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(1/102) Diagnosis and treatment of the acute scrotum.

Testicular torsion must be considered in any patient who complains of acute scrotal pain and swelling. Torsion of the testis is a surgical emergency because the likelihood of testicular salvage decreases as the duration of torsion increases. Conditions that may mimic testicular torsion, such as torsion of a testicular appendage, epididymitis, trauma, hernia, hydrocele, varicocele and Schonlein-Henoch purpura, generally do not require immediate surgical intervention. The cause of an acute scrotum can usually be established based on a careful history, a thorough physical examination and appropriate diagnostic tests. The onset, character and severity of symptoms must be determined. The physical examination should include inspection and palpation of the abdomen, testis, epididymis, scrotum and inguinal region. Urinalysis should always be performed, but scrotal imaging is necessary only when the diagnosis remains unclear. Once the correct diagnosis is established, treatment is usually straightforward.  (+info)

(2/102) Pediatric applications of pinhole magnification imaging.

Pinhole magnification imaging is an important technique for practitioners of pediatric nuclear medicine. This article reviews basic principles of pinhole magnification imaging and ways for optimizing image acquisition with this technique. Applications to skeletal scintigraphy, scrotal scintigraphy and renal cortical scintigraphy are discussed and illustrated.  (+info)

(3/102) Trauma induced testicular torsion: a reminder for the unwary.

Trauma induced testicular torsion is a well recognised entity, the incidence being 4-8% in most studies reporting on testicular torsion. The signs and symptoms of testicular torsion may easily be mistakenly attributed to preceding testicular trauma if there was such an event. A patient is described with trauma induced testicular torsion who presented on three occasions before a decision was made to perform scrotal exploration. Unfortunately, an orchidectomy was the outcome. The message that trauma can and not infrequently does precipitate torsion, needs to be reiterated. Awareness of the entity and constant vigilance is required of clinicians to avoid a delay in definitive treatment.  (+info)

(4/102) Fluctuations in rat testicular interstitial oxygen tensions are linked to testicular vasomotion: persistence after repair of torsion.

Testicular microvascular blood flow is known to exhibit vasomotion, which has been shown to be significantly altered in the short term following the repair of testicular torsion. This loss of vasomotion may ultimately be responsible for the loss of spermatogenesis observed after testicular torsion in rats. In the present study, testicular vasomotion and interstitial oxygen tensions were simultaneously measured prior to, during, and at various time points after repair of testicular torsion in the rat. Testicular torsion was induced by a 720 degrees rotation of the testis for 1 h. Laser-Doppler flowmetry and an oxygen electrode were used to simultaneously measure vasomotion and interstitial oxygen tensions (PO(2)), respectively. Pretorsion control testes had a mean blood flow of 16.3 +/- 1.3 perfusion units (PU) and displayed vasomotion with a cycle frequency of 12 +/- 0.2 cycles per minute and a mean amplitude of 4.2 +/- 0.3 PU. Mean testicular interstitial PO(2) was 12.5 +/- 2.6 mm Hg, which displayed a cyclical variation of 11.9 +/- 0.4 cycles per minute with a mean amplitude of 2.8 +/- 0.8 mm Hg. During the torsion period, both mean blood flow and interstitial PO(2) decreased to approximately zero. Upon detorsion, mean microvascular blood flow and mean interstitial PO(2) values returned to values that were not significantly different from pretorsion values within 30 min; however, vasomotion and PO(2) cycling did not return, even after 24 h. It was 7 days after the repair of torsion before a regular pattern of vasomotion and PO(2) cycling returned. These results demonstrate for the first time a correlation between testicular vasomotion and interstitial PO(2) cycling, and this correlation persists after the repair of testicular torsion.  (+info)

(5/102) Molecular pathway of germ cell apoptosis following ischemia/reperfusion of the rat testis.

