Annals of clinical and laboratory science最新文献

Objective: Pregnancy induced hypertension (PIH) is a common disease in obstetrics. CD4+ T cells can be divided into Th1 and Th2 sub-populations. Imbalance between Th1 and Th2 directly affects body immune status and participates in PIH occurrence and progression. Whether IL-10 affects Th1/Th2 immune balance as a negative regulator of immune response in PIH remains unknown. The aim of the present study was to investigate the role of IL-10 in PIH.

Methods: A total of 52 PIH patients were recruited and divided into mild-moderate and severe PIH groups in parallel with 25 normal pregnant women as a control group. Real-time PCR was used to test mRNA levels of Th1 cytokines IL-2, tumor necrosis factor-α (TNF-α), and Th2 cytokines IL-4, IL-6, and IL-10. Enzyme linked immunosorbent assay (ELISA) tested serum levels of cytokines to analyze their correlation with disease progression.

Results: Our results showed PIH patients had significantly elevated IL-2 and TNF-α levels and decreased IL-4, IL-6, or IL-10 expressions compared with the control group (p<0.05). With disease progression, IL-4, IL-6, and IL-10 expressions were further decreased while IL-2 and TNF-α were increased (p<0.05). Moreover, IL-10 was negatively correlated with Th1 cytokines IL-2 and TNF-α while being positively correlated with Th2 cytokines IL-4 and IL-6. In addition, IL-10 was negatively correlated with PIH severity (p<0.05).

Conclusion: IL-10 can affect Th1/Th2 immune balance and is associated with PIH severity, suggesting IL-10 might be a risk factor for PIH occurrence and progression.

Objective: Multiple myeloma (MM) and Acute myeloid leukemia (AML) are distinct hematologic malignancies originating from different cell lineages. Their coexistence is extremely rare, and current treatment approaches are even more so. Therefore, exploring the clinical features of their coexistence and the promising treatment strategy is worthwhile.

Case report: We described three cases involving the coexistence of MM and DNMT3A-mutant AML, two of which presented simultaneous occurrences, while Case 3 had secondary AML about 70 months after the MM.

Discussion: All cases exhibited DNMT3A mutations, which characterized by one missense mutation and two frameshift mutations; all were likely loss of function mutations. Among them, two patients were treated with Venetoclax-based regimens and achieved favorable effects. The patients were alive for 62,38 and 103 months.

Conclusions: Clonal hematopoiesis of DNMT3A may have a crucial role in the coexistence of MM and AML and Venetoclax-based regimens reveal favorable treatment responses. However, drug resistance still needs to be considered, and further research is required to elucidate the underlying mechanisms and treatment strategies.

Carbapenem-resistant Pseudomonas aeruginosa is a common multidrug-resistant bacterium encountered in clinical practice. This pathogen causes pneumonia, which is difficult to treat owing to the limited choice of antimicrobial drugs, resulting in a relatively high mortality rate. Carrimycin is a new macrolide antibiotic with broad-spectrum antibacterial and potential immunomodulatory effects. Herein, we report a case of severe pneumonia caused by carbapenem-resistant Pseudomonas aeruginosa that presented with septic shock and Acute Respiratory Distress Syndrome (ARDS). Initially, we used piperacillin-tazobactam and ceftazidime-avibactam but without satisfactory results. Finally, we administered carrimycin in combination with piperacillin-tazobactam; the patient's condition improved, and he was successfully weaned off the ventilator. Therefore, the combined use of carrimycin should be considered for patients infected with carbapenem-resistant Pseudomonas aeruginosa who do not respond to conventional anti-infection treatments.

Objective: Self-monitoring blood glucose levels using a blood glucose monitoring system (BGMS) helps minimize mortality and morbidity in patients with diabetes. We evaluated the accuracy of a new BGMS (CareSens S Fit [CaseSens; i-SENS Inc., Seoul, Korea]).

Methods: Patients who visited the Endocrinology Department at Kangbuk Samsung Hospital between July 13, 2021, and August 18, 2021 were included. CareSens was evaluated in accordance with the International Organization for Standardization 2013 (ISO 15197:2013) and the Food and Drug Administration (FDA) standard 2020.

Results: The study included 350 patients. The accuracy evaluation for CareSens, according to ISO 15197:2013 and FDA standard 2020, revealed that >99% of test results are within the allowed range.

Conclusions: The CareSens performed excellently, meeting ISO 15197:2013 and FDA Standard 2020.

