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A young man presented with abdominal pain and vomiting after eating Naphthalene Mothball. He had dyspnea, central cyanosis (SaO2 on air was 67% on air), marked pallor, deep jaundice and dehydration. His urine color was black; and, his plasma in clotted blood sample was brownish. He was treated as methemoglobinemia due to suicidal Naphthalene Mothball poisoning with fluid and electrolyte replacement, ascorbic acid, N-acetylcystine and exchange transfusion twice with four units of whole blood. Dramatic improvement in central cyanosis immediately following exchange transfusion. Psychiatric consultation and counselling were done; he admitted the main reason for committing suicide was socioeconomic stress due to COVID-19.

Glucosamine feeding and genetic activation of the hexosamine biosynthetic pathway (HBP) have been linked to improved protein quality control and lifespan extension in various species. Thus, there is considerable interest in the potential health benefits of dietary supplementation with glucosamine or other HBP metabolites in people. The HBP is a sensor for energy availability and its activation has been implicated in tumor progression and diabetes in higher organisms. As the activation of the HBP has been linked to longevity in lower animals, it is imperative to explore the long-term effects of chronic HBP activation in mammals, which has not been examined so far. To address this issue, we activated the HBP in mice both genetically and through metabolite supplementation, and evaluated metabolism, memory, and survival. GlcNAc supplementation in the drinking water had no adverse effect on weight gain in males but increased weight in young female mice. Glucose or insulin tolerance were not affected up to 20 months of age. Of note, we observed improved memory in the Morris water maze in young male mice supplemented with GlcNAc. Survival was not changed by GlcNAc supplementation. To assess the effects of genetic HBP activation we overexpressed the key enzyme GFAT1 as well as a constitutively activated mutant form in all mouse tissues. We detected elevated UDP-GlcNAc levels in mouse brains, but did not find any effects on behavior, memory, or survival. Together, while dietary GlcNAc supplementation did not extend survival in mice, it positively affected memory and is generally well tolerated.

The aim of this study was to examine the interrelationships between direct (sprint and change-of-direction [COD] velocities) and indirect measures (COD-deficit [CODD], deceleration deficit [DD], and sprint momentum) of speed-related performances in young badminton players. Thirty young male badminton players (age: 16.8 ± 1.4 years; body-mass: 61.5 ± 7.9 kg; height: 170 ± 5.8 cm) performed a 20-m sprint followed by 505 COD tests, on the same day. A Pearson product moment test was applied to determine the relationships among variables. A multiple regression analysis was used to verify whether the combination of CODD and DD increased the capacity to predict COD performance. Large and significant relationships were observed between COD and linear sprint velocity and sprint momentum ( r ranging from 0.62 to 0.84; P < 0.05). COD velocity revealed a moderate significant ( r  = −0.38) and a small non-significant ( r  = 0.29) relationship with CODD and DD, respectively. The multiple regression model combining CODD and DD explained 44% of the variance in COD performance. In summary, young badminton players who sprint faster are equally faster in COD manoeuvres but present higher levels of CODD and DD. Coaches should be aware that faster badminton players may exhibit greater magnitudes of CODD-DD, thus requiring specific interventions to optimize the transition between high deceleration and (re) acceleration phases.

It is well-known that unusual exercise, especially eccentric contraction (ECC), could cause delayed-onset muscle soreness. However, the factors related to the loss of muscle strength and range of motion (ROM) caused by eccentrically damaged muscle, such as increases in muscle soreness, tissue hardness, and pain threshold, have not been investigated in detail. Thus, this study was conducted to investigate the factors related to the loss of muscle strength and ROM caused by eccentrically damaged muscle in a large sample. Fifty-six sedentary healthy young male volunteers were instructed to perform 60 repetitions of ECC exercise. The outcome variables were measured before and 48 h after the ECC exercise. The results showed that a decrease in ROM was correlated to an increase in tissue hardness, whereas a decrease in muscle strength was correlated to an increase in muscle soreness. Our results suggested that tissue hardness must be controlled for ROM loss, and muscle soreness must be controlled for muscle-strength loss.

COVID-19 vaccine-induced thrombotic thrombocytopenia (VITT) is a rare complication of adenoviral vector (ChAdOx1 nCoV-19) vaccine administration. It is presented as thrombocytopenia and thrombotic manifestations in various sites, especially in cerebral veins. Pulmonary emboli have been reported rarely. We present a case of a young male patient who developed severe thrombocytopenia and pulmonary embolism 12 days after the first dose of the vaccine. Severe thrombocytopenia, skin hematomas, and segmental pulmonary emboli were detected. Anti-platelet factor 4 (aPF-4) antibody was highly positive supporting the diagnosis of VITT. Prompt treatment with fondaparinux, intravenous immunoglobulin, and prednisone led to a marked improvement of clinical condition and thrombocytes count. We report the first known case of VITT in Slovakia.

ABSTRACT: Hypertrophic feline muscular dystrophy (HFMD), rarely reported in the literature, is a disease caused by a hereditary recessive dystrophin deficiency linked to the X chromosome, mainly affecting young male cats. Here, we presented the clinical aspects, food management, and clinical evolution of a seven-year-old mixed-breed cat diagnosed with HFMD, having a primary history of progressive tongue protrusion.