Oxidation of chromium(â ¢): A potential risk of using chemical oxidation processes for the remediation of 2-chlorophenol contaminated soils.

Chemical oxidation processes are widely used for the remediation of organically contaminated soils, but their potential impact on variable-valence and toxic metals such as chromium (Cr) is often overlooked. In this study, we investigated the risk of Cr(Ⅲ) oxidation in soils during the remediation of 2-chlorophenol (2-CP) contaminated soils using four different processes: Potassium permanganate (KMnO4), Modified Fenton (Fe2+/H2O2), Alkali-activated persulfate (S2O82-/OH-), and Fe2+-activated persulfate (S2O82-/Fe2+). Our results indicated that the KMnO4, Fe2+/H2O2, and S2O82-/Fe2+ processes progressively oxidized Cr(III) to Cr(Ⅵ) during the 2-CP degradation. The KMnO4 process likely involved direct electron transfer, while the Fe2+/H2O2 and S2O82-/Fe2+ processes primarily relied on HO• and/or SO4•- for the Cr(III) oxidation. Notably, after 4 h of 2-CP degradation, the Cr(VI) content in the KMnO4 process surpassed China's 3.0 mg kg-1 risk screening threshold for Class I construction sites, and further exceeded the 5.7 mg kg-1 limit for Class II construction sites after 8 h. Conversely, the S2O82-/OH- process exhibited negligible oxidation of Cr(III), maintaining a low oxidation ratio of 0.13%, as highly alkaline conditions induced Cr(III) precipitation, reducing its exposure to free radicals. Cr(III) oxidation ratio was directly proportional to oxidant dosage, whereas the Fe2+/H2O2 process showed a different trend, influenced by the concentration of reductants. This study provides insights into the selection and optimization of chemical oxidation processes for soil remediation, emphasizing the imperative for thorough risk evaluation of Cr(III) oxidation before their application.

Network Pharmacology Prediction and Experimental Verification for Anti-Ferroptosis of Edaravone After Experimental Intracerebral Hemorrhage.

Neuronal ferroptosis plays an important role in secondary brain injuries after intracerebral hemorrhage (ICH). Edaravone (Eda) is a promising free radical scavenger that inhibits ferroptosis in neurological diseases. However, its protective effects and underlying mechanisms in ameliorating post-ICH ferroptosis remain unclear. We employed a network pharmacology approach to determine the core targets of Eda against ICH. Forty-two rats were subjected to successful striatal autologous whole blood injection (n=28) or sham operation (n=14). The 28 blood-injected rats were randomly assigned to either the Eda or vehicle group (n=14) for immediate administration and then for 3 consecutive days. Hemin-induced HT22 cells were used for in vitro studies. The effects of Eda in ICH on ferroptosis and the MEK/ERK pathway were investigated in vivo and in vitro. Network pharmacology-based analysis revealed that candidate targets of Eda-treated ICH might be related to ferroptosis; among which prostaglandin G/H synthase 2 (PTGS2) was a ferroptosis marker. In vivo experiments showed that Eda alleviated sensorimotor deficits and decreased PTGS2 expression (all p<0.05) after ICH. Eda rescued neuron pathological changes after ICH (increased NeuN+ cells and decreased FJC+ cells, all p<0.01). In vitro experiments showed that Eda reduced intracellular reactive oxygen species and reversed mitochondria damage. Eda repressed ferroptosis by decreasing malondialdehyde and iron deposition and by influencing ferroptosis-related protein expression (all p<0.05) in ICH rats and hemin-induced HT22 cells. Mechanically, Eda significantly suppressed phosphorylated-MEK and phosphorylated-ERK1/2 expression. These results indicate that Eda has protective effects on ICH injury through ferroptosis and MEK/ERK pathway suppression.

CRISPR/Cas9-mediated knockin of IRES-tdTomato at Ins2 locus reveals no RFP-positive cells in mouse islets.

