This study investigates the transcriptomic variations in the jejunum and liver of Golden Montazah (GM) chickens to better understand the biological mechanisms influencing poultry growth and production. Given the vital role of poultry in fulfilling global protein demands, especially with the rising consumer preference for chicken, it is essential to explore these underlying genetic and molecular factors that drive growth. From a larger cohort of 480 GM chickens, the top 10 males in both the high-weight (HW) and low-weight (LW) groups were selected for RNA sequencing. Tissues from their jejunum and liver were collected for transcriptomic analysis. The results revealed 38 up- and 36 down-regulated genes in the jejunum, while the liver exhibited 109 up- and 74 down-regulated genes. Among these, notable differentially expressed genes (DEGs) such as CHST14 and LOC429682 in the jejunum, alongside RBP2 and STC2 in the liver, appeared to be integral to growth regulation, immune response, and metabolic processes. Functional enrichment analyses using GO and KEGG pathways highlighted processes like cytokine-cytokine receptor interactions in the jejunum and steroid biosynthesis in the liver. Additionally, protein–protein interaction networks identified key hub genes essential for various biological functions. Overall, our findings emphasize the distinct gene expressions profiles associated with body weight in the jejunum and liver, providing valuable insights for genetic improvement in poultry breeding. Understanding these molecular mechanisms paves the way for targeted strategies to enhance growth performance in the poultry industry.

Infective endocarditis (IE) is a severe disease that damages heart valves and can lead to major complications, including heart failure, embolic events, and stroke. It is the third most common fatal infection worldwide. This review examines the clinical burden of IE, its microbial causes, and the ongoing challenges in diagnosis. Particular attention is given to the limitations of traditional blood cultures, especially in detecting culture-negative and fastidious organisms, and to the emerging role of metagenomic approaches. A comprehensive review of the literature was conducted, focusing on diagnostic methods such as blood cultures, molecular assays, and metagenomic sequencing. The role of bacterial biofilms in treatment failure and antibiotic resistance was also explored. Metagenomics, especially cell-free metagenomic DNA (cf-mDNA), shows promise as a non-invasive diagnostic tool that can overcome culture-based limitations. However, standardized protocols and prospective studies are needed to validate its routine clinical application in IE diagnosis and management.

Colorectal cancer (CRC) is a serious public health concern worldwide. Immune checkpoint inhibition medication is likely to remain a crucial part of CRC clinical management. This study aims to create new super paramagnetic iron oxide nano-carrier (SPION) that can effectively transport miRNA to specific CRC cell lines. In addition, evaluate the efficiency of this nano-formulation as a therapeutic candidate for CRC. Bioinformatics tools were used to select a promising tumor suppressor miRNA (mir-497-5p). Green route, using Fusarium oxyporium fungal species, manipulated for the synthesis of SPION@Ag@Cs nanocomposite as a carrier of miR-497-5p. That specifically targets the suppression of PD1/PDL1 and CTLA4pathways for colorectal therapy. UV/visible and FTIR spectroscopy, Zeta potential and MTT were used to confirm the allocation of the miR-497 on SPION@Ag@Cs and its cytotoxicity against CRC cell lines. Immunofluorescence was employed to confirm transfection of cells with miR-497@NPs, and the down- regulation of CTLA4 in HT29, and Caco2 cell lines. On the other hand, PDL1 showed a significant increase in colorectal cell lines (HT-29 and Caco-2) in response to mir497-5p@Nano treatment. The data suggest that the mir-497 -loaded SPION@Ag@Cs nano-formulation could be a good candidate for the suppression of CTLA4in CRC human cell lines. Consequently, the targeting miR-497/CTLA4 axis is a potential immunotherapy treatment strategy for CRC.

