UV-A radiation increases biomass yield by enhancing energy flow and carbon assimilation in the edible cyanobacterium Nostoc sphaeroides.

Ultraviolet (UV) A radiation (315-400 nm) is the predominant component of solar UV radiation that reaches the Earth's surface. However, the underlying mechanisms of the positive effects of UV-A on photosynthetic organisms have not yet been elucidated. In this study, we investigated the effects of UV-A radiation on the growth, photosynthetic ability, and metabolome of the edible cyanobacterium Nostoc sphaeroides. Exposures to 5-15 W m-2 (15-46 µmol photons m-2 s-1) UV-A and 4.35 W m-2 (20 µmol photons m-2 s-1) visible light for 16 days significantly increased the growth rate and biomass production of N. sphaeroides cells by 18%-30% and 15%-56%, respectively, compared to the non-UV-A-acclimated cells. Additionally, the UV-A-acclimated cells exhibited a 1.8-fold increase in the cellular nicotinamide adenine dinucleotide phosphate (NADP) pool with an increase in photosynthetic capacity (58%), photosynthetic efficiency (24%), QA re-oxidation, photosystem I abundance, and cyclic electron flow (87%), which further led to an increase in light-induced NADPH generation (31%) and ATP content (83%). Moreover, the UV-A-acclimated cells showed a 2.3-fold increase in ribulose-1,5-bisphosphate carboxylase/oxygenase activity, indicating an increase in their carbon-fixing capacity. Gas chromatography-mass spectrometry-based metabolomics further revealed that UV-A radiation upregulated the energy-storing carbon metabolism, as evidenced by the enhanced accumulation of sugars, fatty acids, and citrate in the UV-A-acclimated cells. Therefore, our results demonstrate that UV-A radiation enhances energy flow and carbon assimilation in the cyanobacterium N. sphaeroides.IMPORTANCEUltraviolet (UV) radiation exerts harmful effects on photo-autotrophs; however, several studies demonstrated the positive effects of UV radiation, especially UV-A radiation (315-400 nm), on primary productivity. Therefore, understanding the underlying mechanisms associated with the promotive effects of UV-A radiation on primary productivity can facilitate the application of UV-A for CO2 sequestration and lead to the advancement of photobiological sciences. In this study, we used the cyanobacterium Nostoc sphaeroides, which has an over 1,700-year history of human use as food and medicine, to explore its photosynthetic acclimation response to UV-A radiation. As per our knowledge, this is the first study to demonstrate that UV-A radiation increases the biomass yield of N. sphaeroides by enhancing energy flow and carbon assimilation. Our findings provide novel insights into UV-A-mediated photosynthetic acclimation and provide a scientific basis for the application of UV-A radiation for optimizing light absorption capacity and enhancing CO2 sequestration in the frame of a future CO2 neutral, circular, and sustainable bioeconomy.

[Retracted] MicroRNA­139­5p inhibits cell viability, migration and invasion and suppresses tumor growth by targeting HDGF in non­small cell lung cancer.

[This retracts the article DOI: 10.3892/ol.2020.11296.].

Efficient Semi-Artificial Photosynthesis of Ethylene by a Self-Assembled InP-Cyanobacterial Biohybrid System.

Biomanufacturing of ethylene is particularly important for modern society. Cyanobacterial cells are able to photosynthesize various valuable chemicals. A promising platform for next-generation biomanufacturing, the semiconductor-cyanobacterial hybrid systems are capable of enhancing the solar-to-chemical conversion efficiency. Herein, the native ethylene-producing capability of a filamentous cyanobacterium Nostoc sphaeroides is confirmed experimentally. The self-assembly characteristic of N. sphaeroides is exploited to facilitate its interaction with InP nanomaterial, and the resulting biohybrid system gave rise to further elevated photosynthetic ethylene production. Based on chlorophyll fluorescence measurement and metabolic analysis, the InP nanomaterial-augmented photosystem I activity and enhanced ethylene production metabolism of biohybrid cells are confirmed, the mechanism underlying the material-cell energy transduction as well as nanomaterial-modulated photosynthetic light and dark reactions are established. This work not only demonstrates the potential application of semiconductor-N. sphaeroides biohybrid system as a good platform for sustainable ethylene production but also provides an important reference for future studies to construct and optimize nano-cell biohybrid systems for efficient solar-driven valuable chemical production.

