Additional file 1 of Evolution and function analysis of auxin response factors reveal the molecular basis of the developed root system of Zygophyllum xanthoxylum

Additional file 1

Effects of SDF1α on cell morphology, actin filament polymerization and migration capability after hypoxia.

<p>Adhered hippocampal cells were exposed to hypoxia or left untreated (normoxia) on the seventh day of culturing. Then SDF1α (50 ng/ml) was added to medium for 0.5, 1, 12, 24, and 36 hours. A, Cell morphological changes were observed in normoxia and hypoxia with 24 or 36 h stimulation of SDF1α or not. Arrow heads indicate the changes of morphology. Bar = 50 µm. B, Actin filament polymerization was measured by Alexa Fluor 546-conjugated phalloidin under normoxia or hypoxia with SDF1α for 24 h or not. Distribution changes of actin filament polymerization are indicated by arrows. Bar = 50 µm. C, Cell migration induced by SDF1α was determined by a transwell chamber assay. *<i>P</i><0.01, vs normoxia.</p

Expression of ERK1/2 phosphorylation induced by SDF1α after hypoxia with CXCR7 silence.

<p>Cell lysates were obtained with different treatment to detect phosphorylated ERK1/2 (P-ERK) and total ERK1/2 (T-ERK) by western blot. Total ERK was used as a control. A–B, Detection of ERK phosphorylation induced by hypoxia and/or SDF1α was performed. Cells were treated with hypoxia and/or SDF1α (50 ng/ml) for 24 h, or left untreated. *<i>P</i><0.01 vs untreated group. C–D, Detection of ERK1/2 phosphorylation induced by SDF1α after CXCR7 silence was performed. Cells were transfected with CXCR7 ShRNA and/or with application of SDF1α (50 ng/ml) for 24 h, or left untreated. *<i>P</i><0.01 vs untreated group. E–F, Detection of ERK1/2 phosphorylation induced by SDF1α after CXCR7 silencing and hypoxia was performed. Cells were transfected with CXCR7 ShRNA or not, then all of cells were treated with hypoxia with presence or absence of SDF1α (50 ng/ml) for 24 h. *<i>P</i><0.01 vs group with hypoxia exposure.</p

Expression of SDF1α in hippocampal cells after hypoxia.

<p>Adhered hippocampal cells were exposed to hypoxia (3%O₂, 5% CO₂ and 92% N₂) for 4 h or left untreated on the seventh day of culturing. Supernatants and cell lysates were obtained and measured at 0.5, 1, 12, 24, and 36 h after hypoxia for ELISA and western blot respectively. Untreated cells were used as control. A, Concentrations of supernatant SDF1α in the medium were determined by ELISA. *<i>P</i><0.01, vs control. B, Expression of SDF1α in the cells was measured by western blot analysis. GAPDH was used as reference.</p

CXCR7 Silencing Attenuates Cell Adaptive Response to Stromal Cell Derived Factor 1α after Hypoxia

<div><p>Previous studies have shown that chemotactic factor stromal-cell derived factor 1α (SDF1α) promotes cell recovery from hypoxic injury via its main receptor C-X-C chemokine receptor type (CXCR) 4. However, the role of its new receptor CXCR7 on cell repair against hypoxia and cell response to SDF1α remains largely unknown. In this study, neurons induced from hippocampal progenitor cells were pre-conditioned in hypoxia for 4h and subsequently monitored to investigate the function of SDF1α on cell repair after hypoxia. Neurons were assessed for their cell morphology, actin filament polymerization and migration capability. SDF1α protein levels increased significantly 1 h after hypoxia compared to control (<em>P</em><0.01), and it reached a peak at 24 h after hypoxia. Moreover, addition of SDF1α promoted neurite outgrowth and actin filament polymerization both in normoxic and hypoxic cells compared to untreated cells. Cell migration showed a time-dependent increase with SDF1α stimulation in both groups, and hypoxic cells illustrated a significant augment at 0.5 h, 1 h and 12 h after SDF1α application compared to normoxic cells (<em>P</em><0.01). CXCR7 expression also increased with time dependence after hypoxia and demonstrated a two-fold upregulation compared to control at 24 h after hypoxia. With CXCR7 silencing, axon elongation and actin filament polymerization induced by SDF1α were inhibited sharply both in normoxic and hypoxic cells. CXCR7 silencing also leads to reduced hypoxic cell migration at 0.5 h, 1 h, 12 h, 24 h and 36 h after SDF1α application (<em>P</em><0.01), but it failed to reduce normoxic cell migration induced by SDF1α at 0.5 h, 1 h and 12 h (<em>P</em>>0.05). 24 h SDF1α stimulation led to higher ERK1/2 phosphorylation compared to control, and ERK1/2 phosphorylation increased more in hypoxic cells than that in normoxic cells. This study suggested that CXCR7 plays an important role on cell repair processing induced by SDF1α, and CXCR7 silencing attenuates cell adaptive response to acute SDF1α stimulation (≤12 h) after hypoxia.</p> </div

Data_Sheet_1_Characteristics and duties of clinical research nurses: a scoping review.docx

