Objective: The aim of this study is to evaluate the outcome of ablation therapy in our clinic for the treatment of patients with small renal mass Materials and Methods: We retrospectively evaluated the technic and follow-up data of 30 patients with 36 tumors who underwent Radiofrequency Ablation (RFA) and Microwave Ablation (MWA) in our clinic. Demographic data, ablation type, tumor characteristics, peroperative and postoperative complications and treatment success of the patients were evaluated. Results: A total of 36 tumors who underwent ablation treatments, 23 were treated with RFA, 13 with MWA. The mean tumor size was 28.9 ± 6.92 mm in RFA and 29.3 ± 7.70 mm in MWA. 12 (52.1%) of the RFA procedures were applied to the right kidney while 11 (47.8%) were applied to the left kidney. 6 (46.1%) of the MWA procedures were performed on the right kidney and 7 (53.8%) on the left kidney. Of the 36 tumors, 4 (11.1%) were located central and 32 (88.8%) were peripheral. Complications occurred in 2 patients. In one of these patients, acute renal failure and urea creatinine were found to be elevated. In the other patient, local pain was found in the ablation side and minor bleeding was detected at the ablation site in USG. The mean follow-up period was 49.6 ± 24.7 months in patients with RFA and mean follow-up was 16 ± 8,05 months in MWA treatments. The overall success in MWA administration was calculated as 76.9%, while the overall success in RFA was 80%. Conclusion: Long-term oncologic efficacy of RFA appears to be successful in the treatment of T1a renal carcinomas. Further studies can be conducted to elucidate the influence of MWA on long-term oncological outcomes.

COVID-19 pandemic continues to spread across the world in late September 2020. To date, total cases of COVID-19 exceed 33 million including 996.342 deaths according to the WHO data. Although hydroxychloroquine, oseltamivir, remdesivir, favipiravir have been reported as an anti-SARS-CoV-2 effect, it is still unclear the fully effective protective drug and treatment. Herein, we report a woman under Tenofovir diphosphate who live and close contact with his COVID-19 positive husband. Although she had close contact with his husband without measure in the home she did not show any symptoms and signs of COVID-19 and her PCR test along with antibody test negative. Given the high reproduction number of SARS-CoV-2 and long-term close contact of the case, it can be speculated that Tenofovir could interfere with the transmission of COVID-19.

Objectives Diagnostic challenges during the COVID-19 pandemic forced the radiology regulating body to adopt the use of CT Chest as a triage and diagnostic tool, which was subsequently abandoned. The Royal Wolverhampton hospital followed both protocols. Here, we investigate the evidence behind this decision within the context of surgical admissions during the COVID-19 peak in our hospital. Methods Retrospective data collection and analysis of all surgical admissions between the 1st of March to the 31st of May. Data was collected from the radiology and electronic portal looking into patients undergoing CT chest to diagnose the presence of C-19 as well as swab results. Results 78 patients fulfilled our inclusion criteria. The scan either confirmed the presence or absence (4, 63 patients) of C-19 but was sometimes inconclusive (11 patients). Comparing these to the results of the swabs; CT showed sensitivity 42.86 %, Specificity 97.92%, and accuracy 90.91 %. In the inconclusive CT report group, chances of having a positive swab result were 45%: None of the scan results changed any of the surgical planning. Lymphocyte count in the context of surgical presentation did not have any statistical significance to predict the presence of C-19 (P=0.7). Cost implications on our cohort of patients for adding the chest CT is estimated to be around £31,000. Conclusion CT Thorax during the pandemic was a good negative predictor but had limited diagnostic value and did not change patient management. Newer, faster techniques of PCR swabs and antibody testing would be a better and cheaper alternative. Advances in knowledge This paper provides evidence to support the decision from the regulatory bodies not to use CT scan as a screening tool for COVID 19 diagnosis.

