The presence/absence of extracapsular invasion in metastatic lymph nodes has been reported as being significantly correlated with the prognosis in a wide variety of cancers. However, the influence of extracapsular invasion in the metastatic lymph nodes on the prognosis in patients with stage III rectal cancer has not yet been investigated. We investigated the presence/absence of extracapsular invasion in the metastatic nodes of the relevant main/lateral lymph node group in patients with rectal cancer to determine the usefulness of this parameter for stratifying the prognosis of patients with stage III rectal cancer. This was a single-institution study. This study was conducted at a single institution. We enrolled 101 consecutive patients with stage III rectal cancer who had undergone curative surgery with extended lymph node dissection and investigated the presence/absence of extracapsular invasion in the regional metastatic lymph nodes to determine the usefulness of such stratification for a more precise prediction of the patient prognosis. The main outcomes measured were the disease-free and overall survival rates. Univariate analysis revealed a significantly poorer prognosis, in terms of both the disease-free survival rate (p = 0.003) and overall survival rate (p = 0.008), of the pN3-extracapsular invasion-positive cases in comparison with the pN3-extracapsular invasion-negative cases. Multivariate analysis revealed the presence/absence of extracapsular invasion in the metastatic lymph nodes as the only variable that was statistically significantly associated with the disease-free survival rate (p = 0.011). This was a retrospective study in a small number of patients from a single institution. There were no comparator groups. Detailed stratification of pN3 cases based on the presence/absence of extracapsular invasion in metastatic lymph nodes has the potential to contribute significantly to more available prediction of the prognosis of patients with stage III colorectal cancer.

Intrapericardial diaphragmatic hernia (IPDH), defined as prolapse of the abdominal viscera into the pericardium, is a rare clinical condition. This case illustrates the possibility of IPDH after esophagectomy with antethoracic alimentary reconstruction, although such hernias are extremely rare. IPDH often presents with symptoms of bowel obstruction such as abdominal discomfort or vomiting. If not properly treated, life-threatening necrosis and/or perforation of the herniated contents may occur. A 68-year-old Japanese man underwent subtotal esophagectomy with three-field lymph node dissection for treatment of esophageal cancer. Completion gastrectomy with perigastric lymph node dissection was also performed because the patient had previously undergone distal partial gastrectomy for treatment of gastric cancer. The alimentary continuity was reconstructed using the pedicled jejunal limb through the antethoracic route. When we separated the diaphragm from the esophagus and removed xiphoid surgically to prevent a pedicled jejunal limb injury, the pericardium was opened. The patient was readmitted to our hospital because of abdominal discomfort and vomiting 6 months after the esophagectomy. A diagnosis of IPDH after esophagectomy was made. The patient was treated by primary closure of the diaphragmatic defect using vertical mattress sutures and additional reinforcement of the closing defect using a graft harvested from the rectus abdominis posterior sheath. The postoperative course was uneventful, and he was discharged on the seventh day after hernia repair. This patient’s clinical course provides two important clinical suggestions. First, we must be aware of the possibility of iatrogenic IPHD after esophagectomy with antethoracic alimentary reconstruction. Second, a graft from the rectus abdominis posterior sheath is beneficial in the treatment of IPDH.

Inflammation is a tightly regulated process involving immune receptor recognition, immune cell migration, inflammatory mediator secretion, and pathogen elimination, all essential for combating infection and restoring damaged tissue. However, excessive inflammatory responses drive various human diseases. The autonomic nervous system (ANS) is known to regulate inflammatory responses; however, the detailed mechanisms underlying this regulation remain incompletely understood. Herein, we aimed to study the anti-inflammatory effects and mechanism of action of the ANS in RAW264.7 cells. Quantitative PCR and immunoblotting assays were used to assess lipopolysaccharide (LPS)-induced tumor necrosis factor α (TNFα) expression. The anti-inflammatory effects of catecholamines (adrenaline, noradrenaline, and dopamine) and acetylcholine were examined in LPS-treated cells to identify the receptors involved. Catecholamines inhibited LPS-induced TNFα expression by activating the β2 adrenergic receptor (β2-AR). β2-AR activation in turn downregulated the expression of Toll-like receptor 4 (TLR4) by stimulating protein kinase A (PKA) phosphorylation, resulting in the suppression of TNFα levels. Collectively, our findings reveal a novel mechanism underlying the inhibitory effect of catecholamines on LPS-induced inflammatory responses, whereby β2-AR activation and PKA phosphorylation downregulate TLR4 expression in macrophages. These findings could provide valuable insights for the treatment of inflammatory diseases and anti-inflammatory drug development.