The incidence rate of thyroid cancer has been rising in recent years. How to accurately distinguish malignant and benign thyroid nodules before surgery has become an important research direction. Ultrasound, as a non-invasive and fast examination method, has been widely used in clinical practice. Some typical ultrasound features, such as calcification, unclear boundaries, multiple lesions, low echo, and aspect ratio>1, can indicate the occurrence of thyroid cancer before surgery. Further analysis of these ultrasound features is still a focus of current research. This article will review the expression and distribution of calcification, a typical ultrasound feature, in benign and malignant thyroid nodules, in order to provide a basis for predicting the malignancy of thyroid nodules based on the characteristics of calcification under preoperative ultrasound.

Objective:To analyze the effects of shared decision-making in patients with type 2 diabetic mellitus.Methods:Databases including PubMed, Web of Science, Embase, Cochrane Library, CNKI, Wanfang Datebase, COVIP and SinoMed, for randomized controlled trials (RCTs) on the application of shared decision-making in patients with type 2 diabetic mellitus from inception to July 22, 2023, used R Studio software for meta-analysis.Results:A total of 14 RCTs and 2 606 patients with type 2 diabetic mellitus were included. The results of meta-analysis showed that the shared decision-making can alleviate the decision-making conflict of type 2 diabetic mellitus patients ( MD=-3.18, 95% CI -5.36 to -0.99, P<0.05), improve the decision-making self-efficacy ( MD=5.82, 95% CI 2.34 to 9.30, P<0.05), medication compliance ( RR=1.08, 95% CI 1.01 to 1.16, P<0.05), and diabetes-related knowledge ( SMD=0.46, 95% CI 0.16 to 0.75, P<0.05), reduce BMI ( MD=-0.75, 95% CI-1.33 to -0.17, P<0.05) and the HbA1c level ( MD=-0.45, 95% CI -0.65 to -0.24, P<0.05) in the 3-month follow-up. Conclusions:The shared decision-making improves the self-management in patients with type 2 diabetic mellitus. However, the long-term effect and potential risks of this model still need to be further studied. It is suggested that the application of shared decision-making in type 2 diabetic mellitus patients should be optimized in the future, and research on the long-term effects and potential risks of this model should be increased.

Objective:To analyze the evolution of ceftazidime/avibactam (CZA) resistance phenotyes and clinical features of 11 ST11-KL64 carbapenem-resistant Klebsiella pneumoniae (CRKP) isolates carrying bla KPC. Methods:Eleven CRKP isolates, designated K01 to K11, obtained from infected liver transplant patients from June to September 2024 were retrospectively studied. Broth microdilution method, whole genome sequencing (WGS) and plasmid conjugation assays were employed to investigate the antimicrobial susceptibility, resistance mechanisms, and genetic structural characteristics of these CRKP isolates. Clinical data were simultaneously collected and organized to analyze the correlation between bla KPC gene mutations and the clinical efficacy of antimicrobial therapy. Results:All eleven isolates of CRKP exhibited multidrug resistance phenotypes. Among them, K01-K09 and K11 were sensitive to CZA and resistant to carbapenems, while K10 was resistant to CZA and displayed sensitivity or intermediate resistance to carbapenems. WGS analysis showed that all 11 CRKP isolates belonged to the ST11-KL64 clonal type. Among these isolates, the K01-K09 and K11 isolates carry the bla KPC-2 gene, whereas the K10 isolate carries the bla KPC-33 gene. A single nucleotide mutation in bla KPC-2 (G532T) resulted in a substitution of tyrosine (Y) for aspartic acid (D) at Ambler position 179 (D179Y), causing resistance of CRKP to CZA and reduced sensitivity to Imipenem and Meropenem. The conjugative plasmid was successfully constructed, and compared to the parental strain, its minimum inhibitory concentration (MIC) to CZA increased 32 folds. Clinical data revealed that the patient developed the bla KPC-33 mutation after 51 days of CZA treatment. Conclusions:The bla KPC-33 mutation following CZA treatment for CRKP infection exhibits a considerable delay. It is essential to dynamically monitor the evolution of CRKP resistance to ensure timely adjustment of therapeutic strategies in case of the occurrence of mutations such as bla KPC-33.

