Dynamic electrical synapses rewire brain networks for persistent oscillations and epileptogenesis.

One of the very fundamental attributes for telencephalic neural computation in mammals involves network activities oscillating beyond the initial trigger. The continuing and automated processing of transient inputs shall constitute the basis of cognition and intelligence but may lead to neuropsychiatric disorders such as epileptic seizures if carried so far as to engross part of or the whole telencephalic system. From a conventional view of the basic design of the telencephalic local circuitry, the GABAergic interneurons (INs) and glutamatergic pyramidal neurons (PNs) make negative feedback loops which would regulate the neural activities back to the original state. The drive for the most intriguing self-perpetuating telencephalic activities, then, has not been posed and characterized. We found activity-dependent deployment and delineated functional consequences of the electrical synapses directly linking INs and PNs in the amygdala, a prototypical telencephalic circuitry. These electrical synapses endow INs dual (a faster excitatory and a slower inhibitory) actions on PNs, providing a network-intrinsic excitatory drive that fuels the IN-PN interconnected circuitries and enables persistent oscillations with preservation of GABAergic negative feedback. Moreover, the entities of electrical synapses between INs and PNs are engaged in and disengaged from functioning in a highly dynamic way according to neural activities, which then determine the spatiotemporal scale of recruited oscillating networks. This study uncovers a special wide-range and context-dependent plasticity for wiring/rewiring of brain networks. Epileptogenesis or a wide spectrum of clinical disorders may ensue, however, from different scales of pathological extension of this unique form of telencephalic plasticity.

Is extended resection for locally advanced thoracic cancer with cardiopulmonary bypass justified?

BACKGROUND: Resection of intrathoracic tumor with cardiopulmonary bypass (CPB) remains a relatively under-reported intervention in literature, and its role in managing locally advanced mediastinal and lung cancers is a topic of ongoing debate. Our aim was to review our experience and assess the role of CPB for treating locally advanced mediastinal and lung cancers. METHODS: Between 2015 and 2020, this study initially included 10 patients with primary locally advanced thoracic malignancies with apparent adjacent cardiovascular invasion demonstrated by thoracic imaging scans. Operation was performed based on a multidisciplinary tumor board consensus. Eventually, 8 patients (3 primary lung cancers and 5 mediastinal cancers) received either salvage or elective resection with CPB; two completed surgery without requiring CPB. RESULTS: Regarding the extent of adjacent structure involvement, 4 patients presented with involvement of the superior vena cava (SVC), 1 involved the right atrium (RA), 2 involved the SVC and RA, and 1 involved the SVC, the origin of main pulmonary artery, and the ascending aorta. Thirty-day mortality occurred in two of three patients receiving salvage surgery due to respiratory insufficiency. With the long-term follow-up, one patient died of recurrence 25 months postoperatively, one survived with recurrence 30 months postoperatively, and four were alive without recurrence for 35, 36, 49, and 107 months after operations. CONCLUSION: In certain patients, particularly for elective surgical candidates rather than salvage resection, CPB allows for extended resection of locally advanced thoracic cancers with acceptable perioperative safety and survival.

Surface Functional Groups Affect Iron (Hydr)oxide Heterogeneous Nucleation: Implications for Membrane Scaling.

Because of its favorable thermodynamics and fast kinetics, heterogeneous solid nucleation on membranes triggers early-stage mineral scaling. Iron (hydr)oxide, a typical membrane scale, initially forms as nanoparticles that interact with surface functional groups on membranes, but these nanoscale phenomena are difficult to observe in real time. In this study, we utilized in situ grazing incidence small angle X-ray scattering and ex situ atomic force microscopy to examine the heterogeneous nucleation of iron (hydr)oxide on surface functional groups commonly used in membranes, including hydroxyl (OH), carboxyl (COOH), and fluoro (F) groups. We found that, compared to nucleation on hydrophilic OH- and COOH-surfaces, the high hydrophobicity of an F-modified surface significantly reduced the extents of both heterogeneously and homogeneously formed iron (hydr)oxide nucleation. Moreover, on the OH-surface, the high functional group density of 0.76 nmol/cm2 caused faster heterogeneous nucleation than that on a COOH-surface, with a density of 0.28 ± 0.04 nmol/cm2. The F-surface also had the highest heterogeneous nucleation energy barrier (26 ± 0.6 kJ/mol), followed by COOH- (23 ± 0.8 kJ/mol) and OH- (20 ± 0.9 kJ/mol) surfaces. The kinetic and thermodynamic information provided here will help us better predict the rates and extents of early-stage scaling of iron (hydr)oxide nanoparticles in membrane processes.

