J-Net: Improved U-Net for Terahertz Image Super-Resolution.

Terahertz (THz) waves are electromagnetic waves in the 0.1 to 10 THz frequency range, and THz imaging is utilized in a range of applications, including security inspections, biomedical fields, and the non-destructive examination of materials. However, THz images have a low resolution due to the long wavelength of THz waves. Therefore, improving the resolution of THz images is a current hot research topic. We propose a novel network architecture called J-Net, which is an improved version of U-Net, to achieve THz image super-resolution. It employs simple baseline blocks which can extract low-resolution (LR) image features and learn the mapping of LR images to high-resolution (HR) images efficiently. All training was conducted using the DIV2K+Flickr2K dataset, and we employed the peak signal-to-noise ratio (PSNR) for quantitative comparison. In our comparisons with other THz image super-resolution methods, J-Net achieved a PSNR of 32.52 dB, surpassing other techniques by more than 1 dB. J-Net also demonstrates superior performance on real THz images compared to other methods. Experiments show that the proposed J-Net achieves a better PSNR and visual improvement compared with other THz image super-resolution methods.

Wideband SiGe-HBT Low-Noise Amplifier with Resistive Feedback and Shunt Peaking.

In this work, the design of a wideband low-noise amplifier (LNA) using a resistive feedback network is proposed for potential multi-band sensing, communication, and radar applications. For achieving wide operational bandwidth and flat in-band characteristics simultaneously, the proposed LNA employs a variety of circuit design techniques, including a voltage-current (shunt-shunt) negative feedback configuration, inductive emitter degeneration, a main branch with an added cascode stage, and the shunt-peaking technique. The use of a feedback network and emitter degeneration provides broadened transfer characteristics for multi-octave coverage and a real impedance for input matching, respectively. In addition, the cascode stage pushes the band-limiting low-frequency pole, due to the Miller capacitance, to a higher frequency. Lastly, the shunt-peaking approach is optimized for the compensation of a gain reduction at higher frequency bands. The wideband LNA proposed in this study is fabricated using a commercial 0.13 µm silicon-germanium (SiGe) BiCMOS process, employing SiGe heterojunction bipolar transistors (HBTs) as the circuit's core active elements in the main branch. The measurement results show an operational bandwidth of 2.0-29.2 GHz, a noise figure of 4.16 dB (below 26.5 GHz, which was the measurement limit), and a total power consumption of 23.1 mW under a supply voltage of 3.3 V. Regarding the nonlinearity associated with large-signal behavior, the proposed LNA exhibits an input 1-dB compression (IP1dB) point of -5.42 dBm at 12 GHz. These performance numbers confirm the strong viability of the proposed approach in comparison with other state-of-the-art designs.

SNX10-mediated degradation of LAMP2A by NSAIDs inhibits chaperone-mediated autophagy and induces hepatic lipid accumulation.

Rationale: While some non-steroidal anti-inflammatory drugs (NSAIDs) are reported to induce hepatic steatosis, the molecular mechanisms are poorly understood. This study presented the mechanism by which NSAIDs induce hepatic lipid accumulation. Methods: Mouse primary hepatocytes and HepG2 cells were used to examine the underlying mechanism of NSAID-induced hepatic steatosis. Lipid accumulation was measured using Nile-red assay and BODIPY 493/503. The activity of chaperone-mediated autophagy (CMA) was determined by western blotting, qRT-PCR, and confocal imaging. The effect of NSAID on CMA inhibition was evaluated in vivo using diclofenac and CMA activator (AR7) administered mice. Results: All tested NSAIDs in this study accumulated neutral lipids in hepatocytes, diclofenac having demonstrated the most potency in that regard. Diclofenac-induced lipid accumulation was confirmed in both mouse primary hepatocytes and the liver of mice. NSAIDs inhibited CMA, as reflected by the decreased expression of lysosome-associated membrane glycoprotein 2 isoform A (LAMP2A) protein, the increased expression of CMA substrate proteins such as PLIN2, and the decreased activity of photoactivatable KFERQ-PAmCherry reporter. Reactivation of CMA by treatment with AR7 or overexpression of LAMP2A inhibited diclofenac-induced lipid accumulation and hepatotoxicity. Upregulation of sorting nexin 10 (SNX10) via the CHOP-dependent endoplasmic reticulum stress response and thus maturation of cathepsin A (CTSA) was shown to be responsible for the lysosomal degradation of LAMP2A by diclofenac. Conclusion: We demonstrated that NSAIDs induced SNX10- and CTSA-dependent degradation of LAMP2A, thereby leading to the suppression of CMA. In turn, impaired CMA failed to degrade PLIN2 and disrupted cellular lipid homeostasis, thus leading to NSAID-induced steatosis and hepatotoxicity.

