To determine the state of fibroblast during the process of development of hypertrophic scar (HS), 40 specimens of HS in different periods were collected. The expressions of prolifrating cell nuclear antigen (PCNA) and Ag-protein in nucleolar organizer regions (Ag NORs) as well as the content of total amino acids in the tissues were examined. The hypertrophic scar of 1st and 3rd month old, the expression of PCND and Ag NORs were the highest. In the 9th and 12th month old, althrough PCNA was nearly negative, but the expression of Ag NORs was low. The content of total amino acid was increased gradually as HS developed but the increase of amount of hydroxyproline was markedly slowed down in 9 month old HS. It was suggested that: (1) in the developing process of HS the proecess of overproliferation of fibroblasts was short and limitted in 1-3 months period in the process of wound lealing; (2) the synthesis of collagen was nearly stopped at 6 months, but that of other extracellular matrix such as fibronectin and proteoglycan might be continued to aggregate after 12 months.
Analysis of hospital cases of cholelithiasis in every four years of the recent 3 decades clearly shows the tendency of changes of cholelithiasis in clinical appearance in Chengdu.Constituent ratio of gallbladder stone was 12.56% in 70’s,47.54% in 80’s and 81.38% in 90’s.Bill duct stones including acute obstructive suppurative cholangitis was 71.01%, 46.08%,and 15.82% respectively. Biliary ascariasis was 11.67%, 2.75% and 0.68% respectively. Age incidence shows right moving, i.e. old patients increased. Urban patients increased.The influencing factors listed are: improvement of diagnostic methods; improvement of livelihood and diet; increased life expectancy; more health follow up examinations; technical improvements in rural areas and etc.
Objective To investigate the feasibility and effectiveness of thoracodorsal artery perforator (TDAP) flap for repairing serious scar contracture of the opisthenar. Methods Between March 2015 and June 2017, 7 cases of serious scar contracture of opisthenar were repaired with TDAP flaps. There were 5 males and 2 females with an average age of 31 years (range, 11-48 years). The time from injury to operation was 8-67 months, with an average of 42 months. After the relocation of the joint and release of the scar, the size of soft tissue defect ranged from 5 cm×4 cm to 10 cm×8 cm. The size of TDAP flap ranged from 5.5 cm×5.0 cm to 10.5 cm×9.0 cm. Results All flaps survived completely with primary healing at both donor site and recipient site. The flaps of 3 patients were bulky and underwent second-stage skin flap thinning at 3 months after operation. All 7 patients were followed up 6-32 months, with an average of 15 months. The skin flaps were soft and elastic. According to the upper limb function evaluation system recommended by Chinese Society of Hand Surgery, sensory function was classified as \begin{document}$\small{{\rm{S}}_{{{\scriptsize 3}^ + }}}$\end{document} in 2 cases, \begin{document}$\small{{\rm{S}}_{{{\scriptsize 3} }}}$\end{document} in 1 case, \begin{document}$\small{{\rm{S}}_{{{\scriptsize 2} }}}$\end{document} in 3 cases, and \begin{document}$\small{{\rm{S}}_{{{\scriptsize 1} }}}$\end{document} in 1 case. The hand function was excellent in 2 cases, good in 4 cases, and fair in 1 case. There was no significant effect on shoulder movement. Conclusion The TDAP flap is an ideal method for serious scar contracture of opisthenar.
Objective To explore the change of gene expression of stress activated protein kinase (SAPK) and its upstream signalregulated molecule ——mitogen activated protein kinases(MAPKs) (MKK4 and MKK7) in hypertrophic scar and autocontrol normal skin. Methods The total RNA was isolated from 8 hypertrophic scars and 8 auto-control skin, and then mRNA was purified. The gene expressions of MKK4, MKK7 and SAPK were examined with reverse transcriptionpolymerase chain reaction(RT-PCR) method. Results In hypertrophic scar, both MKK7 and SAPK genes weakly expressed. In auto-control skin, the expression of these 2 genes was significantly elevated in comparison with hypertrophic scar (Plt;0.01). The expression levelsof these 2 genes were 1.5 times and 2.6 times as long as those of hypertrophic scar, respectively. Gene expression of MKK4 had no significant difference between autocontrol skin and hypertrophic scar (Pgt;0.05). Conclusion Decreased gene expression of MKK7 and SAPK which results in reducing cell apoptosis might be one of the mechanisms for controlling the formation of hypertrophic scar.
