Antimicrobial susceptibility pattern of aerobic bacteria responsible for post-surgical wound infection of the patients admitted into Khulna Medical College Hospital, Bangladesh.

Resistance against antimicrobial agents is dramatically increasing and gradually impacting treatment costs. Using existing drugs would have helped avoid bacterial infections in various circumstances. The primary objectives of this study were to determine the prevalence of pathogens responsible for postsurgical wound infections and their antimicrobial susceptibility and resistance pattern among the patients admitted to Khulna Medical College Hospital, Khulna Bangladesh. This cross-sectional study involved 250 patients suffering from postsurgical wound infection as respondents. The bacterial pathogens were isolated from pus samples obtained from those patients. The isolated bacterial pathogens were identified through several standard biochemical tests, and finally, the culture sensitivity tests of those bacterial isolates were performed. The study was conducted from August 2019 to June 2020. Data regarding the patient's age, gender, occupation, surgery performed, duration of hospital stay, and comorbidity were also documented using standard questionnaires. Five bacterial pathogens were identified with different frequencies, including Pseudomonas aeruginosa (36 %), Escherichia coli (21.2 %), Staphylococcus aureus (8.8 %), Klebsiella spp. (7.2 %) and Proteus spp. (4.8 %). These bacterial pathogens showed sensitivity to ciprofloxacin (75 %), piperacillin-tazobactam (56.7 %) and gentamicin (50 %). Besides, S. aureus showed sensitivity to linezolid and vancomycin and resistance to cefuroxime, ceftazidime and imipenem. Male patients (68.4 %) suffered more from postsurgical wound infection than female patients (31.6 %). Patients aged 31 to 40 years were more severely affected than patients from other age groups. Postsurgical wound infection was vigorously observed in the patients who underwent hand surgery. Intensive occurrence of this infection was found in the patients who stayed in the hospital from 31 to 40 days. Diabetic patients suffered more from postsurgical wound infection compared to the other patients. Throughout the study, ciprofloxacin has been the best performer against E. coli, Klebsiella spp., and Proteus spp., and gentamicin showed better performance against S. aureus. The antibiotic resistance pattern of these bacterial pathogens reflects the worldwide necessity of rational antibiotic management and proper steps to maintain hospital hygiene in Bangladesh.

A Rare Incidence of Sweating Sickness-Like Symptoms in a Crossbred Holstein Friesian Cow in Chattogram, Bangladesh.

In this report, an incidence of sweating sickness-like symptoms in a crossbred Holstein Friesian cow was diagnosed. The cow was suffering from vaporization of the skin, dehydration, wet hair coat, and matting of hair due to excessive sweating. There were several ticks, flies, and mosquitoes in tail switch and other parts of the body. Blood and urine parameters were tested. We treated the patient successfully with ivermectin as ectoparasite control, ceftiofur sodium antibiotic to treat bacterial infections, ketoprofen as analgesics and antipyretics, chlorpheniramine maleate as H2-blocker, and trichlorfon and povidone-iodine skin spray to prevent fly invasion and prevent opportunistic bacterial infection, respectively. Acyclovir and oil of turpentine were suggested to be sprayed on the floor and wall of the shed for viral and ectoparasitic control. Our treatment regime successfully recovered the cow with no recurrence.

Cathepsin S Knockdown Suppresses Endothelial Inflammation, Angiogenesis, and Complement Protein Activity under Hyperglycemic Conditions In Vitro by Inhibiting NF-κB Signaling.

