Background: Repair of large‑sized bone defects is a challengeable obstacle in orthopedics and evoked the demand for the development of biomaterials that could induce bone repair in such defects. Recently, UiO‑66 has emerged as an attractive metal–organic framework (MOF) nanostructure that is incorporated in biomedical applications due to its biocompatibility, porosity, and stability. In addition, its osteogenic properties have earned a great interest as a promising field of research. Thus, the UiO‑66 was prepared in this study and assessed for its potential to stimulate and support osteogenesis in vitro and in vivo in a rabbit femoral condyle defect model. The nanomaterial was fabricated and characterized using x‑ray diffraction (XRD) and transmission electron microscopy (TEM). Afterward, in vitro cytotoxicity and hemolysis assays were performed to investigate UiO‑66 biocompatibility. Furthermore, the material in vitro capability to upregulate osteoblast marker genes was assessed using qPCR. Next, the in vivo new bone formation potential of the UiO‑66 nanomaterial was evaluated after induction of bone defects in rabbit femoral condyles. These defects were left empty or filled with UiO‑66 nanomaterial and monitored at weeks 4, 8, and 12 after bone defect induction using x‑ray, computed tomography (CT), histological examinations, and qPCR analysis of osteocalcin (OC) and osteopontin (OP) expressions.
Results: The designed UiO‑66 nanomaterial showed excellent cytocompatibility and hemocompatibility and stimulated the in vitro osteoblast functions. The in vivo osteogenesis was enhanced in the UiO‑66 treated group compared to the control group, whereas evidence of healing of the treated bone defects was observed grossly and histologically. Interestingly, UiO‑66 implanted defects displayed a significant osteoid tissue and collagen deposition compared to control defects. Moreover, the UiO‑66 nanomaterial demonstrated the potential to upregulate OC and OP in vivo.
Conclusions: The UiO‑66 nanomaterial implantation possesses a stimulatory impact on the healing process of critical‑sized bone defects indicating that UiO‑66 is a promising biomaterial for application in bone tissue engineering

The current work was undertaken to test the genotoxic potential of chlorpyrifos (CPF), dimethoate, and lambda cyhalothrin
(LCT) insecticides in rat brain and liver using the single cell gel electrophoresis (comet assay). Three groups of adult male Sprague–Dawley rats were exposed orally to one third LD50of CPF, dimethoate, or LCT for 24 and 48 h while the control group received corn oil. Serum samples were collected for estimation of malondialdehyde (MDA) and glutathione peroxidase (GPx); the brain and liver samples were used for comet assay and for histopathological examination. Results showed that signs of neurotoxicity appeared clinically as backward stretching of hind limb and splayed gait in dimethoate and LCT groups, respectively.
CPF, LCT, and dimethoate induced oxidative stress indicated by increased MDA and decreased GPx levels. CPF and LCT caused severe DNA damage in the brain and liver at 24 and 48 h indicated by increased percentage of DNA in tail, tail length, tail moment, and olive tail moment. Dimethoate induced mild DNA damage in the brain and liver at 48 h. Histopathological changes were observed in the cerebrum, cerebellum, and liver of exposed rats. The results concluded that CPF, LCT, and dimethoate insecticides induced oxidative stress and DNA damage associated with histological changes in the brain and liver of exposed rats.

Sepsis is a systemic inflammatory response syndrome (SIRS) that occurs when the body's immunity overreacts to an infection. It is followed by life-threatening medical consequences, including multiple organ failure (MOD). Dexmedetomidine (DEX) is a selective 2 adrenergic agonist that is used as a short-term sedative in the ICU. Apart from improving sepsis prognosis, it is believed to have an organ protecting function. Our study aimed at confirming DEX ameliorative role in sepsis-induced organ damage. We also studied DEX mitigating effect on sepsis-induced acute lung injury (ALI) and elucidated the possible mechanism. Thirty rats were randomly assigned into three groups (n=10): sham, cecal ligation and puncture (CLP)-induced sepsis, or DEX-treated CLP (DEX + CLP). 15 minutes before the CLP procedure, a prophylactic dosage of DEX (5g/kg) was given intraperitoneally (IP). Animals were slaughtered 48 hours after the surgery was completed. Histological examination for tissue samples from lung, liver and kidney. CD54 expression in lung tissue was also investigated. Blood was also taken for hematological analysis. CLP rats showed different pathological lesions in lung, kidney and liver. We reported severe pulmonary tissue damage in CLP group accompanied with enhanced CD54 expression. DEX decreased the severity of histopathological changes in the affected organs and reduced the expression of CD54 in the lung tissue as well. However, DEX could not improve sepsis-induced hematological impairment. DEX attenuated sepsis through decreased CD54 expression in the lung as well as its hepato-renal protective effect in the CLP model.

