Short video platforms as sources of health information about cervical cancer: A content and quality analysis.

BACKGROUND: The development of short popular science video platforms helps people obtain health information, but no research has evaluated the information characteristics and quality of short videos related to cervical cancer. The purpose of this study was to evaluate the quality and reliability of short cervical cancer-related videos on TikTok and Kwai. METHODS: The Chinese keyword "cervical cancer" was used to search for related videos on TikTok and Kwai, and a total of 163 videos were ultimately included. The overall quality of these videos was evaluated by the Global Quality Score (GQS) and the modified DISCERN tool. RESULTS: A total of 163 videos were included in this study, TikTok and Kwai contributed 82 and 81 videos, respectively. Overall, these videos received much attention; the median number of likes received was 1360 (403-6867), the median number of comments was 147 (40-601), and the median number of collections was 282 (71-1296). In terms of video content, the etiology of cervical cancer was the most frequently discussed topic. Short videos posted on TikTok received more attention than did those posted on Kwai, and the GQS and DISCERN score of videos posted on TikTok were significantly better than those of videos posted on Kwai. In addition, the videos posted by specialists were of the highest quality, with a GQS and DISCERN score of 3 (2-3) and 2 (2-3), respectively. Correlation analysis showed that GQS was significantly correlated with the modified DISCERN scores (p<0.001). CONCLUSION: In conclusion, the quality and reliability of cervical cancer-related health information provided by short videos were unsatisfactory, and the quality of the videos posted on TikTok was better than that of videos posted on Kwai. Compared with those posted by individual users, short videos posted by specialists provided higher-quality health information.

Transketolase drives the development of aortic dissection by impairing mitochondrial bioenergetics.

AIM: Aortic dissection (AD) is a disease with rapid onset but with no effective therapeutic drugs yet. Previous studies have suggested that glucose metabolism plays a critical role in the progression of AD. Transketolase (TKT) is an essential bridge between glycolysis and the pentose phosphate pathway. However, its role in the development of AD has not yet been elucidated. In this study, we aimed to explore the role of TKT in AD. METHODS: We collected AD patients' aortic tissues and used high-throughput proteome sequencing to analyze the main factors influencing AD development. We generated an AD model using BAPN in combination with angiotensin II (Ang II) and pharmacological inhibitors to reduce TKT expression. The effects of TKT and its downstream mediators on AD were elucidated using human aortic vascular smooth muscle cells (HAVSMCs). RESULTS: We found that glucose metabolism plays an important role in the development of AD and that TKT is upregulated in patients with AD. Western blot and immunohistochemistry confirmed that TKT expression was upregulated in mice with AD. Reduced TKT expression attenuated AD incidence and mortality, maintained the structural integrity of the aorta, aligned elastic fibers, and reduced collagen deposition. Mechanistically, TKT was positively associated with impaired mitochondrial bioenergetics by upregulating AKT/MDM2 expression, ultimately contributing to NDUFS1 downregulation. CONCLUSION: Our results provide new insights into the role of TKT in mitochondrial bioenergetics and AD progression. These findings provide new intervention options for the treatment of AD.

Protective effect of Cornuside on OGD/R injury in SH-SY5Y cells and its underlying mechanism.