Hyperglycemia plays a key role in the development of microvascular complications, endothelial dysfunction (ED), and inflammation. It has been demonstrated that cathepsin S (CTSS) is activated in hyperglycemia and is involved in inducing the release of inflammatory cytokines. We hypothesized that blocking CTSS might alleviate the inflammatory responses and reduce the microvascular complications and angiogenesis in hyperglycemic conditions. In this study, we treated human umbilical vein endothelial cells (HUVECs) with high glucose (HG; 30 mM) to induce hyperglycemia and measured the expression of inflammatory cytokines. When treated with glucose, hyperosmolarity could be linked to cathepsin S expression; however, many have mentioned the high expression of CTSS. Thus, we made an effort to concentrate on the immunomodulatory role of the CTSS knockdown in high glucose conditions. We validated that the HG treatment upregulated the expression of inflammatory cytokines and CTSS in HUVEC. Further, siRNA treatment significantly downregulated CTSS expression along with inflammatory marker levels by inhibiting the nuclear factor-kappa B (NF-κB) mediated signaling pathway. In addition, CTSS silencing led to the decreased expression of vascular endothelial markers and downregulated angiogenic activity in HUVECs, which was confirmed by a tube formation experiment. Concurrently, siRNA treatment reduced the activation of complement proteins C3a and C5a in HUVECs under hyperglycemic conditions. These findings show that CTSS silencing significantly reduces hyperglycemia-induced vascular inflammation. Hence, CTSS may be a novel target for preventing diabetes-induced microvascular complications.

Targeting an MDM2/MYC Axis to Overcome Drug Resistance in Multiple Myeloma.

BACKGROUND: MDM2 is elevated in multiple myeloma (MM). Although traditionally, MDM2 negatively regulates p53, a growing body of research suggests that MDM2 plays several p53-independent roles in cancer pathogenesis as a regulator of oncogene mRNA stability and translation. Yet, the molecular mechanisms underlying MDM2 overexpression and its role in drug resistance in MM remain undefined. METHODS: Both myeloma cell lines and primary MM samples were employed. Cell viability, cell cycle and apoptosis assays, siRNA transfection, quantitative real-time PCR, immunoblotting, co-immunoprecipitation (Co-IP), chromatin immunoprecipitation (ChIP), soft agar colony formation and migration assay, pulse-chase assay, UV cross-linking, gel-shift assay, RNA-protein binding assays, MEME-analysis for discovering c-Myc DNA binding motifs studies, reporter gene constructs procedure, gene transfection and reporter assay, MM xenograft mouse model studies, and statistical analysis were applied in this study. RESULTS: We show that MDM2 is associated with poor prognosis. Importantly, its upregulation in primary MM samples and human myeloma cell lines (HMCLs) drives drug resistance. Inhibition of MDM2 by RNAi, or by the MDM2/XIAP dual inhibitor MX69, significantly enhanced the sensitivity of resistant HMCLs and primary MM samples to bortezomib and other anti-myeloma drugs, demonstrating that MDM2 can modulate drug response. MDM2 inhibition resulted in a remarkable suppression of relapsed MM cell growth, colony formation, migration and induction of apoptosis through p53-dependent and -independent pathways. Mechanistically, MDM2 was found to reciprocally regulate c-Myc in MM; MDM2 binds to AREs on c-Myc 3'UTR to increase c-Myc mRNA stability and translation, while MDM2 is a direct transcriptional target of c-Myc. MDM2 inhibition rendered c-Myc mRNA unstable, and reduced c-Myc protein expression in MM cells. Importantly, in vivo delivery of MX69 in combination with bortezomib led to significant regression of tumors and prolonged survival in an MM xenograft model. CONCLUSION: Our findings provide a rationale for the therapeutic targeting of MDM2/c-Myc axis to improve clinical outcome of patients with refractory/relapsed MM.

Silicone Implants Immobilized with Interleukin-4 Promote the M2 Polarization of Macrophages and Inhibit the Formation of Fibrous Capsules.