Background Soy protein isolate (SPI) has gained popularity as an alternative to animal proteins. Soy consumption may have a link to rising serum estrogen in humans. This concern is attributed to phytoestrogens, specifically isoflavones present in soy protein, acting as estrogen substitutes and modulators. Objective The objective of this research was to assess the influence of SPI supplementation on estradiol hormone levels and the expression of genes associated with estrogen synthesis in female rats. Materials and methods Female Wistar rats (n=18) were evenly divided into three groups: group 1 (normal control) received oral administration of a saline vehicle. Group 2 (low dose) received 450 mg/kg body weight of SPI for 30 days. Group 3 (high dose) received 900 mg/kg body weight of SPI for 30 days. All administrations were conducted intragastrically. Results and conclusion The results of our study indicate that there was a significant increase in the levels of estradiol hormone in groups receiving low and high doses of SPI when compared with the control group. There was an upregulation in the messenger ribonucleic acid expression of the Cyp19 gene in low-dose and high-dose groups. Moreover, the low-dose group showed upregulation in the expression of the HSD3B gene. These genes are involved in the biosynthesis pathway of estrogen hormone in females. Therefore, the use of SPI should be cautious because it contains phytoestrogens (isoflavones), which have structural similarities to endogenous female estrogen and may cause hormonal disturbance in females.

Polydrug use among teenagers is widespread and emergent either among athletes or non-athletes. It is reported that stanzolol (Stanz) is commonly abused with cannabis (Cann), this combination probably affects the testicular functions negatively. Aim The present study aimed to evaluate the toxic effects of Stanz and or Cann on reproductive hormones and testicular enzymes. Male Wistar rats were administered Stanz (5 mg/kg, s.c., once per week) and Cann (20 mg/kg, i.p., daily) either alone or in combination for two months, in exercise or sedentary conditions. Swimming exercise protocol was applied. Administration of both Stanz and Cann induced testicular damage, as evidenced by altered hormones, oxidative stress, and testicular enzymes. The testis tissue was significantly injured by the combined administration. In serum, levels of free testosterone, follicular stimulating hormone (FSH), lutenizing hormone (LH) were markedly reduced, while sorbitol dehydrogenase level increased. Moreover, tissue malondialdehyde (MDA) was significantly increased, glutathione (GSH) content decreased, testicular N-acetyl-β-glucosaminidase (NAG) and Myeloperoxidase (MPO) were increased. SIRT1 and STS mRNA expression were downregulated. Besides, distinct histopathological changes were detected in testis of Stanz and Cann injected rats. Nevertheless, Stanz, Cann or combined treatment showed a considerable up-regulation of immunoexpression of inducible nitric oxide synthase (iNOS) and caspase-3 in testes tissue. Oxidative stress and inflammation played a significant role in the observed pathological changes. Training was partially ameliorating for the observed effects. Use of the drugs in sedentary rats had more detrimental effects on testes. Although exercise could palliate the damage partially, it was not fully protective.

Soy protein isolate (SPI) is a prevalent ingredient in various dairy, meat products, and health drinks. Concerns have been raised regarding potential adverse effects of soy consumption on male health, such as feminization and infertility. This concern is attributed to phytoestrogens, specifically isoflavones present in soy, acting as estrogen substitutes and modulators. This study aims to investigate the effects of soy protein isolate supplementation on testosterone hormone levels and the expression of genes associated with testosterone synthesis. Male rats (n = 18) were evenly divided into three groups: Group 1 (Normal Control) received oral administration of a saline vehicle. Group 2 (Low Dose) received 450 mg/kg body weight of soy protein isolate for 30 days. Group 3 (High Dose) received 900 mg/kg body weight of soy protein isolate for 30 days. All administrations were conducted intragastrically. Testosterone hormone levels were decreased with a disturbance in the mRNA expression of genes (Hsd17b6, SRD5A1, Akr1c3, Cyp17a1 and Hsd3b) involved in the biosynthesis of testosterone hormone in the low and high dose groups in in comparison to the control group. In the testes of the high dosage group, histopathological analysis showed a noticeable irregularity around the periphery of the seminiferous tubules. Our results have shown damage to testicular tissue and reduced genetic expression of certain genes responsible for the formation of testosterone hormones, followed by a reduction of testosterone hormones in the group of rats that were given a high dose of SPI for 30 days.

