OBJECTIVE To explore comprehensive management and potential issues associated with long-term prescriptions medications of psychiatry， in order to provide a reference for the comprehensive management of long-term prescriptions of psychiatry in psychiatric hospitals and other medical institutions’ pharmacies. METHODS Starting from the applicable principles for long-term prescriptions of psychiatry， this study introduced the standardized assessment and precautions before issuing long-term prescriptions， the formulation and adjustment of the drug list， as well as the rational management of the long-term prescriptions. It also analyzed potential issues that may arise in the comprehensive management of long-term prescription medications and proposed corresponding countermeasures and suggestions. RESULTS & CONCLUSIONS Prior to initiating long-term prescriptions， a standardized assessment should be conducted on patients from the aspects of their psychiatric condition and long-term potential risk factors， pharmacological treatment plans and other non-pharmacological therapies， physical illnesses. Additionally， healthcare providers should fulfill their obligation to inform patients or their family members. The comprehensive management of long-term prescription medications should be jointly established and improved by multiple departments， and the formulation of drug catalogs should avoid including drugs with potential social harm or medication risks while complying with policy requirements. Furthermore， measures such as adding special identifiers to long-term prescriptions， providing patients with reminders about （No.YGLX202537） prescription expiration， or offering online consultations can also effectively enhance the rationality of medication use under long-term prescriptions. Currently， the implementation of long-term prescriptions in psychiatry remains challenged by inconsistencies in prescription duration， incomplete coverage of diagnostic categories， poor patient adherence， and the risk of deviation in clinical assessments. In this regard， measures such as collaborating with multiple departments to strengthen long-term prescription information management， providing matching pharmaceutical services， ensuring the quality and rationality of long-term prescription implementation， and using modern methods to screen high-risk patients can be taken to improve patient medication compliance and safety.

Objective:To construct a recombinant plasmid DNA carrying the decorin( DCN) gene and study its therapeutic effect on hypertrophic scars of rabbit ears. Methods:The human decorin gene fragment amplified by PCR was cloned into plasmid vector pUDK to construct the recombinant plasmid pDCN, which was identified by enzyme digestion and sequencing. pDCN was transfected into 293T cells, and the expression of DCN and TGF-β1 was detected. The therapeutic effect of pDCN on rabbit ear hypertrophic scar model was observed by hypertrophy index, pathological examination and immunohistochemical staining. Results:The decorin gene was successfully inserted into pUDK, which was examined by enzyme digestion and sequencing. The expression level of mRNA and protein of DCN was up-regulated in 293T cells post pDCN transfection, and the expression of TGF-β1 was suppressed. Then the rabbit ear hypertrophic scars were treated with different doses of pDCN, and the results showed that the hypertrophy index of the medium dose (200 μg/cm 2) pDCN group was significantly lower than that of the PBS group ( P<0.05), while there was no significant difference in the hypertrophy index of the low dose and high dose pDCN group compared with the PBS group. The expression of DCN in ears skin in the medium dose pDCN group was significantly higher than that in the PBS group ( P<0.05). The pathological examination showed that inflammatory cell infiltration and fibrous deposition in scar tissue were significantly reduced. These results indicated that the medium-dose pDCN could effectively inhibit the hyperplasia of hypertrophic scar in rabbit ears. Conclusions:pDCN, the plasmid carrying decorin gene, has therapeutic effects on hypertrophic scars of rabbit ears by inhibiting TGF-β1 expression.

Objective:To construct a recombinant plasmid DNA carrying the decorin( DCN) gene and study its therapeutic effect on hypertrophic scars of rabbit ears. Methods:The human decorin gene fragment amplified by PCR was cloned into plasmid vector pUDK to construct the recombinant plasmid pDCN, which was identified by enzyme digestion and sequencing. pDCN was transfected into 293T cells, and the expression of DCN and TGF-β1 was detected. The therapeutic effect of pDCN on rabbit ear hypertrophic scar model was observed by hypertrophy index, pathological examination and immunohistochemical staining. Results:The decorin gene was successfully inserted into pUDK, which was examined by enzyme digestion and sequencing. The expression level of mRNA and protein of DCN was up-regulated in 293T cells post pDCN transfection, and the expression of TGF-β1 was suppressed. Then the rabbit ear hypertrophic scars were treated with different doses of pDCN, and the results showed that the hypertrophy index of the medium dose (200 μg/cm 2) pDCN group was significantly lower than that of the PBS group ( P<0.05), while there was no significant difference in the hypertrophy index of the low dose and high dose pDCN group compared with the PBS group. The expression of DCN in ears skin in the medium dose pDCN group was significantly higher than that in the PBS group ( P<0.05). The pathological examination showed that inflammatory cell infiltration and fibrous deposition in scar tissue were significantly reduced. These results indicated that the medium-dose pDCN could effectively inhibit the hyperplasia of hypertrophic scar in rabbit ears. Conclusions:pDCN, the plasmid carrying decorin gene, has therapeutic effects on hypertrophic scars of rabbit ears by inhibiting TGF-β1 expression.

