Purpose: This study aimed to investigate reproductive concerns among breast cancer patients of reproductive age, analyze the influencing factors, explore the relationship between coping styles, fear of progression (FOP), and reproductive concerns, and identify the multiple effects of coping styles on the relationship between FOP and reproductive concerns among Chinese breast cancer patients. Methods: A cross-sectional, descriptive study was conducted among breast cancer patients in four tertiary grade A hospitals in Fujian, China, from January 2022 to September 2022. A total of 210 patients were recruited to complete paper-based questionnaires, which included the general data questionnaires, the Reproductive Concerns After Cancer Scale (RCACS), the Fear of Progression Questionnaire-Short Form (FOP-Q-SF), and the Medical Coping Modes Questionnaire (MCMQ). Structural equation models were utilized to evaluate the multiple effects of coping styles on FOP and reproductive concerns. Results: Reproductive concerns in breast cancer patients had a mean score of 53.02 (SD, 10.69), out of a total score of 90, and coping styles for cancer (confrontation, avoidance) were closely associated with FOP and reproductive concerns. FOP showed a significant positive correlation with reproductive concerns (r = .52, p < .01). At the same time, confrontation was significantly negatively correlated with both FOP (r = −.28, p < .01) and reproductive concerns (r = −.39, p < .01). Avoidance was positively correlated to both FOP (r = .25, p < .01) and reproductive concerns (r = .34, p < .01). The impact of FOP on reproductive concerns is partially mediated by confrontation and avoidance, with effect sizes of .07 and .04, respectively. These mediating factors account for 22.0% of the total effect. Conclusions The FOP directly impacted reproductive concerns, while coping styles could partially mediate the association between FOP and reproductive concerns. This study illustrates the role of confrontation and avoidance in alleviating reproductive concerns, suggesting that it is necessary to focus on the changes in reproductive concerns among reproductive-age breast cancer patients. Healthcare professionals can improve disease awareness and reduce patients' FOP, thereby promoting positive psychological and coping behaviors and ultimately alleviating reproductive concerns.

A 68-year-old female patient with rheumatic heart disease and auricular fibrillation received warfarin (10.5 mg per week, totally 6 weeks;then 12 mg per week, totally 3 weeks).The international nomalized ratio (INR) was monitored regularly.Her INR was steady and reached the standard during the medication.She took Zhisou Lixiao Wan 12 g daily by herself because of cough on the 10th week.Four days later she found multiple ecchymosis at her front of right leg and the INR was 6.46.Warfarin was withdrawn while Zhisou Lixiao Wan was continued.Three days later, the ecchymosis was absorbed obviously and the INR decreased to 2.96.Zhisou Lixiao Wan was stopped and warfarin was taken by 12 mg weekly.Five days later, her INR was 2.24 and the ecchymosis disappeared completely.

A 74-year-old female patient received oral carbamazepine 0. 1g thrice daily because of epilepsy after acute ischemic stroke. On the third day, the patient suddenly presented drowsiness which gradually aggravated to a state of mild coma within 30 minutes. The electrocardiogram showed that sick sinus syndrome and junctional rhythm with a heart rate of 34 beats per minute. The patient was diagnosed as Adams-Stokes syndrome which may be induced by carbamazepine. She was given an intravenous injection of atropine sulfate 0. 5 mg immediately. Then atropine sulfate 1 mg in 5% glucose injection 500 ml was slowly given by intravenous drip. Two hours later, the patient regained consciousness. The electrocardiogram showed restoration of sinus rhythm with a heart rate of 48 beats per minute. Carbamazepine was withdrawn and disturbance of consciousness did not recur.

A 68-year-old female patient with rheumatic heart disease and auricular fibrillation received warfarin (10.5 mg per week, totally 6 weeks;then 12 mg per week, totally 3 weeks).The international nomalized ratio (INR) was monitored regularly.Her INR was steady and reached the standard during the medication.She took Zhisou Lixiao Wan 12 g daily by herself because of cough on the 10th week.Four days later she found multiple ecchymosis at her front of right leg and the INR was 6.46.Warfarin was withdrawn while Zhisou Lixiao Wan was continued.Three days later, the ecchymosis was absorbed obviously and the INR decreased to 2.96.Zhisou Lixiao Wan was stopped and warfarin was taken by 12 mg weekly.Five days later, her INR was 2.24 and the ecchymosis disappeared completely.

A 74-year-old female patient received oral carbamazepine 0. 1g thrice daily because of epilepsy after acute ischemic stroke. On the third day, the patient suddenly presented drowsiness which gradually aggravated to a state of mild coma within 30 minutes. The electrocardiogram showed that sick sinus syndrome and junctional rhythm with a heart rate of 34 beats per minute. The patient was diagnosed as Adams-Stokes syndrome which may be induced by carbamazepine. She was given an intravenous injection of atropine sulfate 0. 5 mg immediately. Then atropine sulfate 1 mg in 5% glucose injection 500 ml was slowly given by intravenous drip. Two hours later, the patient regained consciousness. The electrocardiogram showed restoration of sinus rhythm with a heart rate of 48 beats per minute. Carbamazepine was withdrawn and disturbance of consciousness did not recur.