HSP90-CDC37 functions as a chaperone for the oncogenic FGFR3-TACC3 fusion.

The FGFR3-TACC3 (F3-T3) fusion gene was discovered as an oncogenic molecule in glioblastoma and bladder cancers, and has subsequently been found in many cancer types. Notably, F3-T3 was found to be highly expressed in both untreated and matched recurrence glioblastoma under the concurrent radiotherapy and temozolomide (TMZ) treatment, suggesting that targeting F3-T3 is a valid strategy for treatment. Here, we show that the F3-T3 protein is a client of heat shock protein 90 (HSP90), forming a ternary complex with the cell division cycle 37 (CDC37). Deprivation of HSP90 or CDC37 disrupts the formation of the ternary complex, which destabilizes glycosylated F3-T3, and thereby suppresses F3-T3 oncogenic activity. Gliomas harboring F3-T3 are resistant to TMZ chemotherapy. HSP90 inhibitors sensitized F3-T3 glioma cells to TMZ via the inhibition of F3-T3 activation and potentiated TMZ-induced DNA damage. These results demonstrate that F3-T3 oncogenic function is dependent on the HSP90 chaperone system and suggests a new clinical option for targeting this genetic aberration in cancer.

Skp2-Mediated RagA Ubiquitination Elicits a Negative Feedback to Prevent Amino-Acid-Dependent mTORC1 Hyperactivation by Recruiting GATOR1.

The regulation of RagA(GTP) is important for amino-acid-induced mTORC1 activation. Although GATOR1 complex has been identified as a negative regulator for mTORC1 by hydrolyzing RagA(GTP), how GATOR1 is recruited to RagA to attenuate mTORC1 signaling remains unclear. Moreover, how mTORC1 signaling is terminated upon amino acid stimulation is also unknown. We show that the recruitment of GATOR1 to RagA is induced by amino acids in an mTORC1-dependent manner. Skp2 E3 ligase drives K63-linked ubiquitination of RagA, which facilitates GATOR1 recruitment and RagA(GTP) hydrolysis, thereby providing a negative feedback loop to attenuate mTORC1 lysosomal recruitment and prevent mTORC1 hyperactivation. We further demonstrate that Skp2 promotes autophagy but inhibits cell size and cilia growth through RagA ubiquitination and mTORC1 inhibition. We thereby propose a negative feedback whereby Skp2-mediated RagA ubiquitination recruits GATOR1 to restrict mTORC1 signaling upon sustained amino acid stimulation, which serves a critical mechanism to maintain proper cellular functions.

Hierarchical multiple regression investigating factors associated with depressive symptoms in the middle-aged and elderly undergoing haemodialysis.

BACKGROUND: Depressive moods are commonly seen in patients who receive haemodialysis. This can cause a lack of compliance in their treatment procedures and increase the rate of hospitalization. This study aimed to investigate the relationship between social support and degree of depression in middle-aged and elderly patients undergoing haemodialysis and the predictors of depressive symptoms. METHODS: A cross-sectional correlational study was designed with a structured questionnaire survey. Patients over 40 years of age were included from five haemodialysis centres. Measures embraced a demographic and clinical characteristics questionnaire, the Centre for Epidemiologic Studies Depression Scale, and the Personal Resource Questionnaire 2000. Statistical analysis was performed using hierarchical multiple regression analysis. RESULTS: A total of 179 patients over 40 years of age were included from five haemodialysis centres in the analysis. The mean CES-D score was 19.0(12.3); the majority of participants (60.3%) had a CES-D score ≥ 15, indicating likely depressive status. The mean PRQ2000 score was 75.7(15.9). The proportional mean of the PRQ2000 was 72.11%, indicating moderate social support for participants in this study. Data disclosed that marital status, number of comorbidities, exercise behaviour, and social support could significantly predict depressive symptoms; total explanatory variance was 31.3%. CONCLUSION: Health care professionals should identify those at high risk of depressive symptoms when they provide care to the middle-aged and elderly patients undergoing haemodialysis. These findings may lead to greater insights into the nursing and rehabilitative care of patients treated by chronic maintenance haemodialysis.