IntroductionThe characteristics and duties of clinical research nurses (CRNs) are constantly developing and changing with the progress of medical technology and increasing needs in patient care. With the continuous deepening and standardization of clinical trials, the importance and status of CRNs during the whole process of clinical trials are also increasingly valued.MethodsA scoping review of studies related to the characteristics and duties of CRNs was conducted to clarify relevant roles and concepts. An electronic search was conducted on three English databases (PubMed, Web of Science, Embase) and two Chinese databases (CNKI and Wanfang database) in December 2023. Two authors independently screened the literature, extracted information from the included literature, and summarized and reported the findings.ResultsA total of 26 articles published between 1991 and 2023 were analyzed, and four characteristics of CRNs were identified as participants and managers of clinical trials, caregivers and protectors of subjects, coordinators of research teams, and educators. Basic knowledge, skills and literacy, communication and coordination ability, and advanced research ability are the competencies required for CRNs.ConclusionFurther studies should focus on the importance of various characteristics of CRNs, so as to improve the quality of clinical trials and promote clinical evidence-based practice.</p

BPAF upregulates the expression of ER and growth factor target genes.

MCF-7 and T47D cells were serum-starved for 48 hours in phenol red-free medium. Then, cells were treated with BPAF (0 or 1 μM) in phenol red-free medium with 5% C.S. FBS for 16 hours, followed by qPCR analysis of the indicated ER and growth factor gene targets. The fold changes for the BPAF-treated samples are graphed relative to the normalized values of the corresponding controls. Values are presented as the means ± S.E. (*PP<0.01 as compared to the corresponding controls).</p

Data_Sheet_1_Effect of emotional stimulus on response inhibition in people with mild cognitive impairment: an event-related potential study.docx

BackgroundA few studies are emerging to explore the issue of how aging promotes emotional response inhibition. However, there is a lack of empirical study concerning the impact of pathological cognitive impairment on emotional response inhibition. The present study investigated the effect of emotion on response inhibition in people with mild cognitive impairment, the stage of cognitive impairment before dementia.MethodsWe used two emotional stop-signal tasks to explore whether the dual competition framework considering limited cognitive resources could explain the relationship between emotion and response inhibition in mild cognitive impairment.ResultsThe results showed that negative emotions prolonged N2 latency. The Go trial accuracy was reduced in the high-arousal negative conditions and the stop-signal reaction time was prolonged under high-arousal conditions. This study also verified impaired response inhibition in mild cognitive impairment and found that negative emotions prolonged P3 latency in mild cognitive impairment.ConclusionEmotional information interferes with response inhibition in mild cognitive impairment populations, possibly because emotional information captures more attentional resources, thus interfering with response inhibition that relies on common-pool resources.</p

Inhibition of EGFR and PI3K blocks BPAF-induced cell growth.

A) MCF-7 and T47D cells were serum-starved for 48 hours in phenol red-free medium. Then, cells were treated with BPAF (1 μM) ± Iressa (2 μM) in phenol red-free medium with 5% C.S. FBS for 5 days. The average percentage of viable cells in each treatment group was determined with an MTT assay. B) MCF-7 and T47D cells were serum-starved for 48 hours in phenol red-free medium. Then, cells were treated with BPAF (1 μM) ± Iressa (2 μM) in phenol red-free medium with 5% C.S. FBS for 21 days, followed by fixation and staining with crystal violet. The graphs in the lower panels present the average number of colonies formed with representative images in the panels above. C) MCF-7 and T47D cells were serum-starved for 48 hours in phenol red-free medium. Then, cells were treated with BPAF (1 μM) ± LY294002 (5 μM) in phenol red-free medium with 5% C.S. FBS for 5 days. The average percentage of viable cells in each treatment group was determined with an MTT assay. D) MCF-7 and T47D cells were serum-starved for 48 hours in phenol red-free medium. Then, cells were treated with BPAF (1 μM) ± LY294002 (5 μM) in phenol red-free medium with 5% C.S. FBS for 21 days, followed by fixation and staining with crystal violet. The graphs in the lower panels present the average number of colonies formed with representative images in the panels above. All values are presented as the means ± S.E. (**P<0.01).</p

Effects of CXCR7 ShRNA on cell morphology and migration capability induced by SDF1α in hypoxic cells.

<p>A, Cell morphology was observed after hypoxia with pre-treatment of CXCR7 ShRNA or not. Some of cells were transfected with CXCR7 ShRNA, or left untreated. Then all of cells were treated with hypoxia followed by stimulation of SDF1α (50 ng/ml) for 24 h. Neuronal cell morphology was observed and photographed under a fluorescence microscope. Arrows indicate the changes of dendrite length and neurite outgrowth formation. Bar = 30 µm. B, Number of migrated cells was counted by transwell chamber analysis. Cells with or without CXCR7 silencing were treated with hypoxia, and then were placed in the upper chamber with SDF1α (50 ng/ml) in the lower chamber for 0.5, 1, 12, 24, and 36 hours respectively. *<i>P</i><0.01, vs hypoxia.</p