Polymerase chain reaction untuk deteksi m. Leprae

ABSTRAK The inability to rapidly identify M. \u27florae is a weak link in the leprosy control program. Arid fast bacilli that are found micoscopically are not always M. leprae. Polymerase Chain Reaction (PCR), which is based on molecular biology, is a new method that is able to multiplyM. feprae DNA under the direction of a specific primer. This method can rapidly idencifyM. leprae. The application of PCR in the leprosy control program can help in the collection of some data (such as, the number of infection sources, the number of infected individuals, healthry or ill), but it cannot help in the evaluation of the effect of treatment. Key Words: PCR, M. leprae, leprosy control program

Multiple mini punch grafts for extensive ulcer: a case report

Multiple mini punch grafts is the placing of mini size of full thickness skins on to ulcer bed. Theyconsist of epidermal and dermal component composed with hair follicles and other skin appendiceswhere epidermal stem cells are located. The epidermal stem cells are the best source of epidermalcells in reconstruction of skin equivalent that is usually used for replacing classic split thicknessskin graft in recovering extensive ulcer. In this article, the application of multiple mini punchgrafts onto extensive ulcer is reported. A case of extensive ulcer was suffered by a 6-year-oldboy whose left foot is injured in a traffic accident. His toes had already been amputated bysurgeon but a classic skin graft failed to recover the ulcer. Multiple mini punch grafts had beenharvested from his inguinal and buttock skin and they were placed onto his ulcer. Pre and postmini punch grafting photographs were reviewed. After eight weeks, placed multiple mini punchtissues onto large ulcer reveals lateral extensions and more than 90% of epithelialization. Multiplemini punch grafts can be used as a method to cover large ulcer.Key words: mini punch grafts-large ulcer-epithelialization-epidermal-stem cell

Transplantation of melanocyte stem cells in vitiliginous skin

Depigmentation in vitiligo occurs as a result of progressive loss of functioning epidermal melanocytes, and currently various modalities have been developed to re-functioning these cells. However, in area with poor melanocytes reservoir, such as old-persistent lesions or lesions on bony prominence, the modalities are hardly to achieve repigmentation. Since spontaneous repigmentation of vitiliginous skins begin mostly in follicular areas, reactivation of melanocyte precursors along the outer root sheath of hair follicle is expected to have better on this pigmentation. Melanocyte precursor came from melanocyte stem cells that originally located on bulge area of hair follicles. The latest surgical intervention in vitiligo is transplantation of melanocyte stem cells. Clinical experiments indicated that the transplantation can be performed either by transplantation of extracted follicular units or single cell suspension harvested from this area. By single cell suspension treatment, a 50 cm2 of vitiliginous skin can be handled by 15 autologous hair follicular units. These procedures are easy and can be performed by any dermatologist especially who has been trained in dermatologic surgery as well as in cellular based therapies

The protective effect of sunscreens against ultraviolet B-induced immunosuppression. A study on Langerhans cell depletion

Ultraviolet B (UVB) radiation can act as immunosuppressant by inducing an epidermal Langerhans cells (LC) depletionwhich could be inhibited by topical sunscreen. Several kinds of sunscreens with various SPF (Sunscreen ProtectionFactor) are now available. The minimal SPF which able to inhibit the immunosuppressive effect of UVB amongpeople with skin photo-type IV has not been established yet. The aim of this study is to determine the minimal SPFcapable to inhibit UVB-induced immunosuppression among people with skin photo-type IV. A simple experimental(post test only experimental) study was conducted among 5 people’s circumsized foreskins with Fitzpatrick’s skinphoto-type IV. Each of them was divided into equal 5 pieces of 0.5 cm2. Each of three pieces of skin was treated bysunscreen SPF 15, SPF 30, and SPF 50, a single piece of skin was treated with placebo, and all of them then weretreated by a single 100 mJ/cm2 of UVB 30 minutes later. A rest single piece of skin was used as control. After 24hours of incubation in incubator of 37O C and 5% CO2, all of them then was fixed by buffer formalin, blocked byparaffin, cut in 2mm of thickness, and then stained with anti CD 1a antibody with AEC as chromogen and Mayer’shematoxylin as counterstaining. The number of LC was counted by Image J Analysis programmed and the mean ofLCwere analyzed by Kruskal-Wallis test dan Mann-Whitney test. There were very significantly different of themean number of LC between UVB placebo group and control group (p 0.05). Sunscreenwith SPF 15 had LC number lower than control group significantly (p<0.05). The lowest SPF for preventing UVBinduced LC depletion among people with skin photo-type IV was 30.Key words : UVB - immunosupression – sunscreens – SPF -CD1aexpressio

