Exotic Animal Practice in East Asia: A Retrospective Study of Species Distribution and Their Common Diseases at 2 Exotics-only Veterinary Clinics in the East Asia Region.

The objective of this clinical retrospective study was to analyze the prevalence and distribution of different avian and exotic animals presented to 2 exotics-only veterinary hospital in Hong Kong and Taiwan over a 1 year period. Exotic companion mammals, predominated by rabbits (Oryctolagus cuniculus) that were often diagnosed with fractures, were the most commonly presented group of patients in the hospital in Hong Kong while second most of that in Taiwan, with dental disease being commonly presented in the species. This study provided a general overview of avian and exotic patients presented to exotics-only practices in the East Asia region.

Bismuth-Containing Quadruple Therapy for Helicobacter pylori Eradication: A Randomized Clinical Trial of 10 and 14 Days.

BACKGROUND: Bismuth-containing quadruple therapy is the first-line treatment for eradicating Helicobacter pylori (H. pylori). The optimal duration for H. pylori eradication using bismuth-containing quadruple therapy remains controversial. Therefore, we aimed to compare the clinical effects of the 10- and 14-day bismuth-containing quadruple treatment regimen to eradicate H. pylori. METHODS: Treatment-naïve patients with H. pylori infection (n = 1300) were enrolled in this multicenter randomized controlled study across five hospitals in China. They were randomized into 10- or 14-day treatment groups to receive bismuth-containing quadruple therapy as follows: vonoprazan 20 mg twice daily; bismuth 220 mg twice daily; amoxicillin 1000 mg twice daily; and either clarithromycin 500 mg twice daily or tetracycline 500 mg four times daily. At least 6 weeks after treatment, we performed a 13C-urea breath test to evaluate H. pylori eradication. RESULTS: The per-protocol eradication rates were 93.22% (564/605) and 93.74% (569/607) (p < 0.001) and the intention-to-treat eradication rates were 88.62% (576/650) and 89.38% (581/650) (p = 0.007) for the 10- and 14-day regimens, respectively. Incidence of adverse effects was lower in patients who received 10- vs. 14 days of treatment (22.59% vs. 28.50%, p = 0.016). We observed no significant differences in the compliance to treatment or the discontinuation of therapy because of severe adverse effects between the groups. CONCLUSION: Compared with the 14-day bismuth-containing quadruple regimens, the 10-day regimen demonstrated a non-inferior efficacy and lower incidence of adverse effects. Therefore, the 10-day regimen is safe and tolerated and could be recommended for H. pylori eradication (NCT05049902).

Fungal metabolite altersolanol a exhibits potent cytotoxicity against human placental trophoblasts in vitro via mitochondria-mediated apoptosis.

Altersolanol A, a fungus-derived tetrahydroanthraquinone, has shown cytotoxic effects on multiple cancer cells. However, its reproductive toxicity in humans has not been well-addressed. The present study was aimed at investigating the cytotoxicity of altersolanol A on human placental trophoblasts including choriocarcinoma cell line JEG-3 and normal trophoblast cell line HTR-8/SVneo in vitro. The results showed that altersolanol A inhibited proliferation and colony formation of human trophoblasts, and the choriocarcinoma cells were more sensitive to the compound than the normal trophoblasts. Altersolanol A induced cell cycle arrest at G2/M phase in JEG-3 cells and S phase in HTR-8/SVneo cells, downregulated the expression of cell cycle-related checkpoint proteins, and upregulated the p21 level. Altersolanol A also promoted apoptosis in human trophoblasts via elevating the Bax/Bcl-2 ratio and decreasing both caspase-3 and caspase-9 levels. Meanwhile, altersolanol A suppressed the mitochondrial membrane potential and induced ROS production and cytochrome c release, which activated the mitochondria-mediated intrinsic apoptosis. Moreover, migration and invasion were inhibited upon altersolanol A exposure with downregulation of matrix metalloproteinase (MMP)-2 in JEG-3 cells and MMP-9 in HTR-8/SVneo cells. Mechanically, altersolanol A supplement decreased the phosphorylation of JNK, ERK, and p38, manifesting the inactivation of MAPK signaling pathway in the human trophoblasts. In conclusion, altersolanol A exhibited potential reproductive cytotoxicity against human trophoblasts via promoting mitochondrial-mediated apoptosis and inhibiting the MAPK signaling pathway.

