Intraperitoneal tuberculous abscess: computed tomography features

AIM: To evaluate the computed tomography(CT) features of intraperitoneal tuberculous abscess(IPTA). METHODS: Eight patients with IPTA confirmed by pathology were analyzed retrospectively. The clinical symptoms, medical images, and surgical findings were evaluated. Involvement of the intestine, peritoneum, viscera, and lymph nodes was also assessed. RESULTS: All 8 patients had a history of abdominal discomfort for 1 to 6 mo. Physical examination revealed a palpable abdominal mass in 6 patients. Three patients had no evidence of pulmonary tuberculosis(TB). All IPTAs(11 abscesses) were seen as a multiseptated, peripherally enhanced, hypodense mass with enlarged, rim-enhanced lymph nodes. The largest abscess diameter ranged from 4.5 cm to 12.2 cm. CT showed 2 types of IPTA: Lymph node fusion and encapsulation. Of the 8 patients, one had liver tuberculosis and one had splenic and ovarian tuberculosis. Two cases showed involvement of the terminal ileum and ileocecal junction. Ascites were found in 4 cases. Three patients had peritonitis and mesenteritis. Three patients showed involvement of the omentum. Three patients had histological evidence of caseating granuloma, and 5 had histological evidence of acid-fast bacilli. CONCLUSION: CT is crucial in the detection and characterization of IPTA. Certain CT findings are necessary for correct diagnosis.

A mutated CRYGD associated with congenital coralliform cataracts in two Chinese pedigrees

AIM:To investigate the causal gene mutation and clinical characteristics for two Chinese families with autosomal dominant congenital coralliform cataract.METHODS:Two Chinese pedigrees with congenital cataract were investigated.Routine ophthalmic examinations were performed on all patients and non-affected family members.Peripheral blood samples were collected,and the genomic DNAs were extracted.The coding regions of proband’s DNAs were analyzed with cataract gene panel.The identified mutation was amplified by polymerase chain reaction,and automated sequencing was performed in other members of two families to verify whether the mutated gene was co-segregated with the disease.RESULTS:Congenital coralliform cataract was inherited in an autosomal dominant mode in both pedigrees.For each family,more than half of the family members were affected.All patients presented with severe visual impairment after birth as a result of bilateral symmetric coralliform lens opacification.An exact the same defect in the same gene,a heterozygous mutation of c.70 C>A(p.P24 T)in exon 2 of γ Dcrystallin gene,was detected in both probands from each family.Sanger sequencing analysis demonstrated that the mutated CRYGD was co-segregated in these two families.CONCLUSION:A c.70 C>A(p.P24 T)variant in CRYGD gene was reconfirmed to be the causal gene in two Chinese pedigrees.It is known that mutated CRYGD caused most of the congenital coralliform cataracts,suggesting that the CRYGD gene is associated with coralliform congenital cataract.

Evaluation of trabecular meshwork-specific promoters in vitro and in vivo using scAAV2 vectors expressing C3 transferase

AIM:To evaluate the potential of two trabecular meshwork(TM)-specific promoters,Chitinase 3-like 1(Ch3L1)and matrix gla protein(MGP),for improving specificity and safety in glaucoma gene therapy based on self-complementary AAV2(scAAV2)vector technologies.METHODS:An scAAV2 vector with C3 transferase(C3)as the reporter gene(scAAV2-C3)was selected.The scAAV2-C3 vectors were driven by Ch3L1(scAAV2-Ch3L1-C3),MGP(scAAV2-MGP-C3),enhanced MGP(scAAV2-eMGP-C3)and cytomegalovirus(scAAV2-CMV-C3),respectively.The cultured primary human TM cells were treated with each vector at different multiplicities of infections.Changes in cell morphology were observed by phase contrast microscopy.Actin stress fibers and Rho GTPases/Rho-associated protein kinase pathway-related molecules were assessed by immunofluorescence staining,real-time quantitative polymerase chain reaction and Western blot.Each vector was injected intracamerally into the one eye of each rat at low and high doses respectively.In vivo green fluorescence was visualized by a Micron III Retinal Imaging Microscope.Intraocular pressure(IOP)was monitored using a rebound tonometer.Ocular responses were evaluated by slit-lamp microscopy.Ocular histopathology analysis was examined by hematoxylin and eosin staining.RESULTS:In TM cell culture studies,the vectormediated C3 expression induced morphologic changes,disruption of actin cytoskeleton and reduction of fibronectin expression in TM cells by inhibiting the Rho GTPases/Rhoassociated protein kinase signaling pathway.At the same dose,these changes were significant in TM cells treated with scAAV2-CMV-C3 or scAAV2-Ch3L1-C3,but not in cells treated with scAAV2-eMGP-C3 or scAAV2-MGP-C3.At lowinjected dose,the IOP was significantly decreased in the scAAV2-Ch3L1-C3-injected eyes but not in scAAV2-MGPC3-injected and scAAV2-eMGP-C3-injected eyes.At highinjected dose,significant IOP reduction was observed in the scAAV2-eMGP-C3-injected eyes but not in scAAV2-MGP-C3-injected eyes.Similar to scAAV2-CMV-C3,scAAV2-Ch3L1-C3 vector showed efficient transduction both in the TM and corneal endothelium.In anterior segment tissues of scAAV2-eMGP-C3-injected eyes,no obvious morphological changes were found except for the TM.Inflammation was absent.CONCLUSION:In scAAV2-transduced TM cells,the promoter-driven efficiency of Ch3L1 is close to that of cytomegalovirus,but obviously higher than that of MGP.In the anterior chamber of rat eye,the transgene expression pattern of scAAV2 vector is presumably affected by MGP promoter,but not by Ch3L1 promoter.These findings would provide a useful reference for improvement of specificity and safety in glaucoma gene therapy using scAAV2 vector.