[The influence of Ras-associated binding protein 23 knockdown on the migration and invasion of esophageal squamous cell carcinoma cells and its mechanism].

Objective: To investigate the role and the mechanism of Ras-associated binding protein23 (RAB23) in the migration and invasion of esophageal squamous cell carcinoma (ESCC) cells. Methods: RAB23 mRNA levels were measured in 16 pairs of ESCC and adjacent normal tissues via real-time polymerase chain reactions. RAB23 mRNA levels in the ESCC and adjacent normal tissues of dataset GSE20347 deposited in the Gene Expression Omnibus (GEO) database were also analyzed. Immunohistochemistry (IHC) was used to detect the RAB23 protein expressions in 106 pairs of ESCC and adjacent normal tissues, as well as in the lymph glands and primary tumor tissues of 33 patients with positive lymph nodes and 10 patients with negative lymph nodes. Endogenous RAB23 expression was transiently depleted using siRNAs (si-NC, si-RAB23-1, and si-RAB23-9) or stably reduced using shRNAs (sh-NC and sh-RAB23) in ESCC KYSE30 and KYSE150 cells, and the knockdown efficiency was tested using Western blot assays. Cell counting kit-8 assays and mouse xenograft models were used to test the proliferation of ESCC cells. Transwell assays and tail vein-pulmonary metastasis models in immunocompromised mice were used to examine the migration and invasion of ESCC cells. Cell adhesion assays were used to test the adhesion of ESCC cells. RNA-seq assays were used to analyze how RAB23 knockdown influenced the expression profile of ESCC cells and the implicated signal pathways were confirmed using Western blot assays. Results: The RAB23 mRNA expression in 16 cases of ESCC tissues was 0.009 7±0.008 9, which was markedly higher than that in adjacent normal tissues (0.003 2±0.003 7, P=0.006). GEO analysis on RAB23 expressions in ESCC and adjacent normal tissues showed that the RAB23 mRNA level in ESCC tissues (4.30±0.25) was remarkably increased compared with their normal counterparts (4.10±0.17, P=0.037). Among the 106 pairs of ESCC and tumor-adjacent normal tissues, 51 cases exhibited low expression of RAB23 and 55 cases showed high expression of RAB23, whereas in the paired tumor-adjacent normal tissues 82 cases were stained weakly and 24 strongly for RAB23 protein. These results indicated that RAB23 expression was markedly increased in ESCC tissues (P<0.001). Additionally, only 1 out of 33 primary ESCC tissues with positive lymph nodes showed low RAB23 protein expression. On the other hand, 7 samples of primary ESCC tissues with negative lymph nodes were stained strongly for RAB23 while its level in the other 3 samples was weak. These results showed that RAB23 expression was remarkably increased in primary ESCC tissues with positive lymph nodes compared with those with negative lymph nodes (P=0.024). Further tests showed that 32 out of 33 positive lymph nodes were stained strongly for RAB23, whereas no negative lymph nodes (n=10) exhibited high expression of RAB23 (P<0.001). Both transient and stable knockdown of endogenous RAB23 expression failed to cause detectable changes in the proliferation of KYSE30 cells in vitro and in vivo, but attenuated the migration and invasion of KYSE30 cells as well as the invasion of KYSE150 cells. RAB23 knockdown was found to significantly decrease the number of adhesive KYSE30 cells in the sh-RAB23 group (313.75±89.34) compared with control cells in the sh-NC group (1 030.75±134.29, P<0.001). RAB23 knockdown was also found to significantly decrease the number of adhesive KYSE150 cells in the sh-RAB23 group (710.5±31.74) compared with the number of control cells in the sh-NC group (1 005.75±61.09, P<0.001). RNA-seq assays demonstrated that RAB23 knockdown using two siRNAs targeting RAB23 mRNA markedly impaired focal adhesion-related signal pathways, and decreased the levels of phosphorylated FAK (p-FAK) and phosphorylated paxillin (p-paxillin) in KYSE30 and KYSE150 cells. Conclusions: Significantly increased RAB23 in ESCC tissues positively correlates with lymph node metastasis. Depleted RAB23 expression attenuates focal adhesion-related signal pathways, thus impairing the invasion, metastasis, and adhesion of ESCC cells.

[Clinical implications of Naples prognostic scores in patients with resectable Siewert type II-III adenocarcinoma of the esophagogastric junction].