Apoptosis induced by oxygen-glucose deprivation/reperfusion (OGD/R) injury is the main cause of neuronal damage. Cornuside, a small-molecule cyclic enol ether terpene glycoside extracted from the dried fruit of mature Cornus officinalis Sieb. et Zucc., has vigorous anti-apoptotic and antioxidant effects. Previous studies have shown that Cornuside can reduce apoptosis and improve mitochondrial energy metabolism in cortical neurons of rats by inhibiting caspase-3 and calcium release. In this study, we treated SH-SY5Y cells with OGD/R to simulated ischemia/reperfusion (I/R) injury. Using high-throughput transcriptome sequencing, differentially expressed genes were analyzed in the OGD/R group versus the OGD/R + Cornuside (10 µmol/L) group to explore the neuroprotective mechanisms of Cornuside. The differentially expressed genes were mainly enriched in apoptosis signaling pathway, cell cycle, DNA damage and repair, and p38/JNK MAPK and p53 signaling pathways. The results showed that OGD/R significantly reduced the survival of SH-SY5Y cells, induced apoptosis, disrupted the nucleus, promoted the release of ROS, and led to cell cycle arrest. Cornuside reversed OGD/R-induced damage. By upregulating MAPK8IP1 and downregulating MAPK14, TP53INP1, and signaling pathway-related proteins (p-p38, p-JNK, and p-p53), Cornuside ameliorated cell damage induced by p38/JNK MAPK and p53 signaling pathways. Cornuside also downregulated apoptosis regulatory proteins (Bax, Bcl-2, caspase-3, caspase-9, and cytochrome c) and cell cycle regulatory proteins (cyclin B1, cyclin E, and p21).

Enhancement of biosynthesis of polyhydroxyalkanoates (PHA) from Taihu blue algae by adding by-product acetic acid.

As an easily obtained organic waste, by-product acetic acid could be an appropriate co-substrate with blue algae wastes (increase C/N ratio of substrates) for co-fermentation of PHA production. However, there are still acrylic acid and other chemicals in by-product acetic acid, which could cause severe inhibition for fermenting microorganisms during PHA production process. The current study represented that alkali pretreatment (pH level of 12) is a more favorable method compared with thermal pretreatment (80 â„ƒ for 30 min) for breaking cell walls of blue algae. It seemed that there was no synergistic effect of the combination of thermal and alkali pretreatment methods (temperature of 80 â„ƒ and pH level of 12). Optimal parameters during electro-fenton process for removal of inhibitors in by-product acetic acid were under current of 0.5 A, pH level of 3 and reaction time of 120 min. Both the highest dry weight of PHA and PHA concentration were achieved by applying blue algae and by-product acetic acid (after pretreatment) as co-substrates (mixed ratio of 3:1, stirring speed of 200 r/min, 24 h), indicating that using by-product acetic acid (after pretreatment) as co-substrate could increase C/N ratio and promote PHA production successfully. The current study could offer new insights for improving PHA production by co-fermentation.

Enhanced nitrogen removal from low C/N municipal wastewater employing algal biochar supported nano zero-valent iron (ABC-nZVI) using A/A/O-MBR: Duration and rehabilitation.

To bridge the organic-dependent barrier on nitrogen from low carbon/nitrogen (C/N) municipal wastewater, employing algal biochar supported nano zero-valent iron (ABC-nZVI) was investigated using A/A/O-MBR. Firstly, it can be seen that adequate carbon source is indispensable for the removal, since total nitrogen (TN) removal reached 77.89 % with the influent C/N of 7.8. Secondly, conducted in batch experiments with different doses of ABC-nZVI with/without active sludge, removal efficiency of total inorganic nitrogen (TIN) and the effective time achieved 84.94 % and 24 h with an ABC-nZVI dose of 300 mg/L, respectively. Thirdly, it was found that the duration of high-efficiency denitrification reached 9 h with the addition of 250 mg/L of ABC-nZVI to the anoxic tank of A/A/O-MBR, and the effluent ammonium nitrogen (NH4+-N) also meet the national discharge standard. Besides, biodiversity of both anoxic and aerobic sludge was apparently promoted with the addition of ABC-nZVI, while the lab-scale A/A/O-MBR could also be fully rehabilitated within 12 h. Finally, predicted through PICRUSt2, relevant abundance of functional genes involved in nitrogen metabolism could be enriched by nZVI addition. As an alternative supporting electron donor and mediator, ABC-nZVI can also be participated in the enhanced nitrogen removal in A/A/O-MBR at low C/N.

Histamine H3R antagonist counteracts the impaired hippocampal neurogenesis in Lipopolysaccharide-induced neuroinflammation.

