Effects of Tai Chi Yunshou on upper-limb function and balance in stroke survivors: A systematic review and meta-analysis.

BACKGROUND AND PURPOSE: Physical rehabilitation plays an important role in the recovery of motor function after a stroke. This study aimed to evaluate the effects of Tai Chi Yunshou (TCY), a form of physical therapy, on upper-limb function and balance in stroke survivors. METHODS: MEDLINE, Embase, CENTRAL and five Chinese databases were retrieved from inception to July 1, 2020 (updated on March 31, 2022). Randomized controlled trials of TCY versus no-treatment for stroke were included. The RoB-2 was used to evaluate the quality of included studies. Upper-limb motor impairment, balance, and activities of daily living (ADLs) were measured by Fugl-Meyer Assessment Upper Extremity Scale (FMA-UE), Berg Balance Scale (BBS), and Barthel Index (BI), respectively. Data synthesis was performed using RevMan (v5.3), and expressed as mean difference (MD) with 95% confidence intervals (CI). RESULTS: Seven studies with 529 participants were included. Compared with no-treatment, TCY improved FMA-UE (MD = 7.31, 95% CI: 5.86-8.77, minimal clinically important difference [MCID]: 9-10), BBS (MD = 4.68, 95% CI: 0.28-9.07, MCID: 4), and BI (MD = 4.12, 95% CI: 3.28-4.96, MCID: 1.85) in stroke survivors. CONCLUSION: TCY may benefit balance and ADLs in rehabilitation after a stroke, but it may not improve upper-limb function clinically.

Knockdown of the DUF647 family member RUS4 impairs stamen development and pollen maturation in Arabidopsis.

ROOT UV-B SENSITIVE4 (RUS4) encodes a Domain of Unknown Function647 (DUF647) protein, whose function is poorly understood. We have previously shown the artificial microRNA knockdown Arabidopsis RUS4 plants, referred to as amiR-RUS4, have severely reduced male fertility with a defect in anther dehiscence. Here, we show that amiR-RUS4 plants are also defective in pollen maturation and germination. Promoter-reporter analysis shows that RUS4 is highly expressed in tapetal layer, developing microspores, mature and germinating pollen, strongly suggesting its role in the process of pollen maturation. As the translational RUS4-GFP fusion protein has been localized to the chloroplasts where the first step of jasmonic acid (JA) biosynthesis takes place, leading to the hypothesis that RUS4 may be involved in JA-mediated stamen development. We show that expression of several JA metabolic genes increased markedly in flower buds of the amiR-RUS4 plants compared to that of the wild-type. We further show that transcript abundance of a clade of the JA-responsive MYB transcript factor genes, especially MYB108, reduced significantly in stamens of amiR-RUS4 plants relative to the wild-type; these MYB transcript factors have been shown to be required for JA-mediated stamen and pollen maturation. Our data suggest that RUS4 may play a role in coordinating anther dehiscence and pollen maturation by affecting the expression of JA-related genes.

CD38 produces nicotinic acid adenosine dinucleotide phosphate in the lysosome.

Nicotinic acid adenosine dinucleotide phosphate (NAADP) is a Ca2+-mobilizing second messenger that regulates a wide range of biological activities. However, the mechanism of its biogenesis remains controversial. CD38 is the only enzyme known to catalyze NAADP synthesis from NADP and nicotinic acid. CD38-mediated catalysis requires an acidic pH, suggesting that NAADP may be produced in acidic endolysosomes, but this hypothesis is untested. In this study, using human cell lines, we specifically directed CD38 to the endolysosomal system and assessed cellular NAADP production. First, we found that nanobodies targeting various epitopes on the C-terminal domain of CD38 could bind to cell surface-localized CD38 and induce its endocytosis. We also found that CD38 internalization occurred via a clathrin-dependent pathway, delivered CD38 to the endolysosome, and elevated intracellular NAADP levels. We also created a CD38 variant for lysosome-specific expression, which not only withstood the degradative environment in the lysosome, but was also much more active than WT CD38 in elevating cellular NAADP levels. Supplementing CD38-expressing cells with nicotinic acid substantially increased cellular NAADP levels. These results demonstrate that endolysosomal CD38 can produce NAADP in human cells. They further suggest that CD38's compartmentalization to the lysosome may allow for its regulation via substrate access, rather than enzyme activation, thereby providing a reliable mechanism for regulating cellular NAADP production.