Objective: To evaluate the clinical value of preoperative Naples prognostic scores (NPS) in patients with resectable Siewert type II-III esophagogastric junction adenocarcinoma (AEG). Methods: In this retrospective observational study we collected and analyzed relevant data of patients with Siewert Type II-III AEG treated in the Department of Gastric Cancer, Tianjin Medical University Cancer Institute and Hospital from January 2014 to December 2018. NPS were calculated using preoperative albumin concentration, total cholesterol concentration, neutrophil/lymphocyte ratio, and lymphocyte/monocyte ratio and used to allocate patients into three groups: NTS-0 (0 points), NTS-1 (1-2 points) and NTS-2 (3-4 points). Kaplan-Meier was used to calculate disease-free survival (DFS) and overall survival (OS) in each NPS group and the log-rank test to compare these groups. Univariate and multivariate survival analyes were performed using the Cox regression model. Time-dependent receiver operating characteristic curves were constructed to compare the relationships between four commonly used tools for evaluating inflammatory responses and nutritional status:NPS, systemic inflammatory response scores, nutrient control status (CONUT), and prognostic nutrition index (PNI). Results: The study cohort comprised 221 patients with AEG of median age 63.0 (36.0-87.0) years. There were 190 men (86.0%) and 31 women (14.0%). As to pTNM stage, 47 patients (21.3%) had Stage I disease, 68 (30.8%) Stage II, and 106 (48.0%) Stage III. One hundred and forty-seven patients (66.5%) had Siewert Type II disease and 74 (33.5%) Siewert type III. There were 45 patients (20.4%) in the NPS-0, 142 (64.2%) in the NPS-1 and 34 (15.4%) in the NPS-2 groups. Higher NPS scores were significantly associated with older patients (χ²=5.056, P=0.027) and higher TNM stages (H=5.204,P<0.001). The median follow-up was 39 (6-105) months; 16 patients (7.2%) were lost to follow-up. The median OS in the NPS-0, NPS-1, and NPS-2 groups were 78.4, 63.1, and 37.0 months, respectively; these differences are statistically significant (P=0.021). Univariate and multivariate Cox regression analysis identified the following as independently and significantly associated with OS in patients with Siewert Type II-III: TNM stage (Stage II: HR=2.182, 95%CI: 1.227-3.878, P=0.008; Stage III: HR=3.534, 95%CI: 1.380-6.654, P<0.001), tumor differentiation (G3: HR=1.995, 95%CI: 1.141-3.488, P=0.015), vascular invasion (HR=2.172, 95%CI: 1.403-3.363, P<0.001), adjuvant chemotherapy (HR=0.326, 95%CI: 0.200-0.531, P<0.001), NPS (NPS-1: HR=2.331, 95%CI: 1.371-3.964, P=0.002; NPS-2: HR=2.494, 95%CI: 1.165-5.341, P=0.019), SIS group (NPS-1: HR=2.170, 95%CI: 1.244-3.784, P=0.006; NPS-2: HR=2.291, 95%CI: 1.052-4.986, P=0.037), and CONUT (HR=1.597, 95% CI: 1.187-2.149, P=0.038). The median DFS in the NPS-0, NPS-1, and NPS-2 groups was 68.6, 52.5, and 28.3 months, respectively; these differences are statistically significant (P=0.009). Univariate and multivariate Cox regression analysis identified the following as independently and significantly associated with DFS in patients with Siewert Type II-III AEG: TNM stage (StageⅡ: HR=2.789, 95%CI:1.210-6.428, P=0.016; Stage III: HR=10.721, 95%CI:4.709-24.411, P<0.001), adjuvant chemotherapy (HR=0.640, 95% CI: 0.432-0.946, P=0.025), and NPS (NPS-1: HR=1.703, 95%CI: 1.043-2.782, P=0.033; NPS-2: HR=3.124, 95%CI:1.722-5.666, P<0.001). Time-dependent receiver operating characteristic curves showed that NPS was more accurate in predicting OS and DFS in patients with Siewert Type II-III AEG than were systemic inflammatory response scores, CONUT, or PNI scores. Conclusion: NPS is associated with age and TNM stage, is an independent prognostic factor in patients who have undergone resection of Siewert type II-III AEG, and is better than SIS, CONUT, or PNI in predicting survival.

[Diagnosis and treatment of intravenous leiomyomatosis].

