Without depleting CD25+ cells, GAD113–132 and GAD265–284 responses were significantly stronger in subjects with diabetes. Although nearly every individual responded to at least one GAD65 epitope, most were seen in less than half of the subjects tested, suggesting that multiple epitopes are recommended for immune monitoring. Type 1 diabetes mellitus (T1D) is associated with antibody and T-cell responses to islet β-cell antigens. These responses lead to the selective destruction of pancreatic β cells, and a profound deficiency in insulin secretion.[1-3] Because T1D is strongly correlated with certain susceptible class

II haplotypes (including HLA-DQ2/DR3 and DQ8/DR4) and because Selleck SB525334 CD4+ T cells have been shown to play a crucial role in animal models of T1D, it is widely held that the presentation of islet-derived epitopes by susceptible HLA class II proteins to pathogenic Vemurafenib cell line CD4+ T cells is a key component of the disease process. Previous studies have identified an array of diabetes-associated self-antigens including insulin, glutamic acid decarboxylase isoform 2 (GAD65), tyrosine phosphatase-like

protein, islet glucose-6-phosphatase catalytic subunit-related protein, the cation efflux transporter ZnT8 and, more recently, chromogranin.[4-6] Among these antigens, insulin and GAD65 have been the most widely studied. GAD65 was identified nearly

20 years ago as a β-cell antigen that reacted with sera from patients with T1D.[7] Subsequent MRIP studies have demonstrated that GAD65 is involved in pathogenesis for animal models of autoimmune diabetes.[8-10] In humans, GAD65 specific auto-antibodies are found in > 70% of patients with new-onset T1D[11, 12] and their presence is an established marker for predicting diabetes risk.[13-15] Several studies have observed CD4+ T-cell responses to epitopes within β-cell antigens in patients with diabetes or in diabetes-susceptible mice. Particularly in the non-obese diabetic (NOD) mouse, adoptive transfer of T cells specific for single epitopes has been sufficient to induce disease.[10, 16] For this reason, a number of human studies have attempted to monitor autoimmune responses or to differentiate between diabetic subjects and healthy controls by measuring CD4+ T-cell responses to one or a small number of epitopes within these antigens.[17] While successful in some settings, this limited approach may not be optimal to capture the dynamics of the disease process in human populations. We hypothesized that susceptible HLAs lead to the generation of diverse repertoires of diabetogenic T cells in humans and that individual subjects respond to subsets of these epitopes.

05. Genotype combinations for IL-1β and IL-10 genes in patients, HHC and HC H 89 mouse were studied by MDR analysis. All the genotypes of IL-1β have shown high risk with GA genotype of IL-10 in patients versus HC and HHC versus HC with GG and AA genotypes. In patients versus HHC, high risk was observed between CC and CT genotypes of IL-1 β and GA genotype of IL-10 (Fig. 2). Host genetic factors may be important determinants of susceptibility to tuberculosis, and several candidate gene polymorphisms have shown variable associations with severity of tuberculosis disease in different populations [22, 23]. IL-1β participates in aberrant immune responses in lung diseases but controls M.tb infection [24]. It regulates inflammatory

reaction and immune response through promoting other cytokine expressions, such as IL-6 and IL-12. In the present study, IL-1β +3954 C/T polymorphism was not found to be associated with tuberculosis susceptibility. The distribution of their genotypes and alleles did not significantly differ between the patients and healthy controls in concordance with studies in London on idiopathic pulmonary fibrosis patients [25], in Gambian population [26] and in Gujarat Asians in east London

with selleck kinase inhibitor tuberculosis [27]. Studies in other diseases like hypogammaglobulinaemia, autoimmunity, cancers [28] and asthma [29] have shown similar results, whereas in contrast to our study IL-1β +3954 C/T polymorphism have shown an association with extrapulmonary tuberculosis in American population [30], in Gambian population with malaria [31] and in Turkish population with behcet’s disease [32]. IL-10 considered as a key mediator of immunosuppression, and tolerance appears to be primarily produced by monocytes and T regulatory lymphocytes. It converts human dendritic cells into macrophage-like cells with increased antimycobacterial activity. Modulation of T cell responses by IL-10 influences the medroxyprogesterone host susceptibility to TB [33]. Our study reported the association of IL-10-1082 G/A polymorphism with tuberculosis. Earlier studies in the Hong Kong, Chinese [34], Colombian [35], Spanish, Turkish and Cambodian populations [36]