Dynamic Resource Allocation for Network Slicing with Multi-Tenants in 5G Two-Tier Networks.

Virtualization is a core 5G network technology which helps telecom companies significantly reduce capital expenditure and operating expenses by deploying multiple services on the same hardware infrastructure. However, providing QoS-guaranteed services for multi-tenants poses a significant challenge due to multi-tenant service diversity. Network slicing has been proposed as a means of addressing this problem by isolating computing and communication resources for the different tenants of different services. However, optimizing the allocation of the network and computation resources across multiple network slices is a critical but extremely difficult problem. Accordingly, this study proposes two heuristic algorithms, namely Minimum Cost Resource Allocation (MCRA) and Fast Latency Decrease Resource Allocation (FLDRA), to perform dynamic path routing and resource allocation for multi-tenant network slices in a two-tier architecture. The simulation results show that both algorithms significantly outperform the Upper-tier First with Latency-bounded Overprovisioning Prevention (UFLOP) algorithm proposed in previous work. Furthermore, the MCRA algorithm achieves a higher resource utilization than the FLDRA algorithm.

The Prognostic Biomarkers of Plasma Trimethylamine N-Oxide and Short-Chain Fatty Acids for Recanalization Therapy in Acute Ischemic Stroke.

Bidirectional communication of the microbiota-gut-brain axis is crucial in stroke. Recanalization therapy, namely intravenous thrombolysis (IVT) and endovascular thrombectomy (EVT), are recommended for eligible patients with acute ischemic stroke (AIS). It remains unclear whether gut microbiota metabolites, namely trimethylamine N-oxide (TMAO) and short-chain fatty acids (SCFAs), can predict the prognosis after recanalization therapy. This prospective study recruited patients with AIS receiving IVT, EVT, or both. The National Institutes of Health Stroke Scale (NIHSS) and modified Rankin scale (mRS) scores were used to assess the severity and functional outcomes of AIS, respectively. A functional outcome of mild-to-moderate disability was defined as a mRS score of 0-3 at discharge. Plasma TMAO and SCFA levels were measured through liquid chromatography with triple-quadrupole mass spectrometry. Fifty-six adults undergoing recanalization therapy for AIS were enrolled. Results showed that TMAO levels were not associated with stroke severity and functional outcomes, while isovalerate levels (one of the SCFAs) were negatively correlated with NIHSS scores at admission and discharge. In addition, high isovalerate levels were independently associated with a decreased likelihood of severe disability. The study concluded that an elevated plasma isovalerate level was correlated with mild stroke severity and disability after recanalization therapy for AIS.

Hyperbaric Oxygen Therapy Alleviates Paclitaxel-Induced Peripheral Neuropathy Involving Suppressing TLR4-MyD88-NF-κB Signaling Pathway.

Paclitaxel (PAC) results in long-term chemotherapy-induced peripheral neuropathy (CIPN). The coexpression of transient receptor potential vanilloid 1 (TRPV1) and Toll-like receptor 4 (TLR4) in the nervous system plays an essential role in mediating CIPN. In this study, we used a TLR4 agonist (lipopolysaccharide, LPS) and a TLR4 antagonist (TAK-242) in the CIPN rat model to investigate the role of TLR4-MyD88 signaling in the antinociceptive effects of hyper-baric oxygen therapy (HBOT). All rats, except a control group, received PAC to induce CIPN. Aside from the PAC group, four residual groups were treated with either LPS or TAK-242, and two of them received an additional one-week HBOT (PAC/LPS/HBOT and PAC/TAK-242/HBOT group). Mechanical allodynia and thermal hyperalgesia were then assessed. The expressions of TRPV1, TLR4 and its downstream signaling molecule, MyD88, were investigated. The mechanical and thermal tests revealed that HBOT and TAK-242 alleviated behavioral signs of CIPN. Immunofluorescence in the spinal cord dorsal horn and dorsal root ganglion revealed that TLR4 overexpression in PAC- and PAC/LPS-treated rats was significantly downregulated after HBOT and TAK-242. Additionally, Western blots showed a significant reduction in TLR4, TRPV1, MyD88 and NF-κB. Therefore, we suggest that HBOT may alleviate CIPN by modulating the TLR4-MyD88-NF-κB pathway.