Correlation Between Maximal Tongue Pressure and Swallowing Function in Spinal and Bulbar Muscular Atrophy.

Background: Spinal and bulbar muscular atrophy (SBMA) is an X-lined motor neuron disease characterized by progressive muscle weakness, bulbar palsy, and dysphagia. Dysphagia is associated with tongue weakness, which is a common manifestation of SBMA. This study aimed to investigate the correlations between tongue pressure and dysphagia in patients with SBMA. Materials and Methods: Thirty-nine genetically confirmed SBMA patients underwent a videofluoroscopic swallowing study (VFSS) and tongue pressure assessment. Then, we analyzed the maximal tongue pressure (MTP), oral transit time, penetration-aspiration scale (PAS), videofluoroscopic dysphagia scale (VDS), amyotrophic lateral sclerosis functional rating scale-revised (ALSFRS-R), and 6-min walk test (6MWT). Pearson and Spearman correlation coefficients were calculated to analyze the association of the MTP with clinical, swallowing, and functional parameters. Results: In the correlation analysis, MTP was negatively correlated with disease duration (r = -0.396, p = 0.013) and VDS (r = -0.426, p = 0.007), and positively correlated with ALSFRS-R (r = 0.483, p = 0.002) and 6MWT (r = 0.396, p = 0.013). The bulbar (r = 0.367, p = 0.022) and gross motor (r = 0.486, p = 0.002) domains of the ALSFRS-R were correlated with MTP. Conclusion: Tongue pressure assessment can be used as a safe and easy tool to assess swallowing function in SBMA patients. Moreover, MTP reflects functional states, including activities of daily living and gait performance, showing it to be a potential biomarker for physical performance in SBMA.

Effects of Self RehAbilitation Video Exercises (SAVE) on Functional Restorations in Patients with Subacute Stroke.

Background: Additional exercise therapy has been shown to positively affect acute stroke rehabilitation, which requires an effective method to deliver increased exercise. In this study, we designed a 4-week caregiver-supervised self-exercise program with videos, named "Self rehAbilitation Video Exercises (SAVE)", to improve the functional outcomes and facilitate early recovery by increasing the continuity of rehabilitation therapy after acute stroke. Methods: This study is a non-randomized trial. Eighty-eight patients were included in an intervention group (SAVE group), who received conventional rehabilitation therapies and an additional self-rehabilitation session by watching bedside exercise videos and continued their own exercises in their rooms for 60 min every day for 4 weeks. Ninety-six patients were included in a control group, who received only conventional rehabilitation therapies. After 4 weeks of hospitalization, both groups assessed several outcome measurements, including the Berg Balance Scale (BBS), Modified Barthel Index (MBI), physical component summary (PCS) and the mental component summary of the Short-Form Survey 36 (SF-36), Mini-Mental State Examination, and Beck Depression Inventory. Results: Differences in BBS, MBI, and PCS components in SF-36 were more statistically significant in the SAVE group than that in the control group (p < 0.05). Patients in the SAVE group showed more significant improvement in BBS, MBI, and PCS components in SF-36 as compared to that in the control group. Conclusions: This evidence-based SAVE intervention can optimize patient recovery after a subacute stroke while keeping the available resources in mind.

Inversion Table Fall Injury, the Phantom Menace: Three Case Reports on Cervical Spinal Cord Injury.