Conversion of primary liver cancer after targeted therapy for liver cancer combined with AFP-targeted CAR T-cell therapy: a case report.

Primary liver cancer (PLC) that originates in the liver is a malignant tumor with the worst prognosis. Hepatocellular carcinoma (HCC) is the most common type of PLC. Most PLC cases are diagnosed at advanced stages mainly due to their insidious onset and rapid progression. Patients with PLC undergo surgical intervention or localized treatment, but their survival is often affected by its high relapse rate. Medical treatment is the primary option for patients with liver cancer, especially with advanced extrahepatic metastases. Molecular targeted therapy exerts an anti-tumor effect by acting on various signaling pathways involved in molecular pathogenesis; however, high drug resistance and low therapeutic responsiveness of PLC to molecular targets challenge the treatment option. In recent years, after surgical intervention, radiotherapy, chemotherapy, and/or molecular targeted therapy, autologous cell immunotherapy has been adopted for PLC. As a typical autologous cell immunotherapy, CAR T-cell therapy uses genetically modified T cells to express tumor-specific chimeric antigen receptors (CARs). Its targeting ability, persistent nature, and tumor-killing function result in a significant impact on the treatment of hematological tumors. However, no breakthrough has happened in the research specific to the curation of lung cancer, liver cancer, breast cancer, and other common solid tumors. In this context, a combination of molecular targeted therapy and CAR T-cell therapy was used to treat a patient with advanced HCC to achieve a partial remission(PR) and facilitate further liver transplantation.

miR-200a-3p- and miR-181-5p-Mediated HOXB5 Upregulation Promotes HCC Progression by Transcriptional Activation of EGFR.

Background: Hepatocellular carcinoma (HCC) remains a worldwide burden. However, the mechanisms behind the malignant biological behavior of HCC remain unclear. The homeobox (HOX) family could act as either promoters or suppressors in different kinds of malignancies. Our study discovered the role of HOXB5 in regulating HCC progression. Methods: The HOXB5 expression was assessed by RT-PCR analysis in human HCC samples and cell lines. HOXB5 transcriptional regulation of the EGFR was verified by the luciferase reporter assay and chromatin immunoprecipitation experiment. The oncogenic role of HOXB5 in HCC progression was analyzed by CCK8, colony-forming, and transwell assays. Results: Upregulation of HOXB5 was found in human HCC, and was strongly correlated with HCC tumor size, tumor-nodule metastasis, TNM stage, and relatively unfavorable OS and DFS. Ectopic expression of HOXB5 promoted the capacity of cell growth and clonogenicity, while the inhibition of HOXB5 decreased the proliferation and clonogenicity potential in vitro by CCK8 and colony-forming assays. In addition, HOXB5 also promoted cell migration by transwell experiment. Mechanism studies elucidated that HOXB5 triggers HCC progression via direct transcriptional activation of EGFR. The upregulation of HOXB5 is regulated by miR-200a-3p and miR-181-5p. Transfection of miR-200a-3p and miR-181-5p mimics blocked the cell proliferation and migration regulated by HOXB5, while overexpression of the 3'-UTR mutant HOXB5 abolished the suppressive effect of miR-200a-3p and miR-181-5p, but not the wild-type HOXB5. Conclusion: HOXB5 is a promising prognostic factor in human HCC. Targeting miR-200a-3p and the miR-181-5p/HOXB5/EGFR signaling pathway may provide new options for the treatment strategies of HCC.

Fabrication of pH/H2O2-responsive polyhedral oligomeric silsesquioxane self-assembled fluorescent vesicles for enhanced in vivo anti-tumor efficacy.

Aim: The rational design of a fluorescence imaging-guided, highly efficient multiresponsive delivery system is important for improving drug delivery efficiency. Materials and methods: Herein, pH/H2O2-responsive polyhedral oligomeric silsesquioxane (POSS) molecule functionalized 4-(phenyl(4-(4,4,5,5-tetramethyl-1,3,2-dioxaborolan-2-yl)-phenyl)amino)benzaldehyde (OTB) copolymer (PEG-POSS-OTB) was synthesized to encapsulate doxorubicin (DOX) for precise drug delivery. Results: The self-assembly fluorescent vesicles exhibited excellent pH/H2O2-responsive drug release properties under physiological conditions and efficient drug-targeting ability. In vitro, compared with the DOX group, PEG-POSS-OTB fluorescent vesicles exhibited improved drug delivery and reduced toxicity. Importantly, we performed a proof-of-concept study demonstrating that PEG-POSS-OTB fluorescent vesicles were a high-efficiency nanoassembly drug-delivery platform for improving drug delivery efficiency. In vivo studies demonstrated that PEG-POSS-OTB vesicles with enhanced stability could be used in targeted drug delivery and controlled intelligent release.