have also shown the same. The GG genotype was significantly associated with the present study and also in Colombian population, whereas in the Tunisian[37], Iranian [38], West African [39], Macedonian [40] Gambian [18], Spanish [41] and Korean population [42], it was not associated. The frequency of GA genotype which is 81% in our study was found to be similar in Iranian population (82.5%). Significant difference was not observed with the allele frequency in our population similar to the Tunisian population. In contrast to our results, other recent reports by Mosaad et al. [43] and Akgunes et al. [44] reported significant association with TB susceptibility. However, A allele was associated with Italian (Sicilian) population [45]. These contradictory findings may be due to ethnical differences in various populations.

Preventing the growth PF-562271 of huge tumour masses by

irradiation or chemotherapy would support CAPRI cell therapy. However, to prevent damage to bone marrow or PBMC, they should be isolated before irradiation or chemotherapy. In summary, we have shown that a treasure of cancer-immunogenic information is stored only in monocytes and is expressed upon stimulation by CD3-activated T cells. Activated monocytes can prime naïve/resting T cells to become powerful cancer-specific CTL against autologous cancers. We raised CAPRI cells against many different types of cancer (Table 3) and did not find a non-immunogenic cancer. Treatment attempts with CAPRI cells as adjuvant treatment for patients with breast cancer showed that almost double the number of patients survived 5 years, but

this needs to be confirmed in standardized clinical studies. With CAPRI cells, many different cancers can be treated within a week and without negative side effects. Future studies should consider analysing the cytokines secreted by the CAPRI cell quartet at different time periods. Treatment with such cytokines may facilitate the treatment for all patients with cancer in a cost-effective and time-sensitive manner. This work was supported in part by the Science Prize of the DGI (Deutsche Gesellschaft für Immungenetik), by the buy Fluorouracil Felix Burda Stiftung, by Immunis e.V and by Annemarie, Max and Karl-Heinz Gansbühler. We thank Dr. M.Levite and Prof. J.P. Johnson for their excellent advice on the style and content of the manuscript. Barbara Laumbacher Acesulfame Potassium and Rudolf Wank pioneered the CAPRI cell procedure over several years. Songhai Gu designed and performed the elegant FACS experiments. All authors participated in writing the manuscript. Barbara Laumbacher and Songhai Gu have no conflicting interests. Rudolf Wank holds European and International patents for the CAPRI procedure. “
“Angioedema (AE) is a clinical syndrome characterized by localised swelling lasting several hours. The swelling is often recurring and can

be lethal if it is located in the laryngeal region. Much progress has been made recently in the treatment of acute episodes, but no consensus has been reached on maintenance treatment. We have performed a national retrospective observational study to assess the use of tranexamic acid (TA) as maintenance treatment for non-histaminergic AE [hereditary AE (HAE) or idiopathic non-histaminergic AE]. Records for 64 cases were collected from 1 October 2012 to 31 August 2013; 37 of these were included (12 HAE with C1-inhibitor deficiency, six with HAE with normal C1-inhibitor and 19 idiopathic non-histaminergic AE). When treated with TA over six months, the number of attacks was reduced by 75% in 17 patients, 10 patients showed a lower level of reduction and 10 had the same number of attacks. In no instances were symptoms increased. No thromboembolic events were observed, and the main side effects were digestive in nature.

It has recently been shown by Caminschi et al. that antigen targeting to DNGR-1 can additionally promote MHC class II presentation and T-cell-dependent Ab production 17. In contrast to CTL priming 9, the Ab responses seen did not require co-administration of adjuvant, suggesting that DNGR-1 targeting to DC might generate intrinsic signals that favor Ganetespib cost CD4+ but not CD8+ T-cell priming 17. In this study, we confirm that antigens targeted to DNGR-1 in the steady state can be presented on MHC class II molecules, and we show that this presentation is restricted to CD8α+ DC. However, we find that, in the absence of adjuvant, Ab responses are weak and show that this form of antigen targeting

does not inevitably lead to CD4+ T-cell priming but, rather, can be used to favor the conversion of antigen-specific naïve CD4+ T cells into Foxp3+ suppressive cells. In contrast, in the presence of adjuvants, the same targeting approach promotes the development of potent Ab and Th1 or Th17 CD4+ T-cell responses. Thus, DNGR-1 acts predominantly as a “neutral” receptor, and antigen targeting to this receptor combined with appropriate immunomodulators can be used to promote a wide range of responses, from dominant tolerance to qualitatively distinct types of immunity. To mark DNGR-1+ cells in vivo, mice were injected i.v. with