The combination effect of triamcinolone acetonide and tamoxifen citrate on fibroblast populated collagen lattice contractions

Background: Keloid is caused by fibroblast hyperproliferation stimulated by transforming growth factor-IH ITGF-131 I, and it is usually treated with triamcinolone acetonide (TAl, which has the ability to inhibit TGF131 synthesis. However, the clinical results is still unsatisfied. Another drug that may inhibit keloid fibroblast TGF-131 synthesis is tamoxifen citrate (TCI, but the effect of the combination on keloid fibroblast activities has never been published.Objective: To find out the effect of combined triamcinolone acetonide and tamoxifen citrate on fibroblast keloid activities in vitro.Methods: It was a parallel post-test only study. The third passage keloid fibroblasts were isolated from a patient with keloid, cultivated in collagen lattice, and treated with several combinations of 5, 10, and 20 pM TA and 10, and 20 pM TC. Lattice contractions were measured based on digital image using scion image.Results: Among TA groups, the best inhibition of lattice contraction was found among 20 pM treated group and among TC groups. The best inhibition of lattice contraction was found among 20 pM TC. The best combination was found in the combination of 20 pM TA plus 20 pM TC.Conclusion: The result indicated that a combination of triamcinolone acetonide and tamoxifen citrate had a significant role in suppressing fibroblast activity, better than triamcinolone acetonid or tamoxifen citrate alone.Key words: tamoxifen - triamcinolone - collagen lattice - keloid fibroblast

α-Lipoic acid inhibit the decrease of collagen deposition in ultravioled B-irradiated cultured normal human skin fibroblasts cell culture

Repeated ultraviolet B (UVB) irradiation on human skin has been considered to be responsible in premature agingprocess because UVB has been proved to inhibit collagen deposition and accelerates collagen degradation. Clinicalstudies showed that topical usage of 5% α-lipoic acid (ALA) improved the clinical appearance of photoaged skin.However, the effect of ALA on collagen deposition and degradation in UVB-irradiated normal human skin fibroblastsculture has not been reported. The aim of the study was to investigate the effect of ALA on collagen deposition anddegradation in UVB-irradiated cultured normal human skin fibroblasts. Culture of normal human skin fibroblasts weretreated with 0, 125, 250, 500 μM ALA diluted in complete Dulbecco’s Modified Eagle’s Medium (DMEM) andirradiated with 300 mJ/cm2 UVB. The mean collagen deposition and degradation’s level were measured by Siriusred assay and read with spectrophotometer at λ 550 nm. Mean difference of collagen deposition as expressed byoptical density (OD) between normal human skin fibroblasts cell after UVB irradiation and without UVB irradiationwas analyzed by Wilcoxon signed-ranks test and Friedman test, while mean difference collagen degradation wasanalyzed by one way analysis of variance (ANOVA) and paired t test with 95% confidence level (p0.05). In conclusion, ALAinhibited the decrease of collagen deposition, but did not inhibit collagen degradation in UVB-irradiated normalhuman skin fibroblasts culture.Key words: α-lipoic acid - collagen - human skin - fibroblasts – UVB - irradiatio

The Combination of suprakeloidal flap and pulsed light heat energy in keloid management: a Case report

The role of chronic tissue hypoxia in the keloid patho-mechanism has been widely accepted. Whereas, the pulsed-light heat energy (LHE) has been developed which has the capacity to generate reactive oxygen species on exposed skin. Although the supra keloidal flap technique has a high recurrence rate, it was used because of its capacity to prevent suturing hypoxia, thereby the formation of lager recurrent keloid after surgery.The combination of supra keloidal flap and pulsed light heat energy was done I the treatment of postvaricella keloid on the right ear lobe of a 9 year old girl. The keloid was excised two times a year ago, but observation one month after the surgery showed a recurrent larger keloid. The performance of supra keloidal technique followed by pulsed-light heat energy treatment in dose 2.5 J/cm2, was administered on day 3

Epigenetic Alterations in Keloid a Possible Method to Find Novel Agents for Keloid Treatment