Objective: To explore the effect of autophagy on process of high phosphate salt induced vascular smooth muscle cell (VSMC) calciifcation in experimental rats. Methods: Rats’ model of VSMC calciifcation was induced by phosphate incubation. VSMC were divided into 3 groups:①Control group,②Calciifcation group which included 3 subgroups as 4-day subgroup, the cells were cultured by 3.2 mmol/L phosphate for 4 days, 6-day subgroup and 8-day subgroup,③Calciifcation+ 3-MA (autophagy inhibitor) group, in which the 8-day cells were cultured with 5mmol/L 3-MA. Calcium nodule formation and calcium deposition in VSMC were measured by Alizarin red staining and o-cresolphthaleincomplexone method, protein expressions of Runx2, α-SMA and LC3 II were examined by Western blot analysis, autophagosome formation in VSMC was measured by transmission electron microscope and the localization and expression of Runx2 and LC3 II in VSMC were observed by immunolfuorescent microscope. Results: Compared with Control group, the cells at 8-day subgroup showed more calcium nodules, higher calcium deposition, increased protein expressions of Runx2, LC3 II, more autophagosome and decreased α-SMA expression, allP<0.05. Compared with 8-day subgroup, the cells in Calcification+3-MA group presented increased calcium deposition, decreased lfuorescence distribution of LC3 II and more cells with positive Runx2 protein expression, all P<0.05. Conclusion: Autophagy has the protective effect on process of phosphate induced VSMC calciifcation in experimental rats.

Objective: To explore the effect of oxidative stress injury on the mechanism of vascular smooth muscle cell (VSMC) calciifcation induced by calcium and phosphorus in experimental rats.
Methods: The VSMC calcification was induced by incubating the cells with calcium chloride (CaCl2) andβ-sodium glycerophosphate (β-GP) for 8 days, and the cells were divided into 4 groups: ① Control group, ② Calcification group,③ Calciifcation+H2O2 group, ④ Calciifcation+catalase group. The calcium nodule formation and calcium deposition in VSMC were detected by Alizarin red staining and o-cresolphthalein complexone method, the reactive oxygen species (ROS) was detected by DCFH-DA probe staining and the protein expression of Runx2 was examined by Western blot analysis.
Results: Compared with Control group, Calciifcation group showed the higher ROS production, more calcium nodule and calcium deposition, higher Runx2 protein expression;while compared with Calciifcation group, the above indexes were even higher in Calciifcation+H2O2 group, P<0.05. The ROS production, calcium nodule, calcium deposition and Runx2 protein expression were lower in Calciifcation+catalase group than those in Calciifcation group and Calciifcation+H2O2 group, but still higher than that in Control group. The protein expression of Runx2 was similar between Calciifcation+catalase group and Control group, P>0.05.
Conclusion: CaCl2 andβ-GP treatment may induce VSMC calciifcation via activating ROS-Runx2 signal pathway in experimental rats.

Objective: To explore the effects of Vitamin K2 (VK2) on theaortic artery calciifcation and oxidative stress injury in experimental rats.
Methods: A total of 24 rats were divided into 4 groups:①Control group,②6-week calciifcation group,③12-week calciifcation group and④6-week calciifcation + 6-week VK2 group;n=6 in each group. The arterial calciifcation was induced by warfarin (WFN) treatment. The calcium nodule and deposition in rat’s theaortic artery were detected by Alizarin red staining and o-cresolphthalein complexone method, the reactive oxygen species (ROS) were measured by DHE probe staining and the morphological changes of mitochondria in smooth muscle cells were detected by transmission electron microscopy.
Results: Calciifcation nodule formed in both 6-week and 12-week calciifcation groups, the calciifcation deposition and ROS were higher than Control group,P<0.01. Compared with both calcification groups, the above indexes were decreased in 6-week calciifcation + 6-week VK2 group,P<0.01. Both calciifcation groups showed mitochondria swelling with unclear structure and cytoplasm vacuoles degeneration in vascular smooth muscle cells. The vascular smooth muscle cell volumes were similar between Control group and 6-week calcification + 6-week VK2 group, and no cytoplasm vacuoles degeneration was observed.
Conclusion: Warfarin induced aortic calciifcation is related to oxidative stress injury which may cause the ultra-micro structural damage in smooth muscle cells; VK2 may reduce the oxidative stress injury and improve the condition of vessel calciifcation in experimental rats.