Skeletal muscle-adipose tissue crosstalk is crucial for developing therapeutic strategies for various metabolic disorders. While obesity is known to disrupt microRNA (miRNA) expression profiles in skeletal muscle, a comprehensive understanding of this phenomenon remains elusive. Therefore, our study aims to investigate the impact of high-fat diet (HFD)-induced obesity on miRNA dysregulation within skeletal muscle tissue at distinct time points. In HFD model, rats received HFD for 2, 4, 6, 8, or 10 weeks. Body weight was determined at 2, 4, 6, 8, and 10 weeks. At the end of each interval, group of animals (n = 8) were sacrificed and skeletal muscle tissues were harvested to assess miRNAs expression levels. HFD administration for 8 and 10 weeks resulted in marked weight changes in comparison to control group. There were not much significant changes in body weight seen in low durations of HFD feeding. Alterations in miR130a, miR30a-5p, miR133a-5p, miR193a-5p, and miR125a-5p expression levels were observed at different time point relative to control rats. While miR let-7 and miR107-5p were upregulated at all-time points compared to control animals. Thus, skeletal muscle miRNA dysregulation likely plays a role in HFD-induced obesity.

Purpose Breast cancer is one of the leading types of cancer diagnosed in women. Despite the improvements in chemotherapeutic cure strategies, drug resistance is still an obstacle leading to disease aggressiveness. The small non-coding RNA molecules, miRNAs, have been implicated recently to be involved as regulators of gene expression through the silencing of mRNA targets that contributed to several cellular processes related to cancer metastasis. Hence, the present study aimed to investigate the beneficial role and mechanism of miRNA-34a-based gene therapy as a novel approach for conquering drug resistance mediated by ATP-binding cassette (ABC) transporters in breast cancer cells, besides exploring the associated invasive behaviors. Material and Methods Bioinformatics tools were used to predict miRNA ABC transporter targets by tracking the ABC transporter pathway. After the establishment of drug-resistant breast cancer MCF-7 and MDA-MB-231 sublines, cells were transfected with the mimic or inhibitor of miRNA-34a-5p. The quantitative expression of genes involved in drug resistance was performed by QRT-PCR, and the exact ABC transporter target specification interaction was confirmed by dual-luciferase reporter assay. Furthermore, flow cytometric analysis was utilized to determine the ability of miRNA-34a-treated cells against doxorubicin uptake and accumulation in cell cycle phases. The spreading capability was examined by colony formation, migration, and wound healing assays. The apoptotic activity was estimated as well. Results Our findings firstly discovered the mechanism of miRNA-34a-5p restoration as an anti-drug-resistant molecule that highly significantly attenuates the expression of ABCC1 via the direct targeting of its 3′- untranslated regions in resistant breast cancer cell lines, with a significant increase of doxorubicin influx by MDA-MB-231/Dox-resistant cells. Additionally, the current data validated a significant reduction of metastatic potentials upon miRNA-34a-5p upregulation in both types of breast cancer-resistant cells. Conclusion The ectopic expression of miRNA-34a ameliorates the acquired drug resistance and the migration properties that may eventually lead to improved clinical strategies and outcomes for breast cancer patients. Additionally, miRNA-34a could be monitored as a diagnostic/prognostic biomarker for resistant conditions.

