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When daytime tropical convection develops away from mesoscale disturbances, it typically transitions gradually from dry to shallow to deep convection on hourly timescales. The transition is commonly associated with the formation of larger horizontal boundary‐layer structures and an increasing level of cloud organization aloft. This study demonstrates that a spectral analysis of the resolved high‐resolution sub‐cloud flow features allows for a robust identification of dominant length scales and the quantification of their growth rates during the transition. Furthermore, it is shown that temperature, moisture, and horizontal winds develop multiple length scales with the largest ones growing up to several kilometers in magnitude. However, the vertical velocity behaves in a distinct manner developing significantly smaller values, comparable over land and ocean. This indicates stronger inherent limits of vertical velocity to self‐organize by size. Plain Language Summary: When tropical storms form away from big weather systems, they usually go through several stages, starting with shallow clouds and then gradually intensifying until deep clouds with anvils develop. As the transition progresses, larger flow patterns form in the air close to the ground, and the clouds above become more organized. This study found that by looking at high‐resolution modeling data in terms of energy distribution per structure size, we can see how these patterns change and grow over time. It also found that the sizes of temperature, moisture, and horizontal wind patterns are similar to each other and can be several kilometers wide. But the patterns of vertical motion behave differently, staying smaller and not growing as much, whether over land or ocean. This indicates natural limits to how big the structures of vertical air movement can get during the formation of local storms. Key Points: Simulated transition to deep convection over both land and ocean is analyzed using a novel method based on spectral analysisDominant sub‐cloud length scales for temperature, moisture, and wind grow linearly until the onset of deep convectionNotably, vertical velocity length scale remains at much lower values, indicating a weaker tendency to self‐organize by size [ABSTRACT FROM AUTHOR]

Non-septic olecranon bursitis (NSOB) is the inflammation of the olecranon bursa, which is usually self-limiting with aseptic clinical manifestations. NSOB can be idiopathic or secondary to repetitive trauma or rheumatological conditions. Septic olecranon bursitis (SOB) is usually caused by bacterial skin colonisers, such as staphylococci and streptococci, and patients tend to present with systemic symptoms requiring medical and/or surgical interventions. Herein we present a case of disseminated cryptococcal infection stemming from bilateral septic olecranon bursitis in a previously healthy immunocompetent 24-year-old female. Fluid cultures were positive for Cryptococcus neoformans . Patient underwent bilateral olecranon bursectomy, washouts and debridement. Moreover, the patient was started on long-term intravenous amphotericin B and later switched to oral flucytosine and fluconazole with good effect. Patient had good clinical outcomes at one-year follow-up.  SOB secondary to unusual pathogens, such as Cryptococcus neoformans , is a rare occurrence, and tends to affect immunocompromised individuals. The clinical course of such infections has shown to be subtle and insidious, which in turn hinders the diagnosis and leads to inappropriate treatment administration. Early follow-up and consideration of these organisms, together with appropriate discussion with microbiologists and/or infectious disease teams is crucial to reduce long-term morbidity and mortality., Competing Interests: Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, Bianco et al.)

Introduction Anterior cruciate ligament (ACL) tears are common injuries that can considerably impact an individual's quality of life and athletic performance. In these cases, surgical reconstruction of the ligament can be considered to restore stability to the knee. This study aims to investigate the time taken for individuals to return to sport post-ACL reconstruction, assess the rate of re-injury and evaluate the reliability of the International Knee Documentation Committee (IKDC) and Knee Injury and Osteoarthritis Outcome Score (KOOS) scoring systems in predicting a return to sport at the pre-injury level. Methods In this retrospective study, a total of 104 patients who underwent ACL reconstruction between January 2016 and December 2022 by one surgical team at Mater Dei Hospital, Malta were evaluated using a self-administered questionnaire. The questionnaire was based on different components including the sport practised at the time of injury, sport engagement classification, return to sport, the ability to return to pre-injury levels of performance and re-injury. The participants then had to fill in IKDC and KOOS evaluation forms. Results In this study, 73% (n=76) of individuals successfully returned to sport after ACL reconstruction, with no significant difference being found between professional and recreational athletes (Chi-squared=0.00455, p=0.95). After reconstruction, 31.7% (n=33) of participants experienced an ipsilateral or contralateral ACL tear, with those returning to sport within six months showing a fivefold increase in re-injury risk compared to individuals who returned at eight or 12 months, suggesting a significant association between return duration and re-injury. The relationship between scoring systems and return to sport at the pre-injury level of performance was analysed using binary logistic regression, revealing that achieving scores of 85.6 or higher in IKDC or 89 or higher in KOOS meant having a 95% probability of returning to sport at the pre-injury level. Conclusions By considering these scoring systems with other post-operative criteria, clinicians can offer a more customised rehabilitation plan tailored to each patient who undergoes ACL reconstruction., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2024, Paris et al.)