Autologous Fat Grafting in Female Genital Area Improves Sexual Function by Increasing Collagenesis, Angiogenesis, and Estrogen Receptors.

BACKGROUND: Vulvovaginal laxity, atrophic vaginitis, and orgasmic dysfunction are not only aesthetic but also sexual problems. Autologous fat grafting (AFG) facilitates tissue rejuvenation through the effects of adipose-derived stem cells; the fat grafts serve as soft-tissue filler. However, few studies have reported the clinical outcomes of patients undergoing vulvovaginal AFG. OBJECTIVES: The aim of this study was to describe a new technique, micro-autologous fat transplantation (MAFT), for AFG in the vulvovaginal area. Posttreatment histologic changes in the vaginal canal that imply improved sexual function were assessed. METHODS: This retrospective study enrolled females who underwent vulvovaginal AFG performed through MAFT between June 2017 and 2020. Assessments were based on the Female Sexual Function Index (FSFI) questionnaire and on histologic and immunohistochemical staining. RESULTS: In total, 20 female patients (mean age, 38.1 years) were included. On average, 21.9 mL of fat was injected into the vagina and 20.8 mL in the vulva and mons pubis area. Six months afterwards, the patients' mean total FSFI score (68.6) was significantly higher than that at baseline (43.8; P < .001). Histologic and immunohistochemical staining of vaginal tissues revealed substantially increased levels of neocollagenesis, neoangiogenesis, and estrogen receptors. By contrast, the level of protein gene product 9.5, which is associated with neuropathic pain, was considerably lower after AFG. CONCLUSIONS: AFG performed through MAFT in the vulvovaginal area may help manage sexual function-related problems in females. In addition, this technique improves aesthetics, restores tissue volume, alleviates dyspareunia with lubrication, and reduces scar tissue pain.

How Can an Na+ Channel Inhibitor Ameliorate Seizures in Lennox-Gastaut Syndrome?

OBJECTIVE: Lennox-Gastaut syndrome (LGS) is an epileptic encephalopathy frequently associated with multiple types of seizures. The classical Na+ channel inhibitors are in general ineffective against the seizures in LGS. Rufinamide is a new Na+ channel inhibitor, but approved for the treatment of LGS. This is not consistent with a choice of antiseizure drugs (ASDs) according to simplistic categorical grouping. METHODS: The effect of rufinamide on the Na+ channel, cellular discharges, and seizure behaviors was quantitatively characterized in native neurons and mammalian models of epilepsy, and compared with the other Na+ channel inhibitors. RESULTS: With a much faster binding rate to the inactivated Na+ channel than phenytoin, rufinamide is distinctively effective if the seizure discharges chiefly involve short bursts interspersed with hyperpolarized interburst intervals, exemplified by spike and wave discharges (SWDs) on electroencephalograms. Consistently, rufinamide, but not phenytoin, suppresses SWD-associated seizures in pentylenetetrazol or AY-9944 models, which recapitulate the major electrophysiological and behavioral manifestations in typical and atypical absence seizures, including LGS. INTERPRETATION: Na+ channel inhibitors shall have sufficiently fast binding to exert an action during the short bursts and then suppress SWDs, in which cases rufinamide is superior. For the epileptiform discharges where the interburst intervals are not so hyperpolarized, phenytoin could be better because of the higher affinity. Na+ channel inhibitors with different binding kinetics and affinity to the inactivated channels may have different antiseizure scope. A rational choice of ASDs according to in-depth molecular pharmacology and the attributes of ictal discharges is advisable. ANN NEUROL 2021;89:1099-1113.

Impact of the CYP2D6 single nucleotide polymorphism on the concentration of and therapeutic response to donepezil in mild-to-moderate Alzheimer's disease.

