A pedigree analysis of Rotor hyperbilirubinemia combined with hepatitis B virus infection in a SLCO1B1 and SLCO1B3 gene mutations patient.

Background: Rotor syndrome (RS, OMIM#237450) is an extremely rare autosomal digenic recessive disorder characterized by mild non-hemolytic hereditary conjugated hyperbilirubinemia, caused by biallelic variation of SLCO1B1 and SLCO1B3 genes that resulted in OATP1B1/B3 dysfunction in the sinusoidal membrane leading to impaired bilirubin reuptake ability of hepatocytes. Methods: One RS pedigree was recruited and clinical features were documented. Whole genome second-generation sequencing was used to screen candidate genes and mutations, Sanger sequencing confirmed predicted mutations. Results: This study detected a homozygous nonsense variant c.1738C > T (p.R580*) in the coding region of the SLCO1B1 (NM006446) gene in a family with RS and hepatitis B virus infection by Variants analysis and Sanger sequencing, and confirmed by Copy Number Variation (CNV) analysis and Long Range PCR that there was a homozygous insertion of intron 5 of the SLCO1B3 gene into intron 5 of long-interspersed element 1 (LINE1). A few cases of such haplotypes have been reported in East Asian populations. A hepatitis B virus infection with fatty liver disease was indicated by pathology, which revealed mild-moderate lobular inflammation, moderate lobular inflammation, moderate hepatocellular steatosis, and fibrosis stage 1-2 (NAS score: 4 points/S1-2) alterations. Heterozygotes carrying p.R580* and LINE1 insertions were also detected in family members (I1, I2, III2, III3), but they did not develop conjugated hyperbilirubinemia. Conclusion: The mutations may be the molecular genetic foundation for the presence of SLCO1B1 c.1738C > T(p.R580*) and SLCO1B3 (LINE1) in this RS pedigree.

Clinical analysis of 114 cases of bronchiolitis in infants.

BACKGROUND: Bronchiolitis is a common lower respiratory tract infection in infants and young children. Severe cases may be accompanied by obvious dyspnea and oxygen saturation decline. AIM: To summarize the clinical features, standard diagnosis, and treatment of bronchiolitis. METHODS: This is a retrospective analysis of 114 pediatric patients (74 males, 40 females) who were first diagnosed as having bronchioles at the Department of Pediatrics of Tongling Maternal and Child Health Hospital from January 2019 to December 2019. The clinical features, imaging features, treatment, and other clinical data were recorded and analyzed. RESULTS: The age of onset of the disease was mainly from 1 mo to 6 mo (75.4%), and the time to hospital visit was mostly from the 2nd day to the 4th day of the course of the disease (75.4%). Lung imaging examination showed increase in lung texture, fuzzy (93.8%). The main treatment was atomization therapy: Budesonide combined with terbutaline (45.6%) and budesonide combined with salbutamol (38.5%). The average hospitalization time was 7.1 ± 2.4 d, and the overall cure rate was 94.7%. In patients without bacterial infection, the use of antibiotics significantly prolonged the length of hospital stay (7.8 ± 2.5 d vs 5.7 ± 1.8 d) and improved the cure rate (98.3% vs 87.9%, P < 0.05). CONCLUSION: Infants with bronchiolitis are mainly male and tend to have a good prognosis. However, the unneeded use of antibiotics may prolong the length of hospital stay significantly, which imposes the burden both on the patients and hospital system.

Hypervirulent Klebsiella pneumoniae detection methods: a minireview.

Hypervirulent Klebsiella pneumoniae (hvKp), characterized by high virulence and epidemic potential, has become a global public health challenge. Therefore, improving the identification of hvKp and enabling earlier and faster detection in the community to support subsequent effective treatment and prevention of hvKp are an urgent issue. To address these issues, a number of assays have emerged, such as String test, Galleria mellonella infection test, PCR, isothermal exponential amplification, and so on. In this paper, we have collected articles on the detection methods of hvKp and conducted a retrospective review based on two aspects: traditional detection technology and biomarker-based detection technology. We summarize the advantages and limitations of these detection methods and discuss the challenges as well as future directions, hoping to provide new insights and references for the rapid detection of hvKp in the future. The aim of this study is to focus on the research papers related to Hypervirulent Klebsiella pneumoniae involving the period from 2012 to 2022. We conducted searches using the keywords "Hypervirulent Klebsiella pneumoniae, biomarkers, detection techniques" on ScienceDirect and Google Scholar. Additionally, we also searched on PubMed, using MeSH terms associated with the keywords (such as Klebsiella pneumoniae, Klebsiella Infections, Virulence, Biomarkers, diagnosis, etc.).

