Posterior dislocation of the sternoclavicular joint: report of two cases,with emphasis on radiologic management and early diagnosis

Posterior dislocations of the sternoclavicular joint are uncommon, but are potentially quite serious. Radiologic diagnosis and management are frequently difficult. The specialized projections available are not widely known, and the role of plain films is poorly understood. The incidence, pathomechanics, and clinical manifestations of such dislocations are presented and the radiologic diagnosis is discussed.     

Cotinine determination by immunoassays may be influenced by other nicotine metabolites

Polyclonal rabbit anticotinine antiserum, which can be used for biomonitoring nicotine uptake by the determination of cotinine in body fluids, was checked by a competitive ELISA for its cross-reactivity with nine nicotine metabolites. The highest percentage of relative crossreactivity (about 30%) was observed with trans-3w1202211463l54w5/xxlarge8242.gif" alt="prime" align="BASELINE" BORDER="0">-hydroxycotinine, a metabolite which is known to be excreted in 3-fold higher amounts than cotinine in the urine of human smokers. Therefore, it is possible that cotinine determinations performed by immunochemical methods — especially in urine — may yield overestimated cotinine concentrations.     

Spectrum of morphological appearance of amyloid deposits in Alzheimer's disease

Summary Immunocytochemical staining with monoclonal antibodies to the w0163080366r561t/xxlarge946.gif" alt="beta" align="MIDDLE" BORDER="0">-protein on tissue sections which have been pretreated with formic acid is not only a very specific but also a highly sensitive method for the detection of amyloid deposits in the brains of Alzheimer's disease victims. We report here a spectrum of morphological appearance of the brain amyloid deposits which are one of the main histopathological correlates of this disorder. Deposits of the w0163080366r561t/xxlarge946.gif" alt="beta" align="MIDDLE" BORDER="0">-protein are not only found in the well-known lesions [congophilic angiopathy and senile (neuritic) plaques] but are also seen under various morphological forms for which the word w0163080366r561t/xxlarge8220.gif" alt="ldquo" align="MIDDLE" BORDER="0">plaquesw0163080366r561t/xxlarge8221.gif" alt="rdquo" align="MIDDLE" BORDER="0"> does not appear an appropriate term: amyloid fibrils are found as large areas of diffuse infiltration of the neuropil, as ribbon-like infiltration in the subpial layer of the cerebral cortex, as granular deposits in the white matter, as diffuse deposits in the molecular layer of the cerebellum and the basal ganglia and as star-shaped deposits in the cerebellar Purkinje cell layer. The morphology of these deposits seems to depend on the cyto-and fibroarchitectonics of the brain region in which they are found, on the amount of amyloid deposited, and also on the type of staining technique used. It is only under specific circumstances that the deposition of amyloid in the neuropil is accompanied by the formation of paired helical filaments in nerve cell processes and their parent perikarya. In conclusion, our studies suggest that the extent of brain amyloidosis in Alzheimer's disease is much wider than so far appreciated.Supported in part by grants 5-AGO-4220-05 and 5-HD-22634-02 from the National Institutes of Heath     

The reduction of water intake in rats caused by a low dose of apomorphine is unaltered by α-methyl-p-tyrosine: are autoreceptors not involved?

Summary Low doses of the dopamine (DA) agonist apomorphine (APO) induces a behavioural syndrome characterized by reduced spontaneous activity, reduced food and water intake and induction of yawning and penile erections. Traditionally these effects of APO have been considered to be caused by a preferential stimulation of DA autoreceptors, causing a decreased amount of transmitter at the postsynaptic receptors. If this is so, it could be hypothesized that 1) the same behavioural effects should be obtained if DA transmission is decreased by some other means, for example by synthesis inhibition, and that 2) the response to APO should be altered if DA transmission is already lowered.It was found that high doses of w8x5867877j7152h/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0">-methyl-p-tyrosine (w8x5867877j7152h/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0">-MPT; 50–200 mg/ kg) did not reduce water intake in thirsty rats, which low doses of APO do. It was further found that pretreatment with w8x5867877j7152h/xxlarge945.gif" alt="agr" align="BASELINE" BORDER="0">-MPT did not alter the response to APO. These results are difficult to reconcile with the DA autoreceptor hypothesis claiming that behavioural effects of low doses of APO are caused by a decreased release of DA. An alternative interpretation is that low doses of APO stimulates a certain population of sensitive postsynaptic D-2 receptors.     

The effects of clonidine and yohimbine on human information processing

The effects of clonidine and yohimbine on human information processing were tested in six normal volunteers ages 18–30 years. Subjects were tested in a pre-post design with sessions conducted at weekly intervals. Three drug conditions were: Placebo (lactose), 0.2 mg clonidine, and 30 mg yohimbine. Two choice reaction time (RT) tasks were used. One was a stimulus evaluation-response selection task (SERS) that has been shown to be sensitive tod-amphetamine, methylphenidate and scopolamine. The other task was to assess stimulus pre-processing and used spatial frequency as a discriminative stimulus. The principle finding was that clonidine slowed RT; this effect was significant for both tasks. In contrast, yohimbine tended to speed RT, but the effects were significant only for the spatial frequency task on some analyses while not for others. RTs to high spatial frequency stimuli were speeded more than for low spatial frequency. The effects of these two NE drugs were compared with findings withd-amphetamine and scopolamine and interpreted within the framework of a serial information processing model proposed by Callaway (1983). Specifically, it is suggested that yohimbine and clonidine affect an early pre-processing stage.     