Intravenous leiomyomatosis is a rare type of tumor that is histologically benign but biologically invasive. It originates from the smooth muscle of the uterine or the uterine vein. It can grow through the uterus and extend into the pelvic cavity, or grow along the veins without invading the wall of the venous vessel itself. The tumors are estrogen-dependent and can metastasize through the bloodstream. Thus, in addition to continuous growth, some tumors exhibit isolated growths in the venous system and heart chambers or show disseminated growth in the lungs, although distant metastasis to other regions usually do not occur. Currently, there is limited research on this disease, the majority of which are case reports, surgical experience summaries, and differentiation from ordinary gynecological myomas in terms of pathogenesis and radiological diagnostic experience. There are two main theories on the origin of the disease: uterine smooth muscle and smooth muscle of the uterine veins. Some studies have verified the role of estrogen, progesterone receptor-related pathways, and angiogenesis in the development of the disease. The clinical symptoms of this disease are varied, depending on the affected area. In the early stages, when the tumor only affects the pelvic cavity, patients show mild symptoms resulting from pelvic organ compression. When it progresses to the inferior vena cava and heart, patients show more complex symptoms resulting from venous return obstruction, cardiac obstruction, and hemodynamics appearing. Different institutions have proposed different disease staging and classification strategies for different clinical purposes. Some are based on the affected area of the lesion; others are based on the size of the tumor. Although surgery remains the main treatment for this disease, the specific surgical approach, adjuvant drug therapy, and prognosis still need further exploration.

Outcome and etiology of fetal pleural effusion, fetal ascites, and hydrops fetalis after fetal intervention: retrospective observational cohort from a single institution.

OBJECTIVES: Nonimmune hydrops fetalis (NIHF) is the pathological accumulation of fluids in fetal compartments without maternal isoimmunisation. Fetal interventions (e.g. shunting, fetal paracentesis, fetal thoracocentesis, and fetal pleurodesis) are used to alleviate the fluid accumulations. The outcomes of fetal interventions are uncertain because the underlying causes of NIHF vary. We explore the etiologies and the long-term outcomes of NIHF after fetal interventions. METHODS: Fetuses with NIHF, defined by the presence of fetal ascites, pleural or pericardial effusion, skin edema and cystic hygroma, or a combination of these features, who underwent fetal interventions at our institution during 2012-2021 were retrospectively reviewed. Clinical surveillance, genetic analyses, and viral infection screening were used to delineate the etiologies. Chart reviews and telephone interviews were conducted to assess the long-term outcomes. RESULTS: A total of 55 fetuses were enrolled and 46 cases had final follow-up data after birth. Etiologies were identified in 33 cases, of which 4 who initially failed to identify the underlying causes using small-gene-panel tests were later diagnosed with monogenic disorders by whole exome sequencing (WES). Twenty-three cases survived with a follow-up period of 2- to 11-year span when submission, 17 of which were healthy. Particularly, all 11 cases initially presented as congenital chylothorax survived with favorable outcomes. CONCLUSIONS: The etiologies of NIHF are heterogeneous, and the long-term (2- to 11-year span) outcomes of fetal interventions vary and are correlated with the underlying etiologies. Genome-wide tests, such as WES, are helpful for prenatal diagnosis and possibly alter the future fetal therapy strategies of NIHF. This article is protected by copyright. All rights reserved.

Prognostic value of multiphase CT angiography: estimated infarct core volume in the patients with acute ischaemic stroke after mechanical thrombectomy.

BACKGROUND AND PURPOSE: Recent studies reported the feasibility of quantifying a reliable infarct core (IC) volume using multiphase computed tomography (mCTA) based on deep learning, however its prognostic value was not fully clarified. Therefore, we aimed to evaluate the prognostic value of mCTA-estimated IC volume in patients with acute ischemic stroke (AIS) after mechanical thrombectomy (MT). MATERIALS AND METHODS: We retrospectively reviewed patients who underwent mCTA and MT for large vessel occlusion in middle cerebral artery and (or) internal carotid artery within 6 hours after symptom onset between January 2018 and November 2019. Patients were dichotomized into good (modified Rankin Scale [mRS] score, 0-2) and poor (mRS, 3-6) outcome groups. mCTA-estimated IC volume were generated based on a multi-scale three-dimensional convolutional neural network. Univariate, multivariate logistic regression and receiver operating characteristic (ROC) curve analyses were used to identify the independent variables, and evaluate their performances in predicting the clinical outcome. RESULTS: Of 44 included patients, 27 (61.4%) patients achieved good outcome. National Institutes of Health Stroke Scale scores at admission [NIHSSpre] (odds ratio [OR], 1.191; 95%confidence interval [CI], 1.028-1.379; P=0.020) and mCTA-estimated IC volume (OR, 1.076; 95%CI, 1.016-1.140; P=0.013) were found to be independently associated with functional outcome in patients with AIS after MT. After integrating NIHSSpre and mCTA-estimated IC volume, optimal performance (area under the ROC curve, 0.874; 95%CI, 0.739-0.954) could be obtained in predicting the clinical outcome. CONCLUSIONS: mCTA-estimated IC volume might be promising for predicting the prognosis, and assisting in making individualized treatment decision in patients with AIS.