Association between PT, PT-INR, and in-hospital mortality in critically ill patients with tumors: A retrospective cohort study.

Objectives: Prothrombin time (PT) and PT-INR are independent predictors of mortality in patients with cancer. The PT and PT-INR of cancer patients are independent predictive variables of mortality. However, whether the PT or PT-INR is related to in-hospital mortality in severely ill patients with tumors remains unknown. Design: This was a case-control study based on a multicenter public database. Settings: This study is a secondary analysis of data extracted from 2014 to 2015 from the Electronic Intensive Care Unit Collaborative Research Database. Participants: The data relevant to seriously ill patients with tumors were obtained from 208 hospitals spread throughout the USA. This research included a total of 200,859 participants. After the samples were screened for patients with combination malignancies and prolonged PT-INR or PT, the remaining 1745 and 1764 participants, respectively, were included in the final data analysis. Primary and secondary outcome measures: The key evaluation methodology was the PT count and PT-INR, and the main outcome was the in-hospital mortality rate. Results: After controlling for confounding variables, we found a curvilinear connection between PT-INR and in-hospital mortality (p < 0.001), and the inflection point was 2.5. When PT-INR was less than 2.5, an increase in PT-INR was positively associated with in-hospital mortality (OR 1.62, 95% CI 1.24 to 2.13), whereas when PT-INR was greater than 2.5, in-hospital mortality was relatively stable and higher than the baseline before the inflection point. Similarly, our study indicated that the PT exhibited a curvilinear connection with in-hospital mortality. On the left side of the inflection point (PT <22), a rise in the PT was positively linked with in-hospital mortality (OR 1.08, 95% CI 1.04 to 1.13, p < 0.001). On the right side of the inflection point, the baseline PT was above 22, and the in-hospital mortality was stable and higher than the PT count in the prior range (OR 1.01, 95% CI 0.97 to 1.04, 0.7056). Conclusion: Our findings revealed that there is a curved rather than a linear link between the PT or PT-INR and in-hospital mortality in critically ill cancer patients. When these two laboratory results are below the inflection point, comprehensive therapy should be employed to reduce the count; when these two laboratory results are above the inflection point, every effort should be made to reduce the numerical value to a value below the inflection point.

Non-linear relationship between basal serum albumin concentration and cardiac arrest in critically ill patients with end-stage renal disease: a cross-sectional study.

OBJECTIVES: The aim of our study was to investigate the association between serum albumin concentration and the risk of cardiac arrest in critically ill patients with end-stage renal disease in the intensive care unit (ICU). DESIGN: This was a secondary analysis. SETTING: The Phillip electronic-ICU collaborative database from 2014 to 2015. PARTICIPANTS: This study included 4990 critically ill patients diagnosed with end-stage renal disease. PRIMARY AND SECONDARY OUTCOME MEASURES: The exposure of interest was serum albumin concentration. The outcome variable was cardiac arrest. RESULTS: A non-linear relationship was observed between serum albumin concentration and risk of cardiac arrest, with an inflection point of 3.26 g/dL after adjusting for potential confounders. The effect sizes and the CIs on the left and right sides of the inflection point were 0.88 (0.65 to 1.19) and 0.32 (0.16 to 0.64), respectively. CONCLUSIONS: Within an albumin range of 3.26-5.6 g/dL, each 1 g/dL increase in serum levels is associated with a 68% decrease of the risk of cardiac arrest in critically ill patients with end-stage renal disease.

CTRP9 induces macrophages polarization into M1 phenotype through activating JNK pathway and enhances VSMCs apoptosis in macrophages and VSMCs co-culture system.