Breast augmentations with silicone implants can have adverse effects on tissues that, in turn, lead to capsular contracture (CC). One of the potential ways of overcoming CC is to control the implant/host interaction using immunomodulatory agents. Recently, a high ratio of anti-inflammatory (M2) macrophages to pro-inflammatory (M1) macrophages has been reported to be an effective tissue regeneration approach at the implant site. In this study, a biofunctionalized implant was coated with interleukin (IL)-4 to inhibit an adverse immune reaction and promoted tissue regeneration by promoting polarization of macrophages into the M2 pro-healing phenotype in the long term. Surface wettability, nitrogen content, and atomic force microscopy data clearly showed the successful immobilization of IL-4 on the silicone implant. Furthermore, in vitro results revealed that IL-4-coated implants were able to decrease the secretion of inflammatory cytokines (IL-6 and tumor necrosis factor-α) and induced the production of IL-10 and the upregulation of arginase-1 (mannose receptor expressed by M2 macrophage). The efficacy of this immunomodulatory implant was further demonstrated in an in vivo rat model. The animal study showed that the presence of IL-4 diminished the capsule thickness, the amount of collagen, tissue inflammation, and the infiltration of fibroblasts and myofibroblasts. These results suggest that macrophage phenotype modulation can effectively reduce inflammation and fibrous CC on a silicone implant conjugated with IL-4.

Functionalization of Silicone Surface with Drugs and Polymers for Regulation of Capsular Contracture.

Breast reconstruction is achieved using silicone implants, which are currently associated with major complications. Several strategies have been considered to overcome the existing limitations as well as to improve their performance. Recently, surface modification has proved to be an effective clinical approach to prevent bacterial adhesion, reduce capsular thickness, prevent foreign body reactions, and reduce other implant-associated problems. This review article summarizes the ongoing strategies for the surface modification of silicone implants in breast reconstruction applications. The article mostly discusses two broad categories of surface modification: drug-mediated and polymer-based. Different kinds of drugs have been applied with silicone that are associated with breast reconstruction. Initially, this article discusses studies related to drugs immobilized on silicone implants, focusing on drug-loading methods and their effects on capsule contracture. Moreover, the pharmacological action of drugs on fibroblast cells is considered in this section. Next, the polymeric modification of the silicone surface is introduced, and we discuss its role in reducing capsule thickness at the cellular and biological levels. The polymeric modification techniques, their chemistry, and their physical properties are described in detail. Notably, polymer activities on macrophages and inflammation are also briefly discussed. Each of the reviewed articles is summarized, highlighting their discussion of capsular thickness, foreign body reactions, and bacterial attachment. The aim of this review is to provide the main points of some research articles regarding the surface modification of silicon, which can lead to a decrease in capsular thickness and provides better patient compliance.

In Vivo Comparison of Three Human Acellular Dermal Matrices for Breast Reconstruction.

BACKGROUND/AIM: Acellular dermal matrices (ADMs) have become popular in implant-based breast reconstruction. The aim of this study was to compare three commonly used ADM products in vivo in an animal model. MATERIALS AND METHODS: The nucleic acid content (residual double-stranded DNA) and the levels of the remaining growth factors after decellularization were measured for each ADM. Cytocompatibility with ADMs was documented using NIH 3T3 mouse fibroblast cells. In vivo, the implanted ADMs were histologically evaluated at 1, 2, 3, and 6 months (n=5) using male 8-week-old Sprague-Dawley rats. RESULTS: Fibroblasts grew in the SureDerm HD and DermACELL with no cytotoxicity. In a rat model, SureDerm HD and DermACELL incorporated more readily into the surrounding host tissue, as measured by rapid cell influx and collagen deposition, and showed more delayed tissue remodeling with decreased matrix metalloproteinases levels compared to AlloDerm. CONCLUSION: SureDerm HD and DermACELL can be used as biological materials for breast reconstruction.

SMAD1 as a biomarker and potential therapeutic target in drug-resistant multiple myeloma.

