Effect of platelet-rich plasma on healing of lower extremity diabetic skin ulcers: A meta-analysis.

The aim of this research is to explore the therapeutic efficacy of platelet-rich plasma (PRP) on the cutaneous ulceration of diabetes mellitus (DM). From the beginning of the database until January 2024, we looked through several databases to obtain randomised, controlled PRP studies to treat the wound healing of DM in adult patients. The Cochrane Collaboration's Risk-Of-Bias Instrument was used to evaluate the risk of bias in randomised, controlled studies. Funnel plots, sensitivity analyses and Egger regression tests were employed to determine the reliability and effectiveness of the meta-analyses. Depending on the degree of heterogeneity, a fixed or random effect model has been used. The statistical significance was determined to be below 0.05. Altogether 281 trials were collected from the database and entered into Endnote Software for screening, and 15 trials were analysed. It was found that PRP was associated with a higher rate of wound healing (OR, 3.23; 95% CI, 2.42, 4.31 p < 0.0001). PRP was associated with a reduction in the risk of post-operative wound infection (OR, 0.46; 95% CI, 0.21, 0.99 p = 0.05). PRP was associated with a reduction in the risk of amputations amongst those with DM (OR, 0.50; 95% CI, 0.30, 0.84 p = 0.009). Overall, PRP treatment for DM is expected to improve the rate of wound healing, decrease the risk of wound infection and decrease the risk of amputations.

Research progress on ferroptosis in the pathogenesis and treatment of neurodegenerative diseases.

Globally, millions of individuals are impacted by neurodegenerative disorders including Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and Alzheimer's disease (AD). Although a great deal of energy and financial resources have been invested in disease-related research, breakthroughs in therapeutic approaches remain elusive. The breakdown of cells usually happens together with the onset of neurodegenerative diseases. However, the mechanism that triggers neuronal loss is unknown. Lipid peroxidation, which is iron-dependent, causes a specific type of cell death called ferroptosis, and there is evidence its involvement in the pathogenic cascade of neurodegenerative diseases. However, the specific mechanisms are still not well known. The present article highlights the basic processes that underlie ferroptosis and the corresponding signaling networks. Furthermore, it provides an overview and discussion of current research on the role of ferroptosis across a variety of neurodegenerative conditions.

Generalized Rayleigh quotient optimization method for inter-channel nonlinearity compensation in coherent optical communication systems.

Inter-channel nonlinearity compensation plays a crucial role in wavelength division multiplexing (WDM) systems for improving transmission capacity and distance. In this work, we propose a novel, to the best of our knowledge, inter-channel nonlinearity compensation method called generalized Rayleigh quotient optimization (GRQO) method with two different working modes. In an 8 × 64 GBaud 16-ary quadrature amplitude modulation (16-QAM) experimental system over 1600 km standard single-mode fiber (SSMF), the proposed method shows a 0.40 dB Q2 factor improvement over nonlinear polarization cross talk canceller (NPCC) with a moderately low computational complexity of about 2000 real multiplications per bit (RMb).

The value of platelet-rich plasma-derived extracellular vesicles in modern medicine.

Platelet-rich plasma (PRP) has been widely used in clinical practice. The mechanism by which PRP promotes tissue repair lies in the release of multiple growth factors upon platelet activation, which accelerates the proliferation and differentiation of repair cells and the synthesis of extracellular matrix. In recent years, as extracellular vesicles (EVs) research has increased and intensified, it has been found that EVs also play an important role in tissue repair. This article provides a comprehensive review of the role of PRP and PRP-derived extracellular vesicles (PRP-EVs) in tissue repair. It discusses the biological characteristics, extraction, identification, activation, and preservation of PRP-EVs. It also reviews their applications in orthopedics and wound repair. The article highlights the importance of PRP-EVs in modern medicine and suggests that they could be a promising natural nanocarrier.

The review discusses extracellular vesicles derived from platelet-rich plasma(PRP-EVs). PRP promotes repair of the body's tissues and has been used in clinical practice for many years. Extracellular vesicles are granules released by cells that facilitate intercellular communication. Studies in recent years have revealed that PRP can also release extracellular vesicles that participate in the repair process of tissues. Here, we elaborate on PRP-EVs. Regarding PRP-EVs, current studies are limited to the animal level and have not yet been used in the clinical setting.

LINC00969 inhibits proliferation with metastasis of breast cancer by regulating phosphorylation of PI3K/AKT and ILP2 expression through HOXD8.

