Relationship between ultra-short heart rate variability and short-term mortality in hospitalized COVID-19 patients.

OBJECTIVE: To assess the association between ultra-short heart rate variability (US-HRV) and short-term mortality in patients with COVID-19 and develop prognostic prediction models to identify high-risk patients as early as possible. METHODS: A retrospective cohort study was performed on 488 patients diagnosed with COVID-19 and hospitalized in the First Affiliated Hospital of Fujian Medical University from December 2022 to January 2023. 10-s electrocardiogram (ECG) data were available for these patients. The US-HRV parameters including standard deviation of all normal-to-normal R-R intervals (SDNN) and root mean square of successive differences between normal-to-normal R-R intervals (rMSSD) were calculated using Nalong ECG software. The endpoint was short-term mortality, including in-hospital mortality or mortality within 1 week after discharge. RESULTS: Of the 488 patients, 76 (15.6%) died. The SDNN and rMSSD in the death group were significantly lower than those in the survival group (P < 0.001). The area under the receiver operating characteristic (ROC) curve (AUC) for SDNN and rMSSD to predict mortality was 0.761 and 0.715, respectively. The combined use of SDNN and rMSSD had an AUC of 0.774. The mortality rate in the group with SDNN ≤7.5 ms was higher than that of SDNN >7.5 ms group (P < 0.05). With the decrease of SDNN, the mortality of patients showed an upward trend, and the mortality of patients with SDNN ≤2 ms was the highest (66.7%). Multivariate logistic regression analysis identified SDNN as an independent predictor of prognosis (odds ratio (OR) = 5.791, 95% confidential interval (CI) 1.615-20.765, P = 0.007). The AUC of Model 1 (simple model) was 0.866 (95% CI 0.826-0.905). The AUC of Model 2 (comprehensive model) was 0.914 (95% CI 0.881-0.947). CONCLUSION: SDNN was associated with short-term mortality and provided the additional discriminatory power of the risk stratification model for hospitalized COVID-19 patients.

Flexible High-Performance and Screen-Printed Symmetric Supercapacitor Using Hierarchical Rodlike V3O7 Inks.

The emergence of the Internet of things stimulates the pursuit of flexible and miniaturized supercapacitors. As an advanced technology, screen printing displays vigor and tremendous potential in fabricating supercapacitors, but the adoption of high-performance ink is a great challenge. Here, hierarchical V3O7 with rodlike texture was prepared via a facile template-solvothermal route; and the morphology, component, and valence bond information are characterized meticulously. Then, the screen-printed inks composed of V3O7, acetylene black, and PVDF are formulated, and the rheological behaviors are studied detailedly. Benefitting from the orderly aligned ink, the optimal screen-printed electrode can exhibit an excellent specific capacitance of 274.5 F/g at 0.3 A/g and capacitance retention of 81.9% after 5000 cycles. In addition, a flexible V3O7 symmetrical supercapacitor (SSC) is screen-printed and assembled on the Ag current collector, exhibiting a decent areal specific capacitance of 322.5 mF/cm2 at 0.5 mA/cm2, outstanding cycling stability of 90.8% even after 5000 cycles, satisfactory maximum energy density of 129.45 µWh/cm2 at a power density of 0.42 mW/cm2, and remarkable flexibility and durability. Furthermore, a single SSC enables the showing of an actual voltage of 1.70 V after charging, and no obvious self-discharge phenomenon is found, revealing the great applied value in supply power. Therefore, this work provides a facile and low-cost reference of screen-printed ink for large-scale fabrication of flexible supercapacitors.

The UBC27-AIRP3 ubiquitination complex modulates ABA signaling by promoting the degradation of ABI1 in Arabidopsis.

Abscisic acid (ABA) is the key phytohormone in plant drought tolerance and stress adaptation. The clade A protein phosphatase 2Cs (PP2Cs) like ABI1 (ABA-INSENSITIVE 1) work as coreceptors of ABA and regulate multiple ABA responses. Ubiquitination of ABI1 has been proven to play important regulatory roles in ABA signaling. However, the specific ubiquitin conjugating enzyme (E2) involved is unknown. Here, we report that UBC27 is an active E2 that positively regulates ABA signaling and drought tolerance. UBC27 forms the E2-E3 pair with the drought regulator RING E3 ligase AIRP3. Both UBC27 and AIRP3 interact with ABI1 and affect the ubiquitination and degradation of ABI1. ABA activates the expression of UBC27, inhibits the proteasome degradation of UBC27, and enhances the interaction between UBC27 and ABI1 to increase its activity. These findings uncover a regulatory mechanism in ABA signaling and drought response and provide a further understanding of the plant ubiquitination system and ABA signaling pathway.

