A Novel Air-Cooled Nd:YAG Laser for the Treatment of the Venous Lakes of the Lips.

Objective: To evaluate the therapeutic effect of a novel air-cooled Nd:YAG laser in the venous lakes of the lips (VLL). Background: The thermal injury is one of the most important issues during laser therapy for venous lakes. Methods: Six pieces of fresh pork livers were used to provide 30 regions with a diameter of 6 mm for experiment in vitro, among which 15 regions were treated by Nd:YAG laser with air cooling until the tissue turned gray-white, whereas the rest were treated without air cooling as control. The operation time of laser irradiation, the degree of temperature increase, and the depth of coagulation tissue were compared between two groups. Then, 60 VLL patients were selected for Nd:YAG laser treatment with or without air cooling. The operation time of laser irradiation, the degree of temperature increase, the postoperative pain visual analog scale (VAS) score, and the percentage of lesions removed within 1 month were compared. Results: In tissue studies, the treated group showed a longer operation time of laser irradiation (p < 0.01), a lower degree of temperature increase (p < 0.01), and there was no significant statistical difference in the depth of coagulation tissue (p = 0.624). In clinical studies, the treated group showed a longer operation time of laser irradiation (p < 0.01), a lower degree of temperature increase (p < 0.01), and a lower VAS score on the 1st and 2nd day, compared with the control group (p < 0.01). Conclusions: Air cooling during Nd:YAG laser for the treatment of VLL can prolong the surgical time, but lowered tissue temperature and reduced patient pain within 2 days under the premise of ensuring the treatment effect.

Understanding the Neural Mechanisms of General Anesthesia from Interaction with Sleep-Wake State: A Decade of Discovery.

The development of cutting-edge techniques to study specific brain regions and neural circuits that regulate sleep-wake brain states and general anesthesia (GA), has increased our understanding of these states that exhibit similar neurophysiologic traits. This review summarizes current knowledge focusing on cell subtypes and neural circuits that control wakefulness, rapid eye movement (REM) sleep, non-REM sleep, and GA. We also review novel insights into their interactions and raise unresolved questions and challenges in this field. Comparisons of the overlapping neural substrates of sleep-wake and GA regulation will help us to understand sleep-wake transitions and how anesthetics cause reversible loss of consciousness. SIGNIFICANCE STATEMENT: General anesthesia (GA), sharing numerous neurophysiologic traits with the process of natural sleep, is administered to millions of surgical patients annually. In the past decade, studies exploring the neural mechanisms underlying sleep-wake and GA have advanced our understanding of their interactions and how anesthetics cause reversible loss of consciousness. Pharmacotherapies targeting the neural substrates associated with sleep-wake and GA regulations have significance for clinical practice in GA and sleep medicine.

Chromium-Modified Ultrathin CoFe LDH as High-Efficiency Electrode for Hydrogen Evolution Reaction.

Hydrogen evolution reaction (HER) has a dominant function in energy conversion and storage because it supplies a most effective way for converting electricity into sustainable high-purity hydrogen. Layered double hydroxides (LDHs) have shown promising performance in the process of electrochemical water oxidation (a half-reaction for water splitting). Nevertheless, HER properties have not been well released due to the structural characteristics of related materials. Herein, a simple and scalable tactics is developed to synthesize chromium-doped CoFe LDH (CoFeCr LDH). Thanks to oxygen vacancy, optimized electronic structure and interconnected array hierarchical structure, our developed ternary CoFeCr-based layered double hydroxide catalysts can provide 10 mA cm-2 current density at -0.201 V vs. RHE with superior long-term stability in alkaline electrolyte. We anticipate that the simple but feasible polymetallic electronic modulation strategy can strengthen the electrocatalytic property of the layered double hydroxides established in the present study, based on a carbon neutral and hydrogen economy.

RN181 regulates the biological behaviors of oral squamous cell carcinoma cells via mediating ERK/MAPK signaling pathway.