Background: Delta9-tetrahydrocannabinol (Delta9-THC) induces analgesic effects and alterations of alertness. It has been reported that propofol increases endocannabinoid levels in the brain, but the effects of Delta9-THC on propofol sedation remain unclear. Our aim was to characterize the interaction between Delta9-THC and propofol in terms of sedation and analgesia., Methods: Sedation was monitored by a rota-rod and analgesia by tail-flick latencies. Twenty mice received intraperitoneal injections of 50 mg/kg Delta9-THC with 50, 75 and 100 mg/kg propofol after baseline values were established for each drug. Control experiments were performed with Delta9-THC and thiopental or Intralipid., Results: Injection of 50 mg/kg propofol caused a rapid onset of sedation with a minimum of 24 s on the rota-rod. Fifty mg/kg Delta9-THC alone had no sedative effects. Administration of Delta9-THC significantly reduced the sedative effect of propofol to at least 60 s on the rota-rod (P < 0.001). After increasing the propofol dose to 100 mg/kg in the presence of Delta9-THC, sedation was re-established with 27 s on the rota-rod. Thiopental sedation was significantly reduced (P < 0.01) in the presence of Delta9-THC., Conclusion: The results indicate a dose-dependent antagonistic interaction between Delta9-THC and propofol, and also between Delta9-THC and thiopental.

Background: Meperidine proved to be more effective in treatment of shivering than equianalgesic doses of other opioids, especially pure mu-agonists. Further, meperidine has well known nonopioid actions including agonistic effects at alpha2-adrenoceptors in vitro. Accordingly, the authors investigated nonopioid receptor-mediated effects of meperidine on thermoregulation using a mice model of nonshivering thermogenesis. To differentiate conceivable alpha2-adrenoceptor subtype specific interactions the authors analyzed wild-type mice and knock-out mice with deletion of the alpha2A-, alpha2B-, or alpha2C-adrenoceptor., Methods: Ten mice per group (n = 60) were injected with saline, meperidine (20 mg/kg), saline plus naloxone (125 microg/kg), meperidine plus naloxone, fentanyl (50 microg/kg) plus naloxone, or meperidine plus atipamezole (2 mg/kg) intraperitoneally. Each mouse was subjected to the six different treatments. Then they were positioned into a plexiglas chamber where rectal temperature and mixed expired carbon dioxide were measured while whole body cooling was performed. Maximum response intensity and thermoregulatory threshold temperature of nonshivering thermogenesis were analyzed., Results: Meperidine decreased the thermoregulatory threshold temperature in wild-type mice and alpha2B- and alpha2C-adrenoceptor knock-out mice. This effect ended after injection of the alpha2-adrenoceptor antagonist atipamezole. In wild-type and alpha2B-adrenoceptor knock-out mice, the decrease of thermoregulatory threshold was not reversible by administration of the opioid receptor antagonist naloxone. In contrast, in alpha2A-adrenoceptor knock-out mice, no decline of thermoregulatory threshold following meperidine injection was detectable. Maximum response intensity of nonshivering thermogenesis was comparable in all groups., Conclusions: The authors' results suggest a major role of alpha2-adrenoceptors, especially the alpha2A subtype, in the mediation of thermoregulatory effects caused by meperidine in mice.

Background: Dexmedetomidine is a potent and selective alpha2-adrenoceptor (alpha2AR) agonist that exhibits a broad pattern of actions, including sedation, analgesia, and neuroprotection. Recent studies have emphasized the role of phosphorylated extracellular signal-regulated protein kinases (pERK1 and 2) in coupling rapid events such as neurotransmitter release and receptor stimulation long-lasting changes in synaptic plasticity and cell survival. Here, the authors hypothesized that dexmedetomidine increases pERK1 and 2 content and examined the mechanisms involved in this effect., Methods: The effects of dexmedetomidine and their sensitivity to various pharmacologic agents on expression of pERK1 and 2 were studied by Western blots in hippocampal slices obtained from rats, wild-type mice, and mice carrying targeted deletions of the alpha2AR subtypes., Results: Dexmedetomidine induced a concentration-related increase in the expression of pERK1 and 2 in rat hippocampal slices (EC50 [95% confidence interval] for pERK1, 0.97 [0.68-1.37] microm; for pERK2, 1.15 [0.62-2.14] microm). This effect was insensitive to the inhibitors of the alpha2AR-mediated signaling pathway, to prazosin, and to PP2, an inhibitor of the focal adhesion kinase-Src kinases. In contrast, it was still present in mice deleted for each of the alpha2AR subtypes and was markedly decreased by the antagonist of the I1-imidazoline receptors efaroxan, by phospholipase C and protein kinase C inhibitors, and by PD 098059, a direct inhibitor of ERK1 and 2 phosphorylation., Conclusion: Dexmedetomidine increases the expression of pERK1 and 2 via mechanisms independent of alpha2AR activation. The I1-imidazoline receptors likely contribute to these effects. The results may be relevant to some long-term effects (e.g., neuroprotective) of dexmedetomidine in the brain.

