We report a patient with a traumatic lung cyst, documenting its radiological evolution: the formation of the pneumatocele, the appearance posteriorly of an intracavitary hematoma, and the spontaneous resolution of the radiological abnormalities.

Adult↗

PubMed1988

Interaction of permanently uncharged dopamine analogs with the D-2 dopaminergic receptor.

The purpose of this study was to determine if structural analogs of dopamine in which the side chain nitrogen has been replaced by a permanently uncharged monomethylsulfide, monomethylselenide or sulfoxide group are capable of binding to the striatal D-2 dopamine receptor and acting as agonists at this receptor. All the permanently uncharged dopamine analogs were found to bind to the D-2 dopamine receptor as evidenced by their abilities to inhibit significantly [3H]spiperone binding to striatal homogenates. However, the inhibition of [3H]spiperone binding by the uncharged dopamine analogs was incomplete and was almost abolished by the addition of NaCl (125 mM) to the incubation medium or by the addition of dopamine or quinpirole at a concentration that that saturates the high-affinity state of the D-2 dopamine receptor. These effects of NaCl, dopamine and quinpirole suggest that the uncharged dopamine analogs bind primarily to the high-affinity state of the D-2 dopamine receptor. Whether the uncharged monomethylsulfide and sulfoxide analogs could function as dopamine agonists at the striatal D-2 dopamine receptor was assessed by determining the abilities of these compounds to inhibit the K+-evoked release of [3H]acetylcholine from striatal slices. Both the monomethylsulfide and sulfoxide analogs inhibited the K+-evoked release of [3H]acetylcholine, but this inhibitory effect does not appear to be due to the activation of the D-2 dopamine receptor since it was not reversed by the selective D-2 dopamine antagonist, sulpiride. Additionally, the uncharged monomethylsulfide and sulfoxide dopamine analogs were found to antagonize the ability of apomorphine to inhibit the K+-evoked release of [3H]acetylcholine, but this antagonistic effect does not appear to be due to the reversible blockade of the D-2 dopamine receptor since it was not reduced by increasing the concentration of apomorphine. Therefore, while the permanently uncharged analogs of dopamine appear to bind to the high-affinity state of the D-2 dopamine receptor, they are not dopamine agonists or antagonists at the striatal D-2 dopamine receptor involved in regulating the release of acetylcholine. These results suggest that a positive charge may be a requirement for the activation of the striatal D-2 dopamine receptor.

Acetylcholine↗

PubMed1987

Interaction of permanently charged analogs of dopamine with the D-2 dopaminergic receptor.

Dopamine can exist in both charged and uncharged forms at physiological pH. At present it is unclear which of these forms is responsible for dopaminergic agonist activity. The purpose of this study was to determine whether permanently charged structural analogs of dopamine containing either a nitrogen, sulfur, or selenium atom in the side chain can bind to and activate the D-2 dopamine receptor. Binding to and activation of the D-2 dopamine receptor were measured by determining the abilities of the permanently charged dopamine analogs to inhibit [3H]spiperone binding to striatal homogenates and to inhibit K+-stimulated [3H]acetylcholine release from striatal slices respectively. The quaternary ammonium, dimethylsulfonium and dimethylselenonium analogs of dopamine were all found to inhibit [3H]spiperone binding to the same extent and in a manner qualitatively similar to the parent amines, dopamine and dimethyldopamine. Thus, [3H]spiperone inhibition curves for dopamine, dimethyldopamine and the permanently charged dopamine analogs were generally shallow and fit best to a two-site binding model as indicated by computer-assisted analyses. The addition of 125 mM NaCl to the incubation medium resulted in a significant decrease in the proportion of high affinity binding sites for both the permanently charged analogs and the parent amines. Similarly, the permanently charged dopamine analogs were found to maximally inhibit the K+-stimulated release of [3H]acetylcholine to the same extent as dopamine and dimethyldopamine. However, the permanently charged analogs were less potent in inhibiting both [3H]spiperone binding and K+-stimulated [3H]acetylcholine release than dopamine and dimethyldopamine. These results show that dopamine analogs possessing a permanent positive charge in the side chain can bind to and activate the D-2 dopamine receptor. The lower potencies of the permanently charged analogs in binding to and activation of the D-2 dopamine receptor suggest that, while the ability of a compound to exist in an uncharged form is not a requirement, both charged and uncharged forms of the agonist molecule appear to play a role in D-2 dopamine agonist activity.

Acetylcholine↗

PubMed1987

Measurement of the nuclear enhancement in high-Et and jet event production.

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Journal Article↗

PubMed1987

Dopamine agonists: effects of charged and uncharged analogues of dopamine.

Dopamine, at physiological pH, may exist as either an uncharged amine or a charged ammonium species. In order to gain insight as to which species is better suited for interaction with the dopamine receptor, we have synthesized dopamine analogues in which the nitrogen atom is replaced with a neutral methyl sulfide, a neutral methyl selenide, a charged dimethylsulfonium iodide, and a charged dimethylselenonium iodide. These analogues were tested for their ability to inhibit the K+-stimulated release of [3H]acetylcholine from striatal slices. At 30 microM concentration, the charged sulfonium and selenonium salts possessed significant agonist activity while the corresponding neutral species were inactive, suggesting that a charged species is optimal for dopamine agonist activity. In addition, the methyl sulfide was converted into the corresponding sulfoxide and sulfone; however, neither of these oxidation products possessed significant activity as dopaminergic agonists.

Acetylcholine↗