The reaction of triphenylphosphine or N-butylimidazole with cyclic sultones gives zwitterions that are subsequently converted into ionic liquids by reaction with trifluoromethane sulfonic acid or p-toluenesulfonic acid. The resulting ionic liquids have cations to which are tethered alkane sulfonic acid groups. These Brønsted acidic ionic liquids are useful solvent/catalysts for several organic reactions, including Fischer esterification, alcohol dehydrodimerization and the pinacol rearrangement. The new ionic liquids combine the low volatility and ease of separation from product normally associated with solid acid catalysts, with the higher activity and yields normally found using conventional liquid acids.

Serotonin (5-HT) plays a key role in early brain development, and manipulation of 5-HT levels during this period can have lasting neurobiological and behavioral consequences. It is unclear how perinatal exposure to drugs, such as selective serotonin reuptake inhibitors (SSRIs), impacts cortical neural network function and what mechanism(s) may elicit the disruption of normal neuronal connections/interactions. In this article, we report on cortical wiring organization after pre-and postnatal exposure to the SSRI citalopram. We show that manipulation of 5-HT during early development in both in vitro and in vivo models disturbs characteristic chemoarchitectural and electrophysiological brain features, including changes in raphe and callosal connections, sensory processing, and myelin sheath formation. Also, drug-exposed rat pups exhibit neophobia and disrupted juvenile play behavior. These findings indicate that 5-HT homeostasis is required for proper brain maturation and that fetal/infant exposure to SSRIs should be examined in humans, particularly those with developmental dysfunction, such as autism.S erotonin (5-HT) has long been postulated to play a trophic role in brain morphogenesis, including cell proliferation, migration, and differentiation. It is also known to be one of the first neurotransmitters to appear in the central nervous system (1, 2). An obvious question that can be raised relates to whether perinatal exposure to antidepressants, such as selective serotonin reuptake inhibitors (SSRIs), can affect cortical circuit development and function. Perhaps one of the most intriguing previous findings related to 5-HT and early cortical organization was the observation from immunohistochemical and 5-HT transporter (SERT) binding studies that, at postnatal days 2-14 (P2-P14), rodent primary sensory cortex (notably layer IV of visual, auditory, and somatosensory areas) is transiently innervated by aggregates of fine grainlooking 5-HT-containing processes (3)(4)(5). Surprisingly, it became clear that, in early brain development, 5-HT is taken up into glutamatergic thalamocortical terminals (6, 7) and used in combination with the 5-HT 1B receptor on layer IV afferents (8). At present, the functional implication of such transient 5-HT expression and targeting, namely the primary sensory thalamocortical afferents during early development, remains unknown.5-HT and Abnormal Brain Development. Interestingly, manipulations of rodent brain 5-HT levels during early development, either through increases (produced in SERT or monoamine oxidase knockout mice) or decreases (produced by parachlorophenylalanine or other treatments), have been shown to produce the downstream effect of interfering with the formation of the whisker (barrel) representation in the primary somatosensory cortex and promoting aggressive and/or anxiety-related behaviors (9-14). Furthermore, early-life modification of 5-HT levels has been shown to cause overreaction to auditory or tactile sensory stimulation (15) and abnormal response properties of cor...

Object Venous thromboembolism (VTE) represents a significant complication after spine surgery, with reported rates as high as 2%–4%. Published institutional practices for VTE prophylaxis are highly variable. In 2008, the authors implemented a departmental protocol for early VTE prophylaxis consisting of combined compressive devices and subcutaneous heparin initiated either preoperatively or on the same day of surgery. In this study, the authors compared the incidence of VTE in spine surgery patients before and after implementing this protocol. Methods An institutional review board–approved retrospective review of outcomes in patients undergoing spine surgery 2 years before protocol implementation (representing the preprotocol group) and of outcomes in patients treated 2 years thereafter (the postprotocol group) was conducted. Inclusion criteria were that patients were 18 years or older and had been admitted for 1 or more days. Before 2008 (preprotocol), VTE prophylaxis was variable and provider dependent without any uniform protocol. Since 2008 (postprotocol), a new VTE-prophylaxis protocol was administered, starting either preoperatively or on the same day of surgery and continuing throughout hospitalization. The new protocol consisted of 5000 U heparin administered subcutaneously 3 times daily, except in patients older than 75 years or weighing less than 50 kg, who received this dose twice daily. All patients also received sequential compression devices (SCDs). The incidence of VTE in the 2 protocol phases was identified by codes of the International Classification of Diseases, Ninth Revision (ICD-9) codes for deep vein thrombosis (DVT) and pulmonary embolus (PE). Bleeding complications arising from anticoagulation treatments were evaluated by the Current Procedural Terminology (CPT) code for postoperative epidural hematoma (EDH) requiring evacuation. Results In total, 941 patients in the preprotocol group met the inclusion criteria: 25 had DVT (2.7%), 6 had PE (0.6%), and 6 had postoperative EDH (0.6%). In the postprotocol group, 992 patients met the criteria: 10 had DVT (1.0%), 5 had PE (0.5%), and 4 had postoperative EDH (0.4%). This reduction in DVT after the protocol's implementation was statistically significant (p = 0.009). Despite early aggressive prophylaxis, the incidence of postoperative EDH did not increase and compared favorably to the published literature. Conclusions At a high-volume tertiary center, an aggressive protocol for early VTE prophylaxis after spine surgery decreases VTE incidence without increasing morbidity.

Infants born to mothers taking selective serotonin reuptake inhibitors (SSRIs) late in pregnancy have been reported to exhibit signs of antidepressant withdrawal. Such evidence suggests that these drugs access the fetal brain in utero at biologically significant levels. Recent studies in rodents have revealed that early exposure to antidepressants can lead to long lasting abnormalities in adult behaviors, and result in robust decreases in the expression of a major serotonin synthetic enzyme (tryptophan hydroxylase) along the raphe midline. In the present investigation, we injected rat pups with citalopram (CTM: 5 mg/kg, 10 mg/kg, and 20 mg/kg) from postnatal Days 8-21, and examined serotonin transporter (SERT) labeling in the hippocampus, ventrobasal thalamic complex, and caudate-putamen when the subjects reached adulthood. Our data support the idea, that forebrain targets in receipt of innervation from the raphe midline are particularly vulnerable to the effects of CTM. SERT-immunoreactive fiber density was preferentially decreased throughout all sectors of the hippocampal formation, whereas the subcortical structures, each supplied by more lateral and rostral aspects of the raphe complex, respectively, were not significantly affected. Reductions in SERT staining were also found to be dose-dependent. These findings suggest that SSRIs may not only interfere with the establishment of chemically balanced circuits in the neonate but also impose selective impairment on higher cortical function and cognitive processes via more circumscribed (i.e., regionally specific) deficits in 5-HT action. Anat Rec, 293:1920Rec, 293: -1932