Butterworth Hospital

Since the outbreak of COVID-19, teaching and learning have experienced various challenges and shifts from normal classroom dimensions to what several scholars regard as the "new normal." This situation disrupted teaching and learning systems, with various institutions trying to find alternative ways to ensure effective curriculum implementation. In the event that COVID-19 seems to be a thing of the past, there is a need to understand how best education actors could navigate the new shift. Therefore, researchers need to continue to work on improving educators' understanding of how best to teach and learn and how students and educational institutions respond to the shift in the post-pandemic classrooms. Based on this, a special issue was initiated to galvanize findings, views, approaches, and strategies to enhance sustainable post-COVID-19 pedagogical needs. Therefore, this special issue plays an essential role in helping students, scholars, educators, policymakers and educational agencies understand the present pedagogical shift and prepare for the future. Keywords: Post COVID-19 Classrooms, teaching and learning, new normal, pedagogical needs.

This article describes how teachers in rural junior secondary schools perceive current programmes for continuing professional teacher development (CPTD). The sample comprised 18 participants and ut...

Recent evidence has suggested that patients with stable chronic heart failure (CHF) may respond favorably to a progressive exercise program. The use of noninvasive hemodynamic monitoring and B-type natriuretic peptide (BNP) measurement in these patients is not well reported. This study investigated the utility of noninvasive hemodynamic monitoring and point-of-care BNP in a cardiac rehabilitation outpatient setting. Patients with stable CHF were assigned to a supervised 12-week exercise program (n = 13) or control (n = 6). At baseline and at the end of the study period, patients were assessed for functional and quality-of-life status. Point-of-care BNP and noninvasive hemodynamic parameters were also obtained. As expected, patients assigned to the exercise group showed significant improvement in quality of life and distance covered by the 6-minute walk test, but control subjects showed no such changes. There was a trend toward improved BNP in the exercise group, with 73% of these patients showing a decrease in comparison with 67% of controls showing an increase. There was a significant improvement in stroke volume in the exercise group but not in the control group. Both BNP and noninvasive hemodynamic monitoring can be utilized in the cardiac rehabilitation outpatient setting and seem to mirror the favorable response to exercise of other functional tests.

ABOUT THE AUTHOR Ann M. Butterworth is aNP with the Senior Campus Physician’s Group at the Charlestown Erickson Retirement Community, Baltimore, Md.

Commercial anthraquinone (AQ) (9,10-anthracenedione) is produced by at least three different production methods worldwide: oxidation of anthracene (AQ-OX), Friedel-Crafts technology (AQ-FC) and by Diels-Alder chemistry (AQ-DA), with the final product varying in color and purity. AQ-OX begins with anthracene produced from coal tar and different lots can contain various contaminants, particularly the mutagenic isomers of nitroanthracene. AQ has been reported to be negative in a variety of genotoxicity tests including numerous Ames Salmonella mutagenicity assays. In addition, we report that AQ-DA is negative in the Salmonella-Escherichia coli reverse mutation assays, the L5178Y mouse lymphoma forward mutation assay, for inducing chromosomal aberrations, polyploidy or endoreduplication in Chinese hamster ovary cells, and in the in vivo mouse micronucleus assay. Further, a previous 18 month bioassay conducted with AQ administered to male and female B6C3F(1) and (C57BL/6xAKR)F(1) mice reported no induction of cancer. Thus, it was somewhat unexpected that in a long-term study conducted by the National Toxicology Program (NTP) AQ-OX induced a weak to modest increase in tumors in the kidney and bladder of male and female F344/N rats and a strong increase in the livers of male and female B6C3F(1) mice. In the studies reported here, a sample of the AQ-OX used in the NTP bioassay was shown to be mutagenic in the Ames tester strains TA98, TA100 and TA1537. Addition of an S9 metabolic activation system decreased or eliminated the mutagenic activity. In contrast, the purified NTP AQ-OX as well as the technical grade samples AQ-FC and AQ-DA were not mutagenic in the Ames test. The chemical structure of AQ does not suggest that the parent compound would be DNA reactive. Therefore, a mutagenic contaminant was present in the NTP bioassay sample that is either directly mutagenic or can be activated by bacterial metabolism. Analytical studies showed that the primary contaminant 9-nitroanthracene (9-NA) was present in the NTP AQ-OX at a concentration of 1200 p.p.m., but not in the purified material. The 9-NA and any other contaminants that might have been present in the NTP AQ-OX induced measurable mutagenicity at 9-NA concentrations as low as 0.15 microg/plate in tester strain TA98, indicating potent mutagenic activity. On the basis of revertants per microgram, 9-NA was more potent than benzo[a]pyrene (B[a]P) and was about equally as potent as the 2-nitrofluorene run concurrently as positive controls. TD(50) quantitative carcinogenicity potency estimates indicate that a carcinogen of a potency in the range between B[a]P and dimethylnitrosamine would be required to produce the observed carcinogenic response at the levels of the contaminants found in the test sample. While recognizing that there are limitations in extrapolating mutagenic potency to potential carcinogenic potency, these estimates do indicate that it is plausible that the 9-NA contaminant might have been responsible for all of the tumor induction observed in the NTP study. In fact, in the absence of reliable cancer data, the genetic toxicology profile indicates that AQ would not be a genotoxic carcinogen. Thus, no conclusion as to the carcinogenic activity of AQ can be made at this time.