Objective: Immune thrombocytopenia (ITP) is a common bleeding disorder. Although global lipidomic analyses have identified a potential role for lipid species in platelet function, there is currently no evidence to support a causal relationship between plasma lipids and ITP. To investigate this further, we conducted a two-sample Mendelian randomization analysis to determine whether there is a genetically predicted causal relationship between 179 plasma lipid groups and ITP.

Methods: Genome-wide association data from 179 plasma lipid species from 7,174 Finnish subjects were used in a preliminary analysis of ITP GWAS data from the GWAS catalogue database (GCST90018865, case=675, control=488,749). Causal analyses were performed using random inverse variance weighting (IVW) with MR-Egger and weighted median as complementary analyses. Sensitivity analyses were conducted using the MR-Egger intercept test, MR-PRESSO, and leave-one-out analysis. To assess the association of lipid metabolites with the risk of developing ITP, multivariate MR analysis was performed. Significant correlations were found. The final identification of lipid metabolites was further evaluated using the Steiger test for chain imbalance.

Results: The results of this study showed that six plasma lipid species, sterol esters (27:1/20:2) (SE) (odds ratio [OR]: 1.30, 95% confidence interval [CI]: 1.06-1.60, p=0.013), phosphatidylethanolamine (18:0_0:0) (PE) (OR: 1. 46, 95% CI: 1.10-1.95, p=0.009), phosphatidylcholine (16:0_18:3) (PC) (OR: 1.51, 95% CI: 1.12-2.02, p=0.006), phosphatidylcholine-ether (O-16:0_16:0) (PCO) (OR: 0.64, 95% CI: 0. 47-0.88, p = 0.005), phosphatidylethanolamine-ether (O-18:2_20:4) (PEO) (OR: 0.71, 95% CI: 0.55-0.93, p=0.013), triacylglycerol (49:1) (TAG) (OR: 1.65, 95% CI: 1.21-2.24, p=0.001), and ITP were all significantly correlated. MVMR analysis showed that genetically predicted phosphatidylcholine ethers may independently influence ITP without dependence on other metabolites. Triacylglycerol may be affected by other plasma liposomal metabolites and is a risk factor for the development of ITP.

Conclusion: The current work provides evidence for a causal role of six plasma lipids in ITP and provides new perspectives for combining genomics and metabolomics to explore the biological mechanisms of ITP. These findings may contribute to the screening, prevention, and treatment of ITP.

Objective: Chlamydia pneumoniae (C. pneumoniae) is a gram-negative intracellular bacterium that causes respiratory infections in humans. C. pneumoniae is responsible for cell activation and production of cytokines that may contribute to inflammatory responses in asthma. Cell-mediated immune responses are important for protective immunity; however, these responses may be impaired in asthma. In this study, we examined cytokine responses (IL-21, IL-12, IL-13) responsible for T helper (Th)1 versus Th2 responses in C. pneumoniae-stimulated PBMC from subjects with or without asthma. These cytokines could be potential biomarkers in the evaluation of past C. pneumoniae infection.

Methods: Peripheral blood mononuclear cells (PBMC) (1×10⁶/mL) from stable adult asthmatic (N=6) and non-asthmatic subjects (N=6) were infected +/- C. pneumoniae TW-183 at a multiplicity of infection (MOI)=0.1, using dose responses (1:10, 1:100), and cultured 48 hrs. Cytokine responses (Interleukin (IL)-21, IL-12, IL-13) were measured in supernatants (ELISA).

Results: Cytokine responses (mean differences: unstimulated-stimulated cells) were significant for IL-12 (1:10, 1:100) (P=0.0005, 0.0005) but not for IL-21 or IL-13 (Wilcoxon signed-rank test). Cytokine levels were higher in asthmatic subjects for IL-13 (mean differences: non-asthma-asthma) (unstimulated, 1:10, 1:100) (-210±167, -140±113, -89±59, respectively) (P=0.05, 0.05, 0.05, respectively) compared with non-asthma. However, IL-21 and IL-12 responses were similar in both groups. When subjects were stratified according to C. pneumoniae IgG antibody status, no significant differences in cytokine responses were observed.

Conclusion: Differential cytokine patterns in subjects with or without asthma may suggest a mechanism for the development of persistent infection with C. pneumoniae.