BACKGROUND: SMAD1, a central mediator in TGF-ß signaling, is involved in a broad range of biological activities including cell growth, apoptosis, development and immune response, and is implicated in diverse type of malignancies. Whether SMAD1 plays an important role in multiple myeloma (MM) pathogenesis and can serve as a therapeutic target are largely unknown. METHODS: Myeloma cell lines and primary MM samples were used. Cell culture, cytotoxicity and apoptosis assay, siRNA transfection, Western blot, RT-PCR, Soft-agar colony formation, and migration assay, Chromatin immunoprecipitation (Chip), animal xenograft model studies and statistical analysis were applied in this study. RESULTS: We demonstrate that SMAD1 is highly expressed in myeloma cells of MM patients with advanced stages or relapsed disease, and is associated with significantly shorter progression-free and overall survivals. Mechanistically, we show that SMAD1 is required for TGFß-mediated proliferation in MM via an ID1/p21/p27 pathway. TGF-ß also enhanced TNFα-Induced protein 8 (TNFAIP8) expression and inhibited apoptosis through SMAD1-mediated induction of NF-κB1. Accordingly, depletion of SMAD1 led to downregulation of NF-κB1 and TNFAIP8, resulting in caspase-8-induced apoptosis. In turn, inhibition of NF-κB1 suppressed SMAD1 and ID1 expression uncovering an autoregulatory loop. Dorsomorphin (DM), a SMAD1 inhibitor, exerted a dose-dependent cytotoxic effect on drug-resistant MM cells with minimal cytotoxicity to normal hematopoietic cells, and further synergized with the proteasomal-inhibitor bortezomib to effectively kill drug-resistant MM cells in vitro and in a myeloma xenograft model. CONCLUSIONS: This study identifies SMAD1 regulation of NF-κB1/TNFAIP8 and ID1-p21/p27 as critical axes of MM drug resistance and provides a potentially new therapeutic strategy to treat drug resistance MM through targeted inhibition of SMAD1.

Pathophysiological roles of myristoylated alanine-rich C-kinase substrate (MARCKS) in hematological malignancies.

The myristoylated alanine-rich C-kinase substrate (MARCKS) protein has been at the crossroads of multiple signaling pathways that govern several critical operations in normal and malignant cellular physiology. Functioning as a target of protein kinase C, MARCKS shuttles between the phosphorylated cytosolic form and the unphosphorylated plasma membrane-bound states whilst regulating several molecular partners including, but not limited to calmodulin, actin, phosphatidylinositol-4,5-bisphosphate, and phosphoinositide-3-kinase. As a result of these interactions, MARCKS directly or indirectly modulates a host of cellular functions, primarily including cytoskeletal reorganization, membrane trafficking, cell secretion, inflammatory response, cell migration, and mitosis. Recent evidence indicates that dysregulated expression of MARCKS is associated with the development and progression of hematological cancers. While it is understood that MARCKS impacts the overall carcinogenesis as well as plays a part in determining the disease outcome in blood cancers, we are still at an early stage of interpreting the pathophysiological roles of MARCKS in neoplastic disease. The situation is further complicated by contradictory reports regarding the role of phosphorylated versus an unphosphorylated form of MARCKS as an oncogene versus tumor suppressor in blood cancers. In this review, we will investigate the current body of knowledge and evolving concepts of the physical properties, molecular network, functional attributes, and the likely pathogenic roles of MARCKS in hematological malignancies. Key emphasis will also be laid upon understanding the novel mechanisms by which MARCKS determines the overall disease prognosis by playing a vital role in the induction of therapeutic resistance. Additionally, we will highlight the importance of MARCKS as a valuable therapeutic target in blood cancers and will discuss the potential of existing strategies available to tackle MARCKS-driven blood cancers.

A preliminary study of micro-RNAs as minimally invasive biomarkers for the diagnosis of prostate cancer patients.

