Hybridization, polyploidization, and morphological convergence make dozens of taxa into one chaotic genetic pool: a phylogenomic case of the Ficus erecta species complex (Moraceae).

The Ficus erecta complex, characterized by its morphological diversity and frequent interspecific overlap, shares pollinating fig wasps among several species. This attribute, coupled with its intricate phylogenetic relationships, establishes it as an exemplary model for studying speciation and evolutionary patterns. Extensive researches involving RADseq (Restriction-site associated DNA sequencing), complete chloroplast genome data, and flow cytometry methods were conducted, focusing on phylogenomic analysis, genetic structure, and ploidy detection within the complex. Significantly, the findings exposed a pronounced nuclear-cytoplasmic conflict. This evidence, together with genetic structure analysis, confirmed that hybridization within the complex is a frequent occurrence. The ploidy detection revealed widespread polyploidy, with certain species exhibiting multiple ploidy levels, including 2×, 3×, and 4×. Of particular note, only five species (F. abelii, F. erecta, F. formosana, F. tannoensis and F. vaccinioides) in the complex were proved to be monophyletic. Species such as F. gasparriniana, F. pandurata, and F. stenophylla were found to encompass multiple phylogenetically distinct lineages. This discovery, along with morphological comparisons, suggests a significant underestimation of species diversity within the complex. This study also identified F. tannoensis as an allopolyploid species originating from F. vaccinioide and F. erecta. Considering the integration of morphological, molecular systematics, and cytological evidences, it is proposed that the scope of the F. erecta complex should be expanded to the entire subsect. Frutescentiae. This would redefine the complex as a continuously evolving group comprising at least 33 taxa, characterized by blurred species boundaries, frequent hybridization and polyploidization, and ambiguous genetic differentiation.

Colchicine ameliorates myocardial injury induced by coronary microembolization through suppressing pyroptosis via the AMPK/SIRT1/NLRP3 signaling pathway.

BACKGROUND: Coronary microembolization(CME)is a common complication in acute coronary syndrome and percutaneous coronary intervention, which is closely related to poor prognosis. Pyroptosis, as an inflammatory programmed cell death, has been found to be associated with CME-induced myocardial injury. Colchicine (COL) has potential benefits in coronary artery disease due to its anti-inflammatory effect. However, the role of colchicine in pyroptosis-related CME-induced cardiomyocyte injury is unclear. This study was carried out to explore the effects and mechanisms of colchicine on myocardial pyroptosis induced by CME. METHODS: The CME animal model was constructed by injecting microspheres into the left ventricle with Sprague-Dawley rats, and colchicine (0.3 mg/kg) pretreatment seven days before and on the day of modeling or compound C(CC)co-treatment was given half an hour before modeling. The study was divided into 4 groups: Sham group, CME group, CME + COL group, and CME + COL + CC group (10 rats for each group). Cardiac function, serum myocardial injury markers, myocardial histopathology, and pyroptosis-related indicators were used to evaluate the effects of colchicine. RESULTS: Colchicine pretreatment improved cardiac dysfunction and reduced myocardial injury induced by CME. The main manifestations were the improvement of left ventricular systolic function, the decrease of microinfarction area, and the decrease of mRNA and protein indexes related to pyroptosis. Mechanistically, colchicine increased the phosphorylation level of adenosine monophosphate-activated protein kinase (AMPK), promoted the expression of silent information regulation T1 (SIRT1), and inhibited the expression of NOD-like receptor pyrin containing 3 (NLRP3) to reduce myocardial pyroptosis. However, after CC co-treatment with COL, the effect of colchicine was partially reversed. CONCLUSION: Colchicine improves CME-induced cardiac dysfunction and myocardial injury by inhibiting cardiomyocyte pyroptosis through the AMPK/SIRT1/NLRP3 signaling pathway.

Immune-related adverse events and outcomes among pan-cancer patients receiving immune checkpoint inhibitors: A monocentric real-world observational study.