Inflammation plays a critical role in the development of atherosclerosis (AS), which has been identified as a major predisposing factor for stroke. Macrophages and VSMCs are associated with plaque formation and progression. Macrophages can dynamically change into two main functional phenotypes, namely M1 and M2, they can produce either pro-inflammatory or anti-inflammatory factors which may affect the outcome of inflammation. As a member of CTRPs family, CTRP9 has been reported play important protective roles in the cardiovascular system. However, whether CTRP9 can regulate macrophage activation status in inflammatory responses and have effect on VSMCs behaviors in co-culture system have not been fully investigated. In the present study, using peritoneal macrophages treated with CTRP9, we found that CTRP9 facilitated macrophages towards M1 phenotype, promoted TNF-α secretion and MMPs expression. CTRP9 showed synergistic effect with LPS in inducing M1 macrophages. In macrophages-VSMCs co-culture system, apoptosis and down-regulated proliferation of VSMCs were accelerated with CTRP9-treated macrophages. Then we attempted to explore the underlying molecular mechanisms of CTRP9 resulting in M1 activation. The c-Jun NH2-terminal kinases (JNK) are members of the mitogen activated protein kinases (MAPK) family, plays a central role in the cell stress response, with outcomes ranging from cell death to cell proliferation and survival. We found JNK expression was upregulated following CTRP9 stimulation, and inhibiting JNK phosphorylation level was associated with decreased expression of M1 markers and TNF-α concentration. Moreover, VSMCs apoptosis were ameliorated after inhibition of JNK. These results suggested that CTRP9 may promote macrophage towards M1 activation status through JNK signaling pathway activation.

CTRP9 induces iNOS expression through JAK2/STAT3 pathway in Raw 264.7 and peritoneal macrophages.

The C1q tumor necrosis factor (TNF)-related proteins 9 (CTRP9), an adipocyte-derived cytokine, affects a number of physiological processes, including immune function and inflammation. We investigated whether CTRP9 affects the expression of inflammation-related genes in Raw 264.7 and peritoneal macrophages. The CTRP9-induced expression of iNOS increased in a time- and dose-dependent manner. LPS and CTRP9 promote the expression of iNOS jointly in Raw 264.7 and peritoneal macrophages. CTRP9 induced the phosphorylation of JAK2 and STAT3 in Raw 264.7 and peritoneal macrophages. VX509 (JAK2 inhibitor) reduced the CTRP9-induced iNOS protein production. In addition, the CTRP9-induced phosphorylation of JAK2 and STAT3 was dramatically reduced by VX509. Collectively, these results suggest that JAK2/STAT3 signaling is involved in the CTRP9-induced expression of iNOS.

Screening of MYH7 gene mutation sites in hypertrophic cardiomyopathy and its significance.

BACKGROUND: There have been few reports of mutations in the beta-myosin heavy chain (MYH7) gene in hypertrophic cardiomyopathy (HCM), which is associated with sudden cardiac death caused by HCM. This study aimed to screen the mutation sites in the sarcomeric gene MYH7 in Chinese patients with HCM. We also planned to analyze the pathogenicity of the mutation site as well as its significance in clinical and forensic medicine. METHODS: From January 2006 to June 2017, autopsy cases were collected from the Department of Pathology, the Affiliated Hospital of Qingdao University. The experiment was to detect MYH7 gene status in formalin-fixed paraffin-embedded tissues from 18 independent autopsy cases who suffered HCM related sudden death (fatal HCM) and 20 cases without cardiomyopathy. Common mutation exon fragments of MYH7 gene were amplified by polymerase chain reaction. The end-of-deoxygenation method and gene cloning method were further performed to analyze the mutation sites. Homologous comparison among mutant sites was conducted using BLAST online database. RESULTS: The 1336th nucleotide of MYH7 gene at exon 14 was converted from T to G in one HCM case, resulting in the conversion of threonine (Thr) at position 446 to proline (Pro). In another case, the 1402th nucleotide at exon 14 was converted from T to C, resulting in the conversion of phenylalanine (Phe) at position 468 to leucine (Leu). Homologous comparison results showed that the two amino acid residues of Thr446 and Phe468 are highly conserved among different species. CONCLUSIONS: Our results showed fatal HCM harbored mutations of Thr446Pro and Phe468Leu in the MYH7 gene. It is significant for clinical and forensic medicine to further explore the functions and detailed mechanisms of these mutations.

Organochlorine pesticides accumulation and breast cancer: A hospital-based case-control study.

