Normal wound healing is a dynamic and complex multiple phase process involving coordinated interactions between growth factors, cytokines, chemokines, and various cells. Any failure in these phases may lead wounds to become chronic and have abnormal scar formation. Chronic wounds affect patients’ quality of life, since they require repetitive treatments and incur considerable medical costs. Thus, much effort has been focused on developing novel therapeutic approaches for wound treatment. Stem-cell-based therapeutic strategies have been proposed to treat these wounds. They have shown considerable potential for improving the rate and quality of wound healing and regenerating the skin. However, there are many challenges for using stem cells in skin regeneration. In this review, we present some sets of the data published on using embryonic stem cells, induced pluripotent stem cells, and adult stem cells in healing wounds. Additionally, we will discuss the different angles whereby these cells can contribute to their unique features and show the current drawbacks.

Purpose: Virulent and resistant Klebsiella pneumoniae strains are considered as one of the most significant causes of hospital-acquired infections. The present investigation was done to study the distribution of virulence factors, capsule serotypes and phenotypic and genotypic evaluation of antibiotic resistance of the K. pneumoniae strains isolated from hospital-acquired infections. Patients Materials and methods: Two hundred and sixty different types of hospital-acquired infections were collected and cultured. Antibiotic resistance pattern of K. pneumoniae isolates and their molecular characterization were studied using disk diffusion and PCR, respectively. Results: One hundred and fifty out of 260 (44.22%) hospital-acquired infections harbored K. pneumoniae . Urine samples (63.75%) had the highest prevalence of K. pneumoniae , while wound (33.33%) had the lowest. K. pneumoniae strains harbored the highest prevalence of resistance against ampicillin (100%), cefuroxime (100%), amoxicillin/clavulanic acid (95.65%) and ceftazidime (95.52%). FimH-1 (93.04%), traT (92.17%), mrkD (84.34%), and entB (80.86%) were the most commonly detected virulence genes. AcrAB (96.52%) and tolC (85.21%) were the most commonly detected antibiotic resistance genes. Prevalence of ompK35 and ompK36 virulence genes were 75.65% and 79.13%, respectively. Prevalence of K1 and K2-positive serotypes were 27.82% and 6.96%, respectively. Conclusions: High prevalence of resistance against several types of antibiotics and simultaneous presence of some virulence factors and multi-drug resistance genes pose an important public health issue.

Survivin is one of the most cancer-specific proteins overexpressed in almost all malignancies, but is nearly undetectable in most normal tissues in adults. Functionally, as a member of the inhibitor of apoptosis family, survivin has been shown to inhibit apoptosis and increase proliferation. The antiapoptotic function of survivin seems to be related to its ability to inhibit caspases directly or indirectly. Furthermore, the role of survivin in cell cycle division control is related to its role in the chromosomal passenger complex. Consistent with its determining role in these processes, survivin plays a crucial role in cancer progression and cancer cell resistance to anticancer drugs and ionizing radiation. On the basis of these findings, recently survivin has been investigated intensively as an ideal tumor biomarker. Thus, multiple molecular approaches such as use of the RNA interfering technique, antisense oligonucleotides, ribozyme, and small molecule inhibitors have been used to downregulate survivin regulation and inhibit its biological function consequently. In this review, all these approaches are explained and other compounds that induced apoptosis in different cell lines through survivin inhibition are also reported.