Using the CRISPR/Cas9 genomic editing technology, we constructed a transgenic mouse model to express specific fluorescent protein in pancreatic ß cells, which harbor tdTomato exogenous gene downstream of the Ins2 promoter in C57BL/6 J mice. The Ins2-specific single-guide RNA-targeted exon2 was designed for the CRISPR/Cas9 system and Donor vector was constructed at the same time. Then Cas9, sgRNA, and Donor vector were microinjected in vitro into the mouse zygotes that were implanted into pseudo-pregnant mice. We obtained homozygotes through mating heterozygotes, and verified the knockin effect through genotype identification, in vivo imaging, and frozen section. Six F0 mice and stable inherited Ins2-IRES-tdTomato F1 were obtained. Genome sequencing results showed that the knockin group had no change in the Ins2 exon compared with the control group, while only the base sequence of tdTomato was added and no base mutation occurred. However, in vivo imaging and frozen section did not observe the expression of red fluorescent protein (RFP), and the protein expression of knockin gene tdTomato was negative. As a result, the expressions of tdTomato protein and fluorescence intensity were low and the detection threshold was not reached. In the CRISP/Cas9 technique, the exogenous fragment of IRES connection would affect the transcription level of the preceding gene, which in turn would lead to low-level expression of the downstream gene and affect the effect of gene insertion.

Predicting value of fibrinogen in identifying cerebrovascular ischemic events in patients with dizziness/vertigo.

PURPOSE: Dizziness and vertigo are caused by multiple etiologies, including cerebrovascular ischemic events. However, identifying cerebrovascular ischemic events as a cause of dizziness and vertigo remains a challenge. We tried to assess the value of fibrinogen (FIB) in identifying of cerebral ischemic event in patients with dizziness/vertigo. METHODS: The study enrolled patients with dizziness/vertigo presented within 72 h in a tertiary hospital. The plasma FIB levels were measured in all participants. According to the final diagnosis, participants were divided into cerebral ischemic events group and non-cerebrovascular diseases group. Multivariate logistic regression was performed to explore the association between FIB and cerebral ischemic events. The receiver operating characteristic curve was performed, and the nomogram was constructed to evaluate the overall prediction ability of FIB in cerebral ischemic event. RESULTS: A total of 298 participants were enrolled in our study, of 126 cerebral ischemic events patients. Multivariate logistic regression analysis showed that FIB was independently associated with cerebral ischemic event in patients with dizziness (OR = 1.84, 95%CI [1.15, 2.92], p = 0.010). The cut-off value of FIB in predicting cerebral ischemic event was 2.43 g/L (AUC = 0.658). The nomogram showed that higher FIB level was associated with a greater risk of cerebral ischemic event (C-index = 0.800). CONCLUSIONS: Our study suggested that FIB may be a useful biochemical parameter for identifying cerebral ischemic event in patients with dizziness/vertigo.

Spata2 Knockdown Exacerbates Brain Inflammation via NF-κB/P38MAPK Signaling and NLRP3 Inflammasome Activation in Cerebral Ischemia/Reperfusion Rats.

Brain inflammation induced by ischemic stroke is an important cause of secondary brain injury. The nuclear factor kappa B (NF-κB), mitogen-activated protein kinase (MAPK), and NLRP3 inflammasome signaling are believed to drive the progression of brain inflammation. Spermatogenesis-associated protein2 (SPATA2) functions as a partner protein that recruits CYLD, a negative regulator of NF-κB signaling, to signaling complexes. However, the role of SPATA2 in the central nervous system remains unclear and whether it is involved in regulating inflammatory responses remains controversial. Rats were subjected to transient middle cerebral artery occlusion followed by reperfusion (tMCAO/R) surgery. The expression and localization of SPATA2 in the brain were investigated. The lentivirus-mediated shRNA was employed to inhibit SPATA2 expression. The inflammatory responses and outcomes of Spata2 knockdown were investigated. SPATA2 was co-localized with CYLD in neurons. SPATA2 expression was reduced in tMCAO/R rats. Spata2 knockdown resulted in increased microglia, increased expression of Tnfa, Il-1ß, and Il-18, decreased Garcia score, and increased infarct volume. Spata2 knockdown resulted in the activation of P38MAPK and NLRP3 inflammasome and the increased activation of NF-κB signaling. These results suggest that SPATA2 plays a protective role against brain inflammation induced by ischemia/reperfusion injury. Therefore, SPATA2 could be a potential therapeutic target for treating ischemic stroke.