High-fat diet induces sarcopenic obesity in natural aging rats through the gut-trimethylamine N-oxide-muscle axis.

INTRODUCTION: The lack of suitable animal models for sarcopenic obesity (SO) limits in-depth research into the disease. Emerging studies have demonstrated that gut dysbiosis is involved in the development of SO. As the importance of microbial metabolites is starting to unveil, it is necessary to comprehend the specific metabolites associated with gut microbiota and SO. OBJECTIVES: We aimed to investigate whether high-fat diet (HFD) causes SO in natural aging animal models and specific microbial metabolites that are involved in linking HFD and SO. METHODS: Young rats received HFD or control diet for 80 weeks, and obesity-related metabolic disorders and sarcopenia were measured. 16S rRNA sequencing and non-targeted and targeted metabolomics methods were used to detect fecal gut microbiota and serum metabolites. Gut barrier function was evaluated by intestinal barrier integrity and intestinal permeability. Trimethylamine N-oxide (TMAO) treatment was further conducted for verification. RESULTS: HFD resulted in body weight gain, dyslipidemia, impaired glucose tolerance, insulin resistance, and systemic inflammation in natural aging rats. HFD also caused decreases in muscle mass, strength, function, and fiber cross-sectional area and increase in muscle fatty infiltration in natural aging rats. 16S rRNA sequencing and nontargeted and targeted metabolomics analysis indicated that HFD contributed to gut dysbiosis, mainly characterized by increases in deleterious bacteria and TMAO. HFD destroyed intestinal barrier integrity and increased intestinal permeability, as evaluated by reducing levels of colonic mucin-2, tight junction proteins, goblet cells and elevating serum level of fluorescein isothiocyanate-dextran 4. Correlation analysis showed a positive association between TMAO and SO. In addition, TMAO treatment aggravated the development of SO in HFD-fed aged rats through regulating the ROS-AKT/mTOR signaling pathway. CONCLUSION: HFD leads to SO in natural aging rats, partially through the gut-microbiota-TMAO-muscle axis.

Diabetes and further risk of cancer: a nationwide population-based study.

BACKGROUND: Individuals with diabetes have a significantly higher risk of developing various forms of cancer, and the potential biological links between these two diseases are not completely understood. METHODS: This was a longitudinal retrospective nationwide cohort study, a study design that allows us to examine the natural course of cancer development over an extended period of time with a large sample size. Initially, 3,111,975 and 22,208,395 eligible patients aged ≥ 20 years with and without diabetes, respectively, were matched by age, sex, and the Charlson comorbidity index. Ultimately, 1,751,457 patients were selected from each group. Stratified populations for diabetic retinopathy (DR) (n = 380,822) and without DR (n = 380,822) as well as proliferative DR (PDR) (n = 141,150) and non-proliferative DR (NPDR) (n = 141,150) were analyzed in this study. The main outcome measure was the first-time diagnosis of cancer during the follow-up period. RESULTS: We observed a 20% higher risk of total cancer incidence [hazard ratios (HR), 1.20; p < 0.001] in the diabetes cohort compared to the non-diabetes cohort. The highest HR was observed for liver and pancreas cancers. Moderately increased risks were observed for oral, colon, gallbladder, reproductive (female), kidney, and brain cancer. Furthermore, there was a borderline significantly increased risk of stomach, skin, soft tissue, female breast, and urinary tract (except kidney) cancers and lymphatic and hematopoietic malignancies. The stratified analysis revealed that the total cancer incidence was significantly higher in the DR cohort compared to the non-DR cohort (HR, 1.31; p < 0.001), and there was a borderline increased risk in the PDR cohort compared to the NPDR cohort (HR, 1.13; p = 0.001). CONCLUSIONS: This study provides large-scale, nationwide, population-based evidence that diabetes is independently associated with an increased risk of subsequent development of total cancer and cancer at specific sites. Notably, this risk may further increase when DR develops.