MicroRNA-455-3p functions as a tumor suppressor by targeting HDAC2 to regulate cell cycle in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is one of the most common cancers. MicroRNA has been studied more and more deeply and may become a new target for the treatment of HCC. Here, we investigated the role of miR-455-3p in HCC progression. Compared with non-tumor tissues and normal human hepatic cells, miR-455-3p expression was significantly downregulated in HCC tissues and cell lines. And overexpression of miR-455-3p inhibited cell proliferation and migration but promoted cell apoptosis in HCC cell lines HepG2 and Huh7. Mechanism studies displayed that miR-455-3p targeted HDAC2 and negatively regulated HDAC2 expression. Moreover, HDAC2 was highly expressed in HCC tissues and cell lines. Overexpression of HDAC2 reversed the inhibitory effects of miR-455-3p on cell proliferation, migration and cell cycle protein (CDK6 and cyclin D1) expression, and neutralized the promotion effects of miR-455-3p on cell apoptosis and the activation of p53 pathway. Furthermore, a p53 inhibitor Pifithrin-α (PFT-α) effectively abolished the effects of miR-455-3p on HCC cell behaviors. Additionally, the role of miR-455-3p in tumorigenesis was evaluated by using a mouse xenograft model, and the data showed that miR-455-3p suppressed tumor growth in vivo. In summary, our results suggested that miR-455-3p targeted HDAC2 to inhibit cell proliferation, migration and promote cell apoptosis via the activation of p53 pathway.

HIPK3 Circular RNA Promotes Metastases of HCC Through Sponging miR-338-3p to Induce ZEB2 Expression.

BACKGROUND: Upregulation of circHIPK3 has been observed in several kinds of malignancies. However, the mechanisms of circHIPK3 in HCC metastases remains unclear. We investigated the role and the mechanisms of circHIPK3 in the development of HCC. METHODS: HCC tissues and paired adjacent non-tumor tissues of surgical patients were used to evaluate circHIPK3 expression. A series of biological experiments had been taken to evaluate the pro-metastatic ability of circHIPK3 during HCC development in vitro and in vivo. The potential mechanisms of circHIPK3 in HCC development were identified by RT-qPCR, Western blot, RIP, and luciferase reporter assays. RESULTS: CircHIPK3 expression is significantly upregulated during HCC development. Overexpression of circHIPK3 promotes cell migration, invasion, and metastases in vitro and in vivo. CircHIPK3 promoted HCC metastases by sponging miR-338-3p to regulate EMT-associated proteins E-cadherin, vimentin, and ZEB2 expression. CONCLUSION: CircHIPK3 plays a regulatory role in metastatic HCC by sponging miR-338-3p to induce ZEB2 expression, thus promoting EMT procession.

The long noncoding RNA OTUD6B-AS1 enhances cell proliferation and the invasion of hepatocellular carcinoma cells through modulating GSKIP/Wnt/ß-catenin signalling via the sequestration of miR-664b-3p.

Ovarian tumour domain containing 6B antisense RNA1 (OTUD6B-AS1), a newly identified long noncoding RNA (lncRNA), has been reported as a key cancer-related lncRNA. However, the detailed relevance of OTUD6B-AS1 in hepatocellular carcinoma (HCC) remains undetermined. This study was designed to determine the functional significance and regulatory mechanism of OTUD6B-AS1 in HCC. We found that the expression of OTUD6B-AS1 was up-regulated in HCC tissues, and patients with high levels of OTUD6B-AS1 expression had shorter survival rates than those with low OTUD6B-AS1 expression. Elevated expression of the lncRNA was also found in multiple HCC cell lines and the silencing of OTUD6B-AS1 significantly decreased proliferation, colony formation and invasion. Correspondingly, OTUD6B-AS1 overexpression had the opposite effect on HCC cell invasion, colony formation and proliferation. Notably, OTUD6B-AS1 was identified as a molecular sponge of microRNA-664b-3p (miR-664b-3p). The down-regulation of miR-664b-3p was detected in HCC tissues and cell lines, and the up-regulation of miR-664b-3p repressed proliferation and invasion in HCC cells by targeting the glycogen synthase kinase-3ß interaction protein (GSKIP). Moreover, OTUD6B-AS1 knockdown or miR-664b-3p up-regulation exerted a suppressive effect on Wnt/ß-catenin signalling via the down-regulation of GSKIP. In addition, GSKIP overexpression markedly reversed OTUD6B-AS1 knockdown- or miR-664b-3p overexpression-induced antitumour effects in HCC. Further data confirmed that OTUD6B-AS1 knockdown exerted a tumour-inhibition role in HCC in vivo. Overall, these findings indicate that the lncRNA OTUD6B-AS1 accelerates the proliferation and invasion of HCC cells by enhancing GSKIP/Wnt/ß-catenin signalling via the sequestration of miR-664b-3p. Our study reveals a novel molecular mechanism, mediated by lncRNA OTUD6B-AS1, which may play a key role in regulating the progression of HCC.