Comparison of biomarkers of endothelial dysfunction and microvascular endothelial function in patients with primary aldosteronism and essential hypertension.

INTRODUCTION: Studies have shown that primary aldosteronism (PA) has a higher risk of cardiovascular events than essential hypertension (EH). Endothelial dysfunction is an independent predictor of cardiovascular events. Whether PA and EH differ in the endothelial dysfunction is uncertain. Our study was designed to investigate the levels of biomarkers of endothelial dysfunction (Asymmetric dimethylarginine, ADMA; E-selectin, and Plasminogen activator inhibitor-1, PAI-1) and assess the microvascular endothelial function in patients with PA and EH, respectively. METHODS: The biomarkers of endothelial dysfunction were measured by enzyme-linked immunosorbent assay (ELISA). Microvascular endothelial function was evaluated by Pulse amplitude tonometry (PAT). RESULTS: Thirty-one subjects with EH and 36 subjects with PA including 22 with aldosterone-producing adenoma (APA) and 14 with idiopathic hyperaldosteronism (IHA) were enrolled in our study. The ADMA levels among the three groups were different (APA 47.83 (27.50, 87.74) ng/ml vs EH 25.08 (22.44, 39.79) ng/ml vs IHA 26.00 (22.23, 33.75) ng/ml; p = 0.04), however, when the APA group was compared with EH and IHA group, there was no statistical significance (47.83 (27.50, 87.74) ng/ml vs 25.08 (22.44, 39.79) ng/ml for EH, p = 0.11; 47.83 (27.50, 87.74) ng/ml vs IHA 26.00 (33.75) ng/ml, p = 0.07). The results of ADMA levels are presented as Median (p25, p75). Whereas, levels of PAI-1 and E-selectin, microvascular endothelial function were not significantly different between PA and EH subjects. CONCLUSIONS: Our study shows no significant differences between PA and EH in terms of biomarkers of endothelial dysfunction and microvascular endothelial function. The microvascular endothelial function of PA and EH patients is comparable.

4-Phenylbutyric acid protects islet ß cell against cellular damage induced by glucocorticoids.

This study, using the MIN6 cell line, examines the effect of glucocorticoids (GCs) on the expression and protein levels of endoplasmic reticulum stress (ERS) related genes. Furthermore, we evaluated the protective role of 4-phenylbutyric acid (4-PBA) on the aforesaid GCs induced changes. Pancreatic islet MIN6 cells were treated with dexamethasone (DEX) at distinct concentrations (0.1 µmol/L and 0.5 µmol/L) for different periods (1 h, 4 h, 12 h, and 24 h). The mRNA and protein levels of ERS related genes were measured using real-time qPCR (qRT-PCR) and western blotting. Similar evaluations were also carried out for the cells treated with 4-PBA combined with DEX. Upon DEX intervention which induces the unfolded protein response (UPR), the expression levels of BIP, ATF6, IRE1, and PERK increased in the MIN6 cells, both in concentration and time-dependent manner. Similarly, ERS associated gene CHOP, which is involved in the apoptotic pathway, also showed increased levels both in concentration and time-dependent manner. However, treatment with 4-PBA decreased the expression levels of ERS related proteins. Quantitative analysis found that all these results were statistically significant (P < 0.05). GCs markedly activates the ERS in the MIN6 cell line in vitro, however, this effect can be significantly alleviated upon treatment with 4-PBA.

Huoxin Pill () Attenuates Cardiac Fibrosis by Suppressing TGF-ß1/Smad2/3 Pathway in Isoproterenol-Induced Heart Failure Rats.

