Research trends and hotspots in the field of electrical impedance tomography for mechanical ventilation: a bibliometric analysis.

Background: Electrical impedance tomography (EIT) is a relatively recent functional imaging technique that is both noninvasive and radiation free. EIT measures the associated voltage when a weak current is applied to the surface of the human body to determine the distribution of electrical resistance within tissues. We performed a bibliometrics-based review to explore the geographic hotspots of current research and future trends developing in the field of EIT for mechanical ventilation. Methods: The Web of Science database was searched from its inception to June 25, 2023. CiteSpace software was used to visualize and analyze the relevant literature and identify the most impactful literature, trends, and hotspots. Results: 363 articles describing EIT use in mechanical ventilation were identified. A fluctuating growth in the number of publications was observed from 1998 to 2023. Germany had the highest number of articles (n=154), followed by Italy (n=53) and China (n=52). A cluster analysis of keyword co-occurrence revealed that "titration", "ventilator-related lung injury", and "oxygenation" were the most actively researched terms associated with the use of EIT in mechanically ventilated patients. Conclusions: Significant progress has been made in EIT research for mechanical ventilation. EIT research is limited to a small number of countries with a present research focus on the prevention and treatment of ventilator-related lung injury, oxygenation status, and prone ventilation. These topics are expected to remain research hotspots in the future.

Rat Liver Mitochondrial Dysfunction Induced by an Organic Arsenical Compound 4-(2-Nitrobenzaliminyl) Phenyl Arsenoxide.

Arsenic is successfully used in cancer chemotherapy and several cancer treatments on account of its apoptogenic effects. However, it is environmentally hazardous with potential for toxicity when distributed in the soil, water, and food, and long exposure to water contaminated with Arsenic may induce cancers. Some research studies have reported that liver is the storage site and an important target organ for Arsenic toxicity. In the present work, a new kind of organic arsenic compound, 4-(2-nitrobenzaliminyl) phenyl arsenoxide (NPA), was synthesized, and its potential involvement of mitochondria was explored. The results presented that the toxicology of NPA, at least in part, mediated mitochondrial function and may thoroughly destroy mitochondrial membrane physiological functions. NPA induced mitochondrial permeability transition pore (mtPTP) opening that induces mitochondrial biochemical abnormalities as evidenced by mitochondrial swelling, mitochondrial membrane potential breakdown, membrane fluidity alterations, and the strikingly remarkable protection of CsA. Meanwhile, both the decreased respiration rate of state 4 and the increased inner membrane H(+) permeabilization revealed that the inner membrane function regarding important energy production chain was destroyed. The toxicity of NPA is due to its interaction with mitochondrial membrane thiol protein. This conclusion is based on the protective effects of RR, DTT, and MBM(+).

Mechanistic studies on the reversible photophysical properties of carbon nanodots at different pH.

The pH-dependent photoluminescence (PL) behavior of carbon nanodots (C-dots) and its mechanism has been exhaustively studied in this work. The PL and UV-vis absorption spectra are reversible in the pH between 3 and 13. We speculate that two kinds of reactions (fast and slow) occurring at the surface of C-dots may contribute to this pH-dependent PL behavior. When C-dots solutions are switched to acidic conditions, they will quickly self-assembled aggregate into larger particles and surface oxygen-related groups of C-dots would be slowly oxidized at room temperature. Moreover, it should be noted that this is the first direct observation of self-assembled aggregation of C-dots under acidic conditions. In addition, the optimal PL spectra of C-dots blue-shift while their sizes increase, so-called 'inverse PL shift' phenomenon is also observed. Meanwhile, as the solution is adjusted to alkaline conditions, a structural tautomerization of C-dots rapidly takes place and hydrogenation/deoxygenation reaction proceeds in a much slower rate. Furthermore, through distinct decay dynamics as well as the characterizations of C-dots at different pHs, the PL properties are proposed to be mainly related to the surface states of C-dots.

[TfR2 mRNA expression in bone marrow mononuclear cells of children with hyperplastic anemia and its implications].