The aim of this study is to detect the accumulation status of organochlorine pesticides in breast cancer patients and to explore the relationship between organochlorine pesticides contamination and breast cancer development. We conducted a hospital-based case-control study in 56 patients with breast cancer and 46 patients with benign breast disease. We detected the accumulation level of several organochlorine pesticides products (ß-hexachlorocyclohexane, γ-hexachlorocyclohexane, polychlorinated biphenyls-28, polychlorinated biphenyls-52, pentachlorothioanisole, and pp'-dichlorodiphenyldichloroethane) in breast adipose tissues of all 102 patients using gas chromatography. Thereafter, we examined the expression status of estrogen receptor, progesterone receptor, human epidermal growth factor receptor-2 (HER2), and Ki-67 in 56 breast cancer cases by immunohistochemistry. In addition, we analyzed the risk of breast cancer in those patients with organochlorine pesticides contamination using a logistic regression model. Our data showed that breast cancer patients suffered high accumulation levels of pp'-dichlorodiphenyldichloroethane and polychlorinated biphenyls-52. However, the concentrations of pp'-dichlorodiphenyldichloroethane and polychlorinated biphenyls-52 were not related to clinicopathologic parameters of breast cancer. Further logistic regression analysis showed polychlorinated biphenyls-52 and pp'-dichlorodiphenyldichloroethane were risk factors for breast cancer. Our results provide new evidence on etiology of breast cancer.

Molecular docking studies of Traditional Chinese Medicinal compounds against known protein targets to treat non-small cell lung carcinomas.

In silico drug design using virtual screening, absorption, distribution, metabolism and excretion (ADME)/Tox data analysis, automated docking and molecular dynamics simulations for the determination of lead compounds for further in vitro analysis is a cost effective strategy. The present study used this strategy to discover novel lead compounds from an in-house database of Traditional Chinese Medicinal (TCM) compounds against epithelial growth factor receptor (EGFR) protein for targeting non-small cell lung cancer (NSCLC). After virtual screening of an initial dataset of 2,242 TCM compounds, leads were identified based on binding energy and ADME/Tox data and subjected to automated docking followed by molecular dynamics simulation. Triptolide, a top compound identified by this vigorous in silico screening, was then tested in vitro on the H2347 cell line carrying wild-type EGFR, revealing an anti-proliferative potency similar to that of known drugs against NSCLC.

Effects of tanshinone IIA on fibrosis in a rat model of cirrhosis through heme oxygenase-1, inflammation, oxidative stress and apoptosis.

Tanshinone IIA is extracted from the root of Salvia miltiorrhiza and used in traditional Chinese medicine for its anti-inflammatory activity and antioxidant effects. The aim of the present study was to investigate the potential protective effects of tanshinone IIA against fibrosis in a rat model of cirrhosis and to elucidate the underlying mechanisms. Male Sprague Dawley rats were used as the model of cirrhosis in the present study. In the cirrhotic rats, the extent of fibrosis, levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), heme oxygenase­1 (HO­1) protein expression, serum levels of nuclear factor (NF)­κB, tumor necrosis factor­α (TNF­α), interleukin (IL)­1ß and IL­6, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH­PX), and the protein expression levels of phosphorylated­p38 mitogen­activated protein kinase (MAPK) were all significantly increased. However, the serum malondialdehyde (MDA) activity and protein kinase B (Akt) protein expression were suppressed in cirrhotic rats compared with the sham (control) group. Compared with the cirrhotic group, administration of tanshinone IIA reduced the extent of fibrosis, levels of ALT and AST, HO­1 protein expression, serum NF­κB, TNF­α, IL­1ß and IL­6 levels, and the activity of SOD, CAT and GSH­PX. Furthermore, administration of tanshinone IIA significantly increased the inhibition of the serum MDA activity and the Akt protein expression in cirrhotic rats compared with those in the cirrhotic group. The protective effect of tanshinone IIA suppresses fibrosis in a rat model of cirrhosis, and reduces inflammation and oxidative stress, via the HO­1, Akt and p38 MAPK signaling pathway.

Inhibition of MAPK and NF-κB signaling pathways alleviate carbon tetrachloride (CCl4)-induced liver fibrosis in Toll-like receptor 5 (TLR5) deficiency mice.