OBJECTIVE: To evaluate the effects of Huoxin Pill (, HXP) on cardiac fibrosis and heart failure (HF) in isoproterenol (ISO)-induced HF rats. METHODS: Thirty Wistar rats were randomly divided into 5 groups including control, HF, isosorbide mononitrate (ISMN), HXP low (HXP-L), and HXP high (HXP-H) groups (n=6 for each group) according to the complete randomization method. Rats were pretreated with ISMN (5 mg/kg daily), low concentration of HXP (10 mg/kg daily) or high concentration of HXP (30 mg/kg daily) or equal volume of saline by intragastric administration for 1 week, followed by intraperitoneal injection of ISO (10 mg/kg, 14 days), and continually intragastric administrated with above medicines or saline for additional 6 weeks. The effects of HXP treatment on the cardiac function, heart weight index (HWI), pathological changes, and collagen content were further assessed. Moreover, the role of HXP on activation of transforming growth factor- ß 1 (TGF-ß 1)/Smads pathway was further explored using immunohistochemistry (IHC) and Western-blot assay. RESULTS: HXP treatment significantly alleviated the decrease of ejection fraction (EF) and fractional shortening (FS), while decreased the elevation of left ventricular end-systolic volume (LVESV) in ISO-induced HF rats (P<0.05). Moreover, HXP treatment obviously attenuated the increase of HWI and serum level of creatine kinase MB (CK-MB, P<0.05), as well as pathological changes in ISO-induced HF rats. Further determination indicated that HXP treatment alleviated the elevation of collagen I and collagen III protein expression in cardiac tissues of ISO-induced HF rats. Furthermore, HXP treatment significantly down-regulated the increase of TGF-ß 1 and p-Smad2/3 protein expression in cardiac tissues of HF rats (P<0.05), while did not affect the expression of total Smad2/3. CONCLUSIONS: HXP attenuated heart failure and cardiac fibrosis in ISO-induced HF rats by suppression of TGF-ß 1/Smad2/3 pathway.

The design of electronic medical records for patients of continuous care.

In order to meet the ever-increasing needs of health care, as well as helping patients who need continuous care after being discharged from the hospital and making modern medical technology better serve humans, the design of electronic medical records for continuous care patients, especially those with malignant tumors, is investigated. In the research process, the idea of Browser/Server (B/S) framework is adopted, and the corresponding electronic medical record system is designed based on the targets and the overall structure of the system; afterward, the black-box testing and white-box testing are carried out to test the functions, reliability, and stability of the designed electronic medical record system; in addition, combined with other research results, the feasibility of the design is proved. It can be seen that the electronic medical record system designed for patients who need continuous care in the study is absolutely feasible, which can be further researched and improved with the development of electronic medical records; therefore, it would make greater contributions to both patients and hospitals in the future.

Empirical Mode Decomposition Based Multi-Modal Activity Recognition.

This paper aims to develop an activity recognition algorithm to allow parents to monitor their children at home after school. A common method used to analyze electroencephalograms is to use infinite impulse response filters to decompose the electroencephalograms into various brain wave components. However, nonlinear phase distortions will be introduced by these filters. To address this issue, this paper applies empirical mode decomposition to decompose the electroencephalograms into various intrinsic mode functions and categorize them into four groups. In addition, common features used to analyze electroencephalograms are energy and entropy. However, because there are only two features, the available information is limited. To address this issue, this paper extracts 11 different physical quantities from each group of intrinsic mode functions, and these are employed as the features. Finally, this paper uses the random forest to perform activity recognition. It is worth noting that the conventional approach for performing activity recognition is based on a single type of signal, which limits the recognition performance. In this paper, a multi-modal system based on electroencephalograms, image sequences, and motion signals is used for activity recognition. The numerical simulation results show that the percentage accuracies based on three types of signal are higher than those based on two types of signal or the individual signals. This demonstrates the advantages of using the multi-modal approach for activity recognition. In addition, our proposed empirical mode decomposition-based method outperforms the conventional filtering-based method. This demonstrates the advantages of using the nonlinear and adaptive time frequency approach for activity recognition.

