Objective:To analyze plaque characteristics of non-culprit coronary lesions with cholesterol crystals in patients with acute myocardial infarction(AMI) by using optical coherence tomography(OCT). We also investigated the potential association between cholesterol crystals with plaque rupture and healed plaque at non-culprit segment.Methods:This study was a retrospective cohort study. Between January 2017 and December 2017, patients with AMI who underwent 3-vessel OCT imaging were included in this study. Patients were divided into two groups according to the presence or absence of cholesterol crystals at the non-culprit lesions. All patients underwent coronary angiography and OCT examination, and non-culprit plaque characteristics were compared between the two groups. The generalized estimating equation log-binomial multirariate regression model was used to assess the relationship between non-culprit lesions with cholesterol crystals and plaque rupture and plaque healing. The follow-up data collection ended in October 2023. Kaplan-Meier survival curves were plotted, and log-rank tests were used to compare the cumulative incidence of major adverse cardiovascular events between the two groups.Results:A total of 173 AMI patients were included (aged (56.8±11.6) years; 124 men (71.7%)). Among 710 non-culprit lesions identified by OCT, there were 102 (14.4%) in cholesterol crystals group and 608 (85.6%) in non-cholesterol crystals group. Compared with non-culprit lesions without cholesterol crystals, those with cholesterol crystals had smaller minimum lumen diameter, severer diameter stenosis, and longer lesion length (all P<0.01). The prevalence of plaque rupture (17.6% (18/102) vs. 4.9% (30/608), P=0.001) and thin-cap fibroatheroma (31.4% (32/102) vs. 11.5% (70/608), P<0.01) was higher in the cholesterol crystals groups than in the non-cholesterol crystals group. In addition, vulnerable plaque characteristics such as (44.1% (45/102) vs. 25.8% (157/608), P<0.01), macrophages were more frequently observed in non-culprit lesions with cholesterol crystals. The generalized estimating equation log-binomial multivariate regression analyses showed that non-culprit cholesterol crystals were positively correlated with healed plaque ( OR=1.583, 95% CI: 1.004-2.495, P=0.048). Conversely, cholesterol crystals were not associated with plaque rupture ( OR=1.632, 95% CI: 0.745-3.576, P=0.221). The follow-up time was 2 142 (1 880, 2 198) days. Non-culprit cholesterol crystals were not related to the major adverse cardiovascular events in patients with AMI (log-rank P=0.558). Conclusions:Among AMI patients, non-culprit lesions with cholesterol crystals presented with severer luminal stenosis and increased plaque vulnerability. The presence of non-culprit cholesterol crystals was associated with rather than plaque rupture.

Objective:To evaluate the efficacy and safety of mitoxantrone hydrochloride liposome injection in the treatment of peripheral T-cell lymphoma (PTCL) in a real-world setting.Methods:This was a real-world ambispective cohort study (MOMENT study) (Chinese clinical trial registry number: ChiCTR2200062067). Clinical data were collected from 198 patients who received mitoxantrone hydrochloride liposome injection as monotherapy or combination therapy at 37 hospitals from January 2022 to January 2023, including 166 patients in the retrospective cohort and 32 patients in the prospective cohort; 10 patients in the treatment-na?ve group and 188 patients in the relapsed/refractory group. Clinical characteristics, efficacy and adverse events were summarized, and the overall survival (OS) and progression-free survival (PFS) were analyzed.Results:All 198 patients were treated with mitoxantrone hydrochloride liposome injection for a median of 3 cycles (range 1-7 cycles); 28 cases were treated with mitoxantrone hydrochloride liposome injection as monotherapy, and 170 cases were treated with the combination regimen. Among 188 relapsed/refractory patients, 45 cases (23.9%) were in complete remission (CR), 82 cases (43.6%) were in partial remission (PR), and 28 cases (14.9%) were in disease stabilization (SD), and 33 cases (17.6%) were in disease progression (PD), with an objective remission rate (ORR) of 67.6% (127/188). Among 10 treatment-na?ve patients, 4 cases (40.0%) were in CR, 5 cases (50.0%) were in PR, and 1 case (10.0%) was in PD, with an ORR of 90.0% (9/10). The median follow-up time was 2.9 months (95% CI 2.4-3.7 months), and the median PFS and OS of patients in relapsed/refractory and treatment-na?ve groups were not reached. In relapsed/refractory patients, the difference in ORR between patients with different number of treatment lines of mitoxantrone hydrochloride liposome injection [ORR of the second-line, the third-line and ≥the forth-line treatment was 74.4% (67/90), 73.9% (34/46) and 50.0% (26/52)] was statistically significant ( P = 0.008). Of the 198 PTCL patients, 182 cases (91.9%) experienced at least 1 time of treatment-related adverse events, and the incidence rate of ≥grade 3 adverse events was 66.7% (132/198), which was mainly characterized by hematologic adverse events. The ≥ grade 3 hematologic adverse events mainly included decreased lymphocyte count, decreased neutrophil count, decreased white blood cell count, and anemia; non-hematologic adverse events were mostly grade 1-2, mainly including pigmentation disorders and upper respiratory tract infection. Conclusions:The use of mitoxantrone hydrochloride liposome injection-containing regimen in the treatment of PTCL has definite efficacy and is well tolerated, and it is a new therapeutic option for PTCL patients.

