Inability to ventilate the lungs of a patient with tracheal anomaly and in prone position

We present the case of an otherwise asymptomatic patient with a rare congenital airway abnormality of the tracheobronchial tree, who developed a complete airway obstruction after being placed in the prone position. The tracheal bronchus, accessory bronchus arising from the trachea superior to its bifurcation at the carina, was identified by fiberoptic bronchoscopic examination. An endotracheal tube can migrate into a tracheal bronchus causing pulmonary atelectasis, hypoxia, or both.     

Transperineal TRUS-guided prostate brachytherapy using loose seeds versus RAPIDStrand: a dosimetric analysis

PURPOSE: An analysis of the effect of stranded (125)I and loose (predominantly (103)Pd) sources on dosimetric outcomes of brachytherapy of the prostate. METHODS AND MATERIALS: Between September 1998 and December 2003, 473 patients were treated with brachytherapy for biopsy-proven carcinoma of the prostate. Of these, 337 (71%) procedures were performed using free seeds placed with a Mick applicator. Beginning in April 2002, a program of stranded (125)I sources (RAPIDStrand) was implemented; 136 (29%) patients were treated via this approach. Dosimetric variables were collected, as were events of urinary retention. RESULTS: Mean V100 values for the stranded (125)I approach were greater than those for free seeds (p < 0.0005), whether (125)I or (103)Pd (p < 0.005). Use of the strand was the most significant determinant of V100 of all variables examined. The stranded (125)I approach was also associated with higher mean D90 values and lower V150-urethral doses. CONCLUSIONS: Use of stranded (125)I was associated with superior dosimetric outcomes in this group of patients.     

Quantitative evaluation of alternative mechanisms of blood and testes disposition of di(2-ethylhexyl) phthalate and mono(2-ethylhexyl) phthalate in rats.

Di(2-ethylhexyl) phthalate (DEHP), a commercially important plasticizer, induces testicular toxicity in laboratory animals at high doses. After oral exposure, most of the DEHP is rapidly metabolized in the gut to mono(2-ethylhexyl) phthalate (MEHP), which is the active metabolite for induction of testicular toxicity. To quantify the testes dose of MEHP with various routes of exposure and dose levels, we developed a physiologically based pharmacokinetic (PBPK) model for DEHP and MEHP in rats. Tissue:blood partition coefficients for DEHP were estimated from the n-octanol: water partition coefficient, while partition coefficients for MEHP were determined experimentally using a vial equilibration technique. All other parameters were either found in the literature or estimated from blood or tissue levels following oral or intravenous exposure to DEHP or MEHP. A flow-limited model failed to adequately simulate the available data. Alternative plausible mechanisms were explored, including diffusion-limited membrane transport, enterohepatic circulation, and MEHP ionization (pH-trapping model). In the pH-trapping model, only nonionized MEHP is free to become partitioned into the tissues, where it is equilibrated and trapped as ionized MEHP until it is deionized and released. All three alternative models significantly improved predictions of DEHP and MEHP blood concentrations over the flow-limited model predictions. The pH-trapping model gave the best predictions with the largest value of the log likelihood function. Predicted MEHP blood and testes concentrations were compared to measured concentrations in juvenile rats to validate the pH-trapping model. Thus, MEHP ionization may be an important mechanism of MEHP blood and testes disposition in rats.     

Long-Term Alterations in Benzodiazepine,Muscarinic and α-Amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) Receptor Density Following Continuous Cocaine Administration

Abstract: Animal models of clinical phenomena, such as stimulant-induced psychosis have focused primarily on persisting alterations that develop in brain after chronic stimulant administration. The present study utilized autoradiographic measures to examine changes in the density of benzodiazepine ([³H] flunitrazepam), muscarinic ([³H] quinuclidinyl benzilate), and non-NMDA glutamatergic (³H α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid: AMPA) receptor binding in rats 21 days following two exposures to cocaine administered continuously for 5 days via subcutaneous pellets. A marked, selective increase in [³H] flunitrazepam binding in both the lateral and medial habenula nucleus was observed. Reduced [³H] quinuclidinyl benzilate binding was observed in various brain areas, including large decreases in the anterior cingulate cortex and ventral thalamus. A reduction in [³H]AMPA binding was observed in the ventral striatum and was suggested in the nucleus accumbens. [³H] Flunitrazepam binding was also examined 12 hr following a single 5 day cocaine exposure to determine if the long-term habenular changes were evident at acute withdrawal. No alterations in [³H] flunitrazepam binding were observed in the habenula or any other structure analyzed at this time point. The relation of these results to persisting alterations in mesocorticolimbic pathways and previous findings of cocaine-induced degeneration in lateral habenula circuitry is discussed.