Background: Keloids are dermal fibro-proliferative disorders due to prolonged wound healing processes with excessive collagen depositions, which produce symptoms of itching and pain, cosmetic disfigurement, and limitation of joint motion. Standard treatment for keloid has not been accepted yet. It may be due to the complexities and poorly understood keloid development that are driven by various factors from systemic to local, genetic to epigenetic. Since genetic factors are difficult to manipulate, an approach to epigenetic factors may be hopeful. Purpose: To review various related reports on epigenetic factors such as DNA methylations, histone modifications, and micro-RNAs, which have significant roles in keloid development and can be used as targets for novel agents in keloid treatment. Review: Various genes in keloid fibroblasts (KFs) are repressed by DNA methylation, and one of them can inhibit the regulation of TGF-β1/Smad signaling, whereas another gene may influence anti-fibrotic events. Either inhibitor of methyl-transferase, inhibitor of histone-acetyltransferase, or histone-deacetylase can reduce TGF-β1/Smad signaling in KFs. Abnormal expressions of pro-fibrotic miRNAs have been identified in KFs and transfection KFs with anti-fibrotic miRNAs such as miRNA-205 and miRNA- 31, evidently can inhibit VEGF signaling. Furthermore, transfection of miRNA-637 into KFs can inhibit KFs in proliferation, migration, and collagen synthesis through TGF-β1/Smad signaling. Apoptosis and cellular senescence in KFs can also be stimulated by miRA-34 and miRNA-30. Conclusion: In the future, targets in epigenetic events such as inhibitors of methyl-transferase, histone-acetyltransferases, and histone-deacetylases, together with various miRNA, may be applied as novel agents for the treatment of keloid

The protective effect of sunscreens against ultraviolet B-induced immunosuppression. A study on Langerhans cell depletion

Ultraviolet B (UVB) radiation can act as immunosuppressant by inducing an epidermal Langerhans cells (LC) depletionwhich could be inhibited by topical sunscreen. Several kinds of sunscreens with various SPF (Sunscreen ProtectionFactor) are now available. The minimal SPF which able to inhibit the immunosuppressive effect of UVB amongpeople with skin photo-type IV has not been established yet. The aim of this study is to determine the minimal SPFcapable to inhibit UVB-induced immunosuppression among people with skin photo-type IV. A simple experimental(post test only experimental) study was conducted among 5 people’s circumsized foreskins with Fitzpatrick’s skinphoto-type IV. Each of them was divided into equal 5 pieces of 0.5 cm2. Each of three pieces of skin was treated bysunscreen SPF 15, SPF 30, and SPF 50, a single piece of skin was treated with placebo, and all of them then weretreated by a single 100 mJ/cm2 of UVB 30 minutes later. A rest single piece of skin was used as control. After 24hours of incubation in incubator of 37O C and 5% CO2, all of them then was fixed by buffer formalin, blocked byparaffin, cut in 2mm of thickness, and then stained with anti CD 1a antibody with AEC as chromogen and Mayer’shematoxylin as counterstaining. The number of LC was counted by Image J Analysis programmed and the mean ofLCwere analyzed by Kruskal-Wallis test dan Mann-Whitney test. There were very significantly different of themean number of LC between UVB placebo group and control group (p 0.05). Sunscreenwith SPF 15 had LC number lower than control group significantly (p<0.05). The lowest SPF for preventing UVBinduced LC depletion among people with skin photo-type IV was 30.Key words : UVB - immunosupression – sunscreens – SPF -CD1aexpressio

The efficacy of captopril and 5-fluorouracil combination in the proliferation and collagen deposition of keloid fibroblast

Keloid is a benign fibroproliferative tissue growth that exceeds the initial wound margins. Captopril has been tested in vitro to reduce fibroblast proliferation and collagen deposition; thus, it has potential for use in the treatment of keloids. Meanwhile, 5‐fluorouracil (5‐FU) has already been used in keloid management. This study aimed to determine the efficacy of the combination of captopril and 5‐FU in keloid fibroblast cultures. Keloid tissues were cultured up to passages 4–7. The study consisted of a control group, captopril in various concentrations (10‐2, 10‐3, 10‐4, and 10‐5 mol/L), 5‐FU 1 mg/mL and a combination of captopril at various concentrations with 5‐FU 1 mg/mL. After 144 hours of treatment, fibroblast proliferation and collagen deposition were measured. The study showed a significant decrease in the mean index of fibroblast proliferation and collagen deposition in the group receiving captopril in various concentrations (10‐2, 10‐3, 10‐4, and 10‐5 mol/L) and the 5‐FU group against the control group (p<0.05). In the combined‐dose group, captopril at a concentration of 10‐2 mol/L and 5‐FU showed a significant reduction in fibroblast proliferation and collagen deposition compared to the 5‐FU group and the captopril at the same dose (p<0.05). In conclusion, the combination of captopril 10‐2 mol/L and 5‐FU 1 mg/mL is better at reducing fibroblast proliferation and collagen deposition in keloid fibroblast cultures than captopril or 5‐FU as a single therapeutic agent