Transcription factors NtNAC028 and NtNAC080 form heterodimers to regulate jasmonic acid biosynthesis during leaf senescence in Nicotiana tabacum.

Plant senescence, as a highly integrated developmental stage, involves functional degeneration and nutrient redistribution. NAM/ATAF1/CUC (NAC) transcription factors orchestrate various senescence-related signals and mediate the fine-tuning underlying plant senescence. Previous data revealed that knockout of either NtNAC028 or NtNAC080 leads to delayed leaf senescence in tobacco (Nicotiana tabacum), which implies that NtNAC028 and NtNAC080 play respective roles in the regulation of leaf senescence, although they share 91.87% identity with each other. However, the mechanism underlying NtNAC028- and NtNAC080-regulated leaf senescence remains obscure. Here, we determined that NtNAC028 and NtNAC080 activate a putative jasmonic acid (JA) biosynthetic gene, NtLOX3, and enhance the JA level in vivo. We found that NtNAC028 and NtNAC080 interact with each other and themselves through their NA-terminal region. Remarkably, only the dimerization between NtNAC028 and NtNAC080 stimulated the transcriptional activation activity, but not the DNA binding activity of this heterodimer on NtLOX3. Metabolome analysis indicated that overexpression of either NtNAC028 or NtNAC080 augments both biosynthesis and degradation of nicotine in the senescent stages. Thus, we conclude that NtNAC028 cooperates with NtNAC080 and forms a heterodimer to enhance NtLOX3 expression and JA biosynthesis to trigger the onset of leaf senescence and impact secondary metabolism in tobacco.

Flexible Needle Steering with Tethered and Untethered Actuation: Current States, Targeting Errors, Challenges and Opportunities.

Accurate needle targeting is critical for many clinical procedures, such as transcutaneous biopsy or radiofrequency ablation of tumors. However, targeting errors may arise, limiting the widespread adoption of these procedures. Advances in flexible needle (FN) steering are emerging to mitigate these errors. This review summarizes the state-of-the-art developments of FNs and addresses possible targeting errors that can be overcome with steering actuation techniques. FN steering techniques can be classified as passive and active. Passive steering directly results from the needle-tissue interaction forces, whereas active steering requires additional forces to be applied at the needle tip, which enhances needle steerability. Therefore, the corresponding targeting errors of most passive FNs and active FNs are between 1 and 2 mm, and less than 1 mm, respectively. However, the diameters of active FNs range from 1.42 to 12 mm, which is larger than the passive steering needle varying from 0.5 to 1.4 mm. Therefore, the development of active FNs is an area of active research. These active FNs can be steered using tethered internal direct actuation or untethered external actuation. Examples of tethered internal direct actuation include tendon-driven, longitudinal segment transmission and concentric tube transmission. Tendon-driven FNs have various structures, and longitudinal segment transmission needles could be adapted to reduce tissue damage. Additionally, concentric tube needles have immediate advantages and clinical applications in natural orifice surgery. Magnetic actuation enables active FN steering with untethered external actuation and facilitates miniaturization. The challenges faced in the fabrication, sensing, and actuation methods of FN are analyzed. Finally, bio-inspired FNs may offer solutions to address the challenges faced in FN active steering mechanisms.

A review of recent advancements in soft and flexible robots for medical applications.

BACKGROUND: Soft and flexible robots for medical applications are needed to change their flexibility over a wide range to perform tasks adequately. The mechanism and theory of flexibility has been a scientific issue and is of interest to the community. METHODS: Recent advancements of bionics, flexible actuation, sensing, and intelligent control algorithms as well as tunable stiffness have been referenced when soft and flexible robots are developed. The benefits and limitations of these relevant studies and how they affect the flexibility are discussed, and possible research directions are explored. RESULTS: The bionic materials and structures that demonstrate the potential capabilities of the soft medical robot flexibility are the fundamental guarantee for clinical medical applications. Flexible actuation that used to provide power, intelligent control algorithms which are the exact executors, and the wide range stiffness of the soft materials are the three important influence factors for soft medical robots. CONCLUSION: Some reasonable suggestions and possible solutions for soft and flexible medical robots are proposed, including novel materials, flexible actuation concepts with a built-in source of energy or power, programmable flexibility, and adjustable stiffness.

