Immediate ultrastructural effects of endothelin-1 on rabbit basilar artery

Summary In this study intra-arterial Endothelin-1 was applied to rabbit basilar arteries and morphological findings were compared between two groups who were either perfusion fixed or immersion fixed. We planned to establish the quantitative dimension of the drug-induced morphological alterations, independent of the fixation technique's effect.There was an abundance of collagenous fibres deposited among the smooth muscle cells which was not observed in control arteries and after immersion fixation. These degenerative changes are similar to the finding following subarachnoid haemorrhage. The only fixation-related difference was the fact that lamina elastica interna was not corrugated in the perfusion fixation group.It is concluded that, the observed changes in the connective tissue of the arterial wall alter the passive elastic properties and so affect the degree of the response to the vasoactive messengers.     

Role of granulocyte colony-stimulating factor in the treatment of mucormycosis

Several problems in the management of life-threatening mucormycosis remain unresolved, necessitating new methods of management. Four patients with histopathologically proven rhinocerebral mucormycosis were treated with high cumulative doses of granulocyte colony-stimulating factor (G-CSF). All had multiple predisposing factors for mucormycosis, particularly leukemia and neutropenia. Two patients refractory to fluconazole therapy were treated with liposomal amphotericin B. The improvement in clinical manifestations was closely related to neutrophil recovery, and all patients were alive at the end of therapy. In addition to surgical debridement and antifungal therapy, G-CSF seems to have played a role in their survival.     

The clinical impact of Prostate Imaging–Reporting and Data System classification in patients with haemospermia undergoing multiparametric magnetic resonance imaging of the prostate

In this study, we evaluated the role of the Prostate Imaging–Reporting and Data System (PI-RADS) classification of multiparametric magnetic resonance imaging (mpMRI) to determine the likelihood of prostate cancer (PCa) in patients with haemospermia. Fifty-one patients presenting with haemospermia between 2018 and 2020 were included in this retrospective study. Forty-two of the patients (82.4%) were over 40 years, and the median prostate-specific antigen (PSA) level was 1.4 ng/ml. Fourteen of the patients (27.5%) had recurrent haemospermia. All patients underwent mpMRI, and assessments were classified according to PI-RADS v2. The mpMRI revealed PI-RADS one to four lesions in 10 (19.6%), 30 (58.8%), 6 (11.8%) and 5 (9.8%) patients respectively. One patient with PI-RADS 3 and five with PI-RADS 4 lesions underwent cognitive fusion prostate biopsy depending on MRI findings, and two patients with PI-RADS 4 lesions were diagnosed with PCa. Patients with haemospermia and risk factors, that is aged over 40 years, a high PSA level or familial history of PCa, need a more thorough evaluation with mpMRI.     

An independent indicator of erectile dysfunction is C-reactive protein/albumin ratio

Research has found that, instead of passive lipid-accumulated vascular damage, atherosclerosis which is the primary cause of erectile dysfunction (ED) can be seen as an active inflammatory cycle and that inflammation has a central role in the entire atherosclerotic process. As an inflammatory marker, serum C-reactive protein (CRP)/albumin ratio (CAR) may link to ED and ED severity. The CAR, demographic features and other criteria of 198 patients with ED who visited our outpatient clinic during March 2019–April 2020 were prospectively evaluated. The research also included healthy control subjects without systemic or infectious diseases. The mean difference of CAR between ED and no ED was statistically significant (0.55 ± 0.27 and 0.79 ± 0.49, p = .002 respectively). On the basis of the ROC analysis, CAR has a good ED diagnostic value with an area under the curve (AUC) of 0.63 (95% CI:0.541–0.714) and better diagnostic performance to distinguish ED severity (AUC:0.73, 95% CI:0.620–0.842). Additionally, mean CAR gradually increased with increasing severity of ED (for all p < .001). The CAR has been described as an independent ED indicator in the multivariate analysis (p = .001OR = 8.934; 95% CI:2.449–32.583). Increased CAR is associated with ED severity and increased ED risk. For CAR predicting ED and ED severity, a considerable cut-off point was identified.     

