Exploring the prognostic significance of iron death­related lncRNAs in colorectal cancer: A systematic review and meta­analysis.

Colorectal cancer is a significant health challenge globally, with its prognosis associated with the profile of molecular biomarkers. Recently, the role of iron death-associated long non-coding (lnc)RNAs in cancer development has garnered attention; however, their expression patterns and prognostic value in colorectal cancer remain poorly elucidated. The present study aimed to assess the expression levels of iron death-related lncRNAs in colorectal cancer tissues and evaluate their relationship with patient outcomes through a comprehensive meta-analysis. Systematic searches were performed across multiple databases, including PubMed, Embase, Web of Science, Cochrane Library, CNKI, Wanfang and VIP databases, to identify studies relevant to the objective of the present study. Selected studies met predetermined inclusion criteria, from which data were extracted. R software version 4.3.1 was used for the meta-analysis, evaluating the association between iron death-related lncRNAs expression and colorectal cancer prognosis. Publication bias was assessed using funnel plot analysis, and Begg's and Egger's test. A total of 11 studies, including 3,984 patients with colorectal cancer, were included in the present meta-analysis. The results demonstrated a significant association between iron death-related lncRNAs and tumor stage classification [odds ratio (OR)=2.00; 95% confidence interval (CI), 1.77-2.24]. Notably, a significant association was also revealed between iron death-related lncRNAs and T stage classification in colorectal cancer (OR=1.82; 95% CI, 1.50-2.20). Furthermore, a statistically significant association was demonstrated between iron death-related lncRNAs and lymph node metastasis in colorectal cancer (OR=1.31; 95% CI, 1.03-1.66). The findings also highlighted a significant association between iron death-associated lncRNA and distant metastasis in colon cancer (OR=2.04; 95% CI, 1.62-2.56). Moreover, a significant association between iron death-related lncRNAs and risk score in colorectal cancer was revealed (OR=1.75; 95% CI, 1.25-2.46). In conclusion, the findings of the present meta-analysis underscore the potential of high ferroptosis-associated lncRNA expression as an indicator of adverse outcomes in colorectal cancer, suggesting their viability as biomarkers for cancer progression and prognosis. This insight opens potential new avenues for clinical application and further research into colorectal cancer management.

Prognostic related gene index for predicting survival and immunotherapeutic effect of hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is the most common malignant liver tumor. It is an aggressive disease with high mortality rate. In this study, we investigated a new prognosis-related gene index (PRGI) that can predict the survival and efficacy of immunotherapy in patients with HCC. RNA-seq data and clinical data of HCC samples were obtained from the cancer genome atlas and ICGC databases. Prognosis-related genes were obtained using log-rank tests and univariate Cox proportional hazards regression. Univariate and multivariate analyses were performed on the overall survival rate of patients with prognosis-related genes and multiple clinicopathological factors, and a nomogram was constructed. A PRGI was then constructed based on least absolute shrinkage and selection operator or multivariate Cox Iterative Regression. The possible correlation between PRGI and immune cell infiltration or immunotherapy efficacy was discussed. Eight genes were identified to construct the PRGI. PRGI can predict the infiltration of immune cells into the tumor microenvironment of HCC and the response to immunotherapy. PRGI can accurately predict the survival rate of patients with HCC, reflect the immune microenvironment, and predict the efficacy of immunotherapy.

Differentially expressed genes PCCA, ECHS1, and HADH are potential prognostic biomarkers for gastric cancer.

Gastric cancer (GC) is one of the most common malignant tumors in the world. As far as we know, no biomarker has been widely accepted for early diagnosis and prognosis prediction of GC. The purpose of this study is to find potential biomarkers to predict the prognosis of GC. The differentially expressed gene (DEG) was analyzed from GSE93774. Enrichr was used to analyze the gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, the enrichment of transcription factors (TF), miRNA, and kinase. GO analysis showed DEGs was enriched in the process of amino acid metabolism. Pathway results showed DEGs was mainly enriched in cell cycle. Propionyl CoA carboxylase alpha (PCCA), Enoyl coenzyme A hydratase short chain 1 (ECHS1), and 3-hydroxyacyl-CoA dehydrogenase (HADH) have prognostic value in patients with GC. ECHS1 and HADH genes were significantly associated with disease-free survival. There was a significant correlation between PCCA and overall survival rate. The results of this study suggest that PCCA, ECHS1, and HADH may be new biomarkers for predicting the prognosis of GC.

[Baicalein attenuates acute lung injury induced by intestinal ischemia/reperfusion via inhibition of nuclear factor-κB pathway in mice].

