Homeopathic Ankle Dislocation for Treatment of Unstable Trimalleolar Fractures Involving Posterior Die-Punch Fragment: A Retrospective Cohort Study.

OBJECTIVES: Unstable trimalleolar fractures are relatively complex and more difficult to manage if die-punch fracture is present. We aimed to evaluate the curative effect of homeopathic ankle dislocation on the unstable trimalleolar fractures involving posterior die-punch fragments. METHODS: A total of 124 patients diagnosed with unstable trimalleolar fractures combined with post-die punch fragment between June 2008 and June 2020 were retrospectively included. Patients who received homeopathic ankle dislocation were named as the experimental group, and patients who accepted conventional treatment were control group. The fracture healing time, wound healing, American Orthopedic Foot and Ankle Society ankle-hindfoot scale (AOFAS), visual analogue scale (VAS), the Kellgren-Lawrence arthritis grading scale (KLAGS) and short-form 36 score (SF-36) scores were collected. Student t-test was used for fracture healing time. Wound healing and SF-36 were compared using the Mann-Whitney test. Repeated measurement analysis of variance (ANOVA) was used for AOFAS and VAS. χ2-test was used for KLAGS. RESULTS: AOFAS showed statistically significant differences between the two groups (p = 0.001). In non-weight-bearing and weight-bearing conditions, VAS scores were significant different between the two groups, and there was an interaction between group and time point (p < 0.001). The experimental group was superior to the control group in terms of physical function (p = 0.022), role-physical (p = 0.018), general health (p = 0.001) and social function (p = 0.042).The operation time of experimental group was shorter than that of control group (p < 0.001). CONCLUSION: Homeopathic ankle dislocation is used for the unstable trimalleolar fractures involving posterior die-punch fragment, which can provide better functional outcomes while shortening the operation time and recovery period.

Rare squamous cell carcinoma of the jejunum causing perforated peritonitis: A case report.

BACKGROUND: Adenocarcinoma has the highest incidence among malignant tumors of the small intestine (SI). Squamous cell carcinoma (SCC) often occurs in organs covered with squamous epithelium. Primary or metastatic SCC originating from the SI is very rare, with very few cases reported in the literature. CASE SUMMARY: This case report involves a 69-year-old man who developed abdominal pain after lunch. After admission, an abdominal computed tomography scan revealed perforation of the alimentary canal and multiple abnormal low-density lesions in the liver. During laparotomy, an approximately 4 cm × 3 cm-sized solid tumor was found in the jejunum, located 30 cm from the Treitz ligament, with a perforation. An intestinal segment of approximately 15 cm was removed, including the perforated portion. The pathological result was SCC. In combination with liver imaging, a diagnosis of SI SCC with multiple liver metastases was considered. The patient died from hepatic failure 1 mo after the operation. CONCLUSION: SI tumors are very rare compared to those originating in other digestive organs. Due to its insidious onset, the diagnosis of this disease is usually delayed. Clinicians must pay close attention to digestive symptoms such as persistent abdominal pain and melena.

rh-ES and Chemotherapy in Advanced Gastrointestinal Cancer in China: A Meta-analysis.

BACKGROUND: The purpose of this study was to evaluate the efficacy and safety of recombinant human endostatin (rh-ES) combined with chemotherapy in advanced gastrointestinal tumors in China. METHODS: A literature search was performed in PubMed, Medline, Springer, Elsevier Science Direct, Weipu, Wanfang, and China National Knowledge Infrastructure (CNKI), with the last report through September 2019. The included research was scored using a modified Jadad scale, and a meta-analysis was performed using RevMan 5.3 software. RESULTS: Twenty articles including 905 participants (experimental group [rh-ES combined with chemotherapy] 459; control group [chemotherapy alone] 446) were considered. The total effective rate for the experimental group in advanced gastrointestinal tumors was higher than that of the control group (P<0.05). No significant difference in adverse reactions was seen between the two groups (P>0.05). CONCLUSIONS: The short-term efficacy of rh-ES combined with chemotherapy for advanced gastrointestinal tumors was better, with fewer adverse reactions.

Crohn's disease with infliximab treatment complicated by rapidly progressing colorectal cancer: A case report.

