bluuebunny/crossref_metadata_2025_split huggingface dataset:
Reversible changes in aqueous outflow facility, hydrodynamics, and morphology following acute intraocular pressure variation in bovine eyes
Authors: ZHU Jing-ying , YE Wen , WANG Ti , GONG Hai-yan 
Published: January 2024

Background
Elevated intraocular pressure (IOP) is primarily due to increased aqueous outflow resistance, but how aqueous outflow resistance is generated and regulated are still not fully understood. The aim of this study is to determine whether changes in outflow facility, outflow pattern, and morphology following acute IOP elevation were reversible when the IOP was returned to a normal level in bovine eyes using a two-color tracer technique to label outflow patterns within the same eye.

Methods
Twelve fresh enucleated bovine eyes were perfused with Dulbecco's phosphate buffer saline (PBS) containing 5.5 mmol/L glucose (DBG) at 30 mmHg first to establish the baseline outflow facility followed by a fixed volume of red fluorescent microspheres (0.5 μm, 0.002% v/v). After the red tracer being replaced with DBG in the anterior chamber, perfusion was continued at 7 mmHg with the same volume of green tracer, followed by a fixative. In two control groups, the eyes were constantly perfused at either 30 mmHg (n=6) or 7 mmHg (n=6) using the same methods. The outflow facility (C, μl·min·-1mmHg-1), was continuously recorded. Confocal images were taken along the inner wall (IW) of the aqueous plexus (AP) in frontal sections. The percent of the effective filtration length (PEFL, PEFL=IW length exhibiting tracer labeling/total length of IW) was measured. Sections with AP were processed and examined by light microscopy. The total length of IW and the length exhibiting separation (SL) in the juxtacanalicular connective tissue (JCT) were measured. A minimum of eight collector channel (CC) ostia per eye were analyzed for herniations.

Results
In the experimental (30-7 mmHg) group, the outflow facility was significantly higher at 7 mmHg ((4.81±1.33) μl·min·-1mmHg-1) than that at 30 mmHg ((0.99±0.15) μl·min·-1mmHg-1, P=0.002), corresponding to a significant increase in the PEFL (P=0.0003). The percent of CC ostia exhibiting herniations in the experimental group ((67.40±8.90) μl·min·-1mmHg-1) decreased significantly compared to that in the control at 30 mmHg ((94.44±3.33) μl·min·-1mmHg-1, P=0.03), but higher than that in the control at 7 mmHg ((29.43±4.60) μl·min·-1mmHg-1, P=0.01). Washout-associated separation between the IW and JCT was found by light microscopy and percent separation length (PSL, PSL=SL/total length of IW) was decreased in the control at 30 mmHg compared to that in the experimental group and control at 7 mmHg.

Conclusions
The pressure-induced morphological and hydrodynamic changes were reversible. Changes (collapse of AP, separation between the JCT and IW, and herniation into CC ostia) influence the effective filtration area that regulates outflow facility.
Mitogen-activated protein kinase-activated protein kinase 2 regulates tumor necrosis factor-induced interleukin-6 expression via human antigen R
Authors: XU Jin , SU Xin , SHI Jia-Xin , SUN He , WU Ting , SHI Yi 
Published: January 2024

Background
Human antigen R (HuR) is a ubiquitously expressed member of the ELAV family, and has relatively high cytoplasmic abundance in lung tissue regenerating after injury. In this study, we investigated whether mitogen-activated protein kinase (MAPK)-activated protein kinase 2 (MK2) and HuR participate in the tumor necrosis factor (TNF)-induced expression of interleukin-6 (IL-6).

Methods
Human pulmonary microvascular endothelial cells were treated with TNF following short interfering RNA-mediated knockdown of MK2 or HuR. Cell supernatants were collected to detect the mRNA and protein expression of IL-6 at different time points. The expression and half-life of IL-6 mRNA were then determined in cells that had been treated with actinomycin D. Finally, after knockdown of MK2, the cytoplasmic expression of HuR protein was analyzed using Western blotting.

