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and the nomogram model incorporating the FF value, age, and BMI can further improve the predictive efficiency to provide a visual modality for predicting early bone mass loss.
To assess the inhibitory effects of aloin on lactate-induced gastric proliferation and migration of cancer cells and explore the underlying molecular mechanism.
Gastric cancer BGC-823 cells were treated with aloin, lactate or the combination of lactate and different doses of aloin. EdU assay was used to detect the proliferation of BGC-823 cells, and colony formation ability of the cells was evaluated with colony forming assay; wound healing and Transwell assays were used to detect the changes in migration ability of the treated cells. The expression levels of cyclin D1, cyclin E1, PCNA, N-cadherin, E-cadherin, MMP-2, MMP-9 and HMGB1 were determined using Western blotting, and ELISA was performed to detect HMGB1 release. HMGB1 expression was knocked down in BGC-823 cells using RNA interference technique, and the effects of HMGB1 knockdown on proliferation and migration of the cells stimulated with lactate for 24 h were examined using EdU and wound healing assays.
Aloin treatment significantly inhibited lssions of proliferation- and migration-related proteins.
To investigate the molecular mechanism by which pirfenidone inhibits scar formation through the TGF-β/Smad pathway.
Cultured rabbit tenon fibroblasts (RTFs) were treated with different concentrations of pirfenidone to determine its initial active concentration and optimum concentration of pirfenidone for inhibiting RTF proliferation using CCK-8 assay. In RTFs treated with pirfenidone at the initial and optimal concentrations, expressions of TGF-β3, collagen I and collagen III were examined with both immunofluorescence assay and Western blotting, and their mRNA expression levels were detected using RT-PCR.
The initial and optimal concentrations of pirfenidone for inhibiting RTF proliferation were 0.1 mg/mL and 0.27 mg/mL, respectively. In RTFs treated with pirfenidone at the two concentrations for 24 h, both immunofluorescence assay and Western blotting showed significantly lowered protein expressions of TGF-β3, collagen I and collagen III as compared with those in the control group (
< 0.05). The mRNA expressions of TGF-β3, collagen I and collagen III in the RTFs were also significantly lowered after treatment with pirfenidone at the initial and optimal concentrations (
< 0.05).
Pirfenidone concentration-dependently inhibits the proliferation of RTFs possibly by down-regulating the expression of TGF-β3 in the TGF-β/Smad pathway.
Pirfenidone concentration-dependently inhibits the proliferation of RTFs possibly by down-regulating the expression of TGF-β3 in the TGF-β/Smad pathway.
To investigate the effect of transforming growth factor (TGF-β) inhibition on functional recovery of spinal cord injury in mice.
Twelve mice were divided into treatment group, control group and sham-operated group (
=4). The mice in the treatment group were subjected to hemisection of the spinal cord and received intraperitoneal injection of TGF-β neutralizing antibody (1D11) 3 times a week (25 μL each time), and those in control group were injected with the vehicle antibody (13C4) following spinal cord hemisection. The sham-operated mice underwent sham operation to expose the spinal cord without hemisection. Four weeks later, the heart of the mice was perfused and 1-2 cm of the spinal cord spanning the injury site was harvested. Immunofluorescence staining of FSP1, fibronectin, and PGP9.5 was performed to assess fibroblast recruitment in the injury area, fibronectin deposition, and neurological recovery. For further verification of the results, we used a mouse model of spinal cord clamp injury to observtion and repair of the injured spinal cord in mice.
To evaluate the efficacy of tunnel technique (TUN) in treatment of teeth with adjacent gingival regression (GR) combined with noncarious cervical lesions (NCCL).
We collected data from 21 patients (79 teeth) undergoing TUN surgery for GR combined with NCCL. According to GR depth (GRD) and lesion depth (LD) of NCCL, the teeth were divided into group 1 with GRD≤3 mm and LD≤1 mm; group 2 with GRD≤3 mm and LD>1mm; group 3 with GRD>3 mm and LD≤1 mm; and group 4 with GRD>3 mm and LD>1 mm. The mean root coverage (MRC) rate, complete root coverage (CRC) rate, keratinized gingival width, and keratinized gingival thickness were compared among the 4 groups after TUN surgery.
The keratinized gingival width and thickness were significantly improved after the surgery in the 4 groups. When the GRD was below 3 mm, the MRC was not significantly different between group 1 and group 2 (8.55%
95.45%,
>0.05); When the GRD was beyond 3 mm, the MRC and CRC rates were both decreased in group 3 and group 4, especially in group 4, where the CRC rate (25%) was significantly lower than those in the other 3 groups (
< 0.01).
In patients with GR combined with NCCL, TUN surgery can obviously improve keratinized gingival width and thickness. GRD has a greater effect on the outcome of root coverage than LD, suggesting that NCCL restoration before TUN surgery may not be necessary. Both GRD and LD should be considered in the evaluation of the clinical efficacy of TUN surgery.
In patients with GR combined with NCCL, TUN surgery can obviously improve keratinized gingival width and thickness. GRD has a greater effect on the outcome of root coverage than LD, suggesting that NCCL restoration before TUN surgery may not be necessary. Both GRD and LD should be considered in the evaluation of the clinical efficacy of TUN surgery.
