[Clinical characteristics and prognostic factors of adult patients with acute respiratory failure due to influenza infection].

OBJECTIVE: To investigate the clinical characteristics and prognostic predictors of adult patients with acute respiratory failure due to influenza infection. METHODS: A retrospective analysis was performed on adult patients with acute respiratory failure due to confirmed influenza infection admitted to intensive care units (ICU) of the First Affiliated Hospital of Zhengzhou University and the Sixth People's Hospital of Zhengzhou between January 2018 and January 2020. The subjects were divided into survival and death groups according to whether the patients died before discharge. Demographic and clinical data including underlying conditions, laboratory variables, therapy and prognostic factors of hospital mortality between the two groups were analyzed. The risk factors of mortality were evaluated by univariate and multivariate Logistic regression analysis. Then, the correlation between lymphocyte (LYM) count and LYM subsets were analyzed. The survival rates of different acute physiologic and chronic health evaluation II (APACHE II) and LYM level subgroups were compared. RESULTS: A total of 104 patients were enrolled. Among them, 67 cases (64.4%) had underlying conditions, 91.3% of the patients (95 cases) were infected by influenza A virus, and the hospital mortality rate was 39.4% (41 cases). Compared with survival group, the patients of death group had higher respiratory rate (times/min: 26.0±5.6 vs. 23.7±5.0), APACHE II score (18.20±4.88 vs. 12.35±4.58), procalcitonin [PCT (µg/L): 0.82 (0.23, 4.63) vs. 0.39 (0.11, 0.92)], higher percentage of cardiovascular disease [24.4% (10/41) vs. 7.9% (5/63)] and invasive mechanical ventilation [63.4% (26/41) vs. 17.5% (11/63), all P < 0.01], but had lower oxygenation index [PaO2/FiO2 (mmHg, 1 mmHg = 0.133 kPa): 131.8±34.5 vs. 181.7±31.6] at ICU admission, LYM (×109/L: 0.53±0.40 vs. 0.92±0.44), hemoglobin [Hb (g/L): 105.66±28.17 vs. 118.29±28.29], platelet count [PLT (×109/L): 135.12±85.40 vs. 199.81±110.11], T lymphocyte count [cells/µL: 181 (131, 275) vs. 319 (238, 528)], CD4+ count [cells/µL: 110 (71, 161) vs. 190 (120, 311)] and CD8+ count [cells/µL: 71 (33, 100) vs. 121 (81, 188), all P < 0.01]. Patients of death group also had a shorter length of hospital stay [days: 7.0 (4.0, 11.0) vs. 12.0 (8.0, 20.0), P < 0.01]. Univariate analysis showed that APACHE II score [odds ratio (OR) = 1.207, 95% confidence interval (95%CI) was 1.094-1.332, P < 0.001], LYM (OR = 0.070, 95%CI was 0.018-0.271, P < 0.001), Hb (OR = 0.984, 95%CI was 0.970-0.999, P = 0.031), PLT (OR = 0.992, 95%CI was 0.987-0.997, P = 0.003), T lymphocyte count (OR = 0.996, 95%CI was 0.993-0.998, P = 0.001) and PaO2/FiO2 (OR = 0.955, 95%CI was 0.938-0.972, P < 0.001) were the risk factors for the prognosis of influenza patients with acute respiratory failure. Further multivariate Logistic analysis also showed that APACHE II score (OR = 1.195, 95%CI was 1.041-1.372, P = 0.011), LYM (OR = 0.063, 95%CI was 0.011-0.369, P = 0.002) and PaO2/FiO2 (OR = 0.953, 95%CI was 0.933-0.973, P < 0.001) were the predictors of mortality. Moreover, patients with peripheral blood LYM < 0.65×109/L or APACHE II score > 14 had a higher risk of poor outcome. There were significantly positive correlation between LYM and LYM subsets (T lymphocyte, CD4+ and CD8+ lymphocyte, r value was 0.593, 0.563, and 0.500, respectively, all P < 0.001). CONCLUSIONS: Influenza patients with acute respiratory failure were critically ill and had a high mortality rate. APACHE II score, PaO2/FiO2 and LYM at ICU admission were independent risk factors affecting the prognosis of patients.

