Clinical determinants of early spontaneous conversion to sinus rhythm in patients with atrial fibrillation.

BACKGROUND: The current standard of care for acute atrial fibrillation (AF) focuses primarily on immediate restoration of sinus rhythm by cardioversion, although AF often terminates spontaneously. OBJECTIVE: To identify determinants of early spontaneous conversion (SCV) in patients presenting at the emergency department (ED) because of AF. METHODS: An observational study was performed of patients who visited the ED with documented AF between July 2014 and December 2016. The clinical characteristics and demographics of patients with and without SCV were compared. RESULTS: We enrolled 943 patients (age 69 ± 12 years, 47% female). SCV occurred within 3 h of presentation in 158 patients (16.8%). Logistic regression analysis showed that duration of AF <24 h [odds ratio (OR) 7.7, 95% confidence interval (CI) 3.5-17.2, p < 0.001], left atrial volume index <42 ml/m2 (OR 1.8, 95% CI 1.2-2.8, p = 0.010), symptoms of near-collapse at presentation (OR 2.4, 95% CI 1.2-5.1, p = 0.018), a lower body mass index (BMI) (OR 0.9, 95% CI 0.91-0.99, p = 0.028), a longer QTc time during AF (OR 1.01, 95% CI 1.0-1.02, p = 0.002) and first-detected AF (OR 2.5, 95% CI 1.6-3.9, p < 0.001) were independent determinants of early SCV. CONCLUSION: Early spontaneous conversion of acute AF occurs in almost one-sixth of admitted patients during a short initial observation in the ED. Spontaneous conversion is most likely to occur in patients with first-onset, short-duration AF episodes, lower BMI, and normal left atrial size.

Proliferation and death of cultured fetal neocortical neurons: effects of ethanol on the dynamics of cell growth.

Neuronal number in the mature CNS is determined by the balance of cell proliferation and death. The effects of ethanol on cell proliferation and death were examined in primary cultures of neocortical neurons derived from 16-day-old rat fetuses. The cells were treated with ethanol (0 or 400 mg/dl) and examined for (1) immunohistochemical identity, (2) cell cycle kinetics using a cumulative bromodeoxyuridine labeling technique, (3) viable cell number via a trypan blue assay, and (4) the incidence of cell death with terminal deoxy-nucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and caspase 3 immunhistochemistry. After two days in culture, most (>85%) cells expressed a neuron-specific antigen(s) whether or not ethanol was added to the culture medium. Ethanol affected the proliferation of the cultured cells, e.g., the length of the cell cycle was greater in the ethanol-treated cells than in controls. The number of trypan blue-negative (viable) cells was profoundly decreased by ethanol exposure. This decrease was accompanied by increases in the frequencies of TUNEL- and caspase 3-positive cells and of cells exhibiting nuclear condensations. Thus, ethanol decreases the number of viable cells in vitro by slowing cell proliferation and increasing the incidence of cell death. The expression of the death indices in untreated cultures is most consistent with a single (apoptotic) pathway of cell death, rather than simultaneous apoptotic and necrotic modes of death. Furthermore, it appears that ethanol initiates an apoptotic death among cultured cortical neurons.

Which is most pungent: isoflurane, sevoflurane or desflurane?

We compared the pungency and tolerability of three inhaled anaesthetics in a randomized, double-blind study. Eighty-one unpremedicated patients (n = 27, each group) inhaled 2 MAC of isoflurane (2.3%), desflurane (12%) or sevoflurane (4%) for 60 s from an anaesthetic breathing circuit via a mask. Two blinded observers recorded coughing, complaints of burning and irritation, and how long the inhalation was tolerated. One sevoflurane patient coughed, but completed the study period, whereas 11 isoflurane patients and 20 desflurane patients coughed, objected verbally or removed the mask forcefully. All sevoflurane, 20 isoflurane and seven desflurane patients completed the study period (average 60, 49 and 33 s, respectively, P < 0.05). The irritability grading was: desflurane > isoflurane > sevoflurane (P < 0.05). Sevoflurane is the least irritating agent for inhalation at 2 MAC concentration.

Cell cycle kinetics and immunohistochemical characterization of dissociated fetal neocortical cultures: evidence that differentiated neurons have mitotic capacity.