[Low-frequency fluctuation amplitude changes in resting-state brain functional magnetic resonance imaging and its correlation with clinical hearing levels in patients with unilateral hearing impairment].

Objective: To investigate low-frequency fluctuation amplitude changes in resting-state brain fMRI and its correlation with clinical hearing levels in patients with clinical hearing level in patients with unilateral hearing impairment. Methods: Forty-five patients with unilateral hearing impairment[12 males and 33 females, aged 36-67 (46.0±9.7) years], and 31 controls with normal hearing[9 males and 22 females, aged 36-67 (46.0±10.1) years], were retrospectively included. All subjects underwent blood oxygen level-dependent (BOLD) resting-state functional magnetic resonance imaging and high-resolution T1-weighted imaging. The patients were divided into the left-sided hearing impaired group(24 cases), and the right-sided hearing impaired group(21 cases). After data being preprocessed, differences in low frequency amplitude (ALFF) metrics between the evaluated patients and controls were calculated and analyzed, and the statistics were corrected for Gaussian random field (GFR). Results: Overall comparative analysis of patients with hearing impairment showed that one-way ANOVA among the three groups showed abnormal ALFF values only in the right anterior cuneiform lobe (GRF adjusted P=0.002). The ALFF value of the hearing impaired group was higher than that of the control group in one cluster (peak coordinates: X=9, Y=-72, Z=48, T=5.82), involving the left occipital gyrus, right anterior cuneiform lobe, left superior cuneiform lobe, left superior parietal gyrus, and left angular gyrus (GRF adjusted P=0.031). The ALFF value of the hearing impaired group was lower than that of the control group in three clusters (peak coordinates: X=57, Y=-48, Z=-24; T=-4.99; X=45, Y=-66, Z=0, T=-4.06; X=42, Y=-12, Z=36, T=-4.03), involving the right inferior temporal gyrus, the right middle temporal gyrus, and the right precentral gyrus (GRF adjusted P=0.009). Compared with the control group, the ALFF value of the left hearing impairment group was significantly higher than that of the control group in one cluster (peak coordinates: X=-12, Y=-75, Z=45, T=5.78), involving the left anterior cuneiform lobe, right anterior cuneiform lobe, left middle occipital gyrus, left superior parietal gyrus, left superior occipital gyrus, left cuneiform lobe, and right cuneiform lobe (P=0.023 after GRF correction). Compared with the control group, the right hearing impairment group had a significantly higher ALFF value in one cluster (peak coordinates: X=9, Y=-46, Z=22, T=6.06), involving the left middle occipital gyrus, right anterior cuneiform lobe, left cuneiform lobe, right cuneiform lobe, left superior occipital gyrus, and right superior occipital gyrus (GRF adjusted P=0.022); The brain area with reduced ALFF values is located in the right inferior temporal gyrus (GRF adjusted P=0.029). Spearman's two-tailed correlation analysis between ALFF values and pure tone average in the abnormal brain regions showed that ALFF values in the abnormal brain regions correlated to some extent with the pure tone average (PTA) only in the left-sided hearing impaired group(PTA=2 000 Hz, r=0.318,P=0.033;PTA=4 000 Hz,r=0.386,P=0.009). Conclusion: The abnormal neural activity within the brain are different in patients with left-sided and right-sided hearing impairment, and the severity of hearing impairment is related to the difference in functional integration of brain regions.

Mouth breathing induces condylar remodelling and chondrocyte apoptosis via both the extrinsic and mitochondrial pathways in male adolescent rats.

The prevalence of mouth breathing is high in children and adolescents. It causes various changes to the respiratory tract and, consequently, craniofacial growth deformities. However, the underlying mechanisms contributing to these effects are obscure. Herein, we aimed to study the effects of mouth breathing on chondrocyte proliferation and death in the condylar cartilage and morphological changes in the mandible and condyle. Additionally, we aimed to elucidate the mechanisms underlying chondrocyte apoptosis and investigate any variations in the related pathways. Subchondral bone resorption and decreased condylar cartilage thickness were observed in mouth-breathing rats; further, mRNA expression levels of Collagen II, Aggrecan, and Sox 9 were lower in the mouth breathing group, while those of matrix metalloproteinase 9 increased. TdT-mediated dUTP nick end labelling staining and immunohistochemistry analyses showed that apoptosis occurred in the proliferative and hypertrophic layers of cartilage in the mouth breathing group. TNF, BAX, cytochrome c, and cleaved-caspase-3 were highly expressed in the condylar cartilage of the mouth-breathing rats. These results suggest that mouth breathing leads to subchondral bone resorption, cartilage layer thinning, and cartilage matrix destruction, inducing chondrocyte apoptosis via both the extrinsic and mitochondrial apoptosis pathways.