As Dr. Thomson eloquently notes in his valuable letter [1], underlying respiratory diseases appear to be less of a risk factor for poor outcome in COVID-19 patients than either underlying cardiovascular disease or diabetes. This intriguing finding emerged from several studies that examined underlying medical conditions in COVID-19 patients.In a single-center retrospective analysis of critically ill adults admitted to the intensive care unit of a hospital from China between late December 2019 and January 26, 2020, 22% of the non-survivors had cerebrovascular disease, 22% had diabetes, and 6% had chronic respiratory disease [2]. The analysis of data from patients with laboratory-confirmed COVID-19 from hospitals in China through January 29, 2020 found that 16.2% of those with serious disease had diabetes, 23.7% had hypertension, and 3.5% had chronic obstructive pulmonary disease [3]. A study of electronical medical records of COVID-19 patients admitted between January 16 and February 3, 2020 to a hospital from Wuhan found that hypertension and diabetes mellitus, the most common comorbidities, were present in 37.9%, 13.8%, of the patients with severe disease, respectively, but only in 3.4% of the patients with chronic obstructive pulmonary disease [4]. Finally, an analysis of all COVID-19 cases reported through February 11, 2020, extracted from the Infectious Disease Information System in China, found that case fatality rates in individuals with cardiovascular disease, chronic respiratory disease, and diabetes were 10.5%, 6.3%, and 7.3% respectively, as compared to 0.9% among patients with no comorbidities [5]. In a case series of COVID-19 patients hospitalized in Wuhan, China, ICU patients were more likely to have underlying diabetes than patients that did not receive ICU care (22.2% vs 5.9%) [6].The studies mentioned above did not stratify patients by therapies they were receiving. However, one commonality between cardiovascular disease and diabetes is that they are often treated with angiotensin-converting enzyme (ACE) inhibitors and angiotensin II type-I receptor blockers (ARBs), widely used to inhibit the formation and action of angiotensin II.ACE shares 42% amino acid identity with ACE2 [7], a membrane-bound aminopeptidase [8] extensively expressed on type II human alveolar cells [9]. The genes encoding these two proteins are thought to have emerged by duplication [10]. ACE2 is distributed on many tissues and shows highest expression levels in the heart, kidney, lung, small intestine, and testis [11]. On the apical surface of polarized respiratory epithelial cells, ACE2 is a crucial and primary receptor for the cellular entry of SARS-CoV, the virus that caused the 2002-2003 SARS outbreak [12-16]. SARS-CoV binding to ACE2 mediates entry into human or animal cells [17]. ACE2 is also the receptor for SARS-CoV-2, the etiologic agent of COVID-19 [18]. Structural analyses indicate that SARS-CoV-2 binds the ACE2 receptor with a 10-20-fold higher affinity than SARS-CoV [19, 20].The entry of SARS-CoV and SARS-CoV-2 into their target cells is mediated by the viral spike (S) glycoprotein, which is located on the outer envelope of the virion [21]. The S glycoprotein has two functional subunits, S1, which binds the cellular receptor, and S2, which contains domains required for the fusion between viral and cellular membranes [22, 23]. Viral binding and membrane fusion represent the initial and critical steps during the infection cycle of the coronavirus [24] and the first step in establishing the infection [25, 26]. Binding is followed by internalization of ACE2 and down‐regulation of its activity on the cell surface [27-29].SARS-CoV binds ACE2 through a region of the viral S1 subunit called the minimal receptor-binding domain (RBD) [17]. RBD is the most important determinant of the SARS-CoV host range, and studies about the “species jump” during the 2002-2003 SARS outbreak revealed that changes of only one or two amino acids in this region were sufficient to make the virus “jump” to a new host [26, 30, 31].ACE and ACE2 are two members of the renin angiotensin system that negatively regulate each other [32, 33] and are distinct in their substrate specificity and function [34]. ACE converts angiotensin I to angiotensin II and mediates aldosterone release, vasoconstriction, sodium retention, cell proliferation, and organ hypertrophy [35]. ACE2 cleaves a single residue from angiotensin I to form angiotensin-(1-9), and a single residue from angiotensin II to form angiotensin-(1-7). In humans, ACE2 has a 400-fold higher catalytic efficiency when it uses angiotensin II as a substrate as compared to when it uses angiotensin I [36]. ACE2 and angiotensin-(1-7), through the Mas receptors, oppose ACE and mediate vasodilation and anti-proliferative, anti-hypertrophic, cardioprotective, and reno-protective effects [8, 35, 37]. ACE2 has physiological and pathological importance [25] and its dysregulation was implicated in heart disease, hypertension, and diabetes [36, 38-40]. ACE2 is not inhibited by ACE inhibitors [32] and several studies indicate that the ACE2/Angiotensin-(1-7)/Mas axis has anti-inflammatory effects [41, 42].It was recently hypothesized that treatment with ACE inhibitors and/or ARBs may lead to ACE2 overexpression and this could increase the risk of severe COVID-19 [43], possibly by increasing the internalization of SARS-CoV-2. Several lines of evidence indicate that pharmacological manipulation of the renin-angiotensin-aldosterone pathway could affect ACE2 receptor levels. In animal studies, the selective blockade of angiotensin II synthesis or activity increased cardiac Ace2 gene expression and activity [44, 45], and treatment with ARBs increased the levels of cardiovascular ACE2 receptors [46-49]. While this link is thought-provoking as a possibility, there isn’t currently sufficient evidence to contemplate changing patients’ existing therapeutic regimens in order to minimize their risk of COVID-19 complications. The first clinical evidence exploring this link indicated that the use of ACEI and ARBs appear to improve the clinical outcome of COVID-19 patients with hypertension [50]. We will only learn about any possible associations, along with their magnitude and direction, from carefully conducted and adequately powered clinical trials.It is also important to consider that an increase in ACE2 levels does not necessarily entail a negative impact for the course of COVID-19. ACE2, by forming angiotensin-(1-7) from angiotensin II, could diminish the deleterious effects of angiotensin II and, consequently, it is also possible that ACE inhibitors or ARBs could, in fact, lower the risk of complications [51]. However, increased ACE2 and the formation of angiotensin-(1-7), by inhibiting COX-2, could exert anti-inflammatory effects [52, 53], underscoring the multitude of possible effects and the need to conduct studies to interrogate these connections. Finally, it is not known whether an increase in the expression of ACE2 would also lead to an increased shedding and increased levels of soluble ACE2, which could act as a decoy receptor and lower viral entry into cells [54]. In support of this, recombinant human ACE2 ameliorated the lung injury induced by the avian influenza H5N1 virus in mice [55]. It is also important to consider that from the relatively limited amount of human data, plasma ACE2 activity does not appear to be statistically different between individuals taking ACE inhibitors or ARBs and those not taking these medications, but these results do not reflect the levels of cellular receptors [56]. Structural analyses indicate that the binding of the SARS-CoV spike protein to ACE2 does not occlude the catalytically active site of the receptor [26, 57], and it was hypothesized that angiotensin II binding to ACE2 could induce a conformational change in the receptor, which will no longer be favorable for SARS-CoV-2 binding [54]. The mining of existing datasets, preclinical studies, and clinical trials will help shed light on these complex and sometimes conflicting scenarios.A decrease in the number of ACE2 receptors appears to be involved in acute lung injury and cardiovascular pathology [58, 59], and may be detrimental during coronavirus infection. A mouse Ace2 knockout developed severe cardiac contractility defects and increased angiotensin II levels, and the additional deletion of Ace rescued this phenotype [60]. In acute lung injury models, the loss of Ace2precipitated severe acute lung failure, and this was attenuated by the exogenous recombinant human ACE2 in both Ace2 knock-out and in wild-type mice [59]. Attenuation of the Ace2 catalytic function perturbed the pulmonary renin-angiotensin-aldosterone system and increased inflammation and vascular permeability [61], and Ace2 overexpression decreased lung inflammation in an animal model of acute lung injury [62]. In vitro and in experimental animals, SARS-CoV and the SARS-CoV spike protein downregulated ACE2 expression [12, 28]. In mice with lung injury, injection of the SARS-CoV spike protein worsened the acute lung failure and caused lung edema, increased vascular permeability, and decreased lung function, and this pathology was attenuated by blocking the renin-angiotensin-aldosterone pathway [12]. Thus, animals infected with SARS-CoV or treated with the spike protein resemble Ace2 knockout animals [12]. It is relevant that a pilot study of patients with acute respiratory distress syndrome reported the accumulation of angiotensin I and the decrease of angiotensin-(1-9), indicating decreased ACE2 activity, among non-survivors [63]. Thus, SARS-CoV and SARS-CoV-2 might contribute to severe respiratory symptomatology partly because the viruses, by binding the ACE2 receptors, also deregulate protective pathways in the lungs.Thus, either increased or decreased numbers of pulmonary ACE2 receptors may be detrimental during SARS-CoV or SARS-CoV-2 infection, most likely for distinct reasons. An increased number of ACE2 receptors may lead to a higher viral load and more severe clinical disease. Diabetes increases ACE2 expression, as shown in several experimental models, and the resulting increased viral load might explain the more severe course of COVID-19 in diabetic patients [64, 65]. Interestingly, in a rodent model of diabetes, ibuprofen inhibited the ACE/angiotensin II/angiotensin type 1 receptor axis and enhanced the ACE2/angiotensin-(1-7)/Mas receptor axis [66]. Too few functional ACE2 receptors, which decrease even more as a result of high viral loads and enhanced receptor internalization [67], might exacerbate acute lung injury, increase angiotensin II levels, and alter the balance between pro- and anti-inflammatory responses. It is relevant that in a study on twelve COVID-19 patients from China, plasma angiotensin II levels were markedly elevated as compared to healthy control individuals, and linearly associated with the viral load and with the lung injury [68]. The animal studies that documented an age-dependent decrease in ACE2 expression in the lung and the aortic might also explain, at least in part, the age-dependent increase in the risk of serious COVID-19 complications [69, 70].SARS-CoV can also bind cells through alternative receptors that include the C-type lectins DC-SIGN (dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin) and/or L-SIGN (liver/lymph node-SIGN) [14, 71-73]. It will be critical to understand the potential involvement of the same, or alternative receptors in the pathogenesis of COVID-19.It has been less clear why SARS-CoV and SARS-CoV-2 lead to severe lung disease [57], in contrast to other, previously known coronaviruses, which usually result in mild upper respiratory infections and cause pneumonia only rarely, mostly in newborn, the elderly, and immunocompromised individuals [74-77]. One of the possibilities advanced for SARS is that the burden of viral replication and the immune status of the host may both shape the severity of the infection [57, 78, 79]. The same might be true for COVID-19, and further exploring the link between viral burden, chronic medical conditions, long-term medication usage, and the severity of the infection will be critical.An important lesson from SARS and MERS is the association between the incubation period and disease severity. For any infectious disease, the incubation period varies among individuals, even for the same outbreak, and depends on the initial infective dose, the speed of pathogen replication within a host, and host defense mechanisms [80]. During the 2002-2003 SARS outbreak, a study in Hong Kong revealed that patients with shorter incubation times developed more severe disease [81]. The same was found in MERS patients from South Korea, where longer incubation times were associated with a lower risk of death [82]. Interestingly, during the SARS outbreak in Hong Kong, healthcare workers, who have a higher infecting dose, had 34% shorter median incubation times than non-healthcare workers [83]. It will be interesting to examine whether the same is true for SARS-CoV-2, and whether the incubation period is different in COVID-19 patients when they are stratified by age, coexisting morbidities, and therapies they receive for chronic diseases. While the association between the incubation period and mortality might simply indicate that the disease was confirmed earlier in patients with longer incubations, and reflect earlier treatment opportunities [82], it is also plausible that high viral loads might mediate the link between the two.Two factors decisive for the successful control of outbreaks are the ability to isolate asymptomatic individuals and the ability to trace and quarantine their contacts [84, 85]. Several studies reported asymptomatic shedding of SARS-CoV-2, indicating that asymptomatic carriers, or individuals with very mild symptoms, may sustain transmission [86-89]. For example, nearly 18% of the passengers who tested positive for SARS-CoV-2 on the Diamond Princess cruise ship were asymptomatic [88]. Another valuable finding that emerged from the COVID-19 outbreak analysis in Singapore, and has a strong impact on infection control, is that after becoming asymptomatic, some patients continued to shed the virus for up to several days. In one instance, a patient continued to have detectable respiratory shedding, as shown by PCR, for eight consecutive days after becoming asymptomatic [90]. Another study revealed that several children with COVID-19 persistently tested positive for viral RNA on fecal swabs after their nasopharyngeal cultures became negative. Even though replication-competent virus was not detected in the fecal swabs, this finding leaves open the possibility of SARS-CoV-2 fecal-oral transmission [91]. These findings illustrate the challenges in understanding SARS-CoV-2 transmission and in identifying infected individuals, tracing their contacts, and implementing preparedness plans. One of the absolute requirements, to clarify these questions and overcome these obstacles, is ensuring the prompt and large-scale testing of symptomatic individuals and of their asymptomatic contacts. This, together with the social distancing measures, are currently our only available assets in facing a pandemic that, even though it was preceded by multiple warnings in recent years, is unlike any other infectious disease that we experienced in modern history.