Carbamazepine-induced sperm disorders can be associated with the altered expressions of testicular KCNJ11/miR-let-7a and spermatozoal CFTR/miR-27a

Male infertility is a global health problem, and the underlying molecular mechanisms are not clearly known. Ion channels and microRNAs (miRNAs), known to function in many vital functions in cells, have been shown to play a significant role in male infertility through changes in their expressions. The study aimed to evaluate the alterations of testicular and/or spermatozoal potassium voltage-gated channel subfamily J member 11 (KCNJ11), Cystic fibrosis transmembrane conductance regulator (CFTR), miR-let-7a and miR-27a expressions in carbamazepine-related male infertility. Here, we showed that carbamazepine reduced sperm motility, increased abnormal sperm morphology, and impaired hormonal balance as well as increased relative testis weight and decreased relative seminal vesicle weight. On the other hand, downregulated KCNJ11 and upregulated miR-let-7a expressions were determined in testis (p < .05). Also, downregulated KCNJ11 and upregulated CFTR and miR-27a expressions were found in spermatozoa (p < .05). Interestingly, altered testicular KCNJ11 and miR-let-7a expressions were correlated with decreased sperm motility and elevated sperm tail defect. Besides, spermatozoal CFTR and miR-27a expressions positively correlated with sperm tail defects. The results indicated a significant relationship between ion channel and/or miRNA expression alterations and impaired sperm parameters due to carbamazepine usage.     

MRI and MRS in HMG-CoA lyase deficiency

3-Hydroxy-3-Methylglutaryl coenzyme A lyase (HMG-CoA) deficiency is a rare inborn error of leucine catabolism. The disease is characterized by recurrent episodes of metabolic acidosis, hyperammonemia without ketosis, hypoglycemia, lethargy, hepatomegaly, and seizures. This study has evaluated the magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) findings of three patients with HMG-CoA deficiency. The common findings on all of the MRI scans were multiple, coalescent, marked lesions in periventricular white matter and arcuate fibers, most prominently in frontal or periatrial regions that were superimposed on diffuse, slightly hyperintense subcortical white matter signal. Involvement of the caudate nucleus and the dentate nucleus were observed in the reported patients. MRS studies by both STEAM and PRESS spectra of all patients revealed a decrease in N-acetylaspartate and elevation in both myoinositol and choline. A pathologic peak at 1.33 ppm, which is compatible with lactate, and a particular peak at 2.42 ppm in all patients were also found. The combination of both MRI and MRS findings could be considered as being specific in patients with HMG-CoA lyase deficiency.     

The Effect of Tizanidine on Chronic Vasospasm in Rats

Summary ? Background. Cerebral vasospasm after subarachnoid hemorrhage (SAH) has remained a major cause of morbidity and mortality in patients with SAH. Excitatory neurotransmitters are gathered in the extracellular space during ischemia due to cerebral vasospasm and initiate or stimulate a series of pathophysiological biochemical processes which consequently lead to neuronal death. Tizanidine (Sandoz compound DS 103–282, 5-chloro-4,2 (2-imidazolin-2-yl-amino)-2,1,3-benzothiazol hydrochloride) is a centrally-acting muscle relaxant and a selective α 2 adrenoreceptor agonist which shows its effect by stimulating presynaptic α 2 adrenoreceptors in central ASPergic and GLUergic system by inhibiting aspartic acid and glutamic acid release. In this study, the effect of Tizanidine on vasospasm was evaluated.  Methods. We used a femoral artery vasospasm model in rats which has been described by Okada et al. 60 rats were examined in three groups. The first group was used as control group (Control) (n=20), in the second group subarachnoid hemorrhage was performed (SAH) (n=20), in the third group Tizanidine was administered in addition to SAH (SAH+Tizanidine administration) (n=20). Animals in SAH+Tizanidine administration group received 0,3 mg/kg/day intraperitoneally for 7 days. Seven days after the experiment, after perfusion-fixation, 10 mm segments of both femoral arteries were removed and the femoral artery was prepared for light microscope examination, scanning and transmission electron microscopy and for morphometric analysis.  Results. There was a statistically significant difference between the electron, scanning and light microscopic observations and morphometric analysis of SAH+Tizanidine administration group and SAH group, and no statistically significant difference between SAH+Tizanidine administration group and control group.  Conclusion. This study has disclosed that Tizanidine administration before the vasospasm reduces ultrastructural and morphometric vasospastic insult significantly. However, the clinical application of Tizanidine as a protective and therapeutic agent in cerebral vasospasm needs further studies including the employment of clinically more relevant SAH models.