BACKGROUND: An inversion device, which is used to suspend one's body and perform traction therapy, was introduced as an inversion table under the name of "Geokkuri" in South Korea. Fall injuries while hanging on inversion tables are among the most devastating spine injuries, as the likelihood of severe neurological sequelae such as tetraplegia increases. However, its enormous danger has been overlooked and this devastating injury has become a common clinical entity over time. The limited number of studies reported imply the lack of interest of researchers in these injuries. We reviewed three cases of spinal cord injury sustained on inversion tables in different environments and report the potential danger associated with the use of inversion tables to facilitate a safer exercise environment.

Alterations of functional connectivity in auditory and sensorimotor neural networks: A case report in a patient with cortical deafness after bilateral putaminal hemorrhagic stroke.

RATIONALE: Cortical deafness is a rare auditory dysfunction caused by damage to brain auditory networks. The aim was to report alterations of functional connectivity in intrinsic auditory, motor, and sensory networks in a cortical deafness patient. PATIENT CONCERNS: A 41-year-old woman suffered a right putaminal hemorrhage. Eight years earlier, she had suffered a left putaminal hemorrhage and had minimal sequelae. She had quadriparesis, imbalance, hypoesthesia, and complete hearing loss. DIAGNOSES: She was diagnosed with cortical deafness. After 6 months, resting-state functional magnetic resonance imaging (rs-fMRI) and diffuse tensor imaging (DTI) were performed. DTI revealed that the acoustic radiation was disrupted while the corticospinal tract and somatosensory track were intact using deterministic tracking methods. Furthermore, the patient showed decreased functional connectivity between auditory and sensorimotor networks. INTERVENTIONS: The patient underwent in-patient stroke rehabilitation therapy for 2 months. OUTCOMES: Gait function and ability for activities of daily living were improved. However, complete hearing impairment persisted in 6 months after bilateral putaminal hemorrhagic stroke. LESSONS: Our case report seems to suggest that functional alterations of spontaneous neuronal activity in auditory and sensorimotor networks are related to motor and sensory impairments in a patient with cortical deafness.

Diclofenac impairs autophagic flux via oxidative stress and lysosomal dysfunction: Implications for hepatotoxicity.

Treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with various side effects, including cardiovascular and hepatic disorders. Studies suggest that mitochondrial damage and oxidative stress are important mediators of toxicity, yet the underlying mechanisms are poorly understood. In this study, we identified that some NSAIDs, including diclofenac, inhibit autophagic flux in hepatocytes. Further detailed studies demonstrated that diclofenac induced a reactive oxygen species (ROS)-dependent increase in lysosomal pH, attenuated cathepsin activity and blocked autophagosome-lysosome fusion. The reactivation of lysosomal function by treatment with clioquinol or transfection with the transcription factor EB restored lysosomal pH and thus autophagic flux. The production of mitochondrial ROS is critical for this process since scavenging ROS reversed lysosomal dysfunction and activated autophagic flux. The compromised lysosomal activity induced by diclofenac also inhibited the fusion with and degradation of mitochondria by mitophagy. Diclofenac-induced cell death and hepatotoxicity were effectively protected by rapamycin. Thus, we demonstrated that diclofenac induces the intracellular ROS production and lysosomal dysfunction that lead to the suppression of autophagy. Impaired autophagy fails to maintain mitochondrial integrity and aggravates the cellular ROS burden, which leads to diclofenac-induced hepatotoxicity.

Prediction of Motor Recovery in Patients with Basal Ganglia Hemorrhage Using Diffusion Tensor Imaging.

Predicting prognosis in patients with basal ganglia hemorrhage is difficult. This study aimed to investigate the usefulness of diffusion tensor imaging in predicting motor outcome after basal ganglia hemorrhage. A total of 12 patients with putaminal hemorrhage were included in the study (aged 50 ± 12 years), 8 patients were male (aged 46 ± 11 years) and 4 were female (aged 59 ± 9 years). We performed diffusion tensor imaging and measured clinical outcome at baseline (pre) and 3 weeks (post1), 3 months (post2), and 6 months (post3) after the initial treatment. In the affected side of the brain, the mean fractional anisotropy (FA) value on pons was significantly higher in the good outcome group than that in the poor outcome group at pre (p = 0.004) and post3 (p = 0.025). Pearson correlation analysis showed that mean FA value at pre significantly correlated with the sum of the Brunnstrom motor recovery stage scores at post3 (R = 0.8, p = 0.002). Change in the FA ratio on diffusion tractography can predict motor recovery after hemorrhagic stroke.

