Experimental and therapeutic medicine最新文献

The 203 patients who underwent laparoscopic common bile duct exploration for choledocholithiasis were retrospectively analyzed. The patients were divided into internal drainage tube group (n=87) and T-tube group (n=116). Total bilirubin, direct bilirubin, alanine aminotransferase (AST), aspartate aminotransferase (ALT), the diameter of common bile duct, number of stones, operation time, intraoperative bleeding, postoperative hospital stay and postoperative complications were compared between the two groups. Possible influencing factors were selected as independent variables, and the operation mode was selected as the dependent variable for multifactor unconditional logistic regression analysis. There were no significant differences in the sex, age, total bilirubin, direct bilirubin, AST, ALT, operation time, intraoperative blood loss, postoperative hospital stay and postoperative biliary leaks between the two groups (P>0.05). The diameter of the common bile duct was smaller and the incidence of multiple stones in the common bile duct was lower in the internal drainage tube group compared with that in the T-tube group (P<0.05). The results of multifactor unconditional logistic regression analysis demonstrated that the diameter of the common bile duct and the number of stones in the common bile duct were associated with the operation mode as influencing factors. In conclusion, Patients with multiple stones in the common bile duct or with a wide diameter of the common bile duct are more likely to have T-tube placed rather than an internal drainage tube.

A desmoid tumor is a fibroblastic proliferation of mesenchymal origin, which has no metastasizing potential but is locally aggressive. Although treatment has shifted to observation and active surveillance for newly diagnosed patients with desmoid tumors, intra-abdominal mesenteric tumors or tumors that persistently grow and provoke symptoms may need prompt surgical treatment. There have only been a small number of case reports that illustrate large sporadic intra-abdominal mesentery-deriving desmoid tumors in which the longest diameter was ≥19 cm. In the present study, an adolescent male patient with a rapidly growing 38-cm long sporadic intra-abdominal desmoid tumor of mesenchymal origin is reported. The patient was treated with chemotherapy followed by surgical resection due to non-responsiveness and progression of symptoms, then with maintenance adjuvant chemotherapy to prevent recurrence due to the large size of the tumor. Despite the rapid growth of the tumor and its high occupancy in the intra-abdominal cavity, an R0 resection was successful with organ preservation. The patient has been recurrence-free for 2 years, and further follow-up is expected in the future.

Subacute combined degeneration (SCD) is a neurological disorder caused by vitamin B12 deficiency, prevalent in the cervical and thoracic medullas, with an insidious onset and a lack of characteristic clinical manifestations. The present study describes a case of a 36-year-old female patient with SCD who demonstrated abnormal changes in the white matter of the brain. The laboratory test results showed a decrease in serum vitamin B12 levels and an increase in homocysteine levels. Magnetic resonance imaging (MRI) of the brain showed that, in addition to abnormal signals in the cervical and thoracic spine, speckled and short-striped abnormal signals were present, symmetrically distributed in the centrum semiovale. After 6 months of follow-up treatment, cranial MRI showed a significant attenuation of the symmetrical speckled and short-striped abnormal signals in the centrum semiovale. Homocysteine and serum vitamin B12 levels of the patient were within the expected range. Although, to the best of our knowledge, there have been no previous reports of alterations in the brain of patients with SCD, if these patients report neurological symptoms, clinicians should consider that these symptoms may be accompanied by inflammatory demyelination of the brain.

The present study aimed to examine the effects of the long non-coding (lnc)RNA expressed by tissue differentiation-inducing non-protein coding RNA (TINCR) on cervical cancer development. For this purpose, adjacent normal and cancer tissues were obtained from patients with cervical cancer and the lncRNA TINCR level was examined using reverse transcription-quantitative PCR (RT-qPCR) and in situ hybridization. The association between lncRNA TINCR and the clinicopathological characteristics and prognosis of patients with cervical cancer was also analyzed. Furthermore, the expression levels of lncRNA TINCR, miRNA-7, mTOR, hypoxia-inducible factor 1 subunit α and VEGF were measured using RT-qPCR and western blot analysis. Cell proliferation, apoptosis, and invasion and migration were examined using MTT assay, 5-ethynyl-2'-deoxyuridine staining, flow cytometry, TUNEL assay, and Transwell and wound healing assays. The association between lncRNA TINCR, miRNA-7 and mTOR was also examined using a luciferase assay. The results revealed that the lncRNA TINCR level was significantly increased in cervical cancer tissues and was associated with the overall survival of patients (low vs. high expression group; P=0.0391). LncRNA TINCR was also associated with the clinicopathological characteristics of patients with cervical cancer. Following the knockdown of lncRNA TINCR using small interfering (si)RNA, cell proliferation was significantly decreased and cell apoptosis was significantly increased (P<0.001 for both); cell invasion and migration were also significantly decreased (P<0.001 for both) following transfection with mimics miRNA-7. Transfection with miRNA-7 antisense oligonucleotide decreased the antitumor effects of si-TINCR in Siha and HeLa cell lines. As shown using the dual-luciferase assay, lncRNA TINCR could target miRNA-7 and miRNA-7 could directly regulate mTOR in HeLa and SiHa cell lines. In conclusion, the present study demonstrated that lncRNA TINCR could promote cervical cancer development via regulation of the miRNA-7/mTOR axis in vitro.

