Angiogenesis in the human corpus luteum

Angiogenesis is important for the formation and development of the corpus luteum and for maintenance of luteal function. Blood vessel regression is an important physiological phenomenon in the corpus luteum, which is associated with tissue involution during structural luteolysis. Angiogenesis actively occurs during the early luteal phase and is completed by the mid-luteal phase. Perivascular cells (pericytes) increase in number from the early luteal phase to the mid-luteal phase, suggesting that blood vessels are gradually stabilized until the mid-luteal phase. In the corpus luteum undergoing luteolysis, blood vessels and pericytes decrease in number, which is related to structural involution. In the corpus luteum of early pregnancy, the number of blood vessels with pericytes increases, suggesting that angiogenesis occurs again, accompanied by blood vessel stabilization. These changes in vasculature of the corpus luteum are regulated by the collaboration with vascular endothelial growth factor, which is involved in proliferation of vascular endothelial cells, and angiopoietins, which are involved in stabilization of blood vessels. This review focuses on angiogenesis, blood vessel stabilization and blood vessel regression during the divergent phases of luteal formation, luteal regression and luteal rescue by pregnancy. (Reprod Med Biol 2008; 7 : 91–103)     

Surgical repair for late-onset hepatic venous outflow block after living-donor liver transplantation

The incidence of hepatic venous complications in partial liver transplantation is more frequent than that in whole liver transplantation. There are no reports of a surgical strategy for hepatic venous outflow block (HVOB) after living-donor liver transplantation. HVOB was diagnosed when the pull-through pressure gradient across the anastomotic site was over 5 mm Hg. Reoperation for venous anastomosis was performed if the angioplasty was unsuccessful. After dissection around the hepatic venous anastomotic site, a patch venoplasty of the anastomosis was performed. When the inferior vena cava was constricted, venoatrial anastomosis was performed. In 6 years, 5 of 223 patients experienced HVOB. Balloon angioplasty was successfully performed in two patients, a patch venoplasty of the anastomosis in two, and venoatrial anastomosis in one. In all patients, the ascites stopped. HVOB must be diagnosed as soon as possible with Doppler ultrasound and venography. Prompt surgical revision can salvage the grafts.     

The p53-independent nuclear translocation of cyclin G1 in degenerating neurons by ischemic and traumatic insults

Cyclin G1 (CG1) was identified as a p53-transactivated target gene, and yet its physiological and pathological roles have been unclear. Here, we demonstrate that CG1 is translocated from cytoplasm to the nuclei of neurons in response to variety of injuries. In the normal matured rodent brain, CG1 immunoreactivity was hardly observed; however, some brain injuries exhibited intense CG1 immunoreactivity in the nuclei of the damaged neurons. Transient common carotid artery occlusion (CCAO) in the gerbil showed strong CG1-like immunoreactivity in the hippocampal CA1 neurons, and permanent middle cerebral artery occlusion (MCAO) in the mouse showed strong CG1-like immunoreactivity in the nuclei of neurons located in the ischemic brain regions. TUNEL staining did not exactly overlap with the CG1-positive cells, but overlapped highly with Fluoro-Jade B staining, a degeneration marker. Brain trauma caused by knife cut, cold injury, and kinate injection also showed CG1 accumulation in the neuronal nuclei located near the injury site. These observations were obtained in p53-deficient mice as well, suggesting that the accumulation of CG1 in the injured neurons is p53-independent. A similar nuclear translocation of endogenous CG1 was confirmed in a primary culture of cortical neurons when a toxic level of N-methyl-D-aspartate (NMDA) was applied. These results demonstrate that nuclear translocation of CG1 from cytoplasmic region occurs in damaged and degenerating neurons in a p53-independent manner, and the CG1 nuclear staining could be a good marker for the neurons received fatal damages.     

Autopsy findings of meningitis associated with multiple brain infarctions in two adult patients

Cerebrovascular complications of meningitis have been extensively documented in the literature. It is little known, however, that paroxysmal, devastating, and potentially fatal complications can occur when the early signs of infection are subtle and missed. We describe the clinical course and neuropathological findings of the occurrence of brain infarctions during two atypical clinical courses of meningitis. In one patient, it was due to Serratia marcescens detected only by an autopsy specimen, and in the other, it was due to Aspergillus detected by a surgical biopsy. Death followed multiple, extensive, and progressively multiplicative infarctions in the basal ganglia, brainstem, and cerebral cortices. Autopsies revealed that the infarctions were caused by severe inflammatory change in the vascular walls, mainly of the arteries of the skull base, including the basilar and carotid arteries. Thrombus formation was also recognized in the lumen of several arteries. A number of characteristic Aspergillus hyphae were recognized in the arterial wall of one patient. Meningitis, which may be associated with severe vasculitis and lead to cerebral infarction, should be considered in the differential diagnosis of these conditions. Early diagnosis and initiation of vigorous therapy should be stressed for therapeutic success.     

Pulmonary embolectomy for acute massive pulmonary thromboembolism

Acute pulmonary thromboembolism is a frequently lethal and acute-onset in-hospital complication after surgery. Absolute indications for surgical embolectomy are acute massive pulmonary embolism with deep shock, refractory circulatory collapse, and continuous hypoxemia. Although thrombolytic therapy is indicated for patients with pulmonary thromboembolism with right ventricular overload, it is contraindicated for patients after major surgery or with stroke due to the high risk of rebleeding. Therefore surgical embolectomy should be considered in those patients. Pulmonary embolectomy relieves the right ventricular overload, and immediate restoration of right ventricular function contributes to the recovery of hemodynamics. A recent study revealed improved outcome for massive pulmonary embolism with early diagnosis with multidetector-row computed tomography, risk stratification using echocardiography, and surgical embolectomy. Surgical pulmonary thromboembolectomy should be considered for critically ill patients with massive pulmonary thromboembolism.     

Hepatic Resection for Metastatic Breast Cancer: Prognostic Analysis of 34 Patients

Liver metastasis of breast cancer is considered a generalized disease, and surgical treatment is rarely discussed. Thirty-four patients who underwent 35 hepatectomies for liver metastases of breast cancer between 1985 and 2003 were analyzed. The median interval between the breast surgery and relapse in the liver was 1.9 years (0–20 years). The liver was the first site of recurrence in 25 patients. Fifteen clinicopathologic factors were evaluated using univariate and multivariate analyses to predict survival after hepatic resection. No patients died because of the surgery. The median survival was 36 months (1 month to 20 years). The overall and disease-free 5-year survival rates after hepatectomy for breast metastases were 21% and 16%, respectively. Four patients survived more than 5 years. The presence of extrahepatic recurrence prior to hepatectomy was the only significant prognostic factor according to the analyses, and the 5-year survival rate of patients without extrahepatic disease was 31%. No patient who had hilar lymph node metastasis survived more than 5 years. In the absence of extrahepatic recurrence, surgical resection of liver metastasis from breast cancer can offer an acceptable prognosis and should not be avoided in selected patients.