Morphine-6beta-glucuronide modulates the expression of inducible nitric oxide synthase

The immunomodulatory effects of morphine are well established; however, suprisingly little is known about the immunomodulatory properties of the major metabolites of morphine. The present study tests the hypothesis that expression of inducible nitric oxide synthase (iNOS) is modulated by the administration of the morphine metabolite, morphine-6w545540m7h27u0j5/xxlarge946.gif" alt="beta" align="MIDDLE" BORDER="0">-glucuronide. The initial study using rats shows that morphine-6w545540m7h27u0j5/xxlarge946.gif" alt="beta" align="MIDDLE" BORDER="0">-glucuronide administration (0, 1.0, 3.163, 10 mg/kg s.c.) results in a pronounced reduction in lipopolysaccharide (LPS)-induced expression of iNOS (inducible nitricoxide synthease) in spleen, lung, and liver tissue as measured by western blotting. Morphine-6w545540m7h27u0j5/xxlarge946.gif" alt="beta" align="MIDDLE" BORDER="0">-glucuronide also produces a reduction in the level of plasma nitrite/nitrate, the more stable end-product of nitric oxide degradation. In a subsequent study, administration of the opioid receptor antagonist, naltrexone (0.1 mg/kg) prior to the injection of morphine-6w545540m7h27u0j5/xxlarge946.gif" alt="beta" align="MIDDLE" BORDER="0">-glucuronide (10 mg/kg) blocks the morphine-6w545540m7h27u0j5/xxlarge946.gif" alt="beta" align="MIDDLE" BORDER="0">-glucuronide induced reduction of iNOS expression and plasma nitrite/nitrite levels indicating that the effect is mediated via the opioid-receptor. This study provides the first evidence that morphine-6w545540m7h27u0j5/xxlarge946.gif" alt="beta" align="MIDDLE" BORDER="0">-glucuronide alters the expression of iNOS.     

Functional mapping of the activity of the R region in the human T-cell leukemia virus type I long terminal repeat to increase gene expression

We previously demonstrated the activity of the R fragment in the long terminal repeat of human T-cell leukemia virus type I for elevation of the level of gene expression. In this study, the fragment was deleted with BAL31 nuclease to determine its functional domain. Series of the shortened R fragments were linked to the simian virus 40 promoter unit, which regulated expression of a reporter gene. Examination with the R fragments deleted from the 5w237l62046070810/xxlarge8242.gif" alt="prime" align="BASELINE" BORDER="0"> and 3w237l62046070810/xxlarge8242.gif" alt="prime" align="BASELINE" BORDER="0"> ends showed that borders of the functional domain were mapped within nucleotide positions 458 to 473 for the 5w237l62046070810/xxlarge8242.gif" alt="prime" align="BASELINE" BORDER="0"> end and nucleotide positions 559 to 594 for the 3w237l62046070810/xxlarge8242.gif" alt="prime" align="BASELINE" BORDER="0"> end, respectively. Thus we conclude that a 136-base-pair fragment corresponding to the second half of the R region was sufficient to allow elevation of the level of gene expression.     

The COX-2 inhibitor, rofecoxib, ameliorates dextran sulphate sodium induced colitis in mice

Objective: We have evaluated the efficacy of the selective cyclo-oxygenase (COX)-2 inhibitor, rofecoxib, for the prevention of experimental colitis.Material and methods: To induce colitis BALB/c mice received 5% dextran sulphate sodium (DSS) in their drinking water continuously for 7 days. Rofecoxib (2.5–10 mg/kg body weight, p.o.) was administered throughout the treatment period with DSS. Colitis was quantified by a clinical damage score, colon length, weight loss, stool consistency and rectal bleeding. Inflammatory response was assessed by neutrophil infiltration, determined by histology and myeloperoxidase (MPO) activity. Interleukin (IL)-1w8455h/xxlarge946.gif" alt="beta" align="MIDDLE" BORDER="0">, prostaglandin (PG)E₂ and PGD₂ levels in colon mucosa and the immunohistochemical expression of COX-1 and –2 were also studied.Results: The COX-2 inhibitor ameliorated severe colitis, reduced the degree of inflammation through reduction of neutrophil infiltration and IL-1w8455h/xxlarge946.gif" alt="beta" align="MIDDLE" BORDER="0"> levels. PGE₂, and PGD₂ synthesis were significantly reduced in DSS-treated groups. Indeed, treatment with rofecoxib diminished the lost of COX-1 caused by DSS in the crypt epithelium whereas expression of COX-2 remained unaffected.Conclusions: Rofecoxib is protective in acute DSS – induced colitis, probably by reducing neutrophil infiltration, inhibiting up-regulation of IL-1w8455h/xxlarge946.gif" alt="beta" align="MIDDLE" BORDER="0"> and returning to normal COX-1 expression in the inflamed colonic mucosa.Received 19 April 2004; returned for revision 17 June 2004; accepted by I. Ahnfelt-Rønne 23 November 2004     