Evaluating a maladaptive personality-informed model of social support and post-traumatic stress disorder.

BACKGROUND: Social support is a robust predictor of post-traumatic stress disorder (PTSD). Although the inverse relationship between perceived social support and PTSD (social causation model) is supported, less is understood about the antecedents of the social causation model. Further, there is limited research in non-Western psychiatric populations that experience elevated rates of trauma and PTSD (e.g., mood disorders). The present study evaluated whether cumulative traumatic life events influenced current PTSD symptoms through maladaptive personality traits and perceptions of social support among Asian patients with mood disorders. METHODS: A total of 200 Asian patients (77.5 % Chinese) with mood disorders were assessed for maladaptive personality traits, perceptions of social support, cumulative traumatic life events, PTSD, and depressive symptoms. Structural equation modelling was conducted to evaluate the extended social causation model. RESULTS: The extended social causation model demonstrated acceptable fit to the data (Comparative Fit Index [CFI] = 0.90; absolute Root Mean Square Error of Approximation [RMSEA] = 0.08). There were significant indirect effects of cumulative traumatic life events on current PTSD symptoms (ß = 0.29, p < .001; 85 % variance explained) and depressive symptoms (ß = 0.28, p < .001; 69 % variance explained). LIMITATIONS: Results may not be generalizable beyond the Singapore population due to the socio-cultural and environmental context. CONCLUSIONS: The present findings provide conceptual support for a maladaptive personality-informed model of social support and PTSD, which could better inform trauma-focused interventions in preventing and treating the debilitating effects of PTSD in psychiatric populations.

Mosaic distal 10q deletion or 46,XY,del(10) (q26.13)/46,XY at amniocentesis and cordocentesis in a pregnancy associated with cytogenetic discrepancy between cultured amniocytes and uncultured amniocytes, perinatal progressive decrease of the aneuploid cell line and a favorable fetal outcome.

OBJECTIVE: We present mosaic distal 10q deletion at prenatal diagnosis in a pregnancy associated with a favorable fetal outcome. CASE REPORT: A 40-year-old, gravida 2, para 0, woman underwent amniocentesis at 16 weeks of gestation because of advanced maternal age. Amniocentesis revealed a karyotype of 46,XY, del(10) (q26.13)[6]/46,XY[17]. Simultaneous array comparative genomic hybridization (aCGH) analysis on the DNA extracted from uncultured amniocytes showed 35% mosaicism for the 10q26.13q26.3 deletion. At 22 weeks of gestation, she underwent cordocentesis which revealed a karyotype of 46,XY,del(10) (q26.13)[16]/46,XY[24]. Prenatal ultrasound findings were normal. At 24 weeks of gestation, she was referred for genetic counseling, and repeat amniocentesis revealed a karyotype of 46,XY,del(10) (q26.13)[4]/46,XY[22]. The parental karyotypes were normal. Molecular genetic analysis on uncultured amniocytes revealed no uniparental disomy (UPD) 10 by quantitative fluorescence polymerase chain reaction (QF-PCR), arr 10q26.13q26.3 × 1.6 (40% mosaicism) by aCGH, and 29.8% (31/104 cells) mosaicism for the distal 10q deletion by interphase fluorescence in situ hybridization (FISH). The woman was advised to continue the pregnancy, and a phenotypically normal 2,900-g male baby was delivered at 39 weeks of gestation. The cord blood had a karyotype of 46,XY,del(10) (q26.13)[6]/46,XY[34], and both the umbilical cord and the placenta had the karyotype of 46,XY. When follow-up at age four months, the neonate was normal in phenotype and development. The peripheral blood had a karyotype of 46,XY,del(10) (q26.13)[5]/46,XY[35], and interphase FISH analysis on buccal mucosal cells showed 8% (8/102 cells) mosaicism for distal 10q deletion. CONCLUSION: Mosaic distal 10q deletion with a normal cell line at prenatal diagnosis can be associated with a favorable fetal outcome and perinatal progressive decrease of the aneuploid cell line.

