycystin-1 (PC1),or PKD2, encoding polycystin-2 (PC2), are causative genes ofPKD. Recent studies indicate that renal cilia, known asmechanosensors, detecting flow stimulation through renaltubules, have a critical function in maintaining homeostasis ofrenal epithelial cells. Because most proteins related to PKD arelocalized to renal cilia or have a function in ciliogenesis.PC1/PC2 heterodimer is localized to the cilia, playing a role incalcium channels. Also, disruptions of ciliary proteins, exceptfor PC1 and PC2, could be involved in the induction ofpolycystic kidney disease. Based on these findings, variousPKD mice models were produced to understand the roles ofprimary cilia defects in renal cyst formation. In this review, wewill describe the general role of cilia in renal epithelial cells,and the relationship between ciliary defects and PKD. We alsodiscuss mouse models of PKD related to ciliary defects basedon recent studies. [BMB Reports 2013; 46(2): 73-79]

Cyst formation is a major characteristic of ADPKD and iscaused by the abnormal proliferation of epithelial cells. Renalcyst formation disrupts renal function and induces diversecomplications. The mechanism of cyst formation is unclear.mIMCD-3 cells were established to develop simple epithelialcell cysts in 3-D culture. We confirmed previously that Mxi1plays a role in cyst formation in Mxi1-deficient mice. Cysts inMxi1 transfectanted cells were showed by collagen or mebiolgels in 3-D cell culture system. Causative genes of ADPKDwere measured by q RT-PCR. Herein, Mxi1 transfectants rarelyformed a simple epithelial cyst and induced cell death.Overexpression of Mxi1 resulted in a decrease in the PKD1,PKD2 and c-myc mRNA relating to the pathway of cystformation. These data indicate that Mxi1 influences cystformation of mIMCD-3 cells in 3-D culture and that Mxi1 maycontrol the mechanism of renal cyst formation. [BMB reports2012; 45(3): 189-193]

Autosomal dominant polycystic kidney disease (ADPKD) is characterized by formation of multiple fluid-filled cysts that expand over time and destroy renal architecture. The proteins encoded by the PKD1 and PKD2 genes, mutations in which account for nearly all cases of ADPKD, may help guard against cystogenesis. Previously developed mouse models of PKD1 and PKD2 demonstrated an embryonic lethal phenotype and massive cyst formation in the kidney, indicating that PKD1 and PKD2 probably play important roles during normal renal tubular development. However, their precise role in development and the cellular mechanisms of cyst formation induced by PKD1 and PKD2 mutations are not fully understood. To address this question, we presently created Pkd2 knockout and PKD2 transgenic mouse embryo fibroblasts. We used a mouse oligonucleotide microarray to identify messenger RNAs whose expression was altered by the overexpression of the PKD2 or knockout of the Pkd2. The majority of identified mutations was involved in critical biological processes, such as metabolism, transcription, cell adhesion, cell cycle, and signal transduction. Herein, we confirmed differential expressions of several genes including aquaporin-1, according to different PKD2 expression levels in ADPKD mouse models, through microarray analysis. These data may be helpful in PKD2-related mechanisms of ADPKD pathogenesis.

Mass effect from polycystic kidney and liver enlargement can result in significant clinical complications and symptoms in autosomal dominant polycystic kidney disease (ADPKD). In this single-center study, we examined the correlation of height-adjusted total liver volume (htTLV) and total kidney volume (htTKV) by CT imaging with hepatic complications (n = 461) and abdominal symptoms (n = 253) in patients with ADPKD. "Mass-effect" complications were assessed by review of medical records and abdominal symptoms, by a standardized research questionnaire. Overall, 91.8% of patients had 4 or more liver cysts on CT scans. Polycystic liver disease (PLD) was classified as none or mild (htTLV < 1,600 mL/m); moderate (1,600 ≤ htTLV

Hibernoma is a rare benign lipogenic tumor of brown fat that develops in a wide variety of locations. Although the features of hibernoma demonstrated by MRI resemble those of liposarcoma, recent FDG-PET/CT studies have documented higher radiotracer uptake than liposarcoma, suggesting that FDG/PET/CT is useful for differentiating hibernoma from liposarcoma. Here we report two cases of hibernoma that showed relatively lower SUVs than those reported previously, lying within the range for liposarcoma. Our findings emphasize that hibernoma needs to be included in the differential diagnosis of any fat-containing tumor showing intense accumulation by FDG-PET/CT. Although it is unlikely that such a rare condition could be reasonably diagnosed on the basis of MRI and FDG-PET/CT alone due to possible SUV overlap between hibernoma and liposarcoma, it is important to recognize this extremely rare lipogenic tumor for accurate diagnosis and appropriate management.

A 55-year-old female presented with bilateral progressive retinal vasculitis. She was on systemic and intravitreal steroids on the basis of uveitis work-up result (negative result including rapid plasma reagin), but her visual acuity continued to deteriorate to light perception only. Ocular examination showed retinal vasculitis, multiple yellow placoid lesions and severe macula edema in both eyes. Repeated work-up revealed positivity of fluorescent treponemal antibody-absorption in serum and subsequently in cerebrospinal fluid. Ocular syphilis was diagnosed. And intravenous penicillin G resulted in rapid resolution of vasculitis and macular edema. To avoid delay in the diagnosis of ocular syphilis, high index of suspicion and repeating serological tests (including both treponemal and non-treponemal tests) are warranted.

Paraoxonase 1 (PON1) is an antioxidant enzyme which plays a central role in various diseases. However, the mechanism and function of PON1 protein in inflammation are poorly understood. Since PON1 protein alone cannot be delivered into cells, we generated a cell permeable PEP-1-PON1 protein using protein transduction domains, and examined whether it can protect against cell death in lipopolysaccharide (LPS) or hydrogen peroxide (H2O2)-treated Raw 264.7 cells as well as mice with 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced skin inflammation. We demonstrated that PEP-1-PON1 protein transduced into Raw 264.7 cells and markedly protected against LPS or H2O2-induced cell death by inhibiting cellular reactive oxygen species (ROS) levels, the inflammatory mediator's expression, activation of mitogen-activated protein kinases (MAPKs) and cellular apoptosis. Furthermore, topically applied PEP-1-PON1 protein ameliorates TPA-treated mice skin inflammation via a reduction of inflammatory response. Our results indicate that PEP-1-PON1 protein plays a key role in inflammation and oxidative stress in vitro and in vivo. Therefore, we suggest that PEP-1-PON1 protein may provide a potential protein therapy against oxidative stress and inflammation.

Deposition of polysilicon (poly-Si) was tried to increase productivity of poly-Si by using two different types of gas nozzle in a monosilane Bell-jar Siemens (MS-Siemens) reactor. In a mass production of poly-Si, deposition rate and energy consumption are very important factors because they are main performance indicators of Siemens reactor and they are directly related with the production cost of poly-Si. Type A and B nozzles were used for investigating gas nozzle effect on the deposition of poly-Si in a MS-Siemens reactor. Nozzle design was analyzed by computation cluid dynamics (CFD). Deposition rate and energy consumption of poly-Si were increased when the type B nozzle was used. The highest deposition rate was 1 mm/h, and the lowest energy consumption was 72 kWh⋅kg-1 in this study.