OBJECTIVE: To investigate the effects of baicalein (Bai) on acute lung injury (ALI) induced by intestinal ischemia/reperfusion (I/R) and its mechanism in mice. METHODS: Twenty-four male C57BL/6J mice were divided into three groups by random number table: namely sham group, I/R group and Bai+I/R group, with 8 mice in each group. Intestinal I/R induced lung injury model was reproduced by clamping superior mesenteric artery for 90 minutes, followed by reperfusion. Bai (100 mg/kg) was intraperitoneally injected 1 hour before ischemic challenge in the Bai+I/R group. The mice in sham group underwent the similar procedure with I/R group but without vascular occlusion. All mice were sacrificed at 4 hours of reperfusion, and blood was collected from inferior vena cava and lung tissues were harvested. Lung tissues were stained with hematoxylin-eosin (HE), and histological changes were examined under light microscope for pathological score. Lung wet/dry (W/D) ratio was calculated. Lung cell apoptosis was determined by TdT-mediated dUTP nick end labeling (TUNEL) technique. Serum levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were determined by enzyme-linked immunosorbent assay (ELISA). The mRNA expressions of TNF-α and IL-6 in lung tissues were determined by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR). The protein expression levels of cytoplasmic inhibitory factor-α of nuclear factor-κB (IκB-α) and nucleus NF-κB were determined by Western Blot. RESULTS: Under light microscope, a normal lung tissue structure was shown in the sham group and no evidence of obvious lung injury was found. In the I/R group, the alveolar structure was seriously damaged. The alveolar wall was widened and there was significant interstitial edema and leukocytes infiltration. In the Bai+I/R group, pathological damage was significantly decreased as indicated by reduced lung tissue edema and leukocytes infiltration. Compared with the sham group, the lung pathological scores, W/D ratio and cellular apoptosis in the I/R group were significantly increased. Both serum TNF-α and IL-6 contents and lung TNF-α and IL-6 mRNA expressions were significantly increased. Furthermore, I/R significantly resulted in a decrease of IκB-α in the cytoplasm and an increase of NF-κB in the nucleus. Notably, Bai treatment significantly attenuated ALI induced by intestinal I/R injury. Compared with the I/R group, the lung pathological scores and W/D ratio in the Bai+I/R group were significantly decreased (lung pathological score: 4.59±1.17 vs. 6.27±1.34, W/D ratio: 3.79±0.28 vs. 4.32±0.57), cellular apoptosis was significantly decreased [(4.85±2.47)% vs. (8.15±2.33)%], both serum TNF-α and IL-6 contents and lung TNF-α and IL-6 mRNA expressions were significantly decreased [serum TNF-α (pg/L): 124.18±30.49 vs. 167.72±38.65, IL-6 (ng/L): 1.65±0.69 vs. 2.43±0.57; lung TNF-α mRNA (2-ΔΔCt): 4.75±2.38 vs. 7.69±2.32, IL-6 mRNA (2-ΔΔCt): 16.45±4.39 vs. 27.69±6.82], additionally, Bai pretreatment significantly increased cytoplasmic IκB-α protein expression (gray value: 0.47±0.11 vs. 0.27±0.09), while decreased nuclear NF-κB protein expression (gray value: 0.57±0.13 vs. 1.07±0.14, all P < 0.05). CONCLUSIONS: Bai could attenuate intestinal I/R injury induced ALI via the inhibition of inflammation and apoptosis.

Predisposition to Schizophrenia: An Update of Current Understanding.

Within the field of mental health, the concept of predisposition or that of being "at risk" has been properly addressed by Mrazek and Haggarty. This period prior to clear diagnosis of psychosis has been referred by several names like 'premorbid' phase, at-risk individuals, predisposed individuals, prodromal phase, etc. The premorbid phase is perhaps the most debated term in this list because this term suggests that the morbidity arises only in the overt illness phase. However, evidences arising from several different lines of observations suggest that this may not be the case. In spite of the fact that it has been generally accepted that the prodromal phase precedes the clinical phase, identification of this phase remains a challenge. The real challenge in identifying the onset of the prepsychotic phase is the differentiation of 'normal' experiences from these 'abnormal' experiences. Much fewer studies have been conducted for the assessment of cognitive functions in prodromal phase or predisposed phases of schizophrenia. Cognitive deficits, particularly in memory and attentional functions, are among the most extensively documented aspects of psychosis. Regarding the somatosensory abnormalities in the high-risk individuals, so far there has been only one study conducted which involved somatosensory evoked potentials in these patients.

[Serum anti-Ku86: a potential biomarker for early detection of hepatocellular carcinoma].