A20-Binding Inhibitor of NF-κB 1 Ameliorates Neuroinflammation and Mediates Antineuroinflammatory Effect of Electroacupuncture in Cerebral Ischemia/Reperfusion Rats.

A20-binding inhibitor of NF-κB 1 (ABIN1) is an inhibitor of NF-κB and exerts anti-inflammatory effect. Electroacupuncture (EA) is considered as a neuroprotective strategy by inhibiting neuroinflammatory damage after cerebral ischemia. This study was performed to explore the role of ABIN1 and investigate whether the ABIN1 is involved in the mechanism of EA in cerebral ischemia/reperfusion (I/R) rats. Male Sprague-Dawley (SD) rats were subjected to middle cerebral artery occlusion/reperfusion (MCAO/R) and received EA after reperfusion once a day. Lentivirus-mediated ABIN1 gene knockdown was used to detect the role of ABIN1 in neuroinflammation after I/R. ABIN1 expression, proinflammatory cytokine levels, microglial activation, neurological function, infarct volumes, and NF-κB activation were assessed. ABIN1 expression was elevated in the peri-infarct cortex and was further upregulated by EA. ABIN1 knockdown increased the levels of proinflammatory cytokines and activation of microglia, worsened neurological deficits, and enlarged the infarct volume. Moreover, ABIN1 was blocked to partially reverse the neuroprotective effect of EA, and this treatment weakened the ability of EA to suppress NF-κB activity. Based on these findings, ABIN1 is a potential suppressor of neuroinflammation and ABIN1 mediates the antineuroinflammatory effect of EA in cerebral I/R rats.

PPAR-γ Mediates Ta-VNS-Induced Angiogenesis and Subsequent Functional Recovery after Experimental Stroke in Rats.

BACKGROUND: Neoangiogenesis after cerebral ischemia in mammals is insufficient to restore neurological function, illustrating the need to design better strategies for improving outcomes. Our previous study has suggested that transcutaneous auricular vagus nerve stimulation (ta-VNS) induced angiogenesis and improved neurological functions in a rat model of cerebral ischemia/reperfusion (I/R) injury. However, the mechanisms involved need further exploration. Peroxisome proliferator-activated receptor-γ (PPAR-γ), well known as a ligand-modulated nuclear transcription factor, plays a crucial role in the regulation of cerebrovascular structure and function. Hence, the present study was designed to explore the role of PPAR-γ in ta-VNS-mediated angiogenesis and uncover the possible molecular mechanisms against ischemic stroke. METHODS: Adult male Sprague-Dawley rats were transfected with either PPAR-γ small interfering RNA (siRNA) or lentiviral vector without siRNA prior to surgery and subsequently received ta-VNS treatment. The expression and localization of PPAR-γ in the ischemic boundary after ta-VNS treatment were examined. Subsequently, neurological deficit scores, neuronal damage, and infarct volume were all evaluated. Additionally, microvessel density, endothelial cell proliferation condition, and the expression of angiogenesis-related molecules in the peri-infarct cortex were measured. RESULTS: We found that the expression of PPAR-γ in the peri-infarct cortex increased at 14 d and reached normal levels at 28 d after reperfusion. Ta-VNS treatment further upregulated PPAR-γ expression in the ischemic cortex. PPAR-γ was mainly expressed in neurons and astrocytes. Furthermore, ta-VNS-treated I/R rats showed better neurobehavioral recovery, alleviated neuronal injury, reduced infarct volume, and increased angiogenesis, as indicated by the elevated levels of brain-derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF), and phosphorylated endothelial nitric oxide synthase (P-eNOS). Surprisingly, the beneficial effects of ta-VNS were weakened after PPAR-γ silencing. CONCLUSIONS: Our results suggest that PPAR-γ is a potential mediator of ta-VNS-induced angiogenesis and neuroprotection against cerebral I/R injury.

Huoxin Pill Attenuates Cardiac Inflammation by Suppression of TLR4/NF-κB in Acute Myocardial Ischemia Injury Rats.