To study the effects of different continuous background noises on auditory response characteristics of primary auditory cortex (A1) neurons in awake mice.
We performed in vivo cell-attached recordings in layer 4 neurons of the A1 of awake mice to investigate how continuous background noises of different levels affected the intensity tuning, frequency tuning and time characteristics of individual A1 neurons. According to the intensity tuning characteristics and types of stimulation, 44 neurons were devided into 4 groups monotonic-intensity group (20 monotonic neurons), nonmonotonic-intensity group (6 nonmonotonic neurons), monotonic-frequency group (25 monotonic neurons) and monotonic-latency group (15 monotonic neurons).
The A1 neurons only had transient spike response within 10 to 40 ms after the onset of continuous wild-band noise stimulation. The noise intensity had no significant effects on the background firing rates of the A1 neurons (
>0.05). The increase of background noise resulted in a sige increase of background noise intensity. An increased background noise leads to compressed frequency band-width, a decreased firing rate and a prolonged spike latency, but the frequency selectivity and the time accuracy of auditory response to the same noise remain stable.
The acoustic response threshold of the A1 neurons increases linearly with the increase of background noise intensity. An increased background noise leads to compressed frequency band-width, a decreased firing rate and a prolonged spike latency, but the frequency selectivity and the time accuracy of auditory response to the same noise remain stable.
To explore the role of extranuclear p53-mediated autophagy suppression by regulating AMPK/mTOR signaling pathway in heat stress (HS)-induced injury of mouse aortic endothelial cells (MAECs).
Primary cultures of MAECs were pretreated with compound C (an AMPK inhibitor), rapamycin (a mTOR inhibitor) or pifithrin-α (PFT, a selective p53 inhibitor) for 1 h before exposure to HS (43 ℃) for 2 h. The changes in cell viability at different time points after HS were examined using CCK-8 assay, and the protein expressions of P53, LC3-II, Beclin-1, p62 and the AMPK/mTOR signaling proteins were detected using Western blotting. In the animal experiment, C57 mice were pretreated with compound C, rapamycin or PFT and exposed to a high temperature at 40 ℃ to induce HS. The pathological changes in the aorta of the mice were observed with HE staining, and cell apoptosis was detected using TUNEL staining.
In cultured MAECs, the cell viability was significantly reduced (
< 0.05) and the mitochondrial fraction of p53 i. Pretreatment with compound C obviously aggravated HS-induced vascular injury and endothelial cell apoptosis, while pretreatment with either rapamycin or PFT significantly alleviated these injuries.
Autophagy inhibition mediated by extranuclear p53
inhibiting AMPK activity and activating mTOR signaling participates in HS-induced injury of MAECs.
Autophagy inhibition mediated by extranuclear p53 via inhibiting AMPK activity and activating mTOR signaling participates in HS-induced injury of MAECs.
To investigate the secondary structure, physicochemical properties and antibacterial activity of Brevinin- 2GHk (BR2GK), an antimicrobial peptide from frog skin, and explore its antibacterial mechanism.
BR2GK was synthesized, purified with high performance liquid chromatography (HPLC) and identified using mass spectrometry. Circular dichroism was used to determine the secondary structure and physicochemical properties of BR2GK. Two-fold dilution method was used to determine the antibacterial activity of BR2GK, and its antibacterial mechanism was explored using laser scanning confocal microscopy (LSCM) and scanning electron microscopy (SEM). The hemolytic activity of BR2GK was analyzed in red blood cells. Isothermal titration calorimetry (ITC) and surface plasmon resonance imaging (SPRi) were employed to detect the binding of BR2GK to lipopolysaccharide (LPS), and the antioxidant activity of BR2GK was evaluated using biochemical kits.
The synthesized BR2GK, with a purity exceeding 95% after purification, antibacterial activity and lower cytotoxicity.
BR2GK, as a broad-spectrum antibacterial peptide with also a strong antioxidant capacity, does not cause hemolysis and is capable of binding to LPS. BR2GK has an important value for future design and synthesis of antimicrobial peptides with stronger antibacterial activity and lower cytotoxicity.
To obtain GH/tPA double transgenic mice, analyze the expression level of tissue plasminogen activator (tPA) in the mammary glands and observe the growth and development of the transgenic mice.
We obtained the offspring mice of 2 tPA single transgenic mice (P03 and P05) mated with a female nontransgenic mouse by microinjection of linearized GH plasmid into the fertilized eggs and embryo transfer. click here PCR was used to detect the gene integration. The expression levels of tPA in single gene and double gene transgenic mice were compared using ELISA and Western blotting. We assessed the effects of GH gene transduction on the growth and development of the transgenic mice by observing body weight changes of the mice at each developmental stage.
A total of 286 fertilized eggs were collected from P03 mice, and after embryo transfer, 77 offspring mice were obtained, including 16 tPA single transgenic mice (7 male, 9 female) and 13 GH/tPA double transgenic mice (8 male, 5 female) as confirmed by PCR. The integration rate of the double genes was 16.