fluorophore-labeled anti-DNGR-1 or isotype-matched control mAb. We then analyzed the labeling of different cell types in secondary lymphoid www.selleckchem.com/products/Dasatinib.html tissues at time points ranging from 5

to 120 min post injection. In mice injected with anti-DNGR-1 mAb but not with the isotype control mAb, we observed rapid and bright staining of the CD8α+CD11c+ population (Supporting Information Fig. 1A and C). In agreement with the previously described pattern of expression of DNGR-1 9, 17, we were unable to detect any labeling of the CD11c− compartment or CD4+ DC, whereas a fraction of pDC was stained, although with reduced intensity and slower kinetics when compared with CD8α+ DC (Supporting Information Fig. 1A, Casein kinase 1 B and 2). Systemic inflammation induced by LPS administration did not change the pattern of targeting by anti-DNGR-1 mAb (Supporting Information Fig. 2). These data confirm that anti-DNGR-1 mAb rapidly and specifically targets CD8α+ DC and, to a lower extent, pDC. To test whether DNGR-1 targeting promotes MHC class II antigen presentation by DC, we covalently conjugated anti-DNGR-1 or isotype-matched control mAb to the OVA323–339 peptide. We then injected B6 mice with 2 μg of either conjugate and, after 4 h, purified different subpopulations of splenocytes. To reveal processed antigen on MHC class II molecules, we cultured increasing number of cells with CFSE-labeled OVA-specific OT-II CD4+ T lymphocytes for 4–5 days. We only observed T-cell division with CD11c+ cells purified from mice injected with anti-DNGR-1 mAb (Fig. 1A). Furthermore, among the CD11c+ cells, only the CD8α+ fraction was able to induce potent OT-II proliferation (Fig.

The dose was adjusted https://www.selleckchem.com/products/INCB18424.html according to serum phosphate concentration. Subjects were enrolled in the study immediately if all inclusion criteria were met. Mean time since transplantation was 1 month. Diet was unrestricted but all patients were encouraged

to consume products rich in phosphorus, such as meat and dairy. After 12 weeks, mean serum phosphate concentration had normalized in both groups. It was found that muscular phosphate content did not correlate with serum phosphate concentrations, though was restored in both groups after 12 weeks. However, the mean proportion of muscular adenosine triphosphate was significantly higher in the treatment group compared with the control group (P < 0.03) after 12 weeks. Metabolic acidosis improved significantly in subjects in the treatment group compared with those in the control group. This study provides level see more III evidence that oral neutral phosphate supplements may normalize serum phosphate concentration and muscle phosphate content after transplantation safely. Such supplementation appears effective in prolonging

phosphaturia and promoting recovery from latent metabolic acidosis observed in kidney transplant recipients early after transplantation. Oral phosphate supplementation does not seem to affect calcium or parathyroid hormone (PTH) metabolism in the early post-transplant period.1 Caravaca et al.5 undertook a prospective study to evaluate the effects of oral phosphorus supplementation on the mineral

Glycogen branching enzyme metabolism of kidney transplant recipients with well-functioning grafts. Thirty-two kidney transplant recipients with stable graft function and serum phosphate levels of <3.5 mg/dL were included in the study. The mean time since transplantation was 41 ± 18 months. After a one-month wash-out period, in which oral phosphate supplements were withdrawn, baseline blood samples were taken and analysed for creatinine, uric acid total calcium corrected to albumin, phosphate, alkaline phosphatase, bicarbonate, PTH, 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol. In a 24 h urine sample, baseline urinary creatinine, calcium and phosphate excretions were determined. Patients then received 1.5 g oral neutral phosphate for 15 days and were advised to continue with their usual diets. After 15 days of treatment serum concentrations of calcium and 1,25-dihydroxycholecalciferol concentrations for the whole group were significantly reduced (P < 0.0003 and P < 0.0006, respectively). There were also significant reductions in urinary calcium excretion (P < 00001). However, there was a significant increase in serum phosphorus; PTH levels; and urinary phosphorus excretion (P < 0.0001; P < 0.0001; and P < 0.0001, respectively). The study provides level IV evidence that phosphate supplements can potentially worsen hyperparathyroidism in the late post-transplantation period.