Huoxin Pill (HXP), a traditional Chinese medicine, has been prescribed widely in the treatment of coronary heart disease, angina pectoris, and other diseases. However, the possible protective mechanisms of HXP on myocardial ischemia remain unclear. In the current study, we investigated the effects and potential mechanism of HXP on myocardial ischemia and cardiac inflammation and the activation of TLR4/NF-κB pathway. Determination of electrocardiogram, echocardiography, and heart weight index (HWI) indicated that HXP treatment obviously attenuated the elevation of ST-segment, end-diastolic volume, and HWI in the AMI rat model. Enzyme-linked immunosorbent assay (ELISA) demonstrated that Huoxin Pill treatment significantly decreased the levels of CTnT, CK-MB, MDA, IL-6, and TNF-α, while it increased SOD content in serum of the AMI rat model. Moreover, hematoxylin and eosin (HE) and immunohistochemistry (IHC) staining revealed that HXP treatment alleviated pathological change, infiltration of inflammatory cells, levels of IL-6 and TNF-α, and expression of TLR4 and p-NF-κB in cardiac tissues of the AMI rat model. In conclusion, HXP treatment significantly improves cardiac function and attenuates cardiac inflammation by suppressing the activation of TLR4/NF-κB pathway in the ISO-induced AMI rat model. This study provides insights into the potential of HXP on prevention and treatment of AMI.

Qingda granules attenuate hypertensive cardiac remodeling and inflammation in spontaneously hypertensive rats.

Qingda granules (QDG) are derived from QingXuanJiangYa Decoction (QXJYD) a traditional Chinese medication that has been used to treat hypertension for more than 60 years. QXJYD has been shown to be effective in rat models of hypertension. However, the effects of QDG on hypertension remain largely unknown. In the current study, baicalin was identified as one of the main components of QDG using Ultra Performance Liquid Chromatography (UPLC) analysis. We investigated the effects of QDG on blood pressure, cardiac remodeling, and cardiac inflammation. QDG (0.8 g/kg/day) treatment attenuated the elevated blood pressure in spontaneously hypertensive rats (SHRs). Moreover, QDG treatment reduced the degree of myocardial fiber disarray, degeneration and necrosis of myocardial cells, expression of ANP and BNP, as well as collagen content of SHRs. Moreover, we further assessed the effect of QDG treatment on cardiac inflammation and found that QDG treatment reduced CD68 protein expression, decreased levels of IL-6 and TNF-α in both serum and cardiac tissues, as well as suppressed activation of NF-κB pathway in cardiac tissues of SHRs. Differential expressed metabolites (DEMs) analysis identified 41 increased and 51 decreased metabolites in the cardiac tissues of SHRs after QDG treatment. In summary, QDG treatment of SHRs attenuated the elevated blood pressure and ameliorated cardiac remodeling and inflammation, in part, through suppression of NF-κB pathway and DEMs, which provide a basis for other therapeutic uses of this TCM.

Suppressing the Spikes in Electroencephalogram via an Iterative Joint Singular Spectrum Analysis and Low-Rank Decomposition Approach.

The novelty and the contribution of this paper consists of applying an iterative joint singular spectrum analysis and low-rank decomposition approach for suppressing the spikes in an electroencephalogram. First, an electroencephalogram is filtered by an ideal lowpass filter via removing its discrete Fourier transform coefficients outside the wave band, the wave band, the wave band, the wave band and the wave band. Second, the singular spectrum analysis is performed on the filtered electroencephalogram to obtain the singular spectrum analysis components. The singular spectrum analysis components are sorted according to the magnitudes of their corresponding eigenvalues. The singular spectrum analysis components are sequentially added together starting from the last singular spectrum analysis component. If the variance of the summed singular spectrum analysis component under the unit energy normalization is larger than a threshold value, then the summation is terminated. The summed singular spectrum analysis component forms the first scale of the electroencephalogram. The rest singular spectrum analysis components are also summed up together separately to form the residue of the electroencephalogram. Next, the low-rank decomposition is performed on the residue of the electroencephalogram to obtain both the low-rank component and the sparse component. The low-rank component is added to the previous scale of the electroencephalogram to obtain the next scale of the electroencephalogram. Finally, the above procedures are repeated on the sparse component until the variance of the current scale of the electroencephalogram under the unit energy normalization is larger than another threshold value. The computer numerical simulation results show that the spike suppression performance based on our proposed method outperforms that based on the state-of-the-art methods.

