[An Important Problem in AdV-36 Seropositive Obesity Patients: Leptin Resistance]. / AdV-36 Seropozitif Olan Obez Hastalarda Önemli Bir Sorun: Leptin Direnci.

Adenoviruses are naked viruses with an icosahedral nucleocapsid containing a 36 kb linear double-stranded DNA genome that encodes 30-40 proteins. The word "obesity" in Latin means "because of feeding". Obesity is an energy metabolism pathology that paves the way for physical and psychological problems with excessive fat accumulation that can impair health. Body mass index (BMI), unaffected by gender and age, is the most useful indicator of overweight and obesity at the population level. The concept of infectobesity was first introduced in 1978 after the data showed that viruses might also play a role in obesity cases. In the same year, adenovirus 36 (AdV-36) was isolated from the stool of a six-year-old girl with diabetes who was admitted to the hospital with the complaint of enteritis. One of the adipokines important for obesity is leptin. Leptin regulates food intake and energy metabolism by having a "negative feedback" effect on the hypothalamus. Leptin acts as a sensor that acutely regulates energy metabolism by creating hunger and satiety signals and it also regulates the amount of body fat and the required weight of the person by adjusting its concentration in the plasma according to the nutritional status. Changes in body weight and metabolic status are often associated with acute or chronic inflammatory processes. Human cells infected by AdV-36 showed greater differentiation and higher lipid accumulation than uninfected control cells, which increases the prevalence of obesity. There are two fractions of serum leptin, protein-bound and free form. The balance between these two fractions depends on serum leptin and soluble leptin receptor (sLR) plasma concentration, which is adversely affected by BMI. AdV-36 infection reduces norepinephrine and leptin levels. These two effects contribute to obesity by increasing appetite and food intake. In this study, it was aimed to determine the presence of immunoglobulin G against AdV-36 in the blood serum of obesity patients (BMI≥ 30) and healthy weight individuals (18.5≤ BMI≤ 25), and also aimed to determine and compare the leptin and soluble leptin receptor levels of these individuals. In this study, 10 ml of blood was collected on an empty stomach from obese individuals (n= 101; BMI≥ 30) and healthy individuals (n= 96; 18.5≤ BMI≤ 25) between the ages of 18-55. All participants consisted of who were not taking any medication and were not immunosuppressed. Blood samples separated into their serum were analyzed for AdV-36 IgG, leptin, and soluble leptin receptor levels. Mean, standard deviation, and percentage values were calculated by descriptive statistical analysis. The data with normal distribution were evaluated with the paired and independent sample t-test and data with abnormal distribution were evaluated with the paired and independent sample Mann-Whitney U test. Findings with a p-value less than 0.05 were considered statistically significant. In conclusion, leptin levels in obese individuals who were not infected with Adv-36 were found to be low, in line with the principle that "insufficient leptin synthesis has a role in the pathophysiology of obesity". When AdV-36 infection is added to the obesity picture, it may be due to the fact that it increases leptin synthesis in patients and the level of soluble leptin receptors increases in response to the increased leptin level, that AdV-36 suppresses the binding of the leptin molecule to its receptor, which leads to leptin resistance.

Strongyloides stercoralis infestation mimicking recurrence of ovarian cancer in the liver.

Ovarian cancer is the most lethal gynecological cancer and can recur in most cases. Surgery is an option for recurrent ovarian cancer. Parasitic infestation disseminated in an immunocompromised host can be fatal. The case is here presented of a female patient diagnosed with early-stage ovarian cancer. Chemotherapy was initiated for treatment. At the follow-up examination, masses in the liver suggestive of recurrence were detected on positron emission tomography computed tomography. Surgery was performed. A Strongyloides stercoralis infestation mimicking relapsing ovarian cancer in the liver was diagnosed.

[Existence of Biofilm and Biofilm-Associated Virulence Genes in Multi-Drug Resistant Invasive Acinetobacter baumannii Isolates]. / Çok Ilaca Dirençli Invaziv Acinetobacter baumannii Izolatlarinda Biyofilm ve Biyofilm Iliskili Virülans Genlerinin Varligi.

Acinetobacter baumannii is a multi-drug resistant (MDR) gram-negative pathogen leading to nosocomial infections. Hospital-acquired infections due to A.baumannii occur especially in patients hospitalized in intensive care units. Important infections related to this bacterium are pneumonia, bacteremia, endocarditis, skin and soft tissue, urinary tract infections and meningitis. Human transmission is usually through the hospital environment or through medical personnel. A.baumannii isolates increases their virulence not only being multiple resistance to antibiotics but as well as the ability to form biofilm. The biofilm formation of A.baumannii isolates were mostly related with genes encoding curli fiber (csgA), the chaperone-usher fimbria (csuE) and the outer membrane (ompA). The aim of this study was to demonstrate biofilm production and virulence genes in MDR invasive A.baumannii isolates. MDR and similarity status previously known invasive A.baumannii (n= 156) isolates were included in the study. Biofilm production was determined by quantitative microplate biofilm method. Virulence genes csgA, csuE, fimH, ompA and blaPER-1 were investigated by polymerase chain reaction (PCR). It was determined that 60.3% (94/156) of all the isolates formed biofilm. Of these 94 isolates, 17 were weak, 33 were medium and 44 were strong. The mean biomass forming capacity of the isolates was found to be 2.23 ± 0.0033. Among the isolates included in the study (n= 156) the frequency of csgA, csuE, ompA, fimH and blaPER-1 genes were 71.2%, 32.1%, 21.8%, 7.1% and 3.2% respectively. The frequency of csgA, ompA, bap, csuE, fimH virulence genes were found to be 41.5%, 24.5%, 20.2% and 5.3% among biofilm positive isolates respectively. Biofilm-forming isolates were most commonly found in pulsotype II 19.1% (18/94), pulsotype IX 17.0% (16/94) and pulsotype VI 12.8% (12/94). In this study, when the distribution of virulence genes were compAred with the isolates that have weak, medium and strong biofilm, all of the studied genes were found to be more abundant in isolates with strong and medium positive biofilm production. This has shown that excluding fimH gene, csgA, csuE and ompA genes have contributed to the biofilm formation in invasive A.baumannii isolates, respectively.