Applying machine learning to assess the morphology of sculpted teeth.

Background/purpose: Producing tooth crowns through dental technology is a basic function of dentistry. The morphology of tooth crowns is the most important parameter for evaluating its acceptability. The procedures were divided into four steps: tooth collection, scanning skills, use of mathematical methods and software, and machine learning calculation. Materials and methods: Dental plaster rods were prepared. The effective data collected were to classify 121 teeth (15th tooth position), 342 teeth (16th tooth position), 69 teeth (21st tooth position), and 89 teeth (43rd tooth position), for a total of 621 teeth. The procedures are divided into four steps: tooth collection, scanning skills, use of mathematical methods and software, and machine learning calculation. Results: The area under the curve (AUC) value was 0, 0.5, and 0.72 in this study. The precision rate and recall rate of micro-averaging/macro-averaging were 0.75/0.73 and 0.75/0.72. If we took a newly carved tooth picture into the program, the current effectiveness of machine learning was about 70%-75% to evaluate the quality of tooth morphology. Through the calculation and analysis of the two different concepts of micro-average/macro-average and AUC, similar values could be obtained. Conclusion: This study established a set of procedures that can judge the quality of hand-carved plaster sticks and teeth, and the accuracy rate is about 70%-75%. It is expected that this process can be used to assist dental technicians in judging the pros and cons of hand-carved plaster sticks and teeth, so as to help dental technicians to learn the tooth morphology more effectively.

Novel quantitative immunohistochemistry method using histone H3, family 3B as the internal reference standard for measuring human epidermal growth factor receptor 2 expression in breast cancer.

BACKGROUND: Immunohistochemistry (IHC) is an essential technique in surgical and clinical pathology for detecting diagnostic, prognostic, and predictive biomarkers for personalized cancer therapy. However, the lack of standardization and reference controls results in poor reproducibility, and a reliable tool for IHC quantification is urgently required. The objective of this study was to describe a novel approach in which H3F3B (histone H3, family 3B) can be used as an internal reference standard to quantify protein expression levels using IHC. METHODS: The authors enrolled 89 patients who had human epidermal growth factor receptor 2 (HER2)-positive breast cancer (BC). They used a novel IHC-based assay to measure protein expression using H3F3B as the internal reference standard. H3F3B was uniformly expressed at the protein level in all tumor regions in cancer tissues. HER2 expression levels were measured with the H-score using HALO software. RESULTS: Kaplan-Meier analysis indicated that, among patients who had HER2-positive BC in The Cancer Genome Atlas data set and the authors' data set, the subgroup with low HER2 expression had a significantly better prognosis than the subgroup with high HER2 expression. Furthermore, the authors observed that HER2 expression levels were precisely evaluated using the proposed method, which can classify patients who are at higher risk of HER2-positive BC to receive trastuzumab-based adjuvant therapy. Dual-color IHC with H3F3B is an excellent tool for internal and external quality control of HER2 expression assays. CONCLUSIONS: The proposed IHC-based quantification method accurately assesses HER2 expression levels and provides insights for predicting clinical prognosis in patients with HER2-positive BC who receive trastuzumab-based adjuvant therapy.

Plant resistance against whitefly and its engineering.

Plants face constant threats from insect herbivores, which limit plant distribution and abundance in nature and crop productivity in agricultural ecosystems. In recent decades, the whitefly Bemisia tabaci, a group of phloem-feeding insects, has emerged as pests of global significance. In this article, we summarize current knowledge on plant defenses against whitefly and approaches to engineer plant resistance to whitefly. Physically, plants deploy trichome and acylsugar-based strategies to restrain nutrient extraction by whitefly. Chemically, toxic secondary metabolites such as terpenoids confer resistance against whitefly in plants. Moreover, the jasmonate (JA) signaling pathway seems to be the major regulator of whitefly resistance in many plants. We next review advances in interfering with whitefly-plant interface by engineering of plant resistance using conventional and biotechnology-based breeding. These breeding programs have yielded many plant lines with high resistance against whitefly, which hold promises for whitefly control in the field. Finally, we conclude with an outlook on several issues of particular relevance to the nature and engineering of plant resistance against whitefly.