Objective: To observe the effect of low-dose azithromycin on pulmonary ventilation function and inflammatory factors IL-6, IL-13 in children with bronchial asthma.

Methods: A total of 80 children with asthma in Pediatric Medicine affiliated to Taizhou Women and Children's Hospital of Wenzhou Medical University from January 2019 to December 2022 were selected and divided into control group (42 cases) and study group (38 cases). The control group regularly inhaled Salmeterol Xinafoate and Fluticasone Propionate inhalation, while the study group was additionally given low-dose azithromycin. After four weeks of treatment, pulmonary function tests including FEV1, FVC were performed and inflammatory indicators including CRP, FeNO, IL-6, IL-13 were measured. The occurrence of adverse reactions during treatment was recorded.

Results: Pulmonary function tests including FEV1%, FEV1/FVC% were improved in all subjects, and the improvement of pulmonary function was more significant in the study group (P<0.05). The levels of CRP, FeNO, IL-6 and IL-13 were decreased in the two groups, especially in the study group (P<0.05). There was no significant difference in the incidence of adverse drug reactions between the two groups (P>0.05).

Conclusion: Low-dose azithromycin can significantly improve the pulmonary function in children with bronchial asthma, reduce the levels of inflammatory factors, control airway mucus secretion and inflammation, and can be used to treat chronic lung diseases such as bronchial asthma.

Objective: To study the therapeutic effect and protective mechanism of granulocyte colony stimulating factor (G-CSF) and neurotrophin receptor (NTR) on cerebral ischemia-reperfusion injury.

Methods: Rat models of permanent focal middle cerebral artery occlusion (MCAO) were constructed by using a modified suture method, and the rats were assigned into three groups such as treatment group (the rats were injected with mixed G-CSF and NTR once), sham operation group and PBS control group. The volume of the cerebral infarction was detected using Triphenyltetrazolium Chloride (TTC) staining method; the motor function in rats was evaluated; and qRT-PCR detection, double immunofluorescence histochemistry and immunohistochemistry were performed to observe various effects.

Results: After G-CSF and NTR treatment, the infarct volume induced by MCAO in the treatment group was significantly lower than that in the PBS control group (P<0.05). The motor function in the treatment group was significantly improved on day 7 and day 14 compared to the PBS control group (P<0.05). The levels of MCP-1, TNF-α, TGF-β and IL-10 mRNA in the treatment group decreased by 22% compared with PBS control group, and the difference was statistically significant (P<0.05). The Bcl-2 protein level in the treatment group was greater than that in the PBS control group, while the Bax level in the treatment group was lower than in the control group; and both the differences were statistically significant (P<0.05). The number of BrdU + cells in the treatment group was significantly greater than that in the PBS control group (P<0.05).

Conclusion: G-CSF can promote the regeneration of neurons, promote the formation of new blood vessels, promote the reconstruction of neural network in rat MCAO models through anti apoptosis, anti-inflammation and mobilization of bone marrow hematopoietic cells to exert its powerful protective effect on neurons, and contribute to the repair of neural function and improvement of prognosis.

Objective: During the progression of chronic idiopathic pulmonary fibrosis (IPF), maladaptive tissue remodeling including excessive extracellular matrix (ECM) deposition occurs, which eventually leads to architectural distortion and loss of organ function in organ fibrosis. ADAM15, which is highly expressed in the developing lungs and kidneys, is a transmembrane-anchored multidomain protein belonging to the family of metalloproteinases. Compared to the extensive studies about functions of matrix metalloproteinases (MMPs), less are discussed about ADAM15, particularly in function and mechanism involving fibrogenesis. Our study aims to fill in this gap.

Methods: We identified ADAM15 as a novel antifibrotic mediator in lung fibrosis. We found that ADAM15 has cross-talks with transforming growth factor-β1 (TGF-β1), which is the most potent profibrotic mediator. We provided molecular and translational evidence that knockdown of ADAM15 accelerated fibrogenic response induced by TGF-β1 and upregulation of ADAM15 rescued TGF-β1-induced myofibroblast activation in part.

Results: Overexpression of ADAM15 ameliorates fibrotic changes and ADAM15 deficiency exacerbates changes from fibroblast to myofibroblast in NIH/3T3. Results were also presented and identified by the intuitive immunofluorescence staining.

Conclusion: In this study, we uncover a new molecular mechanism of tissue fibrogenesis and identify ADAM15 as a potential therapeutic target in the treatment of fibrotic diseases.