BACKGROUND: Real-world evidence on immune-related adverse events (irAEs) are relatively insufficient. Herein patterns and outcomes of irAEs after administration of anti-programmed cell death 1 (PD-1) and its legend 1 (PD-L1) antibodies were investigated. METHODS: Patients treated with anti-PD-1/PD-L1 drugs from January 2018 to September 2021 at Huadong Hospital, Fudan University were included. Common Terminology Criteria for Adverse Events (CTCAE) was used for irAEs evaluation. The primary endpoints were the clinical description of irAEs. RESULTS: Two hundred and forty-one solid tumor patients were included, with lung cancer as the most common tumor type (56%). 187 (77.6%) patients presented any kind of irAEs. The median time to any irAE onset was 28 (95% CI 24-32) days. Skin toxicities are the most common irAEs (46.1%) and the irAEs (36.5%) occurred earliest after immune-checkpoint inhibitors. The most frequently occurred all-grade irAEs were rash (23.7%), myelosuppression (20.7%), and hepatic injury (19.5%). 23 (9.5%) patients died of severe irAEs, which consists of 10 patients with pneumonitis, four colitis, four myocarditis, and one each for gastritis, pulmonary embolism, myelosuppression, hypophysitis, and encephalitis. Patients with any irAE onset had significantly longer progression-free survival (PFS) (p = 0.013) and overall survival (OS) (p = 0.007), respectively, than patients without irAEs. In addition, patients with skin toxicities (p = 0.012) or blood toxicities (p = 0.015) had achieved a longer PFS, than those without corresponding toxitities, respectively. CONCLUSION: Most irAEs are mild and manageable, while some irAEs can present at later time or can be life-threatening, especially pneumonitis as we observed. Patients with any irAE onset may achieve a better prognosis than those without irAEs, and presentation of skin or blood toxicities will indicate a better PFS.

Transketolase Serves as a Biomarker for Poor Prognosis in Human Lung Adenocarcinoma.

Despite apparently having completed surgical resection, approximately half of resected early-stage lung cancer patients relapse and die of their disease. Adjuvant chemotherapy reduces this risk by only 5% to 8%. Thus, there is a need for better identifying the drivers of relapse, who benefits from adjuvant therapy, and novel targets in this setting. Although emerging evidence has suggested a strong link between the pentose phosphate pathway (PPP) and cancer, the role of transketolase (TKT), an enzyme in the nonoxidative branch of the PPP that connects PPP and glycolysis, remains obscure in Lung adenocarcinoma (LUAD). In this study, TKT expression was first identified in The Cancer Genome Atlas (TCGA) and then validated with our database. TKT was upregulated at protein levels in cancer compared with normal tissues (P <0.05), and high TKT expression was associated with advanced tumor stage in our cohorts. Besides, TKT inhibitor promotes tumor cell apoptosis and cell cycle blockade. Clearly, TKT plays a critical role in LUAD progression and prognosis and could be a potential biomarker for prediction of recurrence after lung cancer resection.

TREM2 ameliorates anesthesia and surgery-induced cognitive impairment by regulating mitophagy and NLRP3 inflammasome in aged C57/BL6 mice.

Postoperative cognitive dysfunction (POCD) is a major postoperative complication. Triggering receptor expressed on myeloid cells 2 (TREM2) exerts a neuroprotective function against neuro-inflammatory responses. The present study investigated the role of TREM2 in anesthesia and surgery-induced cognitive impairment and the potential related mechanism. Our results revealed that TREM2 was downregulated, coupled with activation of the NLRP3 inflammasome and subsequent IL-1ß expression on postoperative day 3. A corresponding decline in PSD-95 and BDNF was found at the same time point. The key regulator of mitophagy PINK1 and Parkin protein levels were significantly decreased following surgery and anesthesia. TREM2 overexpression partially reversed postoperative cognitive impairment and enhanced PSD-95 and BDNF expression. TREM2 overexpression also improved mitophagy function and inhibited activation of the NLRP3 inflammasome and associated production of IL-1ß. Our findings demonstrate that TREM2 rescues anesthesia and surgery-induced spatial learning and memory impairment and neuro-inflammation in aged C57/BL6 mice, which may be at least partially mediated through the activation of mitophagy and subsequent inhibition of the NLRP3 inflammasome.