41%) received preoperative statin therapy. The specific type, dosage, and duration of statin therapy were not ABT-199 cost available in most studies. Preoperative statin therapy was associated with a significant risk reduction for cumulative

postoperative AKI (weighted summary odds ratio (OR) 0.87, 95% CI 0.79 to 0.95). The effect of risk reduction was also significant when considering postoperative AKI requiring RRT (OR 0.80, 95% CI 0.72 to 0.90). When restricting the analysis to the five RCTs, preoperative statin therapy did not show significant protective effect on postoperative AKI (OR 0.49, 95% CI 0.22 to 1.09). In patients undergoing major surgery, preoperative statin therapy could associate with a reduced risk for postoperative AKI. However, considerable heterogeneity existed among included studies. Future randomized trials were warranted for this critical clinical question. Acute kidney injury (AKI) is a common complication after major surgery and impacts postoperative morbidity and mortality.[1-4] The reported

incidence of AKI after surgery ranges from 1% to 30%[1-4] and varies largely due to different definitions of AKI. The incidence of postoperative AKI requiring renal replacement therapy (RRT), the most devastating form of AKI, ranges from 0.7% to 1.4%.[1-4] The development of postoperative AKI is associated with increased hospital stay, in-hospital mortality, and long-term mortality.[2, 5-9] The proposed pathophysiology Selleckchem Y-27632 of postoperative

AKI was impaired perfusion related to operation, hypoxic insult to the kidneys, oxidative stress, endothelial dysfunction, and inflammation of the kidneys.[10, 11] Many interventions have been advocated for preventing postoperative AKI, such as N-acetylcystein,[12] steroid,[13] off-pump coronary surgery,[14] and postoperative prophylactic RRT.[15] However, no definitive benefit of these preventive measures has been shown in the literature to date.[16, 17] Statins (HMG-CoA reductase inhibitors) possess the ability not only to lower blood lipid levels, but also to induce anti-inflammation, anti-oxidation, and improvement of endothelial function.[18] The effect of statins to reduce systemic inflammation and improve endothelial function Inositol monophosphatase 1 after surgery has been previously reported.[19] Randomized controlled studies and meta-analyses have demonstrated the benefits of statins on postoperative cardiovascular outcomes.[20-22] There are also animal studies showing that administration of statins before ischaemic reperfusion insult can reduce the incidence of AKI.[23] However, several randomized studies[24-28] and observational studies[29-47] elicited inconsistent results regarding the role of preoperative statins in the prevention of postoperative AKI. Our systematic review and meta-analysis examined the association between preoperative use of statins and postoperative AKI.

Methods:  Lowe syndrome was diagnosed based on the clinical manifestations and laboratory and imaging findings.

Altogether, 164 DNA samples, including samples from three affected subjects, five family members (from two families) and 156 healthy donors, were analyzed to identify the mutations in the OCRL1 gene. Results:  In family 1, proband 1 had a novel nonsense mutation (c.880G>T) in exon 10 of the OCRL1. This mutation led to a premature termination of the OCRL1 protein (p.Glu294X). Galunisertib In family 2, a novel insertion mutation (c.2626dupA) in exon 24 of OCRL1 was found in proband 2 and his affected elder brother. This mutation likely results in the degradation of the OCRL1 protein (p.Met876AsnfsX8). Both probands’ mothers were identified as carriers of the respective mutations. These mutations were not found in the unrelated controls. Conclusions:  Our study suggests that the novel nonsense mutation (c.880G>T) in exon 10 and the novel insertion mutation (c.2626dupA) in exon 24 of the OCRL1 gene cause Lowe syndrome in these two Chinese families. “
“Vascular calcification (VC) is common among patients with chronic kidney disease (CKD) due to the strong prevalence of cardiovascular and CKD-related risk

factors such as diabetes mellitus (DM), hypertension and phosphate retention. Kidney transplantation improves kidney function and abnormal mineral metabolism at the same time. It remains unclear whether kidney transplantation favourably impacts VC in the long-term. The present study examined VC in 132 kidney transplant (KT) recipients Protease Inhibitor Library datasheet who had been transplanted for longer than one year. The severity of VC was compared to 129

