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Gizzard erosion and ulceration syndrome (GEUS) is caused by a fowl adenovirus serotype 1 (FAdV-1) and was first reported in laying hens in Japan in 1993. This syndrome has emerged as an epizootic in Morocco since 2014, causing significant economic losses for the poultry industry, but no involvement of a FAdV has been confirmed. Thus, the objective of this work was to assess GEUS cases that occurred in the country and to determine the role of FAdVs in their occurrence. Investigations were based on a retrospective reassessment of tissue sections and paraffin blocks of gizzards and livers from GEUS cases between 2014 and 2021 coupled with a prospective search of cases in 2022. Gizzards and livers were fixed in 10% neutral buffered formalin for histopathologic examinations according to standard methods and stored at -20 C for molecular analysis. After deparaffinizing, 10-µm-thick tissue sections along with fresh organs were subjected to DNA extraction using a commercial kit. A primer pair specific for the Hexon gene of FAdVs was used in conventional PCR; in contrast, for real-time PCR, a primer pair targeting the 52K gene was employed. In total, 24 flock cases with characteristic GEUS were assessed between 2014 and 2022. They were nine broiler cases aged between 11 and 39 days, 11 layer cases with an age between 17 and 29 wk, two cases in meat-type breeders aged 10 and 27 wk, and two flock cases of turkey poults aged 22 and 23 days. In most cases, microscopic lesions were consistent with an ulcerative and lymphoplasmocytic ventriculitis, and pathognomonic viral intranuclear inclusion bodies within degenerate epithelial cells were identified in four broiler flock cases, four layer cases, and one case in breeders and hence were highly suggestive of a FAdV infection. Among these nine cases that were positive at the histopathologic examination, six cases were found to be FAdV-PCR positive; another four cases were negative to histology but FAdV-PCR positive. Furthermore, a sequencing analysis was conducted, providing the initial evidence of the implication of FAdV-1 from species A as the cause of GEUS in Moroccan poultry. Additionally, a phylogenetic analysis was executed to facilitate a comparison between the strains investigated in this study and those identified in diverse geographic regions and across various time periods.

Background: Knee osteoarthritis (KOA) is a painful degenerative joint disease that may limit activities of daily living. This study aimed to determine the relationship between quadriceps endurance and knee joint position sense (JPS) in KOA individuals and compare the quadriceps endurance and knee JPS with and without KOA., Methods: This comparative cross-sectional study was conducted in medical rehabilitation clinics, King Khalid University, Saudi Arabia. This study recruited 50 individuals diagnosed with unilateral KOA (mean age = 67.10 ± 4.36 years) and 50 asymptomatic individuals (mean age = 66.50 ± 3.63 years). Quadriceps isometric endurance capacity (sec) was measured using a fatigue resistance test, and knee JPS (degrees) were assessed using a digital inclinometer and evaluated in sitting and standing positions., Results: Quadriceps isometric endurance showed a significant moderate negative correlation with knee JPS in 20° of flexion (r = -0.48, p < 0.001); 40° of flexion: r = -0.62, p < 0.001; 60° of flexion: r = -0.58, p < 0.001) in sitting and 20° of flexion (r = -0.25, p = 0.084) in standing position in KOA individuals. When compared to the asymptomatic, the quadriceps endurance was lower (p < 0.001), and knee joint position errors were larger (p < 0.001) in KOA individuals., Conclusion: Results of this study showed that quadriceps endurance capacity is negatively associated with knee JPS. KOA individuals demonstrated lower quadriceps endurance and larger JPS compared to asymptomatic., (© 2022. The Author(s).)