Background: Breast cancer (BC) is a malignancy that is inadequately treated and poses a significant global health threat to females. The aberrant expression of long noncoding RNAs (lncRNAs) acts as a complex with a precise regulatory role in BC progression. LINC00969 has been linked to pyroptotic cell death and resistance to gefitinib in lung cancer cells. However, the precise function and regulatory mechanisms of LINC00969 in BC remain largely unexplored. Methods: Cell proliferation, migration, and invasion of BC cells were evaluated using CCK-8 and Transwell assays. Western blotting was employed to analyze the protein expression levels of HOXD8, ILP2, PI3K, t-AKT, and p-AKT. Results: LINC00969 was drastically reduced in BC tissues LINC00969 overexpression markedly suppressed proliferation, migration, and invasion, and blocked PI3K and p-AKT protein expression in MCF-7 cells. Activation of the PI3K/AKT pathway reversed the suppressive effect of LINC0096 overexpression on the proliferation, migration, and invasion of MCF-7 cells. Moreover, LINC00969 overexpression enhanced HOXD8 and blocked ILP2 protein expression in MCF-7 cells. In contrast, activating the PI3K/AKT pathway had no effect on HOXD8 and blocked ILP2 protein expression in MCF-7 cells overexpressing LINC00969. HOXD8 knockdown enhanced ILP2, PI3K, and p-AKT protein expression, and the proliferation, migration, and invasion of MCF-7 cells co-transfected with si-HOXD8 and ov-LINC00969. LINC00969 regulated HOXD8 via binding to miR-425-5p. Conclusion: LINC00969 inhibits the proliferation and metastasis of BC cells by regulating PI3K/AKT phosphorylation through HOXD8/ILP2.

Intelligent and adaptive intra-channel and inter-channel fiber nonlinearity compensation in coherent optical transmission systems.

Fiber nonlinearity mitigation is a crucial technology for extending transmission reach and increasing channel capacity in high-baud rate wavelength division multiplexing (WDM) systems. In this work, we propose a novel, to the best of our knowledge, architecture that combines learned modified digital back-propagation (L-MDBP) to compensate for intra-channel nonlinearity and a two-stage decision-directed least mean square (DDLMS) adaptive equalizer to mitigate inter-channel nonlinearity. By leveraging globally optimized model parameters and adaptive channel estimation, the proposed scheme achieves superior performance and lower computation complexity compared with conventional DBP. Specifically, in an 8 × 64 Gbaud 16-ary quadrature amplitude modulation (16QAM) experimental system over 1600 km of standard single-mode fiber (SSMF), our approach shows a 0.30-dB Q2-factor improvement and a complexity reduction of 82.3% compared with DBP with 8 steps per span (SPS). Furthermore, we enhance the adaptability of the architecture by introducing an online transfer learning (TL) technique, which requires only 2% of initial training epochs.

Kirenol alleviates diabetic nephropathy via regulating TGF-ß/Smads and the NF-κB signal pathway.

CONTEXT: Kirenol possesses anti-inflammatory, antifibrotic and anti-arthritic effects. However, its reno-protective effects against diabetic nephropathy (DN) have not been evaluated. OBJECTIVE: This study explores the reno-protective effects of kirenol against DN and clarifies the potential mechanisms. MATERIALS AND METHODS: The mesangial cells were treated with 20 µM kirenol and 10 ng/mL human recombinant TGF-ß1 or 30 mM glucose for 24 h. Then the cells were harvested to assay the expression of the target genes or proteins. Thirty C57BL/6J male mice were given high-fat diet with streptozotocin injection to induce diabetes and then were randomized into three groups (n = 10): vehicle administration (DM group), 2 mg/kg kirenol (DM + kirenol group) and 200 mg/kg metformin (Met group) for 3 months, orally. A healthy group (Con, n = 10) was included as the control. RESULTS: Compared to the DM group, kirenol treatment decreased the phosphorylation of Smad2/3 and NF-κB (0.64- and 0.43-fold) as well as the accumulation of FN and Col IV (0.58- and 0.35-fold); moreover, the expression of IκBα was restored to normal level by kirenol treatment both in vivo and in vitro. After kirenol treatment, IL-6 expression was decreased 0.35- and 0.57-fold, and TNF-α expression was decreased 0.34- and 0.46-fold, in vitro and in vivo, respectively. Furthermore, kirenol alleviated the glomerular basement membrane thickness and foot process fusion. DISCUSSION AND CONCLUSIONS: Kirenol could alleviate DN by downregulating the TGF-ß/Smads and the NF-κB signal pathway. Our study provides a potential mechanism for the treatment of DN with kirenol.

