Topographical anatomy of the mandibular foramen in the dromedary camels (Camelus dromedarius): an extraoral approach for the inferior alveolar nerve blocks.

Understanding the clinical anatomy of the head is essential for performing proper inferior alveolar nerve (IAN) block anesthesia to facilitate invasive dental procedures in camels. However, osteometric data related to the IAN in camels are lacking. This study was carried out to accurately locate the mandibular foramen (MF) and the course of the IAN in the camel head and to establish an approach for its localization in clinical practice. To achieve these aims, eight osteometric measurements were used to determine the location of the MF in relation to its surrounding structures in six cadaveric skulls of adult camels. Four camel heads were dissected, and the course of the IAN inside the mandibular canal was studied. In addition, four heads were used as a trial for the extraoral approach to the IAN block using contrast radiographs based on established metric indices. Dissection of the four camel heads revealed that the MF was located near the intersection of two lines passing through the occlusal surface of the mandibular cheek teeth and at the midpoint of the zygomatic process of the temporal bone. Significant differences were not observed between the right and left mandibles. Successful deposition of the contrast medium near the MF was observed in all examined specimens. This study reports a new, simple approach to reaching the IAN at the MF. However, further clinical validation of the proposed technique is required.

Evaluation of anti-cancer effects of carnosine and melittin-loaded niosomes in MCF-7 and MDA-MB-231 breast cancer cells.

Background: We investigated the anti-cancer effect of carnosine-loaded niosomes (Car-NIO) and melittin-loaded niosomes (Mel-NIO) with olaparib in breast cancer cell lines (MCF-7 and MDA-MB-231). Methods: The thin film method was used for preparing the niosomes and characterized in terms of morphology, size, and polydispersity index (PDI). We further evaluated the impact of these peptides on breast cancer cells viability, RT-qPCR assays, malondialdehyde (MDA) activity, and cell cycle progression, to determine if these are linked to carnosine and melittin's anti-proliferative properties. Results: Car-NIO and Mel-NIO in vitro study inhibited cancer cell viability. They have also upregulated the expression of protein 53 (P53), BCL2-Associated X Protein (Bax), caspase-9, caspase-3, programmed cell death 4 (PDCD4), and Forkhead box O3 (FOXO3), while downregulated the expression of B-cell lymphoma 2 (Bcl2), poly (ADP-ribose) polymerase (PARP 1), and MicroRNA-183 (miRNA-183). The MCF-7 cells were arrested at the G2/M phase in Car-NIO, on the other hand, the MDA-MB-231 cells were arrested at the S phase. While the Mel-NIO and olaparib arrested the MCF-7 and MDA-MB-231 cells at the G0/1 phase. Conclusion: Our study successfully declared that Mel-NIO had more anti-cancer effects than Car-NIO in both MCF-7 and MDA-MB-231 breast cancer cells.

Probiotics-loaded nanoparticles attenuated colon inflammation, oxidative stress, and apoptosis in colitis.

Promising therapy is needed for treating inflammatory bowel diseases (IBD) to overcome current treatment that inefficient and associated with unnecessary health risks. Recently, the concept of incorporating natural products into nanocarriers has been intended as a promising therapy for treating IBD via modulating their stability and bioavailability. Thus, we aimed to explore the potential alleviating effects of dietary nano-supplement combined with bacillus strains (Bacillus amyloliquefaciens; BANPs) in colitis model. Rats were orally gavaged by 5% DSS and the efficacy and mechanistic actions of BANPs were evaluated by assessing the severity of clinical signs and inflammatory and apoptosis response, histopathological and immunohistochemistry examination in colonic tissues. The severity of clinical signs was successfully alleviated and fecal Lcn-2 levels, an important colitic marker, were decreased in BANPs then free BA treated groups. In contrast, inflammatory markers overexpression IL-6, IL-1ß, TNFα, COX-2, and iNOS in the colitic group were reduced more prominently in BANPs treated group, unlike free BA. The amelioration of BANPs to colon injury was also correlated with oxidative stress suppression along with restoring total antioxidant capacity. Interestingly, BANPs treatment modulated apoptotic markers as proved by downregulation of cytochrome c, and caspase-3 and upregulation of Bcl-2 and Bax than free BA. The severity of the histopathological alterations in the colon was greatly reduced in BANPs than free BA groups. Remarkably, over-expression of ki67 and IL-6 in colonic tissues were suppressed in BANPs group. These findings together highlighted the beneficial efficacy of BANPs in IBD treatment which are evidenced by colonic inflammation alleviation. Taken together, these results recommend that BANPs is a promising agent that encourages its possible therapeutic role in colitis treatment.

