MR arthrographic findings of SLAP lesion type V

PURPOSE: The purpose of this study was to determine the findings of MR arthrography of the shoulder and to assess the role of MR arthrography in the diagnosis of superior labrum anterior to posterior (SLAP) lesion type V. METHODS AND MATERIALS: Two radiologists retrospectively reviewed fat-suppressed T1-weighted MR arthrography images of six patients who were diagnosed with SLAP lesion type V by arthroscopy. Each imaging plane, including the transverse, oblique coronal, oblique sagittal, and oblique transverse in abductor external rotation (ABER) position were evaluated for the following three findings: tear of the superior labrum at biceps tendon insertion, Bankart lesion, and continuity of the two former findings. RESULTS: Tear of the superior labrum was shown in all patients on oblique coronal images. Bankart lesion was noted in five patients on the transverse images and in four on the oblique sagittal images. On the oblique transverse images in ABER position, Bankart lesion was shown in all patients. The continuity of the two former findings was noted in three patients on the ABER positioned images. Therefore, three patients could be diagnosed as having SLAP lesion type V by MR arthrography in our series. CONCLUSION: It is difficult to detect all three findings of SLAP lesion type V in one imaging plane, however, a combination of multi-directional images may increase the feasibility of MR arthrography in diagnosing SLAP lesion type V.     

Human parathyroid hormone (1-34) increases mass and structure of the cortical shell,with resultant increase in lumbar bone strength,in ovariectomized rats

Estrogen deficiency causes reduction of bone mass and abnormal bone microarchitecture, consequently reducing bone strength. Human parathyroid hormone (hPTH) (1-34) increases bone mass and strength. To clarify the factors that determine the recovery of bone strength in the lumbar vertebrae of ovariectomized rats by intermittent hPTH administration, we analyzed the relationship between skeletal measurements and bone strength. Human PTH (1-34) administration resulted in recovery of cortical bone mineral content (BMC) and cortical bone area to sham the levels, but in resulted in a less pronounced recovery of trabecular BMC and no increase in the total cross-sectional area of the vertebral body. Of the three-dimensional (3D) trabecular bone parameters, hPTH (1-34) increased trabecular thickness (Tb.Th). The cortical shell area of L4, determined by histomorphometry, was also increased. In hPTH-treated rats, the only determinant of the compressive load of L5 was the cortical shell BMC, in the early recovery period (days 42–84). Our data suggest that increased cortical bone mass contributes more than trabecular bone mass and structure to the recovery of bone strength in response to hPTH therapy in the rat lumbar vertebral body after ovariectomy.     

Cross-calibration of ionization chambers in proton and carbon beams

The calibration coefficients of a parallel plate ionization chamber are examined by comparing the coefficients obtained through three methods: a calculation from a 60Co calibration coefficient, N(D, omega, 60Co), a cross-calibration of a parallel plate ionization chamber using a cylindrical ionization chamber at the plateau region of a mono-energetic beam and a cross-calibration of the chamber using a cylindrical chamber at the middle of the SOBP of the therapeutic beams. This paper also examines reference conditions for determining absorbed dose to water in the cases of therapeutic carbon and proton beams. In the dose calibration procedure recommended by IAEA, irradiation fields should be larger than 10 cm in diameter and the water phantom should extend by at least 5 cm beyond each side of the field. These recommendations are experimentally verified for proton and carbon beams. For proton beams, the calibration coefficients obtained by these three methods approximately agreed. For carbon beams, the calibration coefficients obtained by the second method were about 1.0% larger than those obtained by the third method, and the calibration coefficients obtained by cross-calibration using 290 MeV/u beams were 0.5% lower than those obtained using 400 MeV/u beams. The calibration coefficient obtained by the first method agreed roughly with the results obtained by SOBP beams.     

Establishment of a binding assay for protein kinase C isozymes using synthetic C1 peptides and development of new medicinal leads with protein kinase C isozyme and C1 domain selectivity

Conventional and novel protein kinase C (PKC) isozymes contain two cysteine-rich C1 domains (C1A and C1B), both of which are candidate phorbol-12, 13-dibutyrate (PDBu)-binding sites. We synthesized C1 peptides of 50-70 residues corresponding to all PKC isozyme C1 domains using an Fmoc solid-phase strategy. These C1 peptides were successfully folded by zinc treatment, as monitored by electrospray ionization time-of-flight mass spectrometry. We measured the K(d)'s of [3H]PDBu for all PKC C1 peptides. Most of the C1 peptides, except for delta-C1A and theta-C1A, showed strong PDBu binding affinities with K(d)'s in the nanomolar range (0.45-7.4 nM) comparable with the respective whole PKC isozymes. The resultant C1 peptide library can be used to screen for new ligands with PKC isozyme and C1 domain selectivity. Non-tumor-promoting 1-oleoyl-2-acetyl-sn-glycerol and bryostatin 1 showed relatively strong binding to all CIA peptides of novel PKCs (delta, epsilon, and eta). In contrast, the tumor promoters (-)-indolactam-V, ingenol-3-benzoate, and PDBu bound selectively to all C1B peptides of novel PKCs. The preference of tumor promoters for the domain might be related to tumorigenesis since recent investigations proposed the involvement of novel PKCs in tumor promotion in vivo using transgenic or knockout mice. Moreover, we recently have found that a new lactone analogue of benzolactams (6) shows significant selectivity in PKCeta-C1B binding.     