Syntheses, crystal structures and biological relevance of glycolato and S-lactato molybdates.

Glycolato and S-lactato complexes containing the dioxomolybdenum(VI) moiety have been synthesized for studies on the role of the alpha-hydroxycarboxylato anion in the iron molybdenum cofactor of nitrogenase. The ligands in these complexes, vis K2[MoO2(glyc)2].H2O (H2glyc=glycolic acid, C2H4O3) (1) and (Na2[MoO2(S-lact)2])3.13H2O (H2lact=lactic acid, C3H6O3) (2) chelate through their alpha-alkoxyl and alpha-carboxyl oxygen atoms. In contrast, octanuclear K6[(MoO2)8(glyc)6(Hglyc)2].10H2O (3) formed by the reduction of the glycolato complex (1), features three different ligand binding modes: (i) non-bridging and bridging bidentate coordination of alpha-alkoxyl and alpha-carboxyl groups, and (ii) bidentate bridging using alpha-carboxyl group, leaving the alpha-alkoxyl group free. The octanuclear skeleton shows strong metal-metal interactions. The coordination modes in (1) and (2) mimic that of homocitrate to the iron molybdenum cofactor (FeMo-co) of nitrogenase. The bidentate coordination of alpha-alkoxyl and alpha-carboxyl groups shows that bond of alpha-carboxyl group to Mo is less susceptible to the oxidation state of molybdenum compared with the Mo-alpha-alkoxyl bond. This is supported by the dinuclear coordination of alpha-carboxyl group with free alpha-alkoxyl group in glycolato molybdate(V) (3).

Syntheses, spectroscopies and structures of molybdenum(VI) complexes with homocitrate.

Initial investigations into the possible role of homocitric acid in iron molybdenum cofactor (FeMo-co) of nitrogenase lead us to isolate and characterize two tetrameric molybdate(VI) species. The complexes K2(NH4)2[(MoO2)4O3(R,S-Hhomocit)2].6H2O (1) and K5[(MoO2)4O3(R,S-Hhomocit)2]Cl.5H2O (2) (homocitric acid = H4homocit, C7H10O7) are prepared from the reactions of acyclic homocitric acid and molybdates, which represent the first synthetic structural examples of molybdenum homocitrate complexes. The homocitrate ligand trapped by tetranuclear molybdate coordinates to the molybdenum(VI) atom through alpha-alkoxy and alpha-, beta-carboxy groups. The physical properties, structural parameters, and their possible biological relevances are discussed.

Peroxomolybdate(VI)-citrate and -malate complex interconversions by pH-dependence. Synthetic, structural and spectroscopic studies.

The reaction of potassium molybdate(VI) with biologically relevant ligands, citric and malic acids, in the presence of H2O2 was investigated for the effect of pH variations on the product pattern. That with citric acid led to the formation of the monomeric complex K4[MoO(O2)2(cit)].4H2O (1) in the pH range 7-9, and dimer K5[MoO(O2)(2-)(Hcit)H(Hcit)(O2)2OMo].6H2O (2) (H4cit = citric acid) at pH 3-6 through carboxylate-carboxylic acid hydrogen bonding. The relation with the previously identified K4[MoO3(cit)].2H2O (4) and K4[Mo2O5(Hcit)2].4H2O (5) were shown. These and other intermediates were shown to react in the pH range 3-6 to give a more stable species 2; the reaction sequence was demonstrated either by the protonation from 1 or the deprotonation of [MoO(O2)2(H2cit)](2-) (8). Evidence that 2 exists as a dimer in solution is presented. The reaction with (S)-malic acid afforded Delta-K(2n)[MoO(O2)2((S)-Hmal)]n.nH2O (3) (H3mal = malic acid) that was oxidized further to oxalato molybdate (11) by H2O2. The three complexes 1-3 were characterized by elemental analysis, UV, IR and NMR spectroscopies, in addition to the X-ray structural studies that show citrate and malate being coordinated as bidentate ligands via alpha-alkoxyl and alpha-carboxylate groups. The formation of these complexes is dictated by pH and their thermal stabilities varied with the coordinated hydroxycarboxylate ligands.