Mesenchymal stem-cells' exosomes are renoprotective in postmenopausal chronic kidney injury via reducing inflammation and degeneration.

Chronic kidney disease (CKD) is an important global disease its rates are increasing worldwide. CKD is caused by injuries to kidney tissue that exceeds the rate of regeneration, which with time lead to irreversible renal damage and CKD become evident. In females, diminished estrogen supply in the postmenopausal period is associated with greater risk for developing CKD. In this study we isolated exosomes from bone marrow mesenchymal stem/stromal cells (BM-MSCs) and tested their therapeutic effects on post-menopause CKD (PM-CKD) and compared their effects with BM-MSCs. The menopause model was achieved by bilateral ovariectomy in 8-months-old female albino rats, then no treatment, 2 million BM-MSCs or 100 µg of exosomes (Exo) was given intravenously in tail vein to ovariectomized rats and the study continued for 8 weeks post-ovariectomy. Changes in weight, urine volume, urine protein content, kidney function biochemical parameters (creatinine and BUN), Kidney oxidative stress (MDA), kidney antioxidant parameters (SOD, GPx and CAT), histopathological changes, immunohistochemical expression of KIM-1 and, finally, genes related to renal damage (peroxiredoxin-3, KIM-1 and ICAM-1) and inflammation (TNF-α, Cox2 and IL-6) were recorded for all study groups. Post-ovariectomy there was an increased body weight, drastic reduction of estrogen and progesterone levels, reduced urine output, increased urinary protein excretion, elevated serum creatinine and BUN, increased MDA and reduced GPx SOD, and CAT in kidney tissue, chronic inflammation, degenerative and fibrotic lesions in histopathological examination, high expression of KIM-1 immunohistochemically and changes in gene expression analyses all pointing to the development of CKD in the study rats. In the PM-CKD groups receiving BM-MSCs or Exo, the whole chronic inflammatory picture was completely reversed towards a much normal kidney structure and function. The improvements were more observable with Exo compared to BM-MSCs. Overall, our results show for the first time that exosomes isolated from BM-MSCs are more potent in reducing chronic inflammatory changes in the kidney of postmenopausal females compared to the cell-based approach using BM-MSCs. Therefore, MSCs-derived exosomes are a promising therapeutic approach for preserving postmenopausal kidney structure and function and, subsequently, should improve the quality of life of postmenopausal females.

Scanning electron microscopy and morphometric analysis of superficial corneal epithelial cells in dromedary camel (Camelus dromedarius).