Adult neurogenesis in hippocampus dentate gyrus (DG) is associated with numerous neurodegenerative diseases such as aging and Alzheimer's disease (AD). Overactivation of microglia induced neuroinflammation is well acknowledged to contribute to the impaired neurogenesis in pathologies of these diseases and then leading to cognitive dysfunction. Histamine H3 receptor (H3R) is a presynaptic autoreceptor regulating histamine release via negative feedback way. Recently, studies show that H3R are highly expressed not only in neurons but also in microglia to modulate inflammatory response. However, whether inhibition of H3R is responsible for the neurogenesis and cognition in chronic neuroinflammation induced injury and the mechanism remains unclear. In this study, we found that inhibition of H3R by thioperamide reduced the microglia activity and promoted a phenotypical switch from pro-inflammatory M1 to anti-inflammatory M2 in microglia, and ultimately attenuated lipopolysaccharide (LPS) induced neuroinflammation in mice. Additionally, thioperamide rescued the neuroinflammation induced impairments of neurogenesis and cognitive function. Mechanically, the neuroprotection of thioperamide was involved in histamine dependent H2 receptor (H2R) activation, because cimetidine, an H2R antagonist but not pyrilamine, an H1R antagonist reversed the above effects of thioperamide. Moreover, thioperamide activated the H2R downstream phosphorylated protein kinase A (PKA)/cyclic AMP response element-binding protein (CREB) pathway but inhibited nuclear factor kappa-B (NF-κB) signaling. Activation of CREB by thioperamide promoted interaction of CREB-CREB Binding Protein (CBP) to increase anti-inflammatory cytokines (Interleukin-4 and Interleukin-10) and brain-derived neurotrophic factor (BDNF) release but inhibited NF-κB-CBP interaction to decrease pro-inflammatory cytokines (Interleukin-1ß, Interleukin-6 and Tumor necrosis factor α) release. H89, an inhibitor of PKA/CREB signaling, abolished effects of thioperamide on neuroinflammation and neurogenesis. Taken together, these results suggested under LPS induced neuroinflammation, the H3R antagonist thioperamide inhibited microglia activity and inflammatory response, and ameliorated impairment of neurogenesis and cognitive dysfunction via enhancing histamine release. Histamine activated H2R and reinforced CREB-CBP interaction but weakened NF-κB-CBP interaction to exert anti-inflammatory effects. This study uncovered a novel histamine dependent mechanism behind the therapeutic effect of thioperamide on neuroinflammation.

Effect of Dihuang Yinzi on Inflammatory Response in Cerebral Ischemia-Reperfusion Model Rats by Regulating Gut Microbiota.

Dihuang Yinzi, as a classical Chinese medicine prescription, plays an important role for the treatment of ischemic stroke. Gut microbiota play a functional role for the expression of proinflammatory cytokines and anti-inflammatory cytokines, which further affect central nervous system and change brain function. Our research confirmed that Dihuang Yinzi can exert brain protection by inhibiting inflammatory reaction. Dihuang Yinzi can significantly decrease the contents of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and interleukin-17 (IL-17) in brain, serum, and colon tissues and increase the contents of transforming growth factor-ß (TGF-ß) and interleukin-10 (IL-10) in cerebral ischemia-reperfusion model rats. The results of 16s rRNA high-throughput sequencing showed that Dihuang Yinzi had a significant effect on microbiome in rats. The firmicutes, bacteroidetes, and proteobacteria were dominant in Dihuang Yinzi group. The content of firmicutes increased with the increase of dosage of Dihuang Yinzi. Especially, the content of actinomycetes in the high-dose group was higher than other groups. At the genus level, the number of bacteroides in the antibiotic groups was significantly higher than that in the other treatment groups. The results suggest that Dihuang Yinzi may play important roles in treatment of ischemic stroke by regulating the gut microbiota and the inflammatory reaction in the colon tissues, serum, and brain of the model rats, to verify the scientific nature of this prescription in relieving brain inflammatory reaction and brain injury by this way and to reveal the brain-gut related mechanism of Dihuang Yinzi in treating ischemic stroke.

LDHA mediated degradation of extracellular matrix is a potential target for the treatment of aortic dissection.

