Laparoscopic management of second trimester ruptured cornual heterotopic pregnancy with subsequent live birth delivery: A case report and literature review.

OBJECTIVE: Heterotopic pregnancy (HP) is the coexistence of extra- and intrauterine gestation implantation sites. A rare case of a second-trimester ruptured cornual HP (CHP) treated with laparoscopic cornual resection with the primary repair is presented. Risk factors, clinical presentations, treatments, and outcomes of CHPs are also reviewed. CASE REPORT: A 35-year-old pregnant woman with CHP presented with lower abdominal pain with hemoperitoneum and her hemoglobin level dropped. Laparoscopic management of a ruptured HP was performed, leaving the surplus intrauterine fetus intact. She delivered a 2360 g male infant via cesarean section at 34 weeks' gestation due to preterm premature rupture of membranes. We found a well-healed wound over the left uterine cornua during the cesarean section. CONCLUSION: Ruptured CHP is a rare but life-threatening complication of an obstetric emergency. Although the pregnant uterus becomes congested and fragile, using reliable laparoscopic energy devices and barbed sutures, successful treatment is feasible.

Validation of Non-Invasive Preimplantation Genetic Screening Using a Routine IVF Laboratory Workflow.

Embryo selection is needed to optimize the chances of pregnancy in assisted reproduction technology. This study aimed to validate non-invasive preimplantation genetic testing for aneuploidy (niPGT-A) using a routine IVF laboratory workflow. Can niPGT-A combined with time-lapse morphokinetics provide a better embryo-selection strategy? A total of 118 spent culture mediums (SCMs) from 32 couples were collected. A total of 40 SCMs and 40 corresponding trophectoderm (TE) biopsy samples (n = 29) or arrested embryos (n = 11) were assessed for concordance. All embryos were cultured to the blastocyst stage (day 5 or 6) in a single-embryo culture time-lapse incubator. The modified multiple annealing and looping-based amplification cycle (MALBAC) single-cell whole genome amplification method was used to amplify cell-free DNA (cfDNA) from the SCM, which was then sequenced on the Illumina MiSeq system. The majority of insemination methods were conventional IVF. Low cfDNA concentrations were noted in this study. The amplification niPGT-A and conventional PGT-A was 67.7%. Based on this study, performing niPGT-A without altering the daily laboratory procedures cannot provide a precise diagnosis. However, niPGT-A can be applied in clinical IVF, enabling the addition of blastocysts with a better prediction of euploidy for transfer.

The role of bile acid metabolism in the occurrence and development of NAFLD.

Non-alcoholic fatty liver disease (NAFLD) has become one of the important causes of cirrhosis and liver cancer, resulting in a huge medical burden worldwide. Currently, effective non-invasive diagnostic indicators and drugs for NAFLD are still lacking. With the development of metabolomics technology, the changes in metabolites during the development of NAFLD have been gradually revealed. Bile acid (BA) is the main endpoint of cholesterol metabolism in the body. In addition, it also acts as a signaling factor to regulate metabolism and inflammation in the body through the farnesyl X receptor and G protein-coupled BA receptor. Studies have shown that BA metabolism is associated with the development of NAFLD, but a large number of animal and clinical studies are still needed. BA homeostasis is maintained through multiple negative feedback loops and the enterohepatic circulation of BA. Recently, treatment of NAFLD by interfering with BA synthesis and metabolism has become a new research direction. Here, we review the changes in BA metabolism and its regulatory mechanisms during the development of NAFLD and describe the potential of studies exploring novel non-invasive diagnostic indicators and therapeutic targets for NAFLD based on BA metabolism.

Novel mechanism of hepatobiliary system damage and immunoglobulin G4 elevation caused by Clonorchis sinensis infection.

