Long term co-application of biochar and fertilizer could increase soybean yield under continuous cropping: insights from photosynthetic physiology.

BACKGROUND: Photosynthesis is the key to crop yield. The effect of biochar on photosynthetic physiology and soybean yield under continuous cropping is unclear. We conducted a long-term field experiment to investigate the effects of co-application of biochar and fertilizer (BCAF) on these parameters. Five treatments were established: F2 (fertilizer), B1F1 (3 t hm-2 biochar plus fertilizer), B1F2 (3 t hm-2 biochar plus reduced fertilizer), B2F1 (6 t hm-2 biochar plus fertilizer), and B2F2 (6 t hm-2 biochar plus reduced fertilizer). RESULTS: BCAF increased chlorophyll and leaf area, enhancing soybean photosynthesis. The net photosynthetic rate (Pn ), transpiration rate (Tr ), stomatal conductance (Gs ), water use efficiency (WUE) and intercellular carbon dioxide (CO2 ) concentration (Ci ) were enhanced by BCAF. In addition, BCAF improved soybean photosystem II (PSII) photosynthetic performance, driving force, potential photochemical efficiency (Fv /F0 ), and quantum yield of electron transfer (φE0 ). Furthermore, BCAF enhanced the accumulation of photosynthetic products, such as soluble proteins, soluble sugars and sucrose content, resulting in higher leaf dry weight. Consequently, BCAF increased the soybean yield, with the highest increase of 41.54% in B2F1. The correlation analysis revealed positive relationships between soybean yield and chlorophyll, leaf area, maximal quantum yield of PSII (Fv /Fm ), electron transport flux per cross-section at t = 0 (ET0 /CS0 ), trapped energy flux per cross-section at t = 0 (TR0 /CS0 ), composite blade driving force (DFTotal ), and leaf dry weight. CONCLUSIONS: We demonstrated that long-term BCAF enhances soybean photosynthesis under continuous planting, reduces fertilizer use and increases yield. This study reveals a novel way and theory to sustainably increase soybean productivity. © 2023 Society of Chemical Industry.

Could continuous rice cropping increase soil fertility and rice productivity by rice straw carbonized utilization in cold areas? - A 6-year field-located trial.

Biochar amendment can benefit rice growth, but the long-term effects of rice straw carbonized utilization (RSCU, biochar, and biochar-based fertilizer) on rice production in cold areas are still unclear. Herein, we conducted a field experiment over 6 years with four treatments: F (conventional fertilization) as the control, RB1 (biochar, 3 t·ha-1), RB2 (biochar, 6 t·ha-1), and RBF (biochar-based fertilizer, 0.75 t·ha-1). We found that rice straw biochar significantly improved soil physical properties by reducing soil bulk density, increasing soil porosity and liquid and gas phases ratio, and enhancing soil aggregate stability. RSCU also increased soil fertility by improving soil organic carbon (SOC), active organic carbon, and soil nutrients (N, P, K) and their availability, as indicated by an increase in soil C:N and a decrease in soil N:P. Moreover, biochar increased soil microbial biomass carbon (MBC), microbial biomass nitrogen (MBN), and enzyme activities. As a result, RSCU increased rice yield, which was positively correlated with soil total porosity, total phosphorus, available potassium, dissolved organic carbon (DOC), easily oxidizable carbon (EOC), labile fraction of organic carbon (LFOC), and urease activity. RB2 had the highest rice yield (5.94% higher than F). Our study suggests that RSCU can synergistically improve the rice straw utilization rate, soil fertility, and rice productivity in cold areas.

Osteopontin regulates the growth and invasion of liver cancer cells via DTL.

Osteopontin (OPN), a secreted phosphoglycoprotein, has important roles in tumor growth, invasion and metastasis in numerous types of cancers. Denticleless E3 ubiquitin protein ligase homolog (DTL), one of the CUL4-DDB1-associated factors (DCAFs), has also been associated with the invasion and metastasis of cancer cells. In the present study, OPN was found to induce DTL expression in liver cancer cells, and the results obtained using luciferase activity assays demonstrated that OPN could transcriptionally activate DTL expression in liver cancer cells. Furthermore, the results of the present study demonstrated that OPN could increase the expression of DTL via PI3K/AKT signaling. In conclusion, the present study demonstrated that OPN, as an extracellular matrix protein, is able to promote the growth and invasion of liver cancer cells through stimulation of the expression of DTL via the PI3K/AKT signaling pathway.

Isoginkgetin inhibits inflammatory response in the fibroblast-like synoviocytes of rheumatoid arthritis by suppressing matrix metallopeptidase 9 expression.