TOMATO yellow leaf curl disease (TYLCD) is a significant limitation factor in tomato crops and ranks among the top 10 plant viruses affecting the production of many crops, particularly tomatoes, leading to considerable economic losses without an efficient control strategy till now. In this study, PCR technique was used to amplify partial sequences (670 bp) of tomato yellow leaf curl virus (TYLCV) genome, specifically spanning the trans-activator protein (C2), replication enhancer protein (C3) genes, as well as partial parts of replication (Rep) and coat protein (CP) genes. These sequences were obtained from naturally infected tomato plants collected from different governorates in Egypt. The DNA sequence analyses of the current Egyptian isolate was annotated and deposited in the GenBank with an accession ID MZ546492, revealing high nucleotide sequence identities (99.3 %) to TYLCV isolates in the GenBank. The transmission and host range assays confirmed that the whitefly is the sole transmitter, and tomatoes, zucchini, cucumber, pepper, jimsonweed, and common bean as a host for TYLCV. To explore alternative control strategies, an in-silico approach was employed to generate the possible siRNA-producing sequences that could be used to knock down TYLCV in infected plants. The current findings support the development of a rapid, reliable, and robust molecular detection and identification tool of TYLCV in tomato germplasm to ensure the safe and sustainable production of TYLCV-free tomatoes. Additionally, in silico analysis indicated the possibility of using siRNA to control TYLCV.

Alzheimer’s disease (AD) is a neurodegenerative disorder that is clinically characterized by deteriorating cognitive function. Quercetin (Q), a bioflavonoid, has been reported to slow down AD progression. Q at a dose of 50 mg/kg-1 shows an important therapeutic effect in aluminum chloride (AlCl3)-induced Alzheimer’s disease, which has been previously published by us. Here, this study aimed to highlight the neuroprotective effect of quercetin on hallmark genes in AlCl3-induced Alzheimer’s disease in rats. Wistar male rats were subjected to a vehicle group, AlCl3 group, and co-administration with AlCl3 + Q50 for 60 sequential days. Behavioral tests and qPCR were performed to assess the efficacy of Q. The co-administration of quercetin (50 mg kg-1) has a significant effect on memory deficits. Furthermore, AlCl3 + Q50 group resulted in significantly decreased amyloid precursor protein levels (APP), β-amyloid converting enzyme 1 (BACE1), and presenilin I (PSEN1) and increased the expression of ADAM17 in the hippocampus tissue compared to AlCl3 group (p < 0.05). The current study showed that the quercetin’s neuroprotective properties may involve its ability to target the most significant Alzheimer’s disease-related genes and slow the progression of cognitive impairment.

Background and objective Wastewater treatment plants (WWTPs) represent a source of airborne bacteria. The presence of airborne bacteria in the environment of WWTPs could be considered as a potential health hazard for the exposed workers. This study aimed to isolate and identify cultivable bacteria from bioaerosols of different sites in a WWTP using 16S rRNA gene identification, as a first step to identify the pathogenic health hazards among the exposed workers. Materials and methods Air samples were collected from various locations in a selected WWTP. Airborne microorganism samples were collected on the nutrient agar plates by the settle-plate technique and were identified by the 16S rRNA gene sequencing technique. Results A total of 32 bacterial isolates were collected and sequenced. The study identified 25 different bacterial species. Of the 25 different strains, 10 (40%) belonged to pathogenic bacteria. Overall, 40% of the isolated pathogenic species were from the secretary room locations. The isolated bacterial species were Staphylococcus sp., Bacillus sp., Rhodococcus sp., Cellulosimicrobium funkei, Kytococcus sedentarius, and Kocuria rosea. The highest percentage occurrence was Bacillus sp. (37.5%), followed by Staphylococcus sp. (18.75%). Conclusions Disseminated infection can be associated with isolated pathogen, and this result gives a warning of the danger of the spread of pathogenic aerobic bacteria in WWTPs and their existence in indoor environments.

