Purpose: We analyzed the surgical results of patients who were treated and followed up for prostate cancer in our clinic to predict the relationship between periprostatic adipose tissue and patients with and without pathologically upstaged disease. Materials and Methods: The study included patients who had undergone robot-assisted radical prostatectomy and preoperative multiparametric prostate magnetic resonance imaging between 18 February 2019 and 1 April 2022. The patients were divided into two groups, and the surgical and transrectal ultrasound-guided biopsy pathology results were compared according to tumor grade and distribution in 124 patients who met the selection criteria. We analyzed the relationships between upgrading/upstaging and periprostatic adipose tissue thickness (PPATT) and subcutaneous adipose tissue thickness (SATT) as measured in magnetic resonance imaging. Results: The median PPATT was 4.03 mm, whereas the median SATT was 36.4 mm. Upgrading was detected in 45 patients (36.3%), and upstaging was detected in 42 patients (33.9%). A receiver operating characteristic regression analysis revealed that a PPATT >3 mm was a predictive factor for upstaging after radical prostatectomy (area under curve=0.623, 95% confidence interval [CI] 0.519–0.727, p=0.025). Multivariate logistic regression analyses revealed that prostate specific antigen density ≥0.15 ng/mL/cm 3(odds ratio [OR] 5.054, 95% CI 2.008–12.724, p=0.001), International Society of Urological Pathology grade ≥4 (OR 9.369, 95% CI 2.109–21.626, p=0.003) and higher PPATT (OR 1.358, 95% CI 1.081–1.707, p=0.009) were independent risk factors for upstaging after radical prostatectomy. Conclusions We believe that the PPATT may be a predictive indicator for upstaging after robot-assisted laparoscopic radical prostatectomy.

OBJECTIVES: Nerve growth factor (NGF) induces neuron transdifferentiation of adrenal medulla chromaffin cells (AMCCs) and consequently downregulates the secretion of epinephrine (EPI), which may be involved in the pathogenesis of bronchial asthma. Mammalian achaete scute-homologous 1 (MASH1), a key regulator of neurogenesis in the nervous system, has been proved to be elevated in AMCCs with neuron transdifferentiation in vivo. This study aims to explore the role of MASH1 in the process of neuron transdifferentiation of AMCCs and the mechanisms. METHODS: Rat AMCCs were isolated and cultured. AMCCs were transfected with siMASH1 or MASH1 overexpression plasmid, then were stimulated with NGF and/or dexamethasone, PD98059 (a MAPK kinase-1 inhibitor) for 48 hours. Morphological changes were observed using light and electron microscope. Phenylethanolamine-N-methyltransferase (PNMT, the key enzyme for epinephrine synthesis) and tyrosine hydroxylase were detected by immunofluorescence. Western blotting was used to test the protein levels of PNMT, MASH1, peripherin (neuronal markers), extracellular regulated protein kinases (ERK), phosphorylated extracellular regulated protein kinases (pERK), and JMJD3. Real-time RT-PCR was applied to analyze the mRNA levels of MASH1 and JMJD3. EPI levels in the cellular supernatant were measured using ELISA. RESULTS: Cells with both tyrosine hydroxylase and PNMT positive by immunofluorescence were proved to be AMCCs. Exposure to NGF, AMCCs exhibited neurite-like processes concomitant with increases in pERK/ERK, peripherin, and MASH1 levels (all P<0.05). Additionally, impairment of endocrine phenotype was proved by a signifcant decrease in the PNMT level and the secretion of EPI from AMCCs (all P<0.01). MASH1 interference reversed the effect of NGF, causing increases in the levels of PNMT and EPI, conversely reduced the peripherin level and cell processes (all P<0.01). MASH1 overexpression significantly increased the number of cell processes and peripherin level, while decreased the levels of PNMT and EPI (all P<0.01). Compared with the NGF group, the levels of MASH1, JMJD3 protein and mRNA in AMCCs in the NGF+PD98059 group were decreased (all P<0.05). After treatment with PD98059 and dexamethasone, the effect of NGF on promoting the transdifferentiation of AMCCs was inhibited, and the number of cell processes and EPI levels were decreased (both P<0.05). In addition, the activity of the pERK/MASH1 pathway activated by NGF was also inhibited. CONCLUSIONS MASH1 is the key factor in neuron transdifferentiation of AMCCs. NGF-induced neuron transdifferentiation is probably mediated via pERK/MASH1 signaling.
Animals ; Rats ; Adrenal Medulla ; Cell Transdifferentiation ; Chromaffin Cells ; Dexamethasone ; Epinephrine/pharmacology* ; Mammals ; Nerve Growth Factor ; Neurons ; Peripherins ; Protein Kinases ; Tyrosine 3-Monooxygenase

