Bronchogenic cysts originate from abnormal foregut budding during embryogenesis. Two pathogenic mechanisms exist: (1) ectopic migration of tracheobronchial precursors forming cysts in extrapulmonary sites, and (2) retained bronchial buds developing pulmonary cysts through mucus accumulation. Despite anatomical variations, all cysts retain respiratory epithelium with mucinous glands, pathognomonically reflecting their embryological origin. Herein, we report an unusual case of bronchogenic cyst in the posterior wall of the gastric fundus with elevated CEA and CA199 in cystic fluid. CT showed that a kind of circular soft tissue density shadow was visible under the submucosa of the stomach floor, with a size of about 3.9 × 3.7 cm, uniform density, and clear boundary. Pathology after surgical resection of the gastric tumor: the cystic wall‐like tissue was locally lined with ciliated columnar epithelium, the mucosa showed chronic inflammation, and foreign body giant cell reaction, calcification, and ossification were observed in the submucosa. The patient was diagnosed as having a bronchogenic cyst in the posterior wall of the gastric fundus and was followed up for 12 months after the operation, with no obvious discomfort.

Backgrounds: Liver fibrosis (LF) is the pathological basis of various chronic liver diseases. An in-depth understanding of the pathologic alterations leading to LF is of great significance for the future diagnosis and treatment of LF. The objective of this study was to investigate the role of prostaglandin-endoperoxide synthase 2 (PTGS2) in LF and to provide a potential new target for diagnosis and treatment of LF. Methods: Twelve Specific Pathogen Free (SPF)-grade SD rats were randomized into four equal groups. One group was left untreated as the control group. The other three groups were subjected to LF modeling. LF was induced by intraperitoneal injection of a carbon tetrachloride/olive oil mixture twice weekly for 8 weeks. Three groups of LF model rats were then selected. One group was injected with lentiviral vector inhibiting PTGS2 expression (PTGS2 group), one group was injected with PTGS2 empty vector (blank group), and one group was injected with saline (model group). After 24 hours, the liver function of each group was measured, and the body weight and liver weight were obtained to calculate the liver index. Liver tissues were taken for hematoxylin-eosin (HE) staining and histopathologic examination, and the expressions of transforming growth factor-β (TGF-β), α-smooth muscle actin (α-SMA), E-cadherin and N-cadherin were measured. Results: A large number of steatosis and inflammatory cell infiltration, interlobular connective tissue hyperplasia and fibrous septum formation were observed in the liver tissues of rats in the model and blank groups, which were significantly improved in the PTGS2 group. Alanine transaminase (ALT) in the PTGS2 group was significantly lower than in the model and blank groups, but significantly higher than in the control group (p < 0.05). There was no difference in liver index between the PTGS2 and control groups, both of which were lower than the model and blank groups (p < 0.05). TGF-β and α-SMA mRNAs were higher in the PTGS2 group than in the control group and lower than in the model and blank groups (p < 0.05). E-cadherin was decreased, while N-cadherin was increased (p < 0.05), in both the model and blank groups compared to the control and PTGS2 groups. Conclusion: Blocking PTGS2 expression ameliorated hepatic damage and reversed epithelial mesenchymal transition (EMT) in LF rats.

Light chain (AL) amyloidosis is a complex and rare disease characterized by low incidence and diverse clinical manifestations. At the time of diagnosis, most patients exhibit involvement of multiple organs or tissues, leading to severe illness and a poor prognosis. Therefore, early diagnosis, active treatment, and a comprehensive assessment of the disease hold paramount importance. The initial presentation of this rare condition often manifests as gastrointestinal symptoms, posing challenges in clinical identification and differential diagnosis. In this case report, we describe a 70-year-old man with AL amyloidosis, initially misdiagnosed as irritable bowel syndrome and colon polyps. Subsequently, he experienced a series of complications including renal function impairment, pulmonary nodule, pleural effusion, mediastinal lymph node enlargement, spleen enlargement, reduction of white blood cells, red blood cells and platelets, and small intestinal obstruction. Despite multiple pulmonary nodule biopsy and lymph node biopsy, as well as concurrent splenectomy and partial resection of the small intestine, a clear diagnosis remained elusive. Before admission, diarrhea was aggravated, accompanied by emaciation and fatigue. Following the completion of serum immunofixed protein electrophoresis, renal biopsy, bone marrow and rectal biopsy, a conclusive diagnosis of AL amyloidosis involving multiple organs (Mayo 2012 revision stage III) was finally confirmed after a 12-year period. Treatment with proteasome inhibitors, immunomodulators, and glucocorticoids was recommended. The patient underwent methylprednisolone treatment and was discharged after symptom improvement. However, eight months into the follow-up, the patient succumbed to multiple organ failure. The repeated misdiagnoses over the past 12 years were attributed to limited perspectives among some specialists who did not conduct a systematic and detailed medical history analysis or comprehensive physical examinations. Additionally, they did not strictly follow the principle of "monism" in diagnosis. On the contrary, early diagnosis and active treatment of the disease are of great significance to improve the prognosis.