OBJECTIVE: To investigate the clinical value of serum anti-Ku86 in early detection of hepatocellular carcinoma (HCC). METHODS: Expression levels of Ku86 protein in HCC and adjacent normal liver tissues were detected by Western blotting. Serum anti-Ku86 level in 83 patients with early HCC and 124 patients with liver cirrhosis were detected by enzyme-linked immunosorbent assay (ELISA). Chemiluminescence was used to measure the serum level of α-fetoprotein (AFP). RESULTS: Expression of Ku86 protein in HCC was increased when compared with the adjacent normal liver tissues (0.21 ± 0.05 vs. 0.08 ± 0.02, P < 0.01). Serum anti-Ku86 level was significantly elevated in HCC patients compared with that in liver cirrhosis patients (0.47 ± 0.22 vs. 0.22 ± 0.06 Abs at 450 nm, P < 0.01), but there was no significant difference between HBV infection and HCV infection in HCC patients (0.51 ± 0.19 vs. 0.47 ± 0.24, P = 0.267). Of note, serum anti-Ku86 level was significantly decreased after surgical resection of the tumors in the 30 HCC cases tested (P < 0.01). The results of ROC analysis indicated a better performance of anti-Ku86 (0.857) than AFP (0.739) for early detection of HCC. In 83 HCC patients, the positive rate of anti-Ku86 was 61.4% (51/83), significantly higher than that of the AFP positive rate (27.7%, 23/83). The anti-Ku86 level was positive in 37 of 60 HCC cases with negative AFP. Combination assay of AFP and anti-Ku86 could detect 60 of 83 HCC cases (72.3%, 60/83). There was no significant correlation of anti-Ku86 and AFP (r = 0.156, P = 0.161). CONCLUSIONS: Serum anti-Ku86 level is significantly elevated and is not related to HBV and HCV infection in HCC patients. Serum anti-Ku86 antibody may be a potential biomarker for early detection of HCC, and can be used in combination with AFP in clinics.

Poly[bis-[µ(2)-2-(2-pyridylmethyl-amino)ethanesulfonato]cadmium(II)].

The title compound [Cd(C(8)H(11)N(2)O(3)S)(2)](n), is a two-dimensional coordination polymer based on a Cd(2+) atom and deprotonated 2-(2-pyridylmethyl-amino)ethanesulfonic acid (Hpmt). The complex has mol-ecular symmetry C(i) as a consequence of the Cd(II) being located on an inversion centre. Two N atoms of each pmt(-) ligand coordinate to the Cd(2+) ion and its sulfonate O atom bonds to an adjacent Cd(2+) ion. 24-membered (-Cd-N-C-C-S-O-)(4) rings are formed between neighbouring Cd(2+) ions; these are inter-connected, forming a two-dimensional layer structure. In respect to stereogenic amino N atom and the inversion symmetry of the complex, the compound is a 1:1 racemate. The crystal packing is stabilized by inter-molecular N-H⋯O hydrogen bonds and further connected by π-π stacking inter-actions between the pyridyl rings [average inter-planar distance and centroid-centroid separation = 3.582 (1) and 3.634 (1)Å, respectively], forming a three-dimensional supra-molecular architecture.

4,4'-(Propane-1,3-di-yl)dipyridinium tetra-chloridonickelate(II).

The title compound, (C(13)H(16)N(2))[NiCl(4)] or (H(2)bpp)·NiCl(4) [bpp is 1,3-bis-(4-pyrid-yl)propane], is isostructural with its already reported Cu, Zn and Hg analogues. The structure consists of a doubly charged (H(2)bpp)(2+) cation and a tetra-hedral [NiCl(4)](2-) dianion. Both pyridyl N atoms are protonated and form a (H(2)bpp)(2+) cation which adopts an anti-anti conformation with a dihedral angle of 6.287 (7)° between the pyridyl rings. The two pyridyl N atoms are both involved in strong N-H⋯Cl hydrogen bonds, which link both units into a dimer.

Bis[2-(2-pyridylmethyl-amino)ethane-sulfonato-κN,N',O]zinc(II).

The title mononuclear complex, [Zn(C(8)H(11)N(2)O(3)S)(2)], is a zinc salt of 2-(2-pyridylmethyl-amino)ethane-sulfonic acid (Hpmt). The Zn(II) ion is located on an inversion centre and is octahedrally surrounded by four N and two O atoms. The deprotonated pmt(-) anion coordinates in a facial arrangement through its two N atoms and one of the sulfonate O atoms. The crystal packing is determined by inter-molecular N-H⋯O and C-H⋯O hydrogen bonds.

2-(2-Furylmethyl-ammonio)ethane-sulfonate methanol solvate.

