Hanan Hassan Fouad

COVID-19 is one of the deadliest epidemics. This pandemic is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), but the role of dogs in spreading the disease in human society is poorly understood. This review sheds light on the limited susceptibility of dogs to COVID-19 infections which is likely attributed to the relatively low levels of angiotensin-converting enzyme 2 (ACE2) in the respiratory tract and the phylogenetic distance of ACE2 in dogs from the human ACE2 receptor. The low levels of ACE2 affect the binding affinity between spike and ACE2 proteins resulting in it being uncommon for dogs to spread the disease. To demonstrate the role of dogs in spreading COVID-19, we reviewed the epidemiological studies and prevalence of SARS-CoV-2 in dogs. Additionally, we discussed the use of detection dogs as a rapid and reliable method for effectively discriminating between SARS-CoV-2 infected and non-infected individuals using different types of samples (secretions, saliva, and sweat). We considered the available information on COVID-19 in the human-dog interfaces involving the possibility of transmission of COVID-19 to dogs by infected individuals and vice versa, the human-dog behavior changes, and the importance of preventive measures because the risk of transmission by domestic dogs remains a concern.

This study investigated the effect of oral dosing of titanium dioxide nanoparticles (TNPs) and cadmium (Cd) on rat liver and the potential protective role of coenzyme Q10 (CQ10) against TNPs and Cd-induced hepatic injury. Seventy male Sprague Dawley rats were divided into seven groups and orally given distilled water, corn oil, CQ10 (10 mg/kg b.wt), TNPs (50 mg/kg b.wt), Cd (5 mg/kg b.wt), TNPs + Cd, or TNPs + Cd+CQ10 by gastric gavage for 60 successive days. The results showed that individual or mutual exposure to TNPs and Cd significantly increased the serum levels of various hepatic enzymes and lipids, depleted the hepatic content of antioxidant enzymes, and increased malondialdehyde. Moreover, the hepatic titanium and Cd content were increased considerably in TNPs and/or Cd-exposed rats. Furthermore, marked histopathological perturbations with increased immunoexpression of tumor necrosis factor-alpha and nuclear factor kappa B were evident in TNPs and/or Cd-exposed rats. However, CQ10 significantly counteracted the damaging effect of combined exposure of TNPs and Cd on the liver. The study concluded that TNPs and Cd exposure harm hepatic function and its architecture, particularly at their mutual exposure, but CQ10 could be a candidate protective agent against TNPs and Cd hepatotoxic impacts.

This study investigated the effect of oral dosing of titanium dioxide nanoparticles (TNPs) and cadmium (Cd) on rat liver and the potential protective role of coenzyme Q10 (CQ10) against TNPs and Cd-induced hepatic injury. Seventy male Sprague Dawley rats were divided into seven groups and orally given distilled water, corn oil, CQ10 (10 mg/kg b.wt), TNPs (50 mg/kg b.wt), Cd (5 mg/kg b.wt), TNPs + Cd, or TNPs + Cd+CQ10 by gastric gavage for 60 successive days. The results showed that individual or mutual exposure to TNPs and Cd significantly increased the serum levels of various hepatic enzymes and lipids, depleted the hepatic content of antioxidant enzymes, and increased malondialdehyde. Moreover, the hepatic titanium and Cd content were increased considerably in TNPs and/or Cd-exposed rats. Furthermore, marked histopathological perturbations with increased immunoexpression of tumor necrosis factor-alpha and nuclear factor kappa B were evident in TNPs and/or Cd-exposed rats. However, CQ10 significantly counteracted the damaging effect of combined exposure of TNPs and Cd on the liver. The study concluded that TNPs and Cd exposure harm hepatic function and its architecture, particularly at their mutual exposure, but CQ10 could be a candidate protective agent against TNPs and Cd hepatotoxic impacts.

This study investigated the effect of oral dosing of titanium dioxide nanoparticles (TNPs) and cadmium (Cd) on rat liver and the potential protective role of coenzyme Q10 (CQ10) against TNPs and Cd-induced hepatic injury. Seventy male Sprague Dawley rats were divided into seven groups and orally given distilled water, corn oil, CQ10 (10 mg/kg b.wt), TNPs (50 mg/kg b.wt), Cd (5 mg/kg b.wt), TNPs + Cd, or TNPs + Cd+CQ10 by gastric gavage for 60 successive days. The results showed that individual or mutual exposure to TNPs and Cd significantly increased the serum levels of various hepatic enzymes and lipids, depleted the hepatic content of antioxidant enzymes, and increased malondialdehyde. Moreover, the hepatic titanium and Cd content were increased considerably in TNPs and/or Cd-exposed rats. Furthermore, marked histopathological perturbations with increased immunoexpression of tumor necrosis factor-alpha and nuclear factor kappa B were evident in TNPs and/or Cd-exposed rats. However, CQ10 significantly counteracted the damaging effect of combined exposure of TNPs and Cd on the liver. The study concluded that TNPs and Cd exposure harm hepatic function and its architecture, particularly at their mutual exposure, but CQ10 could be a candidate protective agent against TNPs and Cd hepatotoxic impacts.