CKD stages 5-5D patients on a kidney transplant (KT) waiting list. The median KT vintage was 88 months. The prevalence of VC among KT and CKD patients were 54.5% and 62.8%, respectively, (P = 0.2). There Ibrutinib were no differences in age, gender, body mass index (BMI), the prevalence of DM or CVD between the two groups. Among patients with calcification, a more severe degree was observed in KT recipients (P = 0.01). Aging, DM, CVD and dialysis vintage were associated with significant VC in both groups. The degree of VC in KT recipients was more pronounced than that in CKD patients among those who experienced prolonged dialysis vintage (>2 years) (P = 0.04). Among KT recipients, the severity of VC increased with the length of time after transplantation and became more substantial after 5 years. Long-term KT recipients demonstrated a more severe degree of VC compared to matched CKD stages 5-5D patients. The severity of VC became more pronounced among those with longer transplant vintage and was in part influenced by past dialysis experience. “
“Persons receiving haemodialysis (HD) are at increased risk of cognitive impairment (CI).

Importantly, our studies of chemokine induction in monocytes from HIV+ donors represent only a small number of subjects and we have only anecdotally examined responses in viraemic and aviraemic subjects. From our previous studies of CD80 induction MI-503 cost by hBD-3, viraemia does not seem to play a major role in diminished hBD-3 responsiveness;[11] however, this may depend on the functional read-out being investigated.

Assessment of monocyte responses to antimicrobial peptide-mediated stimulation and discernment of the mechanism(s) responsible for monocyte dysfunction may provide new insights into immune deficiencies in HIV-infected persons, including those persons receiving anti-retroviral therapy. This work was supported by a National Institutes of Health grant (DE17335), by the Center for AIDS Research at Case Selleck PF 01367338 Western Reserve University (AI-36219) and by a grant from the James B. Pendleton Charitable Trust. The authors have no competing interests. “
“M.tb is an intracellular pathogen which survives within the phagosomes

of host macrophages by inhibiting their fusion with lysosomes. Here, it has been demonstrated that a lysosomal glycoprotein, CD63, is recruited to the majority of M.tb phagosomes, while RILP shows limited localization. This is consistent with the author’s findings that CD63, but not RILP, is recruited to the phagosomes in macrophages expressing Tacrolimus (FK506) the dominant negative form of Rab7. These results suggest that M.tb phagosomes

selectively fuse with endosomes and lysosomes to escape killing activity while acquiring nutrients. Phagocytosis of infected pathogens by macrophages plays an important role in the early stages of innate immunity. Phagocytosed pathogens are incorporated into phagosomal vacuoles. These phagosomes then interact with endosomal and lysosomal vesicles in a process referred to as phagolysosome biogenesis. During phagolysosome biogenesis, phagosomes acquire degradative and microbicidal properties, leading phagocytosed pathogens to be killed and degraded. M.tb, the causative bacterium of tuberculosis, infects more than one-third of the human population. M.tb is able to survive and proliferate within phagosomes of the host’s macrophages by inhibiting phagolysosome biogenesis (1, 2). However, the exact process by which M.tb blocks phagolysosome biogenesis is not fully understood. Recently, it was reported that phagosomes containing M.tb (M.tb phagosomes) within dendritic cells are associated with lysosomes in the early stages of infection (3). In addition, we have previously demonstrated that LAMP-2, but not cathepsin D, is recruited to M.tb phagosomes in macrophages (4). These results suggest that M.tb phagosomes selectively fuse with lysosomal vesicles which have distinct characteristics.

Many mechanisms that are involved in preventing an effective anticancer immune response have been described, including immunosuppressive and anti-inflammatory factors, such as NO, arginase, TGF-β, and IL-10 that are produced by both classically and alternatively activated macrophages, other myeloid cell subsets, and Treg cells [102, 104-106]. In addition, tumor and stromal cells, including hematopoietic cells, express ligands as the B7 family and PDL1/2 that trigger immune checkpoint receptors on T cells, such as CTLA-4 and GPCR Compound Library PD1, and prevent their antitumor activity (reviewed in [107]). Thus, inflammation and immunity should be considered inherent characteristics of cancer