Inflammatory and invasive fibroblast-like synoviocytes (FLS) contribute to the pathology of rheumatoid arthritis (RA). Isoginkgetin (IGKG) has been identified as having anti-inflammatory properties. This study investigated whether IGKG could be utilized to treat RA. Primary FLS were isolated from synovial tissues derived from six RA patients, which were over-expressed with matrix metallopeptidase 9 and cultured with or without tumor necrosis factor (TNF)-α and then further treated with IGKG. IGKG down-regulated the content of various interleukins (ILs), namely, IL-1ß, IL-6, and IL-8, in RA-FLS supernatant with or without TNF-α stimulation, with diminished migration and invasion properties as assayed by the transwell system. Furthermore, down-regulated inflammatory cytokine secretion and down-regulated migration and invasion properties could be reversed through matrix metallopeptidase 9 overexpression. Dual-luciferase reporter gene assay indicated that IGKG could inhibit nuclear factor kappa B transcription activity. Western blot analysis also demonstrated that IGKG down-regulated the expression of p-IκBα, p-p65, and MMP9. IGKG displayed the ability to inhibit the inflammatory response of RA-FLS through the NF-κB/MMP9 pathway with diminished migration and invasion.

Combination of serum matrix metalloproteinase-3 activity and EBV antibodies improves the diagnostic performance of nasopharyngeal carcinoma.

Objective: Nasopharyngeal carcinoma (NPC) is a malignant head and neck tumor that is highly prevalent in Southeast Asia. The two traditional NPC markers VCA-IgA (EBV viral capsid antigen) and EA-IgA (EBV early antigen) are limited in the screening and diagnosis of NPC. The purpose of present study is to evaluate the diagnostic value of matrix metalloproteinase-3 (MMP3) in NPC. Methods: The levels of 23 secretory MMPs in serum samples from 15 healthy controls and 26 NPC patients were detected by Cytokine Antibody Array 2000. Immunohistochemistry, Real-time PCR and western bolt were used to detect MMP3 mRNA and protein levels in NPC tissues and cell lines. The serum protein levels of MMP3 were further measured by ELISA in healthy control individuals (n = 200) and NPC patients (n = 206). Results: MMP3 can be expressed and secreted by both NPC and fibroblast cell lines, suggesting that the higher expression of MMP3 protein in both tumor nests and stromal of NPC tissues may be the source of circulating MMP3 in NPC patients. Furthermore, we found out both MMP3 concentration and enzymatic activity were significantly increased in the NPC group (n = 206) than the healthy control group (n = 200) (P < 0.001). However, serum MMP3 enzymatic activity, but not MMP3 concentration, was significantly associated with the progression of NPC. In addition, serum MMP3 activity was more valuable in diagnosis of NPC than its concentration (0.86 vs. 0.78, AUC), and MMP3 activity can improve the diagnosis of NPC by combining with EBV-infection biomarkers VCA-IgA and EA-IgA with a sensitivity of 91.5% and a specificity of 92.3%. Conclusions: This study suggested the combination of MMP3 activity and EBV antibodies may be a useful biomarker for screening and diagnosis of NPC.

Fast and robust population transfer with a Josephson qutrit via shortcut to adiabaticity.

We propose an effective scheme to implement fast and robust population transfer with a Josephson qutrit via shortcut to adiabaticity. Facilitated by the level-transition rule, a Λ-configuration resonant interaction can be realized between microwave drivings and the qutrit with sufficient level anharmonicity, from which we perform the reversible population transfers via invariant-based shortcut. Compared with the detuned drivings, the utilized resonant drivings shorten the transfer times significantly. Further analysis of the dependence of transfer time on Rabi couplings is helpful to experimental investigations. Thanks to the accelerated process, transfer operation is highly insensitive to noise effects. Thus the protocol could provide a promising avenue to experimentally perform fast and robust quantum operations on Josephson artificial atoms.

Palmitic Acid Curcumin Ester Facilitates Protection of Neuroblastoma against Oligomeric Aß40 Insult.

