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Biomedical subjects

S G Mulholland

Publications and source records attributed to S G Mulholland.

At least 19 recordsLinked to original sources
PubMed1979

Ultrasonic differentiation of renal pelvic filling defects.

We herein describe 9 patients with non-opaque calculi and 3 patients with soft tissue filling defects in the renal pelvis studied by ultrasound. The calculi varied in size from 1.5 cm. to staghorn calculi. All stones were imaged satisfactorily by ultrasound, allowing the diagnosis of stone to be made with confidence. Ultrasonic differentiation of renal pelvic filling defects proved to be a simple, reliable, non-invasive method to differentiate these clinically perplexing lesions.

Diagnosis, Differential↗
PubMed1979

Venous injury in major urological surgery.

With the increasing use of pelvic node dissection for staging and treating pelvic urological cancer injury to the common, external and internal iliac veins will occur. The sequelae of these injuries are described and the treatment is outlined. A case is described that epitomizes the problems and solutions of this condition.

Aged↗
PubMed1979

Antibacterial activity of bladder surface mucin duplicated by exogenous glycosaminoglycan (heparin).

We have previously shown that the transitional cells lining the urinary bladder are capable of producing glycosaminoglycan (GAG). By use of a quantitative in vivo method of measuring bacterial adherence, we demonstrated that bacterial adherence to the mucosal cells is diminished in the presence of this GAG, rises when it is removed (by acid), and returns to normal when the GAG is resynthesized (in less than 24 h). We also found that this much layer could be removed (with a corresponding rise in bacterial adherence) and that addition of exogenous GAG (heparin) to the bladder prevented the expected rise in bacterial adherence. This study analyzed in depth the manner by which heparin prevents the rise in adherence seen when the mucin is removed. Pretreatment of bacteria with heparin had no effect on adherence, whereas pretreatment of the bladder with heparin inhibited adherence. To corroborate our impression that the heparin was coating the transitional cells, [3H]heparin was added to bladders after removal of mucin. Autoradiography revealed the heparin to be adherent to the surface of the transitional cells.

Animals↗
PubMed1978

Heparin as antibacterial agent in rabbit bladder.

Previous studies performed in our laboratory indicated that the primary antibacterial defense mechanism of the rabbit bladder is the antiadsorptive action of the surface mucopolysaccharide. The increased bacterial adsorption that occurs when the bladder is denuded of this layer was prevented by the instillation of heparin. Additional studies showed that the protective effect of heparin is inhibited by protamine, a further indication that the bladder's "antiadherence factor" is a mucopolysaccharide. Small amounts of heparin, applied directly to the mucoprotein-deficient bladder or to the surface of the inoculated bacteria, produced a statistically significant reduction in bacterial adsorption.

Adsorption↗
PubMed1978

Ultrasonic detection of nonopaque renal calculi.

Four patients with 5 nonopaque renal calculi composed of uric acid were examined by ultrasound. The calculi varied in size from a 1.5 X 1.5-cm intrapelvic stone to a staghorn calculus measuring 4 cm. All stones were satisfactorily imaged by ultrasound, allowing a diagnosis of nephrolithiasis to be made with confidence in each case. In 2 patients with poor excretion on urography, the diagnosis was not suspected prior to the ultrasound examination. The authors feel that ultrasound has great potential value in the investigation of nonopaque filling defects of the renal pelvis and in patients with urographic nonvisualization who have a high risk of uric acid lithiasis.

Adult↗
PubMed1978

Bladder surface mucin. Examination of possible mechanisms for its antibacterial effect.

We have previusly provided physiologic and histochemical data implicating the bladder surface mucin layer as an important new antibacterial defense mechanism. This mucin or its contents seems to act as an "antiadherence factor", inhibiting bacterial adherence to the bladder mucosa and thereby facilitating the removal of bacteria by the voiding process. The present study was designed to investigate three mechanisms by which the mucin might repel bacterial attachment. Our data suggest that neither IgA nor a chelating agent are anti-adherence factors. We did find, however, that pH had a significant effect on the adherence of bacteria to mucosal cells stripped of their mucin layer. This result suggest that electrochemical charge is important in bacterial adherence. We beleive that the mucin layer both provides an electrochemical coat on the bladder surface that is a poor substrate for bacterial adherence and blocks the receptor sites of the transitional cells to which the microbes might adhere.

Adhesiveness↗
PubMed1978

Bladder surface mucin. Its antibacterial effect against various bacterial species.

We previously reported the results of quantitative and histochemical studies implicating the surface mucin of the bladder mucosa as an important antibacterial defense mechanism, which functions by preventing bacteria from adhering to the bladder wall. We call the mucin "anti-adherence factor" and we feel this is a previously undocumented role for mucin as a type of host antibacterial defense. These experiments were conduced with Escherichia coli. In an effort to determine whether the anti-adherence ability of the vesical mucin was a generalized phenomenon, we repeated these studies using unrelated bacterial species, including E coli, Klebsiella pneumoniae, and Staphylococcus aureus. The ability of the vesical mucosa to resist bacterial adherence to its surface was found to be independent of the bacterial species that was investigated.

Animals↗
PubMed1977

Role of urothelial surface mucoprotein in intrinsic bladder defense.

To implicate further the surface mucoprotein as the factor responsible for preventing bacterial attachment to the bladder mucosa, rabbit urothelium was severely disrupted and allowed to regenerate for varying periods of time. Quantitative measurements of the attachment of 14C-labeled Escherichia coli were correlated with the histologic presence of the surface mucoprotein. Control levels of bacterial attachment were observed only when the PAS-positive layer had regenerated, further supporting the role of this layer in the bladder's antibacterial defense.

Adsorption↗
PubMed1977

Role of surface mucin in primary antibacterial defense of bladder.

Histochemical staining of bladder tissue has demonstrated a discrete layer of mucopolysaccharide (mucin) at the surface of rabbit and human bladders. This mucin is disrupted by acid treatment and is probably resynthesized by the transitional cells in less than twenty-four hours and replaced by forty-eight hours. Physiologic data indicate that bladder mucose can resist bacterial attachment, a function that is also disrupted by acid and recovers in less than twenty-four hours. These findings suggest that the surface mucopolysaccharide inhibits bacterial binding and may be the primary antibacterial defense of the urinary tract.

Adsorption↗
PubMed1977

Two-stage urethroplasty for urethral stricture disease.

Of 97 patients who underwent first-stage urethroplasty 23 per cent required at least 1 revision. Sixty-seven patients underwent second-stage reconstruction with a 90 per cent success rate. The various factors influencing the outcome of 2-stage urethroplasty procedures are analyzed critically.

Adolescent↗
PubMed1976

Oral methylene blue and the dissolution of renal calculi.

Oral methylene blue therapy was not effective in dissolving non-obstructive renal calculi in 26 patients but it may prevent new stone formation in patients with metabolically active urolithiasis. The use of methylene blue therapy in combination with other regimens having different mechanisms of stone inhibition is recommended to further improve results.

Administration, Oral↗
PubMed1976

Bladder defense mechanism.

In order for micro-organisms to infect the urinary tract they must adhere to the vesical mucosa so that they remain after voiding. Experiments in our laboratory demonstrated that the bladder has a self-protective mechanism capable of preventing bacterial adherence to the surface. Histochemical staining demonstrated that this substance is a mucopolysaccharide. Treatment of the mucosa with acid disrupted the protective layer and resulted in a 20 to 100-fold increase in bacterial adherence. Within 24 hours this layer reappeared and binding was again reduced to normal. This phenomenon was not related to microbial species or metabolic activity.

Adhesiveness↗