Control of pulmonary vascular smooth muscle tone by sarcoplasmic reticulum ca2+ pump blockers: thapsigargin and cyclopiazonic acid

The effect of thapsigargin (TG) and cyclopiazonic acid (CPA) on the mechanical activity of the rat pulmonary artery were investigated. In chemically (w41u28u7212/xxlarge946.gif" alt="beta" align="MIDDLE" BORDER="0">-escin)-skinned arterial strips, application of TG (0.1–1 w41u28u7212/xxlarge956.gif" alt="mgr" align="MIDDLE" BORDER="0">M) or CPA (0.5–10 w41u28u7212/xxlarge956.gif" alt="mgr" align="MIDDLE" BORDER="0">M) prior and throughout the loading procedure of the internal Ca²⁺ stores (0.3 w41u28u7212/xxlarge956.gif" alt="mgr" align="MIDDLE" BORDER="0">M free Ca²⁺ ions for 8–10 min) concentration dependently inhibited the subsequent contractile response induced by noradrenaline (NA, 10 w41u28u7212/xxlarge956.gif" alt="mgr" align="MIDDLE" BORDER="0">M) or caffeine (25 mM). In intact strips repeatedly incubated in a Ca²⁺-containing solution (2.5 mM for 10 min), followed by incubation in a Ca²⁺-free solution 12 min before NA-stimulation, TG and CPA not only inhibited the NA-induced contraction but also increased the tension which appeared during the exposure time to Ca²⁺. The two phenomena developed with similar time courses. The increase in tension during the readmission of Ca²⁺ ions was not antagonized by verapamil (10 w41u28u7212/xxlarge956.gif" alt="mgr" align="MIDDLE" BORDER="0">M) or nifedipine (1 w41u28u7212/xxlarge956.gif" alt="mgr" align="MIDDLE" BORDER="0">M) but was blocked by La³⁺ (50 w41u28u7212/xxlarge956.gif" alt="mgr" align="MIDDLE" BORDER="0">M) and Co²⁺ (1 mM) ions. The amplitude of the verapamil-insensitive TG (or CPA)-induced contraction was dependent on the external [Ca²⁺] [0.1–10 mM, concentration for half maximal effect (EC₅₀) =0.85 mM], not modified by the reduction of the external [Na⁺] (from 130 to 10 mM) and decreased by depolarization of the strip using K⁺-rich (30–120 mM) solutions. Under the latter condition, 38±9 and 83±4% reduction (n=5) was observed in the presence of 60 and 120 mM K⁺ respectively. This contraction was also concentration dependently inhibited by the tyrosine kinase inhibitors genistein (0.5–50 w41u28u7212/xxlarge956.gif" alt="mgr" align="MIDDLE" BORDER="0">M) and tyrphostin (2–50 w41u28u7212/xxlarge956.gif" alt="mgr" align="MIDDLE" BORDER="0">M). Sr²⁺ ions, which contracted both depolarized intact and skinned strips, failed to replace Ca²⁺ ions in the verapamil-insensitive contraction induced by TG or CPA (n=4). Finally, TG (1 w41u28u7212/xxlarge956.gif" alt="mgr" align="MIDDLE" BORDER="0">M) and CPA (10 w41u28u7212/xxlarge956.gif" alt="mgr" align="MIDDLE" BORDER="0">M) did not modify the pCa tension relationship in skinned strips (n=5). These results show that the main action of TG and CPA in rat pulmonary artery is to prevent the refilling of the internal Ca²⁺ store. TG and CPA also seem to facilitate a Ca²⁺ influx through a specific verapamil-insensitive pathway. The biophysical and molecular characteristics of this pathway remain to be elucitated, although it appears to involve a tyrosine kinase activity.     

Effect of avitaminosis B6 in mice on T-lymphocyte function in vitro

The effect of different degrees of avitaminosis B₆ in mice on the cytolytic activity of T lymphocytes, measured as the quantity of Na₂Cr⁵¹O₄ released from lysed target cells, was studied on a model of the primary immune response in a mixed lymphocyte culture in vitro. Keeping animals for 3 weeks on a diet without pyridoxine did not affect the ability of the lymphocytes to proliferate in vitro or their cytolytic activity. In animals receiving a diet without pyridoxine for 45 days the content of pyridoxal-5w864191x3066/xxlarge8242.gif" alt="prime" align="BASELINE" BORDER="0">-phosphate in the spleen was 55% lower than in the control. Lymphocytes taken from these animals, when cultured in vitro, showed sharply weakened ability to incorporate [³H]thymidine into DNA in response to the alloantigen. The cytolytic activity of these lymphocytes also was reduced. The ability of different forms of pyridoxine to restore the functions of T lymphocytes, when disturbed by avitaminosis B₆, was studied.Laboratory of Systemic Blood Diseases, Oncologic Scientific Center, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR N. A. Kraevskii.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 84, No. 8, pp. 185–188, August, 1977.