Heparin is an effective treatment for preventing liver failure after hepatectomy.

BACKGROUND: Posthepatectomy liver failure (PHLF) is one of the most important causes of death following liver resection. Heparin, an established anticoagulant, can protect liver function through a number of mechanisms, and thus, prevent liver failure. AIM: To look at the safety and efficacy of heparin in preventing hepatic dysfunction after hepatectomy. METHODS: The data was extracted from Multiparameter Intelligent Monitoring in Intensive Care III (MIMIC-III) v1. 4 pinpointed patients who had undergone hepatectomy for liver cancer, subdividing them into two cohorts: Those who were injected with heparin and those who were not. The statistical evaluations used were unpaired t-tests, Mann-Whitney U tests, chi-square tests, and Fisher's exact tests to assess the effect of heparin administration on PHLF, duration of intensive care unit (ICU) stay, need for mechanical ventilation, use of continuous renal replacement therapy (CRRT), incidence of hypoxemia, development of acute kidney injury, and ICU mortality. Logistic regression was utilized to analyze the factors related to PHLF, with propensity score matching (PSM) aiming to balance the preoperative disparities between the two groups. RESULTS: In this study, 1388 patients who underwent liver cancer hepatectomy were analyzed. PSM yielded 213 matched pairs from the heparin-treated and control groups. Initial univariate analyses indicated that heparin potentially reduces the risk of PHLF in both matched and unmatched samples. Further analysis in the matched cohorts confirmed a significant association, with heparin reducing the risk of PHLF (odds ratio: 0.518; 95% confidence interval: 0.295-0.910; P = 0.022). Additionally, heparin treatment correlated with improved short-term postoperative outcomes such as reduced ICU stay durations, diminished requirements for respiratory support and CRRT, and lower incidences of hypoxemia and ICU mortality. CONCLUSION: Liver failure is an important hazard following hepatic surgery. During ICU care heparin administration has been proved to decrease the occurrence of hepatectomy induced liver failure. This indicates that heparin may provide a hopeful option for controlling PHLF.

Ischaemic colitis during pegylated interferon-alpha monotherapy for chronic hepatitis B: A case report.

RATIONALE: Pegylated interferon-alpha (PEG-IFN-α) is available for the treatment of hepatitis B virus infection, which is better than interferon-alpha (IFN-α) for the inhibition of hepatitis B virus replication. Ischemic colitis has been described from non-pegylated IFN-α, which occurs mainly in patients with hepatitis C virus infection. This is the first case of ischemic colitis during pegylated IFN-α monotherapy for chronic hepatitis B. PATIENT CONCERNS: A 35-year-old Chinese man presented with complaints of acute lower abdominal pain and haematochezia, who was receiving PEG-IFN-α-2a monotherapy for chronic hepatitis B. DIAGNOSES: Colonoscopy revealed scattered ulcers and severe mucosal inflammation with edema in the left hemi colon and necrotizing changes in the descending portion. Biopsies revealed focal mucosal chronic inflammation and mucosal erosion. Therefore, the patient was diagnosed with ischemic colitis based on clinical and testing results. INTERVENTIONS: PEG-IFN-α therapy was discontinued and switched to symptomatic management. OUTCOMES: The patient was discharged from the hospital after recovery. Follow-up colonoscopy revealed normal. The temporal association between the resolution of ischemic colitis and cessation of PEG-IFN-α treatment strongly favors the diagnosis of interferon-induced ischemic colitis. LESSONS: Ischaemic colitis is a severe emergency complication of interferon therapy. Physicians should consider this complication in any patient taking PEG-IFN-α who develops abdominal discomfort and hematochezia.

Comprehensive phylogeographic and phylodynamic analyses of global Senecavirus A.