Results
MK2 or HuR knockdown decreased both the mRNA and protein expression of IL-6 in TNF-stimulated cells. In MK2 knockdown cells, the half-life of IL-6 mRNA was reduced to 36 minutes, compared with 67 minutes in the control group. In HuR knockdown cells, the half-life of IL-6 mRNA decreased from 62 minutes to 24 minutes. Further analysis revealed that knockdown of MK2 resulted in reduced HuR protein expression in the cytoplasm.

Conclusions
MK2 regulates the TNF-induced expression of IL-6 by influencing the cytoplasmic levels of HuR.
Role of mitochondrial damage during cardiac apoptosis in septic rats
Authors: Li Li , Hu Bang-chuan , Chen Chang-qin , Gong Shi-jin , Yu Yi-hua , Dai Hai-wen , Yan Jing 
Published: January 2024

Background
Myocardial apoptosis is involved in the pathogenesis of sepsis-related myocardial depression. However, the underlying mechanism remains unknown. This study investigated the role of mitochondrial damage and mitochondria-induced oxidative stress during cardiac apoptosis in septic rats.

Methods
Seventy-two Sprague-Dawley rats were randomly divided into a control group and septic group receiving lipopolysaccharide injection. Heart tissue was removed and changes in cardiac morphology were observed by light microscopy and scanning electron microscopy. In situ apoptosis was examined using terminal transferase-mediated dUTP nick end-labeling assay and nuclear factor-kappa B activation in myocardium by Western blotting to estimate myocardial apoptosis. Appearance of mitochondrial cristae and activation of cytochrome C oxidase were used to evaluate mitochondrial damage. Oxidative stress was assessed by mitochondrial lipid and protein oxidation, and antioxidant defense was assessed by mitochondrial superoxide dismutase and glutathione peroxidase activity.

Results
Sepsis-induced inflammatory cell infiltration, myocardium degeneration and dropsy were time-dependent. Expanded capillaries were observed in the hearts of infected rats 24 hours post-challenge. Compared with sham-treated rats, the percentage of cell apoptosis increased in a time-dependent manner in hearts from septic rats at 6 hours, 12 hours and 24 hours post-injection (P < 0.05). The expression of nuclear factor-kappa B p65 decreased gradually in the cytosol and increased in the nucleus during sepsis, indicating that septic challenge provoked the progressive activation of nuclear factor-kappa B. Mitochondrial cristae and activation of cytochrome C oxidase increased in a time-dependent manner. Both superoxide dismutase and glutathione peroxidase activities decreased, while mitochondrial lipid and protein oxidation increased between 6 and 24 hours after lipopolysaccharide challenge.

Conclusions
Septic challenge induced myocardial apoptosis and mitochondrial damage. Furthermore, mitochondrial damage via alteration of defenses against reactive oxygen species might play an important role in myocardial apoptosis during sepsis.
Propofol may protect PC12 cells from β-amyloid25-35 induced apoptosis through the GSK-3β signaling pathway
Authors: Zhang Rui , Xu Jie , Liu Yan-yong , Zuo Ping-ping , Yang Nan , Ji Chao , Wang Yun , Wang Hui , Wu An-shi , Yue Yun 
Published: January 2024

Background
There are two major pathological hallmarks of Alzheimer's disease. One is the progressive accumulation of beta-amyloid (Aβ) in the form of senile plaques; the other is hyperphosphorylated tau, causing neuronal apoptosis. Some inhalation anesthetics, such as isoflurane and desflurane, have been suggested to induce Aβ accumulation and cause AD-like neuropathogenesis. Whether intravenous anesthetics have similar effects is still unclear. We therefore set out to determine the relationship between propofol and AD-like pathogenesis.