MicroRNA-139-5p inhibits cell viability, migration and invasion and suppresses tumor growth by targeting HDGF in non-small cell lung cancer.

MicroRNA (miRNAs) serve key roles in the progress of various types of cancer. The expression of miRNA (miR)-139-5p is downregulated in several types of tumor and has been recognized as a tumor suppressor. However, the role of miR-139-5p in non-small cell lung cancer (NSCLC) has not been investigated in detail. In the present study, it was demonstrated that miR-139-5p was significantly downregulated in NSCLC cells and tissues, and the overexpression of miR-139-5p in vitro induced apoptosis and significantly inhibited the viability and proliferation of A549 and H1299 cells. In addition, upregulation of miR-139-5p significantly inhibited the migration and invasion of A549 and H1299 cells. Hepatoma-derived growth factor (HDGF) was identified as a direct target of miR-139-5p. Rescue experiments demonstrated that the inhibitory function of miR-139-5p on cell viability, migration and invasion was partially mediated by suppressing HDGF expression. Furthermore, miR-139-5p exhibited efficient inhibition of tumor growth in a xenograft tumor mouse model of A549 cells. In summary, the results from the present study suggested that miR-139-5p may serve an important role in NSCLC by targeting HDGF and causing inhibition of cell viability and metastasis, as well as induction of apoptosis. miR-139-5p may also have the potential to serve as a therapeutic target for the treatment of NSCLC.

Efficacy of transcatheter arterial chemoembolization combined with sorafenib in inhibiting tumor angiogenesis in a rabbit VX2 liver cancer model.

BACKGROUND: The aim of this study was to investigate the effects of transcatheter arterial chemoembolization (TACE) combined with sorafenib on tumor angiogenesis. MATERIALS AND METHODS: Thirty New Zealand rabbit VX2 liver cancer model animals were divided into five groups, which received either normal saline (A), TACE (B), sorafenib (C), sorafenib followed by TACE (D), or TACE followed by sorafenib (E). Serum vascular endothelial growth factor (VEGF) levels were measured before and after TACE via ELISA. Immunohistochemistry for CD34 was performed to evaluate microvessel density (MVD), and ultrasonography was used to access tumor volume. RESULTS: VEGF levels declined in group C but increased significantly on the 3rd post-operative day in groups B, D, and E. Levels decreased after the 7th post-operative day. Peak levels were significantly lower in group D than in groups B and E. On the 14th post-operative day, VEGF levels were the lowest in group C, followed by those in groups D and B. MVD was the lowest in group C followed by that in group D and E, and was the highest in group B. Group D had the smallest tumor volume. HE staining of tumor tissues from group C showed apoptosis in a scattered patchy pattern, whereas in groups B, D, and E, large areas of tumor cell necrosis were visible. CONCLUSION: TACE can up-regulate serum VEGF levels, which in turn accelerates the formation of new blood vessels. Thus, TACE combined with sorafenib inhibits VEGF and angiogenesis, and pre-operative administration of sorafenib has a more superior anti-angiogenic effect than post-operative administration.

ATDC promotes the growth and invasion of hepatocellular carcinoma cells by modulating GSK-3ß/Wnt/ß-catenin signalling.

