Citations

Tube thoracostomy (TT) insertion can serve as a life-saving adjunct for thoracic trauma. Unfortunately, suboptimal positioning using the open, standard of care technique is associated with complications resulting in impaired TT function. Using a porcine model, we aimed to determine whether a magnetic chest tube positioning system (MCTPS) could be utilized to direct the intrathoracic TT position. Using recently deceased cross-bred domestic swine, we performed TT using our MCTPS and the standard of care open technique. The operator held one magnet outside of the thorax. The second magnet was positioned at the distal aspect of the TT. The operator was tasked with positioning the TT to distinct premarked intra-thoracic locations under blinded conditions. The experiment was video-recorded through an open sternotomy incision. As a control, TT was inserted using the standard of care open technique. The utilization of MCTPS successfully directed TT from one premarked location to another in 4 of 5 attempts (80%). Conversely, the control TT without magnetic guidance failed to navigate the premarked intra-thoracic locations with 0 of 5 attempts successful (p = 0.05). Positional flaws after TT placement are common. We demonstrate the feasibility of the MCTPS as an alternative to traditional hand-guided technique under simulated TT insertion conditions. The MCTPS is possibly superior to the current standard of care technique of TT. Additional studies are needed to develop this emerging technology in humans.

Objective: To report the presentation, diagnosis, management, and convalescence of labyrinthine sequestrum (LS) and summarize all previously published cases. Patient(s): Eleven-year-old female with LS. Intervention(s): Multidisciplinary diagnostic evaluation and treatment. Main Outcome Measures: Imaging and laboratory findings, medical and surgical treatment. Results: We describe a case of LS secondary to medically recalcitrant suppurative otitis media in an 11-year-old female and review all eight previously reported cases. The index patient presented after 6 months of otitis media, profound unilateral hearing loss, with symptoms suggesting meningitis. Temporal bone CT demonstrated marked bony destruction of the left otic capsule. Gadolinium-enhanced MRI showed an enhancing process with evidence of meningitis and subdural empyema. The patient was treated with surgical debridement and culture directed antibiotic therapy. Posttreatment imaging showed resolution of intracranial infection with fibrous bony healing of the otic capsule resembling fibrous dysplasia. Conclusion: LS is a rare form of labyrinthitis characterized by centrifugal destruction of the otic capsule. The current index case highlights the importance of combined medical and surgical treatment and describes for the first time in the literature the fibrous ossification of the otic capsule following disease resolution.

Recent studies in cultured cells have provided evidence that a variety of pathobiologic stimuli, including high glucose, angiotensin II, and thromboxane A 2 , trigger a signaling pathway leading to autocrine induction of TGF-β1. TGF-β1 production through this pathway may profoundly affect cell growth, matrix synthesis, and response to injury. This study examines the role of autocrine versus exogenously added TGF-β1 in cellular proliferation and collagen IV production, critical targets of TGF-β1 signaling, using renal cells derived from TGF-β1 knockout (KO) animals or wild-type (WT) controls. Growth of WT and KO cells was assessed by cell counting and [ 3 H]thymidine uptake. Basal and TGF-β1-stimulated collagen production was assessed by Northern and Western blotting; transcriptional activity of the α1(IV) collagen gene was assessed by transient transfection analysis. KO cells grew at a faster rate than WT cells carefully matched for plating density and passage number. This increased growth rate was paralleled by increases in [ 3 H]thymidine uptake. KO cells expressed lower levels of the cell cycle inhibitors p21 and p27 than WT cells. KO cells failed to express TGF-β1, as expected. Basal TGF-β3 mRNA levels were higher in KO cells than in WT cells. WT cells expressed higher basal levels of TGF-β2 mRNA than KO cells. Basal α1(IV) and α2(IV) collagen mRNA and protein expression were significantly lower in KO cells than WT cells. Administration of exogenous TGF-β1 induced collagen IV production in both KO and WT cells. Although basal transcriptional activity of an α1(IV) collagen-CAT construct was lower in KO cells than WT cells, administration of exogenous TGF-β1 was associated with significant increases in transcriptional activity of this construct in both KO and WT cells. These studies provide evidence that autocrine production of TGF-β1 may play a critical role in regulation of growth and basal collagen IV production by renal tubular epithelial cells.