Objective:To analyze the evolution of ceftazidime/avibactam (CZA) resistance phenotyes and clinical features of 11 ST11-KL64 carbapenem-resistant Klebsiella pneumoniae (CRKP) isolates carrying bla KPC. Methods:Eleven CRKP isolates, designated K01 to K11, obtained from infected liver transplant patients from June to September 2024 were retrospectively studied. Broth microdilution method, whole genome sequencing (WGS) and plasmid conjugation assays were employed to investigate the antimicrobial susceptibility, resistance mechanisms, and genetic structural characteristics of these CRKP isolates. Clinical data were simultaneously collected and organized to analyze the correlation between bla KPC gene mutations and the clinical efficacy of antimicrobial therapy. Results:All eleven isolates of CRKP exhibited multidrug resistance phenotypes. Among them, K01-K09 and K11 were sensitive to CZA and resistant to carbapenems, while K10 was resistant to CZA and displayed sensitivity or intermediate resistance to carbapenems. WGS analysis showed that all 11 CRKP isolates belonged to the ST11-KL64 clonal type. Among these isolates, the K01-K09 and K11 isolates carry the bla KPC-2 gene, whereas the K10 isolate carries the bla KPC-33 gene. A single nucleotide mutation in bla KPC-2 (G532T) resulted in a substitution of tyrosine (Y) for aspartic acid (D) at Ambler position 179 (D179Y), causing resistance of CRKP to CZA and reduced sensitivity to Imipenem and Meropenem. The conjugative plasmid was successfully constructed, and compared to the parental strain, its minimum inhibitory concentration (MIC) to CZA increased 32 folds. Clinical data revealed that the patient developed the bla KPC-33 mutation after 51 days of CZA treatment. Conclusions:The bla KPC-33 mutation following CZA treatment for CRKP infection exhibits a considerable delay. It is essential to dynamically monitor the evolution of CRKP resistance to ensure timely adjustment of therapeutic strategies in case of the occurrence of mutations such as bla KPC-33.

Objective:To analyze the effects of shared decision-making in patients with type 2 diabetic mellitus.Methods:Databases including PubMed, Web of Science, Embase, Cochrane Library, CNKI, Wanfang Datebase, COVIP and SinoMed, for randomized controlled trials (RCTs) on the application of shared decision-making in patients with type 2 diabetic mellitus from inception to July 22, 2023, used R Studio software for meta-analysis.Results:A total of 14 RCTs and 2 606 patients with type 2 diabetic mellitus were included. The results of meta-analysis showed that the shared decision-making can alleviate the decision-making conflict of type 2 diabetic mellitus patients ( MD=-3.18, 95% CI -5.36 to -0.99, P<0.05), improve the decision-making self-efficacy ( MD=5.82, 95% CI 2.34 to 9.30, P<0.05), medication compliance ( RR=1.08, 95% CI 1.01 to 1.16, P<0.05), and diabetes-related knowledge ( SMD=0.46, 95% CI 0.16 to 0.75, P<0.05), reduce BMI ( MD=-0.75, 95% CI-1.33 to -0.17, P<0.05) and the HbA1c level ( MD=-0.45, 95% CI -0.65 to -0.24, P<0.05) in the 3-month follow-up. Conclusions:The shared decision-making improves the self-management in patients with type 2 diabetic mellitus. However, the long-term effect and potential risks of this model still need to be further studied. It is suggested that the application of shared decision-making in type 2 diabetic mellitus patients should be optimized in the future, and research on the long-term effects and potential risks of this model should be increased.

Ruxolitinib， a small molecule inhibitor， selectively targets Janus kinase （JAK） by competitively binding to adenosine triphosphate on the catalytic site of the JAK1 and JAK2 domain， thereby inhibiting JAK activation and signal transducer and activator of transcription （STAT） phosphorylation and prevents the expressions of the JAK-STAT signaling pathway. Oral ruxolitinib has demonstrated promising efficacy for myelofibrosis and polycythemia vera. The topical Ruxolitinib cream， approved by the US FDA as the first non-segmental vitiligo home treatment drug， is set to be launched in domestic medical pioneer areas in August 2023 and is expected to bring about a breakthrough in the treatment of vitiligo. Clinical cases have also shown that Ruxolitinib cream has significant curative effects on atopic dermatitis， alopecia areata， and other conditions， indicating great application prospects.

Objective:To investigate the association between plasma anti-Müllerian hormone(AMH) levels and ischemic stroke.Methods:In this case-control study, 93 ischemic stroke patients were randomly selected as the case group from a study on the prevention and treatment of metabolic syndrome, which was conducted in 2018-2019 in Changshu, Jiangsu Province, while 372 nonischemic stroke patients were selected as the control group according to the principle of 1∶4 matching.An enzyme-linked immunosorbent assay was used to measure plasma AMH levels.The conditional logistic regression model and restricted cubic spline were used to analyze the relationship between AMH levels and ischemic stroke.Results:A total of 465 subjects with an average age of (68.7±7.4)years were included in this study, of whom 215(46.2%)were men and 250(53.8%)were women.According to our conditional Logistic regression analysis, the risk of ischemic stroke was reduced by 44% for every unit increase in the log-AMH level( OR=0.56, 95% CI: 0.37-0.85)in the overall population after multivariate adjustment.Compared with the tertile with the lowest AMH level, the risk of ischemic stroke in the tertile with the highest AMH level decreased significantly( OR=0.37, 95% CI: 0.19-0.69). When subgrouped by sex, the tertiles with the highest AMH levels were associated with a 66% lower risk of ischemic stroke in men( OR=0.34, 95% CI: 0.13-0.88)and a 64% lower risk of ischemic stroke in women( OR=0.36, 95% CI: 0.15-0.87), compared with the tertiles with the lowest AMH levels.The results of restricted cubic spline analysis showed that there was a linear dose-response relationship between plasma AMH levels and ischemic stroke both in the general population and in male or female population( Pvalues for linear trends were 0.0002, 0.008 and 0.007, respectively). Conclusions:Higher plasma AMH levels decrease the risk of ischemic stroke with a dose-response pattern.

