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ABSTRACTPurposeIn 2020, the COVID-19 pandemic forced global lockdowns. Herein, we examine the effect of a lockdown exercise programme in a case-study of youth Australian A-league academy football players.MethodsFifty-five u13-u15 age-grade players were provided with a 110 minute exercise programme including technical, tactical, cardiovascular and muscle strengthening exercises to perform 4 per week at home during the 10-week COVID-19 lockdown.ResultsPre/Post lockdown, maximum aerobic speed was determined via the 30–15 intermittent fitness test (IFT). Exercise compliance was high (78.5% CI72.2–83.8) with an average of 3.15 sessions completed each week. All time-loss (TL) and medical attention (MA) injuries were recorded. Pre/Post lockdown, no difference in the mean incidence or burden of total time-loss (TL), match TL, training TL or medical attention (MA) injuries or injury rate ratio (1.21 CI:0.85–2.74) was observed. Similarly, no difference was observed in any injury incidence or burden data or the injury rate ratio (1.53 CI:0.85–2.74) when comparing the 9-week period prior to lockdown with the first 9 weeks post lockdown (9v9 only). A 9.6% (p = <0.01) increase was also observed in Pre/Post 30–15 IFT composite scores (18.7 CI: 18.3–19.1 to 20.5 CI:20–21).ConclusionIn this case study, compliance to the home-based exercise programme was high and no increase in injury was apparent. These findings must however be considered alongside the limitations associated within this case-study.

Hydrogen embrittlement is the limiting factor when it comes to the utilization of advanced highest strength steels in a car body frame. Steels with a tensile strength of greater than 1000 MPa are deemed to be susceptible to hydrogen induced delayed fracture and therefore are not yet widely used. To characterize the deleterious effects of hydrogen embrittlement in advanced highest strength steels the slow strain rate testing in gaseous hydrogen atmosphere is a suitable method for investigating the effect of hydrogen on the materials ductility. Additionally the hydrogen content after slow strain rate testing was measured by means of thermal desorption spectroscopy. By using this technique it is possible to differentiate between diffusible and trapped hydrogen. Diffusible hydrogen may interact with dislocations and therefore changes the fracture behaviour of metals. This was also documented by analysing the fracture surface of the tensile specimen by optical and scanning electron microscopy. The investigations yield a comprehensive view on the susceptibility towards hydrogen induced cracking and allow a comparative view among different steel grades.

The incidence, distribution, size, and histopathology of grossly visible intestinal tumors induced by the parenteral administration of 1,2-dimethylhydrazine dihydrochloride were examined in 32 paired rats fed a nutritionally adequate liquid diet containing 36% of total calories either as ethanol or isocaloric carbohydrates. The liquid diets were begun 4 wk before the first of four weekly injections of 1,2-dimethylhydrazine dihydrochloride. At the time of the subcutaneous application of the procarcinogen, liquid diets were omitted for 3 wk, and were replaced by a standard laboratory diet. This feeding schedule was repeated four times, and after 32 wk the animals were killed. Chronic ethanol ingestion increased the total number of rectal tumors significantly (17 vs. 6, p < 0.02). However, alcohol had no effect on tumor size or histopathology. Chronic ethanol ingestion did not exhibit any cocarcinogenic effect in tissues other than the rectum. A 47% increase in the activity of mucosai alcohol dehydrogenase in the distal colorectum was found between chronically ethanolfed rats and pair-fed controls (0.241 ± 0.019 vs. 0.164 ± 0.020 µmol • mg protein- 1• h-1, p < 0.01). This could in part explain the cocarcinogenic effect of alcohol in this tissue. Fecal bile acids, however, do not play a role as promoters of rectal cancer under the present experimental conditions. The data give experimental support to the epidemiologic findings of an increased incidence of rectal cancer in the alcoholic.

Summary The oral administration of dietary chenodeoxycholic acid (1%), but not of ursodeoxycholic acid (1%), to male Sprague Dawley rats results in a significant increase in the colonic adenylate cyclase activity without any influence on the colonic cyclic-AMP phosphodiesterase activity. No effect of chronic bile acid feeding on the response of colonic adenylate cyclase to prostaglandin E2 and vasoactive intestinal peptide is observed. These data emphasize a dependence of the cyclic-AMP adenylate cyclase activation on the chemical structure of the bile acid. This may be of pathophysiologic relevance with respect to the frequently observed diarrhea as a side effect of oral chenodeoxycholic, but not ursodeoxycholic acid therapy for cholesterol gallstone dissolution in man.

A microsomal ethanol oxidizing system (MEOS) is present in the colonic mucosa of the rat. This MEOS metabolizes ethanol to acetaldehyde at the physiological pH of 7.4. Alcoholdehydrogenase or catalase are not involved in the reaction. The Michaelis Menten constante of the reaction is 13.7±0.3 mM and the maximal velocity is 219±30 pmoles acetaldehyde/mg microsomal protein x min.

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