Neurons in the neocortex (regardless of their developmental state) are considered to be post-mitotic and incapable of dividing. We used dissociated primary cultures derived from the neocortices of 16-day-old fetuses to test the counter-hypothesis, that is, differentiating neocortical neurons can divide. The cultured cells experienced considerable cell death, yet the number of viable cells remained relatively constant over the first 5 days in vitro. The implication was that the cultures contained proliferating cells. This was confirmed with a [(3)H]thymidine ([3H]dT) incorporation study and cumulative bromodeoxyuridine labeling. In fact, over 1/4 of the cells were cycling and the length of the cell cycle was 20.0 h; kinetics which mirror those of the developing cortex in vivo. This population of proliferating cells was eliminated by 48 h treatment with fluorodeoxyuridine. Immunohistochemical procedures determined that most cultured cells (>/=90%) expressed proteins associated with differentiating or mature neurons, e.g., neurofilament (NF) 200 and isoforms of microtubule-associated protein (MAP) 2. Markers for immature neurons (e.g., nestin) were expressed by 10% of the cells. In contrast, markers for glia and their precursors were expressed by

Expression of nerve growth factor, p75, and the high affinity neurotrophin receptors in the adult rat trigeminal system: evidence for multiple trophic support systems.

We hypothesize that discrete trigeminal structures have the components required for autocrine regulation as well as redundant neurotrophin support systems. We examined the expression of nerve growth factor (NGF) and the low affinity (p75) and high affinity (trkA, trkB, and trkC) neurotrophin receptors in the trigeminal system of adult rats. Four sites were examined; the trigeminal ganglion, mesencephalic nucleus, principal sensory nucleus (PSN), and trigeminal motor nucleus. NGF was expressed by more than 60% of neurons in each area studied. NGF immunolabeling may have resulted from exogenous protein incorporated from the microenvironment or from NGF synthesized by the neuron per se. To resolve this issue, in situ hybridization for NGF mRNA was performed. The mRNA was expressed by 2/3 to 7/8 of neurons in trigeminal structures. Moreover, double-labeling studies showed that virtually every ganglion cell that was NGF-immunoreactive also expressed the NGF transcript. Neurotrophin receptors (p75 and trk isoforms) were expressed by more than 60% of the neurons in each trigeminal structure. The only exception was the PSN, where the receptors were expressed by fewer than half of the neurons. Taken together, these data imply that NGF must be elaborated by neurons that co-express both p75 and trkA. Therefore, each trigeminal structure has the machinery for autocrine/paracrine regulation, as well as the capacity for retrograde and/or anterograde trophic support. Furthermore, the co-expression of the specific trk isoforms indicates that trigeminal neurons are sensitive to more than one neurotrophin.

Inhibition of platelet-derived growth factor-mediated signal transduction and tumor growth by N-[4-(trifluoromethyl)-phenyl]5-methylisoxazole-4-carboxamide.

Many reports have cited coexpression of platelet-derived growth factor (PDGF) and its receptors by tumor cells or cells supporting tumor growth, suggesting both autocrine and paracrine mechanisms for PDGF-mediated tumor growth. We found that a small organic molecule, N-[4-(trifluoromethyl)phenyl] 5-methylisoxazole-4-carboxamide (SU101, leflunomide), inhibited PDGF-mediated signaling events, including receptor tyrosine phosphorylation, DNA synthesis, cell cycle progression, and cell proliferation. SU101 inhibited PDGF-stimulated tyrosine phosphorylation of PDGF receptor (PDGFR) beta in C6 (rat glioma) and NIH3T3 cells engineered to overexpress human PDGFRbeta (3T3-PDGFRbeta). SU101 blocked both PDGF- and epidermal growth factor (EGF)-stimulated DNA synthesis. Previously, this compound was shown to inhibit pyrimidine biosynthesis by interfering with the enzymatic activity of dihydroorotate dehydrogenase. In the current study, EGF-stimulated DNA synthesis was restored by the addition of saturating quantities of uridine, whereas PDGF-induced DNA synthesis was not, suggesting that the compound demonstrated some selectivity for the PDGFR pathway that was independent of pyrimidine biosynthesis. Selectivity was further demonstrated by the ability of the compound to block the entry of PDGF-stimulated cells into the S phase of the cell cycle, without affecting cell cycle progression of EGF-stimulated cells. In cell growth assays, SU101 selectively inhibited the growth of PDGFRbeta-expressing cell lines more efficiently than it inhibited the growth of PDGFRbeta-negative cell lines. SU101 inhibited the s.c., i.p., and intracerebral growth of a panel of cell lines including cells from glioma, ovarian, and prostate origin. In contrast, SU101 failed to inhibit the in vitro or s.c. growth of A431 and KB tumor cells, both of which express EGF receptor but not PDGFRbeta. SU101 also inhibited the growth of D1B and L1210 (murine leukemia) cells in syngeneic immunocompetent mice, without causing adverse effects on the immune response of the animals. In an i.p. model of tumor growth in syngeneic immunocompetent mice, SU101 prevented tumor growth and induced long-term survivors in animals implanted with 7TD1 (murine B-cell hybridoma) tumor cells. Because PDGFRbeta was detected on most of the tumor cell lines in which in vivo growth was inhibited by SU101, these data suggest that SU101 is an effective inhibitor of PDGF-driven tumor growth in vivo.