Aortic dissection (AD) is a disease with high mortality and lacks effective drug treatment. Recent studies have shown that the development of AD is closely related to glucose metabolism. Lactate dehydrogenase A (LDHA) is a key glycolytic enzyme and plays an important role in cardiovascular disease. However, the role of LDHA in the progression of AD remains to be elucidated. Here, we found that the level of LDHA was significantly elevated in AD patients and the mouse model established by BAPN combined with Ang II. In vitro, the knockdown of LDHA reduced the growth of human aortic vascular smooth muscle cells (HAVSMCs), glucose consumption, and lactate production induced by PDGF-BB. The overexpression of LDHA in HAVSMCs promoted the transformation of HAVSMCs from contractile phenotype to synthetic phenotype, and increased the expression of MMP2/9. Mechanistically, LDHA promoted MMP2/9 expression through the LDHA-NDRG3-ERK1/2-MMP2/9 pathway. In vivo, Oxamate, LDH and lactate inhibitor, reduced the degradation of elastic fibers and collagen deposition, inhibited the phenotypic transformation of HAVSMCs from contractile phenotype to synthetic phenotype, reduced the expression of NDRG3, p-ERK1/2, and MMP2/9, and delayed the progression of AD. To sum up, the increase of LDHA promotes the production of MMP2/9, stimulates the degradation of extracellular matrix (ECM), and promoted the transformation of HAVSMCs from contractile phenotype to synthetic phenotype. Oxamate reduced the progression of AD in mice. LDHA may be a therapeutic target for AD.

Thioperamide attenuates neuroinflammation and cognitive impairments in Alzheimer's disease via inhibiting gliosis.

Alzheimer's disease (AD) is an age-related neurodegenerative disease, which characterized by deposition of amyloid-ß (Aß) plaques, neurofibrillary tangles, neuronal loss, and accompanied by neuroinflammation. Neuroinflammatory processes are well acknowledged to contribute to the progression of AD pathology. Histamine H3 receptor (H3R) is a presynaptic autoreceptor regulating histamine release via negative feedback way. Recently, studies show that H3R are highly expressed not only in neurons but also in microglia and astrocytes. H3R antagonist has been reported to have anti-inflammatory efficacy. However, whether inhibition of H3R is responsible for the anti-neuroinflammation in glial cells and neuroprotection on APPswe, PSEN1dE9 (APP/PS1 Tg) mice remain unclear. In this study, we found that inhibition of H3R by thioperamide reduced the gliosis and induced a phenotypical switch from A1 to A2 in astrocytes, and ultimately attenuated neuroinflammation in APP/PS1 Tg mice. Additionally, thioperamide rescued the decrease of cyclic AMP response element-binding protein (CREB) phosphorylation and suppressed the phosphorylated P65 nuclear factor kappa B (p-P65 NF-κB) in APP/PS1 Tg mice. H89, an inhibitor of CREB signaling, abolished these effects of thioperamide to suppress gliosis and proinflammatory cytokine release. Lastly, thioperamide alleviated the deposition of amyloid-ß (Aß) and cognitive dysfunction in APP/PS1 mice, which were both reversed by administration of H89. Taken together, these results suggested the H3R antagonist thioperamide improved cognitive impairment in APP/PS1 Tg mice via modulation of the CREB-mediated gliosis and inflammation inhibiting, which contributed to Aß clearance. This study uncovered a novel mechanism involving inflammatory regulating behind the therapeutic effect of thioperamide in AD.

Evaluating the Accuracy of Breast Cancer and Molecular Subtype Diagnosis by Ultrasound Image Deep Learning Model.