Direct detection transmission of a PAM signal with power fading mitigation based on Alamouti coding and dual-drive MZM.

Power-fading impairment induced by fiber dispersion and photodiode detection imposes a fundamental limitation on the intensity-modulation direct-detection (IM-DD) transmission systems. In this work, we propose a cost-effective pulse-amplitude modulation (PAM) signal transmission scheme with power-fading mitigation enabled by Alamouti coding and dual-drive Mach-Zehnder modulator (DDMZM). By interleaving the symbol blocks in the time domain for upper- and lower-arm of the DDMZM, flat end-to-end frequency response can be obtained without spectral nulls after combining the photocurrents at odd and even time slots. For single channel demonstration, we experimentally transmit up to 160Gb/s PAM-4, 140Gb/s PAM-6, and 108Gb/s PAM-8 signals over 80 km standard single-mode fiber (SSMF) with bit-error rates (BERs) below the 20% soft-decision forward error correction (SD-FEC) threshold of 2.0×10-2. For wavelength division multiplexing (WDM) transmission, 8λ×150Gb/s PAM-4 signals spacing at 100 GHz can also achieve 80 km reach. Moreover, we compare the optical signal-to-noise ratio (OSNR) sensitivity with single sideband (SSB) scheme and evaluate the tolerance of bias deviation in numerical simulation. The proposed Alamouti coding-based scheme provides a hardware-efficient and dispersion-tolerant candidate for high-speed inter-data center interconnect (DCI) applications.

Overexpression of HOXD8 inhibits the proliferation, migration and invasion of breast cancer cells by downregulating ILP2 expression.

Breast cancer is one of the most common malignant tumors in women. Although a number of homeobox (HOX) genes are known to serve an important role in breast cancer, the role of HOXD8 in breast cancer remains unclear. The aim of the present study was to investigate the role of HOXD8 in the physiological behaviors of breast cancer cells. The Gene Expression Profiling Interactive Analysis database was used to analyze the expression of HOXD8 in patients with breast cancer and in healthy subjects. Western blotting was performed to determine the expression levels of HOXD8 in several breast cancer cell lines; subsequently, HOXD8 expression was knocked down and overexpressed in MCF-7 cells. Cell Counting Kit-8, colony formation, wound healing and Transwell assays were used to evaluate the effects of HOXD8 on breast cancer cell viability, proliferation, migration and invasion, respectively. Chromatin immunoprecipitation and dual-luciferase reporter assays were conducted to identify the binding sites between HOXD8 and inhibitor of apoptosis-like protein-2 (ILP2). In addition, ILP2 expression levels were knocked down in MCF-7 cells. The results demonstrated that the expression levels of HOXD8 were significantly downregulated in breast cancer tissues and cell lines, and that the overexpression of HOXD8 inhibited the proliferation, invasion and migration of cancer cells. HOXD8 was shown to bind to the ILP2 promoter to regulate the expression of ILP2. Furthermore, ILP2 knockdown reversed the effects of HOXD8 knockdown on breast cancer cell proliferation, invasion and migration. In conclusion, the findings of the present study suggested that HOXD8 may inhibit the proliferation, migration and invasion of breast cancer cells by downregulating ILP2 expression.

Polysaccharides from the Fleshy Fruits of Camellia oleifera Attenuate the Kidney Injury in High-Fat Diet/Streptozotocin-Induced Diabetic Mice.

The fleshy fruits of Camellia oleifera Abel are the immature fruits of C. oleifera, which are infected by Exobasidium vexans Massee and then turn to be intumescent and hollowed. They contain rich trace elements and vitamin C and are eaten directly as wild fruits in the Chinese countryside. Recent studies report that C. oleifera has anti-inflammatory and antioxidative effects. The current study, for the first time, evaluates the renal protective capacity of polysaccharides from the fleshy fruits of C. oleifera (CFFP) in streptozotocin-induced diabetic mice fed high-fat diets. The diabetic mice were orally administered CFFP for 3 months to evaluate the renoprotective function of CFFP. Our results indicated that 250 mg/kg CFFP significantly alleviated diabetes-induced renal injury by decreasing serum creatine, blood urea nitrogen levels, the kidney/body weight ratio, expression of fibronectin and collagen, as well as the secretion of tumor necrosis factor-α and interleukin-6. Additionally, 250 mg/kg CFFP could significantly ameliorate renal oxidative stress through increasing glutathione levels and lowering malondialdehyde contents. We confirmed that CFFP could exert antioxidative, anti-inflammatory, and antifibrosis activities. CFFP might be a potential therapeutic agent, and the fleshy fruits of C. oleifera might be a diet therapy for diabetic patients in the future.