Possible benefits of triamcinolone-assisted pars plana vitrectomy for retinal diseases

PURPOSE: To study the advantages and complications of triamcinolone acetonide (TA)-assisted pars plana vitrectomy (PPV) for various retinal diseases. METHODS: This report is an interventional case series and nonrandomized study. One hundred seventy-seven eyes from 158 patients underwent PPV with or without TA. Group TA(+) consisted of 94 eyes and group TA(-) consisted of 83 eyes. The improvement in vision and postoperative complications were prospectively studied. RESULTS: Sixty-two percent of the eyes in group TA(+) and 49% of the eyes in group TA(-) had improved vision after surgery (P = 0.34). Twelve eyes in group TA(+) and 12 eyes in group TA(-) had an intraocular pressure higher than 21 mmHg after the operation, with no statistically significant difference (P = 0.63). Four eyes with proliferative diabetic retinopathy in group TA(+) and five eyes with proliferative diabetic retinopathy in group TA(-) needed an additional filtering surgery. Group TA(+) (five eyes) had a lower incidence (P = 0.041) of reoperation caused by preretinal fibrous membrane formation than group TA(-) (13 eyes). No apparent corneal disorder or infectious signs were found in any eyes. CONCLUSIONS: Triamcinolone acetonide-assisted PPV appears to be potentially useful to reduce the incidence of reoperation owing to preretinal fibrosis with no serious complications.     

Involvement of noradrenergic system within the central nucleus of the amygdala in naloxone-precipitated morphine withdrawal-induced conditioned place aversion in rats

Rationale We previously reported that the central nucleus of the amygdala (CeA) plays a crucial role in the negative affective, rather than somatic, component of morphine withdrawal. However, numerous studies have reported that the central ascending noradrenergic system is implicated in morphine withdrawal syndrome, although the roles of the noradrenergic system within the CeA in the negative affective component remains less clear. Objectives The possible role of the noradrenergic system within the CeA in the negative affective component of morphine withdrawal was investigated. Methods The extracellular noradrenaline level within the CeA during naloxone-precipitated morphine withdrawal was measured using an in vivo microdialysis experiment on unanesthetized and freely moving rats. The effects of microinjection of β-adrenoceptor antagonists into the bilateral CeA on the naloxone-precipitated morphine withdrawal-induced conditioned place aversion (CPA) and somatic signs were examined. Results The extracellular noradrenaline level within the CeA was transiently elevated during morphine withdrawal. Intra-CeA injections of β-adrenoceptor antagonists propranolol (30 nmol per side) and timolol (10 nmol per side) significantly attenuated the morphine withdrawal-induced CPA. Similarly, β₁-antagonist atenolol (30 nmol per side) or β₂-antagonist butoxamine (30 nmol per side) significantly attenuated the CPA. In contrast, they did not affect morphine withdrawal-induced somatic signs, except for propranolol. Conclusion These results suggest that the activation of the noradrenergic system within the CeA contributes to naloxone-precipitated morphine withdrawal-induced CPA, rather than somatic signs, through β₁- and β₂-adrenoceptors.     

Investigation of the mechanism of drug-induced autoimmune hemolytic anemia in cynomolgus monkeys elicited by a repeated-dose of a humanized monoclonal antibody drug

We investigated the mechanism of hemolytic anemia detected in a repeated-dose toxicity study using cynomolgus monkeys that were treated with a humanized antibody drug. This drug was an IgG1 monoclonal antibody (MoAb) that binds to the human HM1.24 antigen named anti-HM1.24 MoAb. The presence of the HM1.24 antigen on the erythrocyte membranes and the erythrocyte agglutination following the addition of anti-HM1.24 MoAb was examined. In addition, an indirect Coombs' test, a hemolysis assay and the measurement of anti-single stranded-DNA antibodies were performed using test animal serum or plasma. The specific binding of FITC- and 125I-labeled anti-HM1.24 MoAb to the erythrocyte membrane was not observed. HM1.24 antigen was not identified on the erythrocyte membranes. However, a high concentration (more than 713 microg/mL) of anti-HM1.24 MoAb hemagglutinated the erythrocyte suspensions. The cause of this agglutination was unclear, but it is assumed that the non-specific binding and/or adhesion caused the direct agglutination. In the examination using test serum from the anemic monkeys, a positive reaction in the indirect Coombs' test was noted. Moreover, in these Coombs' test-positive animals, the production of anti-single stranded-DNA antibodies was sequentially increased. In the female monkey sacrificed in extremis due to severe anemia, an in vitro hemolytic reaction was detected attributable to complement activation. From these results, the hemolytic anemia detected in the repeated-dose toxicity study was diagnosed as a drug-induced autoimmune hemolytic anemia (AIHA) and the primary cause was assumed to be production of IgG class anti-erythrocyte autoantibodies.