Background: Breast ultrasound is the first choice for breast tumor diagnosis in China, but the Breast Imaging Reporting and Data System (BI-RADS) categorization routinely used in the clinic often leads to unnecessary biopsy. Radiologists have no ability to predict molecular subtypes with important pathological information that can guide clinical treatment. Materials and Methods: This retrospective study collected breast ultrasound images from two hospitals and formed training, test and external test sets after strict selection, which included 2,822, 707, and 210 ultrasound images, respectively. An optimized deep learning model (DLM) was constructed with the training set, and the performance was verified in both the test set and the external test set. Diagnostic results were compared with the BI-RADS categorization determined by radiologists. We divided breast cancer into different molecular subtypes according to hormone receptor (HR) and human epidermal growth factor receptor 2 (HER2) expression. The ability to predict molecular subtypes using the DLM was confirmed in the test set. Results: In the test set, with pathological results as the gold standard, the accuracy, sensitivity and specificity were 85.6, 98.7, and 63.1%, respectively, according to the BI-RADS categorization. The same set achieved an accuracy, sensitivity, and specificity of 89.7, 91.3, and 86.9%, respectively, when using the DLM. For the test set, the area under the curve (AUC) was 0.96. For the external test set, the AUC was 0.90. The diagnostic accuracy was 92.86% with the DLM in BI-RADS 4a patients. Approximately 70.76% of the cases were judged as benign tumors. Unnecessary biopsy was theoretically reduced by 67.86%. However, the false negative rate was 10.4%. A good prediction effect was shown for the molecular subtypes of breast cancer with the DLM. The AUC were 0.864, 0.811, and 0.837 for the triple-negative subtype, HER2 (+) subtype and HR (+) subtype predictions, respectively. Conclusion: This study showed that the DLM was highly accurate in recognizing breast tumors from ultrasound images. Thus, the DLM can greatly reduce the incidence of unnecessary biopsy, especially for patients with BI-RADS 4a. In addition, the predictive ability of this model for molecular subtypes was satisfactory,which has specific clinical application value.

Activation of CREB-mediated autophagy by thioperamide ameliorates ß-amyloid pathology and cognition in Alzheimer's disease.

Alzheimer's disease (AD) is an age-related neurodegenerative disease, and the imbalance between production and clearance of ß-amyloid (Aß) is involved in its pathogenesis. Autophagy is an intracellular degradation pathway whereby leads to removal of aggregated proteins, up-regulation of which may be a plausible therapeutic strategy for the treatment of AD. Histamine H3 receptor (H3R) is a presynaptic autoreceptor regulating histamine release via negative feedback way. Our previous study showed that thioperamide, as an antagonist of H3R, enhances autophagy and protects against ischemic injury. However, the effect of thioperamide on autophagic function and Aß pathology in AD remains unknown. In this study, we found that thioperamide promoted cognitive function, ameliorated neuronal loss, and Aß pathology in APP/PS1 transgenic (Tg) mice. Interestingly, thioperamide up-regulated autophagic level and lysosomal function both in APP/PS1 Tg mice and in primary neurons under Aß-induced injury. The neuroprotection by thioperamide against AD was reversed by 3-MA, inhibitor of autophagy, and siRNA of Atg7, key autophagic-related gene. Furthermore, inhibition of activity of CREB, H3R downstream signaling, by H89 reversed the effect of thioperamide on promoted cell viability, activated autophagic flux, and increased autophagic-lysosomal proteins expression, including Atg7, TFEB, and LAMP1, suggesting a CREB-dependent autophagic activation by thioperamide in AD. Taken together, these results suggested that H3R antagonist thioperamide improved cognitive impairment in APP/PS1 Tg mice via modulation of the CREB-mediated autophagy and lysosomal pathway, which contributed to Aß clearance. This study uncovered a novel mechanism involving autophagic regulating behind the therapeutic effect of thioperamide in AD.

Celastrol attenuates ischemia/reperfusion-mediated memory dysfunction by downregulating AK005401/MAP3K12.