A comparison of the analgesic efficacy of serratus anterior plane block vs. paravertebral nerve block for video-assisted thoracic surgery: a randomized controlled trial.

INTRODUCTION: Patients who undergo video-assisted thoracic surgery (VATS) frequently experience moderate to severe postoperative pain. Serratus anterior plane block (SAPB) is a relatively novel technique that can block the lateral cutaneous branches of the intercostal nerves as well as the long thoracic nerve. AIM: To evaluate the analgesic efficiency of deep serratus plane block (DSPB) and superficial serratus anterior plane block (SSPB) as well as paravertebral nerve block (PVB) in patients undergoing VATS. MATERIAL AND METHODS: A total of 74 patients aged 16-80 undergoing VATS were randomized to receive either DSPB or SSPB as well as PVB. Ultrasound (US) guided DSPB or SSPB as well as PVB was performed preoperatively on the patients according to their groups. All patients were provided with patient-controlled intravenous analgesia (PCIA) for postoperative analgesia. The primary outcomes were the levels of postoperative pain at rest and on coughing evaluated by the visual analog scale (VAS), and intraoperative and postoperative opioid consumption. The secondary outcomes included PCIA pressing times, side effects and satisfaction with analgesia, duration of nerve block, intraoperative hemodynamic changes and vasoactive drug dosage. RESULTS: No significant differences of VAS score were found. During the operation, PVB reduced consumption of opioids (27.23 ±5.10 mg) compared to DSPB (31.20 ±3.80 mg) and SSPB (32.61 ±5.28 mg). The effective pressing times of PCIA in the SSPB group (0.18 ±0.65) were significantly lower compared to the PVB group (1.09 ±1.50) at 12 h postoperatively. Accordingly, SSPB also reduced the dosage of PCIA (26.55 ±4.72 ml) compared to PVB (31.45 ±7.60 ml). Time of the PVB procedure was longer (11.14 ±1.66 min) than DSPB (5.68 ±1.10 min) and SSPB (4.77 ±1.04 min). CONCLUSIONS: DSPB and SSPB are easy to perform and can serve as a promising alternative technique to PVB that may offer comparable analgesic effectiveness for patients undergoing VATS.

Golgi anti-apoptotic proteins redundantly counteract cell death by inhibiting production of reactive oxygen species under endoplasmic reticulum stress.

Maintaining proteostasis in the endoplasmic reticulum (ER) is critical for cell viability and plant survival under adverse conditions. The unfolded protein response (UPR) pathways interact with reactive oxygen species (ROS) to precisely trigger adaptive outputs or cell death under ER stress with varying degrees. However, little information is known about the relationship between UPR signalling and ROS regulation. Here, Arabidopsis GOLGI ANTI-APOPTOTIC PROTEIN1 (GAAP1)-GAAP4 were found to play redundant positive roles under ER stress. Genetic analysis showed that GAAP4 played a role in INOSITOL-REQUIRING ENZYME (IRE1)-dependent and -independent pathways. In addition, GAAPs played negative roles to activate the adaptive UPR under conditions of stress. Quantitative biochemical analysis showed that mutations in GAAP genes decreased the oxidised glutathione content and altered the pattern of ROS and glutathione in early ER stress. When plants were challenged with unmitigated ER stress, mutations in GAAP advanced ROS accumulation, which was associated with a decline in adaptive UPR. These data indicated that GAAPs resist cell death by regulating glutathione content to inhibit ROS accumulation and maintain UPR during ER stress. They provide a basis for further analysis of the regulation of cell fate decision under ER stress.

A comparison of paravertebral block, erector spinae plane block and the combination of erector spinae plane block and paravertebral block for post-operative analgesia after video-assisted thoracoscopic surgery: A randomised controlled trial.