It is likely that superficial corneal epithelial cells (SCECs) of the dromedary camels have a significant role in their survival at arid and semiarid regions. To the best of our knowledge, SCECs of camels' eyes have not been characterized previously using scanning electron microscopy (SEM), combined with morphometric analysis. Therefore, in the current study, we aim to describe the shape, topographical distribution, and density of SCECs associated with morphometric analysis using SEM. Twelve healthy adult camels' corneas were obtained immediately after slaughter. Each cornea has been divided into nine parts: central (C), middle dorsal (MD), middle ventral (MV), middle nasal (MN), middle temporal (MT), peripheral dorsal (PD), peripheral ventral (PV), peripheral nasal (PN), and peripheral temporal (PT). SCECs were distinguished and characterized into light, medium, and dark mosaics. The polygonal cells have been externally covered with microplicae that were more numerous above the light cells. The topographic distribution of light, medium, and dark cells revealed a well-defined concentration of light cells in excess of other cells in all parts as follows: PV (92.5%), PN (78.5%), MN (78%), MT (74.7%), PD (73.8%), PT (70.7%), MV (68.7%), MD (66.3%), and C (19.3%). The PV part recorded the highest density of light cells, while the C portion showed the lowest density for the same cells. We concluded that the light cells extensively predominate in all parts of the camels' cornea except the C part, indicating an adaptive modification to the harsh environment. Additionally, the PV and PN parts represent the permanent and endogenous source as well as a proliferative reserve for SCECs in dromedary camel.

Nano-silica and magnetized-silica mitigated lead toxicity: Their efficacy on bioaccumulation risk, performance, and apoptotic targeted genes in Nile tilapia (Oreochromis niloticus).

Contamination of aquatic systems with heavy metals (HM) is of great concern owing to their deleterious impact on living organism. The current research is focused on application of silica particles with new functionalized properties (magnetic silica; SiMag or Nanoporous silica; SiNPs) and their efficacy to mitigate lead (pb) toxicity in Nile tilapia. One thousand fingerlings were distributed: two control groups (negative; without pb toxicity (NC) positive (with pb toxicity) and other four groups received two silica sources (SiMag or SiNPs) with two levels (400 and 600 mg/kg diet) for 56 days then exposed to pb for 30 days. Before toxicity exposure, maximum growth, and most improved feed conversion ratio and biochemical parameters were noticed with higher SiMag or SiNPs levels. Serum antioxidant enzymes and their transcriptional levels in muscle and liver were boosted in groups received SiMag or SiNPs. After toxicity exposure, hematological and antioxidants biomarkers maintained at adequate levels in SiMag or SiNPs. Prominent reduction of residual pb in gills, liver, kidney, and muscle was observed in SiNPs then SiMag groups. Interestingly, the maximum down-regulation of P450, caspase-3 and HSP-70 and MT were observed in groups received 600 mg/kg diet of SiMag or SiNPs. The higher level of P53 in liver and gills was detected in PC, inversely reduced in SiMag or SiNPs. Severity of the histopathological alterations in examined organs greatly reduced in groups received SiMag or SiNPs, unlike it were induced in PC group. In conclusion, higher SiMag or SiNPs levels not only mitigate negatives impact of pb toxicity in fish but also ensure its safety for human consumption.

Promising Role of Growth Hormone-Boosting Peptide in Regulating the Expression of Muscle-Specific Genes and Related MicroRNAs in Broiler Chickens.

Appropriate skeletal muscle development in poultry is positively related to increasing its meat production. Synthetic peptides with growth hormone-boosting properties can intensify the effects of endogenous growth hormones. However, their effects on the mRNA and miRNA expression profiles that control muscle development post-hatching in broiler chicks is unclear. Thus, we evaluated the possible effects of synthetic growth hormone-boosting peptide (GHBP) inclusion on a chicken's growth rate, skeletal muscle development-related genes and myomiRs, serum biochemical parameters, and myofiber characteristics. A total of 400 one-day-old broiler chicks were divided into four groups supplied with GHBP at the levels of 0, 100, 200 and 300 µg/kg for 7 days post-hatching. The results showed that the highest levels of serum IGF-1 and GH at d 20 and d 38 post-hatching were found in the 200 µg/kg GHBP group. Targeted gene expression analysis in skeletal muscle revealed that the GHBP effect was more prominent at d 20 post-hatching. The maximum muscle development in the 200 µg/kg GHBP group was fostered by the upregulation of IGF-1, mTOR, myoD, and myogenin and the downregulation of myostatin and the Pax-3 and -7 genes compared to the control group. In parallel, muscle-specific myomiR analysis described upregulation of miR-27b and miR-499 and down-regulation of miR-1a, miR-133a, miR-133b, and miR-206 in both the 200 and 300 µg/kg GHBP groups. This was reflected in the weight gain of birds, which was increased by 17.3 and 11.2% in the 200 and 300 µg/kg GHBP groups, respectively, when compared with the control group. Moreover, the maximum improvement in the feed conversion ratio was achieved in the 200 µg/kg GHBP group. The myogenic effects of GHBP were also confirmed via studying myofiber characteristics, wherein the largest myofiber sizes and areas were achieved in the 200 µg/kg GHBP group. Overall, our findings indicated that administration of 200 µg/kg GHBP for broiler chicks could accelerate their muscle development by positively regulating muscle-specific mRNA and myomiR expression and reinforcing myofiber growth.

