Malignant tumors of the liver stemming from mesenchymal origins are rare neoplasms, <1% of primary malignant hepatic lesions. Primary hepatic angiosarcoma (PHA) is the most common (36%). This study describes the incidence and clinical characteristics of this rare tumor in two medical centers, over the past 18 years. We reviewed tumor registry files at Jackson Memorial Hospital and oncology data records at Cedar's Medical Center, 1979-1997. A total of 865 primary hepatic tumors were identified, of which five cases (0.58%) were PHA; four were men, and the median age was 53 years. Symptoms and signs included: pain, anemia, fever of unknown origin, weight loss, abdominal mass, and hemoperitoneum. Median survival was only 6 months. In conclusion, primary hepatic angiosarcomas frequently are symptomatic. The presentation and preexisting factors are valuable in establishing a clinical suspicion to diagnose this rare tumor. Although imaging studies are helpful, they are not conclusive, and liver biopsy is usually required.
Seventy-five percent of all traumatic brain injuries are mild and do not cause readily visible abnormalities on routine medical imaging making it difficult to predict which individuals will develop unwanted clinical sequelae. Microglia are brain-resident macrophages and early responders to brain insults. Their activation is associated with changes in morphology or expression of phenotypic markers including P2Y12 and major histocompatibility complex class II. Using a murine model of unrestrained mild closed head injury (mCHI), we used microglia as reporters of acute brain injury at sites of impact versus sites experiencing rotational stress 24 h post-mCHI. Consistent with mild injury, a modest 20% reduction in P2Y12 expression was detected by quantitative real-time PCR (qPCR) analysis but only in the impacted region of the cortex. Furthermore, neither an influx of blood-derived immune cells nor changes in microglial expression of CD45, TREM1, TREM2, major histocompatibility complex class II or CD40 were detected. Using magnetic resonance imaging (MRI), small reductions in T2 weighted values were observed but only near the area of impact and without overt tissue damage (blood deposition, edema). Microglial morphology was quantified without cryosectioning artifacts using ScaleA2 clarified brains from CX3CR1-green fluorescence protein (GFP) mice. The cortex rostral to the mCHI impact site receives greater rotational stress but neither MRI nor molecular markers of microglial activation showed significant changes from shams in this region. However, microglia in this rostral region did display signs of morphologic activation equivalent to that observed in severe CHI. Thus, mCHI-triggered rotational stress is sufficient to cause injuries undetectable by routine MRI that could result in altered microglial surveillance of brain homeostasis.
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