OBJECTIVE: To explore the role of RN181 in the pathogenesis of oral squamous cell carcinoma (OSCC) cells via mediating ERK/MAPK signaling. METHODS: The expression of RN181 was detected in OSCC tissues and cells. CAL27 and SCC-15 cells were divided into Control, Empty, RN181, si-RN181, U0126 (an inhibitor of ERK/MAPK pathway) and si-RN181 + U0126 groups. MTT was used to determine cell proliferation, flow cytometry to determine cell cycle and apoptosis, Transwell assay and wound healing test to determine cell invasion and migration, respectively. Western blotting was used to measure the protein expression. Furthermore, a xenograft tumor model was established to observe the effect of RN181 on the in vivo growth of OSCC cells. RESULTS: RN181 was down-regulated in OSCC tissues and cells. As compared to the Control group, CAL27 and SCC-15 cells in the RN181 group and U0126 group presented with decreases in the proliferation, invasion and migration, but increases in the cell ratio at the G0/G1 phase and apoptosis, while the p-ERK 1/2/ERK 1/2 was down-regulated. Cells in the si-RN181 group manifested the opposite changes. U0126 could reverse the positive effect of si-RN181 on the growth of OSCC cells. In vivo experiment demonstrated that the tumor growth and weight were reduced in the RN181 group, with decreased Ki67 positive expression and elevated TUNEL positive cells. CONCLUSION: RN181 was down-regulated in OSCC, and it could inhibit the proliferation, invasion and migration, cause the G0/G1 arrest, while promote the apoptosis of OSCC cells via inhibiting ERK/MAPK pathway.

Nucleus accumbens neurons expressing dopamine D1 receptors modulate states of consciousness in sevoflurane anesthesia.

Although general anesthesia (GA) enables patients to undergo surgery without consciousness, the precise neural mechanisms underlying this phenomenon have yet to be identified. In addition to many studies over the past two decades implicating the thalamus, cortex, brainstem, and conventional sleep-wake circuits in GA-induced loss of consciousness (LOC), some recent studies have begun to highlight the importance of other brain areas as well. Here, we found that population activities of neurons expressing dopamine D1 receptor (D1R) in the nucleus accumbens (NAc), a critical interface between the basal ganglia and limbic system, began to decrease before sevoflurane-induced LOC and gradually returned after recovery of consciousness (ROC). Chemogenetic activation of NAcD1R neurons delayed induction of and accelerated emergence from sevoflurane GA, whereas chemogenetic inhibition of NAcD1R neurons exerted opposite effects. Moreover, transient activation of NAcD1R neurons induced significant cortical activation and behavioral emergence during continuous steady-state GA with sevoflurane or deep anesthesia state with constant and stable burst-suppression oscillations. Taken together, our findings uncover that NAcD1R neurons modulated states of consciousness associated with sevoflurane GA and may represent an area for targeting GA-induced changes in consciousness and ameliorating related adverse effects.

Hierarchical iron molybdate nanostructure array for efficient water oxidation through optimizing electron density.

The water oxidation reaction plays a major role in many alternative-energy systems because it provides the electrons and protons required for the use of renewable electricity. We report the tuning of the iron molybdate (FeMoO4) electron structure via a coupled interface between the catalytic centers and the substrate. Our developed FeMoO4 catalysts can provide a 50 mA cm-2 current density at 1.506 V vs. RHE with excellent stability in 1.0 M KOH. The improved performance can be ascribed to the synergy of the optimized electronic structures and hierarchical nanostructure.

MiR-590-5p regulates cell proliferation, apoptosis, migration and invasion in oral squamous cell carcinoma by targeting RECK.

