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Background Development of multiple rib fractures leading to bilateral flail chest in Cronkhite–Canada Syndrome (CCS) has not been reported. Case presentation A 59-year-old man presented with complaints of fatigue, chest pain, respiratory distress and orthopnea requiring ventilatory support to maintain oxygenation. CCS with bilateral anterior and posterior flail chest due to multiple rib fractures (2nd-10th on the right side and 2nd-11th on the left side). He underwent open reduction and anterior and posterior internal fixation using a titanium alloy fixator and a nickel-titanium memory alloy embracing fixator for chest wall reconstruction. He recovered gradually from the ventilator and showed improvement in his symptoms. He gained about 20 kg of weight in the follow up period (6 months after discharge from the hospital). Conclusion CCS is a rare, complex disease that increases the risk of developing multiple rib fractures, which can be successfully treated with open reduction and internal fixation.

Background and Purpose— Intracranial artery calcification detected by computed tomography is associated with ischemic stroke as an indicator of intracranial atherosclerosis. However, little is known about its histopathology. This study aimed to explore the intracranial calcification patterns and their associations with atherosclerotic plaques. Methods— We recruited 32 adult autopsy cases to assess the calcification patterns and distributions in the middle cerebral artery, vertebral artery, and basilar artery. The relationships of calcification patterns with plaque phenotype and luminal stenosis were evaluated. The calcification patterns on computed tomography were correlated with that on histology. Results— Visible calcifications were detected within 37 (39%) segments, including 25 segments with intimal calcification, 6 segments with internal elastic lamina calcification, 3 segments with adventitial calcification, and 3 segments with concurrent calcification. Calcification occurred more often in the vertebral artery (51%), followed by the middle cerebral artery (35%) and basilar artery (14%; P P P Conclusions— Our histological findings indicate that the presence of intracranial artery calcification has 3 patterns, including intimal, internal elastic lamina, and adventitial calcifications. But only intimal calcification is related with progressive atherosclerotic lesions, indicative of a proxy for intracranial atherosclerosis.

BACKGROUND AND PURPOSE Vasa vasorum (VV) have been believed to be rare or non-existent in small-caliber intracranial arteries. In a series of human cerebral artery specimens, we identified and examined the distribution of VV in association with co-existing intracranial atherosclerosis. METHODS We obtained cerebral artery specimens from 32 consecutive autopsies of subjects aged 45 years or above. We scrutinized middle cerebral artery (MCA), vertebral artery (VA), and basilar artery (BA) for the presence of adventitial VV. We described the distribution of VV, and the characteristics of co-existing atherosclerotic lesions. RESULTS Among 157 intracranial arteries, adventitial VV were present in 74 of the 157 specimens (47%), involving MCA (n=13, 18%), BA (n=14, 19%), and VA (n=47, 64%). Although qualitatively these 74 adventitial VV distributed similarly in arteries with or without atherosclerotic lesions (disease-free arteries n=4/8; arteries of pre-atherosclerosis n=17/42; and arteries of progressive atherosclerosis n=53/107), the presence of adventitial VV in intracranial VA was associated with a heavier plaque load (1.72±1.66 mm2 vs. 0.40±0.32 mm2, P

Background and Purpose: Vasa vasorum, which constitutes a network of microvasculature, plays a nutritive and drainable role in vessel walls of arteries. The existence of vasa vasorum within brain vasculature is rarely reported. Based on a series of cerebral artery specimens, we aimed to describe the distribution features of vasa vasorum among intracranial arteries, including middle cerebral arteries (MCAs), basilar arteries (BAs) and vertebral arteries (VAs) and potential effects of vasa vasorum on atherosclerosis morphology. Methods: One hundred and fifty- seven arteries (64 MCAs, 32 Bas and 61 VAs) were obtained from consecutively recruited 32 autopsy cases aged 45 years or above. Routine histology and immunostaining processing were performed to identify the presence of adventitial vasa vasorum and to study the phenotypes and specific components of intracranial atherosclerotic lesions. Results: Among 157 intracranial cerebral arteries, adventitial vasa vasorum were present most frequently in the vertebral arteries (77%), followed by basilar arteries (44%) and middle cerebral arteries (20%). Arteries with adventitial vasa vasorum had greater thickness of tunica adventitia (0.10±0.06 mm vs. 0.06±0.03 mm, p &lt 0.001) and larger size in diameters (3.41± 0.73 mm vs. 2.97± 0.66 mm, p &lt 0.001). The occurrence of adventitial vasa vasorum correlated with high frequency of complicated plaques and higher rate of concentric atherosclerotic lesions (70% vs. 36%, p &lt 0.001). Conclusion: For the first time, our study demonstrated the presence of adventitial vasa vasorum within brain vasculature, especially at vertebral arteries. The correlations between adventitial vasa vasorum and intraplaque hemorrhage, inflammation and calcification suggest that adventitial vasa vasorum may serve as a predictor of unstable atherosclerotic lesions. Further studies are required to explore the biological behavior of adventitial vasa vasorum within cerebral arteries.