Accumulating evidence has suggested that the ataxia telangiectasia group D complementing (ATDC) gene is an emerging cancer-related gene in multiple human cancer types. However, little is known about the role of ATDC in hepatocellular carcinoma (HCC). In this study, we aimed to investigate the expression level, biological function and underlying mechanism of ATDC in HCC. The expression of ATDC in HCC cells was detected by quantitative real-time polymerase chain reaction and western blot analysis. Cell growth was determined by cell counting kit-8 assay and colony formation assay. Cell invasion was assessed by Transwell invasion assay. The activation status of Wnt/ß-catenin signalling was evaluated by the luciferase reporter assay. Functional experiments showed that the silencing of ATDC expression significantly suppressed the growth and invasion of HCC cells, whereas the overexpression of ATDC promoted the growth and invasion of HCC cells in vitro. Moreover, we showed that ATDC overexpression promoted the phosphorylation of glycogen synthase kinase (GSK)-3ß and resulted in the activation of Wnt/ß-catenin signalling. Notably, the inhibition of GSK-3ß activity significantly abrogated the tumour suppressive effect of ATDC silencing, while the silencing of ß-catenin partially reversed the oncogenic effect of ATDC overexpression. Taken together, these findings reveal an oncogenic role of ATDC in HCC and show that the suppression of ATDC impedes the growth and invasion of HCC cells associated with the inactivation of Wnt/ß-catenin signalling. Our study suggests that ATDC may serve as a potential therapeutic target for HCC.

Emergency endoscopic needle-knife precut papillotomy in acute severe cholangitis resulting from impacted common bile duct stones at duodenal papilla.

AIM: To evaluate the efficacy and safety of emergency endoscopic needle-knife precut papillotomy in acute severe cholangitis resulting from impacted common bile duct stones at duodenal papilla. METHODS: Between January 2010 and January 2015, 118 cases of acute severe cholangitis with impacted common bile duct stones at the native papilla underwent emergency endoscopic retrograde cholangiopancreatography (ERCP) and early needle-knife precut papillotomy in a tertiary referral center. Precut techniques were performed according to the different locations of stones in the duodenal papilla. Clinical data about therapy and recovery of the 118 patients were recorded and analyzed. RESULTS: One hundred and eighteen patients underwent emergency ERCP within 24 h after hospitalization, with a total success rate of 100%. The mean operating time was 6.4 ±â€¯4.1 min. Postoperative acute physiology and chronic health evaluation (APACHE) II scores, white blood cell count and liver function improved significantly. The complication rate was 4.2% (5/118); two with hemorrhage and three with acute pancreatitis. There was no procedure-related mortality. CONCLUSION: Emergency endoscopic needle-knife precut papillotomy is effective and safe for acute severe cholangitis resulting from impacted common bile duct stones at the duodenal papilla.

Regulation of cancerous progression and epithelial-mesenchymal transition by miR-34c-3p via modulation of MAP3K2 signaling in triple-negative breast cancer cells.

Emerging but limited data have evidenced an essential involvement of microRNAs (miRNAs) in the development and progression of triple negative breast cancer (TNBC), which empowers these small regulators as an innovative therapeutic approach, especially for this unique tumor subgroup still lacking an efficient and specific therapeutic target. Herein, we reported the down-regulation of miR-34c-3p level in TNBC tissues, and its expression was closely associated with estrogen receptor alpha (ERα), but not other receptors, in well-characterized breast cancer (BCa) cells. Functionally, ectopic expression of miR-34c-3p inhibited migration, invasion and epithelial-mesenchymal transition (EMT) in TNBC cells. From a mechanistic standpoint, bioinformatics coupled with luciferase and gain-of-function, loss-of-function assays showed that miR-34c-3p may regulate TNBC progression by directly targeting the 3'-untranslated region (UTR) of mitogen-activated protein kinase kinase kinase 2 (MAP3K2). Consistently, MAP3K2 overexpression could effectively rescue miR-34c-3p mimics-induced suppression of cell invasion and EMT. In light of these findings, miR-34c-3p may function as a tumor suppressor in regulating of TNBC invasiveness and EMT through negatively modulating MAP3K2 pathway. Future endeavor in this field may help to identify a novel biomarker to predict prognosis and response to therapy in TNBC.

Diagnosis of Acute Appendicitis by Endoscopic Retrograde Appendicitis Therapy (ERAT): Combination of Colonoscopy and Endoscopic Retrograde Appendicography.