BACKGROUND: Reconstruction of the pelvic ring anatomy in unstable anterior pelvic ring injuries is a significant step to reduce the mortality rate associated with these injuries efficiently. There is a debate on using either an anterior subcutaneous pelvis internal fixator (INFIX) or an anterior supra-acetabular external fixator (EXFIX) to manage an unstable anterior pelvic ring fracture.

AIM: To compare the functional and radiological outcomes and complications of INFIX EXFIX in managing unstable pelvic ring injuries.

METHODS: A prospective cohort study included 54 patients with unstable pelvic ring fractures. The patients were divided into two groups; the INFIX group, in which 30 cases were fixed by INFIX, and the EXFIX group, in which 24 patients were treated by EXFIX. The average age in the EXFIX group was 31.17 years (16-57 years), while in the INFIX group, it was 34.5 years (17-53 years). The study included 20 (66.7%) males and 10 (33.3%) females in the INFIX group and 10 (41.7%) males and 14 (58.3%) females in the EXFIX group. The radiological outcomes were evaluated using Matta and Tornetta's score, and the functional outcomes using the Majeed score.

RESULTS: The results revealed a statistically significant difference between both groups ( = 0.013) regarding radiological outcomes, according to Matta and Tornetta's score in favor of the INFIX group. Sitting, standing, and walking abilities were measured at a 3-mo follow-up visit using Majeed score modules. It was significantly better among the INFIX group than the EXFIX group in all three modules. At the final follow-up, both groups had no statistically significant difference according to the Majeed score; 92.35 in the INFIX group and 90.99 in the EXFIX group ( = 0.513). A lower surgical site infection rate was noticed in the INFIX group ( = 0.007).

CONCLUSION: Anterior subcutaneous pelvis INFIX is associated with better radiological outcomes and a lower infection rate than anterior supra-acetabular EXFIX in managing patients with unstable anterior pelvic ring fractures.

OBJECTIVES: To explore current management practices for PMR by general practitioners (GPs) and rheumatologists including implications for clinical trial recruitment.

METHODS: An English language questionnaire was constructed by a working group of rheumatologists and GPs from six countries. The questionnaire focused on: 1: Respondent characteristics; 2: Referral practices; 3: Treatment with glucocorticoids; 4: Diagnostics; 5: Comorbidities; and 6: Barriers to research. The questionnaire was distributed to rheumatologists and GPs worldwide via members of the International PMR/Giant Cell Arteritis Study Group.

RESULTS: In total, 394 GPs and 937 rheumatologists responded to the survey. GPs referred a median of 25% of their suspected PMR patients for diagnosis and 50% of these were returned to their GP for management. In general, 39% of rheumatologists evaluated patients with suspected PMR >2 weeks after referral, and a median of 50% of patients had started prednisolone before rheumatologist evaluation. Direct comparison of initial treatment showed that the percentage prescribing >25 mg prednisolone daily for patients was 30% for GPs and 12% for rheumatologists. Diagnostic imaging was rarely used. More than half (56%) of rheumatologists experienced difficulties recruiting people with PMR to clinical trials.

CONCLUSION: This large international survey indicates that a large proportion of people with PMR are not referred for diagnosis, and that the proportion of treatment-naive patients declined with increasing time from referral to assessment. Strategies are needed to change referral and management of people with PMR, to improve clinical practice and facilitate recruitment to clinical trials.

Osteoarthritis (OA) is a chronic debilitating degenerative disorder leading to structural, and functional anomaly of the joint. The present study tests the hypothesis that overexpression of the basic fibroblast growth factor (FGF-2) via direct rAAV-mediated gene transfer suppresses monosodium iodoacetate (MIA)-induced knee OA in rats relative to control (reporter rAAV-lacZ vector) gene transfer by intra-articular injection. Rats were treated with 20 μl rAAV-hFGF-2 on weekly basis; on days 7, 14, and 21 after single intra-articular injection of MIA (3 mg/50 μl saline). FGF-2 reduced knee joint swelling and improved motor performance and muscle coordination as evidenced by increased distance travelled, mean speed, rearing frequency in open field test (OFT) as well as fall-off latency in rotarod test together with reduced immobility time in OFT. Moreover, FGF-2 attenuated MIA-related radiological and histological alterations. Indeed, FGF-2 decreased knee joint inflammatory biomarker as demonstrated by reduced mRNA expression of toll like receptor (TLR)-4 and its downstream mediators such as tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β) and high motility group box (HMGB) 1. In parallel, FGF-2 attenuated knee joint degradation biomarkers as reflected by the downregulation of ADAMTS-5 mRNA expression and matrix metalloproteinase 13 (MMP-13) content together with the up-regulation of tissue inhibitor of metalloproteinase (TIMP)-1 mRNA expression. These findings suggest a potential therapeutic role for FGF-2 against MIA-induced knee OA in rats via inhibition of TLR4 signaling and activating TIMP-1, resulting in down-regulation of ADAMTS-5 and MMP-13.