Whether Helicobacter pylori (H. pylori) infection is associated with periodontitis has been contested for decades. The relationship between H. pylori genotypes and periodontitis has not been clarified either. The present study provides a novel perspective to better understand the role of H. pylori in the pathogenesis of periodontitis. A total of 53 volunteers were recruited and divided into 3 groups in this cross-sectional study, namely the periodontally healthy group (15 participants), the stage I/II periodontitis group (20 participants) and the stage III/IV periodontitis group (18 participants). DNA from the subgingival plaque of all participants was extracted and PCR was performed using specific primers for the urease C gene and cytotoxin-associated gene A (cagA)/vacuolating cytotoxin gene A (vacA) to detect the presence and genotype of H. pylori. A χ² test and one-way ANOVA were performed on the data. There was no significant difference in sex, age or body mass index between the groups. The detection rate of H. pylori was 39.62% in the total population and increased with the deepening of probing depth and clinical attachment loss. There were significant differences in the detection rate of H. pylori among the three groups, with 13.33, 40.00 and 61.11% in the periodontally healthy, stage I/II periodontitis and stage III/IV periodontitis groups, respectively (χ²=8.760, P<0.001). The cagA^-/vacAs2m2 genotype was most commonly detected in the periodontally healthy group (100%). In the periodontitis group, cagA⁺/vacAs1m2 was the most commonly detected genotype in the stage I/II periodontitis group (37.5%) and cagA⁺/vacAs1m1 in the stage III/IV periodontitis group (36.3%). The results of the present study suggest that the detection rates and genotypes of H. pylori in the subgingival plaque are associated with the status of periodontitis. cagA⁺/vacAs1m1 and cagA⁺/vacAs1m2 may be considered virulence markers of periodontitis. However, given the small sample size and lack of correlation analysis of the study, further larger scale and high-quality clinical trials are required to confirm these findings.

Cucurbitacin B (CuB) is a member of the cucurbitacin family, which has shown potent anticancer pharmacological activity. Prolonged or severe endoplasmic reticulum stress (ERS) induces apoptosis; therefore, the present study investigated whether CuB may activate the ERS pathway to induce apoptosis. HT-29 and SW620 colorectal cancer (CRC) cells were treated with a range of concentrations of CuB for 48 h, and the viability and proliferation of cells were determined using Cell Counting Kit 8 (CCK8) and colony formation assays. Subsequently, the appropriate CuB concentration (5 µM) was selected for treatment of CRC cells for 48 h. Western blot analysis was used to measure the expression levels of ERS-related proteins, flow cytometry was used to evaluate apoptosis, the dichlorodihydrofluorescein diacetate fluorescent probe was used to detect reactive oxygen species (ROS) production, and the relationship between ROS and ERS was determined by western blot analysis. Furthermore, flow cytometry was used to evaluate apoptosis after treatment with the ERS inhibitor 4-phenylbutyric acid, the ROS inhibitor N-acetylcysteine and following knockdown of CHOP expression. In addition, western blot analysis was performed to measure Bax and Bcl2 protein expression levels, and a CCK8 assay was performed to evaluate the viability of cells following knockdown of CHOP. Notably, CuB treatment increased apoptosis and inhibited cell proliferation in CRC cell lines, and these effects were mediated by ROS and ROS-regulated activation of the PERK and XBP1 ERS pathways. In conclusion, CuB may induce apoptosis in HT-29 and SW620 CRC cells via ROS and ERS.

