Notes: Blackarrow: portal vein; white arrow: splenic artery; white arrowhead: splenic venous thrombus; black arrowhead: superior mesenteric vein; white hollow arrow: retroperitoneal lymphoma; black hollow arrow: the third segment of duodenum. (A) splenic vein was replaced by longitudinal hypoattenuating mass, accompanied with splenic artery. (B) The retroperitoneal mass infiltrated the body of pancreas and splenic vein. The confluences of dilated PSPDV and coronary vein into portal vein could be seen. (C) The retroperitoneal mass involved aorta and posterior wall of duodenum. (D, E) After six cycles of chemotherapy, the splenic thrombus shrank significantly and the retroperitoneal mass disappeared. (F) The para-aorta mass and thickening of duodenum disappeared after the sixth cycle of therapy.
Fig. 9 56 year old female, history of alcoholism, fall from standing height. Celiac artery angiogram after proximal splenic artery embolization with an AMPLATZERTM Plug (star a). This shows collateral perfusion to the spleen and distal splenic artery (straight black arrows b-d) via GDA (thin straight white arrow b, c) → right gastroepiploic (curved white arrow b-d) → left gastroepiploic pathway (curved blackarrow b-d). Note that the parenchymal opacification of the spleen is markedly delayed compared to the liver, an expected finding after PSAE (d). Corkscrew intrahepatic arteries and the recannalized periumbilical vein with hepatopedal flow (thick white arrow b, c) are consistent with the patient ’ s known history of alcohol cirrhosis and portal hypertension
Fig. 3. Left unilateral high jugular bulb was demonstrated in the temporal bone HRCTs. 3A. Left JB dehiscence (white arrow), SS-EAC length (a double-tipped blackarrow) in the axial section of the temporal bone HRCTs. 3B. ICA and JB dehiscence in the left (white arrows) in the axial section of the temporal bone HRCTs. 3C. In the axial section of the temporal bone HRCTs, JB-ED length (a double-tipped white arrow) and the manubrium mallei and umbo (white arrow) were shown in the left side. 3D. Left ICA dehiscence (white arrow) was shown in the coronal section of the temporal bone HRCTs. 3E. Left JB dehiscence (white arrow) was shown in the coronal section of the temporal bone HRCTs. SMF – stylomastoid foramen, V – vestibul, IAC – internal acoustic canal, PSCC – posterior semicircular canal, LSCC – lateral semicircular canal, JB – jugular bulb, SS – sigmoid sinus, EAC – external acoustic canal, ICA – internal carotid artery, M – malleus
Visual inspection of the basicranium of the 70 skulls revealed the presence of a pterygoalar bar and the pterygoalar foramen in 5 cases. The pterygoalar bar was located medially or laterally to the foramen ovale, while in one case it crossed the foramen ovale (Fig. 2). Thus, we confirm that the position of the pterygoalar bar differs towards the foramen ovale Figure 1. Inferior (A) and lateral (B) view of the pterygoalar bar (blackarrow) and the ptery-
&E stain (×100) were are followed: (H) Normal control rats showing Normal white pulb containing follicular artery (blackarrow) and normal red pulb containing numerous blood sinusoids (blue arrow). (I) Sections from DH- TENV gel group illustrated normal white pulb (blackarrow) with dilated in sinusoid in red pulb (blue arrow). (J) RA- arthritic rats showing marked atrophy of white pulp (blackarrow). (K) RA group that treated with MIX showed hyperplagia in the white pulb (blue circle), congestion and dilation in sinusoid of the red pulp (blackarrow). (L) Sections from DH - TENV gel group illustrated hyperplasia in white pulb with multiple macrophages indicated immunoreaction (blackarrow). (M) spleen sections of RA- treated gel group showed Hyperplasia in white pulb (blackarrow) and dilation in sinusoid in the red pulb (blue arrow). (N) Rheumatoid arthritis group that treated with oral DH showed marked activation in the macrophage in the white pulb (blackarrow) and nearly normal red pulb (blue arrow). Liver photomicrographs sections obtained from different groups and stained with routine H&E stain (×200) were are followed: (O) Normal control rats showing normal liver with normal central vein (blue arrow) with normal hepatic cords (blackarrow). (P) Sections from DH - TENV gel group illustrated nearly normal liver with normal central vein (blue arrow) and portal area (orange arrow). (Q) RA- arthritic rats showing slight congestion (orange arrow) and edema (blackarrow) together with sever vascular degeneration in the hepatocyte (blue arrow). (R) RA group that treated with MIX showed dilated central vein (blue arrow) and dilation in hepatic sinusoid (blackarrow) with some with vascular degeneration in the hepatocyte (arrow head). (S) Sections from DH - TENV gel group illustrated nearly normal liver except slight congestion in central (blackarrow) and portal vein (blue arrow). (T) liver sections of RA- treated gel group showed slight congestion in both central vein and portal vein (blue arrow) and hepatic cord and hepatocyte appear normally (blackarrow). (U) Rheumatoid arthritis group that treated with DH oral solution showed marked congestion of central veins (blue arrow) with dilated engorged sinusoid (arrow head) and focal coagulative necrosis of sore hepatocyte (blackarrow).
13 Figure 2 Photomicrographs of liver sections of rats in different groups (H&E stain X20) (star: edema, blackarrow: congestion, red arrow: nuclear pyknosis, blue arrow: inflammatory cells infiltration, green arrow: apoptotic hepatic cells, white arrow and circle: area of coagulative necrosis infiltrated by inflammatory cells) A: Control group showing normal tissue architecture of liver. B1,2: CYP group showing edema, congestion of central vein and hepatic sinusoids, inflammatory cells infiltration, hepatic cells with nuclear pyknosis, some apoptotic hepatic cells and multifocal areas of coagulative necrosis infiltrated by inflammatory cells. C: CYP+MS group showing congestion of hepatic sinusoids, some hepatic cells with nuclear pyknosis. D: CYP+RGH group showing mild congestion of central vein and hepatic sinusoids, small area of coagulative necrosis infiltrated by some inflammatory cells. E: CYP+MS+RGH group showing: somewhat normal histological structure of liver parenchyma.