OBJECTIVEEmbryonic movements (EM) and angiogenesis pathways are evolutionarily conserved mechanisms which are essential for proper embryonic development. Deviations in these processes by exposure to cigarette smoke condensate (CSC) may cause vascular and morphogenetic disorders.

METHODSUsing chicken and mouse embryos, we have demonstrated the in vivo effects of CSC on EM, vascular development, and organogenesis.

RESULTSExamination of the CSC exposed chicken embryos revealed a significant reduction in EM, stunted growth, deviated pattern of blood vessels, hemorrhages, and localized necrosis. Likewise, mouse embryos that were exposed to CSC at E8.5 and E9.5 died between E11.5 and E12.5, respectively. These mouse embryos showed defects in morphogenesis and remodeling of the embryonic vasculature, while littermate controls showed normal development.

CONCLUSIONSCigarette smoking during pregnancy is fatal for growing embryos. CSC may induce the remodeling of embryonic vasculature, leading to various pathologies.

Analysis of Variance ; Animals ; Chick Embryo ; Embryonic Development ; drug effects ; Female ; Maternal Exposure ; adverse effects ; Mice ; Mice, Inbred C57BL ; Movement ; drug effects ; Organogenesis ; drug effects ; Pregnancy ; Smoke ; adverse effects ; Tobacco ; Vascular Malformations ; chemically induced

Prosthetic valve endocarditis with aortic root abscess is a serious condition requiring urgent surgical intervention. We present a case caused by an infected Bentall mechanical valve conduit after cardiac surgery in a patient who was referred for a suprasternal pulsatile mass. The patient also had 1 episode of sentinel haemorrhage.
Abscess ; Endocarditis ; Humans ; Thoracic Surgery

Prosthetic valve endocarditis with aortic root abscess is a serious condition requiring urgent surgical intervention. We present a case caused by an infected Bentall mechanical valve conduit after cardiac surgery in a patient who was referred for a suprasternal pulsatile mass. The patient also had 1 episode of sentinel haemorrhage.

Traumatic brain injury (TBI) causes disability and death, accelerating the progression towards Alzheimer’s disease and Parkinson’s disease (PD). TBI causes serious motor and cognitive impairments, as seen in PD that arise during the period of the initial insult. However, this has been understudied relative to TBI induced neuroinflammation, motor and cognitive decline that progress towards PD. Neuronal ubiquitin-C-terminal hydrolase- L1 (UCHL1) is a thiol protease that breaks down ubiquitinated proteins and its level represents the severity of TBI. Previously, we demonstrated the molecular action of glia maturation factor (GMF); a proinflammatory protein in mediating neuroinflammation and neuronal loss. Here, we show that the weight drop method induced TBI neuropathology using behavioral tests, western blotting, and immunofluorescence techniques on sections from wild type (WT) and GMF-deficient (GMF-KO) mice. Results reveal a significant improvement in substantia nigral tyrosine hydroxylase and dopamine transporter expression with motor behavioral performance in GMF-KO mice following TBI. In addition, a significant reduction in neuroinflammation was manifested, as shown by activation of nuclear factor-kB, reduced levels of inducible nitric oxide synthase, and cyclooxygenase- 2 expressions. Likewise, neurotrophins including brain-derived neurotrophic factor and glial-derived neurotrophic factor were significantly improved in GMF-KO mice than WT 72 h post-TBI. Consistently, we found that TBI enhances GFAP and UCHL-1 expression and reduces the number of dopaminergic TH-positive neurons in WT compared to GMF-KO mice 72 h post-TBI. Interestingly, we observed a reduction of THpositive tanycytes in the median eminence of WT than GMF-KO mice. Overall, we found that absence of GMF significantly reversed these neuropathological events and improved behavioral outcome. This study provides evidence that PD-associated pathology progression can be initiated upon induction of TBI.