OBJECTIVE: To collect and review data from consecutive patients admitted to Queen’s Hospital, Burton on Trent for treatment of Covid-19 infection, with the aim of developing a predictive algorithm that can help identify those patients likely to survive. DESIGN: Consecutive patient data was collected from all admissions to hospital for treatment of Covid-19. Data was manually extracted from the electronic patient record for statistical analysis. RESULTS: Data, including outcome data (discharged alive / died) was extracted for 487 consecutive patients, admitted for treatment. Overall, patients who died were older, had very significantly lower Oxygen saturation (SpO2) on admission, and higher CRP as evidenced by a Bonferroni-corrected P<0.0056). Evaluated individually, platelets and lymphocyte count were not statistically significant but when used in a logistic regression to develop a predictive score, platelet count did add predictive value. The prediction algorithm we developed was: P(survival) = ___________________1______________________ 1+e-1(-16.7104-3.3810LN(age)+6.5592LN(SpO2)-0.4584LN(CRP)+0.7183LN(Plt)) CONCLUSION: Age, SpO2 on Admmission, CRP and platelets were an effective marker combination that helped identify patients who would be likely to survive. The AUC under the ROC Plot was 0.737 (95% Conf. Interval 0.689-0.784; P< 0.001). Further research adding extra markers, is underway.