Objective To investigate the risk factors affecting the malignancy of amorphous calcifications in the breast and to establish a predictive nomogram.Methods Patients with amorphous calcifications detected by mammography were retrospectively collected,clinical data were obtained from electronic medical record(EMR),and the mammographic features of the patients were assessed by diagnostic physicians.The risk factors affecting the malignancy of amorphous calcifications were analyzed to develop a predictive model and to assess the performance of the model.Results A total of 153 amorphous calcifications in 144 patients were included in the study,and the overall malignancy rate of calcifications was 20.92％.Patient's age ≥45 years,linear distribution of calcifications,unilateral single or unilateral multiple calcifications,and a larger maximum ratio of calcification extent all predicted a higher probability of malignancy,establishing a nomogram based on these 4 risk factors,with a 3.65％predicted probability of malig-nancy as the cut-off,33.99％(52/153)of patients were allowed to be spared biopsy.Conclusion Patient's age and the distribution,number,and maximum ratio of calcifications may be the risk predictors of malignancy for amorphous calcifications,with nomogram con-struction for distinguishing benignity from malignancy of amorphous calcifications via combining with mammographic features and clinical data.

Objective:To systematically evaluate the risk of bias and applicability of risk prediction models for the progression of diabetic nephropathy (DN) .Methods:A systematic search was conducted in CNKI, CBMdisc, Wanfang, VIP, PubMed, Web of Science, Embase, and CINAHL for literature related to DN progression prediction models, with a search timeline up to April 30, 2023. Two researchers independently screened the literature and extracted data according to a checklist for key assessments of prediction model studies and the PROBAST tool for assessing risk of bias in prediction models.Results:A total of nine articles encompassing 15 models were included. Of these, eight studies were retrospective study, and one was a randomized controlled trial. The area under the receiver operating characteristic curve ( AUC) for these models ranged from 0.626 to 0.986. Three studies conducted external validation, and seven studies conducted internal validation. Commonly repeated predictive factors included eGFR, cystatin C, and glycated hemoglobin (HbA1c). While the overall applicability of the models was good, methodological issues such as inappropriate data acquisition, selection of predictive factors, and neglect of model performance evaluation contributed to a certain risk of bias. Conclusions:The current DN progression risk prediction models demonstrate good discrimination and applicability. However, most models lack comprehensive calibration assessments and exhibit methodological flaws. Future research should focus on developing models with better applicability and lower bias, coupled with effective internal and external validation.

OBJECTIVES: To investigate the role of mitochondrial autophagy disorder caused by deletion of E3 ubiquitin ligase Parkin in neuroinflammation in a mouse model of MPTP-induced Parkinson's disease (PD). METHODS: Wild-type (WT) male C57BL/6 mice and Parkin^-/- mice were given intraperitoneal injections with MPTP or PBS for 5 consecutive days, and the changes in motor behaviors of the mice were observed using open field test. The effects of Parkin deletion on PD development and neuroinflammation were evaluated using immunofluorescence and Western blotting. The changes of the PINK 1/Parkin signaling pathway in the midbrain substantia nigra of the mice were examined to explore the molecular mechanism of Parkin-mediated regulation of mitochondrial autophagy and its effect on neuroinflammation in PD mice. RESULTS: Compared with their WT counterparts, the Parkin^-/- mice with MPTP injections exhibited significant impairment of motor function with decreased TH⁺ neurons, increased α-synuclein (α-syn) accumulation, and increased numbers of GFAP⁺ and I-ba1⁺ cells in the midbrain substantia nigra. Parkin deletion obviously affected PINK1/Parkin-mediated mitochondrial autophagy to result in significantly increased mtDNA and upregulated expressions of STING and NLRP3 inflammatosomes in the midbrain substantia nigra of MPTP-treated transgenic mice. CONCLUSIONS Parkin deletion causes mitochondrial autophagy disorder to accelerate PD progression and exacerbates neuroinflammation in mice by affecting the PINK1/Parkin signaling pathway, suggesting the important role of Parkin in early pathogenesis of PD.
Animals ; Ubiquitin-Protein Ligases/genetics* ; Mice ; Mice, Inbred C57BL ; Male ; Parkinson Disease/genetics* ; Protein Kinases/genetics* ; Mitochondria/metabolism* ; Disease Models, Animal ; Autophagy ; Signal Transduction ; Neuroinflammatory Diseases/metabolism* ; Mice, Knockout ; alpha-Synuclein/metabolism* ; Substantia Nigra/metabolism* ; Mitophagy ; Disease Progression