The clinical and laboratory characteristics in 76 HD patients with or without sarcope- nia are presented in Table 1. The mean age of total participants was 60.39 ± 12.36 years, with 34% of patients aged > 65 years. Among these patients, 36 (47.4%) patients had low HGS, 30 (39.5%) patients had slow gait speed, and 8 (10.5%) patients had low muscle mass. Eight (10.5%) patients were defined as having sarcopenia according to AWGS cri- teria. Compared to the non-sarcopenia group, patients in the sarcopenia group were lower in height (P = 0.014) and weighed less (P < 0.001), had lower waist circumference (P < 0.001), BMI (P < 0.001), body fat mass (P = 0.048), serum TG (P = 0.032), serum creatinine (P = 0.017), serum phosphorus (P = 0.015), leptin level (P = 0.001), ASMM (P < 0.001), and HGS (P = 0.043) while the Kt/V (P < 0.001) and URR (P < 0.001) were higher. Table 2 depicts the subgroup distribution of HD patients with or without sarcopenia. Among the 76 total participants, 24 (31.6%) patients had DM and 35 (46.1%) patients had hypertension. In comparing the sarcopenia with the non-sarcopenia group, there were no statistically signifi- cant differences in distribution by gender, diabetes, hypertension, angiotensin recep- tor blocker, β-blocker, calcium channel blocker (CCB), statin, or fibrate drugs used. Table 3 shows serumleptinlevels and clin- ical characteristics among HD patients. There were no statistical differences on log-leptin level in comparing sex, diabetes, hypertension, and the drugs used (angio- tensin receptor blocker, β-blocker, CCB, statin, or fibrate).
Abstract: Prostate cancer (PCa) is one of the major health care problems in males. It is known that red and pro- cessed meat consumption, fat intake and obesity are risk factors for PCa development. Adiponectin and leptin are adipokines that are synthesized in visceral adipose tissue and associated with obesity. Up to date, the association of serum adiponectin and leptin with PCa largely remains unexplored. Therefore, we studied the concentration of adiponectin and leptin in PCa patients in Chinese population. 92 prospective cases of prostate cancer and 92 matched healthy controls were enrolled in this study. Serum adiponectin and leptinlevels were detected by enzyme- linked immunosorbent assays (ELISA) technique. No statistically significant differences were observed in age, body- mass index (BMI), prostate specific antigen (PSA), fasting blood glucose (FBG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), total cholesterol (TC), triglycerides (TG), creatinine (CRE), and blood urea nitrogen (BUN) in the paired groups. Both serum adiponectin and leptinlevels were significantly higher in patients with PCa compared to healthy controls (P<0.001 for both). Subsequently, there was a positive correla- tion between adiponectin and PSA (r=0.285, P<0.001). Positive significant correlations between BMI, PSA, TG and leptin were also observed in whole group (r=0.270, P<0.001; r=0.348, P<0.001; r=0.170, P=0.021, respectively). However, the serum adiponectin and leptinlevels were not related to the Gleason score of PCa. Receiver operating characteristic curves analysis of the investigated serum adiponectin differentiated cancer patients from the healthy individuals with a sensitivity of 87%, specificity of 56%. Leptinlevels also distinguished patients from the healthy controls with a sensitivity of 69%, specificity of 68%. Our study shows that the serumlevels of adiponectin and leptin in PCa patients were higher than healthy controls. Adiponectin and leptin may be important markers of PCa. For validation, further studies including large cohort studies would be required.
a wide range of initial, predialysis HGF level in serum (153-1011 ng/ml) but there was no cor- relation between these values and change of its concentration during hemodialysis session. There was also no correlationbetween predial- ysis HGF levels and any of the studied parame- ters reflecting the quality of life in the studied patients. We found however that patients with smaller increase of HGF during hemodialysis session reported not only more limitations of the physical activity, and disorders related to renal failure, but also impaired coping with life during last weeks and stronger interference of the renal disease with their life (Table 2). To summarize, our results suggest that lowhemo- dialysis-induced increase of serum HGF corre- lates with reduced quality of life in patients with end stage renal failure and on the replacement therapy.