The present study investigates the molecular apoptotic pathway in germ cells following acute ischemia of the rat testis. Rats were subjected to ischemia-inducing torsion and testes were harvested after reperfusion. Apoptotic cells were identified with an antibody to single-stranded DNA. Seminiferous tubule RNA was examined by RNase protection assay or by reverse transcriptase-polymerase chain reaction (RT-PCR) for the presence and regulation of apoptotic molecules. Proteins from seminiferous tubules were used for Western blot analysis of cytochrome c. Germ cell apoptosis was maximal at 24 h after repair of torsion. Germ cells in stages II-III of the seminiferous epithelium cycle were the predominant early responders. The RNase protection assays revealed that Bcl-X(L) was the prominent mRNA species. Caspases 1, 2, 3, and Bax mRNA were consistently upregulated; however, the time of upregulation after torsion was variable. The Bcl-X(L) and Bcl-X(S) mRNAs were less consistently upregulated and there was no evidence for upregulation of Fas or Bcl-2. Fas ligand (FasL) was not detected by RNase protection assay, but RT-PCR revealed a significant increase in FasL expression 4 h after the repair of torsion. Western blot analysis for cytochrome c release demonstrated a significant increase 4 h after the repair of torsion. Results suggest that germ cell apoptosis following ischemia/reperfusion of the rat testis is initiated through the mitochondria-associated molecule Bax as well as Fas-FasL interactions.  (+info)

(6/102) Inhibition of calpain but not caspase protects the testis against injury after experimental testicular torsion of rat.

Testicular torsion requires emergent release of the twisted spermatic cord. Ischemia/reperfusion (I/R) plays an important role in its pathogenesis, and recent data suggest that germ cells undergo apoptosis during I/R. In a model of torsion/detorsion (i.e., I/R) of the rat testis, involvement of calpain and caspase in necrotic and apoptotic cell death was examined. After 1 h of ischemia followed by 0, 0.5, 1, 6, or 24 h of reperfusion, the germ cells positively stained with in situ TUNEL, and DNA fragmentation, activation of caspase-3, and proteolysis of caspase substrates increased with time of reperfusion, demonstrating apoptosis. In addition, m-calpain activation and proteolysis of alpha-fodrin were increased during reperfusion, and its activation is thought to be involved in the necrosis. A calpain inhibitor, acety-leucyl-leucyl-norleucinal, inhibited the phenomena associated with apoptosis and necrosis induced by I/R, although a caspase inhibitor, Z-Val-Ala-Asp-fluoromethlyketone, only inhibited apoptotic changes. The inhibition of calpain but not caspase ameliorated the injury after 60 days of reperfusion following 1 h of ischemia. The calpain inhibitor injected just before reperfusion effectively suppressed alpha-fodrin proteolysis, suggesting its usefulness in the treatment of testicular torsion.  (+info)

(7/102) The undescended testicle: diagnosis and management.

Early diagnosis and management of the undescended testicle are needed to preserve fertility and improve early detection of testicular malignancy. Physical examination of the testicle can be difficult; consultation should be considered if a normal testis cannot be definitely identified. Observation is not recommended beyond one year of age because it delays treatment, lowers the rate of surgical success and probably impairs spermatogenesis. By six months of age, patients with undescended testicles should be evaluated by a pediatric urologist or other qualified subspecialist who can assist with diagnosis and treatment. Earlier referral may be warranted for bilateral nonpalpable testes in the newborn or for any child with both hypospadias and an undescended testis. Therapy for an undescended testicle should begin between six months and two years of age and may consist of hormone or surgical treatment. The success of either form of treatment depends on the position of the testicle at diagnosis. Recent improvements in surgical technique, including laparoscopic approaches to diagnosis and treatment, hold the promise of improved outcomes. While orchiopexy may not protect patients from developing testicular malignancy, the procedure allows for earlier detection through self-examination of the testicles.  (+info)

(8/102) Neonatal testicular torsion in two brothers.

Two brothers presenting neonatal testicular torsion are reported. The findings suggest an autosomal or X-linked recessive pattern of inheritance for the anatomical underlying anomaly.  (+info)