BACKGROUND: A prostate cancer diagnosis is based on biopsy sampling that is an invasive, expensive procedure, and doesn't accurately represent multifocal disease. METHODS: To establish a model using plasma miRs to distinguish Prostate cancer patients from non-cancer controls, we enrolled 600 patients histologically diagnosed as having or not prostate cancer at biopsy. Two hundred ninety patients were eligible for the analysis. Samples were randomly divided into discovery and validation cohorts. RESULTS: NGS-miR-expression profiling revealed a miRs signature able to distinguish prostate cancer from non-cancer plasma samples. Of 51 miRs selected in the discovery cohort, we successfully validated 5 miRs (4732-3p, 98-5p, let-7a-5p, 26b-5p, and 21-5p) deregulated in prostate cancer samples compared to controls (p ≤ 0.05). Multivariate and ROC analyses show miR-26b-5p as a strong predictor of PCa, with an AUC of 0.89 (CI = 0.83-0.95;p < 0.001). Combining miRs 26b-5p and 98-5p, we developed a model that has the best predictive power in discriminating prostate cancer from non-cancer (AUC = 0.94; CI: 0,835-0,954). To distinguish between low and high-grade prostate cancer, we found that miR-4732-3p levels were significantly higher; instead, miR-26b-5p and miR-98-5p levels were lower in low-grade compared to the high-grade group (p ≤ 0.05). Combining miR-26b-5p and miR-4732-3p we have the highest diagnostic accuracy for high-grade prostate cancer patients, (AUC = 0.80; CI 0,69-0,873). CONCLUSIONS: Noninvasive diagnostic tests may reduce the number of unnecessary prostate biopsies. The 2-miRs-diagnostic model (miR-26b-5p and miR-98-5p) and the 2-miRs-grade model (miR-26b-5p and miR-4732-3p) are promising minimally invasive tools in prostate cancer clinical management.

A biphasic calcium phosphate ceramic scaffold loaded with oxidized cellulose nanofiber-gelatin hydrogel with immobilized simvastatin drug for osteogenic differentiation.

A novel bone scaffold containing bioceramic and biopolymer materials with an osteoinductive simvastatin molecule was developed to enhance bone regeneration. An oxidized cellulose nanofiber (OCNF)-Gelatin (Gel) hydrogel was loaded into a biphasic calcium phosphate (BCP) ceramic in which simvastatin was entrapped, resulting in a scaffold with both osteoconductive and osteoinductive properties. The fabricated scaffold showed interconnected porosity with micro- and macroporous orientation. After loading the OCNF-Gel (HG), the mechanical stability of the ceramic BCP scaffold was increased suitable for the application of hard tissue regeneration. Fourier-transform infrared spectroscopy showed that simvastatin was successfully coated on the BCPHG scaffolds. OCNF, with its slower degradation, may contribute to the sustained release of drug from the scaffold. Initially simvastatin was released from the scaffold at high levels, then was constantly and gradually released for up to 4 weeks. Pre-osteoblast MC3T3E1 cells were seeded on the scaffolds to investigate cell viability, morphology, and differentiation. The simvastatin-loaded BCPHG-S scaffolds showed better cell proliferation and spreading compared to other scaffolds. Immunostaining assays showed the expression of proteins responsible for osteogenic differentiation. Alkaline phosphatase and osteopontin were more highly expressed in the BCPHG-S scaffold than in other scaffolds. These results suggest that simvastatin-loaded BCPHG scaffolds provided physiological environments suitable for better osteogenic differentiation.

Thermal cycling effect on osteogenic differentiation of MC3T3-E1 cells loaded on 3D-porous Biphasic Calcium Phosphate (BCP) scaffolds for early osteogenesis.