Introduction: The approach to thyroid hormone replacement varies across centres but the extent and determinants of variation is unclear. We evaluated geographical variation in levothyroxine (LT4) and liothyronine (LT3) prescribing across General Practices in England and analysed the relationship of prescribing patterns to clinical and socioeconomic factors. Methods: Data was downloaded from the NHS monthly General Practice Prescribing Data in England for the period 2011-2020. Results Overall, 0.5% of levothyroxine treated patients continue to receive liothyronine. All Clinical Commission Groups (CCGs) in England continue to have at least one liothyronine prescribing practice and 48.5% of English general practices prescribed liothyronine in 2019-20. Factors strongly influencing more levothyroxine prescribing (model accounted for 62% of variance) were the CCG to which the practice belonged and the proportion of people with diabetes registered on the practice list plus antidepressant prescribing, with socioeconomic disadvantage associated with less levothyroxine prescribing. For liothyronine prescribing (model accounted for 17% of variance), factors that were associated with increased levels of liothyronine prescribing were antidepressant prescribing and % of type 2 diabetes mellitus individuals achieving HbA1c control of 58mmol/mol or less. Factors that were associated with reduced levels of liothyronine prescribing included smoking and higher obesity rates. Conclusion: In spite of strenuous attempts to limit prescribing of liothyronine in general practice a significant number of patients continue to receive this therapy, although there is significant geographical variation in the prescribing of this as for levothyroxine, with specific general practice and CCG related factors influencing prescribing of both levothyroxine and liothyronine.