Hepatocellular carcinoma (HCC) is a fatal disease, accounting for 75–85% of primary liver cancers. The conclusive research on miR-181c-5p’s role in hepatocarcinogenesis, whether it has oncogenic effects or acts as a tumor repressor, is limited and fluctuating. Therefore, the current study aimed to elucidate the role of miR-181c-5p in HCC in silico and in vivo. The bioinformatics analysis of miR-181c-5p expression data in HCC using several databases strongly shed light on its involvement in HCC development, but also confirmed the fluctuating data around its role. miR-181c-5p was proven here to have an oncogenic role by increasing HepG2 cells’ viability as confirmed by MTT analysis. In addition, miR-181c-5p was upregulated in the HCC positive control group and progressed the HCC development and malignant features by its forced expression in an HCC mouse model by targeted delivery using a LA-PAMAM polyplex. This is indicated by the cancerous gross and histological features, and the significant increase in liver function biomarkers. The functional enrichment bioinformatics analyses of miR-181c-5p-downregulated targets in HCC indicated that miR-181c-5p targets were significantly enriched in multiple pathways and biological processes involved in HCC development. Fbxl3, an example for miR-181c-5p potential targets, downregulation and its correlation with miR-181c-5p were validated by qPCR. In conclusion, miR-181c-5p is upregulated in HCC and has an oncogenic role enhancing HCC progression.

Polycystic ovary syndrome (PCOS) is a multi-factorial endocrine disorder associated with hyperandrogenism. Dehydroepiandrosterone (DHEA) administration to prepubertal rats stimulates androgen biosynthesis and generation of the PCOS model. The present study aimed to evaluate the anti-androgenic effects of quercetin (Q) in comparison with metformin (MET) on hyperandrogenism and ovarian dysfunction in a DHEA-induced PCOS rat model. After induction of PCOS, female rats were allocated into six groups with 7 rats in each group: normal control; PCOS (DHEA), MET (25 mg/kg, oral administration), Q (25 mg/kg, oral administration), DHEA + MET (25 mg/kg, oral administration), and DHEA + Q (25 mg/kg, oral administration) for 28 days. MET and Q individually reduced body weight, serum free testosterone (T) and luteinizing hormone (LH), and LH/follicle-stimulating hormone (FSH) ratio in the PCOS rats. Both treatments elevated estradiol (E2) level, ovarian aromatase protein content, and E2/free T ratio in the PCOS rats. Additionally, MET and Q increased preantral, antral, and preovulatory follicles and corpora lutea counts, while both treatments decreased atretic follicle count and eliminated the formation of cysts in the PCOS rats. MET and Q reduced ovarian Bax and elevated Bcl-2 protein abundance in the PCOS rats. Our study revealed that Q is as effective as MET in reducing hyperandrogenism via decreasing free T level and improving hypothalamic-pituitary-ovarian axis function. The results suggest that MET and Q may enhance E2 concentration, ovarian aromatase protein content, folliculogenesis, and decrease atresia via attenuation of hyperandrogenism in PCOS rats.

Wool has the tendency to turn into felt during agitation in washing machines. Thus, a benign non-polluting method for the production of machine-washable wool was developed herein. Initially, a proteolytic bacteria was isolated from hot region soil. The bacterial isolate was identified as Bacillus safensis FO-36bMZ836779 according to the 16S rRNA gene sequencing. Afterwards, the extracellular protease produced by this isolate was covalently immobilized in order to enhance its stability under non-ambient conditions which are usually adopted in industrial sectors like textile industries. Sericin, which is usually discharged into degumming effluent of natural silk, was utilized to prepare the immobilization carrier. Box–Behnken design was adopted in order to hone the preparation of the sericin–polyethylene–imine–glutaraldehyde activated agar carrier. The pH and temperature profiles of the free and immobilized proteases were compared. Later, wool fibres were bio-treated with both the free and the immobilized enzymes. The effect of process conditions on the resistance of the bio-finished wool to felting was investigated. The alteration in the fibre morphology was monitored using SEM. Amino acid analysis and alkali solubility tests were adopted to assign any change in the chemical structure of the bio-treated wool. The influence of bio-treatment of wool on its inherent properties was assigned. Results revealed that bio-treatment of wool with the said enzyme led to production of machine-washable wool without severe deterioration in the fibres’ properties. In an energy- and water-consuming process, the hot solution from bio-treatment bath was used successfully in dyeing of wool.