The application of heat stress on a defect site during the healing process is a promising technique for early bone regeneration. The primary goal of this study was to investigate the effect of periodic heat shock on bone formation. MC3T3-E1 cells were seeded onto biphasic calcium phosphate (BCP) scaffolds, followed by periodic heating to evaluate osteogenic differentiation. Heat was applied to cells seeded onto scaffolds at 41 °C for 1 h once, twice, and four times a day for seven days and their viability, morphology, and differentiation were analyzed. BCP scaffolds with interconnected porous structures mimic bone biology for cellular studies. MTT and confocal studies have shown that heat shock significantly increased cell proliferation without any toxic effects. Compared to non-heated samples, heat shock enhanced calcium deposition and mineralization, which could be visualized by SEM observation and Alizarin red S staining. Immunostaining images showed the localization of osteogenic proteins ALP and OPN on heat-shocked cells. qRT-PCR analysis revealed the presence of more osteospecific markers, osteopontin (OPN), osteocalcin, collagen type X, and Runx2, in the heat-shocked samples than in the non-heated sample. Periodic heat shock significantly upregulated both heat shock proteins (HSP70 and HSP27) in differentiated MC3T3-E1 cells. The results of this study demonstrated that periodically heat applied especially two times a day was better approach for osteogenic differentiation. Hence, this work provides a define temperature and time schedule for the development of a clinical heating device in future for early bone regeneration during the postsurgical period.

In vitro and in vivo evaluation of bioglass microspheres incorporated brushite cement for bone regeneration.

Bioglass-calcium phosphate cement (CPC) composite materials have recently received increased attention for bone regeneration purposes, owing to their improved properties in term of biocompatibility and bone ingrowths. In this study, an injectable bone substitute (IBS) system which utilizes bioglass microspheres incorporated into brushite based cement, was evaluated. The microspheres were synthesized with a simple and low sintering temperature process; there was no significant phase difference shown from the powder and good interactivity with cells was obtained. Furthermore, physical properties were optimized in microsphere incorporated brushite cement in order to investigate in vitro and in vivo performance. Accordingly, setting time and compressive strength were hardly altered until a microsphere content of 40% (v/v) was reached. The brushite (BR)/bioglass microsphere (BM) system showed excellent bioactivity to the in-vitro simulated body fluid test: dissolution ions from composite materials influenced apatite growth, countered acidic pH, and increased material degradation. In an in-vitro study with preosteoblasts (MC3T3-E1), BR/BM supported cell adhesion and proliferation, while cell differentiation experiments without osteogenic supplements, demonstrated that BR/BM induced osteogenic differentiation. A post-implantation study conducted in femoral defects showed higher materials degradation and bone formation in BR/BM than in BR. The faster dissolution of bioglass microspheres increased BR/BM composite resorption and hence facilitated bone tissue integration. Our findings suggest that bioglass microspheres incorporated in cement could potentially be used as an injectable bone substitute for bone regeneration applications.

miRNAs as Candidate Biomarker for the Accurate Detection of Atypical Endometrial Hyperplasia/Endometrial Intraepithelial Neoplasia.

Endometrial cancer is the most common gynecologic malignancy in developed countries. Estrogen-dependent tumors (type I, endometrioid) account for 80% of cases and non-estrogen-dependent (type II, non-endometrioid) account for the rest. Endometrial cancer type I is generally thought to develop via precursor lesions along with the increasing accumulation of molecular genetic alterations. Endometrial hyperplasia with atypia/Endometrial Intraepithelial Neoplasia is the least common type of hyperplasia but it is the type most likely to progress to type I cancer, whereas endometrial hyperplasia without atypia rarely progresses to carcinoma. MicroRNAs are a class of small, non-coding, single-stranded RNAs that negatively regulate gene expression mainly binding to 3'-untranslated region of target mRNAs. In the current study, we identified a microRNAs signature (miR-205, miR-146a, miR-1260b) able to discriminate between atypical and typical endometrial hyperplasia in two independent cohorts of patients. The identification of molecular markers that can distinguish between these two distinct pathological conditions is considered to be highly useful for the clinical management of patients because hyperplasia with an atypical change is associated with a higher risk of developing cancer. We show that the combination of miR-205, -146a, and -1260b has the best predictive power in discriminating these two conditions (>90%). With the aim to find a biological role for these three microRNAs, we focused our attention on a common putative target involved in endometrial carcinogenesis: the oncosuppressor gene SMAD4. We showed that miRs-146a,-205, and-1260b directly target SMAD4 and their enforced expression induced proliferation and migration of Endometrioid Cancer derived cell lines, Hec1a cells. These data suggest that microRNAs-mediated impairment of the TGF-ß pathway, due to inhibition of its effector molecule SMAD4, is a relevant molecular alteration in endometrial carcinoma development. Our findings show a potential diagnostic role of this microRNAs signature for the accurate diagnosis of Endometrial hyperplasia with atypia/Endometrial Intraepithelial Neoplasia and improve the understanding of their pivotal role in SMAD4 regulation.