Background: The IV anesthetic, etomidate, has structural and clinical similarities to specific alpha2-adrenoceptor agonists such as dexmedetomidine. We investigated whether the sedative effects of etomidate may be mediated by alpha2-adrenoceptors., Methods: The anesthetic potency of etomidate (1-20 microM) was determined in Xenopus laevis tadpoles in the absence and presence of the specific alpha2-adrenoceptor antagonist atipamezole (10 microM). Anesthesia was defined as loss of righting reflex. Nonlinear logistic regression curves were fitted to the data and half-maximal effective concentrations and the slopes of the curves were calculated. Additionally, sedative/ hypnotic effects of etomidate (8 mg/kg IP) were studied by rotarod test in wild-type (WT) mice and mice carrying targeted deletions of the alpha2A-adrenoceptor gene (alpha2A-KO). Data are presented as mean +/- sem., Results: The fraction of anesthetized tadpoles increased with increasing concentrations of etomidate. Atipamezole significantly increased the half-maximal effective concentration of etomidate (4.5 +/- 0.2 microM; slope: 2.6 +/- 0.3) to 8.4 +/- 0.4 microM (slope: 2.3 +/- 0.3). Etomidate resulted in time-dependent sedative effects in all mice, as assessed by rotarod performance. In WT mice, the sedative effects of etomidate were not decreased by atipamezole (2 mg/kg). Consistently, etomidate-induced sedation was not reduced in alpha2A-KO animals compared with WT mice., Conclusions: The sedative effects of etomidate exhibit a species-specific interaction with alpha2-adrenoceptors. Although the decrease in potency of etomidate by atipamezole may be caused by an interaction with alpha2-adrenoceptors in X. laevis tadpoles, results in mice indicate that the hypnotic effect of etomidate does not require alpha2-adrenoceptors.

We performed the current study in mice lacking individual alpha2-adrenoceptor subtypes to elucidate the contribution of alpha(2)-adrenoceptor subtypes to the neuroprotective properties of dexmedetomidine in a model of perinatal excitotoxic brain injury. On postnatal Day 5, wild-type mice and mice lacking alpha2A-adrenoceptor (alpha2A-KO) or alpha2C-adrenoceptor subtypes (alpha2C-KO) were randomly assigned to receive dexmedetomidine (3 microg/kg) or phosphate-buffered saline intraperitoneally. Thirty minutes after the intraperitoneal injection, the glutamatergic agonist ibotenate (10 microg) was intracerebrally injected, producing transcortical necrosis and white matter lesions that mimic perinatal human hypoxic-like lesions. Quantification of the lesions was performed on postnatal Day 10 by histopathologic examination. Dexmedetomidine reduced mean lesion size in the cortex of wild-type mice and alpha2C-KO mice by 44% and 49%, respectively. Ibotenate-induced white matter lesions were reduced by 71% (wild-type mice) and 75% (alpha2C-KO mice) after pretreatment with dexmedetomidine. In contrast, in alpha2A-KO mice, dexmedetomidine did not protect against the cortical excitotoxic insult, and white matter lesions were even more pronounced (82% increase of mean lesion size). Dexmedetomidine provides potent neuroprotection in a model of perinatal excitotoxic brain damage. This effect was completely abolished in alpha2A-KO mice, suggesting that the neuroprotective effect is mediated via the alpha2A-adrenoceptor subtype.

Meperidine has potent antishivering properties. The underlying mechanisms are not fully elucidated, but recent investigations suggest that alpha2-adrenoceptors are likely to be involved. We performed the current study to investigate the effects of meperidine on nonshivering thermogenesis in a model of thermoregulation in mice. After injection (0.1 mL/kg intraperitoneally) of saline, meperidine (20 mg/kg), the specific alpha2-adrenoceptor antagonist atipamezole (2 mg/kg), plus saline or atipamezole plus meperidine, respectively, mice were positioned in a Plexiglas chamber. Rectal temperature and mixed expired carbon dioxide were measured after provoking thermoregulatory effects by whole body cooling. Maximum response intensity of nonshivering thermogenesis and the thermoregulatory threshold for nonshivering thermogenesis, which was defined as the temperature at which a sustained increase in expiratory carbon dioxide can be measured, were investigated. Meperidine significantly decreased the threshold of nonshivering thermogenesis (36.6 degrees C +/- 0.7 degrees C) versus saline (37.9 degrees C +/- 0.6 degrees C) and versus atipamezole plus saline (37.8 degrees C +/- 0.4 degrees C; P <0.01). This effect was abolished after administration of meperidine combined with atipamezole (37.7 degrees C +/- 0.6 degrees C; P <0.05). Meperidine did not decrease the maximum intensity of nonshivering thermogenesis. The results suggest a major role of alpha2-adrenoceptors in the inhibition of thermoregulation by meperidine in mice.