Methods
PC12 cells were cultured in serum-free medium for 12 hours prior to drug treatment. Various concentrations from 5 μmol/L to 80 μmol/L of aggregated Aβ25-35 were added to determine a proper concentration for further study. After exposure to 10 μmol/L Aβ25-35 alone or with 20 μmol/L propofol for 6 hours, PC12 cell viability was determined by MTT assay. Western blotting and immunocytochemical staining were performed to observe the protein expression of the Bcl-2 family, tau phosphorylation at different sites, and tau protein kinases and phosphatases.

Results
Aβ25-35 induced a decrease in PC12 cell viability in a dose-dependent manner. Exposure to 10 μmol/L Aβ25-35 for 6 hours resulted in the mild cell survival, accompanied by a decline in Bcl-2, and an increase in phosphorylation of GSK-3β and tau at different sites. Compared with the Aβ25-35 group, cells treated with propofol alone showed no significant difference, while cells co-incubated with propofol and Aβ25-35 showed a significantly higher survival rate (P <0.01 or P <0.05). Tau phosphorylation at Ser396, Ser404 and Thr231 and the level of GSK-3β in PC12 cells increased after exposure to 10 μmol/L Aβ25-35. Co-incubation with propofol attenuated cellular apoptosis by inhibiting tau phosphorylation.

Conclusions
These data indicate that propofol may protect PC12 cells from Aβ25-35-induced apoptosis and tau hyperphosphorylation through the GSK-3β pathway, therefore it may be a safer anesthesia for AD and elderly patients.
Serum sclerostin levels associated with lumbar spine bone mineral density and bone turnover markers in patients with postmenopausal osteoporosis
Authors: XU Xiao-juan , SHEN Lin , YANG Yan-ping , LU Fu-rong , ZHU Rui , SHUAI Bo , LI Cheng-gang , WU Man-xiang 
Published: January 2024

Background
Sclerostin, expressed exclusively by osteocytes, is a negative regulator of bone formation. To gain insights into the action of sclerostin in postmenopausal osteoporosis, we evaluated serum sclerostin levels in postmenopausal women and investigated its possible associations with bone turnover markers in patients with postmenopausal osteoporosis.

Methods
We detected serum sclerostin, and measured lumbar spine bone mineral density in 650 Chinese postmenopausal women. We also assessed serum levels of β-isomerized C-terminal crosslinking of type I collagen, intact N-terminal propeptide of type I collagen, N-mid fragment of osteocalcin, 25-hydroxyvitamin D, and estradiol.

Results
Serum sclerostin levels were lower in postmenopausal osteoporotic women compared with non-osteoporotic postmenopausal women ((38.79±7.43) vs. (52.86±6.69) pmol/L, P <0.001). Serum sclerostin was positively correlated with lumbar spine bone mineral density (r=0.391, P <0.001) and weakly negatively correlated with β-isomerized C-terminal crosslinking of type I collagen, intact N-terminal propeptide of type I collagen, N-mid fragment of osteocalcin (r= −0.225, P <0.001; r= −0.091, P=0.046; r= −0.108, P=0.018; respectively) in postmenopausal osteoporosis. There was no significant association of serum sclerostin with age, body mass index, 25-hydroxyvitamin D, and estradiol (r= −0.004, P=0.926; r=0.067, P=0.143; r=0.063, P=0.165; r= −0.045, P=0.324; respectively).

Conclusion
Sclerostin may be involved in the pathogenesis of postmenopausal osteoporosis and may play a role in bone turnover.
Impact of imipenem treatment on colonic mycobiota in rats with double-hit sepsis
Authors: Guan Jun , Liu Shao-ze , Lin Zhao-fen , Li Wen-fang , Liu Xue-feng , Chen De-chang 
Published: January 2024

Background
Broad-spectrum antibiotic administration promotes intestinal colonization of exogenous fungal pathogens in healthy animals and has been recognized as one of the risk factors of invasive fungal infection in clinical settings. It is unclear whether broad-spectrum antibiotic treatment would change the intestinal mycobiota without exogenous fungal challenge in the context of sepsis.