The organic mol-ecule of the title compound, C(7)H(11)NO(4)S·CH(3)OH, is a zwitterion and its furan ring displays positional disorder [occupancy 0.563 (5):0.437 (5)]. The crystal structure is extended into a three-dimensional supra-molecular architecture through inter-molecular O-H⋯O and N-H⋯O hydrogen bonds with participation of the methanol solvent mol-ecules.

3,3'-Di-tert-butyl-5,5'-dimethoxy-biphenyl-2,2'-diol.

The title compound, C(22)H(30)O(4), displays twofold rotational symmetry. The two benzene rings are almost perpendicular to each other, forming a dihedral angle of 89.8 (6)°. In the crystal, mol-ecules are linked into an extended one-dimensional chain structure via inter-molecular O-H⋯O hydrogen bonds.

catena-Poly[[diaqua-nickel(II)]-bis-(µ-pyridine-4-sulfinato)-κN,O;κO,N].

In the title coordination polymer, [Ni(C(5)H(4)NO(2)S)(2)(H(2)O)(2)](n), the Ni(II) ion is located on an inversion centre and is octa-hedrally coordinated by two N and two O atoms of four symmetry-related and deprotonated pyridine-4-sulfinate (ps) ligands together with two water mol-ecules in axial positions. The ps(-) anions, acting as µ(2)-bridging ligands, link neighbouring Ni(II) ions into a chain structure along the c axis. These polymeric chains are extended into a three-dimensional framework via inter-molecular O-H⋯O hydrogen bonds with participation of the water mol-ecules.

Poly[[diaqua(µ(2)-4,4'-dipyridyl sulfide-κN:N')(4,4'-dipyridyl sulfide-κN)(2-hydroxy-5-sulfonatobenzoato-κO)nickel(II)] dihydrate].

The asymmetric unit of the title helical coordination polymer, {[Ni(C(7)H(4)O(6)S)(C(10)H(8)N(2)S)(2)(H(2)O)(2)]·2H(2)O}(n), is comprised of an Ni(II) ion, one 5-sulfosalicylic acid dianion (HSSA), two 4,4'-dipyridylsulfide (4,4'-dps) ligands, and two coordinated and two uncoordinated water mol-ecules. The Ni(II) ion is coordinated by two water mol-ecules, one carboxyl-ate O atom of the HSSA dianion and three N atoms from three 4,4'-dps ligands in a distorted octa-hedral environment. Half of the 4,4'-dps ligands are µ(2)-bridging ligands which link adjacent Ni(II) centers, forming a one-dimensional helical structure along the b axis. This helical structure is further stabilized by O-H⋯O intra- and inter-molecular hydrogen bonds.

catena-Poly[[[diaqua-manganese(II)]-µ(3)-pyridine-2,3-dicarboxyl-ato-κN,O:O:O] dihydrate].

In the title coordination polymer, {[Mn(C(7)H(3)NO(4))(H(2)O)(2)]·2H(2)O}(n), the Mn(II) ion is coordinated in a distorted octahedral environment by the O atoms of two water mol-ecules, one N and one O atoms of the chelating pyridine-2,3-dicarboxyl-ate (PDC) dianion, and two axial bridging carboxyl-ate O atoms from two adjacent PDC ligands. The fully deprotonated PDC anion acts a µ(3)-bridging ligand, establishing a chain structure along the a axis. These polymeric chains are connected into a three-dimensional framework via several inter-molecular O-H⋯O hydrogen bonds.

4-(4-Carb-oxy-1,3-thia-zol-2-yl)pyridinium 3-carb-oxy-4-hydroxy-benzene-sulfonate dihydrate.

In the crystal structure of the title compound, C(9)H(7)N(2)O(2)S(+)·C(7)H(5)O(6)S(-)·2H(2)O, an H atom from the 5-sulfosalicylic acid is transferred to the pyridyl N atom, forming a salt. The dihedral angle between the thiazole and pyridinium rings is 5.909 (5)°. The crystal packing is determined by O-H⋯O and N-H⋯O hydrogen bonds involving water mol-ecules.

Di-µ-chlorido-bis-{[2-(2-pyridylmethyl-amino)ethanesulfonato-κN,N',O]copper(II)}.

In the title compound, [Cu(2)(C(8)H(11)N(2)O(3)S)(2)Cl(2)], the Cu atoms are five-coordinated in a distorted square-pyramidal geometry by three donor atoms of the deprotonated anionic 2-(2-pyridylmethyl-amino)ethanesulfonate (pmt) ligand and two Cl atoms. The Cl atoms bridge two Cu atoms, giving a binuclear structure; the centroid of the Cu(2)Cl(2) ring lies on a crystallographic center of inversion. The complex is stabilized by hydrogen bonds and π-π stacking inter-actions [average inter-planar distance = 3.4969 (1) Šand ring-centroid separation distance = 4.1068 (4) Å].