Testicular torsion: Evaluation of contralateral testicular histology

Infertility may occur in patients with unilateral testicular torsion whose contralateral testis is intact. Depending on this observation, the physicians have begun to examine the contralateral testis. In the present prospective study we aimed to examine the histopathologic alterations occurring in the contralateral testicle with time. Sixty adult male albino rats were included in the programme, and following experimental torsion the histopathologic findings, especially those in the contralateral testis, were evaluated after 4–12 weeks. Long-term and high degree torsion of the testicle led to varying degrees of deterioration in the germinal epithelium and interstitial cells of the contralateral testicle. Histopathologic alterations were reversed in 12 weeks. Tubular diameter and testicular volume also decreased in accordance with the histopathologic alteration. In our opinion, orchiectomy following torsion of one testicle will limit potential histopathologic alterations in the contralateral testicle.     

Somatosensory evoked potential monitoring during intracranial surgery

In the neurosurgical approach to intracranial aneurysms which are often accompanied by arterial spasm and cortical ischaemia, monitoring procedures aim to obtain useful information on cerebral function. SEPs evoked by stimulation of the median nerve at the wrist and of the tibial nerve at the medial malleolus were registered in 45 patients with intracranial aneurysms during neurosurgical procedures. Our results show SEP abnormalities during different stages of neurosurgical procedures in 36 patients out of the monitored 45. Significant abnormalities of SEPs with respect to the control group were decrease of the amplitude of N 20-P 25 complex, lengthening of the absolute latency of the waves N 20- and P 25 and lengthening of the central conduction time (CCT) (N 13-N 20). The greatest SEP abnormalities were registered during the neurosurgical approach to aneurysm and during the clipping procedure. However, the changes were reversible in the majority of the patients. The aim of this paper was to focus on early detection of some cerebral function disturbances during the neurosurgical procedure as well as the prevention of possible brain damage.     

Progressive motor syndrome in a welder with pallidal T1 hyperintensity on MRI: A two-year follow-up.

Chronic exposure to manganese (Mn) fume during welding may lead to mainly extrapyramidal syndrome that is resistant to treatment. We present a 32-year-old patient who developed severe postural instability, Parkinsonism, dystonia, and pyramidal signs in the 10th year of welding. The neurological condition of the patient worsened markedly in the following 3 years, resulting in severe disability rendering him to be assisted in all his daily activities and he did not benefit from any dopaminergic agent. T1 sequences of the MRI of the brain showed pallidal hyperintensity symmetrically. Welders in our country often protect their eyes but ignore to use tools that protect them from inhalation of the fume. Since chronic Mn toxicity may cause serious disability and irreversible neurological disturbances, we strongly believe that it is necessary to inform welders and their employers about this potential hazard.     

Strecker stent in stenotic hemodialysis Brescia-Cimino arteriovenous fistulas

Flexible tantalum stents (Strecker) were used as an adjunct to percutaneous transluminal angioplasty (PTA) in the treatment of stenotic arterial or venous limbs of Brescia-Cimino hemodialysis fistulas. The diagnostic procedure was performed using retrograde fistulography. After PTA with unsatisfactory results, stents were placed in 5 patients with significant residual stenoses and poor fistula function. Within the mean follow-up period of 6.4 months (range 3–10 months) all fistulas were functioning. We conclude that Strecker stent is useful in the treatment of stenotic hemodialysis arteriovenous fistulas as an adjunct to PTA.     

Anthracycline-induced cardiotoxicity: Overview of studies examining the roles of oxidative stress and free cellular iron

The risk of cardiotoxicity is the most serious drawback to the clinical usefulness of anthracycline antineoplastic antibiotics, which include doxorubicin (adriamycin), daunorubicin or epirubicin. Nevertheless, these compounds remain among the most widely used anticancer drugs. The molecular pathogenesis of anthracycline cardiotoxicity remains highly controversial, although the oxidative stress-based hypothesis involving intramyocardial production of reactive oxygen species (ROS) has gained the widest acceptance. Anthracyclines may promote the formation of ROS through redox cycling of their aglycones as well as their anthracycline-iron complexes. This proposed mechanism has become particularly popular in light of the high cardioprotective efficacy of dexrazoxane (ICRF-187). The mechanism of action of this drug has been attributed to its hydrolytic transformation into the iron-chelating metabolite ADR-925, which may act by displacing iron from anthracycline-iron complexes or by chelating free or loosely bound cellular iron, thus preventing site-specific iron-catalyzed ROS damage. However, during the last decade, calls for the critical reassessment of this “ROS and iron” hypothesis have emerged. Numerous antioxidants, although efficient in cellular or acute animal experiments, have failed to alleviate anthracycline cardiotoxicity in clinically relevant chronic animal models or clinical trials. In addition, studies with chelators that are stronger and more selective for iron than ADR-925 have also yielded negative or, at best, mixed outcomes. Hence, several lines of evidence suggest that mechanisms other than the traditionally emphasized “ROS and iron” hypothesis are involved in anthracycline-induced cardiotoxicity and that these alternative mechanisms may be better bases for designing approaches to achieve efficient and safe cardioprotection.     

Effects of Nitrous Oxide on the Rat Heart In Vivo: Another Inhalational Anesthetic That Preconditions the Heart?

Background: For nitrous oxide, a preconditioning effect on the heart has yet not been investigated. This is important because nitrous oxide is commonly used in combination with volatile anesthetics, which are known to precondition the heart. The authors aimed to clarify (1) whether nitrous oxide preconditions the heart, (2) how it affects protein kinase C (PKC) and tyrosine kinases (such as Src) as central mediators of preconditioning, and (3) whether isoflurane-induced preconditioning is influenced by nitrous oxide.

Methods: For infarct size measurements, anesthetized rats were subjected to 25 min of coronary artery occlusion followed by 120 min of reperfusion. Rats received nitrous oxide (60%), isoflurane (1.4%) or isoflurane-nitrous oxide (1.4%/60%) during three 5-min periods before index ischemia (each group, n = 7). Control animals remained untreated for 45 min. Additional hearts (control, 60% nitrous oxide alone%, and isoflurane-nitrous oxide [0.6%/60%, in equianesthetic doses]) were excised for Western blot of PKC-[varepsilon] and Src kinase (each group, n = 4).

Results: Nitrous oxide had no effect on infarct size (59.1 +/- 15.2% of the area at risk vs. 51.1 +/- 10.9% in controls). Isoflurane (1.4%) and isoflurane-nitrous oxide (1.4%/60%) reduced infarct size to 30.9 +/- 10.6 and 28.7 +/- 11.8% (both P < 0.01). Nitrous oxide (60%) had no effect on phosphorylation (2.3 +/- 1.8 vs. 2.5 +/- 1.7 in controls, average light intensity, arbitrary units) and translocation (7.0 +/- 4.3 vs. 7.4 +/- 5.2 in controls) of PKC-[varepsilon]. Src kinase phosphorylation was not influenced by nitrous oxide (4.6 +/- 3.9 vs. 5.0 +/- 3.8; 3.2 +/- 2.2 vs. 3.5 +/- 3.0). Isoflurane-nitrous oxide (0.6%/60%, in equianesthetic doses) induced PKC-[varepsilon] phosphorylation (5.4 +/- 1.9 vs. 2.8 +/- 1.5; P < 0.001) and translocation to membrane regions (13.8 +/- 13.0 vs. 6.7 +/- 2.0 in controls; P < 0.05).