Objective: To investigate the effects of tanshinone ⅡA on atherosclerosis plaque formation and adventitial mast cells activation in high-fat-diet induced Apo E^-/- mice model. Methods: Sixteen 8-week-old Apo E^-/-male mice and eight 8-week-old C57BL/6 male mice were randomly allocated into following group: the control group (C57BL/6 + carboxymethyl cellulose per gavage), the atherogenic group (Apo E^-/-+carboxymethyl cellulose per gavage) and the tanshinoneⅡA intervention group (Apo E^-/-+30 mg/kg tanshinone ⅡA per gavage). All three groups were fed with high-fat-diet for 26 weeks. Tanshinone ⅡA/carboxymethyl cellulose was applied by the method of gavage administration 6 weeks before execution. After 26 weeks, tumor necrosis factor-α (TNF-α) andinterleukin (IL)-6 levels in serum were assessed by ELISA. Carotid artery was removed, fixed with paraformaldehyde, embedded with paraffin and sectioned. Percentage of stenosis was evaluated on HE stained sections. Plaque progression was assessed by Movat staining. Toluidine blue staining was used to evaluate mast cells infiltration and activation. Immunochemistry staining was used to assess 5-HT, TNF-α and IL-6 expression. mRNA expression of mast cell marker Fcer1a in adventitial tissue was detected by real time-PCR. Results: After high-fat-diet for 26 weeks, the mice in the atherogenic group showed advanced atherosclerosis, tanshinoneⅡA intervention reduced the percentage of carotid artery stenosis caused by atherosclerotic plaque formation ((58.48±8.07)% vs. (80.31±4.08)%, P<0.05). Compared with the atherogenic group, tanshinone ⅡA intervention group had lower level of TNF-α ((12.39±1.62)pg/ml vs. (17.44±1.42)pg/ml) and IL-6 ((116.24±12.16)pg/ml vs. (166.05±19.09)pg/ml) in serum, lower TNF-α ((20 145±1 556) vs. (25 288±1 671)) and IL-6 ((25 688±1 604) vs. (35 286±4 198)) expression in adventitia (all P<0.05). TanshinoneⅡA intervention also decreased the number of mast cells infiltration and activation, reduced 5-HT expression and mast cell marker Fcer1a mRNA relative expression in adventitia (all P<0.05). Conclusions Tanshinone ⅡA could attenuate induced by high-fat-diet carotid artery atherosclerosis in Apo E^-/- mice. The protective effect of tanshinoneⅡA is probably mediated through reducing the number and activation percentage of mast cells, decreasing the release of inflammatory cytokines and inflammation of carotid artery in adventitia.

Objective To investigate the effects of tanshinoneⅡA on atherosclerosis plaque formation and adventitial mast cells activation in high?fat?diet induced Apo E?/?mice model. Methods Sixteen 8?week?old Apo E?/?male mice and eight 8?week?old C57BL/6 male mice were randomly allocated into following group: the control group (C57BL/6+carboxymethyl cellulose per gavage), the atherogenic group (Apo E?/?+carboxymethyl cellulose per gavage) and the tanshinoneⅡA intervention group (Apo E?/?+30 mg/kg tanshinoneⅡA per gavage). All three groups were fed with high?fat?diet for 26 weeks. TanshinoneⅡA/carboxymethyl cellulose was applied by the method of gavage administration 6 weeks before execution. After 26 weeks, tumor necrosis factor?α (TNF?α) andinterleukin (IL)?6 levels in serum were assessed by ELISA. Carotid artery was removed, fixed with paraformaldehyde, embedded with paraffin and sectioned. Percentage of stenosis was evaluated on HE stained sections. Plaque progression was assessed by Movat staining. Toluidine blue staining was used to evaluate mast cells infiltration and activation. Immunochemistry staining was used to assess 5?HT, TNF?α and IL?6 expression. mRNA expression of mast cell marker Fcer1a in adventitial tissue was detected by real time?PCR. Results After high?fat?diet for 26 weeks, the mice in the atherogenic group showed advanced atherosclerosis, tanshinoneⅡA intervention reduced the percentage of carotid artery stenosis caused by atherosclerotic plaque formation ((58.48±8.07)% vs. (80.31±4.08)%, P<0.05). Compared with the atherogenic group, tanshinoneⅡA intervention group had lower level of TNF?α ((12.39 ± 1.62)pg/ml vs. (17.44 ± 1.42)pg/ml) and IL?6 ((116.24 ± 12.16)pg/ml vs. (166.05 ± 19.09)pg/ml) in serum, lower TNF?α ((20 145±1 556) vs. (25 288±1 671)) and IL?6 ((25 688±1 604) vs. (35 286±4 198)) expression in adventitia (all P<0.05). TanshinoneⅡA intervention also decreased the number of mast cells infiltration and activation, reduced 5?HT expression and mast cell marker Fcer1a mRNA relative expression in adventitia (all P<0.05). Conclusions TanshinoneⅡA could attenuate induced by high?fat?diet carotid artery atherosclerosis in Apo E?/?mice. The protective effect of tanshinoneⅡA is probably mediated through reducing the number and activation percentage of mast cells, decreasing the release of inflammatory cytokines and inflammation of carotid artery in adventitia.