Applications of dental splints with regard to modern techniques of rigid fixation.

Dental splints have been used in the treatment of maxillofacial fractures since the early 1700s. They have recently come into disfavor due to advancements in technology, the development of rigid fixation, and the application of craniofacial techniques. However, dental splints are still indicated in the management of maxillofacial fractures. These splints assist in anatomical reduction of the fractured segments, help immobilize and maintain the reduction prior to and during application of either maxillomandibular or rigid fixation, and act as stabilization during rehabilitation. Once surgeons become familiar with their applications, the time required to construct them is minimal.

Atraumatic enophthalmos: a report of two unusual cases.

There are many causes of enophthalmos other than those directly related to maxillofacial trauma. As plastic surgeons, we should be aware of these, in the event that we are consulted concerning their treatment. We have presented two cases that, while not unique to the literature, are uncommonly seen by plastic surgeons. In both these cases, CT scans were valuable in the preoperative diagnosis, as well as in the surgical treatment planning. We feel that, ideally, orbital volume content measurements would assist in better assessment of each patient. When a patient presents with enophthalmos and denies any history of facial trauma, one needs to be diligent in the investigation of its etiology.

Changing concepts and controversies in the management of mandibular fractures.

The successful treatment of mandibular fractures and the avoidance of complications ultimately depends on sound surgical judgment. Judgments are influenced by an array of variables. Location, degree of complexity or displacement of the fracture, state of dentition, patient cooperativeness, presence of other maxillofacial trauma, and the surgeon's experience and expertise are some of these factors. We have attempted to outline the basic tenets of mandibular fracture management, recognizing that some areas remain controversial. It is hoped that as technology continues to improve, we will have the luxury of being more dogmatic about our approaches to these problems.

Macromastia in adolescence.

Macromastia is a deforming, disabling, and painful condition, especially in the adolescent. Multiple procedures have been advocated and are successful for the reduction of breast tissue. In addition, adjunctive therapy with hormones may prevent relapse. The hormonal influences on breast development and the etiology of macromastia remain complex and not well understood. It is safe to surmise that the pathologic condition is multifactorial, with both inherited and acquired aspects. In the various techniques for reduction, it is important to have a clear understanding of vascular and neural innervation of the breast in order to maintain maximum security in reduction without loss of excessive vital tissue. Although both sensory ability and lactation function are diminished with most procedures and eliminated with some, careful planning and patient counseling in all cases should lead to maximal benefit and optimal results.

Temporomandibular joint dysfunction: evaluation and treatment.

Temporomandibular joint dysfunction is a complicated problem requiring interdisciplinary cooperation for diagnosis and treatment. Functional problems including bruxism and psychological disorders frequently occur with joint dysfunction making evaluation more difficult. Many new diagnostic modalities are now available to supplement the history and physical examination to provide an accurate assessment of the joint. Although conservative treatment is successful in a majority of the patients, some form of surgical treatment remains the only option for those who do not respond to conservative management. We have discussed the etiology, diagnosis, and treatment of the pathological conditions of the TMJ and introduced a new modality of treatment, temporalis fascia interpositional arthroplasty. Further work is necessary to elucidate the etiology of TMJ dysfunction and develop treatment modalities that avoid the use of alloplastic materials.

Absolute ethanol embolization for peripheral arteriovenous malformation: report of two cures.

We have reported two patients in whom absolute ethanol was used to sclerose arteriovenous malformations. Because of its low viscosity, liquid form, and devastating effect when injected intra-arterially, absolute ethanol is effective in treating AVMs, and it has been proven to have curative potential. For these same reasons it is also potentially harmful, particularly to nerves and possibly to skin.