We analyzed mutations and gene copy number changes in nontumor, IEN, and ESCC samples, collected from 70 patients. IEN and ESCCs each had similar mutations and markers of genomic instability, including apolipoprotein B messenger RNA editing enzyme, catalytic polypeptide-like. Genomic changes observed in precancerous lesions might be used to identify patients at risk for ESCC.

Involving the fathers in breastfeeding education could improve the exclusive breastfeeding rate and prolong the duration of exclusive breastfeeding. The mothers appreciated support from the fathers.

BackgroundLoss of STAT1 (Signal Transducer and Activator of Transcription-1) has been implicated in the pathobiology of a number of cancer types. Nonetheless, the biological and clinical significance of STAT1 in esophageal squamous cell carcinomas (ESCC) has not been comprehensively studied.MethodsUsing immunohistochemistry, we detected the STAT1 expression in a cohort of ESCC patients; In-vitro experiments, we used enforced gene transfection of STAT1C into two STAT1- weak/negative ESCC cell lines and siRNA knockdown of STAT1 in two STAT1-strong ESCC cell lines to detect STAT1 function in ESCC.ResultsWe found that the expression of STAT1 was heterogeneous in ESCC, with 64 (49.0%) strongly positive cases, 59 (45.0%) weakly positive cases and 8 (6.1%) negative cases. STAT1 expression inversely correlated with the depth of tumor invasion and tumor size (p=0.047 and p=0.029, respectively, Chi square). Furthermore, patients with STAT1-strong/weak tumors had a significantly longer survival compared to those with STAT1-negative tumors (33.6 months versus 13.1 months, p=0.019). In patients carrying tumors of aggressive cytology (n=50), those with STAT1-strong tumors survived significantly longer than those with STAT1-weak/negative tumors (34.6 months versus 20.5 months, p=0.011). Our in-vitro experiments revealed that STAT1 is proapoptotic and inhibitory to cell-cycle progression and colony formation. Lastly, we found evidence that STAT1 signaling in ESCC cells down-regulated the expression and/or activity of NF-κB and STAT3, both of which are known to have oncogenic potential.ConclusionTo conclude, our findings suggest that STAT1 is a tumor suppressor in ESCC. Loss of STAT1, which is frequent in ESCC, contributes to the pathogenesis of these tumors.

ObjectivesThe purpose of our study is to investigate whether diffusion-weighted imaging (DWI) is useful for monitoring the therapeutic response after neoadjuvant chemotherapy in osteosarcoma of long bones.Materials and methodsConventional magnetic resonance imaging (MRI) and DWI were obtained from 35 patients with histologically proven osteosarcomas. MR examinations were performed in all patients before and after 4 courses of preoperative neoadjuvant chemotherapy. Apparent diffusion coefficients (ADC) were measured. The degree of tumor necrosis was assessed macroscopically and histologically by two experienced pathologists after operation. Student’s t test was performed for testing changes in ADC value. Pearson’s correlation coefficient was used to estimate the correlation between necrosis rate and post- neoadjuvant chemotherapy ADC values. P<0.05 was considered to denote a significant difference.ResultsThe difference of the whole osteosarcoma between pre- neoadjuvant chemotherapy ADC value (1.24±0.17×10−3 mm2/s) and post- (1.93±0.39×10−3 mm2/s) was significant difference (P<0.01). Regarding in patients with good response, the post- neoadjuvant chemotherapy values were significantly higher than the pre- neoadjuvant chemotherapy values (P<0.01). The post- neoadjuvant chemotherapy ADC value in patients with good response was higher than that of poor response (t = 8.995, P<0.01). The differences in post- neoadjuvant chemotherapy ADC between viable (1.03±0.17×10−3 mm2/s) and necrotic (2.38±0.25×10−3 mm2/s) tumor was highly significant (t = 23.905, P<0.01). A positive correlation between necrosis rates and the whole tumor ADC values (r = 0.769, P<0.01) was noted, but necrosis rates were not correlated with the ADC values of necrotic (r = −0.191, P = 0.272) and viable tumor areas (r = 0.292, P = 0.089).ConclusionsDWI can identify residual viable tumor tissues and tumor necrosis induced by neoadjuvant chemotherapy in osteosarcoma. The ADC value can directly reflect the degree of tumor necrosis, and it is useful to evaluate the preoperative neoadjuvant chemotherapy response in patients with osteosarcoma.