BACKGROUND/AIMS: The generation of reactive oxygen species (ROS) caused by amyloid-ß (Aß) is considered to be one of mechanisms underlying the development of Alzheimer's disease. Curcumin can attenuate Aß-induced neurotoxicity through ROS scavenging, but the protective effect of intracellular curcumin on neurocyte membranes against extracellular Aß may be compromised. To address this issue, we synthesized a palmitic acid curcumin ester (P-curcumin) which can be cultivated on the cell membrane and investigated the neuroprotective effect of P-curcumin and its interaction with Aß. METHODS: P-curcumin was prepared through chemical synthesis. Its structure was determined via nuclear magnetic resonance (NMR) and high-resolution mass spectrometry (HRMS). An MTT assay was used to assess Aß cytotoxicity and the protective effect of P-curcumin on SH-SY5Y cells. The effect of P-curcumin on Aß-induced ROS production in vitro and in vivo were assessed based on changes in dichlorofluorescein (DCF) fluorescence. A spectrophotometric method was employed to detect lipid peroxidation. To mimic the interaction of P-curcumin on cell membranes with Aß, liposomes were prepared by thin film method. Finally, the interactions between free P-curcumin and P-curcumin cultivated on liposomes and Aß were determined via spectrophotometry. RESULTS: A novel derivative, palmitic acid curcumin ester was prepared and characterized. This curcumin, cultivated on the membranes of neurocytes, may prevent Aß-mediated ROS production and may inhibit the direct interaction between Aß and the cellular membrane. Furthermore, P-curcumin could scavenge Aß-mediated ROS as curcumin in vitro and in vivo, and had the potential to prevent lipid peroxidation. Morphological analyses showed that P-curcumin was better than curcumin at protecting cell shape. To examine P-curcumin's ability to attenuate direct interaction between Aß and cell membranes, the binding affinity of Aß to curcumin and P-curcumin was determined. The association constants for free P-curcumin and curcumin were 7.66 × 104 M-1 and 7.61 × 105 M-1, respectively. In the liposome-trapped state, the association constants were 3.71 × 105 M-1 for P-curcumin and 1.44× 106 M-1 for curcumin. With this data, the thermodynamic constants of P-curcumin association with soluble Aß (ΔH, ΔS, and ΔG) were also determined. CONCLUSION: Cultivated curcumin weakened the direct interaction between Aß and cell membranes and showed greater neuroprotective effects against Aß insult than free curcumin.

BDNF Contributes to Spinal Long-Term Potentiation and Mechanical Hypersensitivity Via Fyn-Mediated Phosphorylation of NMDA Receptor GluN2B Subunit at Tyrosine 1472 in Rats Following Spinal Nerve Ligation.

Previously we have demonstrated that brain-derived neurotrophic factor (BDNF) contributes to spinal long-term potentiation (LTP) and pain hypersensitivity through activation of GluN2B-containing N-methyl-D-aspartate (GluN2B-NMDA) receptors in rats following spinal nerve ligation (SNL). However, the molecular mechanisms by which BDNF impacts upon GluN2B-NMDA receptors and spinal LTP still remain unclear. In this study, we first documented that Fyn kinase-mediated phosphorylation of GluN2B subunit at tyrosine 1472 (pGluN2BY1472) was involved in BDNF-induced spinal LTP and pain hypersensitivity in intact rats. Second, we revealed a co-localization of Fyn and GluN2B-NMDA receptor in cultured dorsal horn neurons, implying that Fyn is a possible intermediate kinase linking BDNF/TrkB signaling with GluN2B-NMDA receptors in the spinal dorsal horn. Furthermore, we discovered that both SNL surgery and intrathecal active Fyn could induce an increased expression of dorsal horn pGluN2BY1472, as well as pain hypersensitivity in response to von Frey filaments stimuli; and more importantly, all these actions were effectively abrogated by pre-treatment with either PP2 or ifenprodil to respectively inhibit Fyn kinase and GluN2B-NMDA receptors activity. Moreover, we found that intrathecal administration of BDNF scavenger TrkB-Fc prior to SNL surgery, could prevent the nerve injury-induced increase of both pFynY420 and pGluN2BY1472 expression, and also inhibit the mechanical allodynia in neuropathic rats. Collectively, these results suggest that Fyn kinase-mediated pGluN2BY1472 is critical for BDNF-induced spinal LTP and pain hypersensitivity in SNL rats. Therefore, the BDNF-Fyn-GluN2B signaling cascade in the spinal dorsal horn may constitute a key mechanism underlying central sensitization and neuropathic pain development after peripheral nerve injury.

Nicotinic modulation of Ca2+ oscillations in rat cortical neurons in vitro.

The roles of nicotine on Ca(2+) oscillations [intracellular Ca(2+) ([Ca(2+)]i) oscillation] in rat primary cultured cortical neurons were studied. The spontaneous [Ca(2+)]i oscillations (SCO) were recorded in a portion of the neurons (65%) cultured for 7-10 days in vitro. Application of nicotine enhanced [Ca(2+)]i oscillation frequency and amplitude, which were reduced by the selective α4ß2-nicotinic acetylcholine receptors (nAChRs) antagonist dihydro-ß-erythroidine (DHßE) hydrobromide, and the selective α7-nAChRs antagonist methyllycaconitine citrate (MLA, 20 nM). DHßE reduced SCO frequency and prevented the nicotinic increase in the frequency. DHßE somewhat enhanced SCO amplitude and prevented nicotinic increase in the amplitude. MLA (20 nM) itself reduced SCO frequency without affecting the amplitude but blocked nicotinic increase in [Ca(2+)]i oscillation frequency and amplitude. Furthermore, coadministration of both α4ß2- and α7-nAChRs antagonists completely prevented nicotinic increment in [Ca(2+)]i oscillation frequency and amplitude. Thus, our results indicate that both α4ß2- and α7-nAChRs mediated nicotine-induced [Ca(2+)]i oscillations, and two nAChR subtypes differentially regulated SCO.

