Umbilical cord mesenchymal stem cells promote the repair of trochlear groove reconstruction in dogs.

Trochlear groove reconstruction (TGR) is a common treatment for patellar luxation (PL) in dogs. Nevertheless, the prognosis of TGR is poor due to the cartilage damage and secondary inflammation. To study the repair effect of canine umbilical cord mesenchymal stem cells (UC-MSCs) after TGR, 10 experimental dogs were given TGR surgery and then randomized into two groups: Treatment group (1 ml suspension allogeneic UC-MSCs (106 cells/kg) was injected into the cavum articulare on days 0, 7, and 14 after TGR); and the Model group (injected with 1 ml of physiological saline as negative control). The therapeutic effect of UC-MSCs was studied by blood routine examination, inflammatory factor index detection, double-blind knee score, histopathology, and computed tomography (CT) scans. The results showed that the total number of white blood cells and neutrophils in the model group were significantly higher than those in the treatment group on both 7 days and 21 days, postoperatively (P < 0.05); there were no significant changes in the levels of IL-6, MMP-13, and TGF-ß1 between the model group and the treatment group throughout the days of testing. The double-blind knee scores of the treatment group were significantly lower than the model group on 1st, 4th, and 5th days postoperatively (P < 0.05). The treatment group showed low-pain sensation, stable gait, and fast recovery of muscle strength in the knee score, and the wound healing of the treatment group returned to normal on the 5th day after surgery; CT scans and gross observation showed that the cartilage growth in the treatment group was faster than that in the model group. Histological observation of cases showed that fibro chondrocytes were predominantly found in the treatment group, and the distribution of chondrocytes was uneven, while the model group showed a large number of fibrous tissue hyperplasia, fissures, and unequal matrix staining. Intra-articular injection of UC-MSCs after TGR has the effect of relieving pain and promoting the repair of bone defects, making the operative limb recover function earlier, making up for the deficiency of TGR, and improving the effect of PL treatment. Future studies should furthermore explore the dose and frequency of therapy based on the multiple advantages of UC-MSCs and the mechanism of cartilage repair in dogs.

Arylboronic Acid Catalyzed Dehydrative Mono-/Dialkylation Reactions of ß-Ketoacids and Alcohols.

The dehydrative mono-/dialkylation reactions of alcohols and ß-ketoacids were realized under arylboronic acid catalysis, furnishing a series of ß-aryl ketones and ß-ketoesters in yields of 15-99%, with CO2 and H2O being the byproducts. In this context, the decarboxylative alkylation reaction occurred to give ß-aryl ketones at 50 °C, while the decarboxylation was suppressed to generate dialkylated ester products at 0 °C. A possible catalytic cycle was proposed based on control experiments.

Tomato chlorosis virus-encoded p22 suppresses auxin signalling to promote infection via interference with SKP1-Cullin-F-boxTIR1 complex assembly.

Phytohormone auxin plays a fundamental role in plant growth and defense against pathogens. However, how auxin signalling is regulated during virus infection in plants remains largely unknown. Auxin/indole-3-acetic acid (Aux/IAA) is the repressor of auxin signalling and can be recognized by an F-box protein transport inhibitor response 1 (TIR1). Ubiquitination and degradation of Aux/IAA by SKP1-Cullin-F-boxTIR1 (SCFTIR1 ) complex can trigger auxin signalling. Here, with an emerging important plant virus worldwide, we showed that tomato chlorosis virus (ToCV) infection or stable transgenic overexpression of its p22 protein does not alter auxin accumulation level but significantly decreases the expression of auxin signalling-responsive genes, suggesting that p22 can attenuate host auxin signalling. Further, p22 could bind the C-terminal of SKP1.1 and compete with TIR1 to interfere with the SCFTIR1 complex assembly, leading to a suppression of Aux/IAA degradation. Silencing and over-expression assays suggested that both NbSKP1.1 and NbTIR1 suppress ToCV accumulation and disease symptoms. Altogether, ToCV p22 disrupts the auxin signalling through destabilizing SCFTIR1 by interacting with the C-terminal of NbSKP1.1 to promote ToCV infection. Our findings uncovered a previously unknown molecular mechanism employed by a plant virus to manipulate SCF complex-mediated ubiquitin pathway and to reprogram auxin signalling for efficient infection.