BACKGROUND: Crohn's disease (CD) causes a range of digestive symptoms including recurrent diarrhea, abdominalgia, and flatulence, and severely impacts the quality of life of patients. Infliximab, a monoclonal antibody against tumor necrosis factor alpha, has recently been promoted as a therapeutic treatment for CD, but its safety margins remain uncertain. We report a case of rapidly progressive colorectal cancer that was diagnosed in a patient with CD who had previously been treated with infliximab. CASE SUMMARY: This case report refers to a 40-year-old male with a 6-year history of CD. The patient underwent transverse colostomy because of inflammatory ileus in 2017. He subsequently received infliximab treatment in 2018. Ten months later, worsening contracture of the transverse colostomy was observed. Imaging tests indicated that the patient may have developed colon cancer with extensive peritoneal implantation. At the same time, colonoscopy revealed a rectal mass and pathological examination indicated well-differentiated adenocarcinoma. Palliative ileostomy was performed to improve defecation in 2019. During the operation, a small nodular mass in the mesentery of the small intestine was identified and pathological examination of the mass revealed advanced adenocarcinoma. The patient was diagnosed with advanced colorectal cancer and administered palliative chemotherapy. He died in June 2020. CONCLUSION: We stress the importance of recognizing the possible occurrence of malignance in patients with CD receiving infliximab.

Acute appendicitis complicated by mesenteric vein thrombosis: A case report.

BACKGROUND: Acute appendicitis with mesenteric vein thrombosis (MVT) is an uncommon condition and usually lacks specific clinical manifestations, which leads to a high rate of misdiagnosis or delayed diagnosis, especially when it is accompanied by other abdominal diseases. Prompt and accurate recognition is vital for treatment and prognosis. CASE SUMMARY: A 37-year-old woman had a history of acute metastatic right lower abdominal pain, nausea, and fever. A contrast-enhanced computed tomography (CT) scan showed a filling defect in the mesenteric vessels. The patient was diagnosed with acute appendicitis complicated by MVT and was treated with anticoagulation and intravenous antibiotics. The follow-up CT scan showed full resolution of the thrombosis and inflammation. CONCLUSION: Clinical awareness is essential for recognizing MVT, especially when it is accompanied by other common acute abdominal diseases, such as acute appendicitis. Contrast-enhanced CT is helpful for the diagnosis of MVT and is recommended for patients with acute abdominal diseases.

Endogenously Expressed IL-4Rα Promotes the Malignant Phenotype of Human Pancreatic Cancer In Vitro and In Vivo.

Exogenous interleukin-4 (IL-4) has been demonstrated to affect the growth of different human malignancies including pancreatic cancer cells. The aim of our study was to determine the role of endogenously expressed IL-4-receptor-α-chain (IL-4Rα) in pancreatic cancer cells. IL-4Rα-suppression was achieved by generating Capan-1 cells stably expressing shRNA targeting IL-4Rα. The malignant phenotype was characterized by assessing growth properties, directional and non-directional cell movement in vitro and tumor growth in vivo. Signaling pathways were analyzed upon IL-4 and IL-13 stimulation of wildtype (WT) and control-transfected cells compared to IL-4Rα-knockdown cells. Silencing of IL-4Rα resulted in reduced anchorage-dependent cell growth (p < 0.05) and reduced anchorage-independent colony size (p < 0.001) in vitro. Moreover, cell movement and migration was inhibited. IL-4 and IL-13 stimulation of Capan-1-WT cells induced activation of similar pathways like stimulation with Insulin-like growth factor (IGF)-I. This activation was reduced after IL-4Rα downregulation while IGF-I signaling seemed to be enhanced in knockdown-clones. Importantly, IL-4Rα silencing also significantly suppressed tumor growth in vivo. The present study indicates that endogenously expressed IL-4 and IL-4Rα contribute to the malignant phenotype of pancreatic cancer cells by activating diverse pro-oncogenic signaling pathways. Addressing these pathways may contribute to the treatment of the disease.

H19 Overexpression Induces Resistance to 1,25(OH)2D3 by Targeting VDR Through miR-675-5p in Colon Cancer Cells.

The long noncoding (lnc) RNA H19 was involved in the tumorigenesis of many types of cancer. However, the role of H19 in the tumorigenesis of colon cancer has not been fully illustrated. Recent studies suggested a potential relationship between H19 and vitamin D receptor (VDR) signaling. Considering the pivotal role of VDR signaling in the colon epithelium both physiologically and pathologically, the correlation between H19 and VDR signaling may have an important role in the development of colon cancer. In this study, the correlation between H19 and vitamin D receptor (VDR) signaling and the underlying mechanisms in colon cancer were investigated both in vitro and in vivo. The results suggested that VDR signaling was able to inhibit the expression of H19 through regulating C-Myc/Mad-1 network. H19, on the other hand, was able to inhibit the expression of VDR through micro RNA 675-5p (miR-675-5p). Furthermore, H19 overexpression induced resistance to the treatment with 1,25(OH)2D3 both in vitro and in vivo. Together, these results suggested that H19 overexpression might be one of the mechanisms underlying the development of resistance to the treatment with 1,25(OH)2D3 in the advanced stage of colon cancer.