Temporal Dynamic of the Ratio between Monopartite Begomoviruses and Their Associated Betasatellites in Plants, and Its Modulation by the Viral Gene ßC1.

The begomovirus-betasatellite complex constantly threatens crops in Asia. However, the quantitative relationship between begomoviruses and betasatellites remains largely unknown. The quantities of tobacco curly shoot virus (TbCSV) and its betasatellite (TbCSB) and their ratio varied significantly in initial infection, and thereafter, the ratio tended to become constant. The TbCSB/TbCSV ratio in agrobacteria inoculum significantly affected that in plants in the initial infection but not thereafter. Null-mutation of ßC1 that encodes a multifunctional protein important for pathogenesis in TbCSB significantly reduced the TbCSB/TbCSV ratio in plants. Viral inoculum plants with higher TbCSB/TbCSV ratios promoted whitefly transmission of the virus. The expression of AV1 encoded by TbCSV, ßC1 encoded by TbCSB and the ßC1/AV1 ratio varied significantly in the initial infection and thereafter the ratio tended to become constant. Additionally, the temporal dynamics of the ratio between another begomovirus and its betasatellite was similar to that of TbCSV and was positively regulated by ßC1. These results indicate that the ratio between monopartite begomoviruses and betasatellites tend to become constant as infection progresses, and is modulated by ßC1, but a higher betasatellite/begomovirus ratio in virally inoculated plants promotes virus transmission by whiteflies. Our findings provide novel insights into the association between begomoviruses and betasatellites.

Ultrathin ALD Aluminum Oxide Thin Films Suppress the Thermal Shrinkage of Battery Separator Membranes.

Thermal runaway is a major safety concern in the applications of Li-ion batteries, especially in the electric vehicle (EV) market. A key component to mitigate this risk is the separator membrane, a porous polymer film that prevents physical contact between the electrodes. Traditional polyolefin-based separators display significant thermal shrinkage (TS) above 100 °C, which increases the risk of battery failure; hence, suppressing the TS up to 180 °C is critical to enhancing the cell's safety. In this article, we deposited thin-film coatings (less than 10 nm) of aluminum oxide by atomic layer deposition (ALD) on three different types of separator membranes. The deposition conditions and the plasma pretreatment were optimized to decrease the number of ALD cycles necessary to suppress TS without hindering the battery performance for all of the studied separators. A dependency on the separator composition and porosity was found. After 100 ALD cycles, the thermal shrinkage of a 15 µm thick polyethylene membrane with 50% porosity was measured to be below 1% at 180 °C, with ionic conductivity >1 mS/cm. Full battery cycling with NMC532 cathodes demonstrates no hindrance to the battery's rate capability or the capacity retention rate compared to that of bare membranes during the first 100 cycles. These results display the potential of separators functionalized by ALD to enhance battery safety and improve battery performance without increasing the separator thickness and hence preserving excellent volumetric energy.

[Breeding-system comparison between alien invasive Solanum rostratum and its non-invasive congener S. americanum]. / å¤–æ¥å ¥ä¾µæ¤ç‰©é»„èŠ±åˆºèŒ„ä¸Žå ¶è¿‘ç¼˜éžå ¥ä¾µæ¤ç‰©å°‘èŠ±é¾™è‘µç¹è‚²ç³»ç»Ÿçš„æ¯”è¾ƒ.