BACKGROUND: Oxidative stress induces mitochondrial dysfunction, causing memory loss. Long noncoding RNAs influence mitochondrial function and suppress oxidative stress by regulating target protein expression and gene transcription. Celastrol, a natural antioxidant extracted from Tripterygium wilfordii Hook F. ("Thunder of God Vine"), effectively alleviates oxidative stress-mediated tissue injury. In the present study, we examined the effects of celastrol on memory dysfunction induced by ischemia/reperfusion (I/R) and elucidated the mechanisms underlying these effects. METHODS: C57BL/6 mice were used to mimic I/R using the bilateral common carotid clip reperfusion method, and a hippocampal cell line (HT-22) cells were used to establish a model of oxygen-glucose deprivation/reoxygenation (OGD/R). We observed changes in behavior and mitochondrial structure. Cell activity, cell respiration, and antioxidant capacity were measured. MAP3K12, p-JNK, p-c-Jun, p-Akt/Akt, PI3K, Bcl-2, and Bax expression were evaluated. RESULTS: I/R or OGD/R significantly increased AK005401 and MAP3K12 expression, further attenuating PI3K/Akt activation, promoting reactive oxygen species generation and causing mitochondrial dysfunction and cell apoptosis, thereby resulting in memory dysfunction. Celastrol increased antioxidant capacity, inhibited cell apoptosis, and improved mitochondrial function, effectively improving learning and memory by downregulating AK005401 and MAP3K12 and activating PI3K/Akt. CONCLUSIONS: The AK005401/MAP3K12 signaling pathway has an important role in I/R-mediated hippocampal injury, and celastrol can potentially reduce or possibly prevent I/R-induced neuronal injury by downregulating AK005401/MAP3K12 signaling.

Asprosin is associated with anorexia and body fat mass in cancer patients.

PURPOSE: Increasing evidence suggests that many adipokines are involved in cancer-related anorexia and cachexia syndrome (CACS), although the underlying mechanism remains to be clarify. Asprosin is a new peptide hormone mainly secreted by white adipose tissues that can increase appetite and body weight. In this cross-sectional study, we tested whether asprosin may intervene in the development of CACS. METHODS: The fasting plasma asprosin levels were determined via enzyme-linked immune-sorbent assay. Anorexia was determined using the anorexia/cachexia subscale (A/CS) of the functional assessment of anorexia/cachexia therapy (FAACT) questionnaire. The body composition was assessed using bioelectrical impedance analysis. The association of plasma asprosin with anorexia, cachexia, and nutritional status was analyzed. RESULTS: One hundred twenty treatment-naïve patients with pathological confirmed gastrointestinal or lung cancer and 14 mild gastritis patients were recruited. We found no significant difference in asprosin levels between subgroups of patients by age, sex, cancer types or stage. Correlation analysis suggested that asprosin levels were positively associated with body fat mass (r = 0.248, p = 0.043). No correlations were found between asprosin levels and hemoglobin, white blood cell count, blood platelet count, albumin, C-reactive protein, glucose, cholesterol, triglyceride, high density lipoprotein, low density lipoprotein, body mass index, body fat percentage, protein, skeletal muscle, muscle mass, lean body mass, and basal metabolic rate. Furthermore, asprosin levels were not significantly different between patients with or without cachexia. However, patients with anorexia had significantly lower asprosin levels compared with patients without anorexia. No significant difference in asprosin levels between gastritis and gastric cancer patients. Similarly, no significant change of asprosin levels occurred postoperatively in 10 gastric cancer patients. CONCLUSIONS: Patients with anorexia had significantly lower asprosin levels compared with patients without anorexia. We therefore speculated that asprosin might intervene in the development of cancer anorexia and serve as a potential therapeutic target.

Insulin Resistance Promotes the Formation of Aortic Dissection by Inducing the Phenotypic Switch of Vascular Smooth Muscle Cells.

