The changes of nociception and the signal molecules expression in the dorsal root ganglia and the spinal cord after cold water swimming stress in mice

Several studies have previously reported that exposure to stress provokes behavioral changes, including antinociception, in rodents. In the present study, we studied the effect of acute cold-water (4°C) swimming stress (CWSS) on nociception and the possible changes in several signal molecules in male ICR mice.Here, we show that 3 min of CWSS was sufficient to produce antinociception in tailflick, hot-plate, von-Frey, writhing, and formalin-induced pain models. Significantly, CWSS strongly reduced nociceptive behavior in the first phase, but not in the second phase, of the formalin-induced pain model. We further examined some signal molecules' expressions in the dorsal root ganglia (DRG) and spinal cord to delineate the possible molecular mechanism involved in the antinociceptive effect under CWSS.CWSS reduced p-ERK, p-AMPKα1, p-AMPKα2, p-Tyk2, and p-STAT3 expression both in the spinal cord and DRG. However, the phosphorylation of mTOR was activated after CWSS in the spinal cord and DRG. Moreover, p-JNK and p-CREB activation were significantly increased by CWSS in the spinal cord, whereas CWSS alleviated JNK and CREB phosphorylation levels in DRG. Our results suggest that the antinociception induced by CWSS may be mediated by several molecules, such as ERK, JNK, CREB, AMPKα1, AMPKα2, mTOR, Tyk2, and STAT3 located in the spinal cord and DRG.

The changes of nociception and the signal molecules expression in the dorsal root ganglia and the spinal cord after cold water swimming stress in mice

Several studies have previously reported that exposure to stress provokes behavioral changes, including antinociception, in rodents. In the present study, we studied the effect of acute cold-water (4°C) swimming stress (CWSS) on nociception and the possible changes in several signal molecules in male ICR mice.Here, we show that 3 min of CWSS was sufficient to produce antinociception in tailflick, hot-plate, von-Frey, writhing, and formalin-induced pain models. Significantly, CWSS strongly reduced nociceptive behavior in the first phase, but not in the second phase, of the formalin-induced pain model. We further examined some signal molecules' expressions in the dorsal root ganglia (DRG) and spinal cord to delineate the possible molecular mechanism involved in the antinociceptive effect under CWSS.CWSS reduced p-ERK, p-AMPKα1, p-AMPKα2, p-Tyk2, and p-STAT3 expression both in the spinal cord and DRG. However, the phosphorylation of mTOR was activated after CWSS in the spinal cord and DRG. Moreover, p-JNK and p-CREB activation were significantly increased by CWSS in the spinal cord, whereas CWSS alleviated JNK and CREB phosphorylation levels in DRG. Our results suggest that the antinociception induced by CWSS may be mediated by several molecules, such as ERK, JNK, CREB, AMPKα1, AMPKα2, mTOR, Tyk2, and STAT3 located in the spinal cord and DRG.

Clinical Significance of Hepatic Capsular Enhancement in Multi-Directional Computed Tomography with Fitz-Hugh-Curtis Syndrome

OBJECTIVE@#Fitz-Hugh-Curtis syndrome (FHCS) is characterized by perihepatitis in patients with pelvic inflammatory disease. Hepatic capsular enhancement in arterial phase of abdominal computed tomography (CT) is usually required for definite diagnosis. The objective of this study was to assess clinical significance of intensity of hepatic capsular enhancement in CT of patients with FHCS.@*METHODS@#A total of 86 patients who had hepatic capsular enhancement in CT due to FHCS were retrospectively enrolled. The hepatic capsular enhancement was divided into three patterns according to the intensity of enhancement by an expert radiologist: A, partial weak enhancement; B, partial strong or diffuse weak enhancement; and C, diffuse strong enhancement. Other clinical and laboratory parameters such as duration of admission were also evaluated.@*RESULTS@#Hepatic capsular enhancement in CT was classified into pattern A (n=28), pattern B (n=35), and pattern C (n=23). Hospital stay was significantly shorter in pattern A (6.1±2.4 days, P<0.001) than that in pattern B (7.2±2.9 days) or pattern C (7.7±2.2 days). Subjective perihepatic pain duration was well correlated with the degree of hepatic capsular enhancement (P<0.001). In multivariate analysis, the intensity of capsular enhancement was significantly associated with hospital stay after adjusting other factors. However, laboratory inflammation marker was not directly correlated with hepatic capsular enhancement.@*CONCLUSION@#Enhancement pattern of CT scan in patients with FHCS is closely related to its clinical severity and the course of this disease.

A Case of Successful Treatment for Acute Complication Caused by Ingestion of a Large Amount of Glacial Acetic Acid

Glacial acetic acid, a caustic substance of strong acidity, can easily be found in our daily lives; sometimes, it is drunk for the purpose of suicide, or it can be misjudged as a beverage. Glacial acetic acid is corrosive and toxic, therefore, even a tiny amount may cause fatal damage, such as gastrointestinal injury and systemic complication. A 66-year-old male patient, based on the wrong information, that glacial acetic acid is a healthy beverage, ingested 250 mL of 99% glacial acetic acid. Complications included gastric perforation, hemolysis, disseminated intravascular coagulation, acute renal failure, and liver dysfunction. We achieved successful treatment through performance of emergency surgery and hemodialysis on the patient, who had ingested a more than fatal dose of glacial acetic acid; herein, we would like to report on the case along with a review of the literature.

A Case of Ectopic Sebaceous Glands in the Esophagus

Most ectopic sebaceous glands have been reported in the organs of ectodermal origin such as the lips, oral cavity, salivary glands, nipples, palms & soles, and genitals. Ectopic sebaceous glands in the esophagus are extremely rare conditions, because esophagus is an organ of endodermal origin. Whether the histogenesis of these lesions are embryological misplacement or acquired metaplasia remains unclear. We report a case of ectopic sebaceous glands in the esophagus diagnosed by endoscopic biopsy, with a brief review of the histogenesis. This case was followed up after 1 year. There were no significant changes, but the lesions had increased slightly in number compared with the last examination. When the number of lesions increase as in our case, acquired metaplasia is the most likely cause.

A Case of Ectopic Sebaceous Glands in the Esophagus

Most ectopic sebaceous glands have been reported in the organs of ectodermal origin such as the lips, oral cavity, salivary glands, nipples, palms & soles, and genitals. Ectopic sebaceous glands in the esophagus are extremely rare conditions, because esophagus is an organ of endodermal origin. Whether the histogenesis of these lesions are embryological misplacement or acquired metaplasia remains unclear. We report a case of ectopic sebaceous glands in the esophagus diagnosed by endoscopic biopsy, with a brief review of the histogenesis. This case was followed up after 1 year. There were no significant changes, but the lesions had increased slightly in number compared with the last examination. When the number of lesions increase as in our case, acquired metaplasia is the most likely cause.