Evaluation of selective hepatic angiography and embolization in patients with massive hemobilia.

BACKGROUND: Massive hemobilia is a rare but potentially life-threatening cause of upper gastrointestinal hemorrhage. Transarterial embolization is considered the first line of intervention to stop the bleeding for most causes of hemobilia. This study was conducted to evaluate selective hepatic angiography and embolization in the diagnosis and treatment of patients with massive hemobilia. METHODS: The clinical data of 16 patients with massive hemobilia were analyzed retrospectively. These patients underwent emergency celiac and selective right or left hepatic artery angiography and treated by embolization using Gelfoam particles and/or coils. RESULTS: Hepatic artery angiography revealed hepatic artery pseudoaneurysms in 6 patients, cystic artery pseudoaneurysms in 2, diffuse hemorrhage of hepatic artery branches in 5, and right hepatic artery-bile duct fistulae in 3. The patients were diagnosed rapidly by angiography and treated successfully by embolization of the hepatic artery branch proximal to the bleeding point, and hemorrhage was stopped immediately. Two patients were embolized the second time for rebleeding. Neither recurrence of bleeding nor serious complication was found during the follow-up for 3 months to 2 years. The other 2 patients whose hemorrhage failed to be controlled died several days later. CONCLUSION: Being safe, reliable and minimally invasive, selective hepatic artery angiography and embolization are effective in the diagnosis and treatment of massive hemobilia.

Diagnosis and treatment of penetrating craniocerebral injury.

OBJECTIVE: To evaluate the clinical characteristics and present the experience in the treatment of patients with penetrating craniocerebral injury (PCCI). METHODS: The data of 7 cases with PCCI by foreign body were retrospectively studied and compared with associated literatures. The strategies of diagnosis and treatment of PCCI were analyzed. In this series, 3 cases underwent emergency debridements and 4 cases underwent craniotomies. All patients received surgical intervention within 3 hours after admission. RESULTS: Outcomes were good in 3 cases, moderate disability was in 2 cases, severe disability in 1 case and persistent vegetative state in 1 case. One case developed wound and intracranial infection, but made good recovery after treatment. During the follow-up period, one patient died one month after discharge and other six patients (range from 8 months to 3 years) recovered well and no epilepsy, leakage of cerebrospinal fluid (CSF), or traumatic vascular disease occurred. CONCLUSIONS: Early diagnosis and prompt debridement are the fundamental factors affecting the outcome of PCCI. CT scans are the mainstay in evaluating PCCI and three dimensional (3D) images reconstructed from spiral CT scans provide more information. Efficient debridement should be performed as early as possible. Minimizing the degree of surgical management of PCCI is preferred when there is no indication for aggressive operation. It is important to stress the rapid and effective management of CSF leakage in early stage of PCCI. Use of prophylactic broad-spectrum antibiotics is recommended for patients with PCCI. Traumatic vascular injury should be paid attention to after PCCI.

Investigation on apoptosis of neuronal cells induced by Amyloid beta-Protein.

OBJECTIVE: To construct a PC12 cell strain with neuronal differentiation, and observe the apoptosis and proliferation activity effects induced these cells by Amyloid beta-Protein (Abeta-43). METHODS: 1) PC12 cells in logarithmic growth phase were subcultured for 24 h. After the culture fluid was changed, the cells were treated with Rat-beta-NGF and cultured for 9 days. 2) Neuronal differentiation of PC12 cells in logarithmic growth phase were divided into four groups: control group (0), experimental group (1), experimental group (2) and experimental group (3). The concentrations of Abeta in the four groups were 0 micromol/L, 1.25 micromol/L, 2.5 micromol/L and 5 micromol/L, respectively. The cells were harvested at 24, 48 and 72 h later and stained with AnnexinV-FITC/PI after centrifugation and washing. Then flow cytometry was conducted to examine the apoptosis percentage. 3) NGF-induced PC12 cells were selected and Abeta with different concentrations was added. The final concentrations of Abeta were 0 micromol/L, 1.25 micromol/L, 2.5 micromol/L and 5 micromol/L, respectively. After the cells were incubated in an atmosphere of 5% CO2 at 37 degrees C in an incubator for 72 h, the OD values were examined. RESULTS: 1) Neuronal differentiated PC12 cell lines were successfully established. 2) Flow cytometric examination indicated that Abeta (1.25, 2.5, and 5.0 micromol/L) could effectively induce apoptosis of neuronal-differentiated cells at the 24 h, 48 h and 72 h time points. 3) Abeta (0-5.00 micromol/L) had no obvious effect on proliferation or restraining of the neuronal differentiation of the PC12 cells after a 72 h interacting process. CONCLUSION: This investigation revealed successful neuronal differentiation of the PC12 cell strain. The induction of apoptosis of the neurocytes by various concentrations of Abeta was observed and the influence of Abeta on induced proliferation of PC12 cells by Rat-beta-NGF was revealed. This study may provide basis for future research on the molecular cure of AD and interdiction of AD evolution.