Background: Mast cells play a critical role in tumor-associated immune pathways. We aimed to determine whether the urinary mast cell mediators predict the immune response in patients with non-muscle invasive bladder cancer (NMIBC) treated with Bacillus Calmette-Guérin (BCG) immunotherapy. Methods: Nineteen patients who have received immunotherapy due to NMIBC and 19 healthy participants were enrolled. Urine samples were collected to assay N-methylhistamine, histamine, and tryptase levels immediately before the first BCG instillation, immediately after the third and sixth instillations, and four weeks after the sixth instillation in patients with NMIBC and at a single visit in healthy participants. Cystoscopic examinations were performed on the patient with NMIBC at three-month intervals for two years. The changes in urinary markers due to BCC response, BCG instillation, and the presence of NMIBC were assessed. Results: The average age was 56.1 ± 10.5 years in patients with NMIBC. Fourteen patients had high-grade Ta tumors, and 5 had high-grade T1 tumors. While 12 patients responded, 6 presented with recurrence and 1 with progression. There was no correlation between the levels of mast cell mediators and BCG response. The N-methylhistamine and histamine levels were increased significantly with the onset of immunotherapy, and N-methylhistamine levels were significantly decreased when immunotherapy was terminated. Pre-BCG estimated marginal means of N-methylhistamine were significantly higher in patients with NMIBC than healthy participants. Conclusions: Our study is the first study to identify the changes in mast cell mediators with the onset of immunotherapy and with the presence of bladder cancer. However, these mediators were not found to predict the patients’ response to immunotherapy.

Aim: We aimed to investigate the predictor role of the systemic immune-inflammation index (SII) on Bacille Calmette Guerin (BCG) response in patients with high-risk non-muscle invasive bladder cancer (NMIBC). Methods: A total of 96 patients with high-risk NMIBC, who received intravesical BCG, were enrolled in the study. BCG responsive group (group 1) and BCG failure group (group 2) were compared in terms of demographic and pathological data, peripheral lymphocyte, neutrophil, and platelet counts, neutrophile lymphocyte ratio (NLR), platelet lymphocyte ratio (PLR), SII, recurrence free survival (RFS) and progression free survival (PFS). The prognostic ability of the SII for progression was analyzed with multivariate backward stepwise regression models. Results: The mean follow-up time 34.635±14.7 months. Group 2 had significantly higher SII, peripheral lymphocyte, neutrophil, and platelet counts than group 1. A ROC curve was plotted for the SII to predict the BCG failure and the cut-off point was calculated as 672.75. Effect of the SII to the model was statistically significant (p=0.003) and a higher SII increased the progression one-fold. A tumor greater than 30 mm in size and a high SII together increased the progression 3.6 folds. Conclusions: The SII might be a successful, non-invasive and low-cost parameter for prediction of BCG failure in patients with high-risk NMIBC. The cut-off value for SII is 672.75 and above this level BCG failure and progression to MIBC might be anticipated. However, these results should be validated in prospective randomized controlled studies with large patient groups.

Research of Occult Hepatitis B Infection in HIV-infected Patients, Schindler Study ABSTRACT Objective: Occult hepatitis B infection seems to be more prevalent among subjects at high risk for HBV infection and with concomitant liver disease. The aim of this study was to assess the prevalence of OHBI in group of HIV-1+/HBsAg- Turkish patients. Methods: Ten centers in Turkey have been included in the study. Gender, age, occupation, place of residence, treatment status, clinic, immunodeficiency panel, eliza tests, hemogram, biochemistry and coagulation laboratory results of the patients were evaluated retrospectively. Results: The number of HIV-infected patients followed in these centers is 3172. The mean age of the patients was 37.2 ± 13.1, and they were 235 males (84.5%) and 43 (15.5%) females. 278 (99.6%) of the patients are patients who received antiretroviral treatment. included in the s Of the 279 patients included in the study, it was determined that HBsAg was negative in all of them, 169 were positive for Anti HBs and 125 were positive for Anti HBc IgG. HIV RNA (203/278) was detected in 203 of the patients. 4 (1.4%) of the patients were diagnosed with OHB. In our study, no significant difference was found in hemoglobin and bilirubin levels and complete blood count in patients with HIV-OHB co-infection. However, albumin values were found to be <3.5 in three OHD patients (p = 0.043). Conclusion: Reasearch the presence of OHB infection in HIV-infected patients is important in determining treatment options and predicting the survival of patient. Hypoalbuminemia could be showing hepatic failure and we can suggest the importance of treatment that diseases.