Solanum rostratum is a severely invasive alien plant species in China. Using four S. rostratum populations and non-invasive congener S. americanum, we conducted a common garden experiment to compare their breeding systems. No significant difference in average seed set between the two species under open pollination and supplementary pollination conditions. However, under the bagged self-pollination condition, S. rostratum had significantly lower average seed set (29.5%) than S. americanum (47.0%). No fertile seeds were detected in the emasculation treatments for both species, suggesting no autonomous apomixis in them. S. rostratum had a lower average autofertility index (0.38) than S. americanum (0.64). S. rostratum had higher average pollen limitation index (0.29) and average pollinator's contribution index (0.49) than S. americanum (0.08 and 0.31, respectively). S. rostratum was found in 12 provinces of China and in 3835 locations globally, which were lower than S. americanum with 18 Chinese provinces and 10897 locations globally. The invasive alien S. rostratum had lower self-compatibility than the non-invasive alien S. americanum. Thus, the invasiveness of those two species was not significantly correlated with their self-compatibility, but positively correlated with their distribution range.

Correction to: microRNA-124 inhibits bone metastasis of breast cancer by repressing Interleukin-11.

An amendment to this paper has been published and can be accessed via the original article.

Long non-coding RNA DILC suppresses bladder cancer cells progression.

Accumulative researches have demonstrated the critical functions of long non-coding RNAs (lncRNAs) in the progression of malignant tumors, including bladder cancer (BC). Our previous studies showed that lnc-DILC was an important tumor suppressor gene in both liver cancer and colorectal cancer. However, the role of lnc-DILC in BC remains to be elucidated. In the present study, we for first found that lnc-DILC was downregulated in human bladder cancer tissues. Lnc-DILC overexpression suppressed the proliferation, metastasis and expansion of bladder cancer stem cells (CSCs). Mechanically, lnc-DILC suppressed BC cells progression via STAT3 pathway. Special STAT3 inhibitor S3I-201 diminished the discrepancy of growth, metastasis and self-renewal ability between lnc-DILC-overexpression BC cells and their control cells, which further confirmed that STAT3 was acquired for lnc-DILC-disrupted BC cell growth, metastasis and self-renewal. Taken together, our results suggest that lnc-DILC is a novel bladder tumor suppressor and indicate that lnc-DILC inhibits BC progression via inactivating STAT3 signaling.

miR-613 inhibits liver cancer stem cell expansion by regulating SOX9 pathway.

Liver cancer stem cells (CSCs) contribute to tumorigenesis, progression, drug resistance and recurrence of hepatocellular carcinoma (HCC). However, the underlying mechanism for the propagation of liver CSCs remains unclear. Herein, we observed miR-613 expression was downregulated in both chemoresistant and recurrent HCC patients. A remarkable decrease in miR-613 was detected in CD24 or OV6-positive liver CSCs and CSC-enriched hepatoma spheres. Down-regulation of miR-613 facilitated liver CSCs expansion by promoting the dedifferentiation of hepatoma cells and enhancing the self-renewal of liver CSCs. Mechanistically, bioinformatic and luciferase reporter analysis identified SOX9 as a direct target of miR-613. Overexpression of miR-613 inhibited the expression of SOX9 in HCC cells. Special SOX9 siRNA abolished the discrepancy in liver CSCs proportion and the self-renewal capacity between miR-613 overexpression hepatoma cells and control cells, which further confirmed that SOX9 was required in miR-613-inhibited liver CSCs expansion. Furthermore, hepatoma cells with miR-613 overexpression performed more sensitivity to cisplatin or sorafenib treatment. Conclusion: miR-613 could inhibit HCC cell dedifferentiation and liver CSCs expansion by targeting SOX9 signaling and may prove to be a novel therapeutic target for HCC patients.

Long non-coding RNA DILC promotes the progression of gallbladder carcinoma.

Increasing evidence has demonstrated that long non-coding RNAs (lncRNAs) contribute to tumorigenesis, progression and recurrence of various malignancies including Gallbladder carcinoma (GBC). Lnc-DILC is reported to be the tumor suppressor gene to play an important role in liver cancer stem cells (CSCs). However, the role of lnc-DILC in GBC remains to be elucidated. Herein, we show that lnc-DILC is upregulated in gallbladder CSCs and GBC patients' tissues. Knockdown of lnc-DILC attenuates the self-renewal, tumorigenicity, proliferation and metastasis of gallbladder CSCs. Mechanistically, lnc-DILC promotes gallbladder CSCs expansion via Wnt/ß-catenin pathway. Special Wnt/ß-catenin inhibitor FH535 diminishes the discrepancy of self-renewal, growth and metastasis between lnc-DILC interference GBC cells and their control cells. In conclusion, lnc-DILC drives gallbladder CSCs self-renewal, tumorigenicity, proliferation and metastasis by activating Wnt/ß-catenin signaling, and may therefore prove to be a potential therapeutic target for GBC patients.