Interhemispheric Functional Connectivity in the Primary Motor Cortex Assessed by Resting-State Functional Magnetic Resonance Imaging Aids Long-Term Recovery Prediction among Subacute Stroke Patients with Severe Hand Weakness.

This study aimed to evaluate the usefulness of interhemispheric functional connectivity (FC) as a predictor of motor recovery in severe hand impairment and to determine the cutoff FC level as a clinically useful parameter. Patients with stroke (n = 22; age, 59.9 ± 13.7 years) who presented with unilateral severe upper-limb paresis and were confirmed to elicit no motor-evoked potential responses were selected. FC was measured using resting-state functional magnetic resonance imaging (rsfMRI) scans at 1 month from stroke onset. The good recovery group showed a higher FC value than the poor recovery group (p = 0.034). In contrast, there was no statistical difference in FC value between the good recovery and healthy control groups (p = 0.182). Additionally, the healthy control group showed a higher FC value than that shown by the poor recovery group (p = 0.0002). Good and poor recovery were determined based on Brunnstrom stage of upper-limb function at 6 months as the standard, and receiver operating characteristic curve indicated that a cutoff score of 0.013 had the greatest prognostic ability. In conclusion, interhemispheric FC measurement using rsfMRI scans may provide useful clinical information for predicting hand motor recovery during stroke rehabilitation.

Downregulation of PHGDH expression and hepatic serine level contribute to the development of fatty liver disease.

OBJECTIVE: Supplementation with serine attenuates alcoholic fatty liver by regulating homocysteine metabolism and lipogenesis. However, little is known about serine metabolism in fatty liver disease (FLD). We aimed to investigate the changes in serine biosynthetic pathways in humans and animal models of fatty liver and their contribution to the development of FLD. METHODS: High-fat diet (HFD)-induced steatosis and methionine-choline-deficient diet-induced steatohepatitis animal models were employed. Human serum samples were obtained from patients with FLD whose proton density fat fraction was estimated by magnetic resonance imaging. 3-Phosphoglycerate dehydrogenase (Phgdh)-knockout mouse embryonic fibroblasts (MEF) and transgenic mice overexpressing Phgdh (Tg-phgdh) were used to evaluate the role of serine metabolism in the development of FLD. RESULTS: Expression of Phgdh was markedly reduced in the animal models. There were significant negative correlations of the serum serine with the liver fat fraction, serum alanine transaminase, and triglyceride levels among patients with FLD. Increased lipid accumulation and reduced NAD+ and SIRT1 activity were observed in Phgdh-knockout MEF and primary hepatocytes incubated with free fatty acids; these effects were reversed by overexpression of Phgdh. Tg-Phgdh mice showed significantly reduced hepatic triglyceride accumulation compared with wild-type littermates fed a HFD, which was accompanied by increased SIRT1 activity and reduced expression of lipogenic genes and proteins. CONCLUSIONS: Human and experimental data suggest that reduced Phgdh expression and serine levels are closely associated with the development of FLD.

Hepatic upregulation of fetuin-A mediates acetaminophen-induced liver injury through activation of TLR4 in mice.

Acetaminophen (APAP)-induced liver injury (AILI) is initiated by the generation of a reactive metabolite and ultimately leads to hepatocyte necrosis. Necrotic cells secrete damage-associated molecular patterns that activate hepatic nonparenchymal cells and induce an inflammatory response. Fetuin-A is a hepatokine with reported involvement in low-grade inflammation in many diseases, due to acting as an endogenous ligand for TLR4. However, little is known about the role of fetuin-A in AILI. In this study, we showed that fetuin-A is involved in the aggravation of hepatotoxicity during the initial phase of AILI progression. Treatment with APAP increased the expression and serum levels of fetuin-A in mice. Fetuin-A upregulated transcription of pro-inflammatory cytokines and chemokines through activation of TLR4 and also increased monocyte infiltration into the liver, leading to necroinflammatory reactions in AILI. However, these reactions were attenuated with the silencing of fetuin-A using adenoviral shRNA. As a result, mice with silenced fetuin-A exhibited less centrilobular necrosis and liver injury compared to controls in response to APAP. In conclusion, our results suggest that fetuin-A is an important hepatokine that mediates the hepatotoxicity of APAP through production of chemokines and thus regulates the infiltration of monocytes into the liver, a critical event in the inflammatory response during the initial phase of AILI. Our results indicate that a strategy based on the antagonism of fetuin-A may be a novel therapeutic approach to the treatment of acetaminophen-induced acute liver failure.

