Reappraisal of the ligament of Henle (ligamentum inguinale internum mediale; Henle, 1871): a topohistological study using Korean foetuses.

Ligament of Henle is one of muscle-associated connective tissues of the rectus abdominis muscle, but it has been confused with the conjoint tendon (a common aponeurosis for insertion of the inferomedial end of the obliquus internus and transversus abdominis muscles). To reconsider the inguinal connective tissue structures, we examined 20 mid-term foetuses (10 males and 10 females) at approximately 14-20 weeks of gestation (crown rump length 100-170 mm). In female horizontal sections, we consistently found the ligament of Henle asa wing-like aponeurosis extending from the lateral margin of the rectus tendon behind the superficial inguinal ring. The ligament was separated from and located behind the conjoint tendon. In all male foetuses, instead of the ligament, the conjoint tendon was evident behind the superficial ring and it winded around the posterior aspect of the spermatic cord. Therefore, although a limited number of specimens were examined, the ligament of Henle was likely to be a female-specific structure. The ligament of Henle, if developed well, may provide an arch-like structure suitable for a name "falx inguinalis" instead of the inferomedial end ofthe conjoint tendon. In addition, a covering fascia of the iliopsoas muscle joined the posterior wall of the inguinal canal in male, but not in female, specimens.

Changes of antioxidant enzymes in the kidney after cardiac arrest in the rat model.

Globally, cardiac arrest (CA) is a leading cause of death and disability. Asphyxial CA (ACA)-induced kidney damage is a crucial factor in reducing the survival rate. The purpose of this study was to investigate the role of antioxidant enzymes in histopathological renal damage in an ACA rat model at different time points. A total of 88 rats were divided into five groups and exposed to ACA except for the sham group. To evaluate glomerular function and oxidative stress, serum levels of blood urea nitrogen (BUN) and creatinine (Crtn) and malondialdehyde (MDA) levels in renal tissues were measured. To determine histopathological damage, hematoxylin and eosin staining, periodic acid-Schiff staining, and Masson's trichrome staining were performed. Expression levels of antioxidant enzymes including superoxide dismutase-1 (SOD-1), superoxide dismutase-2 (SOD-2), catalase (CAT), and glutathione peroxidase (GPx) were measured by immunohistochemistry (IHC). Survival rate of the experimental rats was reduced to 80% at 6 h, 55% at 12 h, 42.9% at 1 day, and 33% at 2 days after return of spontaneous circulation. Levels of BUN, Crtn, and MDA started to increase significantly in the early period of CA induction. Renal histopathological damage increased markedly from 6 h until two days post-CA. Additionally, expression levels of antioxidant enzymes were significantly decreased at 6 h, 12 h, 1 day, and 2 days after CA. CA-induced oxidative stress and decreased levels of antioxidant enzymes (SOD-1, SOD-2, CAT, GPx) from 6 h to two days could be possible mediators of severe renal tissue damage and increased mortality rate.

Changes of antioxidant enzymes in the kidney after cardiac arrest in the rat model

Globally, cardiac arrest (CA) is a leading cause of death and disability. Asphyxial CA (ACA)-induced kidney damage is a crucial factor in reducing the survival rate. The purpose of this study was to investigate the role of antioxidant enzymes in histopathological renal damage in an ACA rat model at different time points. A total of 88 rats were divided into five groups and exposed to ACA except for the sham group. To evaluate glomerular function and oxidative stress, serum levels of blood urea nitrogen (BUN) and creatinine (Crtn) and malondialdehyde (MDA) levels in renal tissues were measured. To determine histopathological damage, hematoxylin and eosin staining, periodic acid-Schiff staining, and Masson's trichrome staining were performed. Expression levels of antioxidant enzymes including superoxide dismutase-1 (SOD-1), superoxide dismutase-2 (SOD-2), catalase (CAT), and glutathione peroxidase (GPx) were measured by immunohistochemistry (IHC). Survival rate of the experimental rats was reduced to 80% at 6 h, 55% at 12 h, 42.9% at 1 day, and 33% at 2 days after return of spontaneous circulation. Levels of BUN, Crtn, and MDA started to increase significantly in the early period of CA induction. Renal histopathological damage increased markedly from 6 h until two days post-CA. Additionally, expression levels of antioxidant enzymes were significantly decreased at 6 h, 12 h, 1 day, and 2 days after CA. CA-induced oxidative stress and decreased levels of antioxidant enzymes (SOD-1, SOD-2, CAT, GPx) from 6 h to two days could be possible mediators of severe renal tissue damage and increased mortality rate.

Huge abdominal cyst occurred after kidney transplantation.

This case demonstrates continuous ambulatory peritoneal dialysis-related endometrial tissue migration and occurrence of huge cystic endometriosis by the recovery of menstrual period after kidney transplantation.

Factors predicting the usefulness of deceased donors.

BACKGROUND: Preoperative management for deceased donation is important. Deceased donation can failed for several reasons. We analyzed the clinical data of deceased donation after consent for cadaveric donation to evaluate the reasons of failure of organ procurement. MATERIAL AND METHODS: We retrospectively reviewed the medical records of 112 deceased donors in a single institution between January 1998 and September 2012. There were no organs from cardiac death donors. RESULTS: Of 112 deceased donors, 51 (45.5%) were traumatic brain deaths and 33 (29.5%), nontraumatic brain hemorrhages. The overall mean age was 37.2 (±16.6) years with 35 (30.7%) of female gender. There were 15 (13.3%) donation failures for all organs. Significant factors for failure were histories of cardiopulmonary resuscitation (odds ratio [OR], 0.17; 95% confidence interval [CI], 0.05-0.58; P = .005), cardiac arrest (OR, 0.03; 95% CI, 0.006-0.14; P < .001), or acute renal failure (OR, 0.05; 95% CI, 0.006-0.42; P = .006). The nonsignificant factors included the time from intensive care unit to brain death (mean time, 105.1 ± 153.4); diabetes insipidus; hypotension despite inotrophic therapy, hypothermia (<35°C), arrhythmia, infection, metabolic acidosis, disseminated intravascular coagulopathy, and brain death cause. CONCLUSIONS: Failure of deceased donation was associated with cardiac arrest while awaiting organ procurement and the presence of an history of cardiopulmonary resuscitation or presence of acute renal failure.