Vaccine-related axillary nodal enlargement is a common benign condition that many mRNA vaccine receivers experience. However, a false attribution of axillary swelling to vaccination may result in delay in cancer care and potential disease progression, particularly in breast cancer patients presenting with ipsilateral axillary lymphadenopathy. We report the case of a 41-year-old pre-menopausal female who presented with suspicious axillary nodal enlargement and a right breast lump (triple-negative invasive ductal carcinoma) after recent administration of the second dose of Moderna mRNA coronavirus disease 2019 (COVID-19) vaccine. On imaging, bilateral axillary lymph nodes were detected. The ipsilateral rightsided node was proven to be metastatic, whereas contralateral nodes were related to a recent mRNA COVID-19 vaccination. Right-sided lymph node had intense uptake (maximum standardized uptake value [SUVmax] = 5), while the contralateral reactive nodes were mildly avid (SUVmax = 2.6). On magnetic resonance imaging, the right-sided node revealed asymmetric cortical thickening and marked cortical enhancement as opposed to normalappearing left-sided nodes.

Purpose: This study aimed to evaluate the radiation-induced adverse effects on ocular structures in head and neck cancer patients and investigate the radiation dose-volume effects on the cornea, lacrimal gland, retina, optic nerve and chiasm. Materials and Methods: A total of 38 eyes of 19 patients were included in this prospective, cohort study. All patients underwent complete ophthalmological examination in addition to contrast sensitivity, visual field and visual evoked potentials (VEP) tests. Ophthalmological examinations and psychophysical tests were performed in 6th, 12th, 18th, 24th months and in the last visit. The relationship between the ophthalmologic findings, and the radiation doses below and above the cut-off values was evaluated. Results: Contrast sensitivity decrease and visual field deterioration were observed in 42% of the patients in the last visit (median 26 months) whereas a prolonged latency and decreased amplitude of P100 wave in VEP was observed in 58% and 33% of the eyes, respectively at 24th month. Totally 16 patients (84.2%) developed dry eye disease and eight of them received radiotherapy below tolerance doses and had mild to moderate dry eye findings. Radiation-induced retinopathy was observed in three of the eyes in eight patients who received radiation above tolerance dose. Conclusion Head and neck cancers treated with radiotherapy, resulted in various ophthalmic complications. All patients who are treating with radiotherapy should be evaluated by an ophthalmologist in terms of anterior and posterior segment damage, even if the radiation dose is below the tolerance limit.

Objective: In this study, it is aimed to investigate the relationship between the oxytocin level and the rejection sensitivity, childhood mental traumas, and attachment styles in patients diagnosed with borderline personality disorder (BPD). Methods: Participants between the ages of 18–30 were included in the study. The patient group consists of 31 participants and the healthy control group consists of 31 participants. Sociodemographic/Clinical Variables Questionnaire, Relationship Scales Questionnaire, Rejection Sensitivity Questionnaire and Childhood Trauma Questionnaire were administered to the participants included in the study. Serum oxytocin levels of the participants were measured using the Elisa method. Results: The oxytocin levels were found to be significantly lower in patients with BPD than in healthy control subjects, whereas the rejection sensitivity and childhood traumas were found to be significantly higher. No difference was found between the patient and control groups in terms of attachment styles, yet it was determined that there may be differences between the oxytocin levels of the BPD patients according to the attachment styles the patients have. Conclusion In conclusion, the findings of this study revealed that the rejection sensitivity in BPD patients is not associated with oxytocin levels and childhood traumas, indicating the need to assess the BPD patients in terms of other biopsychosocial factors related to the etiopathogenesis of BPD.

