BACKGROUND AND PURPOSE:Carotid angioplasty with stent placement (CAS) is an optional treatment for significant carotid stenosis. Cerebral vasoreactivity (CVR), representing the reserve capacity of cerebral perfusion, usually decreases in patients with severe carotid stenosis. This study aimed to investigate the relationship between the baseline CVR assessed by functional MR imaging (fMRI) and the changes in cerebral blood flow (CBF) after CAS.

Hepatic fibrosis represents a process of healing and scarring in response to chronic liver injury. a-Melanocyte-stimulating hormone (a-MSH) is a 13-amino-acid peptide with potent anti-inflammatory effects. We have previously demonstrated that a-MSH gene therapy protects against thioacetamide (TAA)-induced acute liver failure. Therefore, the aim of this study is to investigate whether a-MSH gene therapy possesses antihepatic fibrogenic effect. Liver fibrosis was induced by long-term TAA administration in mice. a-Melanocyte-stimulating hormone expression plasmid was delivered via electroporation after liver fibrosis was established. Our results showed that a-MSH gene therapy attenuated liver fibrosis in TAA-treated mice. Reverse transcription polymerase chain reaction revealed that a-MSH gene therapy attenuated the liver transforming growth factor-b1, collagen a1 and cell adhesion molecule mRNA upregulation. Following gene transfer, the expression of a-smooth muscle actin and cyclooxygenase-2 were both significantly attenuated. Further, a-MSH significantly increased matrix metalloproteinase (MMP), while tissue inhibitors of matrix metalloproteinase (TIMPs) were inactivated. In summary, a-MSH gene therapy reversed established liver fibrosis in mice and prevented the upregulated fibrogenic and pro-inflammatory gene responses after TAA administration. Its collagenolytic effect might be attributed to MMP and TIMP modulation. Hence, a-MSH gene therapy may be an effective therapeutic modality against liver fibrosis with potential clinical use.

Hypertensive intracerebral hemorrhage has been considered as a one‐time event with rare recurrence. This observation is quite different from our experience in Taiwan. We, therefore, conducted a systematic review of our series of consecutive patients with recurrent bleeding. During a 2‐year period, we encountered 47 patients with recurrent hypertensive intracerebral hemorrhage from a total of 892 consecutive patients with hypertensive hemorrhage (5.3%). There were 25 men and 22 women with a mean age of 59 ± 10 (range: 36–78) years at the onset of the first hemorrhage and 62 ± 9 (range: 39–80) years at the second hemorrhage. The median interval between 2 hemorrhages was 2 years and 4 months (range: 1 month to 8.5 years). All except one recurrent hemorrhages occurred at a site different from the previous one. Of the 38 patients admitted to our hospital for both hemorrhages only 5 were regularly treated with antihypertensive therapy. The outcome for the recurrent bleeding was grave: 26% died and 51% became totally dependent or vegetative. Recurrent hypertensive hemorrhage is not as rare as previously thought; it comprises 5.3% of our patients with hypertensive intracerebral hemorrhage. The recurrent hemorrhage, however, rarely occurs at the same location as the previous one. Uncontrolled hypertension appears to be an important risk factor for the recurrence. Control of blood pressure after the first bleeding should be attempted to prevent recurrent hemorrhage.

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