The application of Compont gel in chronic obstructive jaundice rats model.

PURPOSE: To establish a new rat model, the pathogenesis of which is closer to the clinical occurrence of chronic obstructive jaundice with liver fibrosis. METHODS: 90 SD rats were randomly divided into 3 groups. Group A common bile duct ligation, group B common bile duct injection compont and group C injection saline. The serum of three groups was extracted, and the liver function was detected by ELISA. HE staining, Masson staining and immunohistochemistry were used to detect liver pathology. RESULTS: Group B showed a fluctuant development of jaundice, obstructive degree reached a peak at 2 weeks, and decreased from 3 weeks. HA, LA and PCIII were significantly higher than control group. 3 weeks after surgery, liver tissue fibrosis occurred in group B, and a wide range of fiber spacing was formed at 5 weeks. Immunohistochemistry showed that hepatic stellate cells were more active than the control group. CONCLUSION: Intra-biliary injection of Compont gel is different from the classic obstructive jaundice animal model caused by classic bile duct ligation, which can provide an ideal rat model of chronic obstructive jaundice with liver fibrosis.

Surgery strategy of 13 cases to control bleeding from the liver on laparoscopic repeat liver resection for recurrent hepatocellular carcinoma.

INTRODUCTION: Laparoscopic repeat liver resection (LRLR) is a safe and effective treatment in recurrent hepatocellular carcinoma (rHCC) in particular patients. However, there are less reports about surgery strategy of LRLR for rHCC. The aim of this study was to perform a systematic strategy for bleeding of liver to increase the safety and feasibility of LRLR for rHCC. METHODS: In this study, a total of 13 cases of LRLR for rHCC, including 8 males and 5 females; aged 28-72 years, mean age 54 years, who were received at least one laparotomy due to HCC. We employ to block the local blood flow, ligation of the left or right hepatic artery and/or approach of Pringle according to the assessment of the degree of adhesions in the abdominal and the first hepatic portal, the location of the tumour (edge/central). RESULTS: Three cases were less adhesions, nine cases were dense adhesions but 1 case was serious adhesions. Two cases were employed to block the local blood flow, 3 cases were employed to ligation of the left or right hepatic artery and 7 cases were employed to approach of Pringle. Twelve cases were successfully completed by LRLR whereas 1 case was completed by transfer to the open resection, including massive resection in 3 cases (the diameter of resection ≥3 cm), small hepatectomy in 10 cases (the diameter of resection <3 cm), no severe perioperative complication. The average operative time was (142 ± 34) min, the average intraoperative blood loss was (251 ± 92) ml and the average post-operative hospital time was (9 ± 3) d. The mean follow-up time was 25 months. Until the last follow-up, 11 cases survived while 2 cases died because of tumour recurrence. CONCLUSIONS: It can improve the safety and feasibility of LRLR for rHCC, according to the degree of adhesion of the peritoneal adhesions and the first hepatic portal, then selecting the appropriate technique to control the bleeding of the hepatectomy.

The application of Compont gel in chronic obstructive jaundice rats model

Abstract Purpose: To establish a new rat model, the pathogenesis of which is closer to the clinical occurrence of chronic obstructive jaundice with liver fibrosis. Methods: 90 SD rats were randomly divided into 3 groups. Group A common bile duct ligation, group B common bile duct injection compont and group C injection saline. The serum of three groups was extracted, and the liver function was detected by ELISA. HE staining, Masson staining and immunohistochemistry were used to detect liver pathology. Results: Group B showed a fluctuant development of jaundice, obstructive degree reached a peak at 2 weeks, and decreased from 3 weeks. HA, LA and PCIII were significantly higher than control group. 3 weeks after surgery, liver tissue fibrosis occurred in group B, and a wide range of fiber spacing was formed at 5 weeks. Immunohistochemistry showed that hepatic stellate cells were more active than the control group. Conclusion: Intra-biliary injection of Compont gel is different from the classic obstructive jaundice animal model caused by classic bile duct ligation, which can provide an ideal rat model of chronic obstructive jaundice with liver fibrosis.