BACKGROUND: Acute appendicitis is the most common abdominal emergency, but the diagnosis of appendicitis remains a challenge. Endoscopic retrograde appendicitis therapy (ERAT) is a new and minimally invasive procedure for the diagnosis and treatment of acute appendicitis. AIM: To investigate the diagnostic value of ERAT for acute appendicitis by the combination of colonoscopy and endoscopic retrograde appendicography (ERA). METHODS: Twenty-one patients with the diagnosis of suspected uncomplicated acute appendicitis who underwent ERAT between November 2014 and January 2015 were included in this study. The main outcomes, imaging findings of acute appendicitis including colonoscopic direct-vision imaging and fluoroscopic ERA imaging, were retrospectively reviewed. Secondary outcomes included mean operative time, mean hospital stay, rate of complication, rate of appendectomy during follow-up period, and other clinical data. RESULTS: The diagnosis of acute appendicitis was established in 20 patients by positive ERA (5 patients) or colonoscopy (1 patient) alone or both (14 patients). The main colonoscopic imaging findings included mucosal inflammation (15/20, 75 %), appendicoliths (14/20, 70 %), and maturation (5/20, 25 %). The key points of ERA for diagnosing acute appendicitis included radiographic changes of appendix (17/20, 85 %), intraluminal appendicoliths (14/20, 70 %), and perforation (1/20, 5 %). Mean operative time of ERAT was 49.7 min, and mean hospital stay was 3.3 days. No patient converted to emergency appendectomy. Perforation occurred in one patient after appendicoliths removal was not severe and did not require invasive procedures. During at least 1-year follow-up period, only one patient underwent laparoscopic appendectomy. CONCLUSION: ERAT is a valuable procedure of choice providing a precise yield of diagnostic information for patients with suspected acute appendicitis by combination of colonoscopy and ERA.

Exploration of the value of MRCP combined with tumor marker CA19-9 in the diagnosis of pancreatic cancer.

This paper aims to provide an effective, accurate, and specific diagnostic method for the diagnosis of pancreatic cancer. It discusses the diagnostic value of magnetic res retrograde cholangiopancreatography (MRCP) combined with the detection of tumor marker carbohydrate antigen 19-9 (CA19-9) for pancreatic cancer. A group of confirmed cases of pancreatic cancer in some hospitals were randomly selected and subjected to an MRCP examination as well as serological CA19-9 detection. In addition, a group of patients whose pancreatic cancer was confirmed by surgery and pathology, and who underwent MRCP without the detection of the tumor marker CA19-9, were also selected for research. The experiment found that the rate of accuracy for the group that underwent MRCP combined with CA19-9 detection showed a higher positive value in the diagnosis of pancreatic cancer than in the group that underwent MRCP alone. Therefore, this paper proposes that MRCP combined with CA19-9 detection can be taken as the reliable and effective means for diagnosis of pancreatic cancer.

Outlier detection and removal improves accuracy of machine learning approach to multispectral burn diagnostic imaging.

Multispectral imaging (MSI) was implemented to develop a burn tissue classification device to assist burn surgeons in planning and performing debridement surgery. To build a classification model via machine learning, training data accurately representing the burn tissue was needed, but assigning raw MSI data to appropriate tissue classes is prone to error. We hypothesized that removing outliers from the training dataset would improve classification accuracy. A swine burn model was developed to build an MSI training database and study an algorithm's burn tissue classification abilities. After the ground-truth database was generated, we developed a multistage method based on Z -test and univariate analysis to detect and remove outliers from the training dataset. Using 10-fold cross validation, we compared the algorithm's accuracy when trained with and without the presence of outliers. The outlier detection and removal method reduced the variance of the training data. Test accuracy was improved from 63% to 76%, matching the accuracy of clinical judgment of expert burn surgeons, the current gold standard in burn injury assessment. Given that there are few surgeons and facilities specializing in burn care, this technology may improve the standard of burn care for patients without access to specialized facilities.

Surgical wound debridement sequentially characterized in a porcine burn model with multispectral imaging.

