Merve Civan

Radiation induces pronounced and widespread histopathological damage in the testes, which exhibit a high degree of radiosensitivity; consequently, the utilization of effective radioprotective agents has become increasingly crucial for mitigating radiation-associated toxic outcomes, particularly infertility. The present investigation aimed to comprehensively evaluate the capacity of selenium-L-methionine to mitigate radiation-induced histopathological and molecular alterations within testicular tissue, thereby assessing its potential as a radioprotective agent. Rats were randomized into four groups: Group 1 (control), Group 2 (rad group), which received a single 10 Gy irradiation on day 2; Group 3 (sel group), which received intraperitoneal selenium-L-methionine (4 mg/kg) for six consecutive days; and Group 4 (rad+sel group), which received the same selenium-L-methionine regimen followed by 10 Gy irradiation 30 minutes after the second day's administration. On the seventh day, all animals were euthanized, and testicular tissue and blood samples were collected for biochemical and histopathological analyses. In the testicular tissues of the radiation-exposed groups, deformed and abnormal seminiferous tubule structures, a reduction in germ cell numbers, and sloughing of tubular epithelial cells were observed. Seminiferous tubule diameters, Johnsen's testicular biopsy scores, epididymal sperm motility, and the expression levels of Connexin 43, HSP70, PCNA, StAR, CAT, and SOD were decreased in the irradiated group, whereas TGFB1, IL-6, and MMP9 levels were increased. Selenium-L-methionine treatment largely reversed these radiation-induced changes. The addition of selenium-L-methionine to radiotherapy yielded promising radioprotective outcomes, and this therapeutic effect positions selenium-L-methionine as a potential novel radioprotective agent. Furthermore, the immunohistochemical markers used in the study-including MMP9, Connexin 43, HSP70, PCNA, and StAR served as sensitive indicators for detecting radiation-induced damage in testicular tissue. Nevertheless, larger-scale and long-term studies are required to validate these findings and to further substantiate the potential use of selenium-L-methionine as a radioprotective agent in clinical practice.

The devastating earthquakes in Kahramanmaraş, Türkiye, in February 2024, caused extensive trauma and loss of lives, causing unique challenges in the management of earthquake-related crush syndrome. The current study investigates the prognostic value of pre-earthquake kidney function for mortality prediction in patients diagnosed with crush syndrome. A multi-center retrospective analysis was performed using data from 469 patients treated at 46 nephrology clinics. Pre-earthquake Kidney function, defined by serum creatinine and estimated glomerular filtration rate (eGFR) levels, was obtained from pre-earthquake health records. Clinical findings, laboratory parameters, complications, and survival probabilities were analyzed. Multivariate Cox regression was used to identify independent predictors of in-hospital mortality. The mean age of participants was 42.56 ± 16.92 years (Non-survivors: 50.46 ± 20.03 years, Survivors: 42.34 ± 16.80 years (p = 0.172)). The in-hospital mortality rate was 2.8%. Non-survivors exhibited significantly higher pre-earthquake creatinine levels than survivors (1.04 ± 0.61 mg/dL vs. 0.77 ± 0.33 mg/dL, p = 0.03), with lower eGFR (85.2 ± 34.7 mL/min/1.73 m² vs. 115.8 ± 39.4 mL/min/1.73 m², p = 0.008). Compared with survivors, non-survivors had higher incidences of AKI (92.3% vs. 61.6%, p = 0.037) and more severe metabolic disturbances, including hyperkalemia (5.41 ± 1.72 mmol/L vs. 5.13 ± 0.98 mmol/L, p = 0.008). Regression analysis revealed that pre-earthquake creatinine (HR: 9.121, 95% CI: 2.686–30.970, p < 0.001) and potassium levels at admission (HR: 3.338, 95% CI: 1.540–7.232, p = 0.002) were independent predictors of mortality. Pre-earthquake kidney function significantly predicts mortality in crush syndrome patients, highlighting the importance of baseline kidney assessment in disaster preparedness.

Hypertriglyceridemia is a metabolic condition with multifactorial etiology that may cause life-threatening complications, such as pancreatitis. In pregnant women, hypertriglyceridemia may be secondary to physiological changes during pregnancy or may be exacerbated by medications. The combination of tacrolimus and estradiol is sometimes used in in vitro fertilization (IVF) for women with a history of recurrent implantation failure. This case report discusses a case of acute pancreatitis caused by hypertriglyceridemia secondary to the use of tacrolimus and estradiol.

Otozomal dominant polikistik böbrek hastalığı (ODPBH) en sık görülen kalıtsal böbrek hastalığıdır ve olguların %85’inde PKD1, %10-15’inde ise PKD2 gen mutasyonu görülmektedir. ODPBH da renal 3',5'-siklik adenozin monofosfat ()seviyeleri artarak kist oluşumunda önemli rol oynar. Vazopressin üretiminin, salgılanmasının veya etkisinin sürekli baskılanması kist oluşumunu engelleyerek böbrek fonksiyonunun korunmasını sağladığı gösterilmiştir. Tolvaptan kısa etkili V2R inhibitörü olarak etki eder ve vazopressinin etkisini tamamen bloke ederek kist gelişimini azaltır. Bu vakada ODPBH’ta hastalık progresyonu yavaşlatmak amacıyla tolvaptan tedavisi kullanırken eşzamanlı KVH ve dislipidemi nedeniyle statin tedavisi başlanmış ancak takiplerde hepatotoksisite gelişmesine bağlı tolvaptan tedavisinin aksatılmadan devam edilmesi için statin yerine ezetimib monoterapisi tercih edilen hasta sunulmuştur.

Aqueous humor inflow falls 50% during sleeping hours without proportional fall in IOP, partly reflecting reduced outflow facility. The mechanisms underlying outflow facility cycling are unknown. One outflow facility regulator is matrix metalloproteinase (MMP) release from trabecular meshwork (TM) cells. Because anterior segment temperature must oscillate due to core temperature cycling and eyelid closure during sleep, we tested whether physiologically relevant temperature oscillations drive cycles in the activity of secreted MMP. Temperature of transformed normal human TM cells (hTM5 line) was fixed or alternated 12 hours/12 hours between 33°C and 37°C. Activity of secreted MMP-2 and MMP-9 was measured by zymography, and gene expression by RT-PCR and quantitative PCR. Raising temperature to 37°C increased, and lowering to 33°C reduced, activity of secreted MMP. Switching between 37°C and 33°C altered MMP-9 by 40% ± 3% and MMP-2 by 22% ± 2%. Peripheral circadian clocks did not mediate temperature-driven cycling of MMP secretion because MMP-release oscillations did not persist at constant temperature after 3 to 6 days of alternating temperatures, and temperature cycles did not entrain clock-gene expression in these cells. Furthermore, inhibiting heat shock transcription factor 1, which links temperature and peripheral clock-gene oscillations, inhibited MMP-9 but not MMP-2 temperature-driven MMP cycling. Inhibition of heat-sensitive TRPV1 channels altered total MMP secretion but not temperature-induced modulations. Inhibiting cold-sensitive TRPM-8 channels had no effect. Physiologically relevant temperature oscillations drive fluctuations of secreted MMP-2 and MMP-9 activity in hTM5 cells independent of peripheral clock genes and temperature-sensitive TRP channels.