BACKGROUND: This study was to determine the analgesic effect of ultrasound-guided erector spinae plane block (ESPB) and paravertebral block (PVB) as well as the combination of PVB and ESPB (P + E) after video-assisted thoracoscopic surgery (VATS). PATIENTS AND METHODS: Patients were randomly assigned to receive ESPB, PVB or PVB combined with ESPB with 0.5% ropivacaine (20 ml). The primary outcomes were cumulative hydromorphone consumption and Visual Analogue Scale (VAS) scores at rest and while coughing at 0 h, 12 h, 24 h, 48 h and 72 h postoperatively. The secondary outcomes were effective PCA usage count and rescue analgesia requirement at the same time points. RESULTS: The median (interquartile range) hydromorphone consumption, including converted oxycodone, was significantly different at 48 h postoperatively among the three groups (ESPB, 10.24 [9.53-11.71] mg; PVB, 9.94 [9.19-10.75] mg; P + E, 9.44 [8.96-9.97] mg; P = 0.011). Hydromorphone consumption in P + E group was lower compared with that in ESPB group at 12 h, 24 h and 48 h (P < 0.001, P = 0.004 and P = 0.003, respectively). VAS scores at rest were significantly higher for ESPB group compared to P + E group at 0 h postoperatively (P = 0.009). VAS scores while coughing were significantly higher for ESPB group compared to P + E group at 0 h and 12 h postoperatively (P = 0.015 and P < 0.001) and to the PVB group at 12 h postoperatively (P = 0.002). The effective PCA usage count in P + E group was lower than in ESPB group in 0-12 h (P < 0.001). More patients needed rescue analgesia in ESPB group compared to those in P + E group in 0-12 h, 0-24 h and 0-48 h (P = 0.022, 0.035 and 0.035, respectively). CONCLUSIONS: Ultrasound-guided PVB combined with ESPB provided superior analgesia to ESPB for VATS. The combination of PVB and ESPB had a similar analgesic effect compared with PVB alone.

LncRNA RP11-116G8.5 promotes the progression of lung squamous cell carcinoma through sponging miR-3150b-3p/miR-6870-5p to upregulate PHF12/FOXP4.

BACKGROUND: Lung squamous cell carcinoma (LUSC) is one of the commonest malignancies worldwide. Long noncoding RNAs (lncRNAs) have been revealed to engage in cancer development. LncRNA RP11-116G8.5 is a new founded lncRNA that has not been clearly elucidated in LUSC. MATERIALS AND METHODS: Expression levels of RNAs in LUSC cells were measured through qRT-PCR. To identify the functions of RP11-116G8.5, CCK-8 assay, colony formation assay and EdU assay were conducted in indicated LUSC cells. Mechanism experiments, including RNA pull down assay, Ago2-RIP assay and luciferase reporter assay were performed to demonstrate the interaction between RP11-116G8.5 and miR-3150b-3p/miR-6870-5p. Meanwhile, the interaction between miR-3150b-3p/miR-6870-5p and their downstream targets PHD finger protein 12 (PHF12), and forkhead box P4 (FOXP4) were also proven in the same methods. RESULTS: RP11-116G8.5 was expressed at high level in LUSC cell lines. Down-regulated RP11-116G8.5 repressed cell proliferation, migration and invasion, but accelerated apoptosis. Furthermore, it was proven that RP11-116G8.5 could act as sponges for miR-3150b-3p and miR-6870-5p these miRNAs were found to act as cancer suppressors in LUSC cells. PHF12 and FOXP4 were verified as the target gene of miR-3150b-3p and miR-6870-5p separately. Overexpression of PHF12 and FOXP4 could reverse the repressive effect of RP11-116G8.5 knockdown on LUSC progression. Additionally, Paired Box 5 (PAX-5) was proven to be the transcription factor for RP11-116G8.5 in LUSC cells. CONCLUSIONS: LncRNA RP11-116G8.5 promotes malignant behaviors of LUSC through sponging miR-3150b-3p/miR-6870-5p to upregulate PHF12/FOXP4 expression. AVAILABILITY OF DATA: The research data is confidential.

Dexamethasone alleviates pemetrexed-induced senescence in Non-Small-Cell Lung Cancer.