Abstract: Objective: To analyze the correlation of serumlevels of visfatin, leptin, resistin, and adiponectin (APN) with glycolipid metabolism and inflammatory factors in obese patients with periodontal disease. Methods: 116 obese adults (OB), of whom 78 participants were diagnosed with different degrees of chronic periodontitis (CP), and 50 healthy adults were recruited into the study. Fasting peripheral venous blood was extracted to determine serumlevels of adipocytokines (e.g., visfatin, leptin, resistin, and APN), glucolipid metabolism (e.g., fasting blood glucose (FBG), fasting insulin (FINS), C-peptide (C-P), cortisol (Cor), homeostasis model of assessment for insulin resistance index (HOMA-IR), glycosylated hemoglobin (HbA1c), triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and non-high-density lipoprotein cholesterol (non- HDL)), and micro-inflammation-related indexes like C-reactive protein (CRP), interleukin (IL)-1β, IL-6, IL-10, and tu- mor necrosis factor (TNF)-α. Correlationbetweenlevels of adipocytokines and levels of glucolipid metabolism and inflammatory factors was further analyzed. Results: Assays for plasma levels of adipocytokines showed that both the OB group and the OB with CP group had significantly higher serumlevels of visfatin, leptin, and resistin than the normal control group and significantly lower serumlevels of ANP than the normal control group (P<0.05). Detection of serum glucolipid metabolism levels showed that FBG, FINS, C-P, Cor, HOMA-IR, TG, TC, LDL-C, HDL-C, Non-HDL-C of OB group, and OB with CP patients were significantly higher than those of normal patients (P<0.05). Assay for plasma levels of inflammatory factors showed that both the OB group and the OB with CP group had significantly higher serumlevels of CRP, IL-1β, IL-6, and TNF-α than the normal control group and significantly lower serumlevels of IL-10 than the normal control group. Spearman’s correlation analysis revealed that serumlevels of visfatin, leptin, resistin, and APN were significantly correlated with concentrations of FBG, FINS, C-P, Cor, TG, TC, LDL-C, HDL-C, Non- HDL-C, CRP, IL-1β, IL-6, IL-10, and TNF-α. Conclusions: There were high expression levels of inflammatory factors and glucolipid metabolism disorder in obese patients with periodontal disease and excessively expressed adipocy- tokines may be important factors of persistent and worsened obesity and of periodontitis.
Abstract: Objective: The aim of the current study was to investigate correlationlevelsbetweenserum total bile acid and occurrence of coronary heart disease. Methods: Patients that underwent coronary angiographies in Linyi people’s Hospital, between December 2015 to December 2016, were selected. Patients with coronary artery dis- ease (diagnosed by coronary angiographies) were included in the observation group (102 cases). Patients with no significant abnormalities were included in the control group (80 cases). Basic information of the patients was col- lected and levels of total cholesterol (TC), triacylglycerol (TG), high density lipoprotein-cholesterol (HDL-C), low den- sity lipoprotein-cholesterol (LDL-C), glucose (Glu), and total bile acid (TBA) were measured. Results were analyzed statistically. Results: Levels of TC, TG, LDL-C, TBA, and Glu in the observation group were significantly higher than those in the control group. HDL-C was significantly lower than that in the control group (all P < 0.05). The abnormal rate of TBA (72.55%) was significantly higher than that of TC, HDL-C, and LDL-C in the observation group (all P < 0.05). Pearson’s linear correlation analysis showed that TC, TG, and LDL-C levels were positively correlated with TBA expression levels and negatively correlated with HDL-C expression levels (all P < 0.05). Logistics multivariate analy- sis showed that smoking, hypertension, diabetes, hyperlipidemia, and TBA are independent risk factors for coronary heart disease. Conclusion: Serum total bile acid was closely related to occurrence of coronary heart disease and could be a good response to the metabolic statuses of coronary heart disease patients. Thus, it is worthy of promo- tion as an auxiliary indicator of coronary heart disease detection.