INTRODUCTION: Multispectral imaging (MSI) is an optical technique that measures specific wavelengths of light reflected from wound site tissue to determine the severity of burn wounds. A rapid MSI device to measure burn depth and guide debridement will improve clinical decision making and diagnoses. METHODOLOGY: We used a porcine burn model to study partial thickness burns of varying severity. We made eight 4 × 4 cm burns on the dorsum of one minipig. Four burns were studied intact, and four burns underwent serial tangential excision. We imaged the burn sites with 400-1000 nm wavelengths. RESULTS: Histology confirmed that we achieved various partial thickness burns. Analysis of spectral images show that MSI detects significant variations in the spectral profiles of healthy tissue, superficial partial thickness burns, and deep partial thickness burns. The absorbance spectra of 515, 542, 629, and 669 nm were the most accurate in distinguishing superficial from deep partial thickness burns, while the absorbance spectra of 972 nm was the most accurate in guiding the debridement process. CONCLUSION: The ability to distinguish between partial thickness burns of varying severity to assess whether a patient requires surgery could be improved with an MSI device in a clinical setting.

Identification of a novel thylakoid protein gene involved in cold acclimation in cyanobacteria.

In cyanobacteria, genes involved in cold acclimation can be upregulated in response to cold stress with or without light. By inactivating 17 such genes in Synechocystis sp. PCC 6803, slr0815 (ccr2) was identified to be a novel gene required for survival at 15 °C. It was upregulated by cold stress in the light. Upon exposure to low temperature, a ccr2-null mutant showed greatly reduced photosynthetic and respiratory activities within 12 h relative to the wild-type. At 48 h, the photosystem (PS)II-mediated electron transport in the mutant was reduced to less than one-third of the wild-type level, and the duration of electron transfer from the Q(B) binding site of PSII to PSI was increased to about eight times the wild-type level, whereas the PSI-mediated electron transport remained unchanged. Using an antibody against GFP, a Ccr2-GFP fusion protein was localized to the thylakoid membrane rather than the cytoplasmic and outer membranes. Homologues to Ccr2 can be found in most cyanobacteria, algae and higher plants with sequenced genomes. Ccr2 is probably representative of a group of novel thylakoid proteins involved in acclimation to cold or other stresses.

Transjugular intrahepatic portosystemic shunt vs endoscopic therapy in preventing variceal rebleeding.

AIM: To compare early use of transjugular intrahepatic portosystemic shunt (TIPS) with endoscopic treatment (ET) for the prophylaxis of recurrent variceal bleeding. METHODS: In-patient data were collected from 190 patients between January 2007 and June 2010 who suffured from variceal bleeding. Patients who were older than 75 years; previously received surgical treatment or endoscopic therapy for variceal bleeding; and complicated with hepatic encephalopathy or hepatic cancer, were excluded from this research. Thirty-five cases lost to follow-up were also excluded. Retrospective analysis was done in 126 eligible cases. Among them, 64 patients received TIPS (TIPS group) while 62 patients received endoscopic therapy (ET group). The relevant data were collected by patient review or telephone calls. The occurrence of rebleeding, hepatic encephalopathy or other complications, survival rate and cost of treatment were compared between the two groups. RESULTS: During the follow-up period (median, 20.7 and 18.7 mo in TIPS and ET groups, respectively), rebleeding from any source occurred in 11 patients in the TIPS group as compared with 31 patients in the ET group (Kaplan-Meier analysis and log-rank test, P = 0.000). Rebleeding rates at any time point (6 wk, 1 year and 2 year) in the TIPS group were lower than in the ET group (Bonferroni correction α' = α/3). Eight patients in the TIPS group and 16 in the ET group died with the cumulative survival rates of 80.6% and 64.9% (Kaplan-Meier analysis and log-rank test χ(2) = 4.864, P = 0.02), respectively. There was no significant difference between the two groups with respect to 6-wk survival rates (Bonferroni correction α' = α/3). However, significant differences were observed between the two groups in the 1-year survival rates (92% and 79%) and the 2-year survival rates (89% and 64.9%) (Bonferroni correction α' = α/3). No significant differences were observed between the two treatment groups in the occurrence of hepatic encephalopathy (12 patients in TIPS group and 5 in ET group, Kaplan-Meier analysis and log-rank test, χ(2) = 3.103, P = 0.08). The average total cost for the TIPS group was higher than for ET group (Wilcxon-Mann Whitney test, 52 678 RMB vs 38,844 RMB, P < 0.05), but hospitalization frequency and hospital stay during follow-up period were lower (Wilcxon-Mann Whitney test, 0.4 d vs 1.3 d, P = 0.01; 5 d vs 19 d, P < 0.05). CONCLUSION: Early use of TIPS is more effective than endoscopic treatment in preventing variceal rebleeding and improving survival rate, and does not increase occurrence of hepatic encephalopathy.