Diosmetin as a promising natural therapeutic agent: In vivo, in vitro mechanisms, and clinical studies.

Diosmetin, a natural occurring flavonoid, is primarily found in citrus fruits, beans, and other plants. Diosmetin demonstrates a variety of pharmacological activities, including anticancer, antioxidant, anti-inflammatory, antibacterial, metabolic regulation, cardiovascular function improvement, estrogenic effects, and others. The process of literature search was done using PubMed, Web of Science and ClinicalTrials databases with search terms containing Diosmetin, content, anticancer, anti-inflammatory, antioxidant, pharmacological activity, pharmacokinetics, in vivo, and in vitro. The aim of this review is to summarize the in vivo, in vitro and clinical studies of Diosmetin over the last decade, focusing on studies related to its anticancer, anti-inflammatory, and antioxidant activities. It is found that DIO has significant therapeutic effects on skin and cardiovascular system diseases, and its research in pharmacokinetics and toxicology is summarized. It provides the latest information for researchers and points out the limitations of current research and areas that should be strengthened in future research, so as to facilitate the relevant scientific research and clinical application of DIO.

The clinical significance of emotional urgency in bipolar disorder: a scoping review.

BACKGROUND: Emotional urgency, defined as a trait concept of emotion-based impulsivity, is at least moderately associated with general psychopathology. However, its clinical significance and associations with clinically relevant features of bipolar disorder remain unclear. This scoping review aims address this gap by determining the extent of evidence in this niche scope of study. METHODS: Evidence of between-group differences of positive and negative urgency, its associations with mood severity, and all peripheral associations related to illness and psychosocial outcomes were synthesized based on PRISMA checklists and guidelines for scoping reviews (PRISMA-ScR). DESIGN: Electronic databases were searched for articles published between January 2001 and January 2024. A total of 1013 entries were gathered, and a total of 10 articles were included in the final selection after the removal of duplicates and ineligible articles. RESULTS: Differences in urgency scores between bipolar disorder and healthy controls were large (Cohen's d ranged from 1.77 to 2.20). Negative urgency was at least moderately associated with overall trauma, emotional abuse, neglect, suicide ideation, neuroticism, and irritable/cyclothymic temperament, whereas positive urgency was at least moderately associated with various aspects of aggression and quality of life. Positive but not negative urgency was associated with quality of life in bipolar disorder. CONCLUSION: Large between-group differences found for emotional urgency in bipolar disorder imply large clinical significance. Emotional urgency was associated with worse clinical features and outcomes. Given the high clinical heterogeneity of the disorder, emotional urgency may be an important phenotype indicative of greater disorder severity.

Ferroptosis Mediates Pulmonary Fibrosis: Implications for the Effect of Astragalus and Panax notoginseng Decoction.

Objective: To investigate the mechanism through which Astragalus and Panax notoginseng decoction (APD) facilitates the treatment of ferroptosis-mediated pulmonary fibrosis. Materials and Methods: First, the electromedical measurement systems were used to measure respiratory function in mice; the lungs were then collected for histological staining. Potential pharmacologic targets were predicted via network pharmacology. Finally, tests including immunohistochemistry, reverse transcription-quantitative polymerase chain reaction, and western blotting were used to evaluate the relative expression levels of collagen, transforming growth factor ß, α-smooth muscle actin, hydroxyproline, and ferroptosis-related genes (GPX4, SLC7A11, ACSL4, and PTGS2) and candidates involved in the mediation of pathways associated with ferroptosis (Hif-1α and EGFR). Results: APD prevented the occurrence of restrictive ventilation dysfunction induced by ferroptosis. Extracellular matrix and collagen fiber deposition were significantly reduced when the APD group compared with the model group; furthermore, ferroptosis was attenuated, expression of PTGS2 and ACSL4 increased, and expression of GPX4 and SLC7A11 decreased. In the APD group, the candidates related to the mediation of ferroptosis (Hif-1α and EGFR) decreased compared with the model group. Discussion and Conclusions. APD may ameliorate restrictive ventilatory dysfunction through the inhibition of ferroptosis. This was achieved through the attenuation of collagen deposition and inflammatory recruitment in pulmonary fibrosis. The underlying mechanisms might involve Hif-1α and EGFR.