BACKGROUND: Insulin resistance (IR) plays a key role in the development of type 2 diabetes mellitus (T2DM) and is one of its most important characteristics. Previous studies have shown that IR and T2DM were independent risk factors for a variety of cardiovascular and cerebrovascular diseases. However, there are few studies on the relationship between IR and aortic dissection (AD). The goal of this research was to find evidence that IR promotes the occurrence of AD. METHODS: Through the statistical analysis, we determined the proportion of glycosylated hemoglobin (HbA1c) abnormalities (HbA1c > 5.7) in people with acute thoracic aortic dissection (ATAD) and compared the difference of messenger RNA (mRNA) and protein expression of GluT1 in the thoracic aorta of normal people and those with ATAD to find evidence that IR is a causative factor in AD. The mouse model of IR and AD and the IR model of human aortic vascular smooth muscle cells (HA-VSMC) were established. Real time-PCR (RT-PCR) and Western blotting were used to study the mRNA and protein expression. Hematoxylin and eosin (H&E), Masson, and elastic fiber staining, and immunofluorescence were used to study the morphological structure. RESULTS: The proportion of HbA1c abnormalities in patients with ATAD was 59.37%, and the mRNA and protein expression of GluT1 were significantly lower than that in normal people. Fasting glucose concentration (FGC), serum insulin concentration (SIC), and the homeostasis model assessment of insulin resistance (HOMA-IR) of mice was obviously increased in the high-fat diet group and the protein expressions of Glut1 and GluT4 were reduced, indicating that the mouse IR model was successfully established. The incidence of AD was different between the two groups (IR: 13/14, Ctrl: 6/14), and the protein expression of MMP2, MMP9, and OPN were upregulated and SM22 and α-SMA were downregulated in mice. The expressions of mRNA and protein of GluT1 and SM22 in HA-VSMCs with IR were reduced and OPN was increased. CONCLUSION: Combined results of clinical findings, mouse models, and cell experiments show that IR induced the phenotypic switching of vascular smooth muscle cells (VSMCs) from contractile to synthetic, which contributes to the occurrence of AD. It provides a basis for further research on the specific mechanism of how IR results in AD and a new approach for the prevention and treatment of AD.

Rooting ability of rice seedlings increases with higher soluble sugar content from exposure to light.

Rooting ability of rice seedling for mechanical transplanting has a large impact on grain yield. This study explored the relationship between endogenous soluble sugar content and rooting ability of rice seedlings. We placed 15-day-old rice seedlings in controlled environment cabinets with stable light and sampled after 0, 3, 6, 9, 12, and 24 hours of light to measure their soluble sugar content, nitrate content, starch content, soluble protein content and rooting ability. The soluble sugar content of the rice seedlings before rooting increased rapidly from 65.1 mg g-1 to 126.3 mg g-1 in the first 9 hours of light and then tended to stabilize; however, few significant changes in the other physiological indices were detected. With the light exposure time increasing from 3 hours to 12 hours, the rooting ability measured with fresh weight, dry weight, total length, and number of new roots increased by 91.7%, 120.0%, 60.6% and 30.3%, respectively. Rooting ability was related more closely to soluble sugar content than to nitrate-nitrogen content of rice seedlings before rooting and their correlation coefficients were 0.8582-0.8684 and 0.7045-0.7882, respectively. The stepwise regression analysis revealed that the soluble sugar content before rooting explained 73.6%-75.4% of the variance, and the nitrate-nitrogen content explained an additional 7.3%-14.2% of the variance in rooting ability, indicating that compared with nitrate-nitrogen content, soluble sugar content of rice seedlings before rooting was more dominant in affecting rooting ability. This study provides direct evidence of the relationship between the rooting ability and endogenous soluble sugar content of rice seedlings.

Hepatoprotection by Traditional Essence of Ginseng against Carbon Tetrachloride-Induced Liver Damage.

The peroxide produced in the lipid metabolic process attacks liver cells and causes liver injury. Ginsenosides have been shown to have anti-oxidation abilities and to mend myocardial damage. This study evaluated the effect of traditional ginseng essence (TEG) in preventing chemical liver damage induced by carbon tetrachloride (CCl4). Forty 8-week-old male Sprague Dawley (SD) rats were divided into five groups: control, liver injury (CCl4), and TEG by oral gavage at 0.074, 0.149, or 0.298 g/kg/day for nine weeks. Liver injury biochemical indicators, antioxidant enzyme activity, and lipid contents in liver tissues were evaluated. The liver appearance was observed, and histopathological tests were conducted to estimate whether TEG-antagonized oxidants further ameliorated liver injury. The results show that, after supplementation of TEG for nine consecutive weeks and CCl4-induced liver injury for eight weeks, the levels of liver injury biochemical indicators in animal serum decreased significantly, and, in liver tissue, antioxidant activity was significantly improved and accumulation of lipids was decreased. Pathological sections exhibited reduced liver lipid accumulation and fibrosis. As discussed above, TEG can increase the antioxidant capacity in the liver and the maintenance of hepatocyte function, protecting the liver from chemical injury and improving healthcare.