Establishment and Evaluation of a Novel Method Based on Loop-Mediated Isothermal Amplification for the Rapid Diagnosis of Thalassemia Genes.

PURPOSE: Currently, thalassemia is commonly detected using gap-polymerase chain reaction (PCR) and deoxyribonucleic acid (DNA) reverse dot blot, which have high requirements of space, instruments, and personnel. Therefore, it is necessary to develop a new method for thalassemia detection with high sensitivity, low cost, and simple and fast operation. In this study, we aimed to design and evaluate a new method for detecting three α-thalassemia genes including -Southeast Asian (SEA), -α3.7, and -α4.2 and five ß-thalassemia genes including 654M, 41/42M, -28M, 17M, and 27/28M based on loop-mediated isothermal amplification (LAMP). METHODS: Primer sequences were designed using Primer Explorer V4 software. Blood samples (5 mL) were collected from all participants in EDTA. DNA was extracted using Chelex 100 and was subjected to LAMP. LAMP products were detected by fluorescence development in ultraviolet light. RESULTS: We found that LAMP assays for positive samples of thalassemia reached a plateau before 60 minutes, whereas the negative control samples entered the plateau after 70 minutes or showed no amplification. The concentration range of positive reactions was between 20-60 pg/µL and 20-60 ng/µL. Additionally, there were no cross-reactivities among 8 thalassemia subtypes. For clinical samples, the positive sample tube showed strong green fluorescence, whereas the negative tube showed light green fluorescence. According to these results, the LAMP method has high sensitivity for detecting thalassemia (252/254). However, 43 false-positive results were obtained in the LAMP test. The LAMP assay was also of low cost and with simple and fast operation. CONCLUSION: The novel LAMP assay can be completed within 60 min using a heating block or a water bath, and the result can be read visually based on color change to detect thalassemia. The LAMP assay fulfills the requirements of field application and resource-limited areas, especially those with primary hospitals and rural areas.

GdCl3 attenuates the glomerular sclerosis of streptozotocin (STZ) induced diabetic rats via inhibiting TGF-ß/Smads signal pathway.

Diabetic nephropathy (DN) is the most serious end-stage renal disease which characterized by renal glomerular sclerosis including glomerular hypertrophy, glomerular basement membrane (GBM) thickening, mesangial expansion and renal fibrosis. TGF-ß/Smads signal pathway plays a crucial role in the development of renal fibrosis. In this study, we found that GdCl3 which was an agonist of Calcium-sensing receptor (CaSR) could repress the activation of TGF-ß/Smads signal pathway induced by TGF-ß1 or high glucose and then alleviated the accumulation of extracellular matrix (ECM) in mesangial cells and the kidney of type1 diabetic rats. Further study indicated that GdCl3 could induce the binding of CaSR and TßR II and then both of these two receptors translocated from cell membrane to cytoplasm, in this case, TßR II on the cell membrane was decreased and then desensitized to the stimulation of its ligand TGF-ß1, so that the activation of its downstream factors such as Smad2 and Smad3 were blocked, finally, ECM expression in mesangial cells were inhibited. We concluded that GdCl3 could alleviate the accumulation of ECM in mesangial cells via antagonizing TGF-ß/Smads signal pathway in diabetes mellitus.

Inhibitor of apoptosis protein-like protein-2 as a novel serological biomarker for breast cancer.

Inhibitor of apoptosis protein-like protein-2 (ILP-2) has only been detected in the testis and in lymphoblastoid cells. Although previous studies have not reported the presence of ILP-2 in breast cancer tissues, this study indicates the presence of ILP-2 in breast cancer serum samples. To validate whether ILP-2 is a novel serological biomarker for breast cancer, we conducted two-dimensional gel electrophoresis (2DE) and matrix-assisted laser desorption/ionization-time of flight mass spectrometry analysis on 400 breast cancer serum samples and 40 non-cancer serum samples (i.e., healthy controls). We then performed a Western blot analysis of 10 breast cancer serum samples and 10 non-cancer serum samples. Finally, we analyzed 35 serum samples from healthy controls or subjects with breast cancer, other types of cancer, galactophore hyperplasia or breast cancer post-surgery by using 2DE and enzyme-linked immunosorbent assay. Our results indicate that ILP-2 is a novel breast cancer biomarker in the peripheral blood.