Pemetrexed (PEM) is a novel and multi-targeted antifolate used as an antineoplastic agent for non-small cell lung cancer (NSCLC) and pleural mesothelioma. Although glucocorticoid was often used with PEM to reduce toxicity during the chemotherapy, it is not clear yet whether glucocorticoid co-administration could affect PEM efficacy in NSCLC. Here we established NSCLC cell lines and examined the effects of dexamethasone (DEX) on PEM sensitivity in vitro and in xenograft models. DEX co-administration reduced chemotherapy sensitivity to PEM in xenograft models. DEX co-administration promoted cell growth and weakened senescence growth arrest, such as altered secretions of proinflammatory and mitogenic cytokines, reminiscent of a senescence associate secretory phenotype (SASP). CSCs in DEX co-administration group were subsequently found to be less sensitive towards PEM treatment as measured by cell proliferation and generation of tumor spheres in the presence of PEM. Survival molecule B-cell lymphoma-2 (Bcl-2) may involve in this process and blockage of Bcl-2 could reverse altered senescence and CSCs abilities, thus alleviated PEM insensitivity. As such, DEX might suppress the antitumor activity of PEM through altered SASP level that had induced traits similar to CSCs.

Clinical effect of trimetazidine on prevention of contrast-induced nephropathy in patients with renal insufficiency: An updated systematic review and meta-analysis.

BACKGROUND: With the continuous development of cardiac interventional medicine, the incidence of contrast-induced nephropathy (CIN) is increasing every year, which is a serious threat to people's physical and mental health. Trimetazidine (TMZ) is a type of anti-ischemic drug developed in recent years, which can significantly reduce the incidence of CIN. At present, a systematic review and meta-analysis was conducted to evaluate the clinical effect of TMZ on prevention of CIN in patients with renal insufficiency. However, the study did not include patients from other countries and speaking different languages. So we conducted this study to update the previous meta-analysis that investigated the effects of TMZ on prevention of CIN in patients with renal insufficiency, and provided some theoretical reference for clinical. METHODS: By searching PubMed, Embase, the Cochrane Library, Web of Science, CBM, CNKI, VIP database, and Wang Fang database for randomized controlled trial, which is comparing TMZ versus conventional hydration for prevention of CIN. Two researchers independently screened literature, and then evaluated the quality of literature and extracted the relevant data. Stata 11.0 software was used for statistical analysis. RESULTS: Finally, this updated review showed that 3 studies that were not included in the previous meta-analysis were included in our study (3 articles were published in the Chinese Journal, 1 study for CIN, 1 study for CIN, serum creatinine (Scr), and superoxide dismutase, 1 study for CIN and Scr), and 1 outcome (Scr) reflecting the change of renal function was additionally included in our study. Of the 932 studies, 6 randomized controlled trials met the criteria, including 377 patients in TMZ group and 387 patients in control group. This meta-analysis for all studies showed that TMZ can significantly reduce the incidence of CIN (relative risk 0.27, 95% confidence interval [CI] 0.16, 0.46, P = 0.000), and can decrease the level of Scr after operation, including Scr of postoperative 24 hours (standardized mean difference [SMD] -0.30, 95% CI -0.51, -0.09, P = 0.005), Scr of postoperative 48 hours (SMD -0.66, 95% CI -1.23, -0.10, P = 0.022), and Scr of postoperative 7 days (SMD -0.74, 95% CI -1.36, -0.11, P = 0.021). However, the Scr of postoperative 72 hours between TMZ group and control group has no statistical significance (P = 0.362). CONCLUSION: Our study showed that when comparing with conventional hydration, TMZ can significantly reduce the incidence of CIN and the level of postoperative Scr. Therefore, we could suggest that TMZ was superior to conventional hydration for the treatment of CIN in patients with renal insufficiency. However, due to the restriction of quality and number of included articles, it still needs to carry out multicenter, randomized, double-blind clinical trials to confirm this conclusion in the future.

The effect of alprostadil on preventing contrast-induced nephropathy for percutaneous coronary intervention in diabetic patients: A systematic review and meta-analysis.