Germline mutations in 40 cancer susceptibility genes among Chinese patients with high hereditary risk breast cancer.

Multigene panel testing of breast cancer predisposition genes have been extensively conducted in Europe and America, which is relatively rare in Asia however. In this study, we assessed the frequency of germline mutations in 40 cancer predisposition genes, including BRCA1 and BRCA2, among a large cohort of Chinese patients with high hereditary risk of BC. From 2015 to 2016, consecutive BC patients from 26 centers of China with high hereditary risk were recruited (n = 937). Clinical information was collected and next-generation sequencing (NGS) was performed using blood samples of participants to identify germline mutations. In total, we acquired 223 patients with putative germline mutations, including 159 in BRCA1/2, 61 in 15 other BC susceptibility genes and 3 in both BRCA1/2 and non-BRCA1/2 gene. Major mutant non-BRCA1/2 genes were TP53 (n = 18), PALB2 (n = 11), CHEK2 (n = 6), ATM (n = 6) and BARD1 (n = 5). No factors predicted pathologic mutations in non-BRCA1/2 genes when treated as a whole. TP53 mutations were associated with HER-2 positive BC and younger age at diagnosis; and CHEK2 and PALB2 mutations were enriched in patients with luminal BC. Among high hereditary risk Chinese BC patients, 23.8% contained germline mutations, including 6.8% in non-BRCA1/2 genes. TP53 and PALB2 had a relatively high mutation rate (1.9 and 1.2%). Although no factors predicted for detrimental mutations in non-BRCA1/2 genes, some clinical features were associated with mutations of several particular genes.

Long non-coding RNA DILC suppresses cell proliferation and metastasis in colorectal cancer.

Colorectal cancer (CRC) is one of the most common malignant tumors and one of the leading causes of cancer-related death in both men and women. The prognosis of CRC remains poor due to the advanced stage and cancer metastasis at the time of diagnosis. However, the exact mechanism of tumorigenesis in CRC remains unclear. Long non-coding RNAs (lncRNAs), which refer to transcripts longer than 200 nucleotides that are not translated into protein, are known to play important roles in multiple human cancers. Lnc-DILC is reported to be an important tumor suppressor gene and its inactivation is closely associated with liver cancer stem cells. However, the role of lnc-DILC in CRC remains to be elucidated. In the present study, we observed that lnc-DILC overexpression inhibited the growth and metastasis of CRC cells. Consistently, lnc-DILC knockdown facilitated the proliferation and metastasis of CRC cells. Mechanically, lnc-DILC suppressed CRC cell progression via IL-6/STAT3 signaling inactivation. More importantly, the specific STAT3 inhibitor S3I-201 and IL-6R inhibitor tocilizumab abolished the discrepancy of growth and metastasis capacity between lnc-DILC-interference CRC cells and control cells, which further confirmed that IL-6/STAT3 signaling was required in lnc-DILC-disrupted CRC cell growth and metastasis. Taken together, our results suggest that lnc-DILC is a novel CRC suppressor and may prove to be an inhibitor of CRC progression by inactivating IL-6/STAT3 signaling.

microRNA-124 inhibits bone metastasis of breast cancer by repressing Interleukin-11.