Identification and Characterization of P0 Protein as a Vaccine Candidate Against Babesia divergens, Blood Parasite of Veterinary and Zoonotic Importance.

The molecular identification and antigenic characterization of P0 protein in Babesia divergens, a blood parasite of veterinary and zoonotic importance, were carried out in this study for use in developing subunit vaccines against B. divergens infection. Recombinant protein encoding P0 (BdP0) was developed in Escherichia coli, and its antiserum was generated in mice for further molecular characterization. Anti-rBdP0 serum had a specific interaction with the corresponding legitimate B. divergens protein, as confirmed by Western blotting and indirect fluorescent antibody tests. ELISA was used to assess the immunogenicity of BdP0 in a group of 68 bovine field samples, and significant immunological reactivity was found in 19 and 20 positive samples of rBdp0 and B. divergens lysate, respectively. The in vitro growth of B. divergens cultures treated with anti-rBdP0 serum was significantly inhibited (p < 0.05). Furthermore, after 6 h of incubation with 2 mg/ml anti-rBdP0 serum, the ability of pre-incubated free merozoites to invade bovine erythrocytes was reduced by 59.88%. The obtained data suggest the possible use of rBdP0 as diagnostic antigen and may serve as a vaccine candidate against babesiosis caused by B. divergens either in animal or human.

Antioxidant response element activator, BTZO-1, improves the developmental competence of bovine oocytes.

Increased reactive oxygen species (ROS) generation may disrupt the oocytes function and their competence. In this study, we introduced BTZO-1, a new supplement that can regulate the oxidative stress. Addition of BTZO-1 during IVM of bovine oocytes improved their developmental competence in the term of improvement of blastocyst rates. In addition, the quality of the produced embryos was improved by decreasing the apoptosis level by showing a decreased number of TUNNEL positive cells.

Normal magnetic resonance anatomy of the hind foot of Egyptian buffalo (Bubalus bubalis): A correlative low-field T1- and T2-weighted MRI and sectional anatomy atlas.

Buffaloes represent a major source of milk production, especially in developing countries including Egypt. The buffalo foot is frequently involved in a large proportion of lameness cases. The relatively small size and complexity of its structures often render the radiographic evaluation of the foot challenging. Magnetic resonance imaging (MRI) is a noninvasive imaging technique that is regarded as both safe and accurate for assessment of the foot disorders in both man and animals. The purpose of the current investigation was to describe the MRI anatomy of buffalo foot using cadaveric hind feet. The feet were subjected to consecutive MRI scanning using a 0.3 Tesla scanner. Both T1-weighted (T1-W) and T2-weighted (T2-W) spin-echo pulse sequences were applied in dorsal, sagittal and transverse planes. The heterogeneity of signal intensities noted amongst foot components allowed for clear differentiation of bones, tendons, ligaments, adipose tissue and synovial fluid. The T1-W images provided an excellent overview of the foot. They were valuable for visualizing the bones and the alignment of tendons and ligaments. The T2-W images were particularly useful for the evaluation of synovial structures such as tendon sheaths and joint cavities. A communication between the two plantar sacs of the metatarsophalangeal (fetlock) joints was evident in T2-W images. MRI findings were further confirmed using relevant gross anatomical sections. The present study establishes a detailed MRI anatomic reference of buffalo foot that could help veterinary researchers, clinicians and surgeons for increasing the accuracy of interpretation of foot MRI scans of both healthy and diseased animals.

