Child inflammatory myofibroblastic tumor of the kidney misdiagnosed as Wilms' tumor: case report.

Inflammatory myofibroblastic tumor (IMT) is a rare mesenchymal tumor with recurrent potential, most commonly occurring in the lung but rarely in the kidney with nonspecific clinical symptoms and radiographic features, thus may be misdiagnosed as primary malignant lesions. We described a 6-year-old boy with renal IMT misdiagnosed as Wilms' tumor and then treated with right nephrectomy. It should be emphasized that in addition to the most common renal tumors in children, IMT should also be taken as a differential diagnosis. It is therefore mandatory to carry out clinical interpretation, careful histologic examination, and immunohistochemical studies collectively to make solid diagnosis.

Asymptomatic adult Wilms' tumor: A case report.

Wilms' tumor, also called nephroblastoma, is an extremely uncommon kidney tumor of adulthood. We reported a adult man with a left kidney mass diagnosed as Wilms' tumor. Case presentation: A 25-year-old man was hospitalized due to injury of the anterior cruciate ligament of the right knee. Preoperative imaging accidentally revealed a mass measuring 53 × 46 mm involving the middle and lower segments of the left kidney without evidence supporting the invasion of the surrounding structures or metastasis. The patient didn't show any symptom commonly occurred in Wilms' tumor, such as flank pain or hematuria. After nephrectomy, the diagnosis of adult Wilms' tumor was confirmed based on the tumor morphology and immunohistochemical findings. Conclusion: In adult patients without any clinical manifestations or favorable imaging findings for low-stage renal cell carcinoma, the diagnosis of Wilms' tumor should be taken into consideration.

Computed Tomography and Magnetic Resonance Imaging Appearances of Abdomen and Pelvis Gossypibomas at the Varied Durations After Cesarean Section.

The incidence of gossypiboma is considerably higher in open cavity surgeries, among which cesarean section ranks number one. However, it is difficult to diagnose abdomen or pelvic gossypibomas after cesarean section. We retrospectively analyzed the clinical and imaging data of three pathologically confirmed gossypiboma patients at varied durations after cesarean section. In case one, at four months after cesarean section, a gossypiboma near the small intestine caused fistula and intestinal obstruction. Soft tissue density lesion along the intestinal canal made the "segmental honeycomb sign" and "truncation" with metal markings on the edge on computed tomography (CT). Magnetic sensitivity artifacts were demonstrated as hypointensity on T1 weighted image (T1WI) and T2 weighted image (T2WI), while hyperintensity was seen on the diffusion weighted image (DWI). In case two, a gossypiboma in the peritoneal and intestinal space was revealed with MRI at 18 months after cesarean section. It was featured as a cystic and solid lesion, with "vortex like sign" and obvious ring enhancement on contrast-enhanced MRI scan. In case three, five years after cesarean section, a mass was palpated in the right middle and lower abdomen. MRI revealed a round mass of T1 hypointensity with mixed T2 signal, as well as swirling hypointensity in T2WI, T2WI-fat suppression (FS), and DWI. In CT and MRI examinations for suspected gossypiboma after cesarean section, "honeycomb sign" and "vortex like sign" are the characteristic appearances; gauze translocated into the intestine may show the "truncation sign". Accurate diagnosis is based on the surgery history, symptoms, and imaging features.

Cytosine 5-hydroxymethylation regulates VHL gene expression in renal clear cell carcinoma.

Cytosine5-hyxymethylation (5hmC)which is a new epigenetic modification form plays important roles in the development and progression of tumors. In the present study, we observed that levels of 5hmC in the promoter region of Von Hippel-Lindau (VHL) were lower in 97 samples of renal clear cell carcinoma tissue than in matched adjacent benign tissues. Moreover, when the cancer tissue samples were divided based on pathological staging, VHL expression and the level of 5hmC in the VHL promoter were both lower in pathological grade III tumors than in grades I or II. Correspondingly, expression of TET1, which catalyzes the formation of 5hmC, was also lower in grade III renal clear cell carcinomas than in grade I or II disease. These findings suggest the 5hmC level on VHL is a key determinant of the gene's expression and may participate in the occurrence and development of renal clear cell carcinoma. Thus the 5hmC level may be a useful indicator for early diagnosis and appropriate treatment of renal clear cell carcinoma.

TGF-beta1 reverses inhibition of COX-2 with NS398 and increases invasion in prostate cancer cells.