Clonorchis sinensis infection is still a major public health problem. It is estimated that more than 15 million people worldwide are infected, especially in Northeast China, Taiwan, South Korea, and North Vietnam. The detection of Clonorchis sinensis eggs in feces and bile is still the only gold standard for the diagnosis of Clonorchis sinensis infection, and new detection methods are needed to improve the detection rate. After Clonorchis sinensis invades the human body, it mainly parasitizes the hepatobiliary tract. Therefore, it is closely related to hepatobiliary diseases such as cholangitis, bile duct stones, liver fibrosis, and cholangiocarcinoma. The increase in immunoglobulin G4 (IgG4) caused by Clonorchis sinensis infection is rare and there are few reports about the relevant mechanism. It may be related to the inflammatory factors interleukin (IL)-4, IL-10, and IL-13 produced by human phagocytes, T cells, B cells, and other immune cells in the process of resisting the invasion of Clonorchis sinensis. However, this finding still needs further clarification and confirmation. This article reviews the epidemiology, clinical manifestations, serology, imaging, pathogenic mechanism, and control measures of Clonorchis sinensis infection to help establish the diagnostic process for Clonorchis sinensis. We report novel mechanisms of IgG4 elevation due to Clonorchis sinensis infection to provide more experience and a theoretical basis for clinical diagnosis and treatment of this infection.

Eosinophilic pancreatitis: a review of the pathophysiology, diagnosis, and treatment.

Eosinophilic pancreatitis (EP) is an extremely rare disease caused by purely eosinophilic infiltration of the pancreas. EP is prone to being misdiagnosed as pancreatic cancer, causing unnecessary economic and physical harm to the patient. We report three cases of EP that were cured by steroids without relapse from 2017 to now. The clinical data of the three patients, including clinical manifestations, serological manifestations, imaging (ultrasound, computed tomography, and MRI), pathological diagnosis and treatment, and telephone follow-up of all patients, were retrospectively analysed. In addition, a literature search was conducted on the Web of Science and PubMed databases using key terms related to EP, considering case reports with no restrictions on the date of publication or language. In conclusion, we analysed 19 cases and determined the diagnostic criteria for EP. The diagnostic algorithm for EP can be used to diagnose EP easily. We hope that our standards and algorithm can reduce the rate of misdiagnosis and contribute to clinical diagnosis and treatment. In addition, we expect to evaluate more EP cases to test our diagnostic criteria and design a systematic diagnostic flow chart.

Distinctive gut microbial dysbiosis between chronic alcoholic fatty liver disease and metabolic-associated fatty liver disease in mice.

The gut microbiota, which may affect normal physiological and biochemical functions, has an important role in the development of human liver diseases. The aim of the present study was to investigate differences in the gut microbiota between chronic alcoholic fatty liver disease (AFLD) and metabolic-associated fatty liver disease (MAFLD). AFLD was induced by chronic alcohol administration and MAFLD was induced by a Western-style diet in C57BL/6 mice. After 8 weeks, the levels of plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglyceride (TG), total cholesterol (TC), lipopolysaccharide (LPS), tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1ß and IL-10 were assessed and H&E staining of mouse liver tissue was performed. High-throughput sequencing of 16S ribosomal DNA from the intestinal contents was used to analyze the different effects of AFLD and MAFLD on the gut microbiota. Differences in the gut microbiota composition were assessed by the t-test. The results revealed increases in LPS, ALT, AST, TG, IL-1ß and TNF-α in the AFLD group. Compared with those in the MAFLD control group, the MAFLD group exhibited increased plasma ALT, TG, TC, IL-6, IL-1ß and TNF-α levels and decreased plasma IL-10 levels. In addition, the α- and ß-diversities revealed that the AFLD and MAFLD groups exhibited obvious changes in the gut structure (with an increase in abundance in the AFLD group and a decrease in abundance in the MAFLD group). In comparison to the AFLD control group, Enterococcaceae were the most abundant bacteria at the family level and Enterococcus and Streptococcus were the most abundant bacteria at the genus level in the AFLD group. However, in the MAFLD group, Lachnospiraceae was the most abundant at the family level, with increases in Erysipelatoclostridium, Gordonibacter and Streptococcus at the genus level and a decrease in the genus Bifidobacterium. In conclusion, the present study confirmed that the AFLD and MAFLD groups harbored differences in the gut microbiota. The marked differences in the gut microbiota at the family and genus levels may contribute to the development process of FLD.

Pituitary stalk interruption syndrome and liver changes: From clinical features to mechanisms.