Activation of AMPK by berberine induces hepatic lipid accumulation by upregulation of fatty acid translocase CD36 in mice.

Emerging evidence has shown that berberine has a protective effect against metabolic syndrome such as obesity and type II diabetes mellitus by activating AMP-activated protein kinase (AMPK). AMPK induces CD36 trafficking to the sarcolemma for fatty acid uptake and oxidation in contracting muscle. However, little is known about the effects of AMPK on CD36 regulation in the liver. We investigated whether AMPK activation by berberine affects CD36 expression and fatty acid uptake in hepatocytes and whether it is linked to hepatic lipid accumulation. Activation of AMPK by berberine or transduction with adenoviral vectors encoding constitutively active AMPK in HepG2 and mouse primary hepatocytes increased the expression and membrane translocation of CD36, resulting in enhanced fatty acid uptake and lipid accumulation as determined by BODIPY-C16 and Nile red fluorescence, respectively. Activation of AMPK by berberine induced the phosphorylation of extracellular signal-regulated kinases 1/2 (ERK1/2) and subsequently induced CCAAT/enhancer-binding protein ß (C/EBPß) binding to the C/EBP-response element in the CD36 promoter in hepatocytes. In addition, hepatic CD36 expression and triglyceride levels were increased in normal diet-fed mice treated with berberine, but completely prevented when hepatic CD36 was silenced with adenovirus containing CD36-specific shRNA. Taken together, prolonged activation of AMPK by berberine increased CD36 expression in hepatocytes, resulting in fatty acid uptake via processes linked to hepatocellular lipid accumulation and fatty liver.

Inhibition of homocysteine-induced endoplasmic reticulum stress and endothelial cell damage by l-serine and glycine.

Hyperhomocysteinemia is an independent risk factor for several cardiovascular diseases. The use of vitamins to modulate homocysteine metabolism substantially lowers the risk by reducing plasma homocysteine levels. In this study, we evaluated the effects of l-serine and related amino acids on homocysteine-induced endoplasmic reticulum (ER) stress and endothelial cell damage using EA.hy926 human endothelial cells. Homocysteine treatment decreased cell viability and increased apoptosis, which were reversed by cotreatment with l-serine. l-Serine inhibited homocysteine-induced ER stress as verified by decreased glucose-regulated protein 78kDa (GRP78) and C/EBP homologous protein (CHOP) expression as well as X-box binding protein 1 (xbp1) mRNA splicing. The effects of l-serine on homocysteine-induced ER stress are not attributed to intracellular homocysteine metabolism, but instead to decreased homocysteine uptake. Glycine exerted effects on homocysteine-induced ER stress, apoptosis, and cell viability that were comparable to those of l-serine. Although glycine did not affect homocysteine uptake or export, coincubation of homocysteine with glycine for 24h reduced the intracellular concentration of homocysteine. Taken together, l-serine and glycine cause homocysteine-induced endothelial cell damage by reducing the level of intracellular homocysteine. l-Serine acts by competitively inhibiting homocysteine uptake in the cells. However, the mechanism(s) by which glycine lowers homocysteine levels are unclear.

Increased hepatic Fatty Acid uptake and esterification contribute to tetracycline-induced steatosis in mice.