Analysis of sterilizer allocation and related factors in dental health-care settings in Yunnan Province, China: a cross-sectional study.

OBJECTIVE: To investigate the status and related factors of sterilizers in dental health-care settings in Yunnan Province, with the aim of providing a theoretical basis for the health administrative department to formulate regional quality control programs and systems, proposing reasonable suggestions for optimizing the allocation of sterilizer resources in Yunnan's dental health-care settings, thereby improving resource utilization efficiency. METHODS: This cross-sectional survey was conducted in 2600 dental health-care settings in Yunnan Province in March 2020. Uni-variable linear regression, multi-variable linear regression, curve fitting and threshold effect analysis were used to understand the relationship between dental units and sterilizers. RESULTS: A total of 2600 dental health-care settings were included. The disinfection and sterilization work were mainly completed by the dental department in 1510(58.1%) institutions. 44(1.7%) institutions were not allocated sterilization equipment, and 1632 (62.8%) had only one sterilizer. The median allocation of sterilizers was 1.0. Uni-variable linear regression showed significant differences in covariates such as dental unit, dental handpiece, disinfection equipment, dentist, and dental assistant, which were more sensitive (p < 0.001) and statistically significant. The adjusted model was more stable in the multi-variable linear regression, and the differences in covariates between different settings were statistically significant. Curve fitting revealed an S-shaped curvilinear relationship between the number of dental units and sterilizers in oral healthcare settings. CONCLUSION: The disinfection and sterilization work was mainly completed by the dental department in dental health-care settings in Yunnan Province. Sterilizer allocation increases with the number of dental units, but some institutions have insufficient allocation of sterilizer and manpower resources, resulting in certain risks of infection control. Thus, it is necessary to strengthen supervision, inspection and regional quality control work in infection control of dentistry.

CA1 Modulates the Osteogenic Differentiation of Dental Follicle Stem Cells by Activating the BMP Signaling Pathway In Vitro.

BACKGROUND: Carbonic anhydrase 1 (CA1) has been found to be involved in osteogenesis and osteoclast in various human diseases, but the molecular mechanisms are not completely understood. In this study, we aim to use siRNA and lentivirus to reduce or increase the expression of CA1 in Dental follicle stem cells (DFSCs), in order to further elucidate the role and mechanism of CA1 in osteogenesis, and provide better osteogenic growth factors and stem cell selection for the application of bone tissue engineering in alveolar bone fracture transplantation. METHODS: The study used RNA interference and lentiviral vectors to manipulate the expression of the CA1 gene in DFSCs during in vitro osteogenic induction. The expression of osteogenic marker genes was evaluated and changes in CA1, alkaline phosphatase (ALP), Runt-related transcription factor 2 (RUNX2), and Bone morphogenetic proteins (BMP2) were measured using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting (WB). The osteogenic effect was assessed through Alizarin Red staining. RESULTS: The mRNA and protein expression levels of CA1, ALP, RUNX2, and BMP2 decreased distinctly in the si-CA1 group than other groups (p < 0.05). In the Lentivirus-CA1 (LV-CA1) group, the mRNA and protein expressions of CA1, ALP, RUNX2, and BMP2 were amplified to varying degrees than other groups (p < 0.05). Apart from CA1, BMP2 (43.01%) and ALP (36.69%) showed significant upregulation (p < 0.05). Alizarin red staining indicated that the LV-CA1 group produced more calcified nodules than other groups, with a higher optical density (p < 0.05), and the osteogenic effect was superior. CONCLUSIONS: CA1 can impact osteogenic differentiation via BMP related signaling pathways, positioning itself upstream in osteogenic signaling pathways, and closely linked to osteoblast calcification and ossification processes.

Tumor necrosis factor receptor-associated factor 5 protects against intimal hyperplasia by regulation of macrophage polarization via directly targeting PPARγ.