A novel antifungal protein of Bacillus subtilis B25.

Bacillus subtilis B25 was isolated from banana rhizosphere soil. It has been confirmed for B25 to have stronger antagonism against Fusarium oxysporum f.sp.cubense, Additionally B25 has good inhibitory to plant pathogens, including Corynespora cassiicola, Alternaria solani, Botrytis cinerea and Colletotrichum gloeosporioides on potato dextrose agar (PDA) plates. The antagonistic substance can be extracted from cell-free culture broth supernatants by 70% (w/v) (NH4)2 SO4 saturation. Clear blank band was observed between the protein and a pathogen. The examination of antagonistic mechanism under light microscope showed that the antifungal protein of B25 appeared to inhibit pathogens by leading to mycelium and spores tumescence, distortion, abnormality. The isolation procedure comprised ion exchange chromatography on DEAE-Sephadex Fast Flow and gel filtration chromatography on SephadexG-100. The purified antifungal fraction showed a single band in sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The active fraction was identified by NanoLC-ESI-MS/MS The amino acid sequences of 17 peptides segments were obtained. The analysis of the protein suggested that it was a hypothetical protein (gi154685475), with a relative molecular mass of 38708.67 Da and isoelectric point (pI) of 5.63.

Arabidopsis ubiquitin conjugase UBC32 is an ERAD component that functions in brassinosteroid-mediated salt stress tolerance.

Plants modify their growth and development to protect themselves from detrimental conditions by triggering a variety of signaling pathways, including the activation of the ubiquitin-mediated protein degradation pathway. Endoplasmic reticulum (ER)-associated protein degradation (ERAD) is an important aspect of the ubiquitin-proteasome system, but only a few of the active ERAD components have been reported in plants. Here, we report that the Arabidopsis thaliana ubiquitin-conjugating enzyme, UBC32, a stress-induced functional ubiquitin conjugation enzyme (E2) localized to the ER membrane, connects the ERAD process and brassinosteroid (BR)-mediated growth promotion and salt stress tolerance. In vivo data showed that UBC32 was a functional ERAD component that affected the stability of a known ERAD substrate, the barley (Hordeum vulgare) powdery mildew O (MLO) mutant MLO-12. UBC32 mutation caused the accumulation of bri1-5 and bri1-9, the mutant forms of the BR receptor, BRI1, and these mutant forms subsequently activated BR signal transduction. Further genetic and physiological data supported the contention that UBC32 plays a role in the BR-mediated salt stress response and that BR signaling is necessary for the plant to tolerate salt. Our data indicates a possible mechanism by which an ERAD component regulates the growth and stress response of plants.

The endoplasmic reticulum-associated degradation is necessary for plant salt tolerance.

Eukaryotic organisms have quality-control mechanisms that allow misfolded or unassembled proteins to be retained in the endoplasmic reticulum (ER) and subsequently degraded by ER-associated degradation (ERAD). The ERAD pathway is well studied in yeast and mammals; however, the biological functions of plant ERAD have not been reported. Through molecular and cellular biological approaches, we found that ERAD is necessary for plants to overcome salt stress. Upon salt treatment ubiquitinated proteins increased in plant cells, especially unfolded proteins that quickly accumulated in the ER and subsequently induced ER stress responses. Defect in HRD3A of the HRD1/HRD3 complex of the ERAD pathway resulted in alteration of the unfolded protein response (UPR), increased plant sensitivity to salt, and retention of ERAD substrates in plant cells. Furthermore, we demonstrated that Ca(2+) release from the ER is involved in the elevation of UPR and reactive oxygen species (ROS) participates the ERAD-related plant salt response pathway.

[Study on inducing an artemisinin-resistant line of Plasmodium berghei].

OBJECTIVE: To induce a line of Plasmodium berghei with resistance to artemisinin. METHODS: The major methods included blood transmission from passage to passage and progressive increase of drug pressure. RESULTS: The resistant lines were developed by different protocols: (A) The initial dosage of artemisinin was 126.2 mg/kg which was increased by 60 mg/kg for the next passage and boosted by 126.2 mg/kg for every other passage. As developed to passage 60 and 76, the resistant index was 18.39:1 and 14.89:1 respectively, then decreased gradually. For passage 108, the dosage was 8,862.5 mg/kg, but the resistant index was only 10.49:1. (B) Using passage 66 from (A) as the source, a dosage of 4,000 mg/kg was given each week, the resistance of the passage 40 increased significantly with an index of 27.5:1. (C) Using passage 19 of (B) as the source, drug was administered at the dose of 2,000 mg/kg each week. The resistant index of passage 15 was 17.41:1. CONCLUSION: Line of P. berghei with medium level resistance to artemisinin was established.