Introduction. Locking the humanity in their homes, COVID-19 forced people to use the technology at hand to keep informed about the outbreak and to keep close to their loved ones. During this time, even if physical health is theoretically unaffected, keeping calm and sane can be challenging. The aim of this research was to evaluate whether exposure to COVID-19 information available in the digital space has a different impact on the mental condition of Romanian medical staff, compared to general population, particularly searching for depression and anxiety symptoms. Materials and methods. An online survey was conducted from April 6 to 16, 2020 within the Romanian users of Social Media platforms. The questionnaire assessed depression with the WHO-Five Well-Being Index, anxiety with the Generalized Anxiety Disorder Scale and Social Media exposure by asking how often the respondents saw COVID-19 related information on the most popular Social Media channels in Romania. Information about: gender, age, educational level, occupation, area of living and risk category was also collected. The risk categories were defined as no risk, medium risk, and medical staff. Results. Almost 90% of the 402 participants received daily through at least one Social Media channel information related to the COVID-19 outbreak. The Social Media Exposure significantly associated with the risk group only for Facebook and LinkedIn. However, exposure to information regarding COVID-19 was neither associated with anxiety nor depression. No significant association was identified neither between age class and self-assessed anxiety nor self-assessed depression. The self-assessment of depression was significantly more frequent as compared to self-assessment of anxiety. Conclusion. The results of this research are opposite to most of the already published literature. Depression and anxiety could not be correlated with the context of lockdown and excessive COVID-19-related information.

Background: COVID-19 pandemic has caused fear all around the world. With people avoiding hospitals, there has been a significant decrease in outpatient clinics. In this study, we aimed to compare and explore the first-peak of the pandemic period by studying its effects on patient applications, new diagnoses, and treatment approaches in a non-infected hospital. Methods: We collected data from the first peak of the pandemic period in Turkey, from the pandemic’s declaration (March 11, 2020) to social normalization (June 1, 2020), and compared it with data from a pre-pandemic period with a similar length of time. We analyzed the data of breast cancer patients from application to surgery. Results: The data of 34,577 patients were analyzed for this study. The number of patients who applied to outpatient clinics decreased significantly during the pandemic period. After excluding control patients and benign disorders, a figure was reached for the number of patients who had a new diagnosis of breast cancer (146 vs 250), were referred to neoadjuvant treatment (18 vs 34), and were treated with surgery (121 vs 229). All numbers decreased during the pandemic period, except for surgeries after neoadjuvant treatment (29 vs 27). Surgical treatment approaches also changed. However, the rate of newly diagnosed breast cancer patients treated with surgery was similar in both periods. None of these patients were diagnosed with COVID-19 or died during the pandemic. Conclusion: This study shows that non-infected hospitals can be useful in avoiding delays in the surgical treatment of cancer patients.

Background/aim: The aim of this study was to evaluate the effects of general anesthesia and ultrasonography-guided interscalene block on pain and oxidative stress evaluated by thiol–disulphide balance and C-reactive protein levels in patients undergoing shoulder arthroscopy. Materials and methods: A total of 42 patients aged 18–75 years who were scheduled to undergo shoulder arthroscopy were randomized into interscalene block group (Group-IB, n = 20) and general anesthesia group (Group-GA, n = 22). All patients received patient-controlled analgesia during the postoperative period. Additional analgesics were administered to patients with a visual analog scale score of > 4. Native -thiol, total -thiol, disulphide and C-reactive protein levels were measured. Patients’ visual analog scale scores, morphine and additional analgesic consumption were recorded. A shift in thiol–disulphide balance toward decreased thiol and increased disulphide levels was regarded as an indicator of oxidative stress. Results: Pain level, morphine and additional analgesic consumption were higher in Group-GA. Native-thiol and total-thiol levels were higher in Group-IB postoperatively and also disulphide levels were lower at postoperative 18 hours. C-reactive protein levels were similar in both the groups. Conclusion: Interscalene block induced less oxidative stress during the postoperative period, as evaluated by thiol–disulphide balance.