[Effect of basic fibroblast growth factor on endogenous neural stem cell in rat cerebral cortex with global cerebral ischemia-reperfusion].

The present paper is aimedto investigate the effect of basic fibroblast growth factor (bFGF) on proliferation, migration and differentiation of endogenous neural stem cell in rat cerebral cortex with global brain ischemia-reperfusion. A global brain ischemia-reperfusion model was established. Immunohistochemistry was used to observe the pathological changes and the expression of BrdU and Nestin in cerebral cortex. RT-PCR was used to measure the NSE mRNA in brain tissue. The results of measurements indicated that in sham operation group, there was no positive cell in cerebral cortex, and the content of NSE mRNA did not change. In the operation group, the expression of BrdU and Nestin increased significantly at the end of the 3rd day, and peaked on the 7th day. NSE mRNA expression did not significantly increase. In bFGF group, compared with sham operation group and model group, the number of BrdU-positive and Nestin-positive cells increased significantly at each time point (P<0. 05), and peaked at the end of the 11th day, and the content of NSE mRNA increased significantly (P<0. 05). This research demonstrated that the proliferation of endogenous neural stem cells in situ could be induced by global cerebral ischemia and reperfu- sion, and could be promoted and extended by bFGF. In additiion, bFGF might promote endogenous neural stem cells differentiated into neurons.

Humanin rescues cultured rat cortical neurons from NMDA-induced toxicity not by NMDA receptor.

Excitatory neurotoxicity has been implicated in many pathological situations and there is no effective treatment available. Humanin is a 24-aa peptide cloned from the brain of patients with Alzheimer's disease (AD). In the present study, excitatory toxicity was induced by N-methyl-D-aspartate (NMDA) in primarily cultured rat cortical neurons. MTT assessment, lactate dehydrogenase (LDH) release, and calcein staining were employed to evaluate the protective activity of humanin on NMDA induced toxicity. The results suggested that NMDA (100 µmol/L, 2.5 hr) triggered neuronal morphological changes, lactate dehydrogenase (LDH) release (166% of the control), reduction of cell viability (about 50% of the control), and the decrease of living cell density (about 50% of the control). When pretreated with humanin, the toxicity was suppressed. The living cells' density of humanin treated group was similar to that of control. The cell viability was attenuated dose-dependently (IC50 = 0.132 nmol/L). The LDH release was also neutralized in a dose-dependent manner. In addition, the intracellular Ca(2+) overloading triggered by NMDA reverted quickly and humanin could not inhibit it. These findings indicate that humanin can rescue cortical neurons from NMDA-induced toxicity in rat but not through interfering with NMDA receptor directly.

Melatonin ameliorates injury and specific responses of ischemic striatal neurons in rats.

Studies have confirmed that middle cerebral artery occlusion (MCAO) causes striatal injury in which oxidative stress is involved in the pathological mechanism. Increasing evidence suggests that melatonin may have a neuroprotective effect on cerebral ischemic damage. This study aimed to examine the morphological changes of different striatal neuron types and the effect of melatonin on striatal injury by MCAO. The results showed that MCAO induced striatum-related dysfunctions of locomotion, coordination, and cognition, which were remarkably relieved with melatonin treatment. MCAO induced severe striatal neuronal apoptosis and loss, which was significantly decreased with melatonin treatment. Within the outer zone of the infarct, the number of Darpp-32+ projection neurons and the densities of dopamine-receptor-1 (D1)+ and dopamine-receptor-2 (D2)+ fibers were reduced; however, both parvalbumin (Parv)+ and choline acetyltransferase (ChAT)+ interneurons were not significantly decreased in number, and neuropeptide Y (NPY)+ and calretinin (Cr)+ interneurons were even increased. With melatonin treatment, the loss of projection neurons and characteristic responses of interneurons were notably attenuated. The present study demonstrates that the projection neurons are rather vulnerable to ischemic damage, whereas the interneurons display resistance and even hyperplasia against injury. In addition, melatonin alleviates striatal dysfunction, neuronal loss, and morphological transformation of interneurons resulting from cerebral ischemia.