Pituitary stalk interruption syndrome (PSIS) is a rare congenital abnormality characterized by thinning or disappearance of the pituitary stalk, hypoplasia of the anterior pituitary and an ectopic posterior pituitary. Although the etiology of PSIS is still unclear, gene changes and perinatal adverse events such as breech delivery may play important roles in the pathogenesis of PSIS. PSIS can cause multiple hormone deficiencies, such as growth hormone, which then cause a series of changes in the human body. On the one hand, hormone changes affect growth and development, and on the other hand, they could affect human metabolism and subsequently the liver resulting in nonalcoholic fatty liver disease (NAFLD). Under the synergistic effect of multiple mechanisms, the progression of NAFLD caused by PSIS is faster than that due to other causes. Therefore, in addition to early identification of PSIS, timely hormone replacement therapy and monitoring of relevant hormone levels, clinicians should routinely assess the liver function while managing PSIS.

Pathogenesis of liver injury in Takayasu arteritis: advanced understanding leads to new horizons.

Liver injury in Takayasu arteritis (TA) is a rare phenomenon. Most symptoms are nonspecific, and the exact pathogenesis remains to be elucidated. Early diagnosis and new treatment methods are important for an improved prognosis. A summary of the clinical information and mechanistic analyses may contribute to making an early diagnosis and development of new treatment methods. A PubMed search was conducted using the specific key words "Takayasu arteritis" and "liver" or "hepatitis" or "hepatic". Symptoms and treatment of TA with an accompanying liver injury were reviewed retrospectively. Many factors are presumed to be involved in the mechanism of TA with liver injury, including the immune response, genes, infections, and gut microbiota. There are several lines of evidence indicating that immune dysfunction is the main pathogenic factor that triggers granuloma formation in TA patients. However, the role of genetics and infections has not been fully confirmed. Recently, the gut microbiota has emerged as an essential component in the process. We reviewed in detail the current concepts that support the complex pathogenesis of TA accompanied by liver injury, and we presented recent theories from the literature. Finally, we discussed future research directions of liver injury in TA.

Mesh-related complications in single-incision transvaginal mesh (TVM) and laparoscopic abdominal sacrocolpopexy (LASC).

OBJECTIVE: Few studies have investigated the long-term impact of synthetic mesh reconstructive surgery for pelvic organ prolapse (POP) on patient outcomes. This study aimed to examine the incidence and risk factors of mesh exposure and the subsequent requirement for surgical interventions due to mesh-related complications. MATERIALS AND METHODS: This retrospective study was conducted from November 2010 to April 2018. We recruited women with Pelvic Organ Prolapse Quantification (POP-Q) stage 3 or 4 who underwent mesh reconstructive surgery for POP, and enrolled 487 women who received transvaginal mesh (TVM) and 110 women who received laparoscopic abdominal sacrocolpopexy (LASC). Assessments included mesh exposure rate and mesh-related complications requiring surgical interventions in both groups. RESULTS: In the LASC group, the overall mesh-related complication rate was 8.18% over a mean follow-up period of 18 months. Concomitant laparoscopic-assisted vaginal hysterectomy was associated with mesh exposure (OR = 9.240; 95% CI = 1.752-48.728). No patients in the concurrent supracervical hysterectomy group were exposed to mesh. In the single-incision TVM group, the overall rate of mesh-related complications was 3.29% over a mean follow-up period of 19 months. Concomitant total vaginal hysterectomy was also a risk factor for mesh exposure (OR = 4.799; 95% CI = 1.313-17.359). CONCLUSION: Preserving the cervix or uterus decreased the rate of mesh exposure in those undergoing TVM and LASC surgery. The overall rate of mesh-related complications was low after up to 8 years of follow-up.

Evaluating Ternary Metal Oxide (TMO) core-shell nanocomposites for the rapid determination of the anti-neoplastic drug Chlorambucil (Leukeran™) by electrochemical approaches.