Aim: The cognate receptor expression of AGE (RAGE; receptor for AGE) on malignant tissues in diabetic patients has been suggested as a co-factor in determining the clinical course and prognosis. We aimed to search this relationship between RAGE expression and clinicopathological features of prostate neoplasia. Methods: A total of 197 patients; 64 (diabetic n=24; non-diabetic n=40) with benign prostate hyperplasia, and 133 (diabetic n=71; non-diabetic n=62) with localized (LPCa)/metastatic prostate cancer (MetPCa) were included the study. The expression of RAGE was studied by immunohistochemically on prostate specimens. The RAGE score was assessed in the specimens according to the extent of immunoreactivity and staining intensity. Results: The RAGE scores of BPH patients (diabetic and non-diabetic) were found as negative. Patients with both LPCa and MetPCa showed significantly higher scores, respectively (LPCa and MetPCa vs. BPH; p<0.01). RAGE scores of diabetic patients with LPCa and MetPCa were found to be 4.71±3.14 and 4.97±3.69, respectively. RAGE scores of the non-diabetic patients who had LPCa and MetPCa were 1.52±1.87 and 1.69±1.58, respectively. When compared both groups with LPCa, RAGE scores of the diabetic patients were significantly higher than that of the non-diabetics (p=0.01). Similar results were revealed as for the patients with MetPCa (4.97±3.69 vs. 1.69±1.58 (diabetic vs. non-diabetic), respectively (p<0.01). Conclusion: We found a high rate of RAGE expression in malign prostate neoplasias to the BPH. Furthermore, as expected, higher scores were demonstrated in those with diabetes than non-diabetics. Disease progression and survival parameters were worse in the patients with high RAGE levels. RAGE may be useful in the diagnosis of prostate cancer and in determining its prognosis.

Abstract Aims: Recurrent pregnancy loss (RPL) is usually defined by two or more consecutive clinical miscarriages, which causes psychological trauma for couples. In this study, we aimed to investigate the predictive role of Fibrinogen to albumin ratio (FAR) in patients with RPL. Methods: Pregnant women in their first trimester of pregnancy were included in the study and divided in to two groups as RPL patients (n:44) and patients with no previous recurrent miscarriage (n:60) as control group. Demographical parameters and routine blood parameters (fibrinogen, D-dimer, fibrinogen to albumin ratio (FAR), neutrophil to lymphocyte ratio (NLR), platelet count, main platelet volume (MPV), and red cell distribution width (RDW) values) were compared between the RPL group and the control group. Results: The groups were determined to be statistically different in regards to gravidity and parity (p<0.05). The difference between the groups was statistically different in regards to fibrinogen (mg/dl), albumin (g/dl), FAR (%), NLR (%), RDW-coefficient of variation (CV) (%), RDW-standard deviation (SD) (fL), and platelet counts (10-3/ uL). However, MPV (fL) and D-dimer (ug/L) levels were similar in both groups. The receiver operating characteristic (ROC) curve analysis revealed that the NLR levels were 84.1% sensitive and 75% specific with a cut-off value of 4.27 and the FAR levels were 79.5% sensitive and 88.3% specific with a cut-off value of 105.69 for predicting RPL. Conclusion: Our results indicate that the FAR and NLR levels seem to be effective parameters for predicting RPL with high sensitivity and specificity.

Objective:After radical prostatectomy,prostate-specific antigen(PSA) value measuring ≥0.1ng/ml is defined as persistent PSA(pPSA) and in many studies,it was found to be associated with aggressive disease and poor prognosis.Our aim in this study is to point out the pathological and clinical factors affecting pPSA among the patients who underwent robot-assisted radical prostatectomy(RARP) in an experienced academic center and to make a nomogram,predicting pPSA value based on operative data,useful. Methods:We examined records of 1273 patients who underwent RARP retrospectively. Preoperative,operative,and postoperative data were collected.Based on the PSA values (ng/ml) measured after 4-to-8 weeks of RARP,patients were divided into 2 groups as pPSA group (Group1)(n=97) with PSA values ≥0.1ng/ml and undetectable PSA group (Group2)(n=778) with PSA values <0.1ng/ml.Later on,Group1 was further divided into Group1a (PSA:0.1-0.2ng/ml) and Group 1b (PSA≥0.2ng/ml) to evaluate biochemical recurrence(BCR). Results:Multivariate logistic regression analyses of the collected data revealed that PSA>20ng/ml,operation time,a postoperative international society of urological pathology (ISUP) grade of ≥4, pT 3-4, and pN were independently associated with pPSA.According to the results, a nomogram predicting pPSA was developed(Table 4).By looking at the nomogram pPSA was found in 98.9% of the cases with a PSA value of ≥20ng/ml, an operation time of 150 minutes, a postoperative ISUP grade of 4-5, a positive lymphovascular invasion (LVI) status, pT3-T4, and pN+; while pPSA was found in 25.5% of the cases with a PSA value of <20 ng/ml, an operation time of 100 minutes, a postoperative ISUP grade of <4-5, a negative LVI status, pT<3-4, and pN-.The estimated BCR-free survival time was 16.3 months in Group 1a and 57.0 months in Group2 (p<0.001).Adjuvant treatment ratio was 64.9% in Group1 and 7.1% in Group2 (p<0.001). Conclusion:For the patients who underwent RARP,factors associated with aggressive disease can predict the PSA persistence.To plan our treatment modalities accurately,an applicable nomogram in daily practice would be useful.