Objective::Microchannels are associated with the progression of atherosclerotic vulnerable plaques. However, in patients with culprit optical coherence tomography (OCT)-defined plaque erosion, the knowledge of microchannels and culprit lesion vulnerability is limited. The aim of this study was to investigate culprit lesion characteristics in patients with ST-segment elevated myocardial infarction (STEMI) caused by plaque erosion with and without microchannels using OCT.Methods::In all, 348 STEMI patients with plaque erosion who underwent OCT of the culprit lesion at the 2 nd Affiliated Hospital of Harbin Medical University (Harbin, China) from August 2014 to December 2017 were included and divided into the microchannel group ( n= 116, 33.3%) and no-microchannel group ( n = 232, 66.7%). The clinical characteristics and OCT-derived plaque features were compared between both groups. Results::Among the 348 STEMI patients with plaque erosion, culprit lesions with microchannels had higher incidence of lipid plaque (59.5% vs. 45.3%, P= 0.012); calcification (41.4% vs. 24.6%, P= 0.002); spotty calcification (30.2% vs. 18.1%, P= 0.014); macrophages accumulation (72.4% vs. 45.7%, P < 0.001); and cholesterol crystals (32.8% vs. 14.2%, P < 0.001) than those without microchannels. In addition, minimal lumen area was smaller ((1.9 ± 0.9) mm 2vs. (2.8 ± 2.3) mm 2, P < 0.001) and lumen area stenosis was greater ((71.3% ± 13.4%) vs. (65.3% ± 19.3%), P= 0.001) in the microchannel group than in the no-microchannel group. Conclusion::In patients with STEMI caused by plaque erosion, one-third manifested typical microchannel characteristics, and those with microchannels were associated with more severe luminal stenosis and more vulnerable plaque features than those without microchannels.

Objective::Microchannels are associated with the progression of atherosclerotic vulnerable plaques. However, in patients with culprit optical coherence tomography (OCT)-defined plaque erosion, the knowledge of microchannels and culprit lesion vulnerability is limited. The aim of this study was to investigate culprit lesion characteristics in patients with ST-segment elevated myocardial infarction (STEMI) caused by plaque erosion with and without microchannels using OCT.Methods::In all, 348 STEMI patients with plaque erosion who underwent OCT of the culprit lesion at the 2 nd Affiliated Hospital of Harbin Medical University (Harbin, China) from August 2014 to December 2017 were included and divided into the microchannel group ( n= 116, 33.3%) and no-microchannel group ( n = 232, 66.7%). The clinical characteristics and OCT-derived plaque features were compared between both groups. Results::Among the 348 STEMI patients with plaque erosion, culprit lesions with microchannels had higher incidence of lipid plaque (59.5% vs. 45.3%, P= 0.012); calcification (41.4% vs. 24.6%, P= 0.002); spotty calcification (30.2% vs. 18.1%, P= 0.014); macrophages accumulation (72.4% vs. 45.7%, P < 0.001); and cholesterol crystals (32.8% vs. 14.2%, P < 0.001) than those without microchannels. In addition, minimal lumen area was smaller ((1.9 ± 0.9) mm 2vs. (2.8 ± 2.3) mm 2, P < 0.001) and lumen area stenosis was greater ((71.3% ± 13.4%) vs. (65.3% ± 19.3%), P= 0.001) in the microchannel group than in the no-microchannel group. Conclusion::In patients with STEMI caused by plaque erosion, one-third manifested typical microchannel characteristics, and those with microchannels were associated with more severe luminal stenosis and more vulnerable plaque features than those without microchannels.

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Thioredoxin is one of important disulfide bond reductases in cells ,which plays important role in antioxi‐dant stress of cells and maintaining reduced state of intracellular protein and its normal functioning .The present ar‐ticle set forth the possible biological function of thioredoxin in atherosclerosis from its antioxidation ,anti－apopto‐sis ,anti－inflammation and regulation of blood lipid and glucose metabolism etc .,aiming at providing new targets for prevention and treatment of atherosclerosis .