Objective: To explore the possible effects of naringin on acrylamide-induced nephrotoxicity in rats. Methods: Sprague-Dawley rats weighing 200-250 g were randomly divided into five groups. The control group was given intragastric (i.g.) saline (1 mL) for 10 d. The acrylamide group was given i.g. acrylamide in saline (38.27 mg/kg titrated to 1 mL) for 10 d. The treatment groups were administered with naringin in saline (50 and 100 mg/kg, respectively) for 10 d and given i.g. acrylamide (38.27 mg/kg) 1 h after naringin injection. The naringin group was given i.g. naringin (100 mg/kg) alone for 10 d. On day 11, intracardiac blood samples were obtained from the rats when they were under anesthesia, after which they were euthanized. Urea and creatinine concentrations of blood serum samples were analyzed with an autoanalyzer. Enzyme-linked immunosorbent assay was used to quantify malondialdehyde, superoxide dismutase, glutathione, glutathione peroxidase, catalase, tumor necrosis factor-β, nuclear factor-κB, interleukin (IL)-33, IL-6, IL-1β, cyclooxygenase-2, kidney injury molecule-1, mitogen-activated protein kinase-1, and caspase-3 in kidney tissues. Renal tissues were also evaluated by histopathological and immunohistochemical examinations for 8-OHdG and Bcl-2. Results: Naringin attenuated acrylamide-induced nephrotoxicity by significantly decreasing serum urea and creatinine levels. Naringin increased superoxide dismutase, glutathione, glutathione peroxidase, and catalase activities and decreased malondialdehyde levels in kidney tissues. In addition, naringin reduced the levels of inflammatory and apoptotic parameters in kidney tissues. The histopathological assay showed that acrylamide caused histopathological changes and DNA damage, which were ameliorated by naringin. Conclusions: Naringin attenuated inflammation, apoptosis, oxidative stress, and oxidative DNA damage in acrylamide-induced nephrotoxicity in rats.

Purpose: Accurate restaging of the axilla after neoadjuvant chemotherapy (NAC) is an important issue to ensure deescalating axillary surgery in patients with initial metastatic nodes. We aimed to present our results of targeted axillary biopsy (TAB) combined with sentinel lymph node biopsy (SLNB) for axillary restaging after NAC. Methods: In 64 breast cancer patients who underwent NAC, biopsy-proven positive nodes were marked with clips before NAC, and ultrasound-guided wire localization of clip-marked nodes was performed after NAC. Patients underwent TAB and SLNB for post-NAC axilla restaging. Results: Identification rates of post-NAC TAB and SLNB were 98.4% and 87.5%, respectively (P = 0.033). Histopathology revealed a nodal pathologic complete response (pCR) rate of 47% in which axillary lymph node dissection (ALND) was avoided. TAB alone and SLNB alone detected residual disease in 29 (85.3%) and 20 (58.8%) patients (P = 0.029), respectively. Whereas rates of up to 97% had been achieved with a combination of TAB and SLNB. The pCR rates after NAC were 64.3% for human epidermal growth factor receptor 2 positive and triple-negative tumors and 13.6% in luminal tumors (P = 0.0002). Conclusion Pathologic analysis following TAB combined with SLNB revealed the pCR rates to NAC in a considerable number of patients that provided de-escalation of axillary surgery. A combination of SLNB and TAB was found to be an accurate procedure in establishing residual nodal disease. This combined procedure in patients with initially positive nodes was a reliable method for post-NAC axillary restaging.

Purpose: Accurate restaging of the axilla after neoadjuvant chemotherapy (NAC) is an important issue to ensure deescalating axillary surgery in patients with initial metastatic nodes. We aimed to present our results of targeted axillary biopsy (TAB) combined with sentinel lymph node biopsy (SLNB) for axillary restaging after NAC. Methods: In 64 breast cancer patients who underwent NAC, biopsy-proven positive nodes were marked with clips before NAC, and ultrasound-guided wire localization of clip-marked nodes was performed after NAC. Patients underwent TAB and SLNB for post-NAC axilla restaging. Results: Identification rates of post-NAC TAB and SLNB were 98.4% and 87.5%, respectively (P = 0.033). Histopathology revealed a nodal pathologic complete response (pCR) rate of 47% in which axillary lymph node dissection (ALND) was avoided. TAB alone and SLNB alone detected residual disease in 29 (85.3%) and 20 (58.8%) patients (P = 0.029), respectively. Whereas rates of up to 97% had been achieved with a combination of TAB and SLNB. The pCR rates after NAC were 64.3% for human epidermal growth factor receptor 2 positive and triple-negative tumors and 13.6% in luminal tumors (P = 0.0002). Conclusion Pathologic analysis following TAB combined with SLNB revealed the pCR rates to NAC in a considerable number of patients that provided de-escalation of axillary surgery. A combination of SLNB and TAB was found to be an accurate procedure in establishing residual nodal disease. This combined procedure in patients with initially positive nodes was a reliable method for post-NAC axillary restaging.

