Primary amyloidosis of the urinary bladder.

Amyloidosis is a systemic disease that usually occurs in the gastrointestinal tract or in muscular or adipose tissue. Primary amyloidosis of the urinary bladder is a rare disease that can mimic bladder cancer on cystoscopic examination as well as in its clinical presentation of painless gross hematuria. This report describes a 49-year-old male with repeated painless gross hematuria, who underwent transurethral resection of a suspected bladder tumor. Pathologic examination revealed papillary urothelial hyperplasia with vascular ectasia and no signs of malignancy. Massive gross hematuria occurred 2.5 years later. Cystoscopy showed multiple papillary lesions with yellowish-brown submucosal plaques on the posterior bladder wall. A second transurethral tumor resection was performed and histologic examination revealed plasma cell infiltration and eosinophilic amorphous deposits in the subepithelial stroma and vascular wall. The deposits were positive for Congo red and apple-green birefringence under polarized light examination but negative for Masson's trichrome stain, indicating that they were not fibrotic in nature. Hence, the diagnosis of amyloidosis of the urinary bladder was confirmed. Screening for amyloidosis was negative in other organ systems and the patient has remained disease-free up to the last follow-up 4 years after the second transurethral resection. Amyloidosis should be considered in the differential diagnosis of patients with recurrent hematuria who have symptoms characteristic of bladder cancer but negative pathologic study for malignancy. Correct diagnosis relies on clinical alertness and the use of a special staining technique during pathologic examination.     

自体腹白线片修补十二指肠溃疡穿孔(附13例报告)

目的探讨用游离自体腹白线片修补急性十二指肠溃疡穿孔的应用价值。方法从2006年1月至2006年7月对13例用自体腹白线片修补急性十二指肠溃疡穿孔的病人的临床资料和随访情况进行回顾性分析,其中2例穿孔大于2cm2,平均手术时间60分钟,平均失血量20ml,平均住院天数9±1天。结果游离自体腹白线片修补急性十二指肠溃疡穿孔13例均痊愈出院。随访15天至6个月,无手术并发症。结论本方法操作较简单、安全、效果好,其适应症广,是一种可行的新方法。     

Angiopoietin1/Tie2 and VEGF/Flk1 induced by MSC treatment amplifies angiogenesis and vascular stabilization after stroke.

Bone marrow stromal cells (MSCs) increase vascular endothelial growth factor (VEGF) expression and promote angiogenesis after stroke. Angiopoietin-1 (Ang1) and its receptor Tie2 mediate vascular integrity and angiogenesis as does VEGF and its receptors. In this study, we tested whether MSC treatment of stroke increases Ang1/Tie2 expression, and whether Ang1/Tie2 with VEGF/ vascular endothelial growth factor receptor 2 (VEGFR2) (Flk1), in combination, induced by MSCs enhances angiogenesis and vascular integrity. Male Wistar rats were subjected to middle cerebral artery occlusion (MCAo) and treated with or without MSCs. Marrow stromal cell treatment significantly decreased blood-brain barrier (BBB) leakage and increased Ang1, Tie2, and occludin (a tight junction protein) expression in the ischemic border compared with MCAo control. To further test the mechanisms of MSC-induced angiogenesis and vascular stabilization, cocultures of MSCs with mouse brain endothelial cells (MBECs) or astrocytes were performed. Supernatant derived from MSCs cocultured with MBECs significantly increased MBEC expression of Ang1/Tie2 and Flk1 compared with MBEC alone. Marrow stromal cells cocultured with astrocytes also significantly increased astrocyte VEGF and Ang1/Tie2 expression compared with astrocyte culture alone. Conditioned media from MSCs alone, and media from cocultures of MSCs with astrocytes or MBECs, all significantly increased capillary tube-like formation of MBEC compared with control Dulbecco's modified Eagle's medium media. Inhibition of Flk1 and/or Ang1 significantly decreased MSC-induced MBEC tube formation. Knockdown of Tie2 expression in MBECs significantly inhibited MSC-induced tube formation. Our data indicate MSC treatment of stroke promotes angiogenesis and vascular stabilization, which is at least partially mediated by VEGF/Flk1 and Ang1/Tie2.     

Neuropathological study 16 years after autologous adrenal medullary transplantation in a Parkinson's disease patient.

To date, there is no clinicopathological correlation of adrenal medullary transplant cases in patients with survival beyond a few years. Postmortem examination of a brain from a patient with Parkinson's disease (PD), 16 years after autologous adrenal medullary transplant, was performed using tyrosine hydroxylase (TH) and chromogranin A. The patient experienced a four-year initial improvement in motor function followed by resumption of the progressive nature of her disease that continued until her death. She expired 16 years following grafting. At autopsy, TH stain of the brain revealed severe loss of TH-immunoreactivity in the substantia nigra and Lewy bodies, confirming the diagnosis of PD. The transplant site was identified by the presence of scarring and there was complete absence of any TH staining cells at the site of the transplant. There were few surviving cells staining with chromogranin A. The absence of TH-staining cells in the transplant 16 years after surgery provides further evidence that adrenal medullary transplants do not survive in the long term.     