Increased expression of TNFRSF14 indicates good prognosis and inhibits bladder cancer proliferation by promoting apoptosis.

Despite advances in management, bladder cancer remains a principal cause of cancer­associated complications. Tumor necrosis factor receptor superfamily member 14 (TNFRSF14) is dysregulated in certain types of cancer; however, limited data are available on the expression and function of TNFRSF14 in bladder cancer. In the present study, the aim was to evaluate the expression and biological functions of TNFRSF14 in bladder cancer. Firstly, the expression levels of TNFRSF14 in bladder cancer tissue were examined using The Cancer Genome Atlas (TCGA) database. Secondly, reverse transcription­quantitative polymerase chain reaction was utilized to investigate the expression levels of TNFRSF14 in the T24, SW780 and EJ­M3 bladder cancer cell lines. Transfection and Cell Counting kit­8 (CCK­8) assay was used to evaluate whether TNFRSF14 overexpression or silencing would have an effect on cell proliferation of T24 and EJ­M3 cells. In addition, TNFRSF14­induced apoptotic cells were identified using Annexin V­fluorescein isothiocyanate and propidium iodide staining. Western blot analysis was used to detect proteins associated with the phosphatidylinositol 3­kinase pathway. According to the TCGA dataset, the expression levels TNFRSF14 were decreased in bladder cancer tissue compared with in normal control samples. Patients with bladder cancer exhibiting low expression levels of TNFRSF14 had a worse prognosis compared to those with high expression levels of TNFRSF14. Overexpression of TNFRSF14 in T24 cells led to increased apoptosis and inhibited cell proliferation in vitro. Western blotting demonstrated that TNFRSF14 overexpression increased the expression levels of caspase3­p17 in T24 cells, but significantly decreased the expression levels of phosphorylated (p)­protein kinase B (AKT) and P70 S6 kinase (P70). TNFRSF14 silencing in EJ­M3 cells enhanced cell growth, inhibited cell apoptosis, increased the expression levels of p­AKT and P70, and decreased the expression levels of caspase3­p17. In conclusion, TNFRSF14 may serve a tumor suppressive role in bladder cancer by inducing apoptosis and suppressing proliferation, and act as a novel prognostic biomarker for bladder cancer.

[Radiobiological characteristics and MRN complex expression of human nasopharyngeal carcinoma cell lines].

OBJECTIVE: To study the radiobiological characteristic of human nasopharyngeal carcinoma cell lines CNE1 and CNE2 and the changes in expression MRN (Mre11-Rad50-Nbs1) complex in the cell lines exposed to irradiation. METHODS: CNE1 and CNE2 were irradiated by a linear accelerator. Radiobiological characteristics were detected by colony assay and MTT assay. MRN complex expression were examined by Western blot. RESULTS: Surviving fraction at 2 Gy (SF2), quasi-threshold Dose (Dq), and mean lethal dose (Do) of CNE1 were 0.56, 1.449 Gy and 1.480 Gy; SF2, Dq, and Do of CNE2 were 0.44, 0.776 Gy and 1.685 Gy, respectively. Survival fraction of CNE1 at the day 6 after 4 Gy irradiation was 0.59 and that of CNE2 was 0.79 when compared with control, with the up-regulated expressions of Rad50 in CNE1 and Mre11, Rad50 and Nbs1 in CNE2 (P < 0.05). CONCLUSIONS: CNE1 and CNE2 were sensitive to radiation, but there were radioresistance cells in CNE2. The expressions of some components of MRN complex were up-regulated to repair DNA lesions induced by radiation.