OBJECTIVE: To discover the role of miR-590-5p in oral squamous cell carcinoma (OSCC) progression and the corresponding mechanism via the targeting RECK. METHODS: OSCC (n=85) and normal oral tissues (n=60) were collected to quantify the miR-590-5p expression by using qRT-PCR. Then SCC-15 and OEC-M1 cells were selected and divided into Mock, inhibitor NC, miR-590-5p inhibitor, si-RECK and miR-590-5p inhibitor + si-RECK groups. Dual-luciferase reporter gene assay was used to verify if miR-590-5p could target RECK. The biological behaviors of OSCC cells were evaluated by MTT, Wound-healing, Transwell and Flow cytometry. The expression of miR-590-5p and RECK was measured by qRT-PCR and Western blotting , respectively. RESULTS: Overexpression of miR-590-5p was found in OSCC tissues. The expression of miR-590-5p was significantly associated with the clinical TNM stage, differentiation degree, and lymph node metastasis of OSCC. RECK was identified as a direct target of miR-590-5p. Compared with the Mock group, cells in the miR-590-5p inhibitor group were decreased in terms of proliferation, invasion, and migration, and increased in cell apoptosis, accompanied by down-regulated miR-590-5p, Bcl-2/Bax and MMP-9, and up-regulated RECK. By contrast, si-RECK group presented completely opposite changes, and si-RECK reversed the inhibitory effect of miR-590-5p inhibitor on the OSCC cell growth. CONCLUSION: MiR-590-5p expression was obviously increased in OSCC, and inhibiting miR-590-5p enhanced the expression of its target gene RECK, thereby suppressing proliferation, migration and invasion of OSCC cells and promoting apoptosis of OSCC cells.

Ultrafast formation of an FeOOH electrocatalyst on Ni for efficient alkaline water and urea oxidation.

We report FeOOH supported on Ni foam which enables highly efficient UOR electrocatalysis and can be readily produced through a hydrolysis reaction. Our developed UOR catalyst as the anode can provide a current density of 200 mA cm-2 at 1.427 V vs. RHE, as well as remarkable operational stability, representing the best yet reported noble metal-free urea electrolyser.

Diketopyrrolopyrrole (DPP)-Based Materials and Its Applications: A Review.

Diketopyrrolopyrrole (DPP) and its derivatives have been widely studied in the past few years due to its intrinsic physical and chemical properties, such as strong electron-withdrawing, deep color, high charge carrier mobility, strong aggregation, good thermal-/photo-stability. In the 1970s, DPP was developed and used only in inks, paints, and plastics. Later, DPP containing materials were found to have potential other applications, typically in electronic devices, which attracted the attention of scientists. In this feature article, the synthesis pathway of DPP-based materials and their applications in organic field-effect transistors, photovoltaic devices, sensors, two photo-absorption materials, and others are reviewed, and possible future applications are discussed. The review outlines a theoretical scaffold for the development of conjugated DPP-based materials, which have multiple potential applications.

LncRNA DANCR regulates the growth and metastasis of oral squamous cell carcinoma cells via altering miR-216a-5p expression.

The study aims to investigate how DANCR can alter the growth and metastasis of oral squamous cell carcinoma (OSCC) cells by regulating miR-216a-5p. The expression of DANCR and miR-216a-5p in OSCC patients and cells were measured. SCC15 and CAL-27 cells were selected to divide into Control, sh-NC, DANCR shRNA, DANCR, miR-216a-5p mimic, and DANCR + miR-216a-5p mimic groups. Dual-luciferase reporter gene assay was performed for the verification of the targeting relationship between miR-216a-5p and DANCR/Bcl-2/KLF12. We also quantified the abilities of OSCC cells regarding proliferation, invasion, migration and apoptosis, and the expression levels of apoptosis-related proteins were measured. Finally, the tumor-bearing nude mice were established to verify the effect of DANCR in vivo. Up-regulated DANCR expression and down-regulated miR-216a-5p expression were observed in both OSCC tissues and cells, and they were proven strongly correlated to the histological grade, clinical staging and lymph node metastasis of OSCC patients. Dual-luciferase reporter gene assay showed a target relationship between DANCR and miR-216a-5p, as well as between miR-216a-5p and Bcl-2/KLF12. Both DANCR shRNA and miR-216a-5p mimic decreased proliferative, migration and invasive abilities of OSCC cells with increased cell apoptosis. However, DANCR group showed completely opposite trends. Moreover, miR-216a-5p mimic could reverse the role of DANCR in promoting tumor growth. In-vivo experiment confirmed the inhibitory role of DANCR shRNA in tumor growth and metastasis. We concluded that DANCR may promote the growth and metastasis of OSCC cells and suppress OSCC cell apoptosis by sponging miR-216a-5p.