The oral-facial-digital syndromes (OFDS) have in common minor facial and oral anomalies (including tongue lobulation and/or hamartomas, accessory frenula, and alveolar anomalies) and variable digital defects such as polydactyly. The classification based on the presence of additional findings [Toriello, 1988, 1993] is not perfect, as many reported examples of a particular OFDS have some other condition. Here we describe six children, all diagnosed as having OFDS IV (OFDS with tibial defects), whose manifestations illustrate the apparent genetic heterogeneity. Am. J. Med. Genet. 69:250–260, 1997. © 1997 Wiley-Liss, Inc.

These studies examined the effect in rats of carnitine supplementation on variables of fat metabolism altered by administration of sodium pivalate, a compound which induces a carnitine deficiency. Weanling male rats received 20 mmol/L sodium pivalate or 20 mmol/L sodium bicarbonate in their drinking water for 2 wk. They were food-deprived for 24 h, and to maximize fatty acid oxidation, were cold-stressed for 4 h. In Experiment 1, group 1 received the bicarbonate, group 2 received the pivalate, group 3 received the pivalate and 0.46 mmol L-carnitine in the diet/d, while group 4 received the pivalate and 0.95 mmol L-carnitine in the diet/d. In Experiment 2, group 1 received unsupplemented drinking water, group 2 received the bicarbonate, group 3 received the pivalate, and group 4 received the pivalate and 0.95 mmol L-carnitine in the diet/d. Pivalate-treated rats given the low carnitine diet had plasma and liver triglyceride levels (Experiment 1), plasma β-hydroxybutyrate concentrations (Experiments 1 and 2) and urinary dicarboxylic acid excretion (Experiment 2) significantly greater than those of controls (P < 0.05). The reduced tissue carnitine concentrations, starvation ketosis and lipid accumulation in the liver are findings also reported for human secondary carnitine deficiency due to organic acidurias. Supplementing the diet with L-carnitine at the level of 0.95 mmol/d significantly raised plasma and tissue carnitine concentrations and reduced the plasma β-hydroxybutyrate and liver triglyceride concentrations to levels not significantly different than control values. Carnitine supplementation ameliorates the degree of liver lipid accumulation and exaggerated starvation ketosis induced by pivalate.

Source Citation Shaw LJ, Eagle KA, Gersh BJ, Miller DD. Meta-analysis of intravenous dipyridamole-thallium-201 imaging (1985 to 1994) and dobutamine echocardiography (1991 to 1994) for risk stratif...