Long non-coding RNA lncTCF7 activates the Wnt/ß-catenin pathway to promote metastasis and invasion in colorectal cancer.

Long non-coding RNA (Lnc)TCF7 is a novel lncRNA that is involved in tumorigenesis. Previous studies have revealed that lncTCF7 serves an essential role in maintaining cancer stem cell self-renewal; however, the functions of lncTCF7 in colorectal cancer (CRC) remain unknown. Therefore, the present study aimed to investigate the role of lncTCF7 in CRC. LncTCF7 was upregulated in 52/58 CRC tissues, and its expression correlated with tumor size, lymph metastasis and tumor-node-metastasis stage in CRC. Knocking down lncTCF7 in colon cancer cell lines decreased cell proliferation, migration and invasion, while lncTCF7 overexpression showed opposite changes. In addition, lncTCF7 promoted cell proliferation in vivo. LncTCF7 activated the Wnt/ß-catenin signaling pathway, which is essential for cancer development. Survival analysis revealed that patients with higher expression of lncTCF7 had significantly worse prognosis compared with patients with low expression. These findings indicate that lncTCF7 regulates CRC progression and support the notion of lncTCF7 as a CRC prognostic marker.

GYY4137 ameliorates intestinal barrier injury in a mouse model of endotoxemia.

Intestinal barrier injury has been reported to play a vital role in the pathogenesis of endotoxemia. This study aimed to investigate the protective effect of GYY4137, a newly synthesized H2S donor, on the intestinal barrier function in the context of endotoxemia both in vitro and in vivo. Caco-2 (a widely used human colon cancer cell line in the study of intestinal epithelial barrier function) monolayers incubated with lipopolysaccharide (LPS) or TNF-α/IFN-γ and a mouse model of endotoxemia were used in this study. The results suggested that GYY4137 significantly attenuated LPS or TNF-α/IFN-γ induced increased Caco-2 monolayer permeability. The decreased expression of TJ (tight junction) proteins induced by LPS and the altered localization of TJs induced by TNF-α/IFN-γ was significantly inhibited by GYY4137; similar results were obtained in vivo. Besides, GYY4137 promoted the clinical score and histological score of mice with endotoxemia. Increased level of TNF-α/IFN-γ in the plasma and increased apoptosis in colon epithelial cells was also attenuated by GYY4137 in mice with endotoxemia. This study indicates that GYY4137 preserves the intestinal barrier function in the context of endotoxemia via multipathways and throws light on the development of potential therapeutic approaches for endotoxemia.

SPARC expression is negatively correlated with clinicopathological factors of gastric cancer and inhibits malignancy of gastric cancer cells.

Secreted protein acidic and rich in cysteine (SPARC) is a glycoprotein which plays multiple roles in different types of cancer. Our previous study showed that SPARC overexpression inhibited the growth and angiogenesis of tumors, and reduced expression of vascular endothelial growth factor (VEGF). However, the relationship between SPARC expression and clinicopathological factors of gastric cancer (GC) is controversial, and the role of SPARC in GC remains unclear. We evaluated expression of SPARC in 65 human GC tissues using immunohistochemistry (IHC). The results indicated that SPARC expression was negatively correlated with clinicopathological factors of GC. In vitro assay showed that SPARC overexpression decreased proliferation and clonogenicity by suppressing CD44 expression. In addition, SPARC overexpression inhibited VEGF induced proliferation and arrested cell cycle of GC cells by reducing the activation of VEGFR2, ERK1/2 and AKT signaling pathways. SPARC suppressed the invasion and migration of GC by reducing MMP-7, MMP-9, N-cadherin, Sp1 and p-ERK1/2 expression. In the in vivo assay, cancer metastasis mouse models were established by tail vein injection. The results revealed that the lung metastases of SPARC-overexpressing GC cells in the mice were much fewer than those of control cells.

Puerarin inhibits iNOS, COX-2 and CRP expression via suppression of NF-κB activation in LPS-induced RAW264.7 macrophage cells.