Bone-derived transforming growth factor (TGF)-beta1 leads to tumor growth, osteoblastic lesions and more invasion. Degradation of basement membranes caused by cyclooxygenase (COX)-2 is known as a distinctive feature of invasive cells. We investigated inhibition of COX-2 with NS398 in PC-3 and LNCaP cell lines. TGF-beta1 and dmPGE2 were added in NS398 treated or untreated cells. COX-2 did not express in PC-3, after treatment with TGF-beta1, COX-2 appeared and accompanied with enhanced invasion. COX-2 expressed in LNCaP, undetectable after addition of NS398 along with decreased invasion. Addition of TGF-beta1 reversed inhibition of NS398 in both cell lines. DmPGE2 augmented invasion in both cell lines without alteration of COX-2. These results suggest that TGF-beta1 can increase invasion and reverse inhibition of COX-2 induced by NS398. We indicate that bone-derived TGF-beta1 might contribute to clinical unsatisfied effect of NSAIDs or COX-2 specific inhibitors adjuvant therapies. Our data provide a new potential therapy for fighting against prostate cancer.

[Cigarette smoking affects cyclogeny of spermatogenic cells in rats].

OBJECTIVE: To determine the effects of cigarette smoking on the cyclogeny of spermatogenic cells in rats. METHODS: Rat models of passive smoking were established using a self-made smoking device, and then allocated randomly into two passive smoking groups (A and B, n = 10) and two corresponding control groups (C and D, n = 10). Groups A and B were exposed to cigarette smoke for 8 weeks, followed by the sacrifice of the rats in Groups A and C. And the animals in Groups B and D were killed 48 days after the cessation of passive smoking. The spermatogenesis cycle of each group of rats was detected by flow cytometry, the levels of testosterone (T) and luteinizing hormone (LH) measured by radio-immunity method, and the testis histopathology analyzed by HE staining and transmission electron microscopy. RESULTS: Compared with Group C, Group A showed a significant decrease in the number of spermatids, spermatozoa ([18.76 +/- 3.58]%) and primary spermatocytes ([5.71 +/- 1.18]%) (P < 0.01), but an obvious increase in the spermatogonias ([55.98 +/- 5.35]%, P < 0.01), with a markedly decreased proliferation index ( P < 0.01). The rats of Group A also exhibited pycnosis of spermatocytes, nucleus aberration of Leydig cells, expansion and degranulation of the endoplasmic reticulum, decreased Golgi apparatus, increased lysosomes and fat drops of Sertoli cells, as well as a reduction in the thickness of the wall and the layers of seminiferous tubules and the number of spermatogonia. The T and LH levels were significantly lower in Group A than in C (P < 0.01). After the cessation of passive smoking, a remarkable increase was observed in the percentage of spermatozoa and primary spermatocytes and the levels of serum T and LH in Group B, although the latter were still lower than those of Group D. CONCLUSION: Smoking damages spermatogenic epithelia, Leydig cells and Sertoli cells, reduces the T and LH levels, and block the proliferation of spermatogenetic cells. These changes can be partially reversed after cessation of smoking.

Expressions of voltage-gated K+ channel 2.1 and 2.2 in rat bladder with detrusor hyperreflexia.

BACKGROUND: Voltage-gated K+ channel (Kv) plays a critical role in the modulation of detrusor contraction. This study was conducted to investigate the expressions of Kv2.1 and Kv2.2 in rat bladder with detrusor hyperreflexia (DH). METHODS: Thirty adult female Sprague-Dawley rats (200-220 g) were randomly divided into the control group and the experimental group. The experimental group was subjected to spinal cord injury (SCI). In the controls, the surgical procedure was identical with the exception that dura and spinal cord were transected. Four weeks after SCI, in vivo cystometry and mechanical pulling tests of isolated detrusor strips were performed. mRNA was extracted from the detrusors of normal and DH rats for the detection of expression of Kv2.1 and Kv2.2 by RT-PCR. Differences in expression between normal and overactive detrusors were identified by gel imaging. RESULTS: Fourteen rats in the experimental group exhibited uninhibited bladder contraction (>8 cmH2O) before voiding after SCI. One rat died from infection. The frequency of DH in the experimental group was significantly different from that in the control group with or without treatment with 4-aminopyridine (4-AP) (P < 0.05), while the amplitude of DH did not change markedly. The rates of variation of the automatic contractile frequency and amplitude were (66.8 +/- 12.4)% and (42.6 +/- 12.6)% respectively in the control group, and (38.4 +/- 9.8)% and (28.0 +/- 4.6)% respectively in the DH group. 4-AP increased the automatic contractile frequency apart from the automatic contractile amplitude in both the control and DH groups (P < 0.05). 4-AP increased the rate of variation of the automatic contractile frequency more markedly in the control group than in the DH group (P < 0.05). Significant expression of Kv2.2 was not detected in bladders in the control group. Compared to the mRNA levels of beta-actin, the mRNA level of Kv2.1 was 1.26 +/- 0.12 in the control group and 0.66 +/- 0.08 in the DH group. SCI significantly reduced the mRNA level of Kv2.1 in rat bladders with DH (P < 0.05). CONCLUSIONS: Our study showed that the mRNA level of Kv2.1 decreased significantly in rat bladder with DH, which was one of the important pathogenetic mechanisms for DH, and suggested that Kv2.1 might be one of the therapeutic targets for bladder overactivity.