Tetracycline induces microvesicular steatosis, which has a poor long-term prognosis and a higher risk of steatohepatitis development compared with macrovesicular steatosis. Recent gene expression studies indicated that tetracycline treatment affects the expression of many genes associated with fatty acid transport and esterification. In this study, we investigated the role of fatty acid transport and esterification in tetracycline-induced steatosis. Intracellular lipid accumulation and the protein expression of fatty acid translocase (FAT or CD36) and diacylglycerol acyltransferase (DGAT) 2 were increased in both mouse liver and HepG2 cells treated with tetracycline at 50 mg/kg (intraperitoneal injection, i.p.) and 100 µM, respectively. Tetracycline increased the cellular uptake of boron-dipyrromethene-labeled C16 fatty acid, which was abolished by CD36 RNA interference. Oleate-induced cellular lipid accumulation was further enhanced by co-incubation with tetracycline. Tetracycline downregulated extracellular signal-regulated kinase (ERK) phosphorylation, which negatively regulated DGAT2 expression. U0126, a specific ERK inhibitor, also increased DGAT2 expression and cellular lipid accumulation. DGAT1 and 2 knock-down with specific small interfering (si)-RNA completely abrogated the steatogenic effect of tetracycline in HepG2 cells. Taken together, our data showed that tetracycline induces lipid accumulation by facilitating fatty acid transport and triglyceride esterification by upregulating CD36 and DGAT2, respectively.

Torsade de pointes in liver transplantation recipient after induction of general anesthesia: a case report.

Torsade de pointes (TdP) is an uncommon and specific form of polymorphic ventricular tachycardia, associated with a prolonged QT interval. Prolongation of the QT interval is the most widely recognized electrophysiological abnormality in patients with liver cirrhosis. We observed a case of TdP leading to cardiopulmonary resuscitation after the induction of general anesthesia, in a patient with liver cirrhosis scheduled for emergency cadaveric donor liver transplantation. The patient had mild QT prolongation on preoperative electrocardiography with a corrected QT (QTc) interval of 455 ms. Drugs used in the preoperative period can elongate cardiac repolarization. Sevoflurane and 5-hydroxytryptamine type 3 receptor antagonists such as palonsetron, used during general anesthesia may have triggered further QT prolongation, producing a fatal condition such as TdP. More caution and consideration in selecting drugs for anesthetic management are necessary for liver cirrhosis patients, especially in patients with preoperative QT prolongation.

The effects of single-dose intravenous dexmedetomidine on hyperbaric bupivacaine spinal anesthesia.

PURPOSE: Dexmedetomidine, a selective α2-adrenoceptor agonist, has analgesic and sedative effects. The purpose of this study was to investigate the effects of small, single-dose intravenous dexmedetomidine administration after hyperbaric bupivacaine spinal anesthesia. METHODS: Sixty adult patients classified as American Society of Anesthesiologists physical status 1 or 2 and scheduled for lower extremity surgery under spinal anesthesia were studied. Patients were randomly assigned to one of three groups and administered hyperbaric intrathecal bupivacaine 12 mg. 5 min after spinal anesthesia, patients in groups 1, 2, and 3 received normal saline 10 ml, dexmedetomidine 0.25 µg/kg, and dexmedetomidine 0.5 µg/kg, respectively, over 10-min intravenous administration. The onset time, maximum block level, two-dermatome sensory regression time, duration of motor and sensory anesthesia, and side effects were assessed. RESULTS: The two-dermatome sensory regression time was significantly increased in groups 2 and 3. The duration of motor and sensory anesthesia was significantly increased in group 3. Onset time, maximum block level, level of sedation, and incidence of hypotension and treatment-needed bradycardia were no different among the groups. CONCLUSION: Single-dose intravenous dexmedetomidine 0.25-0.5 µg/kg, administered 5 min after intrathecal injection of hyperbaric bupivacaine, improved the duration of spinal anesthesia without significant side effects. This method may be useful for increasing the duration of spinal anesthesia, even after intrathecal injection of local anesthetics.

Spontaneous retropharyngeal hematoma - a case report -.

Spontaneous retropharyngeal hematoma is rare and difficult to diagnosis early. A 23-year-old male spontaneously developed acute onset of neck pain, limitation of neck motion, and mild dysphagia. Magnetic resonance imaging demonstrated blood products in prevertebral space from C2 to C4, suggesting a diagnosis of retropharyngeal hematoma. We report a rare case of spontaneous retropharyngeal hematoma causing neck pain.