[Hepatic echinococcus granulosus: a clinicopathological analysis of thirteen cases].

Objective: To investigate the clinicopathologic characteristics of hepatic echinococcus granulosus (HEG). Methods: Thirteen cases of HEG were collected from Linzhi People's Hospital between January 2017 to October 2020, and their clinicopathologic features, ultrasound classification, immunophenotype and histochemical data were analyzed, retrospectively and the relevant literature was reviewed. Results: Thirteen patients (5 male patients, 8 female patients) were included in this cohort, and the mean age was 40 years. The most common clinical presentation was mild abdominal distention and pain (9/13). Based on WHO-IWGE ultrasound standardized classification, these cases were classified into 5 types, including type CL (1 case), type CE1 (2 cases), type CE2 (4 cases), type CE3 (3 cases) and type CE4 (3 cases). Gross examination revealed a solitary cyst localized in the liver, varying from 2.7 to 13.5 cm in diameter, and most of them(10/13)were more than 10 cm. Histopathologically, these cysts possessed a thin inner germinal layer and outer adventitial layer, and a central cavity filled with a clear"hydatid"fluid. The germinal layer was continuous and generated brood capsules and protoscoleces. The laminated membranes were clearly demonstrated by elastic fiber and Gomori's stains. Inside the"mother"cyst, there were a varying number of"daughter"vesicles of variable sizes. The inflammatory reaction around the cyst consisted of eosinophils, mononuclear cells immediately next to the cyst layer and sometimes formed granuloma and giant cells resembling the Langhan's type giant cells. The lymphoid cells were positive for CD20 and CD3. The CD68 immunohistochemistry clearly demonstrated epithelioid cells of granuloma in two cases. Moreover, immunohistochemistry revealed plasma cells were locally positive for CD38, IgG and IgG4, but not meeting the criteria for IgG4 related lesion. Conclusions: Hepatic echinococcus granulosus is a zoonotic parasitic disease prevalent in pastoral areas such as Tibet. It is important to understand its clinical features, ultrasound characteristics and histological morphology.

[Expression and clinical significance of moesin and E-cadherin in invasive carcinoma of breast, no specific type].

OBJECTIVE: To investigate the correlation of moesin and E-cadherin with biological behavior of breast cancer and its mechanism by comparing expression of moesin and E-cadherin in breast invasive carcinoma of no specific type(BIC-NST), breast ductal carcinoma in situ(BDCIS) and normal breast tissues adjacent to carcinoma. METHODS: Breast cancer cases of the Huizhou Municipal Center People Hospital were collected between Jan 2008 and Dec 2010, expression of moesin and E-cadherin in 104 cases of BIC-NST, 84 cases of BDCIS and 53 cases of normal breast tissues adjacent to carcinoma were detected by tissue-microarray and SP immunohistochemical staining. Western blot was used to detect moesin expression of 16 BIC-NST fresh tissues. RESULTS: Expression rate of moesin in BIC-NST and BDCIS were significantly higher than normal tissues(P<0.01), but the expression rate of E-cadherin in BIC-NST and BDCIS were significantly lower than those of normal tissues(P<0.01). Expression rate of moesin in BIC-NST grade Ⅲ group was significantly higher than that of the grade Ⅰ group.There was a significantly positive correlation between histological grade and moesin expression(P<0.05). However, E-cadherin expression rate in BIC-NST grade Ⅲ group was significantly lower than that in grade Ⅰ group , and there was a significantly negative correlation between histological grade and E-cadherin expression(P<0.05). Moreover, no significant correlation was observed between moesin and E-cadherin expression in BDCIS tissues. Expression of moesin in clinical stage Ⅱ + Ⅲ BIC-NST was significantly higher than that in stage Ⅰ(P<0.01) . Expression of moesin was significantly associated with lymph node metastasis (P<0.01). But no significant correlation was observed between moesin expression and age, tumor size and vascular invasion . However, expression of E-cadherin in clinical stage Ⅱ+ Ⅲ BIC-NST was significantly lower than that in stage Ⅰ(P<0.01). Expression of E-cadherin was significantly associated with lymph node metastasis and vascular invasion (P<0.01). But no significant correlation was observed between E-cadherin expression, age and tumor size. There was a negative correlation between expression of moesin and E-cadherin in BIC-NST(P=0.021)and BDCIS(P=0.032). CONCLUSION: Higher moesin and lower E-cadherin signal transduction is closely related to the recurrence and development of breast carcinoma, therefore moesin and E-cadherin might provide new targets for gene therapy in breast carcinoma.

Individualization of transfer function in estimation of central aortic pressure from the peripheral pulse is not required in patients at rest.

Central aortic pressure gives better insight into ventriculo-arterial coupling and better prognosis of cardiovascular complications than peripheral pressures. Therefore transfer functions (TF), reconstructing aortic pressure from peripheral pressures, are of great interest. Generalized TFs (GTF) give useful results, especially in larger study populations, but detailed information on aortic pressure might be improved by individualization of the TF. We found earlier that the time delay, representing the travel time of the pressure wave between measurement site and aorta is the main determinant of the TF. Therefore, we hypothesized that the TF might be individualized (ITF) using this time delay. In a group of 50 patients at rest, aged 28-66 yr (43 men), undergoing diagnostic angiography, ascending aortic pressure was 119 +/- 20/70 +/- 9 mmHg (systolic/diastolic). Brachial pressure, almost simultaneously measured using catheter pullback, was 131 +/- 18/67 +/- 9 mmHg. We obtained brachial-to-aorta ITFs using time delays optimized for the individual and a GTF using averaged delay. With the use of ITFs, reconstructed aortic pressure was 121 +/- 19/69 +/- 9 mmHg and the root mean square error (RMSE), as measure of difference in wave shape, was 4.1 +/- 2.0 mmHg. With the use of the GTF, reconstructed pressure was 122 +/- 19/69 +/- 9 mmHg and RMSE 4.4 +/- 2.0 mmHg. The augmentation index (AI) of the measured aortic pressure was 26 +/- 13%, and with ITF and GTF the AIs were 28 +/- 12% and 30 +/- 11%, respectively. Details of the wave shape were reproduced slightly better with ITF but not significantly, thus individualization of pressure transfer is not effective in resting patients.