Objective To investigate the effects of asiaticoside onthe proliferation and the Smad signal pathway of the hypertrophic scar fibroblasts.Methods The hypertrophic scar fibroblasts were cultured with tissue culture method. The expressions of Smad2 and Smad7 mRNA after asiaticoside treatment were determined by reverse transcriptionpolymerase chain reaction 48 hours later. Thecell cycle, the cell proliferation, the cell apoptosis and the expression of phosphorylated Smad2 and Smad7 with(experimental group) or without(control group) asiaticoside were detected with flow cytometry, immunocytochemistry and Western blot. Results Asiaticoside inhibited the hypertrophic scar fibroblasts from phase S to phase M. The Smad7 content and the expression of Smad7 mRNA were (1.33±1.26)% and (50.80±22.40)% in experimental group, and (9.15±3.36)% and (32.18±17.84)% in control group; there were significant differences between two groups (P＜0.05). While the content and the mRNA expression of Smad2 had no significant difference between two groups. Conclusion Asiaticoside inhibits the scar formation through Smad signal pathway.
Objective To investigate the effect of different degrees of wound eversion on scar formation at the donor site of anterolateral thigh flaps by a prospective clinical randomized controlled study. MethodsAccording to the degree of wound eversion, the clinical trial was designed with groups of non-eversion (group A), eversion of 0.5 cm (group B), and eversion of 1.0 cm (group C). Patients who underwent anterolateral femoral flap transplantation between September 2021 and March 2023 were collected as study subjects, and a total of 36 patients were included according to the selection criteria. After resected the anterolateral thigh flaps during operation, the wound at donor site of each patient was divided into two equal incisions, and the random number table method was used to group them (n=24) and perform corresponding treatments. Thirty of these patients completed follow-up and were included in the final study (group A n=18, group B n=23, and group C n=29). There were 26 males and 4 females with a median age of 53 years (range, 35-62 years). The body mass index was 17.88-29.18 kg/m2 (mean, 23.09 kg/m2). There was no significant difference in the age and body mass index between groups (P>0.05). The incision healing and scar quality of three groups were compared, as well as the Patient and Observer Scar Assessment Scale (POSAS) score [including the observer component of the POSAS (OSAS) and the patient component of the POSAS (PSAS)], Vancouver Scar Scale (VSS) score, scar width, and patient satisfaction score [visual analogue scale (VAS) score]. Results In group C, 1 case had poor healing of the incision after operation, which healed after debridement and dressing change; 1 case had incision necrosis at 3 months after operation, which healed by second intention after active dressing change and suturing again. The other incisions in all groups healed by first intention. At 6 months after operation, the PSAS, OSAS, and patient satisfaction scores were the lowest in group B, followed by group A, and the highest in group C. The differences between the groups were significant (P<0.05). There was no significant difference between the groups in the VSS scores and scar widths (P>0.05). ConclusionModerate everted closure may reduce the formation of hypertrophic scars at the incision site of the anterior lateral thigh flap to a certain extent.
OBJECTIVE To repair facial and neck scar using tissue expanding technique. METHODS From January 1991 to January 1995, 16 cases with facial and neck scar were treated. Multiple tissue expanders were put under the normal skin of facial and neck area, after being fully expanded, the scars were excised and the expended skin flaps were transplanted to cover the defects. The size and number of tissue expanders were dependent on the location of the scars. Normally, 5 to 6 ml expanding volume was needed to repair 1 cm2 facial and neck defect. The incisions should be chosen along the cleavage lines or in the inconspicuous area, such as the nasolabial fold or submandibular region. The design of flap was different in the face and in the neck. In the face, direct advanced flap was most common used, whereas in the neck, transposition flap was often used. Appropriate tension was needed to achieve smooth and cosmetic effect. It was compared the advantages and disadvantages of several methods for repair of the defect after facial and neck scar excision. RESULTS Fifteen cases had no secondary deformity after scar excision. Among them, 1 case showed blood circulation disturbance and cured through dressing change. Ten cases were followed up and showed better color and texture in the flap, and satisfactory appearances. CONCLUSION Tissue expanding technique is the best method for the repair of facial and neck scar, whenever there is enough expandable normal skin.
