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ObjectiveTo investigate the association between portal vein pressure drop gradient in patients with cirrhotic portal hypertension treated by transjugular intrahepatic portosystemic shunt (TIPS) and clinical prognosis, as well as the ideal range of portal vein pressure drop. MethodsA total of 58 patients who underwent TIPS in Xinqiao Hospital of Third Military Medical University from November 2013 to December 2015 were enrolled. All the patients underwent TIPS and embolization of the gastric coronary vein and the short gastric veins, and the change intervals of portal vein pressure gradient were monitored. The follow-up time ranged from 3 days to 2 years, and the association of portal vein pressure drop gradient with postoperative liver function, splenic function, rebleeding rate, hepatic encephalopathy, and portal hypertensive gastrointestinal diseases was analyzed. The paired t-test was used for comparison of parameters before and after treatment. ResultsThe patients had a significant reduction in liver function on day 3 after surgery. At 2 month after surgery, the levels of TBil was rised and had significant changes［(49.81±27.82)μmol/L vs (31.64±17.67) μmol/L,t=5.372,P＜0.001］. At 6 months after surgery, red blood cell count and platelet count had no significant changes，but，white blood cell count was reduced［(3.79±1.37）×109/L vs (4.57±2.24)×109/L，t=2.835，P=0.006］. There was a 23% reduction in portal vein pressure after surgery (from 30.62±3.56 mmHg before surgery to 21.21±2.90 mmHg after surgery, t=23.318，P＜0.001). All the patients had varying degrees of relief of gastrointestinal symptoms associated with portal vein hypertension, such as abdominal distension, poor appetite, and diarrhea. Of all patients, none experienced in-stent restenosis or occlusion and 13 experienced hepatic encephalopathy after surgery, which tended to occur at the time when postoperative portal vein pressure was reduced to 14.7-25.7 mmHg, i.e., a 36%-40% reduction in portal vein pressure. The results of splenic venography performed immediately after surgery showed that varicose veins almost disappeared and that there were no collateral varices. Gastroscopy was performed again within 1 month after surgery and 5 patients had no significant changes in esophageal varices. The other patients were followed up for 2 years, and the severity of esophageal and gastric varices gradually changed from severe varices with red color sign to moderate and mild varices and even disappeared. The proportion of patients with mild and disappeared varices increased from 22% on day 3 after surgery to 52% in the second year after surgery. No patients experienced rebleeding within 1 month after surgery. Six patients each experienced rebleeding at 2, 6, 10, 14, 16, and 24 months after surgery, and in one patient, duodenal bulbar ulcer and bleeding was not excluded; the other 5 patients experienced gastric variceal bleeding again, with a median portal vein pressure of 36.46 mmHg before surgery and 24.8 mmHg after surgery, with a 32% reduction in portal vein pressure. ConclusionTIPS has a good clinical effect in hemostasis and prevention of rebleeding in patients with cirrhotic portal hypertension and can control the portal vein pressure below 21.21±2.90 mmHg, and the degree of reduction in portal vein pressure is below 36%-40%. It can reduce the incidence of postoperative rebleeding and avoid the development of hepatic encephalopathy. TIPS can cause liver impairment within a short period of time after surgery, and liver function can return to normal within 1-6 months after surgery, but splenic function does not recover significantly.

Owing to outstanding properties of two-dimensional electron gas (2DEG) and GaN-base material, such as high electron mobility and high critical electric field, AlGaN/GaN high electron mobility transistors (HEMTs) have been considered as the next-generation power semiconductor devices with high power conversion efficiency, high switching frequency and high-temperature operation capability. For power switching applications, enhancement mode (e-mode, or say normally-off) transistors are desired for fail-safe operation and silicon-compatible gate drive circuit. However, e-mode operation is difficult for AlGaN/GaN-based HEMTs because of the natural existence of 2DEG. To achieve e-mode operation, several approaches have been reported, including gate recess structure, fluorine plasma ion implantation, p-type gate structure and selective channel regrowth, etc. This paper reports normally-off AlGaN/GaN HEMTs with a recessed MOS-gate. After mesa isolation and Source and drain metal, the gate recess process used inductively coupled plasma (ICP). In order to avoid severe etching damage and obtain high drain current density, etching power was carefully optimized. The etching rate is slow for accurate etching depth control to leverage the current density and threshold voltage. After that, an O2 plasma treatment was applied using a plasma asher to oxidize the damaged semiconductor surface. The oxide layer was then removed in HCl: DI-water (1: 3). The next step is an atomic layer deposition (ALD) of Al 2 O 3 as the gate dielectric to increase the breakdown voltage. Follow after that, gate metal and pad metal. By the process, our team made three kinds of HEMTs with different recessed gate depths. The first one, which has been report before, exhibits a high threshold voltage of +4.6V, a specific on-resistance of 4mΩ-cm⁁2 and a drain current density of 108 mA/mm. This paper will show the others fabricated in the later researches. The device transfer curves show that this normally-off recessed MOS-gate AlGaN/GaN HEMTs exhibit threshold voltage of +0.9V and +2.1V, respectively. Additionally, the specific on-resistance and saturation drain current density of the device with 0.9V threshold voltage are 2.26mΩ-cm⁁2 and 326mA/mm, while 2.1V-Threshold Voltage-device are 3.03mΩcm⁁2 and 173mA/mm. Both of the two HEMTs have a breakdown voltage over 400V.

The transcription factor forkhead box protein A1 (FOXA1) plays a critical role in the proliferation of human breast cancer cells, particularly estrogen receptor alpha (ERα)-positive luminal breast cancer cells. However, genetic studies of the requirement for Foxa1 in mammary tumor formation in mice have been hampered by the lack of a conditional gene ablation. We examined three mouse models of mammary-specific ablation of Foxa1 in ductal epithelial cells to identify the best system for complete and mammary-specific ablation of Foxa1. We found that MMTV-Cre and MMTV-rtTA;Tet-On-Cre led to partial deletion of Foxa1 and attenuated mammary duct formation, whereas Krt14-Cre led to complete ablation of Foxa1 and abolished mammary duct formation, in Foxa1(loxP/loxP) mice. These results demonstrate that Foxa1 is essential for mammary duct formation, and reveal a series of mouse models in which mammary expression of Foxa1 can be attenuated or completely blocked. Our study also suggests a potentially powerful model for complete ablation of Foxa1 in mammary epithelial cells using Krt14-driven Cre expression in an inducible manner, such as Krt14-rtTA;Tet-On-Cre. This model system will facilitate further in vivo functional studies of Foxa1 or other factors in mammary gland development and tumor formation and progression. genesis 54:277-285, 2016. © 2016 Wiley Periodicals, Inc.