Symptomatic pulmonary bullet emboli should be managed with endovascular retrieval when available or operative therapy. Asymptomatic intravascular bullet emboli may be managed conservatively as seen in our patient.

The CACNA1C gene that encodes the L-type Ca channel (LTCC) Ca1.2 subunit has emerged as a candidate risk gene for multiple neuropsychiatric disorders including bipolar disorder, major depressive disorder, and schizophrenia, all marked with depression-related symptoms. Although cacna1c heterozygous (HET) mice have been previously reported to exhibit an antidepressant-like phenotype, the molecular and circuit-level dysfunction remains unknown. Here we report that viral vector-mediated deletion of cacna1c in the adult prefrontal cortex (PFC) of mice recapitulates the antidepressant-like effect observed in cacna1c HET mice using the sucrose preference test (SPT), forced swim test (FST), and tail suspension test (TST). Molecular studies identified lower levels of REDD1, a protein previously linked to depression, in the PFC of HET mice, and viral-mediated REDD1 overexpression in the PFC of these HET mice reversed the antidepressant-like effect in SPT and TST. Examination of downstream REDD1 targets found lower levels of active/phosphorylated Akt (S473) with no change in mTORC1 phosphorylation. Examination of the transcription factor FoxO3a, previously linked to depression-related behavior and shown to be regulated in other systems by Akt, revealed higher nuclear levels in the PFC of cacna1c HET mice that was further increased following REDD1-mediated reversal of the antidepressant-like phenotype. Collectively, these findings suggest that REDD1 in cacna1c HET mice may influence depression-related behavior via regulation of the FoxO3a pathway. Cacna1c HET mice thus serve as a useful mouse model to further study cacna1c-associated molecular signaling and depression-related behaviors relevant to human CACNA1C genetic variants.

Plant growth regulators are naturally biosynthesized chemicals in plants that influence physiological processes. Their synthetic analogous trigger numerous biochemical and physiological processes involved in the growth and development of plants. Nowadays, due to changing climatic scenario, numerous biotic and abiotic stresses hamper seed germination, seedling growth, and plant development leading to a decline in biological and economic yields. However, plant growth regulators (PGRs) can potentially play a fundamental role in regulating plant responses to various abiotic stresses and hence, contribute to plant adaptation under adverse environments. The major effects of abiotic stresses are growth and yield disturbance, and both these effects are directly overseen by the PGRs. Different types of PGRs such as abscisic acid (ABA), salicylic acid (SA), ethylene (ET), and jasmonates (JAs) are connected to boosting the response of plants to multiple stresses. In contrast, PGRs including cytokinins (CKs), gibberellins (GAs), auxin, and relatively novel PGRs such as strigolactones (SLs), and brassinosteroids (BRs) are involved in plant growth and development under normal and stressful environmental conditions. Besides, polyamines and nitric oxide (NO), although not considered as phytohormones, have been included in the current review due to their involvement in the regulation of several plant processes and stress responses. These PGRs are crucial for regulating stress adaptation through the modulates physiological, biochemical, and molecular processes and activation of the defense system, upregulating of transcript levels, transcription factors, metabolism genes, and stress proteins at cellular levels. The current review presents an acumen of the recent progress made on different PGRs to improve plant tolerance to abiotic stress such as heat, drought, salinity, and flood. Moreover, it highlights the research gaps on underlying mechanisms of PGRs biosynthesis under stressed conditions and their potential roles in imparting tolerance against adverse effects of suboptimal growth conditions.

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