BACKGROUND Hepatocellular carcinoma (HCC) is the fifth most common cancer. Differential expression of microRNAs (miRNAs)-326, miRNA-424, and miRNA-511 has been associated with the diagnosis and prognosis of HCC in different populations. However, limited information is available regarding their expression in Egyptian HCC patients. AIM To assess the role of circulating miRNAs-326, miRNA-424, and miRNA-511 in Egyptian HCC patients. METHODS This prospective observational study included 70 HCC patients and 25 healthy controls. The circulating levels of these three miRNAs were evaluated by real-time PCR. Receiver operating characteristic curve analysis was used to test the diagnostic accuracy of microRNA expression levels. RESULTS All miRNAs were differentially expressed in HCC patients; miRNAs326 and miRNA-424 were upregulated, while miRNA-511 was downregulated. Both miRNA-326 and miRNA-424 showed sensitivity and specificity of 97%, 71.4%, and 52%, 60%, respectively, to differentiate HCC from controls. Moreover, miRNA-326 was associated with survival and could differentiate between Child grades (A vs B); miRNA-424 significantly differentiated early vs intermediate stages of HCC; while miRNA-511 was significantly correlated with response to modified Response Evaluation Criteria in Solid Tumors (mRECIST). CONCLUSION We conclude that miRNA-326, miRNA-424, and miRNA-511 have diagnostic and prognostic roles in Egyptian patients with hepatitis C virus-related HCC and should be considered for better disease management.

Background Genetic variants of Patatin-like phospholipase domain-containing protein 3 (PNPLA3) and transmembrane 6 superfamily member 2 (TM6SF2) genes have been reported with the development of hepatocellular carcinoma (HCC). This study aims to explore the role of The PNPLA3 rs738409 and TM6SF2 rs58542926 single-nucleotide polymorphisms (SNPs) on the incidence and survival of HCV-induced HCC in Egyptians. Methods and results This case-control study included (120) HCC and (144) hepatitis C virus (HCV) patients. Baseline clinical, laboratory, tumor characteristics data, HCC recurrence, and overall survival were collected. PNPLA3 rs738409 and TM6SF2 rs58542926 polymorphism were detected by TaqMan allelic discrimination assay. We found that HCC patients were significantly older with male predominance. A significant difference between the TT genotypes of TM6SF2 frequency was observed in HCC compared with HCV patients. Moreover, the T allele of TM6SF2 distributions revealed a significant contribution to the different stages of HCC ( p =0.03). Both PNPLA3 rs738409 and TM6SF2 rs58542926 variants showed a significant relation with treatment response according to the modified RECIST criteria. Age and diabetes mellitus were the independent factors associated with the development of HCC by multivariate regression analysis. Conclusions TM6SF2 rs58542926 polymorphism, not PNPLA3 rs738409, could be implicated in the development of HCV-induced HCC and its progression.

Aim: The aim was to investigate the expression profile of miR-516a-3P and its correlation with the PNPLA3 rs738409 polymorphism in Egyptian hepatitis C virus (HCV) and hepatocellular carcinoma (HCC) patients. Materials & methods: miR-516a-3P was quantified and rs738409 was genotyped by quantitative reverse transcription PCR. Results: miR-516a-3P was significantly upregulated in HCC patients compared with HCV patients (p = 0.001). Receiver operating characteristic curve analysis confirmed that miR-516a-3P discriminates HCC from HCV (p = 0.001). A significant (p = 0.015) correlation between miR-516a-3p level and PNPLA3 rs738409 genotypes was recorded in HCV patients, yet it was not recorded in either healthy individuals or HCC patients. miR-516a-3p level was significantly (p = 0.001) higher in HCV patients carrying the rs738409 GG genotype than in those carrying the CC genotype. Conclusion: miR-516a-3P is a potential biomarker in HCC. PNPLA3 rs738409 GG carriers affect miR-516a-3P expression in HCV, and this may highlight a new mechanism in liver disease.