Effects of Different Ligands in the Notch Signaling Pathway on the Proliferation and Transdifferentiation of Primary Type II Alveolar Epithelial Cells.

Background: Transdifferentiation of type II alveolar epithelial cells (AECII) into type I alveolar epithelial cells (AECI) is involved in neonatal respiratory distress syndrome (NRDS). Different ligands of the Notch pathway could have different effects on AECII transdifferentiation. Objective: To investigate the effects of Dlk1 and Jagged1 on the proliferation and transdifferentiation of AECII. Methods: Fetal AECIIs (19 days of gestation) were divided: control group, Dlk1 group, rhNF-κB group. Proliferation was tested using the MTT assay. Expression of surfactant protein C (SP-C) and aquaporin 5 (AQP5) was examined by immunofluorescence. mRNA and protein levels of SP-C, AQP5, Nortch1, Dlk1, Jagged1, and Hes1 were examined by RT-PCR and western blot. Results: In response to Dlk1, cell number and proliferation were increased (P < 0.05), and mRNA and protein levels of SP-C, Dlk1, Notch1, and Hes1 were up-regulated, while AQP and Jagged1 were decreased. In response to rhNF-κB, the cell number and proliferation were reduced, and mRNA and protein levels of Jagged1 and Notch1 were up-regulated, while Dlk1, and SP-C were downregulated. In the Dlk1 group, SP-C, and AQP5 expression patterns suggested that the cells were still transdifferentiating by 96 h, while in the rhNF-κB group, most cells had transdifferentiated by 72 h and were close to apoptosis by 96 h. Conclusion: These results suggest that Dlk1 promoted proliferation of AECIIs and inhibited cell transdifferentiation, while Jagged1 treatment inhibited proliferation of AECIIs and promoted transdifferentiation to AECIs. These results provide some clue for the eventual management of NDRS.

Safflor Yellow B Attenuates Ischemic Brain Injury via Downregulation of Long Noncoding AK046177 and Inhibition of MicroRNA-134 Expression in Rats.

Stroke breaks the oxidative balance in the body and causes extra reactive oxygen species (ROS) generation, leading to oxidative stress damage. Long noncoding RNAs (lncRNAs) and microRNAs play pivotal roles in oxidative stress-mediated brain injury. Safflor yellow B (SYB) was able to effectively reduce ischemia-mediated brain damage by increasing antioxidant capacity and inhibiting cell apoptosis. In this study, we investigated the putative involvement of lncRNA AK046177 and microRNA-134 (miR-134) regulation in SYB against ischemia/reperfusion- (I/R-) induced neuronal injury. I/R and oxygen-glucose deprivation/reoxygenation (OGD/R) were established in vivo and in vitro. Cerebral infarct volume, neuronal apoptosis, and protein expression were detected. The effects of SYB on cell activity, cell respiration, nuclear factor erythroid 2-related factor 2 (Nrf2), antioxidant enzymes, and ROS were evaluated. I/R or OGD/R upregulated the expression of AK046177 and miR-134 and subsequently inhibited the activation and expression of CREB, which caused ROS generation and brain/cell injury. SYB attenuated the effects of AK046177, inhibited miR-134 expression, and promoted CREB activation, which in turn promoted Nrf2 expression, and then increased antioxidant capacities, improved cell respiration, and reduced apoptosis. We suggested that the antioxidant effects of SYB were driven by an AK046177/miR-134/CREB-dependent mechanism that inhibited this pathway, and that SYB has potential use in reducing or possibly preventing I/R-induced neuronal injury.