Methods
We established a rat model of double-hit sepsis using burn injury and endotoxin challenge. Rats with burn injury or double-hit sepsis received imipenem treatment for 3 days or 9 days, and their colon contents were sampled for selective fungal culture and isolation counts.

Results
Imipenem treatment promoted the overgrowth of the commensal fungus Geotrichum capitatum in rats with burn injury. Imipenem treatment also promoted colon colonization by exogenous fungi in rats with burn injury and double-hit sepsis, including Trichosporon cutaneum, Candida albicans, Candida krusei, and Candida glabrata. A longer duration of imipenem treatment had a stronger impact on colon colonization by exogenous fungi.

Conclusion
Imipenem treatment facilitates the overgrowth of commensal fungi and colonization by exogenous, potentially pathogenic fungi in the colons of rats with burn injury or double-hit sepsis.
Human decorin regulates proliferation and migration of human lung cancer A549 cells
Authors: LIANG Shuo , XU Jin-fu , CAO Wei-jun , LI Hui-ping , HU Cheng-ping 
Published: January 2024

Background
Decorin is a small leucine-rich proteoglycan and it plays an important role in regulation of cell growth and migration in various tumor cell lines. Decorin was found down-regulated in non-small cell lung cancer tissue and may be involved in regulation of lung cancer development.

Methods
In this study, lentivirus-mediated RNA interference and over expression were employed to change the expression levels of decorin in lung cancer A549 cells. We tested the cell cycle of A549 cells and the expression of transforming growth factor (TGF)-β1, cyclin D1, epidermal growth factor receptor (EGFR), P53, and P21.

Results
We found that up-regulation of decorin could inhibit proliferation, block cell cycle at G1 and decrease invasive activity of A549 cells. Moreover, we also show that up-regulation of decorin induced significant decreases of TGF-β1, cyclin D1 expression, phosphorylation of EGFR, and increases of P53 and P21 expression. Opposite results were observed in A549 cells with down-regulation of decorin.

Conclusion
Our results suggest that decorin is a key regulator involved in proliferation and migration of A549 cells.
In vitro cartilage production using an extracellular matrix-derived scaffold and bone marrow-derived mesenchymal stem cells
Authors: ZHAO Yan-hong , YANG Qiang , XIA Qun , PENG Jiang , LU Shi-bi , GUO Quan-yi , MA Xin-long , XU Bao-shan , HU Yong-cheng , ZHAO Bin , ZHANG Li , WANG Ai-yuan , XU Weng-jing , MIAO Jun , LIU Yue 
Published: January 2024

Background
Cartilage repair is a challenging research area because of the limited healing capacity of adult articular cartilage. We had previously developed a natural, human cartilage extracellular matrix (ECM)-derived scaffold for in vivo cartilage tissue engineering in nude mice. However, before these scaffolds can be used in clinical applications in vivo, the in vitro effects should be further explored.

Methods
We produced cartilage in vitro using a natural cartilage ECM-derived scaffold. The scaffolds were fabricated by combining a decellularization procedure with a freeze-drying technique and were characterized by scanning electron microscopy (SEM), micro-computed tomography (micro-CT), histological staining, cytotoxicity assay, biochemical and biomechanical analysis. After being chondrogenically induced, the induction results of BMSCs were analyzed by histology and Immunohisto-chemistry. The attachment and viability assessment of the cells on scaffolds were analyzed using SEM and LIVE/DEAD staining. Cell-scaffold constructs cultured in vitro for 1 week and 3 weeks were analyzed using histological and immunohistochemical methods.