Nickel oxide nanoparticles induced pulmonary fibrosis via TGF- ß1 activation in rats.

Nano nickel oxide (NiO), widely used in industry, has recently been discovered to have pulmonary toxicity. However, no subchronic exposure studies about nano NiO-induced pulmonary fibrosis have been reported. The objective of this study was to investigate pulmonary fibrosis induced by nano NiO and its potential mechanism in rats. Male Wistar rats ( n = 40, 200-240 g) were randomized into control group, nano NiO groups (0.015, 0.06, and 0.24 mg/kg), and micro NiO group (0.024 mg/kg). All rats were killed to collect lung tissue after intratracheal instillation of NiO particles twice a week for 6 weeks. To identify pulmonary fibrosis, Masson trichrome staining, hydroxyproline content, and collagen protein expression were performed. The results showed widespread lung fibrotic injury in histological examination and increased content of hydroxyproline, collagen types I and III in rat lung tissue exposed to nano NiO. To explore the potential pulmonary fibrosis mechanism, transforming growth factor beta 1 (TGF- ß1) content was measured by enzyme-linked immunosorbent assay, and the messenger RNA expression of key indicators was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The TGF- ß1 content was increased in nano NiO exposure groups, as well as the upregulated gene expression of TGF- ß1, Smad2, Smad4, matrix metalloproteinase, and tissue inhibitor of metalloproteinase. The findings indicated that nano NiO could induce pulmonary fibrosis, which may be related to TGF- ß1 activation.

Association of Epstein-Barr virus with lymphoepithelioma-like carcinoma of the lung in southern China.

Having reviewed the data on 3,663 consecutive cases of primary lung carcinoma in southern China, we found that 32 cases could meet the criteria for lymphoepithelioma-like carcinoma (LELC) of the lung. To study the relationship between pulmonary LELC and Epstein-Barr virus (EBV) infection, we used in situ hybridization and immunohistochemistry techniques to detect the EBV-encoded small nonpolyadenylated RNA (EBER), latent membrane protein 1 (LMP1), and viral capsid antigen (VCA) in 32 cases of LELC and 19 cases of non-LELC lung carcinoma. Of the 32 cases, 30 (94%) showed EBER positivity. Of the 30 EBER-positive pulmonary LELC cases, 16 and 7 expressed LMP1 and VCA, respectively. In contrast with LELC, none of the 19 cases of non-LELC lung carcinoma showed EBER-, LMP1-, or VCA-positive signals in carcinoma cells. The results demonstrate that there is a close relationship between EBV infection and pulmonary LELC. EBV infection may have an essential role in the tumorigenesis of pulmonary LELC. EBV latent infection is the main status in pulmonary LELC except for individual EBV entering into a lytic cycle.

Lymphoepithelioma-like carcinoma of the lung with a better prognosis. A clinicopathologic study of 32 cases.

The purpose of our study was to clarify the prognosis of lymphoepithelioma-like carcinoma (LELC) of the lung, which is rare. We analyzed the clinicopathologic features of 32 cases of pulmonary LELC and compared the cases with 84 cases of pulmonary non-LELC with available long-term follow-up information. The results show that LELC of the lung as a distinct entity has a better prognosis than non-LELC. We found a significant difference in the survival rates between patients with LELC and patients with non-LELC in stage II and stages III and IV, respectively. Tumor recurrence and necrosis (5% or more of tumor) are associated with a poor prognosis. It seems that the histologic typing (Regaud type and Schmincke type) of pulmonary LELC is of no clinical value.

[Gene chip technology and its advances in medical science].

Gene (DNA) chip or DNA microarray is a new technique developed during human genomic research programs. When DNA chip containing thousands of DNA or oligonucleotide are hybridized to labeled samples, gene expression, DNA sequencing as well as DNA mutation and polymorphism can be analyzed with high efficiency in large scale. We are able to perform this technique on dozens of specimens at once in tumor differentiation, tumor typing, tumor diagnosis, tumorigenesis, and new tumor-associated genes discovery.

[Primary giant cell malignant fibrous histiocytoma of the lung].

A case of primary giant cell malignant fibrous histiocytoma (MFH) of the lung was reported. Gross findings showed two well demarcated isolated nodules located in the right lower lobe of the lung appeared yellowish-gray and gray-red on gross section with areas of focal calcifications, hemorrhage and necrosis. Microscopic findings showed that the tumor consisted of diffuse neoplastic histiocytes and spindle-shaped fibroblasts arranged in a prominent storiform pattern intermingled with numerous multinucleated tumor giant cells and osteoclast-like multinucleated giant cells. Focal osteoid tissue was mainly located at the periphery of the tumor. In addition, a number of scattered apoptotic multinucleated giant cells were observed. Tumor cells were positive for vimentin, alpha-1-antitrypsin, lysozyme and mac387, but negative for cytokeratin, actin, S-100, NSE, and NF. Primary giant cell MFH of the lung is a very rare malignant tumor. This tumor should be treated by prompt radical surgery.