Background: Many Jordanian university students complain of the behavior of some teaching staff. Also, they complain of the grading systems in universities. Aim: This study concerns the occurrence of different forms of student mistreatment and student mistrust of the grading system in the Jordan University of Science and Technology (JUST) as an example of universities in Jordan. Method: A total of 500 students in five health related faculties in JUST responded to a questionnaire. Results: Our results were as follow: (i) 61% of the students had experienced at least one form of mistreatment; (ii) perceived mistreatment most often (52%) had taken the form of psychological mistreatment (shouting and humiliation); (iii) other forms of mistreatment such as physical harm (32%), mistreatment related to religion (36%), mistreatment related to external appearance (35%), sexual harassment (33%) and mistreatment related to specialty (29%) were also common; (iv) with the exception of mistreatment related to specialty which was high among the nursing students, perceived mistreatment did not vary significantly between the different faculties; (v) the male students (66%) complain more than female students (56%); (vi) perceived mistreatment was exceptionally high among the Israeli Arabs, 83% compared to 59% for the Jordanians and 65% for other nonJordanian Arabs; (vii) fellow students (44%), professors (37%) and laboratory technicians (19%) were cited as major sources of mistreatment. Many students (66%) believe that grading system in JUST is unfair. Ninety seven percent of the Israeli Arabs did not trust the grading system compared to 64% of the Jordanians and 66% of the non-Jordanian Arabs. Conclusions: This study suggests that, feelings of mistreatment among university students is strong while their trust of the university grading system is low. Perceived mistreatment and an unfair grading system may be a major source of stress among our students and may affect the process of teaching and learning in our country. This should alert the university administration to face these issues and try to solve them.

Allopurinol, a competitive inhibitor of xanthine oxidase, was found to have a protective effect on ischemic myocardium. Its mechanism of action is still controversial. We used Langendorff isolated rat heart preparation to test the hypothesis that allopurinol could maintain a level of the adenine nucleotide pool (ATP, ADP, and AMP) that would protect and improve the functional activity of the heart during a period of hypoxia. Hearts were initially perfused for 30 min until steady state was attained. This was followed by 20 min of experimental perfusion divided into 5 min of control perfusion followed by 15 min of hypoxic perfusion with or without allopurinol in the perfusate. Hearts were quick-frozen and enzymatically analyzed for adenine nucleotides and creatine phosphate at the end of the hypoxic period. Left ventricular pressure, heart rate, and coronary flow were measured in all preparations. Allopurinol (0.1 mM) treated hearts had greater levels of ATP (12.3 +/- 0.8 vs. 9.3 +/- 0.8 micromol/g dry weight; p < 0.01). This improvement occurred in the presence as well as the absence of glucose. Total adenine nucleotides improved from 17 +/- 1 to 20.3 +/- 2.4 micromol/g dry weight (p < 0.01). This improvement also occurred in the presence as well as in the absence of glucose in the perfusate. It also improved cell energy state significantly in the presence as well as the absence of glucose. There was insignificant change in creatine phosphate. Allopurinol improved left ventricular pressure from 38 +/- 7% to 55 +/- 9% (p < 0.002) in the presence of glucose and from 8 +/- 3% to 27 +/- 6.3% (p < 0.001) in the absence of glucose. Coronary flow improved from 110 +/- 5% to 120 +/- 8% (p < 0.04) in the presence of glucose. These results support the suggestion that allopurinol at 0.1 mM exerts its protective effect on rat heart during hypoxia by enhancing the adenine nucleotide pool.

The purpose of this study was to examine the effects of exercise on anterior pituitary hormones (adrenocorticotropic hormone (ACTH), leutinizing hormone (LH) and growth hormone) as well as on cortisol at low altitude (350 meters below the sea level) and to compare these effects with those at a moderate level altitude (620 meters above the sea level). Ten male athletes with running experience participated in a 21-Km competitive race. Serum levels of ACTH, LH, growth hormone and cortisol were measured before and after the race at each of the altitudes. A significant increase in the serum levels of ACTH and growth hormone were observed in response to this exercise at low altitude. Similar exercise at 620 meters above the sea level resulted in a significant increase only in the serum levels of growth hormone. Serum levels of LH were not affected by this kind of exercise at both altitudes. Serum cortisol levels were increased following exercise at both altitudes. Altogether, these observations show a differential response of the anterior pituitary to exercise at low and normal altitudes. These data suggest that ACTH may have a role in the acclimatization to exercise at low altitudes. The role of growth hormone and LH in this conditioning process seems to be insignificant. The changes in serum cortisol levels in response to exercise at both altitudes correlate well with the effect of exercise on energy metabolism.

Objectives: To investigate the effects of Ramdan fasting on plasma levels of ACTH and cortisol in athletic students living in the Jordan Valley (JV) and compare them to those living at above sea level in Ramtha City (RC). Methods: Sample collection and measurements were done in November 1998 from non-fasting and in December 1998 from fasting people. Results: ACTH levels in non-fasting subjects in the JV were 36 ± 4 IU/ml compared to 43 ± 3 IU/ml for those in RC. Cortisol levels were 483 ± 76 (JV) and 539 ± 89 nmol/l (RC). Fasting led to an increase in ACTH (49 ± 6 (JV) and 58 ± 5 IU/ml (RC)) and cortisol levels (637 ± 101 (JV) and 805 ± 72 nmol/l (RC)). Conclusion: Fasting increases ACTH and cortisol levels in an altitude-independent fashion.

Rett syndrome (RTT) is a rare disability causing female-oriented pediatric neurodevelopmental unmet medical need. RTT was recognized in 1966. However, over the past 56 years, the United States Food and Drug Administration (USFDA) has authorized no effective treatment for RTT. Recently, Trofinetide was approved by the USFDA on 10 March 2023 as the first RTT treatment. This article underlines the pharmaceutical advancement, patent literature, and prospects of Trofinetide. The data for this study were gathered from the PubMed database, authentic websites (Acadia Pharmaceuticals, Neuren Pharmaceuticals, and USFDA), and free patent databases. Trofinetide was first disclosed by Neuren Pharmaceuticals in 2000 as a methyl group containing analog of the naturally occurring neuroprotective tripeptide called glycine-proline-glutamate (GPE). The joint efforts of Acadia Pharmaceuticals and Neuren Pharmaceuticals have developed Trofinetide. The mechanism of action of Trofinetide is not yet well established. However, it is supposed to improve neuronal morphology and synaptic functioning. The patent literature revealed a handful of inventions related to Trofinetide, providing excellent and unexplored broad research possibilities with Trofinetide. The development of innovative Trofinetide-based molecules, combinations of Trofinetide, patient-compliant drug formulations, and precise MECP2-mutation-related personalized medicines are foreseeable. Trofinetide is in clinical trials for some neurodevelopmental disorders (NDDs), including treating Fragile X syndrome (FXS). It is expected that Trofinetide may be approved for treating FXS in the future. The USFDA-approval of Trofinetide is one of the important milestones for RTT therapy and is the beginning of a new era for the therapy of RTT, FXS, autism spectrum disorder (ASD), brain injury, stroke, and other NDDs.