Current researches showed that TLR family plays an important role in liver fibrosis, yet the molecular mechanism by which this occurs is not fully explained. In this study, we investigated the role of TLR5 in carbon tetrachloride-induced liver fibrosis, and further examined wether TLR5 knockout attenuated tetrachloride-induced liver fibrosis by inhibiting hepatic stellate cells activation via modulating NF-κB and MAPK signaling pathways. Our results found that carbon tetrachloride induced liver function injury in WT mice with a inflammatory responses through the activation of NF-κB and MAPK signaling pathways, resulting in hepatic stellate cells activation. In contrast, TLR5 deficiency mice after carbon tetrachloride administration reduced NF-κB and MAPK signaling pathways activation, which down regulated hepatic stellate cells activation. In addition, alpha smooth muscle-actin as marker of hepatic stellate cells further indicated that TLR5 knockout mice have a lower collagen accumulation in liver tissue than WT mice after carbon tetrachloride administration, resulting in inhibition of NF-κB and MAPK signaling pathways activation. Moreover, in vitro experiment of hepatic stellate cells challenged with LPS or TGF-ß, further indicated that NF-κB and MAPK were involved in liver fibrosis development, leading to α-SMA expression and inflammation infiltration. However, cells from TLR5(-)(/-) may weaken phosphorylation levels of signal pathways, finally suppress progress of collagen accumulation and inflammatory responses. These results suggest a new therapeutic approach or target to protect against fibrosis caused by chronic liver diseases.

LECT2 protects mice against bacterial sepsis by activating macrophages via the CD209a receptor.

Leukocyte cell-derived chemotaxin 2 (LECT2) is a multifunctional cytokine and reduced plasma levels were found in patients with sepsis. However, precise functions and mechanisms of LECT2 remain unclear. The aim of the present study was to determine the role of LECT2 in modulating immune responses using mouse sepsis models. We found that LECT2 treatment improved outcome in mice with bacterial sepsis. Macrophages (MΦ), but not polymorphonuclear neutrophils, mediated the beneficial effect of LECT2 on bacterial sepsis. LECT2 treatment could alter gene expression and enhance phagocytosis and bacterial killing of MΦ in vitro. CD209a was identified to specifically interact with LECT2 and mediate LECT2-induced MΦ activation. CD209a-expressing MΦ was further confirmed to mediate the effect of LECT2 on sepsis in vivo. Our data demonstrate that LECT2 improves protective immunity in bacterial sepsis, possibly as a result of enhanced MΦ functions via the CD209a receptor. The modulation of MΦ functions by LECT2 may serve as a novel potential treatment for sepsis.

[Molecular cloning, sequence analysis and expression of ayu complement component C9 gene].

C9, a component of the membrane attack complex, participates in the final stage of the complement cascade which lyses foreign organisms by disrupting the integrity of their cell membranes. In the present study, a full-length ayu C9 (aC9) cDNA was cloned which contains 2,125 nucleotides and encodes a protein of 592 amino acids. A signal peptide was deposited in the N-terminal 22 residues. The deduced amino acid sequence of aC9 showed 56.8% identity to the C9 of rainbow trout, and 40.9% to 53.8% identity to the C9 of other teleosts. RT-PCR analysis demonstrated that the mRNA of aC9 was expressed in the liver, spleen, intestine, gill and muscle of healthy ayu fish with the highest level in the liver. Quantitative RT-PCR analysis showed that aC9 transcripts were significantly up-regulated in the liver at 4 h post Listonella anguillarum infection, peaked at 16 h post injection. Western blotting analysis revealed that serum aC9 significantly increased in Listonella anguillarum infected ayu fish. Our results suggested that aC9 may play an important role in fish immune response of anti-bacteria.

Influence of acute cadmium exposure on the liver proteome of a teleost fish, ayu (Plecoglossus altivelis).

Cadmium (Cd) is a toxic heavy metal that causes the disruption of a variety of physiological processes. In this study, the effect of Cd on liver proteome of ayu, Plecoglossus altivelis, was investigated by two-dimensional gel electrophoresis (2-DE) and matrix assisted laser desorption ionization time-of-flight tandem mass spectrometry (MALDI-TOF-MS/MS). Twenty-three altered protein spots were successfully identified. They were involved in oxidative stress response, metal metabolism, methylation, and so on. The mRNA expression of 60S acidic ribosomal protein P0, heat shock protein 70, apolipoprotein A-I, betaine-homocysteine S-methyltransferase, parahox cluster neighbor, and transferrin was subsequently determined by real-time PCR. The mRNA expression of these genes was consistent with proteomic results. These findings enrich our knowledge on the influence of Cd toxicity to teleost fish, and may be worthy of further investigation to develop biomarkers.