Background: Sadat-Habdan Mesenchymal Stimulating Peptide (SHMSP) was discovered and patented with USPTO in 2008. Studies have shown that SHMSP works as an angiogenesis factor. This study was done to evaluate pharmacokinetics (PK) in rats and toxicology studies in goats and rats., Methods: In 80 skeletally mature Sprague Dawley rats 5 milligram/kg body weight of SHMSP was injected intramuscularly. Blood samples were collected at 0, 30, 60, 120, 240, 320 minutes and 480 minutes. The plasma calibration curves were prepared at concentrations of 6.25, 3.12, 1.56, 0.78 and 0.39 ng/mL by spiking 190 µL of rat plasma with 10µL of working standard and 200 µL of deionized water. Samples were vortexed for five seconds, centrifuged at 14000 rpm for 30 minutes at 4°C and the supernatant was collected analyzed using High-performance liquid chromatography (HPLC). After injection of 20 µL sample, the peptide was eluted with 15ml linear gradient up to 36% of eluent A. The time between injections was 25 min. and the eluent was monitored at a wavelength of 215 nm. The concentration of peptide present in the rat plasma samples collected at different time intervals were quantified using standard curve method. The goats were injected deep intramuscularly 100 mg/kg-body weight of the SHMSP dissolved in injection solution. In 10 Sprague Dawley rats of ≥250 grams of weight, 20 mg/kg/day SHMSP was injected for 7 consecutive days. All the animals were kept at a close watch. Clinical observation at least once daily and as necessary was undertaken. After 2 weeks animals were euthanized and major organs were harvested and histopathology samples were obtained and processed., Results: There were no deaths is either of the study and control group of animals. The gross observations of the various organs appeared normal and histopathological studies did not show any toxicity in the organs tested.  The plasma concentration-time profile of SHMSP after intramuscular injection, the level of SHMSP in an initial high phase reaching the highest at 30 minutes 2.3184 ng/ml and 60 minutes 1.7447 ng/ml at 60 minutes. The lowest level was at 360 minutes of 0.0879 ng/ml., Conclusions: The dose of SHMSP at 20 times the recommended dose was not toxic and secondly the peak time and level was at 30 minutes to 120 minutes and the plasma half-life of SHMSP was 90 minutes.

Background: Most studies of the skin and how it responds to local heat have been conducted with either water, thermodes, or dry heat packs. Very little has been accomplished to look at the interaction between air humidity and temperature on skin temperature and blood flow. With variable air temperatures and humidity's around the world, this, in many ways, is a more realistic assessment of environmental impact than previous water bath studies., Material/methods: Eight young and 8 older subjects were examined in an extensive series of experiments where on different days, air temperature was 38, 40, or 42°C. and at each temperature, humidity was either 0%, 25%, 50%, 75%, or 100% humidity. Over a 20 minute period of exposure, the response of the skin in terms of its temperature and blood flow was assessed., Results: For both younger and older subjects, for air temperatures of 38 and 40°C., the humidity of the air had no effect on the blood flow response of the skin, while skin temperature at the highest humidity was elevated slightly. However, for air temperatures of 42°C., at 100% humidity, there was a significant elevation in skin blood flow and skin temperature above the other four air humidity's (p<0.05). In older subjects, the blood flow response was less and the skin temperature was much higher than younger individuals for air at 42°C. and 100% humidity (p<0.05)., Conclusions: Thus, in older subjects, warm humid air caused a greater rise in skin temperature with less protective effect of blood flow to protect the skin from overheating than is found in younger subjects.

Background: Endothelial function is known to be impaired in response to heat in people with diabetes, but little has been done to see how air humidity alters the skin blood flow response to heat., Methods: Seventeen male and female subjects were divided in two groups, one with type 2 diabetes and the other the control subjects without diabetes, age-matched to the diabetes group. All subjects participated in a series of experiments to determine the effect of the warming of the skin by air on skin temperature and skin blood flow. On different days, skin temperature was warmed with air that was 38°C, 40°C, or 42°C for 20 min. Also, on different days, at each temperature, the air humidity was adjusted to 0%, 25%, 50%, 75%, or 100% humidity. Skin blood flow and temperature were measured throughout the exposure period. This allowed the interactions between air humidity and temperature to be assessed., Results: For the control subjects, the moisture in the air had no different effect on skin blood flow at air temperatures of 38°C and 40°C (analysis of variance, P>0.05), although skin blood flow progressively increased at each air temperature that was applied. But for the warmest air temperature, 42°C, although the four lower humidities had the same effect on skin blood flow, air at 100% humidity caused the largest increase in skin blood flow. In contrast, in the subjects with diabetes, blood flow was always significantly less at any air temperature applied to the skin than was observed in the control subjects (P<0.05), and skin blood flow was significantly higher for the two higher humidities for the two higher air temperatures. Skin temperature paralleled these findings., Conclusion: These data show that individuals with diabetes do not tolerate moist, warm air above 50% humidity as well as controls without diabetes.