The role of frataxin in doxorubicin-mediated cardiac hypertrophy.

Doxorubicin (DOX) is a highly effective anti-neoplastic agent; however, its cumulative dosing schedules are clinically limited by the development of cardiotoxicity. Previous studies have attributed the cause of DOX-mediated cardiotoxicity to mitochondrial iron accumulation and the ensuing reactive oxygen species (ROS) formation. The present study investigates the role of frataxin (FXN), a mitochondrial iron-sulfur biogenesis protein, and its role in development of DOX-mediated mitochondrial dysfunction. Athymic mice treated with DOX (5 mg/kg, 1 dose/wk with treatments, followed by 2-wk recovery) displayed left ventricular hypertrophy, as observed by impaired cardiac hemodynamic performance parameters. Furthermore, we also observed significant reduction in FXN expression in DOX-treated animals and H9C2 cardiomyoblast cell lines, resulting in increased mitochondrial iron accumulation and the ensuing ROS formation. This observation was paralleled in DOX-treated H9C2 cells by a significant reduction in the mitochondrial bioenergetics, as observed by the reduction of myocardial energy regulation. Surprisingly, similar results were observed in our FXN knockdown stable cell lines constructed by lentiviral technology using short hairpin RNA. To better understand the cardioprotective role of FXN against DOX, we constructed FXN overexpressing cardiomyoblasts, which displayed cardioprotection against mitochondrial iron accumulation, ROS formation, and reduction of mitochondrial bioenergetics. Lastly, our FXN overexpressing cardiomyoblasts were protected from DOX-mediated cardiac hypertrophy. Together, our findings reveal novel insights into the development of DOX-mediated cardiomyopathy.

Cardioprotective HIF-1α-frataxin signaling against ischemia-reperfusion injury.

Previous studies have demonstrated the protective signaling of hypoxia-inducible factor (HIF)-1 α against ischemia-reperfusion (I/R) injury in the heart. In the present study, we provide further evidence for a cardioprotective mechanism by HIF-1α against I/R injury exerted via the mitochondrial protein frataxin, which regulates mitochondrial Fe-S cluster formation. Disruption of frataxin has been found to induce mitochondrial iron overload and subsequent ROS production. We observed that frataxin expression was elevated in mice hearts subjected to I/R injury, and this response was blunted in cardiomyocyte-specific HIF-1α knockout (KO) mice. Furthermore, these HIF-1α KO mice sustained extensive cardiac damage from I/R injury compared with control mice. Similarly, reduction of HIF-1α by RNA inhibition resulted in an attenuation of frataxin expression in response to hypoxia in H9C2 cardiomyocytes. Therefore, we postulated that HIF-1α transcriptionally regulates frataxin expression in response to hypoxia and offers a cardioprotective mechanism against ischemic injury. Our promoter activity and chromatin immunoprecipitation assays confirmed the presence of a functional hypoxia response element in the frataxin promoter. Our data also suggest that increased frataxin mitigated mitochondrial iron overload and subsequent ROS production, thus preserving mitochondrial membrane integrity and viability of cardiomyocytes. We postulate that frataxin may exert its beneficial effects by acting as an iron storage protein under hypoxia and subsequently facilitates the maintenance of mitochondrial membrane potential and promotes cell survival. The findings from our study revealed that HIF-1α-frataxin signaling promotes a protective mechanism against hypoxic/ischemic stress.