Five different genes, Eif4a1, Cd68, Supl15h, Sox15 and Fxr2h, are clustered in a 40 kb region of mouse chromosome 11.

We characterized a region of the mouse genome disrupted by integration of a gene trap (GT) vector in ES cells. On 5' rapid amplification of cDNA ends analysis of the fusion transcripts containing the GT vector, we identified the eukaryotic protein synthesis initiation factor 4A1 gene (Eif4a1) as a promoter-trapped gene. Plasmid rescue was used to show that the other end of the integrated vector disrupted the murine homolog of the human fragile X mental retardation syndrome-related protein 2 gene (Fxr2h). Structural analysis of P1 clones, isolated from the wild-type mouse genome by PCR with Eif4a1-specific primers, indicated that the integration of the GT vector was accompanied by the deletion of about 35 kb of genomic DNA and that the disrupted region also included three genes, Cd68, Supl15h and Sox15, the latter two of which are transcribed in opposite directions with overlapping 3' ends. These five different genes at least, Eif4a1, Cd68, Supl15h, Sox15 and Fxr2h, are clustered in a 40 kb region. The chromosomal location of this region was mapped by means of interspecific backcross panel DNAs to the central part of mouse chromosome 11, exhibiting a known region of synteny with human chromosome 17.

[Expression of proteinase inhibitors in the human trabecular meshwork].

We examined the distribution and expression of three proteinase inhibitors, alpha 1-proteinase inhibitor (alpha 1-PI), alpha 1-antichymotrypsin (alpha 1-ACT), and alpha 2-macroglobulin (alpha 2-M) in the human trabecular meshwork. Immunohistochemistry, in situ hybridization, and reverse transcription-polymerase chain reaction (RT-PCR) were used. By immunostaining, all three inhibitors were identified in the human trabecular meshwork with enhanced staining in the uveal meshwork. In situ hybridization showed mild but positive accumulation of the silver grains on the trabecular meshwork cells, which indicates mRNA expression. Specific distribution or cell selectivity were not detectable probably due to weak expression of these inhibitors in this tissue. Instead mRNAs for alpha 1-PI, alpha 1-ACT, and alpha 2-M as well as antithrombin III, plasminogen activator inhibitor-1 could be identified by RT-PCR using trabecular meshwork culture cells. In this study, we concluded that some proteinase inhibitors were distributed in the human trabecular meshwork as well as in the cornea and the ciliary body. At least part of these were probably produced by the trabecular meshwork cells. The balance between proteinases and proteinase inhibitors might play an important role even in the human trabecular meshwork to maintain the outflow route. The alterations in the primary or secondary glaucomatous eyes are curious.

X-ray evidence for the elongation of thin and thick filaments during isometric contraction of a molluscan smooth muscle.

The elongation of thin and thick filaments during isometric contraction of a molluscan smooth muscle was studied by measuring spacing changes of meridional reflections in the medium-angle X-ray diffraction pattern. X-ray patterns from the anterior byssus retractor muscle of Mytilus edulis in the resting, active, and catch states were taken from the same part of a muscle bundle at a fixed specimen-to-detector distance, using imaging plates and 10 s exposure to synchrotron radiation. The third-order reflection (9.2 A) of the axial period of actin, and the fourteenth-order reflection (10.4 A) of the axial subunit-repeat of the thick filament are increased in spacing in the active and catch states. From accurately measured changes in the axial distance of the 9.2 A layer line from the origin, thin filament elongations in the active and catch states are estimated to be 0.48 and 0.32%, respectively, in a muscle that maintains a tension of 12.2 kg cm-2 in the active state and 9.8 kg cm-2 in the catch state. Thick filament elongations in the active and catch states are similarly estimated to be 0.33, and 0.28%, respectively, based on the axial shift of the 10.4 A reflection. The 0.48% elongation of the thin filament in the active state agrees with an elongation that is presumed by White and Thorson (1973) to estimate the lower limit of the thin-filament stiffness. It seems that in the catch state the activated and resting thin filament structures are intermixed. The activated parts of the thin filament are probably more elongated than the apparent value, 0.32%.

[A case of rheumatoid arthritis complicated with pseudotumor around odontoid process successfully treated by methotrexate].

A 69-year-old-female with a history of rheumatoid arthritis since 1975 had suffered from dysesthesia of extremities since October 1989. Radiating pain and weakness occurred when she tried to stand up on Dec. 25 in 1989. She was admitted to our hospital in October 1990. Physical examination showed emaciation, hypesthesia of extremities, hypesthesia over the right chest and back, impaired vibration and position sense, and hyperreflexia. Laboratory findings revealed that the erythrocyte sedimentation rate was elevated to 46mm/hr, rheumatoid factor (RF) to 83.1IU/ml and CRP to 3.7mg/dl. Her blood sugar was high and she was diagnosed as having diabetes mellitus. Cervical X ray film showed atlanto-axial subluxation. A pseudotumor around the odontoid process bulging into the spinal canal and compression of the upper cervical cord was observed by MRI. In spite of administration of bucillamine (100mg/day), the size of pseudotumor did not change. Methotrexate (MTX) at a dose of 5mg/week was started in February 1991 and the pseudotumor decreased in size with a concurrent reduction of ESR, RF and CRP. However, the high intensity lesion by T2 weighed image did not change and dysesthesia persisted. The pseudotumor was thought to be due to pannus and it was revealed that MTX was effective for reduction. The persistent dysesthesia was probably due to the degeneration of the upper cervical cord, although diabetic neuropathy may also have played a role.