Background: Since the pathophysiology of medically unexplained symptoms (MUS) remains unclear, health care providers often struggle with these patients, especially with a different ethnic and/or cultural background. These challenges are insufficiently addressed in their training and in the organization of care. Aim: To improve health care provider-patient interaction focused on MUS patients in general and in ethnic minorities and refugees in particular through a systematic review of syndromal definitions and epidemiology and organization of care of MUS patients. Methods: Screening of PubMed, Web of Science, Cinahl and Cochrane Library on the keywords ‘Medical unexplained (physical) symptoms (MUPS)’, ‘Somatoform disorder’, ‘Functional syndrome’, ‘Diversity’, ‘Migrants’, ‘Ethnicity’, ‘Care models’, ‘Medical education’, ‘Communication skills’, ‘Health literacy’ Results: Different case definitions result in markedly different epidemiologic estimates for MUS patients. Nevertheless, they are prevalent in a wide range of health care settings. Literature offers evidence of the effectiveness of structural frameworks in approaching MUS patients. Organization of MUS care needs to transcend different levels of care: specialist tertiary and secondary care and primary care involving different qualifications of caregivers need to be aligned. Conclusion: The systematic review identified significant gaps and shortcomings in organization of care. These need to be addressed in order to improve outcomes. Keywords: Medical unexplained (physical) symptoms (MUPS), Somatoform disorder, Functional syndrome, Diversity, Migrants, Ethnicity, Care models Message for the clinic: - Medically unexplained symptoms are highly prevalent but case definitions hamper both recognition and a proper approach. - MUS are ill understood in both the general population as in migrants and refugees. - Interdisciplinary and integrated care through a biopsychosocial model is mandatory.

Aim & Objective: Silent information Regulators (SIRT1) gene stimulates the expression of antioxidants and repairs damaged cells. It affects the mitochondrial activity within the oocytes to overcome the oxidant stress. We aimed to assess an association of SIRT1 polymorphism (Tag SNPs rs10509291 and rs12778366) with fertility, and assess serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol, progesterone, manganese superoxide (MnSOD) and SIRT1. Material and Methods: In this cross-sectional study, 207 fertile and 135 infertile subjects between the ages of 18-45 year were recruited. Polymerase chain reaction (PCR) was performed; products were electrophoresed in a 2% agarose gel. Descriptive analysis of continuous variables was expressed as mean ± standard deviation. Mann-Whitney test was performed for comparison of groups, p value <0.001 was considered significant. Single Nucleotide Polymorphism (SNP) data was analyzed by applying chi-squared statistics. Results: All subjects were age matched (p = 0.896). SIRT1 levels were significantly lower in infertile females when compared with fertile subjects (p<0.001). AA (rs10509291) and CC (rs12778366) variant frequency was higher in the infertile than fertile subjects (p<0.01). Similarly, the frequency of A allele (rs10509291) and C allele (rs12778366) was higher in infertile subjects (p<0.001). Infertile females (29%) showed existence of SNP rs10509291 while 49% demonstrated genetic variation of rs12778366. MnSOD and SIRT1 levels were found to be lower in these subjects. Conclusion: Presence of SIRT1 genetic variants (rs10509291 and rs12778366) apparently disturbs the expression of SIRT1 deteriorating mitochondrial antioxidant function within the oocytes, instigating oxidative stress within. Their probable effect on modulating oocyte maturation may be the cause of infertility in females.

Psoriasis is one of the most common chronic cutaneous skin disorders, having genetic and immunological components. It is currently unknown what exactly triggers it, or how far reaching are the etiological factors, although great strides have been made in uncovering the pathophysiological cascade. Presently, there is a wide diversity of treatment methods for psoriasis, yet not all are applicable for each patient. Selection of both drug and dosage depends on both the knowledge and experience of the treating dermatologist, but also on the specific characteristics of each patient. Therefore, the treating physicians should be made aware of the management possibilities, their advantages, as well as their side effects. Current therapies are divided into topical, systemic, and biological agents. In the following manuscript, we present an updated version of these therapies, alongside their indications, posology and most common side effects, a guide that may be useful for every practitioner in this field.