μPADS were fabricated by inkjet printing of permanent marker ink on filter paper, followed by evaporation of solvent.

Practical application of wearable gas-sensing devices has been greatly inhibited by the poorly sensitive and specific recognition of target gases. Rapid charge transfer caused by rich sensory neurons in the biological olfactory system has inspired the construction of a highly sensitive sensor network with abundant defect sites for adsorption. Herein, for the first time, we demonstrate an in situ formed neuron-mimic gas sensor in a single gas-sensing channel, which is derived from lattice deviation of S atoms in Bi2S3 nanosheets induced by gold quantum dots. Due to the favorable gas adsorption and charge transfer properties arising from S vacancies, the fabricated sensor exhibits a significantly enhanced response value of 5.6–5 ppm NO2, ultrafast response/recovery performance (18 and 338 s), and excellent selectivity. Furthermore, real-time visual detection of target gases has been accomplished by integrating the flexible sensor into a wearable device.

No abstract

Pain is prevalent in advanced malignancies; however, some patients cannot get adequate pain relief by conservative routes of analgesic administration or experience serious side effects related to high dose of opioids. For those who have exhausted multimodal conservative analgesic, intrathecal drug delivery is an alternative intervention for truly effective pain management. The objective of this study was to evaluate the clinical efficacy and safety of intrathecal drug delivery system (IDDS) for the treatment of intractable pain in advanced cancer patients.A prospective cohort study was performed between July 2015 and October 2016. Fifty-three patients undergoing intractable cancer-related pain or intolerable drug-related adverse effects were recruited and received IDDS therapy with a patient-controlled intrathecal analgesia pump. The assessment was conducted during admission, in titration period, and followed up monthly to death by scheduled refill visits. Pain numeric rating scale scores, comprehensive toxicity scores, quality of life scores, systemic opioid use (basal and breakthrough dose), intrathecal morphine use (basal and patient-controlled intrathecal analgesia dose), and complications were recorded to evaluate the curative effect and safety.Between baseline and all subsequent follow-ups, statistically significant decreases in pain numeric rating scale scores and comprehensive toxicity scores were verified. A statistical improvement in quality of life scores was found after starting IDDS therapy. Both basal and breakthrough doses of systemic opioid showed a significant decrease during the follow-up period. And there was a modest escalation in the intrathecal morphine dose throughout the duration of study. No infective, device-related, and catheter-related complications were observed.The findings showed that IDDS therapy allowed for rapid and highly effective pain relief with less toxicity in comparison to conservative medications. Patients with advanced malignancies would also benefit from an improvement in the life quality after the procedure. IDDS therapy represented a valuable option for intractable cancer-related pain management.

The NLRC4 inflammasome, a member of the nucleotide-binding and oligomerization domain-like receptor (NLR) family, amplifies inflammation by facilitating the processing of caspase-1, interleukin (IL)–1β, and IL-18. We explored whether NLRC4 knockdown alleviated inflammatory injury following intracerebral hemorrhage (ICH). Furthermore, we investigated whether NLRC4 inflammasome activation can be adjusted by the regulator of G protein signaling 2/leucine-rich repeat kinase-2 pathway. Fifty microliters of arterial blood was drawn and injected into the basal ganglion to simulate the ICH model. NLRC4 small interfering RNAs (siRNAs) were utilized to knockdown NLRC4. An LRRK2 inhibitor (GNE7915) was injected into the abdominal cavity. Short hairpin (sh) RNA lentiviruses and lentiviruses containing RGS2 were designed and applied to knockdown and promote RGS2 expression. Neurological functions, brain edema, Western blot, enzyme-linked immunosorbent, hematoxylin and eosin staining, Nissl staining, immunoprecipitation, immunofluorescence assay and Evans blue dye extravasation and autofluorescence assay were evaluated. It was shown that the NLRC4 inflammasome was activated following ICH injury. NLRC4 knockdown extenuated neuronal death, damage to the blood-brain barrier, brain edema and neurological deficiency 3 days after ICH. NLRC4 knockdown reduced myeloperoxidase (MPO) cells as well as tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β and IL-18 following ICH. GNE7915 reduced pNLRC4 and NLRC4 inflammasome activation. RGS2 suppressed the interaction of LRRK2 and NLRC4 and NLRC4 inflammasome activation by regulating pLRRK2. Our study demonstrated that the NLRC4 inflammasome may aggravate the inflammatory injury induced by ICH and that RGS2/LRRK2 may relieve inflammatory injury by restraining NLRC4 inflammasome activation.

Objective: This study aimed to estimate risk factors associated with recurrence after radiofrequency thermocoagulation (RFT) of the Gasserian ganglion among a large sample of patients with trigeminal neuralgia (TN) during a long-term follow-up. Materials and Methods: We performed a multicenter retrospective analysis of data from 1481 patients with TN who underwent RFT from 2005 through 2017. Recurrence-free survival (RFS) was assessed by the Kaplan-Meier method. Risk factors of all patient characteristics were determined by using univariate and multivariate Cox regression analysis. Prognostic value was determined by prognostic index (PI) with regression coefficients and receiver-operating characteristic curve model. Results: The median of RFS was 136 months (95% confidence interval [CI]: 123.5-148.5). The rate of RFS was 85.3% (95% CI: 83.5%-87.1%) at 1 year, 74.6% (95% CI: 72.2%-77.0%) at 3 years, 68.0% (95% CI: 65.5%-70.5%) at 5 years, and 54.9% (95% CI: 51.6%-58.2%) at 10 years. Multivariate analysis showed that atypical facial pain (hazard ratio [HR]=16.914, 95% CI: 13.117-21.808, P<0.001), Barrow Neurological Institute (BNI) Class II/III facial hypesthesia before undergoing RFT (HR=2.47, 95% CI: 1.52-4.016, P<0.001)/(HR=3.288, 95% CI: 1.035-10.433, P=0.044), and history of previous microvascular decompression/RFT/neurosurgeries≥2 (HR=1.642, 95% CI: 0.941-2.863, P=0.041)/(HR=2.808, 95% CI: 1.819-4.334, P<0.001)/(HR=3.83, 95% CI: 1.802-8.146, P<0.001) were independently associated with RFS. Patients with PI>0.764 were identified as high-risk patients for TN recurrence with a median RFS of 36 months (95% CI: 23.9-48.1) compared with those with PI<0.764 (HR=6.785, 95% CI: 5.371-8.573, P<0.001). Discussion: Our results indicated the patients with a higher risk for recurrence after RFT for the treatment of TN. In addition, our findings might provide support for clinical decision-making before the RFT procedure.

No abstract

This is an open access article under the CC BY-NC license. www.medicaljournals.se/acta