Senecavirus A (SVA) is a member of the genus Senecavirus in the family Picornaviridae that infects pigs and shows symptoms similar to foot and mouth diseases and other vesicular diseases. It is difficult to prevent, thus, causing tremendous economic loss to the pig industry. However, the global transmission routes of SVA and its natural origins remain unclear. In this study, we processed representative SVA sequences from the GenBank database along with 10 newly isolated SVA strains from the field samples collected from our lab to explore the origins, population characteristics, and transmission patterns of SVA. The SVA strains were firstly systematically divided into eight clades including Clade I-VII and Clade Ancestor based on the maximum likelihood phylogenetic inference. Phylogeographic and phylodynamics analysis within the Bayesian statistical framework revealed that SVA originated in the United States in the 1980s and afterward spread to different countries and regions. Our analysis of viral transmission routes also revealed its historical spread from the United States and the risk of the global virus prevalence. Overall, our study provided a comprehensive assessment of the phylogenetic characteristics, origins, history, and geographical evolution of SVA on a global scale, unlocking insights into developing efficient disease management strategies.

Clinical sequencing uncovers the genomic characteristics and mutation spectrum of the 2018 African swine fever virus in Guangdong, China.

African swine fever (ASF) outbreak have caused tremendous economic loss to the pig industry in China since its emergence in August 2018. Previous studies revealed that many published sequences are not suitable for detailed analyses due to the lack of data regarding quality parameters and methodology, and outdated annotations. Thus, high-quality genomes of highly pathogenic strains that can be used as references for early Chinese ASF outbreaks are still lacking, and little is known about the features of intra-host variants of ASF virus (ASFV). In this study, a full genome sequencing of clinical samples from the first ASF outbreak in Guangdong in 2018 was performed using MGI (MGI Tech Co., Ltd., Shenzhen, China) and Nanopore sequencing platforms, followed by Sanger sequencing to verify the variations. With 22 sequencing corrections, we obtained a high-quality genome of one of the earliest virulent isolates, GZ201801_2. After proofreading, we improved (add or modify) the annotations of this isolate using the whole genome alignment with Georgia 2007/1. Based on the complete genome sequence, we constructed the methylation profiles of early ASFV strains in China and predicted the potential 5mC and 6mA methylation sites, which are likely involved in metabolism, transcription, and replication. Additionally, the intra-host single nucleotide variant distribution and mutant allele frequency in the clinical samples of early strain were determined for the first time and found a strong preference for A and T substitution mutation, non-synonymous mutations, and mutations that resulted in amino acid substitutions into Lysine. In conclusion, this study provides a high-quality genome sequence, updated genome annotation, methylation profile, and mutation spectrum of early ASFV strains in China, thereby providing a reference basis for further studies on the evolution, transmission, and virulence of ASFV.

Relaxation Effect of Schisandra Chinensis Lignans on the Isolated Tracheal Smooth Muscle in Rats and Its Mechanism.

Schisandra chinensis (S. chinensis) is one of the core drugs used for relieving cough and asthma in traditional Chinese medicine. However, there are few basic studies on the treatment of respiratory diseases with S. chinensis in modern pharmacology, and the material basis and mechanism of its antiasthmatic effect are still unclear. Lignans are the main active components of S. chinensis. The aim of this study was to observe the relaxation effect of S. chinensis lignans (SCL) on the tracheal smooth muscle of rats by in vitro tracheal perfusion experiments, and to explore the mechanism by preincubation with L-type calcium channel blocker verapamil, four potassium channel blockers glibenclamide, tetraethylamine, 4-aminopyridine and barium chloride (BaCl2), ß-adrenoceptor blocker propranolol, nitric oxide synthase inhibitor Nω-nitro-L-arginine methyl ester (L-NAME), and the cyclooxygenase inhibitor indomethacin, respectively. The results showed that SCL (0.25-1.75 mg/mL) reduced the contraction of isolated tracheal smooth muscle induced by acetylcholine, the preincubation with verapamil and glibenclamide could attenuate the relaxation effect, whereas propranolol, 4-aminopyridine, BaCl2, tetraethylamine, L-NAME, and indomethacin had no such effect. These results suggest that SCL has a significant relaxation effect on the isolated tracheal smooth muscle of rats, and the mechanism may be related to the inhibition of extracellular calcium influx and intracellular calcium release from the sarcoplasmic reticulum, as well as the activation of ATP-sensitive potassium channels. These findings may provide a pharmacological basis for the traditional use of S. chinensis to treat asthma.

[Treatment and analysis of the early postoperative complications of tibial plateau fractures].