Purpose: To describe state laws that govern the optometric practice of glaucoma management in the United States and to correlate those laws with state demographics upto 2015. Materials and Methods: We performed a cross-sectional ecological study of the 50 United States and the District of Columbia. Regulations governing optometric scope of practice as written by each state Board of Optometry were reviewed. Specific optometric privileges assessed included: ability to manage glaucoma independently, use of diagnostic pharmaceutical agents, use of therapeutic pharmaceutical agents (including topical and oral steroids and other oral pharmaceutical agents), IV injections, intraocular injections, therapeutic lasers, presence of defined referral, and comanagement guidelines, and hours of yearly continuing education needed for glaucoma management. Optometric privilege was compared with demographic and employment information for each state. Results: Optometrists in all states, except for Massachusetts, and the District of Columbia are allowed to manage glaucoma; 16 states have defined comanagement guidelines. Therapeutic lasers are allowed in 3 states: Kentucky, Louisiana, and Oklahoma. States with defined comanagement guidelines had a mean of 6.9±1.9 ophthalmologists per 100,000 people, significantly more than the 5.3±1.1 in states without defined comanagement of glaucoma (P<0.01). Binary logistic regression showed that, accounting for population and area, the higher the number of optometrists in a state, the less likely there is to be defined comanagement [β (SE)=−0.008 (0.003), P=0.02] and the greater the number of ophthalmologists in a given state, the more likely a state has defined comanagement [β (SE)=−0.13 (0.006)]. Conclusions: There is a diversity of regulations that govern optometric management of glaucoma in each of the 50 states and the District of Columbia. The number of optometrists and ophthalmologists in a state may influence state regulations governing optometric practice and referral guidelines.

AbstractObjectivesThis study sought to compare the clinical outcomes of percutaneous coronary interventions (PCIs) performed by sleep deprived and non‐sleep deprived operators.BackgroundInterventional cardiologists are at risk for sleep deprivation as they often have to perform emergent procedures at night, but the effects of sleep deprivation on clinical outcomes have received limited study.MethodsWe examined the frequency, clinical characteristics, and outcomes of daytime PCIs performed by sleep deprived and non‐sleep deprived operators at a tertiary medical center. Operators were considered sleep deprived when performing a daytime (7 am–11:59 pm) procedure preceded by a nighttime (12 am–6:59 am) procedure on the same date.ResultsOf the 12,680 daytime PCIs performed from 6/29/09 to 12/30/2016, 367 (2.9%) were performed by sleep deprived operators. Patients undergoing PCI performed by a sleep deprived operator were more likely to be younger, white, and to present with ST‐elevation acute myocardial infarction (STEMI). The incidence of in‐hospital death (1.1% vs. 1.3%, P = 1.0) and bleeding within 72 hr (3.9% vs. 2.9%, P = 0.29) were similar for procedures performed by sleep‐deprived and non‐sleep deprived operators. When the sleep deprived group was further stratified based on degree of sleep deprivation or length of sleep interruption, differences in mortality and total bleeding remained non‐significant.ConclusionsIn this large single center study, operator sleep deprivation did not appear to adversely impact PCI outcomes.

The aims of these experiments were to determine in vitro whether colonic distension releases acetylcholine, vasoactive intestinal polypeptide (VIP), and substance P in the guinea pig inferior mesenteric ganglia (IMG) and whether cholinergic and peptidergic mechanosensory nerves projecting from the colon to the IMG receive cholinergic input from other enteric neurons. Colonic distension significantly increased the release of [3H]-acetylcholine, VIP-like immunoreactivity, and substance P-like immunoreactivity in the IMG. Nicotinic receptor blockade in the colon diminished the increase in [3H]acetylcholine release, abolished the increase in VIP-like immunoreactivity release during distension, but had no effect on the release of substance P-like immunoreactivity. Nicotinic receptor blockade in the colon also decreased fast mechanosensory input and significantly reduced by 54% the slow excitatory postsynaptic potential amplitude evoked by colonic distension. The data suggest that enteric cholinergic and VIP mechanosensory neurons that project from the colon to sympathetic neurons in the IMG receive peripheral cholinergic input from other enteric neurons. There was no evidence for enteric cholinergic input to the mechanosensory substance P pathway.

Signaling via release of Ca2+from intracellular stores is mediated by several systems, including the inositol 1,4,5-trisphosphate (IP3) and cADP-ribose (cADPR) pathway. We recently discovered a high capacity for cADPR synthesis in rat glomeruli and cultured mesangial cells (MC). We sought to determine whether 1) cADPR synthesis in MC is regulated by cytokines and hormones, 2) ryanodine receptors (RyRs) are expressed in MC, and 3) Ca2+is released through RyRs in response to cADPR. We found that ADP-ribosyl cyclase, a CD38-like enzyme that catalyzes cADPR synthesis, is upregulated in MC by tumor necrosis factor-α, interleukin-1β, and all- trans retinoic acid (atRA). [3H]ryanodine binds to microsomal fractions from MC with high affinity in a Ca2+-dependent manner; binding is enhanced by specific RyR agonists and blocked by ruthenium red and cADPR. Western blot analysis confirmed the presence of RyR in MC. Release of45Ca2+from MC microsomes was stimulated by cADPR; release was blocked by ruthenium red and 8-bromo-cADPR. ADPR (non-cyclic) was without effect. In MC, TNF-α and atRA amplified the increment of cytoplasmic Ca2+elicited by vasopressin. We conclude that MC possess elements of a novel ADP-ribosyl cyclase→cADPR→RyR→Ca2+-release signaling pathway subject to regulation by proinflammatory cytokines and steroid superfamily hormones.