(reviewed in [81]), and “avoiding immune destruction” and “tumor promoting inflammation” are now listed among the hallmarks of cancer [108]. Figure 1 schematically depicts the different levels at which inflammation has been described

to affect carcinogenesis, tumor progression, comorbidity, and response to therapy. As discussed below, the commensal microbiota sets an inflammatory/immune tone in the organism and thus modulates the response of the host to oncogenic pathogens, intrinsic inflammation, and tumor-induced tissue damage, and is therefore likely to play a major role in modulating inflammation and immunity to cancer at all of these levels. Approximately 16% of human cancers worldwide are related to infectious agents or infection-associated chronic inflammation, with higher percentages in less developed countries (22.9%) than in more developed countries (7.4%) [109]. Oncogenic viruses, seven of which are Ulixertinib nmr known to be associated with human cancer, represent an important infectious cause of cancer (reviewed in [110]). Two of the human oncogenic viruses are herpesviruses: Epstein-Barr virus (EBV), which

is associated with Burkitt’s lymphoma, nasopharyngeal carcinoma, and a subset of gastric carcinoma, 2-hydroxyphytanoyl-CoA lyase and Kaposi’s sarcoma-associated herpesvirus/human herpesvirus type 8, which causes Kaposi’s sarcoma and other pathologies in immunosuppressed individuals [110]. The two hepatitis viruses among the tumorigenic viruses, hepatitis B virus and hepatitis C virus (HBV and HCV), are associated with hepatocellular carcinoma (HCC) [111]. High-risk oncogenic strains of human papillomaviruses are associated with anogenital cancers, a subset of head and neck cancers and skin cancers [112, 113]. Human T-cell lymphoma virus is the pathogenic determinant of the T-cell lymphomas prevalent in certain geographical regions [114, 115]. Rounding out the list of seven, the recently identified Merkel cell polyomaviruses are associated with aggressive skin cancer in immunosuppressed individuals [116, 117]. With the exception of HCV, all the known human oncogenic viruses encode at least one oncogene and may directly transform healthy cells to tumor-forming cells (reviewed in [118]).

From December 2009 to August 2012,

we used this ALT chimeric flap to reconstruct two separate defects in upper extremity on five patients (mean age: 36.6 years; range: 15∼47 years). The locations of defect were check details palm and fingers in four patients and forearm in the other patient. The sizes of defect ranged from 4.5 × 1.5 cm to 20 × 10 cm. A minimum of two separate perforator vessels in the flap were identified. The skin paddle was then split between the two perforators to shape two separate paddles with a common vascular supply. There were no cases of flap failure or re-exploration. Four donor sites were directly closed and one was covered by a skin graft. Donor-site morbidity was negligible. The ALT chimeric flap provides customized cover for two separate defects in upper extremity. © 2013 Wiley Periodicals, Inc. Microsurgery 33:631–637, 2013. “
“Elbow reconstruction is challenging for reconstructive surgeons. The purpose of this report is to present the results of the use of freestyle perforator-based propeller flap designed from the medial arm region Lorlatinib cell line for elbow reconstruction. The defects following soft tissue sarcoma resection at the medial and posterior elbow were repaired in

two patients. The dimensions of the defects were 11 × 7 cm2 and 10 × 7 cm2. Two perforators were identified in each case using Doppler ultrasound probe in the medial arm, adjacent to the defect. The perforator with visible pulsation was chosen as the pedicle vessel, which was 12-cm and 7-cm proximal to the medial epicondyle. An elliptical flap, extending almost the full length of arm, was raised

and rotated 180° to repair medial elbow defects. The sizes of the flaps were 17 × 8 cm2 and 11 × 7 cm2. The donor sites were closed directly. Both flaps survived; temporary Tolmetin venous congestion occurred in one case. There were no other postoperative complications. These cases illustrated that the medial arm flap might be used for reconstruction of medial elbow defects with this freestyle perforator-based propeller flap design. © 2014 Wiley Periodicals, Inc. Microsurgery, 2014. “
“Skin graft is still a method of choice for the coverage of temporal defects. But there are some disadvantages like a “patch” appearance, the need of dressing or longer healing time. Numbers of local flaps have been described for closing skin defects on temporal region. Yet, they may cause distortion of the surrounding tissues, especially in the temporal hairline and eyebrow. We present a series of seven local flaps based on small branches (SB) of the superficial temporal artery (STA) for the coverage of temporal defects, and discuss their advantages. Supermicrodissection of SB of the STA was performed to obtain local flaps for reconstruction of temporal defects after skin cancer excisions in seven patients.