© 2017 Yang, Fisher, Zheng, Niu, Paganini-Hill, Zhao, Xu, Wong, Ng and Chen. Background: Anterior and posterior circulation atherosclerosis differ in vascular risk factors and stroke mechanisms. However, few studies have compared the pathological features between these lesions. Using a series of intracranial artery specimens, we characterized the intracranial atherosclerotic lesions and compared pathological features among different arteries of the intracranial vasculature. Methods: Intracranial large arteries of 32 consecutively recruited autopsy cases of Chinese adults aged 45 years or older were examined pathologically using routine histology and immunostaining, to characterize the pathological features of the atherosclerotic lesions. We analyzed middle cerebral arteries (MCAs) (both left and right), vertebral arteries (VAs) (side more affected), and basilar arteries (BAs). Results: Progressive atherosclerotic lesions were present in 91(71%) of the 128 arteries examined. Features of complicated plaques were infrequently detected: plaque hemorrhage was encountered in 12%, neovasculature in 12%, lumen thrombi in 13%, macrophage infiltration in 20%, and calcification in 25% of arteries. Luminal narrowing of MCA was the most severe, followed by VA; the BA least stenotic (37 ± 25 vs. 30 ± 24 vs. 20 ± 20%, all p < 0.05). MCA had more eccentric (vs. concentric) plaques than VA (69 vs. 25%, p = 0.003) and BA (69 vs. 38%; p = 0.03). Lumen thrombi were more frequent in BA, and calcification most commonly occurred in VA atherosclerotic lesions. Conclusion: Intracranial atherosclerotic plaques were commonly present in this sample, but the lesions generally lacked features of complicated plaques. MCA lesions had demonstrable differences compared with VA and BA lesions. Further studies are needed to determine whether these characteristics indicate a distinctive atherosclerotic phenotype for the intracranial vasculature.

Objective: Macrophage migration inhibitory factor (MIF) and CD74 emerge as important players in pathogenesis and angiogenesis of several types of malignant tumors. The purpose of this study was to evaluate the expression of MIF and CD74 in cervical squamous cell carcinoma and explore the potential roles they play in cervical tumor angiogenesis. Methods: Macrophage migration inhibitory factor and CD74 expression was assessed by immunohistochemistry in 209 cases with various degrees of cervical epithelial lesions, including 40 normal cervical epithelia, 43 mild cervical intraepithelial neoplasia 1 (CIN 1), 41 moderate-severe cervical intraepithelial neoplasia (CIN 2 to 3), and 85 cervical squamous cell carcinomas (SCCs). CD34 staining was used for counting microvessel density. Semiquantitative reverse transcription polymerase chain reaction and Western blot were used to detect messenger RNA and protein levels of MIF and CD74 in normal and malignant cervical tissues and cervical cancer cell lines SiHa and C-33A. The concentration of vascular endothelial growth factor (VEGF) in the conditioned media of cervical cancer cells was analyzed by enzyme-linked immunosorbent assay. Results: Immunohistochemical analysis showed that MIF and CD74 expression was significantly higher in CIN than in the normal samples and higher in SCC than in CIN. The overexpression of MIF was correlated with deep stromal infiltration but not with the other clinicopathologic features of SCC. Correlation analyses revealed that MIF was positively related to CD74, and both protein levels were associated with microvessel density. Exogenous MIF induced VEGF secretion in SiHa and C-33A cells in a dose-dependent manner, which can be inhibited by MIF-specific inhibitor (ISO-1) or anti-CD74 antibody. Conclusion: Overexpression of MIF and CD74 in SCC and its precancerous lesions and the up-regulation of VEGF secretion in cervical cancer cells indicate that MIF and CD74 may play critical roles in the pathogenesis and angiogenesis of cervical cancer.