Puerarin (7,4'-dihydroxy-8-C-glucosylisoflavone) is the most abundant isoflavone-C-glucoside extracted from Radix puerariae, and it has been used for various medicinal purposes in traditional oriental medicine for thousands of years. In the present study, the ability of the puerarin to modulate inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and C reactive protein (CRP) expression and induce changes in the nuclear factor κB (NF-κB) pathway in RAW264.7 macrophage cells was examined. The protein and mRNA levels of lipopolysaccharide (LPS)-induced iNOS, COX-2 and CRP were determined in RAW246.7 macrophage cells. Inhibitor κB (I-κB) phosphorylation and p65NF-κB expression in RAW246.7 macrophage cells were also detected under our experimental conditions. The results indicated that puerarin inhibited the expression of LPS-induced iNOS, COX-2 and CRP proteins and also suppressed their mRNAs from RT-PCR experiments in RAW264.7 cells. Subsequently, we determined that the inhibition of iNOS, COX-2 and CRP expression was due to a dose-dependent inhibition of phosphorylation and degradation of I-κB, which resulted in the reduction of p65NF-κB nuclear translocation. These data suggested that the effect of puerarin-mediated inhibition of LPS-induced iNOS, COX-2 and CRP expression is attributed to suppressed NF-κB activation at the transcriptional level.

A random forest of combined features in the classification of cut tobacco based on gas chromatography fingerprinting.

We applied the random forest method to discriminate among different kinds of cut tobacco. To overcome the influence of the descending resolution caused by column pollution and the subsequent deterioration of column efficacy at different testing times, we constructed combined peaks by summing the peaks over a specific elution time interval Deltat. On constructing tree classifiers, both the original peaks and the combined peaks were considered. A data set of 75 samples from three grades of the same tobacco brand was used to evaluate our method. Two parameters of the random forest were optimized using out-of-bag error, and the relationship between Deltat and classification rate was investigated. Experiments show that partial least squares discriminant analysis was not suitable because of the overfitting, and the random forest with the combined features performed more accurately than Naïve Bayes, support vector machines, bootstrap aggregating and the random forest using only its original features.

Puerarin inhibits C-reactive protein expression via suppression of nuclear factor kappaB activation in lipopolysaccharide-induced peripheral blood mononuclear cells of patients with stable angina pectoris.

Puerarin (4'-7-dihydroxy-8-beta-D-glucosylisoflavone), the most abundant isoflavone-C-glucoside extracted from the root of the plant Pueraria lobata, has demonstrated anti-inflammatory activity in cellular models of inflammation. In this report, we examined the ability of puerarin to modulate C-reactive protein (CRP) expression and key molecules in the nuclear factor kappa B (NF-kappaB) pathway to determine its molecular target. The protein and mRNA levels of CRP were determined in lipopolysaccharide (LPS)-induced peripheral blood mononuclear cells of patients with unstable angina pectoris. Also, we detected the I-kappaBalpha phosphorylation and the p65NF-kappaB expression in peripheral blood mononuclear cells under our experimental condition. The results indicated that puerarin inhibited the expression of the protein and mRNA levels of CRP in LPS-induced peripheral blood mononuclear cells. Subsequently, we determined that the inhibition of CRP expression was because of a dose-dependent inhibition of phosphorylation and degradation of inhibitor kappaB(I-kappaB), which resulted in a reduction of p65NF-kappaB nuclear translocation. We conclude that puerarin acts as an anti-inflammatory agent by blocking NF-kappaB signalling, and may possibly be developed as a useful agent for the chemoprevention of atherosclerosis.

Puerarin inhibits adhesion molecule expression in tnf-alpha-stimulated human endothelial cells via modulation of the nuclear factor kappaB pathway.

BACKGROUND: The isoflavone puerarin is the most abundant isoflavone-C-glucoside extracted from the root (radix puerariae) of the plant Pueraria lobata and possesses many biological activities. In this report, the ability of puerarin to modulate intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and endothelial leukocyte adhesion molecule 1 (E-selectin), and to induce changes in the nuclear factor kappaB (NF-kappaB) pathway in human umbilical vein endothelial cells (HUVECs) was examined. METHODS: The protein and mRNA levels of tumor-necrosis-factor-alpha (TNF-alpha)-induced ICAM-1, VCAM-1 and E-selectin were determined in HUVECs. Inhibitor kappaB (I-kappaB) phosphorylation and p65 NF-kappaB expression in HUVECs were also examined. RESULTS: Puerarin inhibited the expression of TNF-alpha-induced ICAM-1, VCAM-1 and E-selectin proteins and mRNAs in HUVECs. Subsequently, we determined that the inhibition of ICAM-1, VCAM-1 and E-selectin expression was due to a dose-dependent suppression of phosphorylation and degradation of I-kappaB, which resulted in a reduction of p65 NF-kappaB nuclear translocation. CONCLUSION: These data suggested that the effect of puerarin-mediated inhibition of TNF-alpha-induced ICAM-1, VCAM-1 and E-selectin expression is attributed to suppressed NF-kappaB activation on the transcriptional level.