A functional ternary nanocomposite (MnO2@NiFe2O4) with hierarchically grown flower-like core-shell assembly has been prepared through a simple two-step hydrothermal methodology. The crystallographic information of the sample was obtained via X-ray diffraction. The morphological details of spherical NiFe2O4 (core) and flower-like MnO2 (shell) were examined over FE-SEM and TEM; finally, the XPS confirms the successful formation of MnO2@NiFe2O4 ternary nanocomposite. The surface area of finely grown hierarchical MnO2 flowers on NiFe2O4 nanoparticles was measured through BET isothermal studies. The ternary nanocomposite was employed for the specific and sensitive detection of anticancer drug Chlorambucil. Under the well-optimized condition, the graphically plotted calibration curve was attained at MnO2@NiFe2O4/GCE towards the detection of anticancer drug Chlorambucil, which possesses the wider linear range of 0.025-574.5 µM, with the minimal detection limit of 4.68 nM. The feasibility of the sensitive layer has also been inspected on the pharmaceutical sample (oral tablets) and the biological matrix (human urine), whereas the appreciable spike recoveries were obtained.

One-pot sonochemical synthesis of Bi2WO6 nanospheres with multilayer reduced graphene nanosheets modified electrode as rapid electrochemical sensing platform for high sensitive detection of oxidative stress biomarker in biological sample.

4-Nitroquinoline N-oxide (4-NQO) is an important tumorigenic organic compound with high adverse effect in the human body. In this study, a novel Bismuth Tungstate nanospheres (Bi2WO6) decorated reduced graphene oxide (Bi2WO6/rGOS) nanocomposite have been designed through a sonochemical method. The as-synthesized Bi2WO6/rGOS was characterized through the HRTEM, FESEM, XPS, EIS and XRD. Furthermore, the nanocomposite modified glassy carbon electrode (GCE) was developed for the determination of 4-NQO. The results showed that the Bi2WO6/rGOS nanocomposite modified electrode exhibit valuable responses and excellent electrocatalytic activity. The fabricated sensor was facilitated the analysis of 4-NQO with a nanomolar detection limit (6.11 nM). Further, the as-synthesized Bi2WO6/rGOS modified electrode has been applied to sensing of 4-NQO in human blood and urine samples with satisfactory recovery.

Role of CYP1A2 1F polymorphism in cancer risk: evidence from a meta-analysis of 46 case-control studies.

BACKGROUND: Emerging evidence showed that the common polymorphism (CYP1A2 1F, rs762551 C→A) in the promoter region of the CYP1A2 gene might be associated with susceptibility to cancer in humans. But individually published results were inconclusive. The aim of this meta-analysis is to investigate the association between CYP1A2 1F polymorphism and cancer risk. METHODS: The Pubmed, Embase, Web of Science and Chinese BioMedical databases were searched for all articles published up to September 1st, 2012. Statistical analyses were performed using the STATA 12.0 software. RESULTS: Forty-six case-control studies were included with a total of 22,993 cancer cases and 28,420 healthy controls. Meta-analysis results showed that the A allele of CYP1A2 1F polymorphism was associated with a decreased cancer risk (odds ratio [OR]=0.92, 95% confidence interval [CI]: 0.87-0.98, P=0.013). In the subgroup analysis by cancer types, the A allele of CYP1A2 1F polymorphism may increase the risk of breast cancer (OR=1.05, 95% CI: 1.01-1.10, P=0.024), and is also associated with a decreased risk of ovarian cancer (OR=0.70, 95% CI: 0.54-0.89, P=0.004). However, similar results were not found in lung, colorectal, bladder, endometrial, pancreatic and gastric cancers. Further subgroup analysis by ethnicity also showed a significant association between the A allele of CYP1A2 1F polymorphism and a decreased cancer risk among Caucasian populations (OR=0.91, 95% CI: 0.84-0.98, P=0.014); but no significant associations were observed among Asian populations. CONCLUSIONS: Results from the current meta-analysis indicate that the A allele of CYP1A2 1F polymorphism may be associated with breast and ovarian cancer risk, especially among Caucasian populations.

XRCC1 Arg399Gln polymorphism contributes to increased risk of colorectal cancer in Chinese population.

