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Based on a molecular phylogenetic analysis and morphological comparison, a new species of mountain pitviper, Ovophis jenkinsi sp. nov., is described. The new species was collected in Yingjiang County, Yunnan Province, China. It can be distinguished from congeneric species by the following characters: (1) internasals in contact or separated by one small scale; (2) second supralabial entire and bordering the loreal pit; (3) dorsal scales in 23 (25)–21 (23, 25)–19 (17, 21) rows; (4) 134–142 ventrals; (5) 40–52 pairs of subcaudals; (6) third supralabial larger than fourth in all examined specimens of Ovophis jenkinsi sp. nov.; (7) deep orange-brown or dark brownish-grey markings on dorsal head surface; (8) background color of dorsal surface deep orange-brown or dark brownish-grey; (9) both sides of dorsum display dark brown trapezoidal patches; (10) scattered small white spots on dorsal surface of tail.

Abstract Background Acute kidney injury (AKI) is a common clinical disorder with complex etiology and poor prognosis, and currently lacks specific and effective treatment options. Mitochondrial dynamics dysfunction is a prominent feature in AKI, and modulation of mitochondrial morphology may serve as a potential therapeutic approach for AKI. Methods We induced ischemia–reperfusion injury (IRI) in mice (bilateral) and Bama pigs (unilateral) by occluding the renal arteries. ATP depletion and recovery (ATP-DR) was performed on proximal renal tubular cells to simulate in vitro IRI. Renal function was evaluated using creatinine and urea nitrogen levels, while renal structural damage was assessed through histopathological staining. The role of Drp1 was investigated using immunoblotting, immunohistochemistry, immunofluorescence, and immunoprecipitation techniques. Mitochondrial morphology was evaluated using confocal microscopy. Results Renal IRI induced significant mitochondrial fragmentation, accompanied by Dynamin-related protein 1 (Drp1) translocation to the mitochondria and Drp1 phosphorylation at Ser616 in the early stages (30 min after reperfusion), when there was no apparent structural damage to the kidney. The use of the Drp1 inhibitor P110 significantly improved kidney function and structural damage. P110 reduced Drp1 mitochondrial translocation, disrupted the interaction between Drp1 and Fis1, without affecting the binding of Drp1 to other mitochondrial receptors such as MFF and Mid51. High-dose administration had no apparent toxic side effects. Furthermore, ATP-DR induced mitochondrial fission in renal tubular cells, accompanied by a decrease in mitochondrial membrane potential and an increase in the translocation of the pro-apoptotic protein Bax. This process facilitated the release of dsDNA, triggering the activation of the cGAS-STING pathway and promoting inflammation. P110 attenuated mitochondrial fission, suppressed Bax mitochondrial translocation, prevented dsDNA release, and reduced the activation of the cGAS-STING pathway. Furthermore, these protective effects of P110 were also observed renal IRI model in the Bama pig and folic acid-induced nephropathy in mice. Conclusions Dysfunction of mitochondrial dynamics mediated by Drp1 contributes to renal IRI. The specific inhibitor of Drp1, P110, demonstrated protective effects in both in vivo and in vitro models of AKI.

Abstract The mechanism underlying acute kidney injury (AKI) and AKI-to-Chronic kidney disease (CKD) transition remains unclear, but mitochondrial dysfunction may be a key driving factor. Literature reports suggest that dual-specificity phosphatase 1 (DUSP1) plays a critical role in maintaining mitochondrial function and structural integrity. In this study, ischemic Acute Kidney Injury (AKI) and post-ischemic fibrosis models were established by clamping the renal pedicle with different reperfusion times. To investigate the role of DUSP1, constitutional Dusp1 knockout mice and tubular-specific Sting knockout mice were used. Mitochondrial damage was assessed through electron microscopy observation, measurements of mitochondrial membrane potential, mtDNA release, and BAX translocation. We found that Dusp1 expression was significantly upregulated in human transplant kidney tissue and mouse AKI tissue. Dusp1 gene deletion exacerbated acute ischemic injury, post-ischemic renal fibrosis, and tubular mitochondrial dysfunction in mice. Mechanistically, DUSP1 could directly bind to JNK, and DUSP1 deficiency could lead to aberrant phosphorylation of JNK and BAX mitochondria translocation. BAX translocation promoted mitochondrial DNA (mtDNA) leakage and activated the cGAS-STING pathway. Inhibition of JNK or BAX could inhibit mtDNA leakage. Furthermore, STING knockout or JNK inhibition could significantly mitigate the adverse effects of DUSP1 deficiency in ischemic AKI model. Collectively, our findings suggest that DUSP1 is a regulator for the protective response during AKI. DUSP1 protects against AKI by preventing BAX-induced mtDNA leakage and blocking excessive activation of the cGAS-STING signaling axis through JNK dephosphorylation.