Aqua-{tris-[(1H-benzimidazol-2-yl-κN)meth-yl]amine}-zinc 5-(dimethyl-amino)-naphthalene-1-sulfonate perchlorate 2.5-hydrate.

In the title compound, [Zn(C(24)H(21)N(7))(H(2)O)](C(12)H(12)NO(3)S)(ClO(4))·2.5H(2)O, the Zn(II) ion is in a distorted trigonal-bipyramidal coordination geometry. In the crystal, N-H⋯O and O-H⋯O hydrogen bonds connect the components into a two-dimensional network parallel to (001). In addition, there are weak C-H⋯O hydrogen bonds.

(Nitrato-κO){N,N,N',N'-tetra-kis-[(1H-benzimidazol-2-yl-κN)meth-yl]cyclo-hexane-1,2-diamine}-lead(II) hemiaqua-{N,N,N',N'-tetra-kis-[(1H-benzimidazol-2-yl-κN)meth-yl]cyclo-hexane-1,2-diamine}-lead(II) trinitrate dihydrate.

In the title compound, [Pb(NO(3))(C(38)H(38)N(10))][Pb(C(38)H(38)N(10))(H(2)O)(0.5)](NO(3))(3)·2H(2)O, both Pb(II) ions are coordinated in a distorted trigonal-prismatic environment by a hexa-dentate N,N,N',N'-tetra-kis-[(1H-benzimidazol-2-yl)meth-yl]cyclo-hex-ane-1,2-diamine ligand. A nitrate and a half-occupancy water ligand form long coordination bonds to the Pb(II) ions capping the trigonal-prismatic environment. In the crystal, the components are linked by N-H⋯O and O-H⋯O hydrogen bonds, forming a three-dimensional network. C-H⋯O inter-actions also occur.

[Alteration on the expression of ayu coagulation factor X gene upon Listonella anguillarum infection].

Coagulation factor X (FX) plays an important role in the immune response of mammals. In this study, the full length cDNA sequence of the ayu FX gene, 1817 bp in length excluding 3'-polyA tail, was determined for the first time. The sequence contained an open reading frame, which encoded a protein of 453 amino acids with a molecular weight of 5.07×10(4). The predicted protein had motifs typical of animal FX, and its N-terminal 24 residues were the signal peptides. Sequence comparison showed that ayu FX shared 53% amino acid sequence identity with zebrafish FX. In healthy ayu, FX mRNA was expressed mainly in the liver and weakly in the brain and gill. After Listonella anguillarum infection, liver FX transcriptions significantly increased, and peaked at 16 h post infection. The serine protease motif of ayu FX was expressed in Escherichia coli and was subsequently used for antiserum preparation. Western blotting analysis revealed that serum FX significantly increased in bacterially infected ayu fish. In conclusion, the ayu FX gene expression was significant in the progress of bacterial infection, which suggests FX's role in fish immune response.

4-[1-(4-Hy-droxy-3-meth-oxy-benz-yl)-1H-benzimidazol-2-yl]-2-meth-oxy-phenol.

In the title mol-ecule, C(22)H(20)N(2)O(4), the dihedral angles between the benzimidazole ring system and the benzene rings are 44.26 (2) and 82.91 (2)°. Intra-molecular O-H⋯O hydrogen bonds occur. In the crystal, O-H⋯N and O-H⋯O hydrogen bonds connect the mol-ecules into a two-dimension network parallel to (10[Formula: see text]) and weak inter-molecular C-H⋯O hydrogen bonds complete the formation of a three-dimensional network.

Dichlorido[tris-(benzimidazol-2-ylmeth-yl)amine]-indium(III) chloride ethanol solvate dihydrate.

In the title complex, [InCl(2)(C(24)H(21)N(7))]Cl·C(2)H(5)OH·2H(2)O, the In(III) ion is coordinated by four N atoms from the tris-(benz-imidazol-2-ylmeth-yl)amine (NTB) ligand and two Cl atoms in a distorted octa-hedral environment. In the crystal structure, inter-molecular N-H⋯O, O-H⋯O, O-H⋯Cl and weak C-H⋯Cl hydrogen bonds connect the cations, anions and solvent mol-ecules into a three-dimensional network. The ethanol solvent mol-ecule is disordered over two sites with refined occupancies of 0.54 (2) and 0.46 (2).