ABSTRACT
Objective Incontinence-associated dermatitis(IAD) is a common skin disease, but there is still lack of evidence on which kind of skin proctectant can provide effective prevention and cost reduction. The article aimed to explore the clinical effect and cost-effectiveness of two skin protectants based on structured skin care regimens in the nursing care of incontinent patients and provide evidence for effective prevention of IAD.Methods A total of 124 patients with incontinence were randomly selected and divided into observation group (62 cases) and control group (62 cases). On the basis of the structured skin care program which focused on incontinence management, cleansing and protection, the patients in the observation group were treated with the composite zinc oxide ointment for 7 days, while patients in control group were treated with ostomy powder combined with skin barrier film for 7 days. The main observation indicators were the incidence of IAD and the cost of nursing materials.Results All 62 patients in the observation group completed the study, while in the control group 2 patients fell off because of death and discharge from hospital and 60 patients completed the study. The per-protocol analysis showed that the incidences of IAD in two groups were 6.45% and 20.00%, the intention-to-treat analysis showed 6.45% and 22.58%, and there was significant difference between groups (P<0.05). The nursing cost of the observation group (239.71±48.55) was lower than that of control group (264.35±61.55), and the difference was statistically significant (P<0.05).Conclusion The use of the composite zinc oxide ointment based on a structured skin care regimen can improve the preventive effect of IAD and reducing costs.
ABSTRACT
·AIM: To analyze the curative effect and safety in early stage primary open angle glaucoma (POAG) between simple Ex-PRESS shunt implantation and its combination with biological amniotic membrane implantation. ·METHODS: The clinical data of 53 cases for POAG treated with simple EX-PRESS shunt implantation (22 cases,34 eyes) as control group and its combination with biological amniotic membrane implantation (31 cases,38 eyes) as experimental group were retrospectively analyzed. Intraocular pressure (IOP) preoperatively and postoperatively were statistically evaluated. Filtering bleb and incidences of postoperative complications were observed in our hospital during the period of January of 2015 to April of 2017. ·RESULTS: At each time point after the operation, the mean IOP of the experimental group and the control group decreased distinctly respectively, the difference was statistically significant (P< 0. 05). There was no significant difference on the mean IOP between the experimental group and the control group at 1d and 1wk after operation (P<0.05). The mean IOP in the control group was higher than experimental group at 3 and 6mo (P<0. 05). The rate of functional filtration blebs were different between experimental group and control group during at postoperatively 3mo ( P < 0. 05 ). The complications included shallow anterior chamber, hemorrhage, posterior synechia of the iris, and corneal edema after surgery, and its incidences was not different between two groups (P<0.05). · CONCLUSION: EX - PRESS shunt combined with biological amniotic membrane implantation can effectively and safely reduce intraocular pressure, and improve the condition of filtering bleb after operation, and has long-term effect on IOP.
ABSTRACT
<p><b>OBJECTIVE</b>To study the mutation of PMP22 gene of an early-onset family with Charcot-Marie-Tooth disease (CMT) and the genetic features of the disease.</p><p><b>METHODS</b>Two patients with CMT, fifteen unaffected members in the family and 20 healthy controls were enrolled. STR-PCR and gene scanning were used to detect PMP22 duplication mutation.</p><p><b>RESULTS</b>The mutations of PMP22 were found in the two patients and other five unaffected members in the family. The mutations were located in the STR locus D17S921 in 5 cases and in the STR locus D17S4A in 2 cases. The other members in the family and 20 healthy controls did not show the mutations of PMP22.</p><p><b>CONCLUSIONS</b>The gene causing CMT in the family is found in the 17p11.2-p12 region containing PMP22 gene duplication mutation, resulting in the subtype CMT1A.</p>