Aluminum (Al) exposure is one of the environmental factors involved in the pathogenesis of male infertility as a global health problem. Quercetin (Q) is a naturally occurring flavonol that improved testosterone (T) level and spermatogenesis against heavy metals-, diabetes-, and cancer-induced testicular intoxication in male rats. The present study aimed to investigate the therapeutic potential of Q against aluminum chloride (AlCl3)-induced testicular dysfunction in rats through evaluation of hormones of the pituitary-testicular axis, sperm parameters in the epididymis, and histological alterations in rat testis. After induction of testicular dysfunction in male rats by oral administration of AlCl3 (50 mg/kg) for 28 days, the therapeutic Q dose (50 mg/kg) was orally administered to rats for 28 days. The rats were divided into four groups (each group comprising eight rats): Normal control (NC), Q, AlCl3, and Q+ AlCl3. Q administration increased final body weight and genital organs' relative weight, and serum free testosterone (T), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) in the AlCl3-treated rats. Also, Q increased sperm count, motility, and progressive motility in the epididymis in AlCl3-treated rats. Further, Q administration to AlCl3-treated rats caused regeneration of the germinal epithelium in the seminiferous tubules and increased spermatocytes within the lumen. The current study suggests that Q administration may provide a significant therapeutic effect against AlCl3-induced testicular dysfunction in rats via improving the pituitary-testicular axis hormones, leading to increased sperm count and motility in the epididymis; and amelioration of histological alterations observed in the testes of AlCl3-rats.

Hepatocellular carcinoma (HCC) is one of most common causes of cancer death worldwide. MicroRNA (miRNA) replacement gene therapy is a novel approach for HCC management. MiR-218 is a promising tumor suppressor miRNA that is down-regulated in HCC. Here, our aim was the targeted delivery of miR-218 expressing DNA plasmid (pmiR-218) to suppress HCC in vitro and in vivo. Hyperbranched polyamidoamine was synthesized via simple and economically one-pot reaction followed by decoration with lactobionic acid (LA-PAMAM) to selectively deliver and restore miR-218 expression in HCC. In vitro cytotoxicity investigations revealed the high biocompatibility of LA-PAMAM. Furthermore, decoration of hyperbranched polymer with LA moieties enabled LA-PAMAM to deliver pmiR-218 more efficiently to HepG2 cells compared to both PMAMA and naked pmiR-218. Such efficient delivery of miR-218 resulted in suppression of HepG2 proliferation and down-regulation of its oncogenic HOXA1 target. In vivo, LA-PAMAM/pmiR-218 treatment of HCC induced by DEN and CCl4 in mice leads to an obvious decrease in the number and size of HCC nodules. In addition, LA-PAMAM/pmiR-218 significantly improved the liver histological features, as well as down-regulated the HOXA1 in liver tissue. In conclusion, this study showed the potential of LA-PAMAM carrier for the targeted delivery of tumor suppressor miR-218 as a therapeutic candidate for HCC.

The hydrophobic nature of wool induced by its surface lipid barrier hinders its wettability during processing. Scouring of wool is conducted to remove this lipid barrier and facilitate any wet processes. Scouring of wool is conducted using soda ash followed by rinsing with huge amount of water to ensure complete removal of alkali. This work aimed at utilization of thermophilic lipase enzyme for removal of wool surface lipid barrier without deterioration on the fibre interior. A thermally stable lipase enzyme was produced from thermophilic microorganism; namely Bacillus aryabhattai B8W22, and was utilized in bio-scouring of wool. The produced enzyme was immobilized on sericin-based discs to enhance its stability and to make it reusable. The activity of both free and immobilized lipase enzymes at different conditions was assessed. The effects of bio-scouring of wool on its dyeability with acid, basic, and reactive dyes, as well as on some of its inherent properties, were monitored. Results showed that the bio-scoured wool exhibits enhanced dyeability with the said classes of dyes more than that of conventionally scoured samples. One-bath scouring and dyeing of wool fibres in two successive steps was conducted to reduce consumption of water and energy during wet processing of wool.