OBJECTIVE: To analysis the early complications of tibial fracture and its related factors, and propose a solution. METHODS: From December 2003 to December 2013,38 patients with early complications of tibial plateau fracture after operation were retrospectively analyzed. There were 35 males and 3 females, aged from 37 to 69 years old (averaged 42.3 years). According to Schatzker classification, 3 cases were classified as type II, 2 cases as type III, 2 cases as type IV, 19 cases as type V, 12 cases as type VI. The intervals between injury and operation ranged from 9 hours to 9 days, 26 cases within 3 days. Fifteen cases were treated with internal fixation of plates and 23 were treated by plate fixation and bone transplantation. Early complications included skin necrosis in 15 cases, infection in 6 cases, osteofascial compartment syndrome in 3 cases, common peroneal nerve injury in 2 cases, the superficial peroneal nerve injury in 3 cases, popliteal artery injury in 2 cases, loss of reduction in 7 cases. RESULTS: The wound of 14 cases healed at the first stage and 24 cases healed delay. Hospitalization days ranged from 7 to 67 days (averaged 25.6 days). All patients were followed up for 12 to 36 months with an average of 16.4 months. The fracture healing time ranged from 3 to 9 months (averaged 6.9 months). According to Merchant knee function evaluation criteria, the results were excellent in 19 cases, good in 12, fair in 5 and poor in 2. CONCLUSION: Early complications of tibial fracture after operation is closely associated with the severe fracture complexity and related with preoperative preparation, surgical timing, operation incision selection and surgical technique. Early detection and timely processing reduce damage.

RECK overexpression reduces invasive ability in ameloblastoma cells.

BACKGROUND: Ameloblastoma is a frequent odontogenic neoplasm characterized by local invasiveness and high risk of recurrence. Reversion-inducing cysteine-rich protein with Kazal motifs (RECK) is a tumor suppressor that inhibits metastasis and angiogenesis. The aim of this study was to investigate effects of RECK overexpression on invasive potential in ameloblastoma cells. METHODS: Lentiviral vectors containing human RECK gene were created and subsequently stably transfected into immortalized ameloblastoma cell line hTERT(+) -AM. Functional characteristics of hTERT(+) -AM cells with stable RECK overexpression included proliferation, migration, invasion, and regulation of matrix metalloproteinases (MMP)-2, MMP-9 measured by zymography or commercially available assays. RESULTS: The stable and higher expression of RECK mRNA and protein (P < 0.01) was detected in RECK-transfected hTERT(+) -AM cells. RECK overexpression caused a decrease in migration and invasion (P < 0.01) for hTERT(+) -AM cells and a decrease in activity of MMP-2, MMP-9 (P < 0.01). Proliferation was not affected by RECK overexpression (P > 0.05). CONCLUSIONS: Overexpression of RECK gene significantly inhibited cell invasive ability of hTERT(+) -AM cells, suggesting RECK may be a new target for ameloblastoma treatment.

Extracellular matrix metalloproteinase inducer expression in salivary gland tumors: a correlation with microvessel density.

The purpose of this study was to investigate the expression pattern of extracellular matrix metalloproteinase inducer (EMMPRIN) as well as the correlation between EMMPRIN and microvessel density (MVD) in salivary gland tumors. Extracellular matrix metalloproteinase inducer expression and MVD were examined immunohistochemically on paraffin-embedded tissue specimens from 95 patients with salivary gland tumors, who underwent surgical resection from 1998 to 2006. Reverse transcription-polymerase chain reaction was used to monitor EMMPRIN mRNA expression in frozen samples. Extracellular matrix metalloproteinase inducer expression in mucoepidermoid carcinomas and adenoid cystic carcinomas was significantly higher than in normal salivary gland tissues and pleomorphic adenomas (P < 0.05). The MVD of mucoepidermoid carcinomas and adenoid cystic carcinomas was significantly higher compared with pleomorphic adenomas (P < 0.05). The MVD of the EMMPRIN-positive expression group was significantly higher than the MVD of the EMMPRIN-negative expression group (P < 0.05). Extracellular matrix metalloproteinase inducer mRNA expression in malignant salivary gland tumors was higher than that in pleomorphic adenomas (P < 0.05). This study suggests that EMMPRIN expression is an important feature of malignant salivary gland tumors and can be used as a biologic marker to characterize salivary gland tumors. Extracellular matrix metalloproteinase inducer is also a positive angiogenic factor in salivary gland tumors.

