ENCEPHALOMYELONEURITIS WITH MEDIASTINAL GERM CELL TUMOR A Paraneoplastic Condition ?

An unusual case of encephalomyeloneuritis associated with germ cell tumor with mature and immature teratoma arising in the mediastinum is presented. There was an unusually long interval from the onset of neurologic symptoms to the development of malignancy. The histopathology, characterized by limbic encephalitis, brain stem encephalitis, cortical cerebellar degeneration and myeloneuritis, was similar to that of paraneoplastic encephalomyeloneuritis previously described in the literature. Virological and immunological studies failed to demonstrate any causative agents or autoantibodies reacting with brain tissue. The causal relationship between the malignant neoplasm and encephalomyeloneuritis thus seems to be very complex.     

Synthesis and side-chain crystallization of comb-like polymers obtained from isopropenyl-1,3,5-triazines carrying two,three, and four long alkyl groups

Monomers containing several octadecyl groups, e.g., 2-isopropenyl-4,6-bis(octadecylamino)-1,3,5-triazine ( 2 ), 2-dioctadecylamino-4-isopropenyl-6-octadecylamino-1,3,5-triazine ( 3 ) and 2,4-bis(dioctadecylamino)-6-isopropenly-1,3,5-triazine ( 4 ) were prepared by the alkylation reaction of 2,4-diamino-6-isopropenyl-1,3,5-triazine ( 1 ) with 1-bromooctadecane in the presence of sodium hydride. In the free-radical homopolymerization of these monomers, the polymer yield of 3 was lower than that of 2 due to a decrease in the ceiling temperature, and the polymerization of 4 did not proceed. Copolymerizations of these monomers with styrene or methyl methacrylate were carried out and the monomer reactivity ratios (r₁ and r₂) were determined. The monomer reactivity decreased with increasing the number of octadecyl groups in the monomers. Crystallinity of the octadecyl side chains in the resulting comb-like polymers was evaluated by differential scanning calorimetry.     

Allelic homogeneity due to a founder mutation in Japanese patients with lattice corneal dystrophy type IIIA

Lattice corneal dystrophies (LCDs) are caused by mutations of the transforming growth factor beta-induced gene (TGFBI, formerly betaig-h3). LCD type IIIA (LCDIIIA) has been reported mostly from Japan. In this study, we demonstrate allelic homogeneity for Japanese patients with LCDIIIA, using intragenic polymorphic markers. When exon 11 of TGFBI was analyzed, all 18 patients examined were found to be heterozygous for both a P501T mutation and an IVS10-3C --> T variation. On the other hand, none of 54 normal Japanese control subjects had the P501T, and 5 of the controls were heterozygous for IVS10-3C --> T. Haplotype analysis of the patients revealed that both P501T and IVS10-3C --> T were located on the same chromosome, and a significant linkage disequilibrium (P < 0.001, Fisher's exact probability test) was observed between LCDIIIA (P501T) and IVS10-3C --> T. When exon 8 of the gene was analyzed, all these patients possessed the "G allele" of a 1028G/A polymorphism. A significant linkage disequilibrium (P < 0.003; chi-square test) was also observed between P501T and the G allele in the patients. These results suggest that allelic homogeneity seen in Japanese patients with LCDIIIA may result from a single founder mutation.     

Can random bladder biopsies be eliminated after bacillus Calmette–Guérin therapy against carcinoma in situ?

Purpose

Intravesical bacillus Calmette–Guérin (BCG) is the standard of care for bladder carcinoma in situ (CIS). The response to BCG therapy against CIS is generally assessed by random bladder biopsy (RBB). In this study, we examined the necessity of routine RBB after BCG therapy.

Methods

We retrospectively identified 102 patients who were initially diagnosed with CIS with or without papillary tumor and received subsequent 6–8-week BCG therapy. Thereafter, all patients underwent voiding cytology analysis, cystoscopy, and RBB to evaluate the effects of BCG therapy. We evaluated the association between clinical parameters (voiding cytology and cystoscopy findings) and the final pathological results by RBB specimens.

Results

According to the pathological results of RBB, 30 (29%) patients had BCG-unresponsive disease (remaining urothelial carcinoma was confirmed pathologically) and 20 were diagnosed with CIS. Positive/suspicious voiding cytology and positive cystoscopy findings were well observed in patients who had BCG-unresponsive disease compared with their counterparts (p?=?0.116, and p?<?0.001, respectively). The sensitivity (Sen.), specificity (Spe.), positive predictive value (PPV), and negative predictive value (NPV) of voiding cytology were 50%, 68%, 39%, and 77%, respectively. The values for cystoscopy findings were as follows: Sen.: 87%, Spe.: 57%, PPV: 46%, and NPV: 91%. The values for their combination (having either of them) were as follows: Sen.: 100%, Spe.: 44%, PPV: 43%, and NPV: 100%.

Conclusion

RBB after BCG therapy for patients with negative voiding cytology and negative cystoscopy may be omitted because their risk of BCG-unresponsive disease is significantly low (NPV: 100%).

     

Periodic isorhythmic dissociation during enflurane anesthesia in a patient with Sinus Bradycardia

Key words  dysrhythmia - isorhythmic dissociation - oscillation     

Inhibition of Ca2+ channel current by μ- and κ-opioid receptors coexpressed in Xenopus oocytes: desensitization dependence on Ca2+ channel α1 subunits

1. Desensitization of μ- and κ-opioid receptor-mediated inhibition of voltage-dependent Ca²⁺ channels was studied in a Xenopus oocyte translation system.
2. In the oocytes coexpressing κ-opioid receptors with N- or Q-type Ca²⁺ channel α₁ and β subunits, the κ-agonist, U50488H, inhibited both neuronal Ca²⁺ channel current responses in a pertussis toxin-sensitive manner and the inhibition was reduced by prolonged agonist exposure.
3. More than 10 min was required to halve the inhibition of Q-type channels by the κ-agonist. However, the half-life for the inhibition of N-type channels was only 6±1 min. In addition, in the oocytes coexpressing μ-opioid receptors with N-type or Q-type channels, the uncoupling rate of the μ-receptor-mediated inhibition of N-channels was also faster than that of Q-type channels.
4. In the oocytes coexpressing both μ- and κ-receptors with N-type channels, stimulation of either receptor resulted in a cross-desensitization of the subsequent response to the other agonist. Treatment of oocytes with either H-8 (100 μM), staurosporine (400 nM), okadaic acid (200 nM), phorbol myristate acetate (5 nM) or forskolin (50 μM) plus phosphodiesterase inhibitor did not affect either the desensitization or the agonist-evoked inhibition of Ca²⁺ channels.
5. These results suggest that the rate of rapid desensitization is dependent on the α₁ subtype of the neuronal Ca²⁺ channel, and that a common phosphorylation-independent mechanism underlies the heterologous desensitization between opioid receptor subtypes.