OBJECTIVES: Intimal hyperplasia is a serious clinical problem associated with the failure of therapeutic methods in multiple atherosclerosis-related coronary heart diseases, which are initiated and aggravated by the polarization of infiltrating macrophages. The present study aimed to determine the effect and underlying mechanism by which tumor necrosis factor receptor-associated factor 5 (TRAF5) regulates macrophage polarization during intimal hyperplasia. METHODS: TRAF5 expression was detected in mouse carotid arteries subjected to wire injury. Bone marrow-derived macrophages, mouse peritoneal macrophages and human myeloid leukemia mononuclear cells were also used to test the expression of TRAF5 in vitro. Bone marrow-derived macrophages upon to LPS or IL-4 stimulation were performed to examine the effect of TRAF5 on macrophage polarization. TRAF5-knockout mice were used to evaluate the effect of TRAF5 on intimal hyperplasia. RESULTS: TRAF5 expression gradually decreased during neointima formation in carotid arteries in a time-dependent manner. In addition, the results showed that TRAF5 expression was reduced in classically polarized macrophages (M1) subjected to LPS stimulation but was increased in alternatively polarized macrophages (M2) in response to IL-4 administration, and these changes were demonstrated in three different types of macrophages. An in vitro loss-of-function study with TRAF5 knockdown plasmids or TRAF5-knockout mice revealed high expression of markers associated with M1 macrophages and reduced expression of genes related to M2 macrophages. Subsequently, we incubated vascular smooth muscle cells with conditioned medium of polarized macrophages in which TRAF5 expression had been downregulated or ablated, which promoted the proliferation, migration and dedifferentiation of VSMCs. Mechanistically, TRAF5 knockdown inhibited the activation of anti-inflammatory M2 macrophages by directly inhibiting PPARγ expression. More importantly, TRAF5-deficient mice showed significantly aggressive intimal hyperplasia. CONCLUSIONS: Collectively, this evidence reveals an important role of TRAF5 in the development of intimal hyperplasia through the regulation of macrophage polarization, which provides a promising target for arterial restenosis-related disease management.

Mechanically Adaptive Polymers Constructed from Dynamic Coordination Equilibria.

Designing materials capable of adapting their mechanical properties in response to external stimuli is the key to preventing failure and extending their service life. However, existing mechanically adaptive polymers are hindered by limitations such as inadequate load-bearing capacity, difficulty in achieving reversible changes, high cost, and a lack of multiple responsiveness. Herein, we address these challenges using dynamic coordination bonds. A new type of mechanically adaptive material with both rate- and temperature-responsiveness was developed. Owing to the stimuli-responsiveness of the coordination equilibria, the prepared polymers, PBMBD-Fe and PBMBD-Co, exhibit mechanically adaptive properties, including temperature-sensitive strength modulation and rate-dependent impact hardening. Benefitting from the dynamic nature of the coordination bonds, the polymers exhibited impressive energy dissipation, damping capacity (loss factors of 1.15 and 2.09 at 1.0 Hz), self-healing, and 3D printing abilities, offering durable and customizable impact resistance and protective performance. The development of impact-resistant materials with comprehensive properties has potential applications in the sustainable and intelligent protection fields.

[Clinical effect of allogeneic peroneal bone marrow support combined with plate fixation for the treatment of Neer type â £ proximal humeral fractures].