ObjectiveRice blast is considered as the most destructive disease that threatens global rice production and causes severe economic losses worldwide. The detection of rice blast in an early manner plays an important role in resistance breeding and plant protection. At present, most studies on rice blast detection have been devoted to its symptomatic stage, while none of previous studies have used solar-induced chlorophyll fluorescence (SIF) to monitor rice leaf blast (RLB) at early stages. This research was conducted to investigate the early identification of RLB infected leaves based on solar-induced chlorophyll fluorescence at different leaf positions.MethodsGreenhouse experiments and field trials were conducted separately in Nanjing and Nantong in July and August, 2021, in order to record SIF data of the top 1th to 4th leaves of rice plants at jointing and heading stages with an Analytical Spectral Devices (ASD) spectrometer coupled with a FluoWat leaf clip and a halogen lamp. At the same time, the disease severity levels of the measured samples were manually collected according to the GB/T 15790-2009 standard. After the continuous wavelet transform (CWT) of SIF spectra, separability assessment and feature selection were applied to SIF spectra. Wavelet features sensitive to RLB were extracted, and the sensitive features and their identification accuracy of infected leaves for different leaf positions were compared. Finally, RLB identification models were constructed based on linear discriminant analysis (LDA).Results and DiscussionThe results showed that the upward and downward SIF in the far-red region of infected leaves at each leaf position were significantly higher than those of healthy leaves. This may be due to the infection of the fungal pathogen Magnaporthe oryzae, which may have destroyed the chloroplast structure, and ultimately inhibited the primary reaction of photosynthesis. In addition, both the upward and downward SIF in the red region and the far-red region increased with the decrease of leaf position. The sensitive wavelet features varied by leaf position, while most of them were distributed in the steep slope of the SIF spectrum and wavelet scales 3, 4 and 5. The sensitive features of the top 1th leaf were mainly located at 665-680 nm, 755-790 nm and 815-830 nm. For the top 2th leaf, the sensitive features were mainly found at 665-680 nm and 815-830 nm. For the top 3th one, most of the sensitive features lay at 690 nm, 755-790 nm and 815-830 nm, and the sensitive bands around 690 nm were observed. The sensitive features of the top 4th leaf were primarily located at 665-680 nm, 725 nm and 815-830 nm, and the sensitive bands around 725 nm were observed. The wavelet features of the common sensitive region (665-680 nm), not only had physiological significance, but also coincided with the chlorophyll absorption peak that allowed for reasonable spectral interpretation. There were differences in the accuracy of RLB identification models at different leaf positions. Based on the upward and downward SIF, the overall accuracies of the top 1th leaf were separately 70% and 71%, which was higher than other leaf positions. As a result, the top 1th leaf was an ideal indicator leaf to diagnose RLB in the field. The classification accuracy of SIF wavelet features were higher than the original SIF bands. Based on CWT and feature selection, the overall accuracy of the upward and downward optimal features of the top 1th to 4th leaves reached 70.13%、63.70%、64.63%、64.53% and 70.90%、63.12%、62.00%、64.02%, respectively. All of them were higher than the canopy monitoring feature F760, whose overall accuracy was 69.79%, 61.31%, 54.41%, 61.33% and 69.99%, 58.79%, 54.62%, 60.92%, respectively. This may be caused by the differences in physiological states of the top four leaves. In addition to RLB infection, the SIF data of some top 3th and top 4th leaves may also be affected by leaf senescence, while the SIF data of top 1th leaf, the latest unfolding leaf of rice plants was less affected by other physical and chemical parameters. This may explain why the top 1th leaf responded to RLB earlier than other leaves. The results also showed that the common sensitive features of the four leaf positions were also concentrated on the steep slope of the SIF spectrum, with better classification performance around 675 and 815 nm. The classification accuracy of the optimal common features, ↑WF832,3 and ↓WF809,3, reached 69.45%, 62.19%, 60.35%, 63.00% and 69.98%, 62.78%, 60.51%, 61.30% for the top 1th to top 4th leaf positions, respectively. The optimal common features, ↑WF832,3 and ↓WF809,3, were both located in wavelet scale 3 and 800-840nm, which may be related to the destruction of the cell structure in response to Magnaporthe oryzae infection.ConclusionsIn this study, the SIF spectral response to RLB was revealed, and the identification models of the top 1th leaf were found to be most precise among the top four leaves. In addition, the common wavelet features sensitive to RLB, ↑WF832,3 and ↓WF809,3, were extracted with the identification accuracy of 70%. The results proved the potential of CWT and SIF for RLB detection, which can provide important reference and technical support for the early, rapid and non-destructive diagnosis of RLB in the field.

Summary: Background: Earlier Omicron subvariants including BA.1, BA.2, and BA.5 emerged in waves, with a subvariant replacing the previous one every few months. More recently, the post-BA.2/5 subvariants have acquired convergent substitutions in spike that facilitated their escape from humoral immunity and gained ACE2 binding capacity. However, the intrinsic pathogenicity and replication fitness of the evaluated post-BA.2/5 subvariants are not fully understood. Methods: We systemically investigated the replication fitness and intrinsic pathogenicity of representative post-BA.2/5 subvariants (BL.1, BQ.1, BQ.1.1, XBB.1, CH.1.1, and XBB.1.5) in weanling (3–4 weeks), adult (8–10 weeks), and aged (10–12 months) mice. In addition, to better model Omicron replication in the human nasal epithelium, we further investigated the replication capacity of the post-BA.2/5 subvariants in human primary nasal epithelial cells. Findings: We found that the evaluated post-BA.2/5 subvariants are consistently attenuated in mouse lungs but not in nasal turbinates when compared with their ancestral subvariants BA.2/5. Further investigations in primary human nasal epithelial cells revealed a gained replication fitness of XBB.1 and XBB.1.5 when compared to BA.2 and BA.5.2. Interpretation: Our study revealed that the post-BA.2/5 subvariants are attenuated in lungs while increased in replication fitness in the nasal epithelium, indicating rapid adaptation of the circulating Omicron subvariants in the human populations. Funding: The full list of funding can be found at the Acknowledgements section.