[Explore the influence of vitamin D supplementation on clinical efficacy and drug retention rate of vedolizumab in patients with ulcerative colitis].

Objectives: To analyze the influence of vitamin D supplementation on clinical efficacy and drug retention rate of vedolizumab (VDZ) in patients with ulcerative colitis (UC). Methods: Retrospective study. By retrieving the clinical database of the Second Affiliated Hospital of Wenzhou Medical University, the patients with moderately to severely active UC were collected, who underwent VDZ treatment from January 2020 to June 2022. The modified Mayo score and Mayo endoscopic score (MES) were employed to evaluate disease activity and intestinal inflammation in UC patients, respectively. According to whether vitamin D was supplemented during VDZ treatment, the patients were divided into supplementary group and non-supplementary group. According to baseline serum 25(OH) D level, UC patients were divided into vitamin D deficiency group and non-deficiency group. According to whether vitamin D was supplemented, the patients of each group were divided into supplementary subgroup and non-supplementary subgroup, respectively. The clinical response rate, clinical remission rate and mucosal healing rate at week 30 after receiving VDZ treatment and the retention rate of VDZ at the 72nd week were observed. The effect of baseline serum 25 (OH) D level on the efficacy of vitamin D supplementation was analyzed by chi-square test. The effects of vitamin D supplementation on the clinical efficacy and drug retention of VDZ in UC were analyzed by chi-square test and Kaplan-Meier curve, respectively. Results: A total of 80 patients with moderately to severely active UC, who were aged (39.4±13.0) years(18-75 years), 37 male and 43 female, were included. There were 43 cases in supplementary group and 37 cases in non-supplementary group. There were 59 cases in the deficiency group, including 32 cases in the supplementary subgroup and 27 cases in the non-supplementary subgroup. There were 21 cases in the non-deficiency group, including 11 cases in the supplementary subgroup and 10 cases in the non-supplementary subgroup. At week 30, the average level of serum 25(OH) D was shown to be higher in supplementary group than that at week 0 [(24.5±5.4) vs (17.7±6.7) µg/L, P<0.001]. At week 30, in contrast with non-supplementary group, erythrocyte sedimentation rate(ESR)[75.0% (24.3%, 86.7%) vs 32.7% (-2.6%, 59.3%), P=0.005] and modified Mayo score [(4.7±2.8) vs (2.3±2.7) points, P<0.001] and MES score [(1.2±1.1) vs (0.4±0.9) points, P=0.001] were significantly reduced, clinical response rate [79.1%(34/43) vs 56.8%(21/37), P=0.032], clinical remission rate [67.4%(29/43) vs 29.7%(11/37), P=0.001] and mucosal healing rate [72.1%(31/43) vs 37.8%(14/37), P=0.002] were higher. At week 72, drug retention rate of VDZ was shown to be higher in supplementary group than in non-supplementary group [55.8%(24/43) vs 27.0%(10/37), P=0.004]. The further analysis showed that vitamin D supplementation could only improve clinical response rate[71.9%(23/32) vs 44.4%(12/27), P=0.033], clinical remission rate[62.5%(20/32) vs 14.8%(4/27), P<0.001], mucosal healing rate[68.8%(22/32) vs 22.2%(6/27), P<0.001] and drug retention rate [53.1%(17/32) vs 13.8%(4/27), P=0.001] in the patients with vitamin D deficiency. Conclusion: Vitamin D supplementation contributes to improving clinical response rate, clinical remission rate, mucosal healing rate and drug retention rate of VDZ in UC patients.

Whole-genome sequencing enables molecular dissection and candidate gene identification of the rust resistance gene R12 in sunflower (Helianthus annuus L.).