Objective To investigate the serological patterns of hepatitis B, understand the prevalence of hepatitis B infection in neonates, infants and preschool children based on hospital data in Zhejiang province and provide a basis for prevention and control of local pediatric hepatitis B infection. Methods Five serological markers were detected on electrochemiluminescence analyzer Roche E601. The results of all serological markers in children with hepatitis B from 2006 to 2010 were exported from laboratory information system and 24 892 (15 810 boys and 9 082 girls) cases were selected for further analysis according to the exclusion criterion including duplicate analysis, children older than 7 years and children living out of Zhejiang province. SPSS13.0 software and EXCEL 2003 were employed for statistical analysis in this study. Results Average HBV vaccination coverage rates among 15 413 boys and 8 840 girls were 99. 16%(98. 87% -99. 45%) and 99. 17% (98. 29% -99. 53%), respectively. Seventeen serological patterns of hepatitis B were observed, and "anti-HBs(+)alone"(64. 997%) was the dominant patterns followed by "negative" (18. 231%), "anti-HBc(+)anti-HBs(+)"(9.911%) and "anti-HBe(+)antiHBc(+) anti-HBs(+)"(4.395%), and the positive rates for other patters were 0. 004% -0. 992%. There were significant difference of detection rates for "anti-HBc(+)alone" and "anti-HBe(+)anti-HBs(+)"patterns between male and female (χ2=7.143,8.123, all P＜0.01), and there were no significant difference of detection rates for the other 15 patterns between male and female (all P ＞0.05). Ninety-four HBsAg positive cases were detected, accounting for 0.38%. Totally 19 899 anti-HBs positive cases were detected, accounting for 79.94%. Totally 16 187 cases were "anti-HBs(+) alone", accounting for 81.3%of the total anti-HBs(+) cases. The group of 1-2 years and 2 day-2 week had the highest and lowest rate for anti-HBs(+)alone respectively. The ratios in three groups with different anti-HBs levels (10-100 mIU/ml,100-1000 mIU/ml and ＞ 1000 mIU/ml) in 16 178 anti-HBs(+) children were 23. 64%, 27.66% and 13. 70%, respectively. Totally 3 904 cases with anti-HBc(+) were detected, accounting for 15.68%. The highest positivity rate and lowest positivity rate were in the group of 2-4 week and 3-4 week respectively. In total 1 565 cases with negative results, the lowest negativity rate and highest negativity rate were in the group of 9-12 month (3. 25%) and 6-7 age (36. 21%) respectively. Conclusions The dominant serological patterns of hepatitis B in local young children is "anti-HBs (+) alone" and most of the anti-HBs concentrations ranged from 100 to 1000 mIU/ml, followed by "negative". The total positive rate of HBsAg is mild. The rate of hepatitis B serological patterns in children is associated with ages but independent of gender. For interpretation of serological patterns of HBV in children below 12 months (especially in 3 months) the status of their mothers' HBV infection should also be taken into consideration.

Objective To report the method for repair of the heel and ankle.Method On the basis of applied anatomy,the reversed island flap based on sural neurovascular pedicle has been designed for repair of heel and ankle defects.Results The flaps have been used in 14 cases,the maximum size 9 cm×15 cm,and all flaps were survival compeletely except partial necrosis in one flap.Conclusion The blood supply of the flap is good.The length of pedicle can reach 12 cm.It is an effective method for repair of heel and ankle defects.