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Judit Sandbank

Publications and source records attributed to Judit Sandbank.

2 recordsLinked to original sources

Mesangial cells initiate compensatory renal tubular hypertrophy via IL-10-induced TGF-beta secretion: effect of the immunomodulator AS101 on this process.

The present study investigated the role of IL-10 produced by the mesangial cells in postnephrectomy compensatory renal growth and the effect of the immunomodulator AS101 on this process. One hundred forty unilateral nephrectomized and sham-operated male Sprague-Dawley rats were treated by AS101 or PBS before and after surgery. The results show that secretion of IL-10 and TGF-beta by mesangial cells isolated from the remaining kidneys was increased significantly, compared with those of control and sham animals. Moreover, TGF-beta secretion by mesangial cells was increased after the addition of exogenous recombinant IL-10 and inhibited in the presence of neutralizing anti-IL-10 antibodies. In vivo, compensatory growth of the remaining kidneys was associated with significant increase in IL-10 content in renal tissues and plasma. Immunohistochemical studies show that IL-10 was produced by mesangial cells. Elevated IL-10 levels were followed by the rise in TGF-beta content in plasma and renal tissue. AS101 treatment decreased IL-10 and TGF-beta expression in plasma and kidney tissues and results in 25% reduction in the fresh and fractional kidney weight and decreased hypertrophy of tubular cells (protein/DNA ratio, morphometric analysis). Taken together, these data demonstrate that TGF-beta production by mesangial cells is IL-10 dependent. Mesangial cells are the major source of IL-10 in kidneys. AS101, by inhibiting the activity of IL-10, decreases TGF-beta production by mesangial cells, thus limiting compensatory tubular cell hypertrophy.

Animals↗

[Acute epididymitis].

Epididymitis may be acute (symptoms last less than 6 weeks) or chronic (more than 3 months). Acute epididymitis is almost always unilateral. In sexually active men under 35 years of age, acute epididymitis is frequently caused by Chlamydia trachomatis and less frequently by Neisseria gonorrhoeae and is usually associated with overt or subclinical urethritis. Acute epididymitis in older men, children or following urinary tract instrumentation is commonly caused by gram-negative bacilli. The epididymis is sometimes the site of metastatic infection, such as tuberculosis. It is important to differentiate epididymitis from other causes for acute scrotum, such as testicular torsion and tumor. The cause of acute scrotum especially in children cannot always be identified. Therefore, Doppler ultrasonography and radionuclide scans are often used. In infants and young boys, genitourinary abnormalities are causative factors, and therefore should be excluded by imaging. Supportive measures and antimicrobial agents are the mainstay of therapy.

Acute Disease↗