BACKGROUND: Familial Mediterranean fever (FMF) is an autoinflammatory disease that has self-limiting inflammatory attacks during polyserositis. Hepcidin is a protein, and interleukin-6 stimulation increases hepcidin levels. Calprotectin (CLP) is a recently defined cytokine released from monocytes and neutrophils in response to tissue trauma and inflammation. There are studies in the literature showing that it can be used as a biomarker in rheumatic diseases such as ankylosing spondylitis and rheumatoid arthritis. Here, we compared the levels of hepcidin and CLP in healthy individuals and FMF patients during an attack-free period and show its relation to genetic mutations.METHODS: This is a cross-sectional study. Between July 2017 and December 2017, 60 patients diagnosed with FMF an admitted to the Cumhuriyet University Faculty of Medicine Department of Internal Medicine Rheumatology as well as 60 healthy volunteers without any rheumatic, systemic, or metabolic diseases were enrolled in this study. Blood was collected from a peripheral vein to measure serum CLP and hepcidin levels. Blood tests were examined by ELISA; the study protocol was approved by the local ethics committee.RESULTS: Median serum hepcidin level was 468.1 (210.3–807.8) pg/mL in FMF group and 890.0 (495.0–1,716.9) pg/mL in the healthy control (HC) group. There was a statistically significant difference between the two groups (P < 0.001). The median serum levels of CLP in the FMF group were measured as 1,331.4 (969.3–1,584.6 pg/mL and 73.8(45.0–147.9) pg/mL in the HC group. There was a statistically significant difference between the two groups (P < 0.001). Receiver operating characteristic analysis showed that the sensitivity was 66.7% and the specificity was 71.7% at serum hepcidin < 581.25 pg/mL (P < 0.05); the sensitivity was 96.7% and specificity was 100% at CLP > 238 pg/mL (P < 0.05). There was no significant difference between serum hepcidin and CLP levels in FMF patients with M694V homozygous and M694V heterozygous (P > 0.05). There was no significant difference in serum hepcidin levels between FMF patients with and without arthritis, proteinuria, and amyloidosis (P < 0.05). There was no significant correlation between laboratory findings, gender, age, and serum CLP and hepcidin levels (P > 0.05, r < 0.25).CONCLUSION: Serum CLP levels in FMF patients during an attack-free period are significantly higher than in the HC groups. Serum hepcidin levels in FMF patients are significantly lower than in the HC group. Low levels of hepcidin may be explained by including FMF patients during an attack-free period in the study. CLP may be an important biomarker in FMF. A better understanding of the role of these biomarkers in the diagnosis of FMF is needed to evaluate the results in a more comprehensive way.

Psychiatric diseases are the manifestations that result from the individual’s genetic structure, physiology, immunology and ways of coping with environmental stressors. The current psychiatric diagnostic systems do not include any systematic characterization in regard to neurobiological processes that reveal the clinical picture in individuals who got psychiatric diagnosis. It is obvious that further research in different areas is needed to understand the psychopathology. The problems in the functions of immune system and the correlation of neuroinflammatory processes with psychiatric disorders have been one of the main research topics of psychiatry in recent years and have contributed to our understanding of psychopathology. Recent advances in the fields of immunology and genetics as well as rapidly increasing knowledge on the effects of immunological processes on brain functions have drawn attention to the correlations between psychiatric disorders and immune system dysfunctions. There are still unfilled gaps in the biology, pathophysiology, and treatment of major depressive disorder, which is quite prevalent among the psychiatric disorders, can lead to significant disability, and frequently has a recurrent course. It appears that low-grade chronic neuroinflammation plays a key role in forming a basis for the interaction between psychological stress, impaired gut microbiota and major depressive disorder. In this review, the role of neuroinflammation in the etiopathogenesis of depression and the mechanism of action of the gut-brain axis that leads to this are discussed in the light of current studies.