crucial role in insulin resistance and modula- tion of systemic lipid and glucose metabolism . Our study revealed significantly higher serum A-FABP levels in female KT, DM KT and hypertensive KT patients. Several studies pro- duced the same results of higher A-FABP levels in female populations [33-35], because femal- es have comparatively higher percentages of body fat than males . No relationship was found betweenserum A-FABP levels and the other factors, including the transplantation model and immunosuppressive agents used. Our study revealed a positive association be- tween serum A-FABP levels and the indicators of adiposity including waist circumference, BMI, and body fat mass. It was suggested that adi- pocytes were the major site for A-FABP secre- tion in KT patients. The involvement of serum A-FABP in the development of hyperinsulinemia, hyperglycemia, and insulin resistance [32, 36] is consistent with our results of a positive cor- relation between A-FABP and log-insulin, log- glucose, log HOMA-IR, and DM. A previous study demonstrated that serum A-FABP level was positively correlated with TG , and a similar finding was obtained in this study. The positive correlationbetween A-FABP and Cre as well as the negativecorrelationbetween A-FABP and GFR were noted in type 2 DM patients . Our results revealed a coherent negativecorrelation in A-FABP and GFR, but no relationship was found in A-FABP and Cre. A-FABP played an important role in obesity- related cardiovascular disease and endothelial dysfunction by increasing cholesterol and TG accumulation; therefore, it was positively as- sociated with atherosclerosis [23, 36]. After multivariate forward stepwise linear regression analysis of the significant variables showed that SBP and TG were independent predictors of fasting serum A-FABP levels.
Serum HbA1c was detected by micro-column chromatography with a DCA2000 instrument (Bayer Company, Leverkusen, Germany) (re- agent was provided by Bayer Company). The detection process was conducted in accor- dance with the kit instructions for operation. The best-corrected visual acuity was respec- tively tested based on the international stan- dard visual acuity chart. The chart consisted of 14 lines of the word “E” in various sizes and opening direction, and the measurements ranged from 0.1-1.5 (or from 4.0-5.2). Each line was labeled, and patients’ eyesight was paral- lel to the 1.0 line. The testing distance was 5 m and the best-corrected visual acuity was recorded using decimal notation. The foveal retinal thickness was inspected and scanned with 3D-OCT (Topcon Medical Systems, Inc., Paramus, NJ, USA) in darkroom conditions. Scanning modes included the horizontal, verti- cal, and oblique axis, and the scanning length was 4 mm. Based on OCT software, the dis- tance from the inside of the retinal pigment epithelium band to the inside of the strata neu- ro-epitheliale was measured using an artificial calibration method. After OCT, fundus fluores- cein angiography (FFA) was performed by the combined Heidelberg retina angiograph (HRA2). Patients with a negative allergy test were in- jected 100 g/l sodium fluorescein (5 ml) within 6 seconds through the anterior brachial vein, and FFA was observed for more than 10 min- utes. All of the FFA examinations were interpret- ed by an experienced fundus physician. Laser photocoagulation therapy
Fasting blood samples (approximately 5 ml) from all the participants were immediately cen- trifuged at 3,000×g for 10 min after collection. Serumlevels of albumin, blood urea nitrogen (BUN), creatinine, fasting glucose, glycated hemoglobin (HbA1c), total cholesterol (TCH), tri- glyceride (TG), high-density lipoprotein choles- terol (HDL-C), low-density lipoprotein choles- terol (LDL-C), and high-sensitivity C-reactive protein (hs-CRP) were measured using an auto- analyzer (Siemens Advia 1800, Siemens Healt- hcare GmbH, Henkestr, Germany) [6-8]. Serumleptin concentrations were determined using a commercially available enzyme immunoassay (EIA) (SPI-BIO, Montigny le Bretonneux, France) [3, 9-11, 13]. Serum insulin levels were mea- sured using a commercially available enzyme- linked immunosorbent assay (ELISA) (Labor Diagnostika Nord, Nordhorn, Germany) [11, 14, 15]. Insulin resistance was evaluated using
Abstract: Anemia is a frequent complication in the maintenance hemodialysis (MHD) patients. However, data on se- rum hepcidin level as a guide in MHD patients are limited. We aimed to investigate the clinical significance of serum hepcidin level on erythropoiesis-stimulating agents (ESAs) and/or intravenous iron therapy among MHD patients. A total of 32 MHD patients receiving ESAs and iron therapy were enrolled; 30 age-and gender-matched healthy subjects were selected as controls. Serumlevels of hepcidin, ferritin, iron, transferrin saturation, and erythropoietin were determined. Serum hepcidin level was significantly higher in MHD patients than the control group (424±174.2 ng/mL and 72.4±12.3 ng/mL; P<0.01). Serum hepcidin level in MHD patients was positively correlated with serum iron (r=0.68, P=0.005), serum ferritin (r=0.62, P=0.0045), and transferrin saturation (r=0.7, P=0.001). A negativecorrelation was observed between hepcidin and reticulocyte count (r=-0.63, P=0.015). Moreover, serum hepcidin almost restored to normal level after hemodialysis. EPIAO alone but not intravenous iron sucrose could effectively reduce hepcidin level. In conclusion, serum hepcidin level is increased in MHD patients. Hepcidin may involve in the disturbance of iron metabolism and regulation of erythropoiesis in these patients. Reduction of hepcidin level and sufficient ESAs supplementation can improve erythropoiesis and restore iron homeostasis.