Results
SEM and micro-CT revealed a 3-D interconnected porous structure. The majority of the cartilage ECM was found in the scaffold following the removal of cellular debris, and stained positive for safranin O and collagen II. Viability staining indicated no cytotoxic effects of the scaffold. Biochemical analysis showed that collagen content was (708.2±44.7) μg/mg, with GAG (254.7±25.9) μg/mg. Mechanical testing showed the compression moduli (E) were (1.226±0.288) and (0.052±0.007) MPa in dry and wet conditions, respectively. Isolated canine bone marrow-derived stem cells (BMSCs) were induced down a chondrogenic pathway, labeled with PKH26, and seeded onto the scaffold. Immunofluorescent staining of the cell-scaffold constructs indicated that chondrocyte-like cells were derived from seeded BMSCs and excreted ECM. The cell-scaffold constructs contained pink, smooth and translucent cartilage-like tissue after 3 weeks of culture. We observed evenly distributed cartilage ECM proteoglycans and collagen type II around seeded BMSCs on the surface and inside the pores throughout the scaffold.

Conclusion
This study suggests that a cartilage ECM scaffold holds much promise for in vitro cartilage tissue engineering.
Is prophylactic somatostatin effective to prevent post-endoscopic retrograde cholangiopancreatography pancreatitis or hyperamylasemia? A randomized, placebo-controlled pilot trial
Authors: WANG Zi-kai , YANG Yun-sheng , CAI Feng-chun , WANG Yong-hua , SHI Xiao-lin , DING Chen , LI Wen 
Published: January 2024

Background
Effects of prophylactic somatostatin on post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis (PEP) and hyperamylasemia remain inconclusive. This study aimed to examine whether high-dose, long-term continuous infusion of somatostatin can reduce the incidence of PEP and post-ERCP hyperamylasemia.

Methods
This was a randomized, placebo-controlled pilot trial. One hundred and twenty-four patients scheduled for ERCP from December 2008 to May 2010 randomly received one of the following three interventions: pre-ERCP somatostatin (0.5 mg/h for 24 hours, starting 1 hour prior to ERCP; n=36), post-ERCP somatostatin (0.5 mg/h for 24 hours, starting 1 hour after ERCP; n=47), or placebo (saline for 24 hours, starting 1 hour prior to ERCP; n=41). Serum amylase and lipase concentrations were measured 1 to 3 hours prior to ERCP and 6, 24, and 48 hours after ERCP.

Results
The three groups did not differ in age, gender, medical history, or ERCP procedure (catheterization using contrast or guidewire, pancreatic duct visualization, procedure time, or procedure type). The rate of PEP was 13.7% (17/124) in the overall study sample and 16.7% (6/36), 10.6% (5/47), and 14.6% (6/41) in the pre-ERCP somatostatin, post-ERCP somatostatin, and placebo groups, respectively (P=0.715). The rate of post-ERCP hyperamylasemia was 19.4% (7/36), 21.3% (10/47), and 46.3% (19/41) in the pre-ERCP somatostatin, post-ERCP somatostatin, and placebo groups, respectively (P=0.011).

Conclusions
High-dose, long-term continuous infusion (0.5 mg/h for 24 hours) of somatostatin, performed as either a pre- or post-ERCP, can reduce the incidence of hyperamylasemia, but not PEP.
Device related complications of the Coflex interspinous process implant for the lumbar spine
Authors: ZANG Lei , DU Peng , HAI Yong , SU Qing-jun , LU Shi-bao , LIU Tie 
Published: January 2024

Background
Coflex, a type of interspinous process implant, can provide intervertebral dynamic stability for surgical segments and effectively relieve lumbocrural pain. However, few studies have described therapeutic strategies and the avoidance of Coflex implant complications.

Methods
Coflex implant complications in this study included intraoperative or postoperative spinous process fracture, aggravated postoperative lumbocrural pain, dislodgment and malposition. The complications were analyzed, and therapeutic strategies were applied according to the specific complication. The Visual Analogue Scale and Oswestry Disability Index scores were evaluated by using the paired-samples test from SPSS 12.0.

Results
Conservative treatment was provided to seven patients who experienced aggravated lumbocrural pain even though their devices remained in the correct position, and pedicle screw treatment was used as an alternative in four cases. The Visual Analogue Scale and Oswestry Disability Index scores showed evident improvement in these patients. The Visual Analogue Scale and Oswestry Disability Index scores of two patients who underwent revision were also improved.