[Prognostic value of combining preoperative serum tumor markers and peripheral blood routine indexes in patients with colorectal cancer].

OBJECTIVE: To investigate the prognostic value of preoperative serum tumor markers combined with peripheral blood routine indexes in colorectal cancer patients. METHODS: From January 2010 to March 2013, clinicopathological data of colorectal cancer patients receiving surgery treatment at the Third Affiliated Hospital of Sun Yat-sen University were collected. INCLUSION CRITERIA: (1) histologically confirmed adenocarcinoma; (2) primary cancer resected; (3) intact clinical data; (4) no signs of clinical infection. Patients with intestinal perforation or obstruction, hematological diseases or other malignant tumors were excluded. Informations were recorded containing sex, age, tumor location, degree of differentiation, tumor size, vascular tumor thrombus, nerve invasion, depth of infiltration, lymph node metastasis, distant metastasis, TNM stage, peripheral serum CEA, CA199, number of neutrophil, monocyte, platelet and lymphocyte. Positive CEA was defined as ≥5 µg/L, CA199 as ≥35 U/L; while NLR (neutrophil-to-lymphocyte ratio), MLR (monocyte-to-lymphocyte ratio), PLR (platelet-to-lymphocyte ratio) greater than their cut-off values were defined as positive. ROC curve was used to determine the cut-off values (with greatest area under curve) of NLR, MLR and PLR. The prognostic values of these indexes were analyzed using Kaplan-Meier regression and log-rank test. COX regression was used to perform risk factor analysis. RESULTS: A total of 312 colorectal cancer patients were enrolled, including 192 males and 120 females with median age of 61 (15-85) years. Till March 11, 2018, during median follow-up period of 65 months(2-96), the follow-up rate was 90.4% with loss of 30 cases and the mortality was 37.2% with 116 death. Univariate analysis found that colorectal cancer patients with positive CEA, CA199, NLR (>2.32), MLR (>0.24) and PLR (>164.1) had poor prognosis (all P<0.01). When combining CEA, CA199 with NLR, MLR, PLR, the survival analysis showed that patients with both negative indexes had the best prognosis, one positive the worse and both positive were the worst (all P<0.01). COX regression revealed that CEA(HR= 1.702,95%CI:1.148-2.522, P<0.01), combination of CA199 and MLR (HR=2.292, 95%CI:1.426-3.683, P<0.01) were independent risk factors for colorectal cancer. CONCLUSION: Combination of preoperative serum tumor markers and peripheral blood routine indexes can provide prognostic information for the patients with colorectal cancer.

Human colorectal cancer progression correlates with LOX-induced ECM stiffening.

Some solid tumors are characterized by extracellular matrix (ECM) remodeling and stiffening, which is related to solid tumor progression and aggression. However, the relationship between ECM stiffness and colorectal cancer (CRC) remains unclear. In this study, we investigated the relevance of ECM stiffness to clinicopathologic features using human CRC tissue microarrays. The results demonstrate that the expression of ECM components in CRC tissues is closely correlated with CRC progression and poor prognosis, which indicates that ECM stiffness may be associated with CRC development. We further studied lysyl oxidase (LOX) expression in CRC tissue and demonstrated that LOX expression is closely correlated with CRC progression. Previous studies showed that P-selectin-mediated platelet accumulation in CRC tissue may up-regulate LOX expression. Our findings indicate that P-selectin-mediated platelet aggregation may up-regulate LOX expression and enhance the remodeling and stiffening of the tumor ECM, which may promote the progression of colorectal cancer. Therefore, LOX may be a potential effective therapeutic target to treat colorectal cancer.