BACKGROUND: At present, there are a lot of research about the effect of Alprostadil on preventing contrast-induced nephropathy for percutaneous coronary intervention (PCI) in diabetic patients, but the clinical efficacy is not consistent, so we conduct this study and therefore determine the dominant strategy for the treatment of PCI in diabetic patients based on the best evidence currently. METHODS: An electronic database search was conducted in MEDLINE, Embase, Cochrane library, CBM, CNKI, VIP, and WanFang to retrieve randomized controlled trial (RCT) comparing Alprostadil versus hydration on preventing CIN for PCI in diabetic patients. Reference lists of relevant articles were also screened manually to retrieve additional ones. Two investigators independently assessed the eligibility of retrieved articles using predefined inclusion and exclusion criteria. All characteristics as well as outcome variables including incidence of CIN, blood urea nitrogen (BUN), cystatin C (CysC), glomerular filtration rate (GFR), serum creatinine (Scr), serum beta 2-microspheres (ß2-MG) presented in each included study were extracted. Heterogeneity was thought to be significant when I > 50%. All of the meta-analytic procedures were performed by using Review Manager software, version 5.3. RESULTS: Finally, data from 8 articles including 969 patients were included into this meta-analysis, among them, 487 patients in the experience group, and 482 patients in the control group. Meta analysis showed that the incidence of CIN in the experimental group was significantly lower than that in the control group (OR = 0.28,95%CI[0.18,0.42]). The incidence of adverse reactions in the experimental group was significantly lower than that in the control group (OR = 0.46,95%CI[0.24,0.85]). The BUN of 24 hours, 48 hours, and 72 hours in the experimental group were significantly lower than that of control group (MD = -0.77, 95%CI [-1.22, -0.32]; MD = -1.38, 95%CI [-1.83,-0.92]; MD = -2.43, 95%CI [-2.68,-2.19], respectively). The CysC of 24 hours, 48 hours, and 72 hours in the experimental group were significantly lower than that of control group (MD = -0.30, 95%CI [-0.40, -0.21]; MD = -0.54, 95%CI [-0.68,-0.41]; MD = -0.49, 95%CI [-0.63, -0.35], respectively). The GFR of 24 hours, 48 hours, and 72 hours in the experimental group were significantly higher than that of control group (MD = 7.86, 95%CI [4.44, 11.29], MD = 18.23, 95%CI [13.76,22.69], MD = 12.81, 95%CI [8.51,17.11], respectively). The Scr of 24 hours, 48 hours, and 72 hours in the experimental group were significantly lower than that of control group (MD = -9.09, 95%CI [-12.67, -5.51], MD = -19.14, 95%CI [-23.61, -14.66], MD = -6.50, 95%CI [-8.29, -4.71], respectively). The ß2-MG of 24 hours, 48 hours, and 72 hours in the experimental group were significantly lower than that of control group (MD = -0.12, 95%CI [-0.27, 0.03], MD = -0.55, 95%CI [-0.71, -0.39], MD = -0.50, 95%CI [-0.60, -0.39], respectively). CONCLUSION: Our result suggested that comparing with conventional Hydration, Alprostadil can significantly reduce the incidence of CIN, adverse reaction, and protect renal function in PCI in diabetic patients. Due to the limitations of the quality and quantity of the articles, this conclusion still needs further research to confirm.

Proteomic study of benign and malignant pleural effusion.

BACKGROUND: Lung adenocarcinoma can easily cause malignant pleural effusion which was difficult to discriminate from benign pleural effusion. Now there was no biomarker with high sensitivity and specificity for the malignant pleural effusion. PURPOSE: This study used proteomics technology to acquire and analyze the protein profiles of the benign and malignant pleural effusion, to seek useful protein biomarkers with diagnostic value and to establish the diagnostic model. METHODS: We chose the weak cationic-exchanger magnetic bead (WCX-MB) to purify peptides in the pleural effusion, used matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS) to obtain peptide expression profiles from the benign and malignant pleural effusion samples, established and validated the diagnostic model through a genetic algorithm (GA) and finally identified the most promising protein biomarker. RESULTS: A GA diagnostic model was established with spectra of 3930.9 and 2942.8 m/z in the training set including 25 malignant pleural effusion and 26 benign pleural effusion samples, yielding both 100 % sensitivity and 100 % specificity. The accuracy of diagnostic prediction was validated in the independent testing set with 58 malignant pleural effusion and 34 benign pleural effusion samples. Blind evaluation was as follows: the sensitivity was 89.6 %, specificity 88.2 %, PPV 92.8 %, NPV 83.3 % and accuracy 89.1 % in the independent testing set. The most promising peptide biomarker was identified successfully: Isoform 1 of caspase recruitment domain-containing protein 9 (CARD9), with 3930.9 m/z, was decreased in the malignant pleural effusion. CONCLUSIONS: This model is suitable to discriminate benign and malignant pleural effusion and CARD9 can be used as a new peptide biomarker.