Chronic encapsulated intracerebral haematoma.

We report a rare chronic encapsulated intracerebral haematoma (CEICH). A 52-year-old man had two seizures. Unenhanced computed tomography scanning of the head revealed a hypodense tumour with clusters of calcification in the left temporal lobe. Magnetic resonance imaging of the brain showed a left temporal tumour with a hypointense centre and hyperintense periphery on T(1)-weighted imaging and heterogeneous hypointensity on T(2)-weighted imaging. The tumour was heterogeneously enhanced after gadolinium injection. Craniotomy was carried out and a CEICH in the left temporal lobe was completely excised. No vascular anomaly was found. The tumour was histologically confirmed to be a CEICH. The patient recovered well after the operation. In this report, we describe this rare case and discuss the characteristics of CEICH.     

Protein ubiquitination in postsynaptic densities after transient cerebral ischemia.

The mechanisms underlying neurologic deficits and delayed neuronal death after ischemia are not fully understood. In the present study, we report that transient cerebral ischemia induces accumulation of ubiquitinated proteins (ubi-proteins) in postsynaptic densities (PSDs). By immunoelectron microscopy, we demonstrated that ubi-proteins were highly accumulated in PSD structures after ischemia. On Western blots, ubi-proteins were markedly increased in purified PSDs at 30 minutes of reperfusion, and the increase persisted until cell death in the CA1 region after ischemia. In the resistant DG area, however, the changes were transient and significantly less pronounced. Deposition of ubi-proteins in PSDs after ischemia correlates well with PSD structural damage in the CA1 region as viewed by electron microscopy. These results suggest that the ubiquitin-proteasome system fails to repair and remove damaged proteins in PSDs. The changes may demolish synaptic neurotransmission, contribute to neurologic deficits, and eventually lead to delayed neuronal death after transient cerebral ischemia.     

Reduced expression of CD69 and adhesion molecules of T lymphocytes in asthmatic children receiving immunotherapy

T lymphocytes play a fundamental role in the initiation and regulation of chronic inflammatory responses in patients with asthma. CD69 is an early marker of T‐cell activation. The levels of intercellular adhesion molecule‐1 (ICAM‐1, CD54) and L ‐selectin have been reported to increase in patients with allergic diseases and asthma. The present study was therefore undertaken to investigate the expression of CD69, CD54, and L ‐selectin by T lymphocytes of children with asthma, before and after immunotherapy. Eighteen children newly diagnosed with asthma, 11 good and nine poor responders to immunotherapy, and 16 normal subjects, were enrolled in this study. The percentages of CD69⁺, CD54⁺, and CD62L⁺ cells in T lymphocytes were measured by using flow cytometry. The levels of CD69, CD54, and CD62L in serum and culture supernatants were determined by using enzyme‐linked immunosorbent assay (ELISA). The expression of CD69 and CD54 on CD3⁺ T lymphocytes was significantly higher in children with asthma than in control patients. All the patient groups expressed (spontaneously and following stimulation with phorbol myristate acetate and ionomycin together with mite‐extract proteins) greater amounts of CD69 and CD54 than did control subjects. With long‐term immunotherapy, the percentages of CD69⁺ and CD54⁺ T lymphocytes were significantly lower in patients with a good response to immunotherapy. Our results also showed significantly lower serum L ‐selectin levels following immunotherapy. In conclusion, successful immunotherapy resulted in decreased expression and production of CD69 and CD54. These results may explain, in part, the clinical efficacy of immunotherapy.     

Ureteral obstruction caused by L-asparaginase-induced pancreatitis in a child with acute lymphoblastic leukemia.

L-asparaginase, an effective antileukemia and antilymphoma agent, is toxic to many organ systems. We report a case of ureteral obstruction caused by L-asparaginase via the inflammatory complication of acute pancreatitis. The patient was an 11-year-old boy with acute lymphoblastic leukemia. Six days after completing a 4-week induction therapy containing 9 doses of L-asparaginase, severe left abdominal pain developed. Abdominal computed tomography showed phlegmon formation anterior to the pancreatic head and in the left posterior pararenal space. The strands of inflammatory soft tissues encased the upper third of the left ureter, causing left hydroureter and left hydronephrosis. The ureteral obstruction resolved after insertion of a double-J catheter that remained in place for 66 days. This case suggests that L-asparaginase may play a role in the pathogenesis of ureteral obstruction in children receiving chemotherapy.