The current work was undertaken to evaluate the nephrotoxic effect of Ketoprofen on adult male rats. Eighteen rats were divided into two groups. Ketoprofen- received group (I) included 10 rats were administered Ketoprofen at a therapeutic dose of 13.5 mg/kg by I/M injection daily for 4 successive weeks. Five rats were randomly selected from group I and sacrificed at 2 and 4 weeks of the experiment. The control group (II) that received olive oil included 8 rats, where 4 rats were sacrificed after 2 weeks and the rest of rats were sacrificed after 4 weeks. Tissue specimens from kidneys of all groups were collected for histopathological examination as well as the serum was obtained for the determination of biochemical parameters. The histopathological examination of group I showed glomerular changes such as expanding of glomerular matrix, glomerular sclerosis and congestion of glomerular capillary in the cortex. Renal tubular degeneration and necrosis accompanied with infiltration of inflammatory cells in interstitial tissue in both cortex and medulla were also observed. The biochemical results revealed that animals in group I showed a significant increase in malondialdehyde, creatinine, and urea compared to the control group, while total antioxidant capacity was numerically decreased. In conclusion, the therapeutic dose of Ketoprofen caused damage in kidney tissue even if was taken for a short period as well as altered biochemical parameters.

Aim: The study aimed at studying the hepatoprotective effect of L-carnitine against lead (Pb) acetate-induced
hepatocellular injury, emphasizing the role of caspase-3 and glycogen synthase kinase-3β in hepatocellular
apoptosis and inflammation.
Materials and methods: Male Wistar rats were used. The experimental approach involved estimation of the liver
enzymes' serum levels. Oxidative and inflammatory biomarkers were measured in hepatic tissue homogenates.
Paraffin-embedded hepatic sections were prepared for histopathology and immunohistochemistry. Quantitative
determination of the phosphorylated glycogen synthase kinase-3 beta was performed.
Key findings: The serum showed a significant elevation in ALT, AST, and LDH; tissue homogenates showed significant
elevation in lipid peroxide and inflammatory biomarkers with significant reduction in reduced glutathione
in the Pb acetate-treated group. Co-administration of L-carnitine with Pb acetate produced significant
reduction in liver enzymes with significant improvement in oxidant, antioxidant and inflammatory markers.
Lead acetate treatment significantly reduced the phosphorylated glycogen synthase kinase-3 beta, while Lcarnitine
enhanced its phosphorylation. Histopathological examination showed inflammatory reaction around
blood vessels with fatty degeneration in hepatocytes of the Pb acetate intoxicated group. L-Carnitine caused a
decrease in hepatic damage with minimal vascular alterations in central vein. Caspase-3 expression in hepatocytes
was decreased in Pb-treated group supplemented with L-carnitine.
Significance: Our study reveals that oxidative stress and inflammation participate in Pb acetate-induced hepatocellular
injury. Glycogen synthase kinase-3β and caspase-3 play role in Pb acetate-induced hepatic damage. LCarnitine
shows significant protective effects against hepatocellular apoptosis and inflammation induced by Pb
acetate through antioxidant, anti-inflammatory and anti-apoptotic pathways in part mediated by GSK-3β
inhibition.

According to the American College of Cardiology/American Heart Association (ACC/AHA), both aspirin
and statin are used in the primary prevention of cardiovascular diseases. Aspirin (ASA) is contraindicated
if there is gastrointestinal bleeding because it will exaggerate the condition. In this study, the effect of
surfactant; sodium lauryl sulfate (SLS), in enhancing the in vitro dissolution of simvastatin (SIM) and
ASA, as well as gastric irritation and upset, was studied. Oral tablets containing both ASA and SIM with
and without the SLS were manufactured using the direct compression technique. The prepared tablets
were characterized with respect to hardness, friability, uniformity of dosage units, in vitro disintegration,
and dissolution. The effect of the addition of SLS in reducing the in vivo irritation and protection of gastric
mucosa were also investigated. The results showed that the compressed tablets possessed sufficient
hardness, acceptable friability, and are uniform with respect to disintegration, drugs contents, and tablet
weight. The results showed that SIM alone exhibited a gastroprotective effect on the induced irritation. In
addition, the incorporation of the SLS in the tablets containing SIM and ASA significantly enhanced the
dissolution rates of both drugs and significantly decreased the gastric irritation and the ulcer index.
The ulcer index of aspirin was decreased from 2.3 for tablets manufactured without SLS to 0.8 for tablets
containing SLS. In a conclusion, the addition of pH modifier surfactant; SLS could enhance the dissolution
rate of poorly soluble acidic drugs, reduce gastric upset and irritation without any effect on the main
characters of the tablets. Moreover, the addition of SLS is very useful in improving the therapeutic activities
and reducing the side effects of ASA and SIM for patients who require long-term administration of
these drugs.