Evidence has shown that mild therapeutic hypothermia (MTH) could improve survival and neurological outcome in patients following cardiac arrest. But this therapy may cause some adverse effects. The authors sought to take a systematic approach to describe the safety aspects and outcome of MTH following cardiac arrest to help clinical practice. MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials, BIOSIS Previews and clinicaltrials.gov were searched up to June 2011. Bibliographies of relevant studies were also reviewed. Comparative studies reporting the mortality or any other studies reporting any kind of adverse events in patients undergoing MTH after cardiac arrest and published in English were included. Of 1742 abstracts, 63 studies were included. Most adverse events potentially associated with therapeutic hypothermia were not significantly different between the hypothermia therapy and the normothermia groups. No significant difference was found in the inhospital mortality, bleeding, pneumonia and bradycardia events between surface and endovascular-cooled groups in this study. Cooling device-related adverse events were generally mild. Serious adverse events potentially attributable to therapeutic hypothermia were seldom reported. MTH was associated with reduced inhospital mortality, mortality at 1 month and at 6 months. Evidence about the safety of MTH in children has been limited. These results suggest that while it may result in some adverse events, MTH is generally safe in patients following cardiac arrest and could improve the short-term and long-term survival of comatose patients after cardiac arrest. But awareness of these adverse events should be kept in mind in clinical practice.

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Increasing evidence suggests that the ubiquitin-binding histone deacetylase-6 (HDAC6) plays an important role in the clearance of misfolded proteins by autophagy. In this study, we treated PC-12 cells over-expressing human mutant (A53T) a-synuclein (a-syn) and SH-SY5Y cells with MPP + . It was found that HDAC6 expression significantly increased and mainly colocalized with a-syn in the perinuclear region to form aggresome-like bodies. HDAC6 deficiency blocked the formation of aggresome-like bodies and interfered with the autophagy in response to MPP + -induced stress. Moreover, misfolded a-syn accumulated into the nuclei, resulting in its reduced clearance, and finally, the number of apoptotic cells significantly increased. Taken together, HDAC6 participated in the degradation of MPP + -induced misfolded a-syn aggregates by regulating the aggresome-autophagy pathway. Understanding the mechanism may disclose potential therapeutic targets for synucleinopathies such as Parkinson's disease.

The purpose of our study was to investigate the temporal malignant tumor incidence rates among the 70,000 residents at the relatively isolated Nanao Island in South China Sea. The data on all malignant tumor cases from Nanao Cancer Registry during 1995-2004 were coded, computerized, and analyzed using the software SPSS10.0. The tumor incident cases, crude incident rate, age-standardized incidence rate, their sex distribution and temporal trend were assessed. A total of 1450 new cancer cases (990 males and 460 females) were identified. The annual average age-standardized incidence rate (ASR) of malignant tumors was 208.18/100,000. The age-standardized incidence rate of the ten leading cancers in both sexes combined per 100,000 population were 74.47 for esophageal cancer (EC), 34.81 for cardiac cancer (CC), 25.66 for liver cancer, 26.01 for lung cancer, 18.52 for stomach cancer, 4.45 for nasopharyngeal cancer, 3.91 for breast cancer, 2.53 for colon/rectum cancer, 2.45 for bladder cancer and 1.92 for pancreatic cancer. These ten types of cancers make up to 93% of all cancer cases, with EC and CC being the most prevalent and making up 52% of the total cases. The incidence rates of esophagus, liver, lung, breast, nasopharyngeal, and colon/rectum cancers showed increasing trends during the period from 1995 to 2004 in Nanao Island. Astounding the EC ASR were 72-150/100,000 among male and 26-64/100,000 among female in Nanao Island during 1995-2004. The EC incidence rate in Nanao population is among the highest across the world, which suggests that there are potential genetic and/or environmental factors affecting this particular population.