Objective To explore the effect of connective tissue growth factor on the pathogenesis of hypertrophic scar and keloid tissue. Methods The content of hydroxyproline was determined and the expression of connective tissue growth factor gene was detected by the reverse transcription-polymerase chain reaction and image analysis technique in 5 normal skins, 15 hypertrophic scars and 7 keloid tissues. Results The contents of hydroxyproline in the hypertrophic scar(84.10±1.76) and keloid tissue (92.38±2.04) were significantly higher than that of normal skin tissue (26.52 ± 4.10) (P lt; 0.01). The index of connective tissue growth factor mRNA in the hypertrophic scar (0.78 ± 0.63) and keloid tissue (0.84 ± 0.04) were higher than that of normal skin tissue ( 0.09 ± 0.25) (P lt; 0.01). Conclusion Connective tissue growth factor may play an important role in promoting the fibrotic process of hypertrophic scar and keloid tissue.
OBJECTIVE: To localize the distribution of basic fibroblast growth factor (bFGF) and transforming growth factor-beta(TGF-beta) in tissues from dermal chronic ulcer and hypertrophic scar and to explore their effects on tissue repair. METHODS: Twenty-one cases were detected to localize the distribution of bFGF and TGF-beta, among them, there were 8 cases with dermal chronic ulcers, 8 cases with hypertrophic scars, and 5 cases of normal skin. RESULTS: Positive signal of bFGF and TGF-beta could be found in normal skin, mainly in the keratinocytes. In dermal chronic ulcers, positive signal of bFGF and TGF-beta could be found in granulation tissues. bFGF was localized mainly in fibroblasts cells and endothelial cells and TGF-beta mainly in inflammatory cells. In hypertrophic scar, the localization and signal density of bFGF was similar with those in granulation tissues, but the staining of TGF-beta was negative. CONCLUSION: The different distribution of bFGF and TGF-beta in dermal chronic ulcer and hypertrophic scar may be the reason of different results of tissue repair. The pathogenesis of wound healing delay in a condition of high concentration of growth factors may come from the binding disorder of growth factors and their receptors. bFGF may be involved in all process of formation of hypertrophic scar, but TGF-beta may only play roles in the early stage.
To investigate the inhibitory effect of Col I A1 antisense ol igodeoxyneucleotide (ASODN) transfection mediated by cationic l iposome on Col I A1 expression in human hypertrophic scar fibroblasts. Methods Scar tissue was obtained from volunteer donor. Human hypertrophic scar fibroblasts were cultured by tissue block method. The cells at passage 4 were seeded in a 6 well cell culture plate at 32.25 × 104 cells/well, and then divided into 4 groups: group A, l iposomeand Col I A1 ASODN; group B, Col I A1 ASODN; group C, l iposome; group D, blank control. At 8 hours, 1, 2, 3 and 4 days after transfection, total RNA of the cells were extracted, the expression level of Col I A1 mRNA was detected by RT-PCR, the Col I A1 protein in ECM was extracted by pepsin-digestion method, its concentration was detected by ELISA method. Results Agarose gel electrophoresis detection of ampl ified products showed clear bands without occurrence of indistinct band, obvious primer dimmer and tailing phenomenon. Relative expression level of Col I A1 mRNA: at 8 hours after transfection, group A was less than groups B, C and D (P lt; 0.05), and groups B and C were less than group D (P lt; 0.05), and no significant difference was evident between group B and group C (Pgt; 0.05); at 1 day after transfection, groups A and B were less than groups C and D (P lt; 0.05), and there was no significant difference between group A and group B, and between group C and group D (P gt; 0.05 ); at 2 days after transfection, there were significant differences among four groups (P lt; 0.05); at 3 and 4 days after transfection, group A was less than groups B, C and D (P lt; 0.05), group B was less than groups C and D (P lt; 0.05), and no significant difference was evident between group C and group D (P gt; 0.05). Concentration of Col I protein: at 8 hours after transfection, group A was less than groups B, C and D (P lt; 0.05), groups B and C were less than group D (P lt; 0.05), and no significant difference was evident between group B and group C (P gt; 0.05); at 1 day after transfection, significant differences were evident among four groups (P lt; 0.05); at 2, 3 and 4 days after tranfection, groups A and B were less than groups C and D (P lt; 0.05), and no significant difference was evident between group A and group B (P gt; 0.05). Conclusion Col I A1 ASODN can inhibit mRNA and protein expression level of Col I A1. Cationic l iposome, as the carrier, can enhance the inhibition by facil itating the entry of ASODN into cells and introducing ASODN into cell nucleus.