BACKGROUND: Most patients with breast cancer in advanced stages of the disease suffer from bone metastases which lead to fractures and nerve compression syndromes. microRNA dysregulation is an important event in the metastases of breast cancer to bone. microRNA-124 (miR-124) has been proved to inhibit cancer progression, whereas its effect on bone metastases of breast cancer has not been reported. Therefore, this study aimed to investigate the role and underlying mechanism of miR-124 in bone metastases of breast cancer. METHODS: In situ hybridization (ISH) was used to detect the expression of miR-124 in breast cancer tissues and bone metastatic tissues. Ventricle injection model was constructed to explore the effect of miR-124 on bone metastasis in vivo. The function of cancer cell derived miR-124 in the differentiation of osteoclast progenitor cells was verified in vitro. Dual-luciferase reporter assay was conducted to confirm Interleukin-11 (IL-11) as a miR-124 target. The involvement of miR-124/IL-11 in the prognosis of breast cancer patients with bone metastasis was determined by Kaplan-Meier analysis. RESULTS: Herein, we found that miR-124 was significantly reduced in metastatic bone tissues from breast cancers. Down-regulation of miR-124 was associated with aggressive clinical characteristics and shorter bone metastasis-free survival and overall survival. Restoration of miR-124 suppressed, while inhibition of miR-124 promoted the bone metastasis of breast cancer cells in vivo. At the cellular level, gain of function and loss-of function assays indicated that cancer cell-derived miR-124 inhibited the survival and differentiation of osteoclast progenitor cells. At the molecular level, we demonstrated that IL-11 partially mediated osteoclastogenesis suppression by miR-124 using in vitro and in vivo assays. Furthermore, IL-11 levels were inversely correlated with miR-124, and up-regulation IL-11 in bone metastases was associated with a poor prognosis. CONCLUSIONS: Thus, the identification of a dysregulated miR-124/IL-11 axis helps elucidate mechanisms of breast cancer metastases to bone, uncovers new prognostic markers, and facilitates the development of novel therapeutic targets to treat and even prevent bone metastases of breast cancer.

The HLF/IL-6/STAT3 feedforward circuit drives hepatic stellate cell activation to promote liver fibrosis.

BACKGROUND AND AIMS: Liver fibrosis is a wound-healing response that disrupts the liver architecture and function by replacing functional parenchyma with scar tissue. Recent progress has advanced our knowledge of this scarring process, but the detailed mechanism of liver fibrosis is far from clear. METHODS: The fibrotic specimens of patients and HLF (hepatic leukemia factor)PB/PB mice were used to assess the expression and role of HLF in liver fibrosis. Primary murine hepatic stellate cells (HSCs) and human HSC line Lx2 were used to investigate the impact of HLF on HSC activation and the underlying mechanism. RESULTS: Expression of HLF was detected in fibrotic livers of patients, but it was absent in the livers of healthy individuals. Intriguingly, HLF expression was confined to activated HSCs rather than other cell types in the liver. The loss of HLF impaired primary HSC activation and attenuated liver fibrosis in HLFPB/PB mice. Consistently, ectopic HLF expression significantly facilitated the activation of human HSCs. Mechanistic studies revealed that upregulated HLF transcriptionally enhanced interleukin 6 (IL-6) expression and intensified signal transducer and activator of transcription 3 (STAT3) phosphorylation, thus promoting HSC activation. Coincidentally, IL-6/STAT3 signalling in turn activated HLF expression in HSCs, thus completing a feedforward regulatory circuit in HSC activation. Moreover, correlation between HLF expression and alpha-smooth muscle actin, IL-6 and p-STAT3 levels was observed in patient fibrotic livers, supporting the role of HLF/IL-6/STAT3 cascade in liver fibrosis. CONCLUSIONS: In aggregate, we delineate a paradigm of HLF/IL-6/STAT3 regulatory circuit in liver fibrosis and propose that HLF is a novel biomarker for activated HSCs and a potential target for antifibrotic therapy.

Sentinel lymph node biopsy after neoadjuvant chemotherapy for breast cancer: retrospective comparative evaluation of clinically axillary lymph node positive and negative patients, including those with axillary lymph node metastases confirmed by fine needle aspiration.