Different expression of FoxM1 in human benign and malignant pleural effusion.

The aims of this study were as follows: to analyze the forkhead box M1 (FoxM1) expression in benign and malignant pleural effusion by reverse transcription-polymerase chain reaction assay (RT-PCR); to explore the role of FoxM1 in formation and progress in malignant pleural effusion, and whether there is significant difference in expression level of FoxM1 between benign and malignant pleural effusion; to seek a gene marker diagnostically useful to identify benign and malignant pleural effusion in diagnosis and treatment of pleural effusion; and to collect expression level data of FoxM1 in 23 malignant pleural effusion samples (17 adenocarcinoma samples, four squamous carcinoma samples and two small cell lung carcinoma samples) and 15 benign pleural effusion samples (11 inflammatory pleural effusions, two transudates, two tuberculous pleural effusions) by RT-PCR. Among all 38 samples, average FoxM1 expression level of benign pleural effusions is (235.09 ± 59.99), while malignant pleural effusions (828.77 ± 109.76). Among 23 malignant samples, average FoxM1 expression level is (529.27 ± 75.85) in samples without cytological diagnostic evidence, while (1,218.12 ± 167.21) in samples with cytological diagnostic evidence. Differences of FoxM1 expression level between benign pleural effusions and malignant ones have statistical significance. There is an area of 0.881 under the receiver-operating characteristic curve, which verifies the accuracy of using FoxM1 expression level as diagnostic index to identify benign and malignant pleural effusions. According to our study, diagnostic sensitivity and specificity for FoxM1 expression level at 418.1 were 82.6 and 86.7 %, respectively, while 47.8 and 100 %, respectively, at 768.7. FoxM1 expression level in malignant pleural effusions is significantly higher than in benign ones. This study provides a new approach in clinical diagnosis, with FoxM1 as a specific molecule marker to identify benign and malignant pleural effusions. FoxM1 expression level could provide evidence for diagnosis and treatment of malignant pleural effusions and lung cancer.

Rapid generation of rice mutants via the dominant negative suppression of the mismatch repair protein OsPMS1.

Mismatch repair (MMR) is a conservative pathway for maintaining the genome integrity of different organisms. Although suppression of MMR has resulted in various mutation phenotypes in Arabidopsis, the use of this strategy for mutation breeding in major crops has not been reported. Here, we overexpressed a truncated version of the OsPMS1 protein in rice; this approach is expected to suppress the rice MMR system through a dominant negative mechanism. We observed a wide spectrum of mutation phenotypes in the progeny of the transgenic plants during seed germination and the plant growth stages. Genomic variations were detected with inter-simple sequence repeat (ISSR), and sequencing of the differential ISSR bands revealed that the mutation occurred as a point mutation or as microsatellite instability at high frequencies. Plant lines with agronomically important traits, such as salt and drought tolerance, various tiller number, and early flowering, were obtained. Furthermore, we obtained mutants with important traits that are free of the transgene. Together, these results demonstrate that MMR suppression can be used as an efficient strategy for mutation breeding in rice.

RecQ helicase enhances homologous recombination in plants.

RecQ helicase is a key component in the RecF pathway of Escherichia coli for initiation of homologous recombination. Here, we demonstrate that transient expression of RecQ gene in rice embryogenic cell increases the homologous recombination efficiency as much as 4-fold. Further experiments reveal that this effect is influenced by the RecQ dosage. Stable expression of RecQ in rice dramatically increases the homologous recombination events 20- to 40-fold in leaf tissue from different transgenic lines. This is the first evidence indicating that overexpression of RecQ gene can stimulate homologous recombination in plants.