KEY MESSAGE: We finely mapped the rust resistance gene R12 to a 0.1248-cM region, identified a potential R12 candidate gene in the XRQ reference genome, and developed three diagnostic SNP markers for R12. Rust is a devastating disease in sunflower that is damaging to the sunflower production globally. Identification and utilization of host-plant resistance are proven to be preferable means for disease control. The rust resistance gene R12 with broad-spectrum specificity to rust was previously localized to a 2.4 Mb region on sunflower chromosome 11. To understand the molecular mechanism of resistance, we conducted whole-genome sequencing of RHA 464 (R12 donor line) and reference genome-based fine mapping of the gene R12. Overall, the 213 markers including 186 SNPs and 27 SSRs' were identified from RHA 464 sequences and used to survey polymorphisms between the parents HA 89 and RHA 464. Saturation mapping identified 26 new markers positioned in the R12 region, and fine mapping with a large population of 2004 individuals positioned R12 at a genetic distance of 0.1248 cM flanked by SNP markers C11_150451336 and S11_189205190. One gene, HanXRQChr11g0348661, with a defense-related NB-ARC-LRR domain, was identified in the XRQr1.0 genome assembly in the R12 region; it is predicted to be a potential R12 candidate gene. Comparative analysis clearly distinguished R12 from the rust R14 gene located in the vicinity of the R12 gene on chromosome 11. Three diagnostic SNP markers, C11_147181749, C11_147312085, and C11_149085167, specific for R12 were developed in the current study, facilitating more accurate and efficient selection in sunflower rust resistance breeding. The current study provides a new genetic resource and starting point for cloning R12 in the future.

Introgression and targeting of the Pl37 and Pl38 genes for downy mildew resistance from wild Helianthus annuus and H. praecox into cultivated sunflower (Helianthus annuus L.).

KEY MESSAGE: Two new downy mildew resistance genes, Pl37 and Pl38, were introgressed from wild sunflower species into cultivated sunflower and mapped to sunflower chromosomes 4 and 2, respectively Downy mildew (DM), caused by the oomycete pathogen Plasmopara halstedii (Farl.) Berl. & de Toni, is known as the most prevalent disease occurring in global sunflower production areas, especially in North America and Europe. In this study, we report the introgression and molecular mapping of two new DM resistance genes from wild sunflower species, Helianthus annuus and H. praecox, into cultivated sunflower. Two mapping populations were developed from the crosses of HA 89/H. annuus PI 435417 (Pop1) and CMS HA 89/H. praecox PRA-417 (Pop2). The phenotypic evaluation of DM resistance/susceptibility was conducted in the BC1F2-derived BC1F3 populations using P. halstedii race 734. The BC1F2 segregating Pop1 was genotyped using an Optimal GBS AgriSeq™ Panel consisting of 768 mapped SNP markers, while the BC1F2 segregating Pop2 was genotyped using a genotyping-by-sequencing approach. Linkage analysis and subsequent saturation mapping placed the DM resistance gene, designated Pl37, derived from H. annuus PI 435417 in a 1.6 cM genetic interval on sunflower chromosome 4. Pl37 co-segregated with SNP markers SPB0003 and C4_5738736. Similarly, linkage analysis and subsequent saturation mapping placed the DM resistance gene, designated Pl38, derived from H. praecox PRA-417 in a 0.8 cM genetic interval on sunflower chromosome 2. Pl38 co-segregated with seven SNP markers. Multi-pathotype tests revealed that lines with Pl37 or Pl38 are immune to the most prevalent and virulent P. halstedii races tested. Two germplasm lines, HA-DM15 with Pl37 and HA-DM16 with Pl38, were developed for use in sunflower DM-resistance breeding.

The association between glucose fluctuation with sarcopenia in elderly patients with type 2 diabetes mellitus.

OBJECTIVE: Growing evidence shows that sarcopenia is more prevalent in patients with type 2 diabetes mellitus (T2DM) than in the normal population. However, currently, data on the relationship between blood glucose fluctuation and sarcopenia in elderly patients with T2DM are still limited. PATIENTS AND METHODS: In this study, 280 patients ≥ 60 years with T2DM were divided into sarcopenic group and non-sarcopenic group, according to the diagnostic criteria of the 2019 Asian Working Group for Sarcopenia. They wore MeiQi to acquire the indexes including time in range (TIR), time above range (TAR), time below range (TBR), mean amplitude of glycemic excursion (MAGE), coefficient of Variation (CV), blood glucose standard deviation (SD), largest amplitude of glycemic excursions (LAGE) and mean glucose (MG). The prevalence rate of sarcopenia was statistically analyzed and the different indicators of glucose fluctuation between the two groups were compared. We analyzed the indexes of glucose fluctuation and appendicular skeletal muscle mass index (ASMI), handgrip strength, the time of five times sit to stand test (FTSST) with Spearman's correlation analysis. Logistic regression was used to analyze the influence factors for sarcopenia. RESULTS: The prevalence of sarcopenia was 15.36%. TIR, MG and TAR were correlated with ASMI, handgrip strength, the time of FTSST. MG and TAR were risk factors for sarcopenia, while TIR was the protective factor of sarcopenia. After adjusting mixing factors, logistic regression analysis showed that TIR was an independent protective factor. The result of the Chi-square test showed that the incidence of sarcopenia in different TIR ranges was different: the proportion of patients with sarcopenia was 40.48% (TIR ≤50%), 20.41% (50%70%). CONCLUSIONS: TIR is associated with sarcopenia in elderly T2DM patients. Furtherly, the incidence rate of sarcopenia decreases with the increase of TIR.