Inflammation plays an integral role in the complications of sickle cell disease (SCD), which can lead to vaso-occlusive crisis and extreme pain. SCD is accompanied by numerous complications, including cardiovascular disease, cognitive decline and endothelial dysfunction, contributing to mortality. As disease severity increases with age, the present study aimed to assess if age is also correlated with a definite pattern of progression of the two inflammatory markers, high-sensitivity C-reactive protein (hsCRP) and total homocysteine (tHCY). The findings of the present study could lead to an improved understanding of the threshold levels of these inflammatory markers and timely interventions to delay complications. In an observational study, levels of hsCRP and tHCY were analyzed in 70 patients (35 male and 35 female patients) with SCD aged between 5 and 16 years. hsCRP levels were in the high-risk range in 64.29% (n=45) of all male and female patients. A sex-wise distribution showed that, of the 35 male patients, 74.28% (n=26) were in the high-risk range, and of the 35 female patients, 54.28% (n=19) were in the high-risk range. An age-wise distribution showed that of the 41 patients in the 5-10-years age group, 70.73% (n=29), were in the high-risk range. In comparison, of the 29 patients in the 11-16-years age group, 55.17% (n=16) were in the high-risk range. tHCY levels were observed to be in the normal range in 98.57% (n=69) of all children, as compared with 1.43% (n=1) in the high-risk range. Furthermore, a sex-wise distribution showed that female patients in the high-risk group of hsCRP had higher concentrations of tHCY as compared with the male patients in that risk group. An age-wise distribution of hsCRP concentration also showed that the risk of CVD in patients in the 11-16-years age group was higher with increased concentrations of tHCY. A weak negative correlation was observed between age and hsCRP concentrations (r-value=-0.280; P=0.026) and a weak positive correlation was detected between tHCY and age (r-value=0.259; P=0.036). In conclusion, the results of the present study indicated that higher levels of hsCRP could be a useful marker in children with SCD, and levels of tHCY may be an adjunct marker as the disease progresses with age.

The present paper aimed to investigate the altered angiogenetic mechanisms in hypoxic conditions in patients with prostate tumours, in correlation with common clinicopathologic variables. A case-control study was developed and included 87 patients with prostate tumours [40 diagnosed with benign prostatic hyperplasia (BPH) and 47 diagnosed with prostate cancer (PCa), using prostate transrectal biopsy] and 40 healthy subjects. The following parameters were evaluated in the serum of volunteers: Hypoxia-inducible factor (HIF)-1α, fibroblast growth factor (FGF)-2, vascular endothelial growth factor (VEGF), matrix metalloproteinase (MMP)-2 and -9, thrombospondin (TSP)-1 and soluble VEGF-1 receptor. Experimental data analysis demonstrated increasing amounts of inflammation in patients with PCa (IL-6, 18.1±4.7 ng/ml) and BPH (IL-6, 16.3±5.1 ng/ml) vs. control (IL-6, 4.1±1.2 ng/ml); overregulation of HIF1α in patients with PCa (129.3±21.8 ng/ml) compared with patients with BPH (65.6±18.2 ng/ml) and control (61.3±12.7 ng/ml); angiogenesis abnormalities in patients with PCa (upregulation of FGF-2, VEGF, MMP-2 and -9, suppression of TSP-1 and soluble VEGR-1) and BPH (upregulation FGF-2 and VEGF) compared with the control group. In conclusion, a greater understanding of the biological mechanism, the pathological roles and the clinical significance of various proangiogenic parameters and angiogenic-suppressor proteins seem useful in clinical practice for establishing an early diagnosis of prostate pathology and finding an individualized therapeutic approach.

Lymphatic metastasis is the primary type of cervical cancer metastasis and is associated with an extremely poor prognosis in patients. The tumor microenvironment primarily includes cancer-associated fibroblasts, tumor-associated macrophages, myeloid-derived suppressor cells, immune and inflammatory cells, and blood and lymphatic vascular networks, which can promote the establishment of lymphatic metastatic sites within immunosuppressive microenvironments or promote lymphatic metastasis by stimulating lymphangiogenesis and epithelial-mesenchymal transformation. As the most important feature of the tumor microenvironment, hypoxia plays an essential role in lymph node metastasis. In this review, the known mechanisms of hypoxia, and the involvement of stromal components and immune inflammatory cells in the tumor microenvironment of lymphatic metastasis of cervical cancer are discussed. Additionally, a summary of the clinical trials targeting the tumor microenvironment for the treatment of cervical cancer is provided, emphasizing the potential and challenges of immunotherapy.