BACKGROUND/PURPOSE: Donepezil was approved for the treatment of Alzheimer's disease (AD) but causes variable therapeutic responses. Thus, identifying specific genetic polymorphisms, which can predict a therapeutic response to donepezil, would enable a development of personalized strategy to treatment for patients with AD. The research aimed to exam the impact of the cytochrome P450 2D6 (CYP2D6) single nucleotide polymorphism (SNP) rs1080985 on the concentration of and therapeutic response to donepezil in AD. METHODS: In total, 40 newly diagnosed AD patients who had a clinical dementia rating (CDR) of 0.5-2 and who were on donepezil were enrolled and followed up. Plasma concentrations of donepezil were determined after 6 months of donepezil treatment. Cognitive and functional statuses were evaluated annually during follow-up. The response to therapy was defined based on the change in CDR. RESULTS: At a mean of 21.8 ± 5.7 months of follow-up, 10 of 40 patients (25.0%) were nonresponders to donepezil treatment. Patients who were homozygous for the G allele exhibited a higher concentration of donepezil and concentration-to-dose ratio than those with other genotypes. Furthermore, a significantly higher proportion of patients with the G/G genotype were responders than nonresponders (90.0% vs 50.0%, P = 0.015, effect size of V: 0.457) to donepezil treatment. Conversely, patients carrying the C allele had a significantly high risk of poor responses to donepezil treatment (odds ratio: 9.00, 95% confidence interval: 1.611-50.275). CONCLUSION: The CYP2D6 SNP rs1080985 might be a useful pharmacogenetic marker of the long-term therapeutic response to donepezil in patients with AD.

Thoracoscopic Repair of Adult-Onset Congenital Tracheoesophageal Fistula Using a Polyglycolic Acid Sheet-Buttressed Stapler.

Congenital tracheoesophageal fistula (TEF) without esophageal atresia is usually diagnosed and treated in the neonatal period. It is uncommon to occur in adulthood. Conventional treatment of adult-onset TEF involves repair by either cervicotomy or thoracotomy. We reported the case of a 31-year-old male patient with clinical and radiographic evidence of congenital H-type TEF. Although this fistula was located at the level of the second thoracic vertebra, the repair of the anomaly was performed successfully using a thoracoscopic approach with the novel use of a polyglycolic acid sheet reinforcement.

Concurrence of Marjolin's Ulcer in the Lower Limb in a Patient with Idiopathic Multicentric Castleman Disease: A Case Report.

Idiopathic multicentric Castleman disease (iMCD) is characterized by the benign proliferation of lymphoid cells in multiple regions. However, the co-occurrence of epithelial malignancy and idiopathic multicentric Castleman disease (iMCD) is rarely reported. Herein, we present a case of iMCD mimicking lymph nodal metastasis of Marjolin's ulcer in the lower extremity. A 53-year-old male presented with an unhealed chronic ulcer on the left lower leg and foot accompanied by an enlarged mass in the left inguinal region. Intralesional biopsy was performed, and pathological examination showed squamous cell carcinoma (SCC). Imaged studies revealed left calcaneus bone invasion, and lymph nodal metastasis was suspected by the cancer TNM staging of T4N2M0 pre-operatively. The patient received below-knee amputation and lymph node dissection; intraoperative histological examination showed no lymphatic nodal malignancy and diagnosed the patient as having iMCD with lymphadenopathy. The patient recovered uneventfully and was referred to a hematologist for further treatment.

Glutamate transmission rather than cellular pacemaking propels excitatory-inhibitory resonance for ictogenesis in amygdala.