A hybrid composite system of biphasic calcium phosphate granules loaded with hyaluronic acid-gelatin hydrogel for bone regeneration.

An ideal bone substitute should be made of biocompatible materials that mimic the structure, characteristics, and functions of natural bone. Many researchers have worked on the fabrication of different bone scaffold systems including ceramic-polymer hybrid system. In the present study, we incorporated hyaluronic acid-gelatin hydrogel to micro-channeled biphasic calcium phosphate granules as a carrier to improve cell attachment and proliferation through highly interconnected porous structure. This hybrid system is composed of ceramic biphasic calcium phosphate granules measuring 1 mm in diameter with seven holes and hyaluronic acid-gelatin hydrogel. This combination of biphasic calcium phosphate and hyaluronic acid-gelatin retained suitable characteristics for bone regeneration. The resulting scaffold had a porosity of 56% with a suitable pore sizes. The mechanical strength of biphasic calcium phosphate granule increased after loading hyaluronic acid-gelatin from 4.26 ± 0.43 to 6.57 ± 0.25 MPa, which is highly recommended for cancellous bone substitution. Swelling and degradation rates decreased in the hybrid scaffold compared to hydrogel due to the presence of granules in hybrid scaffold. In vitro cytocompatibility studies were observed by preosteoblasts (MC3T3-E1) cell line and the result revealed that biphasic calcium phosphate/hyaluronic acid-gelatin significantly increased cell growth and proliferation compared to biphasic calcium phosphate granules. Analysis of micro-computed tomography data and stained tissue sections from the implanted samples showed that the hybrid scaffold had good osseointegration and better bone formation in the scaffold one and two months postimplantation. Histological section confirmed the formation of dense collagenous tissue and new bone in biphasic calcium phosphate/hyaluronic acid-gelatin scaffolds at two months. Our study demonstrated that such hybrid biphasic calcium phosphate/hyaluronic acid-gelatin scaffold is a promising system for bone regeneration.

microRNA: Diagnostic Perspective.

Biomarkers are biological measures of a biological state. An ideal marker should be safe and easy to measure, cost efficient, modifiable with treatment, and consistent across gender and ethnic groups. To date, none of the available biomarkers satisfy all of these criteria. In addition, the major limitations of these markers are low specificity, sensitivity, and false positive results. Recently identified, microRNAs (miRNAs) are endogenous, evolutionarily conserved small non-coding RNA (about 22-25 nt long), also known as micro-coordinators of gene expression, which have been shown to be an effective tools to study the biology of diseases and to have great potential as novel diagnostic and prognostic biomarkers with high specificity and sensitivity. In fact, it has been demonstrated that miRNAs play a pivotal role in the regulation of a wide range of developmental and physiological processes and their deficiencies have been related to a number of disease. In addition, miRNAs are stable and can be easily isolated and measured from tissues and body fluids. In this review, we provide a perspective on emerging concepts and potential usefulness of miRNAs as diagnostic markers, emphasizing the involvement of specific miRNAs in particular tumor types, subtypes, cardiovascular diseases, diabetes, infectious diseases, and forensic test.