Previous studies investigating the association between X-ray repair cross-complementation group 1 (XRCC1) Arg399Gln polymorphism and colorectal cancer risk in Chinese provided inconsistent findings. To assess the association in Chinese population, a meta-analysis was performed. Eligible studies were searched in Pubmed, Emabse, and China National Knowledge Infrastructure databases. Odds ratios (OR) with the corresponding 95 % confidence intervals (95 %CI) were pooled to assess the association. Seven case-control studies involving a total of 2136 colorectal cancer cases and 3168 controls were finally included in the meta-analysis. Our analysis suggested that the variant genotypes of XRCC1 Arg399Gln were associated with an increased risk of colorectal cancer in Chinese population (Gln vs. Arg: random effect model OR = 1.24, 95 %CI = 1.01-1.52, P = 0.041; GlnGln vs. ArgArg: random effect model OR = 1.52, 95 %CI = 1.07-2.15, P = 0.019; and Recessive model: fixed effect model OR = 1.37, 95 %CI = 1.12-1.67, P = 0.002). There was low risk of publication bias in present meta-analysis. Our meta-analysis provides an evidence for the association between XRCC1 Arg399Gln polymorphism and colorectal cancer risk in Chinese population, and XRCC1 Arg399Gln variant genotypes contribute to increased risk of colorectal cancer in Chinese.

CYP2E1 RsaI/PstI polymorphism and liver cancer risk among east Asians: a HuGE review and meta-analysis.

Published data on any association between the CYP2E1 RsaI/PstI (c1/c2) polymorphism and liver cancer risk among east Asians are inconclusive. The aim of this Human Genome Epidemiology (HuGE) review and meta- analysis was to derive a more precise estimation of the relationship. A literature search of Pubmed, Embase, Web of science and CBM databases from inception through July 2012 was conducted. Twelve case-control studies were included with a total of 1,552 liver cancer cases and 1,763 healthy controls. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association under five genetic models. When all the eligible studies were pooled into the meta-analysis, the results showed that the c2 allele and the c2 carrier (c2/c2 + c2/c1) of RsaI/PstI polymorphism were associated with decreased risk of liver cancer among east Asians (c2 vs. c1: OR = 0.75, 95%CI: 0.59-0.95, P = 0.016; c2/c2 + c2/c1 vs. c1/c1: OR = 0.76, 95%CI: 0.58-1.00, P = 0.050). In the stratified analysis by country, significant associations were observed between RsaI/PstI polymorphism and decreased risk of liver cancer among the Chinese population (c2 vs. c1: OR = 0.70, 95%CI: 0.54-0.91, P = 0.007; c2/c2 + c2/c1 vs. c1/c1: OR = 0.72, 95%CI: 0.54-0.95, P = 0.020), but not among Japanese and Korean populations. Results from the current meta-analysis indicates that the c2 allele of CYP2E1 RsaI/PstI (c1/c2) polymorphism may be a protective factor for HCC among east Asians, especially among China populations.

CDH1 promoter polymorphism and stomach cancer susceptibility.

The relationship of stomach cancer susceptibility and the presence of E-cadherin (CDH1) promoter -160 C/A polymorphism had been reported with conflicting results. To further explore the association of this polymorphism with stomach cancer susceptibility, we performed an extensive search of relevant studies and carried out a meta-analysis to obtain a more precise estimate. A total of 16 studies including 2,611 cases and 3,788 controls were involved in this meta-analysis. When all studies involved, the meta-analysis results suggest no statistically significant association between CDH1 -160 C/A polymorphism and stomach cancer risk (CA vs. CC: OR = 1.01, 95% CI: 0.85-1.19; AA vs. CC: OR = 1.05, 95% CI: 0.75-1.46; dominant model: OR = 1.02, 95% CI: 0.86-1.20; recessive model: OR = 1.04, 95% CI: 0.76-1.41). When subgroup analyses were performed by ethnicity, the A-allele carriers conferred a decreased stomach cancer risk in Asians (AA vs. CC: OR = 0.67, 95% CI: 0.47-0.96; dominant model: OR = 0.85, 95% CI: 0.72-0.99), but no statistically significant association was found in Caucasians. In conclusion, this meta-analysis suggests that CDH1 -160 A-allele may play a protective role of stomach cancer development in Asians but not in Caucasians.

Human herpesvirus 8 viral FLICE-inhibitory protein retards cell proliferation via downregulation of Id2 and Id3 expression.

