Correlation of 18F-FDG PET/CT metabolic parameters with the expression of immune biomarkers in the tumour microenvironment in lung adenocarcinoma.

AIM: To explore the association between metabolic parameters evaluated by integrated 2-[18F]-fluoro-2-deoxy-d-glucose (FDG) positron-emission tomography (PET)/computed tomography (CT) and the expression of immune biomarkers in the tumour microenvironment in lung adenocarcinoma. MATERIALS AND METHODS: This study included 134 patients. Metabolic parameters were obtained by PET/CT. Immunohistochemistry analysis was used for FOXP3-TILs (transcription factor forkhead box protein 3 tumour-infiltrating lymphocytes), CD8-TILs, CD4-TILs, CD68-TAMs (tumour-associated macrophages) and galectin-1 (Gal-1) tumour expression. RESULTS: There were significant positive associations between FDG PET metabolic parameters and the median percentage of immune reactive areas (IRA%) covered by FOXP3-TILs and CD68-TAMs. Negative associations with the median IRA% covered by CD4-TILs and CD8-TILs were observed: maximal standardised uptake value (SUVmax), metabolic tumour volume (MTV), total lesion glycolysis (TLG), and IRA% for FOXP3-TILs (rho = 0.437, 0.400, 0.414; p<0.0001 for all parameters); SUVmax, MTV, TLG, and IRA% for CD68-TAMs (rho = 0.356, 0.355, 0.354; p<0.0001 for all parameters); SUVmax, MTV, TLG, and IRA% for CD4-TILs (rho = -0.164, -0.190, -0.191; p=0.059, 0.028, 0.027, respectively); SUVmax, MTV, TLG, and IRA% for CD8-TILs (rho = -0.305, -0.316, -0.322; p<0.0001 for all parameters). There were significant positive associations between tumour Gal-1 expression and the median IRA% covered by FOXP3-TILs and CD68-TAMs (rho = 0.379; p<0.0001; rho = 0.370; p<0.0001, respectively), and a significant negative association with the median IRA% covered by CD8-TILs (rho = -0.347; p<0.0001) was observed. Tumour stage (p=0.008), Gal-1 expression (p=0.008), and median IRA% covered by CD8-TILs (p=0.054) were independent risk factors for overall survival. CONCLUSION: FDG PET may facilitate a comprehensive evaluation of the tumour microenvironment and predict response to immunotherapy.

[A case of pulmonary barotrauma complicated with cerebral arterial air embolism in a diver].

Pulmonary barotrauma is a kind of disease caused by the injury of lung tissue or blood vessel when the gas pressure of lung is too high or too lower than the external pressure of the body, which causes the air to enter the blood vessel and adjacent tissue. It could be happened in the escape of the divers with the light diving equipment or the sailors from submarine. Generally, the decompression chamber was used to treating the disease, and the minimum air pressure of 0.5 MPa recompression therapeutic schedule was used to selecting. In November 2019, a patient with pulmonary barotrauma combined with cerebral arterial gas embolism caused by improper underwater escape with light diving equipment was admitted to the General Hospital of Eastern War Zone. He was treated with 0.12 MPa oxygen inhalation recompression scheme in the oxygen chamber pressurized with air. 7 days later, the patient recovered and discharged.

[A case of decompression sickness complicated with multiple organ failure treated by hyperbaric oxygen therapy sequential with continuous renal replacement therapy and extracorporeal membrane oxygenation].

Objective: To discuss the new idea of on-the-spot recompression treatment and multidisciplinary treatment (MDT) for patients with unstable vital signs of type II decompression sickness. To provide reference for the nearby treatment of patients with critical decompression sickness. Methods: The clinical data of a case of a multi-disciplinary collaborative treatment of type II decompression sickness complicated with multiple organ dysfunction syndrome (MODS) admitted to a third-class A hospital in January 2020 were analyzed and summarized. Results: The patient suffered from consciousness disturbance and shock after 3 min of diver's blow-up out of the water. CT examination showed gas accumulation in the systemic multi-organ venous system, and laboratory examination suggested MODS. The oxygen inhalation regimen was given in the session of recompression treatmen by 0.12-0.18 MPa. Intravenous fluid was the total of 8900 ml in the session, and the total recompression treatment time was 9 h 45 min. The patient was still in unconscious when he finished the session. CT re-examination confirmed the elimination of venous bubbles, and laboratory examination indicated multiple organ failure (MOF) . The patient was given comprehensive supporting treatment by mechanical assisted breathing and following by continuons renal replacement therapy (CRRT) and extrocorporeal membrane oxygenation (ECMO) in the intensive care unit, and was discharged after 32 d of hospitalization. Conclusion: Critical decompression sickness patients with unstable vital signs are taken to a local general hospital with hyperbaric oxygen chamber and intensive care unit. The successful treatment can be achieved by organizing diving medicine, hyperbaric oxygen medicine and critical medical personnel for MDT.

Induction of esophageal cancers by nitenpyram (NIT) in rats.

OBJECTIVE: This study was made to investigate and evaluate the safety and carcinogenicity of nitenpyram (NIT) in rats. MATERIALS AND METHODS: A totally 50 male and 50 female SD rats were treated with NIT at 0, 800, 2400, and 7200 ppm, respectively, for 104 w. The growth, clinical signs, and survival rates, as well as the body and organ weights of these animals, were analyzed. Histopathological examination was also performed. RESULTS: Compared with the control group, survival rates at 104 w were significantly decreased in the 7200 ppm dose group, for both the male and female animals. The occurrence of esophageal squamous papilloma (ESP) was significantly increased in the treated animals. The occurrences of ESP for the 0, 800, 2400, and 7200 ppm NIT treatment groups were 0/39, 0/39, 3/35, and 9/27 for the male animals, and 0/43, 0/43, 6/49, and 12/33 for the female animals, respectively. For pre-neoplastic lesion of ESP, the occurrences of esophageal squamous hyperplasia for the 0, 800, 2400 and 7200 ppm NIT treatment groups were 0/39, 1/39, 10/35, and 9/27 for the male animals, and 0/43, 2/43, 15/49, and 17/33 for the female animals, respectively. The basal cell hyperplasia from mild to severe degrees was observed in the treatment groups. CONCLUSIONS: NIT exhibits carcinogenicity of ESP in the male and female rats after the two-year treatment.