Epileptic seizures are automatic, excessive, and synchronized neuronal activities originating from many brain regions especially the amygdala, the allocortices and neocortices. This may reflect a shared principle for network organization and signaling in these telencephalic structures. In theory, the automaticity of epileptic discharges may stem from spontaneously active "oscillator" neurons equipped with intrinsic pacemaking conductances, or from a group of synaptically-connected collaborating "resonator" neurons. In the basolateral amygdalar (BLA) network of pyramidal-inhibitory (PN-IN) neuronal resonators, we demonstrated that rhythmogenic currents are provided by glutamatergic rather than the classic intrinsic or cellular pacemaking conductances (namely the h currents). The excitatory output of glutamatergic neurons such as PNs presumably propels a novel network-based "relay burst mode" of discharges especially in INs, which precondition PNs into a state prone to burst discharges and thus further glutamate release. Also, selective activation of unilateral PNs, but never INs, readily drives bilateral BLA networks into reverberating discharges which are fully synchronized with the behavioral manifestations of seizures (e.g. muscle contractions). Seizures originating in BLA and/or the other structures with similar PN-IN networks thus could be viewed as glutamate-triggered erroneous network oscillations that are normally responsible for information relay.

Effects of MoS2 Layer Thickness on Its Photochemically Driven Oxidative Dissolution.

The distinctive optical and electronic properties of two-dimensional (2D) molybdenum disulfide (MoS2) make it a promising photocatalyst and photothermal agent in aqueous applications. In terms of environmental stability, MoS2 has been considered insoluble, but 2D MoS2 nanosheets can be susceptible to dissolution, owing to their large surface areas and highly accessible reactive sites, including defects at the basal plane and edge sites. Under light illumination, the dissolution of 2D MoS2 nanosheets can be further accelerated by their photochemical reactivity. To elucidate MoS2 reactivity in the environment, here we investigated the thickness-dependent dissolution of MoS2 under illumination. To synthesize nanoscale thicknesses of MoS2, we exfoliated bulk MoS2 by ultrasonication and controlled the layer thickness by iterative cascade centrifugation, producing MoS2 nanosheets averaging either ∼18 nm or ∼46 nm thick, depending on the centrifugation rate. Under simulated sunlight, MoS2 dissolution was accelerated, the Mo6+ composition increased, and the solution pH decreased compared to those in the dark. These results suggest that light exposure promotes the oxidation of MoS2, causing faster dissolution. Importantly, 18 nm thick MoS2 exhibited faster dissolution than either 46 nm or bulk MoS2, driven by the superoxide radical (O2•-) generation promoted by its relative thinness. These findings highlight the important role of the thickness-dependent photochemistry of MoS2 nanosheets in their dissolution, which is directly linked to their environmental behavior and stability.

Simultaneous hyperbaric oxygen therapy during systemic chemotherapy reverses chemotherapy-induced peripheral neuropathy by inhibiting TLR4 and TRPV1 activation in the central and peripheral nervous system.

BACKGROUND AND OBJECTIVES: Chemotherapy-induced peripheral neuropathy (CIPN) is considered one of the most common sequelae in patients with cancer who experience consistent abnormal sensations or pain symptoms during or after paclitaxel (PAC) chemotherapy. Transient receptor potential vanilloid 1 (TRPV1) and toll-like receptor 4 (TLR4) have been reported to interact in the nervous system in patients with CIPN. The antinociceptive effects of hyperbaric oxygen therapy (HBOT) on CIPN was demonstrated in this study through behavior tests. Using a CIPN rat model, we examined the effects of simultaneous HBOT (SHBOT) administration during chemotherapy and discovered that SHBOT achieved better reversal effects than chemotherapy alone. MATERIALS AND METHODS: Twenty-four rats were randomly allocated to four groups: control, PAC, SHBOT, and HBOT after PAC groups. Behavior tests were performed to evaluate mechanical allodynia and thermal hyperalgesia status. Tissues from the spinal cord and dorsal root ganglions were collected, and TLR4 and TRPV1 expression and microglial activation were investigated through immunofluorescence (IF) staining. RESULTS: The mechanical and thermal behavior tests revealed that HBOT intervention during PAC treatment led to the early alleviation of CIPN symptoms and inhibited CIPN deterioration. IF staining revealed that TLR4, TRPV1, and microglial activation were all upregulated in PAC-injected rats and exhibited early and significant downregulation in SHBOT-treated rats. CONCLUSION: This study is the first to demonstrate that the use of SHBOT during PAC treatment has potential for the early suppression of CIPN initiation and deterioration, indicating that it can alleviate CIPN symptoms and may reverse CIPN in patients undergoing systemic chemotherapy.