[Intervention effects of drugs on GSH and SOD enzyme activity of rats kidney acutely poisoned by nickel carbonyl].

Objective: To evaluate the intervention effect of various drugs on glutathione (GSH) and superoxide dismutase (SOD) enzyme activity of rats kidney with acute nickel carbonyl poisoning. Methods: In January 2019, The 250 SPF male SD rats were randomly divided into normal control group (n=10) , poisoned group (n=40) and treatment groups (n=200) according to the random number table method. And the treatment groups were divided into methylprednisolone group (20 mg/kg) , DDC group (100 mg/kg) , sodium selenite group (10 µmol/kg) , Shenfu huiyang decoction group (0.25 ml) and methylprednisolone combined with DDC group (100 mg/kg) , with 40 mice in each group. Except for the normal control group, rats in the other groups were exposed to nickel carbonyl for 30 min, at 4 h and 30 h after exposure, the rats in each treatment group were intraperitoneally injected with corresponding drugs, and kidney tissues were collected 3 d and 7 d after administration, with 10 mice in each group. The activities of GSH and SOD in kidney were measured by enzyme-linked immunosorbent assay, and using electron microscopy observe ultrastructure changes. Results: Compared to the control group, the activities of GSH and SOD enzyme of poisoned group were significantly decreased at 3 d or 7 d after 4 h or 30 h exposure, and the difference was statistically significant (P=0.000, 0.031, 0.001, 0.033) , the epithelial nuclei of proximal convoluted tubules were pyknosis and lysosome hyperplasia in the cytoplasm. And compared to poisoned group, the activities of GSH and SOD enzyme of methylprednisolone+DDC group were significantly increased at treatment with 7 d after 4 h exposure, the difference was statistically significant (P=0.022, 0.000) , and the activities of GSH and SOD enzyme of methylprednisolone and enzyme of methylprednisolone+DDC group were significantly higher at 7 days than at 3 days, the difference was statistically significant (P=0.020, 0.017, 0.018, 0.033) . The results of electron microscopy showed that the cell nuclei and cytoplasmic organelles of proximal convolute tubule were almost restored to normal tissue level of both methylprednisolone group and methylprednisolone+DDC group. Conclusion: The methylprednisolone and methylprednisolone+DDC have obvious repair effect on renal enzyme activity level of rats with acute nickel carbonyl poisoning, and the treatment effect is better for a long time of medication.

Bacterial antibiotic resistance among cancer inpatients in China: 2016-20.

BACKGROUND: The incidence of infections among cancer patients is as high as 23.2-33.2% in China. However, the lack of information and data on the number of antibiotics used by cancer patients is an obstacle to implementing antibiotic management plans. AIM: This study aimed to investigate bacterial infections and antibiotic resistance in Chinese cancer patients to provide a reference for the rational use of antibiotics. DESIGN: This was a 5-year retrospective study on the antibiotic resistance of cancer patients. METHODS: In this 5-year surveillance study, we collected bacterial and antibiotic resistance data from 20 provincial cancer diagnosis and treatment centers and three specialized cancer hospitals in China. We analyzed the resistance of common bacteria to antibiotics, compared to common clinical drug-resistant bacteria, evaluated the evolution of critical drug-resistant bacteria and conducted data analysis. FINDINGS: Between 2016 and 2020, 216 219 bacterial strains were clinically isolated. The resistance trend of Escherichia coli and Klebsiella pneumoniae to amikacin, ciprofloxacin, cefotaxime, piperacillin/tazobactam and imipenem was relatively stable and did not significantly increase over time. The resistance of Pseudomonas aeruginosa strains to all antibiotics tested, including imipenem and meropenem, decreased over time. In contrast, the resistance of Acinetobacter baumannii strains to carbapenems increased from 4.7% to 14.7%. Methicillin-resistant Staphylococcus aureus (MRSA) significantly decreased from 65.2% in 2016 to 48.9% in 2020. CONCLUSIONS: The bacterial prevalence and antibiotic resistance rates of E. coli, K. pneumoniae, P. aeruginosa, A. baumannii, S. aureus and MRSA were significantly lower than the national average.