BACKGROUND: To evaluate the accuracy of sentinel lymph node biopsy (SLNB) after neoadjuvant chemotherapy (NAC) in breast cancer patients with axillary lymph node (ALN) metastasis. METHODS: A total of 122 patients with operable breast cancer were enrolled in this single-center retrospective study. Eighty patients were clinically diagnosed with a positive axillary lymph node (ALN) via imaging or physical examination (including 66 patients with biopsy-proven metastasis). The other 42 cases had a clinically negative ALN. After four sessions of neoadjuvant chemotherapy, patients were assigned to an ALN-positive or -negative group. The identification rate (IR) and false negative rate (FNR) were determined in the ALN-negative group. RESULTS: ALN changed from positive to negative after NAC in 48 patients. Among them, 46 had at least one SLN resected (total IR = 95.8 %). Eight of the 46 SLN-negative patients had pathologically confirmed metastasis of at least one non-SLN (FNR = 36 %). Fifty-five of the 56 patients with a biopsy-proven negative ALN remained ALN negative. Furthermore, 54 of the 56 patients had at least one SLN resected (IR =98.2 %). Three SLN-negative patients of the 54 had at least one positive non-SLN (FNR = 10.7 %). CONCLUSIONS: Due to its high FNR, post-NAC SLNB is not recommended for breast cancer patients with ALN metastasis confirmed by biopsy, though their ALN may become negative after NAC. However, for operable breast cancer with negative ALN, post-NAC SLNB is feasible if the ALN remains clinically negative after NAC. TRIAL REGISTRATION: Retrospective evaluation.

Chemical Composition and Insecticidal Activities of the Essential Oil of Clinopodium chinense (Benth.) Kuntze Aerial Parts against Liposcelis bostrychophila Badonnel.

Water-distilled essential oil from Clinopodium chinense (Labiatae) aerial parts at the flowering stage was analyzed by gas chromatography-mass spectrometry. Thirty-five compounds, accounting for 99.18% of the total oil, were identified, and the main components of the essential oil of C. chinense were spathulenol (18.54%), piperitone (18.9%), caryophyllene (12.04%), and bornyl acetate (8.14%). Based on bioactivity-directed fractionation, bornyl acetate, caryophyllene, and piperitone were identified from the essential oil. The essential oil possessed fumigant toxicity against booklice (Liposcelis bostrychophila) with a 50% lethal concentration (LC50) value of 423.39 µg/liter, while the isolated constituents, bornyl acetate and piperitone, had LC50 values of 351.69 and 311.12 µg/liter against booklice, respectively. The essential oil also exhibited contact toxicity against L. bostrychophila with an LC50 value of 215.25 µg/cm(2). Bornyl acetate, caryophyllene, and piperitone exhibited acute toxicity against booklice with LC50 values of 321.42, 275.00, and 139.74 µg/cm(2), respectively. The results indicated that the essential oil and its isolated constituents have potential for development into natural insecticides or fumigants for control of insects in stored grains.

PTPN11/Shp2 overexpression enhances liver cancer progression and predicts poor prognosis of patients.

BACKGROUND & AIMS: We have previously reported that Shp2, a tyrosine phosphatase previously known as a pro-leukemogenic molecule, suppresses the initiation of hepatocellular carcinoma (HCC). However, the role of Shp2 in HCC progression remains obscure. METHODS: Shp2 expression was determined in human HCC using real-time PCR, immunoblotting and immunohistochemistry. Clinical significance of Shp2 expression was analyzed in 301 HCC tissues with clinico-pathological characteristics and follow-up information. Short hairpin RNA was utilized to investigate the function of Shp2 in hepatoma cell behavior. Role of Shp2 in HCC progression was monitored through nude mice xenograft assay. Kinase activity assay and co-immunoprecipitation were used for mechanism analysis. RESULTS: Elevated expression of Shp2 was detected in 65.9% (394/598) of human HCCs, and its levels were even higher in metastasized foci. Overexpression of Shp2 correlated well with the malignant clinico-pathological characteristics of HCC and predicted the poor prognosis of patients. Interference of Shp2 expression suppressed the proliferation of hepatoma cells in vitro and inhibited the growth of HCC xenografts in vivo. Down-regulation of Shp2 attenuated the adhesion and migration of hepatoma cells and diminished metastasized HCC formation in mice. Our data demonstrated that Shp2 promotes HCC growth and metastasis by coordinately activating Ras/Raf/Erk pathway and PI3-K/Akt/mTOR cascade. Moreover, down-regulation of Shp2 enhanced the sensitivity of hepatoma cells upon sorafenib treatment, and patients with low Shp2 expression exhibited superior prognosis to sorafenib. CONCLUSIONS: Shp2 promotes the progression of HCC and may serve as a prognostic biomarker for patients.