Supercritical Carbon Dioxide-decellularized Porcine Acellular Dermal Matrix combined with Autologous Adipose-derived Stem Cells: Its Role in Accelerated Diabetic Wound Healing.

Diabetes mellitus (DM) causes impaired wound healing by affecting one or more of the biological mechanisms of hemostasis, inflammation, proliferation, and remodeling and a large number of cell types, extracellular components, growth factors, and cytokines. Interventions targeted toward these mechanisms might accelerate the wound healing process. To evaluate the wound healing efficacy of supercritical carbon dioxide (scCO2)-decellularized porcine acellular dermal matrix (ADM) combined with autologous adipose-derived stem cells (ASCs) in streptozotocin (STZ)-induced DM rats. DM was induced by injecting rats with STZ; dorsal full-thickness skin (5 × 5 cm2) was created and treated with and without ASCs-scCO2-treated ADM to evaluate the wound healing rate through histological examination, fluorescence microscopic observation, and immunohistochemical analysis. In the present study, complete decellularization of the porcine dermal matrix was achieved through scCO2. Isolation of ASCs was conducted and evaluated using CD29+/CD31-/CD45-/CD90+ markers in flow cytometry, which indicated that more than 90% of cells were ASCs. The percentage of cells labeled with CD29+ and CD90+ was found to be 97.50% and 99.69%, respectively. The wound healing rate increased in all groups relative to the group with the DM wound without treatment. DM wound treated with ADM-ASCs showed significantly higher (p < 0.01) wound healing rate than DM wound without treatment. ADM-ASC-treated rats showed significantly increased epidermal growth factor, Ki67, and prolyl 4-hydroxylase and significantly decreased CD45 compared with the group with the DM wound without treatment. The intervention comprising ADM decellularized from porcine skin by using scCO2 and ASCs was proven to improve diabetic wound healing. ADM-ASCs had a positive effect on epidermal regeneration, anti-inflammation, collagen production and processing, and cell proliferation; thus, it accelerated wound healing.

Reconstruction for Defects of Total Nail Bed and Germinal Matrix Loss with Acellular Dermal Matrix Coverage and Subsequently Skin Graft.

Background and Objectives: Nail bed and germinal matrix loss due to wide excision for fingertip tumors or malignancy are occasionally encountered complications. These defects also result from severely comminuted fingertip crush injuries. Large-area dorsal finger or toenail bed defects, which usually present with phalangeal bone exposure, remain challenging regardless of the usage of different reconstruction strategies. This study aimed to evaluate the clinical outcome of a staged operation with an acellular dermal matrix coverage and subsequent skin graft as reconstruction for defects of total nail bed, germinal matrix loss, and bone exposure. Materials and Methods: From April 2018 to October 2019, four patients with total nail bed, germinal matrix, and bone exposure loss after surgery were enrolled in our series. A staged operation of the acellular dermal matrix coverage with subsequent skin graft was performed on these patients. Skin graft take rate, oncological prognosis, and cosmetic outcome were evaluated. Patients were followed up for 5-13 months. An excellent skin graft take rate with a satisfying aesthetic result without local malignancy recurrence was noted. Minimal functional deficit and donor site morbidity were reported. Results: A staged operation with acellular dermal matrix coverage and subsequent skin graft proves to serve as a feasible strategy for patients who experience total nail bed, germinal matrix loss, and bone exposure after surgery. Conclusions: This reconstruction method provides a reliable repair result, satisfying aesthetic outcomes, as well as having minimal functional deficits and donor site morbidity.

Hybrid light field head-mounted display using time-multiplexed liquid crystal lens array for resolution enhancement.

In recent years, head-mounted display technologies have greatly advanced. In order to overcome the accommodation-convergence conflict, light field displays reconstruct three-dimensional (3D) images with a focusing cue but sacrifice resolution. In this paper, a hybrid head-mounted display system that is based on a liquid crystal microlens array is proposed. By using a time-multiplexed method, the display signals can be divided into light field and two-dimensional (2D) modes to show comfortable 3D images with high resolution compensated by the 2D image. According to the experimental results, the prototype supports a 12.28 ppd resolution in the diagonal direction, which reaches 82% of the traditional virtual reality (VR) head-mounted display (HMD).