Objective: To design and make a mind map of enterostomy health education and provide a reference for health education of patients with enterostomy. Methods: The mental map group was set up, and the contents of health education for patients with enterostomy were initially established by referring to the literature and combining with the clinical practice. The first draft of mental health education mentality of enterostomy was made by drawing software. After consulting and verifying by experts finalized. Results: The formed intestinal orifice health education mind map consisted of 4 parts of admission education, preoperative education, postoperative education, discharge guidance and small modules contained in each part. Conclusions The mind map is comprehensive and can be used for health education of patients with enterostoma.

Objective To study the effects of chronic exposure to inorganic arsenic (iAs) in drinking water on bone mineral density (BMD) in mice and its underlying mechanisms.Methods Five-month-old female C57BL/6 mice were randomly divided into sham groups and ovarectomy (OVX) groups (n =19 mice each group),which were further randomly assigned into control group (distilled water) and iAs exposure groups [5 mg/L and 20 mg/L,inorganic arsenite (iAsⅢ):inorganic arsenate (iAsv) =1 ∶ 1].Following 3 months of exposure to iAs,BMD of the mice were determined by the dual energy X-ray detector.RAW 264.7 cell line and bone marrow hematopoietic stem cells (BMHSC) primarily isolated from C57BL/6 mice were used to study the in vitro effects of iAs on osteoclast differentiation and underlying mechanisms.During differentiation induced by receptor activator of nuclear factor-κ B ligand (RANKL,50 μg/L) and macrophage colony-stimulating factor (M-CSF,30 μg/L),RAW 264.7 cell line were treated with 0.00,0.25,0.50,0.75,1.00,1.50 μmol/L iAsⅢ,while BMHSC with 0.0,0.2,0.4,0.6,0.8,1.0 μmol/L iAsⅢ for 6 days.Based on the effect of iAsⅢ on the differentiation of RAW cells,RAW 264.7 cell line were treated by 0.6 μmol/L iAsⅢ combined with 0,5,10 mmol/L of N-acetyl-cysteine (NAC).Tartrate resistant acid phosphatase (TRAP)-positive red-colored cells with 3 or more nuclei were considered mature osteoclast.Results The femoral BMD of the mice [(80.04 ± 4.06) mg/cm2] that had been exposed to 20 mg/L of iAs for 3 months was substantially decreased compared to that of sham control mice [(84.44 ± 4.40) mg/cm2].As expected,the BMD of the OVX group [(76.36 ± 3.36) mg/cm2] was significant decreased compared to that of the sham control group (P ＜ 0.05).However,the BMD among the OVX groups showed no significant difference [5 mg/L:(77.74 ± 4.91) mg/cm2;20 mg/L:(75.56 ± 3.71) mg/cm2,P ＞ 0.05].In vitro studies,the iAsⅢ evidently affected the osteoclast differentiation in a concentration-dependent fashion.Low concentrations of iAs Ⅲ exposure significantly augmented osteoclast differentiation in the two cell models while high concentrations showed inhibitory effect.In RAW 264.7 cells,the number of osteoclasts in different groups was significantly different (F =1 522,P ＜ 0.05),in the 0.50 μmol/L iAs Ⅲ group the number of osteoclasts reached the peak.In the BMHSC,the nmnber of osteoclasts in different groups was also significantly different (F =1 781,P ＜ 0.05),in the 0.6 μmol/L iAsⅢ group the number of osteoclasts reached the peak.NAC pretreatment significantly abolished low-level iAsⅢ(0.6 μmol/L)-induced augmentation of osteoclast differentiation in a concentration-dependent fashion (0 mmol/L:109.33 ± 3.06;5 mmol/L:56.00 ± 2.65;10 mmol/L:22.67 ± 0.58,F =1 940,P ＜ 0.05).Conclusions The inhibitory effect of iAs on bone metabolism is dependent on the availability of ovary function,suggesting that iAs may interfere with estrogen metabolism and/or function to disturb bone metabolism.Oxidative stress induced by iAs exposure stimulates osteoclast differentiation,and the increased osteoclast differentiation may be involved in the reduction of BMD caused by chronic iAs exposure.These preliminary findings suggest that antioxidant intervention may be an effective approach to prevent osteoporosis induced by chronic iAs exposure.

Metabolic syndrome (MS)is a clinical syndrome featured by glucose and lipid metabolic disorders,hyper- tension and obesity etc.,whose key links are insulin resistance and abdominal obesity.MS is closely related with cor- onary atherosclerosis,every link of MS can lead to occurrence and development of atherosclerosis.The present arti- cle mainly stated research progress of the correlation between MS and coronary atherosclerosis in recent years.

The present study used optical coherence tomography (OCT) to observe the relationship between inhibitor of monocyte chemoattractant protein-1 (MCP-1) and coronary in-stent restenosis after stenting ,and proved that MCP-1 is a key inflammatory factor causing in-stent restenosis after stenting .