The aim of this study was to investigate the expression of transferrin receptor 2 (TfR2) mRNA in bone marrow mononuclear cells (BMMNC) of children with hyperplastic anemia (HA), to analyze the correlation of TfR2 mRNA expression level with Hb level, bone marrow erythroid hyperplasia, iron status in body and underlying diseases, and to evaluate the role of TfR2 in erythroid hemopoiesis and the useful value in diagnosis of HA. The experiment was divided into 2 groups: test group, in which 40 patients with HA were enrolled, and control group in which 10 patients without erythroid disorders and hematological malignancies confirmed by bone marrow examination were enrolled. The bone marrow samples of patients in mentioned above 2 groups were collected, the TfR2 mRNA expression in BMMNC of patients with HA was detected by fluorescence-quantitative PCR, the correlation of HA with bone marrow erythroid hyperplasia, iron status of body and underlying diseases was analyzed. The results showed that the relative level of TfR2 mRNA expression in HA patients was significantly higher than that in control patients. The TfR2 mRNA expression level negatively correlated with Hb level in peripheral blood (r = -0.715), while it positively correlated with ratio of bone marrow erythroblasts (r = 0.533). It is concluded that TfR2 mRNA expression in HA patients increases and closely correlates with hyperplasia status of bone marrow and anemia level in peripheral blood.

[Expression of transferrin receptor 2 in mononuclear cells from children with acute leukemia].

OBJECTIVE: To study the expression of TFR2 mRNA in mononuclear cells of bone marrow and peripheral blood from children with acute lymphoblastic leukemia, and to explore possible correlations between TFR2 expression and a panel of prognostic/risk factors. METHODS: Bone marrow or peripheral mononuclear cells were isolated from 56 children with newly diagnosed acute lymphoblastic leukemia (ALL) and 15 normal children as control. TFR2 mRNA expression level in mononuclear cell was determined by real-time fluorescence quantitative RT-PCR. RESULTS: Relative expression level of TFR2 mRNA in prednisone good responders (median: 0.0848) was significantly higher than that in prednisone poor responders (median: 0.0126) (P = 0.038). The medians of TFR2 mRNA expression levels in low-risk, moderate-risk and high-risk ALL were 0.1677, 0.0728 and 0.0125 respectively (P = 0.003). The medians of TFR2 mRNA expression levels in three ALL groups with initial WBC counts less than 50 x 10(9)/L, from 50 x 10(9)/L to 100 x 10(9)/L and more than 100 x 10(9)/L were 0.0974, 0.0294 and 0.0078 (P = 0. 013). In addition, the relative TFR2 mRNA level in B-lineage ALL was significantly higher than that in T-ALL, with medians of 0.0636 and 0.0065 respectively (P = 0.004). Ranked correlation analysis revealed that TFR2 expression was negatively correlated to initial white blood cell count, percentage of blast cells and absolute numbers of blasts in peripheral blood, with ranked correlation coefficients of -0.398, -0.307 and 0.421 respectively (correponding P values were 0.003, 0.022 and 0.001). CONCLUSION: TFR2 might be a novel prognostic factor for ALL.

[Comparative study on clinical features between TEL-AML1 positive and negative childhood acute lymphoblastic leukemia].