Expression and role of metalloproteinase-2 and endogenous tissue regulator in ameloblastoma.

BACKGROUND: Ameloblastoma is a frequently encountered odontogenic benign tumor characterized by local invasiveness and high risk of recurrence. Matrix metalloproteinase (MMP)-2 can degrade type IV collagen, one of the major components in the basement membrane, resulting in the promotion of tumor invasion, whereas it is under the influence of an activator, membrane type 1-MMP-14 and the tissue inhibitor of metalloproteases (TIMP)-2. The aim of this study was to investigate combinatorial role played by MMP-2, TIMP-2 and MMP-14 in ameloblastoma. METHODS: Transcriptional expression of MMP-2, TIMP-2 and MMP-14 in tissue extracts of 42 ameloblastomas and 10 dental follicles was detected using reverse transcription-polymerase chain reaction, and compared difference in clinical type and local recurrence of ameloblastoma. RESULTS: MMP-2, TIMP-2 and MMP-14 mRNA were detected in all investigated ameloblastoma tissues. While MMP-2 mRNA was only expressed in eight of 10 odontotheca tissues and TIMP- 2 and MMP-14 were not found in all odontotheca tissues. The mRNA expression of MMP-2, TIMP-2 and MMP-14 were significantly higher in ameloblastoma tissues than in odontotheca tissues. The mRNA levels of TIMP-2 and MMP-14 were significantly higher in recurrent and solid/multicystic ameloblastoma tissues than in primary and unicystic ameloblastoma tissues respectively. CONCLUSIONS: Of the MMP-2/TIMP-2/MMP-14 complex, a high expression of MMP-2, TIMP-2 and MMP-14 mRNA levels may contribute to the local invasive characteristics of ameloblastoma, whereas the local invasive capacity of ameloblastoma is more likely related to a high transcriptional levels of TIMP-2 and MMP-14.

Expression of RECK and matrix metalloproteinase-2 in ameloblastoma.

BACKGROUND: Ameloblastoma is a frequent odontogenic benign tumor characterized by local invasiveness, high risk of recurrence and occasional metastasis and malignant transformation. Matrix metalloproteinase-2 (MMP-2) promotes tumor invasion and progression by destroying the extracellular matrix (ECM) and basement membrane. For this proteolytic activity, the endogenous inhibitor is reversion-inducing cysteine rich protein with Kazal motifs (RECK). The aim of this study was to characterize the relationship between RECK and MMP-2 expression and the clinical manifestation of ameloblastoma. METHODS: Immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) were employed to detect the protein and mRNA expression of RECK and MMP-2 in keratocystic odontogenic tumor (KCOT), ameloblastoma and ameloblastic carcinoma. RESULTS: RECK protein expression was significantly reduced in KCOT (87.5%), ameloblastoma (56.5%) and ameloblastic carcinoma (0%) (P < 0.01), and was significantly lower in recurrent ameloblastoma compared with primary ameloblastoma (P < 0.01), but did not differ by histological type of ameloblastoma. MMP-2 protein expression was significantly higher in ameloblastoma and ameloblastic carcinoma compared with KCOT (P < 0.01). RECK mRNA expression was significantly lower in ameloblastoma than in KCOT (P < 0.01), lower in recurrent ameloblastoma than in primary ameloblastoma, and was negative in ameloblastic carcinoma. MMP-2 mRNA expression was significantly higher in ameloblastoma compared with KCOT (P < 0.01), but was no different in recurrent ameloblastoma versus primary ameloblastoma. RECK protein expression was negatively associated with MMP-2 protein expression in ameloblastoma (r = -0.431, P < 0.01). CONCLUSION: Low or no RECK expression and increased MMP-2 expression may be associated with negative clinical findings in ameloblastoma. RECK may participate in the invasion, recurrence and malignant transformation of ameloblastoma by regulating MMP-2 at the post-transcriptional level.