Death receptor-mediated apoptosis is potently inhibited by viral FLIP (FLICE/caspase 8 inhibitory protein) through reduced activation of procaspase 8. In this study, we show that the human herpesvirus 8-encoded vFLIP retards cell proliferation. Overexpression of vFLIP caused cell cycle arrest, with an apparent decrease of cells in the S phase. The Id (inhibitor of DNA binding) proteins are considered as dominant negative regulators of differentiation pathways, but positive regulators of cellular proliferation. The mechanisms by which Id proteins promote the cell cycle are diverse, but appear to involve affecting the expression of cell cycle regulators. RT-PCR results demonstrated that the expression of vFLIP decreased the expression levels of Id2 and Id3 as well as cyclin E and cyclin A compared with the vFLIP-null cells. These indicate that vFLIP affects cell proliferation by decreasing the expression levels of cell cycle regulatory proteins.

Loss of heterozygosity on 10q23.3 and mutation of tumor suppressor gene PTEN in gastric cancer and precancerous lesions.

AIM: To investigate the loss of heterozygosity (LOH) and mutation of tumor suppressor gene PTEN in gastric cancer and precancerous lesions. METHODS: Thirty cases of normal gastric mucosa, advanced and early stage gastric cancer, intestinal metaplasia, atrophic gastritis, and atypical hyperplasia were analyzed for PTEN LOH and mutations within the entire coding region of PTEN gene by PCR-SSCP denaturing PAGE gel electrophoresis, and PTEN mutation was detected by PCR-SSCP sequencing followed by silver staining. RESULTS: LOH rate found in respectively atrophic gastritis was 10% (3/30), intestinal metaplasia 10% (3/30), atypical hyperplasia 13.3% (4/30), early stage gastric cancer 20% (6/30), and advanced stage gastric cancer 33.3% (9/30), None of the precancerous lesions and early stage gastric cancer showed PTEN mutations, but 10% (3/30) of the advanced stage gastric cancers, which were all positive for LOH, showed PTEN mutation. CONCLUSION: LOH of PTEN gene appears in precancerous lesions, and PTEN mutations are restricted to advanced gastric cancer, LOH and mutation of PTEN gene are closely related to the infiltration and metastasis of gastric cancer.

Growth, invasion, metastasis, differentiation, angiogenesis and apoptosis of gastric cancer regulated by expression of PTEN encoding products.

AIM: To investigate expression of PTEN in gastric cancer and to explore its roles in tumorigenesis and progression of gastric cancer. METHODS: Formalin-fixed and paraffin-embedded tissues of adjacent non-tumor mucosa and primary foci from 113 cases of gastric cancers were studied for the expression of PTEN and Caspase-3 and microvessel density (MVD) by streptavidin-peroxidase (S-P) immunohistochemistry with antibodies against PTEN, Caspase-3, and CD34. The relationship between PTEN and Caspase 3 expression and clinicopathological parameters of tumors was compared. RESULTS: Primary gastric cancer cells expressed PTEN less frequently than adjacent epithelial cells of primary foci (54.9 % vs 89.4 %; P=0.000, chi(2)=33.474). PTEN expression was significantly associated with invasive depth (P=0.003, rs=0.274), metastasis (P=0.036, rs=0.197), growth pattern (P=0.008, rs=0.282), Lauren's classification (P=0.000, rs=0.345), and histological classification (P=0.005, rs=0.262) of tumors, but not with tumor size (P=0.639, rs=0.045), Borrmann's classification (P=0.544, rs=0.070) or TNM staging (P=0.172, rs=0.129). PTEN expression was negatively correlated with MDV in primary gastric cancer (P=0.020, F=5.558). Primary gastric cancer cells showed less frequent immunoreactivity to Caspase-3 than adjacent epithelial cells of primary foci (32.7 % vs 50.4 %; P=0.007, chi(2)=7.286). Caspase-3 expression was dependent of PTEN expression in primary gastric cancer cells (P=0.000, chi(2)=15.266). CONCLUSION: Down-regulated expression of PTEN plays an important role in tumorigenesis, progression, growth, differentiation and angiogenesis of gastric cancer. Low expression of PTEN can decrease expression of Caspase-3 to disorder apoptosis of tumor cells, which might explain the molecular mechanisms of PTEN contributions to tumorigenesis and progression of gastric cancer.