OBJECTIVE: To explore clinical effect of allogeneic peroneal bone marrow support combined with plate internal fixation in treating Neer type Ⅳproximal humeral fractures. METHODS: From December 2017 to December 2020,12 patients with Neer type Ⅳ proximal humeral fractures were treated with allogeneic peroneal bone marrow support combined with plate internal fixation,including 7 males and 5 females,aged from 56 to 78 years old;the time from injury to operation ranged from 1 to7 days. Operative time,fracture healing time and complications during follow-up were observed,and clinical efficacy was evaluated by Constant-Murley score at the latest follow-up. RESULTS: All patients were obtained follow up for 20 to 29 months. All patients got bone healing and incisicons were healed at stageⅠ,operative time ranged from 95 to 138 min,blood loss ranged from 210 to 275 ml,fracture healing time ranged from 14 to 18 weeks. Two patients occurred postoperative shoulder stiffness and recovered after 2 weeks of passive exercise. There were no complications such as infection,poor wound healing,and failure (fracture and loosening) of internal fixators occurred. Constant-Murley shoulder function score ranged from 69 to 89 at the latest follow up,2 patients got excellent results,9 good and 1 fair. CONCLUSION: The application of allogeneic fibular bone marrow placement could provide effective support for medial humerus,which is conducive to assisting reduction of fracture end,reducing occurrence of internal fixation failure caused by collapse of humerus head and screw perforation,and significantly improving function of shoulder joint.

Management of retroperitoneal high-grade serous carcinoma of unknown origin: A case report.

BACKGROUND: Retroperitoneal high-grade serous carcinoma (HGSC) of unknown origin is a sporadic tumor that can originate from ovarian cancer. Herein, we report the case of a woman with retroperitoneal HGSC of unknown origin and describe how she was diagnosed and treated. CASE SUMMARY: A 71-year-old female presented with the tumor marker CA125 elevated to 1041.9 U/mL upon a regular health examination. Computed tomography revealed retroperitoneal lymph node enlargement. Subsequently, positron emission tomography scanning revealed lesions with increased F-18 fluorodeoxyglucose uptake at the nodes. As a result, she underwent laparoscopic lymph node resection, and pathology revealed metastatic adenocarcinoma with CK7(+), PAX8(+), WT1(+), PR(-), and p53 mutational loss of expression, indicating that the origin may be from the adnexa. The patient was admitted to our ward and underwent laparoscopic staging; however, the pathological results were negative. Under the suspicion of retroperitoneal HGSC of unknown origin, chemotherapy and targeted therapy were initiated. Tumor marker levels decreased after treatment. CONCLUSION: We present a case of HGSC of unknown origin managed using retroperitoneal lymphadenectomy, staging surgery, chemotherapy, and targeted therapy.

Disruption of the gastric epithelial barrier in Correa's cascade: Clinical evidence via confocal endomicroscopy.

BACKGROUND: Gastric epithelial barrier disruption constitutes a crucial step in gastric cancer (GC). We investigated these disruptions during the Correa's cascade timeline to correlate epithelial barrier dysfunction. MATERIALS AND METHODS: This study was conducted as a single-center, non-randomized clinical trial in China from May 2019 to October 2022. Patients with chronic atrophic gastritis (CAG), gastric intestinal metaplasia (GIM), low-grade intraepithelial neoplasia (LGIN), high-grade intraepithelial neoplasia (HGIN), and intramucosal carcinoma underwent probe-based confocal laser endomicroscopy (pCLE). The pCLE scoring system was used to assess gastric epithelial barrier disruption semi-quantitatively. RESULTS: We enrolled 95 patients who underwent a pCLE examination. The control group consisted of 15 individuals, and the experimental group included 17 patients with CAG, 27 patients with GIM, 20 patients with LGIN, and 16 patients with early gastric cancer (EGC). Apart from CAG, which showed no significant difference compared to the control group, a significantly higher incidence of gastric epithelial barrier damage was found in the GIM, LGIN, and EGC groups compared to the control group (Kruskal-Wallis H test = 69.295, p < 0.001). There is no difference in LGIN patients between GIM and LGIN areas, and there is no difference between the two groups compared with the EGC group. The intestinal metaplasia area in LGIN patients causes more severe gastric epithelial damage compared to that in non-LGIN patients. Additionally, compared to control group, a significant difference (p < 0.001) was noted between individuals with Helicobacter pylori-positive atrophic gastritis and those with IM, whereas no significant difference (p > 0.05) was observed among individuals with H. pylori-negative atrophic gastritis. CONCLUSIONS: The gastric epithelial barrier remains dysfunctional from the initiation of H. pylori infection to GC progression. Beyond the "point of no return," subsequent carcinogenesis processes may be attributed to other mechanisms.