OBJECTIVE: To determine the incidence of TEL-AML1 fusion gene in childhood acute lymphoblastic leukemia (ALL) and to compare the clinical features between TEL-AML1 positive and negative patients. METHODS: Samples of bone marrow or peripheral blood were collected from 95 newly diagnosed ALL children and the TEL-AML1 fusion gene was detected using nested reverse transcription-polymerase chain reaction (RT-PCR). The ALL patients were stratified into TEL-AML1 positive and negative groups and the clinical features were compared. RESULTS: Among 95 patients, 20 (21.05%) were TEL-AML1 positive. The median age of TEL-AML1 positive patients was 5.9 years old and M/F ratio was 1.22:1. There were significant differences between TEL-AML1 positive and negative patients in hepatomegaly (2.75 cm vs. 4 cm below costal arch, P=0.006), splenomegaly (0 cm vs. 3 cm below costal arch, P < 0.001), initial white blood cell count (median 7.40 x 10(9)/L vs.18.70 x 10(9)/L, P=0.011), initial peripheral blood blast (median 2.45 x 10(9)/L vs.11.66 x 10(9)/L, P=0.013), hemoglobin level [(61.45 +/- 13.46) g/L vs. (75.89 +/- 23.11) g/L, P=0.003] and serum lactate dehydrogenase [(621.47 +/- 335.85) U/L vs.(1566.64 +/- 1720.45) U/L, P=0.020], while no differences were found between two groups in age, gender ratio, initial platelet count, percentage of blast in bone marrow, immunophenotypes and the expression of myeloid antigen CD13, CD33 and CD34. The prednisone sensitivity test showed that all 12 TEL-AML1 positive patients were good responders, while there were 11 prednisone poor responders among 40 negative patients (27.50%, P < 0.05). Bone marrow examination on day 15 showed no difference in the rate of complete remission between TEL-AML1 positive and negative patients. CONCLUSION: The incidence of TEL-AML1 fusion gene in cases of ALL is 21.05%. The load of leukemia cells in TEL-AML1 positive patients is significantly smaller than its counterparts, and the blast cells in TEL-AML1 positive patients are more sensitive to prednisone, indicating childhood ALL with TEL-AML1 fusion gene has a favorable prognosis.

[Expression of mitochondrial ferritin in K562 leukemic cell during TPA-induced cell differentiation].

Mitochondrial ferritin (MtF), a new player in iron metabolism, first identified in 2001, is highly homologous to ferritin both structurally and functionally. Preliminary studies have suggested that MtF might play very important roles in the regulation of mitochondrial iron homeostasis. Leukemic cells, just like other malignant cells, demand more iron for their greater proliferation potential. However, little is known about what roles MtF might play in leukemic cell iron metabolism and cell proliferation. The aim of this study was to investigate the expression of MtF, transferrin receptor 1 (TfR1) and ferritin (Fn) mRNAs in K562 leukemic cells during TPA-induced cell differentiation and to explore the interrelationship between the expression levels of these iron metabolism-related molecules. K562 cells cultured with or without TPA (16 nmol/L) were collected at 24, 72 and 120 hours respectively. Cell differentiation toward monocyte lineage was confirmed by microscopic study (Wright's staining) and flow cytometry. Semiquantitative RT-PCR was performed to determine mRNA expression, with house-keeping gene beta-actin as control reference. This study revealed that over 95% of K562 cells showed morphological features of monocyte/macrophage, and the expression of CD64 on cell surface increased significantly at day 5 with TPA treatment. K562 cells could express a certain level of MtF before TPA-induced differentiation. With increase of TPA-induced cell differentiation, MtF mRNA expressions were downregulated progressively. After 5 days of induced cell differentiation, expression levels of MtF and TfR1 mRNA were just 50.3% and 68.2% of that before TPA treatment. While Fn mRNA expression increased to 1.97 folds of that before TPA treatment. It is concluded that MtF expression is downregulated during TPA-induced K562 cell differentiation, with concomitant downregulation of TfR1 and upregulation of Fn. The coordinated expression regulation of these key iron metabolism-related molecules during cell differentiation may in turn inhibit TfR1-mediated iron uptake via endocytosis and thus adversely affect cell proliferation potential.

Interaction of an organic selenium compound with human serum albumin: a spectroscopic study.

The interaction between 4,4'-diselenadibenzoic acid and human serum albumin (HSA) was investigated by fluorescence and absorption spectroscopy. The quenching mechanism of fluorescence of HSA by 4,4'-diselenadibenzoic acid was discussed. It is proved that the fluorescence quenching of HSA by 4,4'-diselenadibenzoic acid is a result of the formation of the HSA-4,4'-diselenadibenzoic acid complex. The binding sites number n, apparent corporation constant K, and corresponding thermodynamic parameters, deltaH(theta), deltaG(theta), and deltaS(theta) were calculated. Results indicate that the electrostatic interactions forces played major role in the reaction.