MRI-based radiomics analysis in differentiating solid non-small-cell from small-cell lung carcinoma: a pilot study.

AIM: To investigate the ability of a T2-weighted (W) magnetic resonance imaging (MRI)-based radiomics signature to differentiate solid non-small-cell lung carcinoma (NSCLC) from small-cell lung carcinoma (SCLC). MATERIALS AND METHODS: The present retrospective study enrolled 152 eligible patients (NSCLC = 125, SCLC = 27). All patients underwent MRI using a 3 T scanner and radiomics features were extracted from T2W MRI. The least absolute shrinkage and selection operator (LASSO) logistic regression model was used to identify the optimal radiomics features for the construction of a radiomics model to differentiate solid NSCLC from SCLC. Threefold cross validation repeated 10 times was used for model training and evaluation. The conventional MRI morphology features of the lesions were also evaluated. The performance of the conventional MRI morphological features, and the radiomics signature model and nomogram model (combining radiomics signature with conventional MRI morphological features) was evaluated using receiver operating characteristic (ROC) curve analysis. RESULTS: Five optimal features were chosen to build a radiomics signature. There was no significant difference in age, gender, and the largest diameter. The radiomics signature and conventional MRI morphological features (only pleural indentation and lymph node enlargement) were independent predictive factors for differentiating solid NSCLC from SCLC. The area under the ROC curves (AUCs) for MRI morphological features, and the radiomics model, and nomogram model was 0.69, 0.85, and 0.90 (ROC), respectively. CONCLUSIONS: The T2W MRI-based radiomics signature is a potential non-invasive approach for distinguishing solid NSCLC from SCLC.

[A preliminary study on the improved efficacy of mesalazine combined with vitamin D3 in ulcerative colitis].

Objective: To analyze the influence of vitamin D3 supplementation on the clinical efficacy of mesalazine in patients with ulcerative colitis (UC). Methods: From January 2015 to December 2020, patients with mild-to-moderate active UC were retrospectively and continuously enrolled, who accepted mesalazine treatment for at least 12 months at the Second Affiliated Hospital of Wenzhou Medical University. According to simultaneous supplement of vitamin D3 (125 IU/d), the patients were divided into study group and control group. Demographic and disease characteristics, serum 25-hydroxyvitamin D[25(OH)D] levels and other information were collected through retrieving hospital database. Student's t-test, Mann-Whitney U test and Chi-square test were applied for comparison of disease characteristics. The changes of modified Mayo scores[ΔMayo] and 25(OH)D[Δ25(OH)D] were compared before and after treatment by paired t-test, Wilcoxon signed rank test and Chi-square test. Multiple linear regression model was used to analyze the independent factors affecting ΔMayo and Δ25(OH)D, and variables with P-values less than 0.20 in the univariate analysis were allowed for further multivariate analysis. Results: A total of 74 UC patients (44 males, 30 females), with median age (range) 39.5 (20-76) years old, were analyzed and respectively assigned into study group (n=36) and control group (n=38). In study group, the average level of serum 25(OH)D was significantly increased at month 12 compared with that at baseline [(22.87±7.30) µg/L vs. (18.15±7.48) µg/L,P<0.001]. However, no significant elevation of serum 25(OH)D was found in control group [(19.17±8.49) µg/L vs. (19.82±9.47) µg/L,P=0.466]. Furthermore, there was a significant decrease of modified Mayo score [-3(-4.75, -1.25) vs.-2(-3.25, 0), P=0.034] and a higher clinical remission rate (55.6% vs. 28.9%, P=0.020) at month 12 in study group than those in control group. In addition, according to the baseline level of serum 25(OH)D before mesalazine treatment, 74 UC patients were divided into vitamin D deficiency group (n=38, serum 25(OH)D<20 µg/L) and non-deficiency group (n=36, serum 25(OH)D≥20 µg/L). At month 12 in vitamin D deficiency group, patients with vitamin D3 supplementation had a greater decline in modified Mayo score [-4(-5.75, -2) vs.-2(-4, 0), P=0.048] and a higher clinical remission rate (60.0% vs. 22.2%, P=0.019) compared with those without. Conclusions: In patients with mild-to-moderate active UC receiving mesalazine treatment, vitamin D3 supplementation may improve the clinical efficacy, especially in patients with vitamin D deficiency.