[Expression of NK cells receptor NKG2D from peripheral blood in patients with primary hepatic carcinoma and its clinical significance].

OBJECTIVE: To investigate the expression of NK cells receptor NKG2D from peripheral blood in patients with primary hepatic carcinoma and the relationship between NKG2D expression and cytotoxicity of NK cells. METHODS: Flow cytometry was used to determine the number of NK cells and the expression of NK cells receptor NKG2D from peripheral blood in patients with primary hepatic carcinoma (20 cases), hepatitis B cirrhosis (23 cases), hepatitis B (20 cases) and healthy control (20 cases). The microplate reader was used to detect cytotoxicity of NK cells in all cases. RESULTS: Among killing rate of NK cell for K562 cell, the expression rate of NKG2D in NK cells, the number of NKG2D(+)NK cells, NKG2D expression level of NK cells and the number of NK cells, the liver cancer group [(25 +/- 7)%, 6%, 0.7 x 10(7)/L, 15, (1.1 +/- 0.6) x 10(8)/L] decreased significantly as compared with the healthy group [(63 +/- 7)%, 36%, 8.3 x 10(7)/L, 116, (2.7 +/- 1.1) x 10(8)/L] and the hepatitis B group [(41 +/- 8)%, 16%, 2.8 x 10(7)/L, 49, (1.9 +/- 1.1) x 10(8)/L] (P < 0.05); and there was a slight decrease as compared with the hepatitis B cirrhosis group [(29 +/- 10)%, 7%, 0.6 x 10(7)/L, 29, (1.5 +/- 1.2) x 10(8)/L] (all P > 0.05 except NKG2D expression level of NK cells P < 0.05). The activity of NK cells showed a obvious positive correlation with the number of NK cell and the positive rate of NKG2D in NK cells, the number of NKG2D(+)NK cells and NKG2D expression level of NK cells (r = 0.657, 0.770, 0.927, 0.734, all P < 0.01). CONCLUSION: The cytotoxicity and the NKG2D expression of NK cells decreased significantly from peripheral blood in patients with primary hepatic carcinoma. The activity of NK cells was closely related to the NKG2D expression level of NK cells. Enhancing the NKG2D expression level of NK cell may provide a new idea for adoptive immunotherapy of primary hepatic carcinoma.

Zinc oxide nanoparticles inhibit murine photoreceptor-derived cell proliferation and migration via reducing TGF-ß and MMP-9 expression in vitro.

OBJECTIVES: To investigate behaviour and expression of transforming growth factor-ß (TGF-ß) and matrix metalloproteinases (MMP-9) in murine photoreceptor-derived cells (661W) after incubation with zinc oxide (ZnO) nanoparticles. MATERIALS AND METHODS: We explored effects of ZnO nanoparticles on 661W cells using a real-time cell electronic sensing system, flow cytometry, multiple function microplate reading, real-time quantitative PCR detection system and enzyme-linked immunosorbent assay respectively. RESULTS: Our results indicate that ZnO nanoparticles induced overload of calcium and reactive oxygen species within cells, causing formation of apoptotic bodies, disruption of cell cycle distribution, and reduction in expression of TGF-ß and MMP-9, to suppress cell proliferation and migration. Our findings show that disruption of intracellular calcium homoeostasis and overproduction of reactive oxygen species were closely associated with reduction of TGF-ß and MMP-9 in 661W cells under ZnO nanoparticle treatment. CONCLUSIONS: Results of our study indicate that ZnO nanoparticles suppressed cell proliferation and migration, and reduced production of TGF-ß and MMP-9 at both gene and protein levels. Our findings contribute to the understanding of the molecular mechanisms that reduced TGF-ß and MMP-9 levels inhibit cell proliferation and migration under ZnO nanoparticle influence.

piRNA, the new non-coding RNA, is aberrantly expressed in human cancer cells.

BACKGROUND: Piwi-interacting RNAs (piRNAs) are a novel class of non-coding single strand RNAs. They are involved in germline development, in silencing of selfish DNA elements, and in maintaining germline DNA integrity. The relationship between piRNAs and carcinogenesis has not been shown yet. METHODS: The relationship between piRNAs and carcinogenesis was identified by microarray screening and real-time quantitative reverse transcription-polymerase chain reaction technology. The piR-651 inhibitor was transfected into gastric cancer cells to assess its influence on cell growth. Cell cycle analysis was used to reveal the cellular mechanisms of piR-651 in the genesis of gastric cancer. RESULTS: piR-651 expression was upregulated in gastric cancer tissues compared with paired non-cancerous tissues. The levels of piR-651 were associated with TNM stage (P=0.032). The expression of piR-651 in gastric, colon, lung, and breast cancer tissues was higher than that in paired non-cancerous tissues. The upregulated expression of piR-651 was confirmed in several cancer cell lines including gastric, lung, mesothelium, breast, liver, and cervical cancer cell lines. The growth of gastric cancer cells was inhibited by a piR-651 inhibitor and arrested at the G(2)/M phase. CONCLUSION: piR-651 might be involved in the development of gastric cancer and other cancers, and is a potential marker for cancer diagnosis.

[Treatment of congenital hypertrophic pyloric stenosis with endoscopic pyloromyotomy].

OBJECTIVE: To evaluate the effect of the treatment of congenital hypertrophic pyloric stenosis (CHPS) with endoscopic pyloromyotomy. METHOD: Nine consecutive infants (7 boys, 2 girls; age range 26 - 70 days; weight range 2.65 - 6.10 kg), with a diagnosis of CHPS according to typical clinical manifestations, transabdominal ultrasound (US), gastroenterography and gastroscope. All the cases had accompanying malnutrition, anaemia, metabolic alkalosis, and some were complicated with congenital heart disease. In gastroscope operating room, all the patients were given pentobarbital and midazolam intravenously. A gastroscope with an outer diameter of 5.9 mm was passed through mouth, stomach, pylorus to the descending segment of duodenum. Under gastroscopy, two incisions were made along the anterior and posterior wall of pylorus from the duodenal bulb to the antrum by using endoscopic electrosurgical needle knife and an arch sphincter sarcosome. Incisions were deepened by 2 to 3 procedures until the longitudinal muscle was exposed, about 2 to 4 mm according to transabdominal US performed before operation. The incision depth was 2 - 3 mm if pylorus wall was 4 - 6 mm in thickness; or 3 - 4 mm when the wall was thicker than 6 mm. RESULT: The endoscope was easily passed through the pylorus to the duodenum post-operation. The transabdominal US and gastroenterography showed that liquid easily flew through pylorus. All patients were able to have regular feeding about 2 to 10 hours after the operation. Vomiting in all patients was significantly decreased in frequency and amount, and in 8 infants vomiting stopped within 1 week, in one case it did not stop until 1 month after the treatment. Some cases showed slight adverse reaction, no perforation or massive haemorrhage in stomach or intestines occurred in any of the patients during and post-operation. Eight infants were doing well at follow-up (range 2 to 9 months). One girl had recurred vomiting at normal feeding after a period of 1 month postoperation without vomiting. This case was cured by second endoscopic pyloromyotomy. CONCLUSIONS: Endoscopic pyloromyotomy is effective, safe, simple, and offers several advantages: no need for open-abdomen surgery, feeding can be initiated rapidly.