Background: The reaction of vascular endothelial cells to occlusion and heat in Southeast Asian Indians (SAI) compared to Caucasians (C) has not been studied, although genetic differences are found in endothelial cells between the races., Material/methods: Ten C and Ten SAI (<35 years old) male and female subjects participated. There was no difference in the demographics of the subjects except that the SAI group had been in the United States for 6 months; C was natives to the US. Endothelial function was assessed by the response of the circulation (BF) to local heating and the response to vascular occlusion. The effects of local heat on circulation in the skin on the forearm was assessed by applying heat for 6 minutes at temperatures, 38, 40 and 42°C on 3 separate days. On different days, vascular occlusion was applied for 4 minutes to the same arm and skin blood flow was measured for 2 minutes after occlusion; skin temperature was either 31°C or 42°C., Results: When occlusion was applied at a skin temperature of 31°C, the BF response to occlusion was significantly lower in the SAI cohort compared to C (peak BF C = 617 ± 88.2 flux, SAE = 284 ± 73 flux). The same effect was seen at skin temperatures of 42°C. The circulatory response to heat was also significantly less in SAI compared to C at each temperature examined (p<0.05)(for temperatures of 38, 40 and 42°C, peak blood flow for C was 374.7 ± 81.2, 551.9 ± 91.3 and 725.9 ± 107 flux respectively and 248.5 ± 86.2, 361.4 ± 104.3 and 455.3 ± 109.7 flux respectively for SAI. (p<0.05)., Conclusions: Thus there seems to be big differences in these 2 populations in endothelial response to these stressors. The difference may be due to genetic variations between the 2 groups of subjects.

In response to a thermal stress, skin blood flow (BF) increases to protect the skin from damage. When a very warm, noxious, heat source (44 °C) is applied to the skin, the BF increases disproportionately faster than the heat stress that was applied, creating a safety mechanism for protecting the skin. In the present investigation, the rate of rise of BF in response to applied heat at temperatures between 32 °C and 40 °C was examined as well as the thermal transfer to and from the skin with and without BF in younger and older subjects to see how the skin responds to a non-noxious heat source. Twenty male and female subjects (10 - 20-35 years, 10 - 40-70 years) were examined. The arms of the subjects were passively heated for 6 min with and without vascular occlusion by a thermode at temperatures of 32, 36, 38 or 40 °C. When occlusion was not used during the 6 min exposure to heat, there was an exponential rise in skin temperature and BF in both groups of subjects over the 6-min period. However, the older subjects achieved similar skin temperatures but with the expenditure of fewer calories from the thermode than was seen for the younger subjects (p<0.05). BF was significantly less in the older group than the younger group at rest and after exposure to each of the three warmest thermode temperatures (p<0.05). As was seen for noxious temperatures, after a delay, the rate of rise of BF at the three warmest thermode temperatures was faster than the rise in skin temperature in the younger group but less in the older group of subjects. Thus, a consequence of ageing is reduced excess BF in response to thermal stress increasing susceptibility to thermal damage. This must be considered in modelling of BF., (Copyright © 2011 Informa UK, Ltd.)

Lipoatrophy (LA) is a rare complication of insulin treatment in type 1 diabetes mellitus. The pathogenesis of insulin-induced LA is still unknown. Many theories suggest immunological reactions. We report a 4-yr-old Saudi girl with LA probably induced by lispro insulin. A review of the literature on the clinical features, pathophysiology, differential diagnosis, and treatment is briefly discussed.