Background: Castration is a husbandry practice raising important questions on the welfare and physiological status
of farm animals. Searching for effective castration methods that minimally compromise the body physiology is
worthy of attention. Therefore, this study aimed to evaluate the differential response of biological systems in
donkeys to surgical castration versus the chemical one by CaCl2 with special emphasis on stress, lipid profile, and
oxidative stress biomarkers. Donkeys were divided randomly and equally into two groups; the chemical (Ch) and
surgical (S) groups (n = 6). The Ch group was chemically castrated by intratesticular injection of 20% CaCl2 dissolved
in absolute ethanol. Blood samples were collected prior to castration and at 15, 30, 45, and 60 days after the
beginning of experiment.
Results: Surprisingly, the Ch group at the end of the experiment was characterized by significantly higher cortisol
level compared to the S group. TC and LDL-C levels in the S group significantly decreased at day 45, while TG
levels significantly increased at days 45 and 60 in comparison with day 0. HDL-C levels at days 30 and 60 in the Ch
group significantly increased in comparison with day 0. At day 30 post-castration, HDL-C was significantly higher
and LDL-C was significantly lower in the Ch group than the S group. A significant elevation in TC and LDL-C was
observed at day 45 and in HDL-C at the end of experimental duration in the Ch group when compared with the S
group. TPX level was significantly lower and TAC was significantly higher in the Ch group at day 45 than the S
group.
Conclusion: Surgical castration evoked less stress and minor changes in lipid profile and oxidant/antioxidant
balance relative to chemical castration by intratesticular 20% CaCl2 dissolved in absolute ethanol.
Keywords: Surgical castration, Chemical castration, Physiology, Stress, Lipid profile, Oxidative stress

The one-humped camel (Camelus dromedarius) or dromedary is an economically important domestic animal. However, infectious diseases, including those caused by vector-borne hemopathogens, frequently compromise the health and production of camels. In this study, we examined infections caused by Babesia, Theileria, Trypa-
nosoma, and Anaplasma species in camels in Egypt. We analyzed blood DNA samples from 148 camels reared in six Egyptian governorates (Giza, Asyut, Sohag, Qena, Luxor, and the Red Sea) using pathogen-specific Poly-
merase Chain Reaction (PCR) assays. Our results indicated that 29 (19.6%), 22 (14.9%), 1 (0.7%), 2 (1.4%), 1 (0.7%), 2 (1.4%), and 28 (18.9%) of the surveyed animals were infected with Babesia bovis, B. bigemina, Babesia sp. Mymensingh, Theileria sp. Yokoyama, Theileria equi, Trypanosoma evansi, and Anaplasma marginale, respec-
tively. We found that a total of 68 (45.9%) animals were infected with at least one of the detected hemopath-
ogens. Sequencing analyses of PCR amplicons confirmed our diagnostic results. This study is the first to report Theileria sp. Yokoyama and Babesia sp. Mymensingh in Egypt. This is also the first report of infection with these two species in one-humped camel. In conclusion, this study found that camels in Egypt are infected with several vector-borne hemopathogens, including novel parasite species.

The study was carried out to determine the residual levels of heavy metals (zinc, iron, copper, lead, and cadmium) in tissues (meat, liver and kidney), serum and hair of 3 camel breeds (Magaheem, Maghateer and Wadha) collected from Al-Omran slaughterhouse, eastern province, Saudi Arabia by using Atomic Absorption Spectrometer. Camel breed influenced Zinc (Zn) accumulation and distribution in organs, muscle, and arranged in descending manner as follows: hair> liver> muscle > kidney> serum. The iron content in all male camel samples was considerably greater than in female camel. Furthermore, significant strong positive correlation between muscle and serum iron was established. All examined samples contained copper (Cu), the highest value was 17.78 ± 0.85 mg kg–1 detected in liver samples of Maghateer breed. The descending manner of Cu as follows: liver > muscle > hair > kidney > serum. In addition, the female liver contained significantly higher Cu than the male liver. Lead (Pb) residue was detected in all examined samples among different breeds except muscle samples of Maghateer and Magaheem breeds. The cadmium (Cd) values ranged from 0.0001 mg kg–1 in the muscle of the Maghateer breed to 4.5113 mg kg–1 in the hair of the Wadham breed. The meat and offal of all examined breeds contained lower Pb and Cd levels than the maximum permissible limit. The estimated daily intake (EDI) due to consumption of camel meat below the tolerable daily intake (TDI). In addition, the hazard ratio (HR) and hazard indices (HIs) values were far below one for adults.