A preliminary analysis of microRNA as potential clinical biomarker for schizophrenia.

MicroRNAs (miRNA, miR) have been implicated as promising blood-based biomarkers for schizophrenia patients. This study aimed to clinically validate miRNA as potential schizophrenia biomarkers. Plasma levels of 10 miRNAs were analyzed using qPCR in a cohort of 61 schizophrenia patients and 62 normal controls, as well as 25 patients particularly selected for a six-week antipsychotic treatment course. Positive And Negative Syndrome Scale (PANSS), Global Assessment Scale (GAS) and Clinical Global Impression (CGI) were administered to assess the clinical symptoms. The results demonstrated that a panel of miRNAs consisting of miR-30e, miR-181b, miR-34a, miR-346 and miR-7 had significantly increased expression levels with significant combined diagnostic value (AUC:0.713; sensitivity:35.5%; specificity:90.2%). In response to pharmacological treatment, expression levels of miR-132, miR-181b, miR-432 and miR-30e were significantly decreased. In addition, the improvement of clinical symptomatology was significantly correlated with the changes of miR-132, miR-181b, miR-212 and miR-30e expression levels. Furthermore, the decreases of plasma levels of miR-132 and miR-432 were significantly greater in high-effect subgroup than those in low-effect subgroup after six-week treatment course. We conclude that miR-30e, miR-181b, miR-34a, miR-346 and miR-7 combined as a panel are potentially useful non-invasive biomarkers for schizophrenia diagnosis. Markers miR-132, miR-181b, miR-30e and miR-432 are potential indicators for symptomatology improvements, treatment responses and prognosis for schizophrenia patients.

Epidemiology and outcome analysis of severe extensive burns: a 12-year summary of 103 cases in a burn center in China.

The purpose of this article is to improve the treatment of severe extensive burns (SEB) patients by summarizing treatment experience in recent 12 years in China and analyzing the follow-up quality of life (QOL) in these patients. Clinical data and rescue measures of 103 SEB patients (≥70% TBSA) admitted in a burn center in Shanghai between 1997 and 2009 were reviewed, and QOL and hand function of those who survived more than 2 years were assessed by Brief Version of Burn Specific Health scale-B and Michigan Hand Outcome Questionnaire. Of these, 76.7% were caused by flames and 15.5% caused by scald. The median burn area was 87.5% (interquartile range, 77.0-95.0%) TBSA, of which third-degree burns accounted for 56.5% (interquartile range, 25.8-80.0%) TBSA; 71.8% were complicated by inhalation injury. The occurrence of in-hospital complications was 75.7%, with the respiratory system complications predominating (49.5%). The fatality rate was 28.2%, mainly due to sepsis and multiple organ dysfunction syndrome. Work, body image, and heat sensitivity got the lowest Brief Version of Burn Specific Health scale-B scores in all nine domains, and Michigan Hand Outcome Questionnaire scores were also relatively poor. Flame burns remain to be the main cause of SEB in China in recent 12 years. Treatment is still challenged because of the depth and extensive burn area and high occurrence of multiple system complications. How to ameliorate QOL of SEB patients, intensify the functional rehabilitation, and improve their physical appearance in particular remain to be a crux.