Conclusions
Coflex implants should be avoided in patients with osteoporosis, a narrow interspinous space and intervertebral coronal spondylolysis, or sagittal instability. Furthermore the device choice, depth of implantation, and clamping intensity should be appropriate. Conservative treatment can be provided to patients with symptoms if the device remains in the correct position; however, revisions and salvages should be undertaken with internal fixation of pedicle screws for patients with device malposition, intraoperative implantation failure, or device intolerance.
Triple antithrombotic therapy versus double antiplatelet therapy after percutaneous coronary intervention with stent implantation in patients requiring chronic oral anticoagulation: a meta-analysis
Authors: Jayswal Saheb K , DENG Bing-qing , HU Qing-song , XIE Shuang-lun , GENG Deng-feng , NIE Ru-qiong 
Published: January 2024

Background
Whether an addition of OAC to double antiplatelet therapy for patients with an indication of chronic oral anticoagulation undergoing PCI-S may improve clinical outcomes is still debated. This meta-analysis aimed to update and re-compare the benefits and risks of triple antithrombotic therapy (TT) with double anti-platelet therapy (DAPT) after in patients who requiring oral anticoagulation after percutaneous coronary interventions with stenting (PCI-s).

Methods
Ten reports of observational retrospective or prospective studies were retrieved, including a total of 6296 patients, follow-up period ranging from 1 year to 2 years.

Results
Baseline characteristics were similar in both groups. The main finding of this study is the overall incidence of major adverse cardiovascular events (MACE), myocardial infarction (MI) and stent thrombosis was comparable between two groups. Patients with TT was associated with significant reduction in ischemic stroke (OR: 0.27; 95% CI: 0.13-0.57; P=0.0006) as compared to DAPT. We reaffirmed triple therapy significantly increased the risk of major bleeding (OR: 1.47; 95% CI: 1.22-1.78; P <0.0001) and minor bleeding (OR: 1.55; 95% CI: 1.07-2.24; P=0.02).

Conclusions
Triple therapy is more efficacious in reducing the occurrence of ischemic stroke in PCI-s patients with an indication of chronic oral anticoagulation (OAC), compared with DAPT. However, it significantly increased major and minor risk of bleeding. It is imperative that further prospective randomized controlled trials are required to define the best therapeutic strategy for patients with an indication of chronic OAC undergoing PCI-s.
Gender disparity in early death after ST-elevation myocardial infarction
Authors: ZHANG Bo , ZHANG Wei , HUANG Rong-chong , ZHANG Yan , LIU Jun , ZHENG Zheng-guo , JIANG Da-ming , SUN Yu-jiao , REN Li-na , ZHOU Xu-chen , QI Guo-xian 
Published: January 2024

Background
Females with acute myocardial infarction (AMI) have a higher risk of adverse outcomes because of receiving less evidence-based medical care. Our aim was to investigate the gender disparity in early death after ST-elevation myocardial infarction (STEMI) in the current era.

Methods
A total of 1429 consecutive patients with STEMI in the Liaoning district were analyzed. We compared hospital care and cardiac event data by sex for in-patients with acute STEMI within 24 hours of symptom onset.

Results
In the emergency reperfusion group (n=754), in-hospital mortality occurred in 4.2% of the males and 11.2% of the females (P=0.001). In the non-emergency reperfusion group (n=675), in-hospital mortality occurred in 13.0% of the males and 22.9% of the females (P=0.001). Multivariate Logistic regression analysis revealed female sex as an independent risk factor of death for STEMI patients during hospitalization (OR=1.691, P=0.007). After controlling for patients who died within 24 hr after admission, female sex was no longer an independent risk factor (OR=1.409, P=0.259).

Conclusion
Female sex was an independent risk factor for in-hospital mortality of STEMI patients, which is explained by an excess of very early deaths.