In general, serumleptinlevels are significantly ele- vated in patients with renal failure, particularly when compared to age, gender and body mass index (BMI)- matched controls [13,14]. However, the role of hyperlep- tinemia in ESRD patients is somewhat unconventional. In contrast with its anorexogenic effects recognized in the general population  and even in experimental models of uremia (in subtotal nephrectomized and lep- tin receptor-deficient [db/db] mice) , leptin has not been reported to affect perceived appetite and nutrient intake in dialysis patients [16,17]. Although in some observational studies, increased serumleptin concentra- tions were observed in ESRD patients in parallel with loss of lean body mass [18,19] or with hypoalbuminemia and low protein intake , some others failed to find any correlationbetween hyperleptinemia and weight change  or lean mass  in this population. More- over, several clinical studies suggested that leptin is a negative acute phase protein  and can serve as a marker of adequate nutritional status, rather than an appetite-reducing uremic toxin in hemodialysispatients [23-25]. Finally, the relationship between elevated serumleptinlevels and clinical outcomes in ESRD has not been fully defined. In one small prospective cohort of hemodialysispatients, lower baseline serumleptinlevels predicted mortality , but neither changes in leptin over time were measured, nor were leptinlevels normal- ized to body fat mass in this study.
Leptin is a pleiotropic hormone, exclusively pro- duced in adipocytes, that regulates energy expenditure and food intake . Circulating leptinlevels are elevated in patients with renal failure  and correlated with weight chang- es in dialysis patients [26-29]. Moreover, loss of lean body mass has been found to be corre- lated with increased serumleptinlevels in some observational studies [26, 27]. Adipone- ctin, another adipocytokines produced by vis- ceral fat, can increase insulin sensitivity and decrease glucose intolerance and diabetes [30, 31]. Plasma adiponectin levels have been found to have a negativecorrelation with BMI and waist-to-hip ratio in overweight/obese Asian subjects without chronic kidney disease . In dialysis patients, data has consistently demonstrated that plasma adiponectin levels are inversely associated with visceral fat, total body fat, and lean body mass [9, 33, 34]. Delgado et al. stratified BMIs into 6 groups with 5 kg/m 2 increments (from <20 to > 40 kg/m 2 )
A sixth and a seventh mutation were originally de- scribed in 2011 in individuals stemming from consan- guineous Pakistani pedigrees . In a child, a deletion of a thymine-cytosine-adenine triplet at positions 10839 to 10841 of the leptin gene (g.10839_10841 del TCA) cor- responding to positions 104 to 106 of the transcript, re- spectively, (c.104_106 del TCA) was detected . This in turn resulted in the deletion of the isoleucine at position 35 of the protein (p.I35 del ) . In this patient, Fatima et al. originally observed low, but still detectable serumleptinlevels as measured by an ELISA (3.6 ng/ml) . In a later publication, Saeed et al. also reported a child with a p.I35 del mutation, probably the very same pa- tient, in which they could not detect any leptin in the serum using an ELISA . Fatima et al. hypothesized that the deletion of this highly conserved isoleucine at position 35 of the protein and thus resulting loss of hydrophobicity in the N-terminal region of the protein might result in defective intracellular transport and secretion . Furthermore, these authors proposed that the p.I35 del mutation might also result in a loss of the biological activity of the secreted protein as the N- terminal region of leptin has been proposed to be involved in the binding of leptin to the leptin receptor .
The cohort contained 13 men and 8 women age ranging from 16 to 45 years. The mean age of the patients was 28.38±9.38 years. The body mass index of the cohort was 22.09±2.48 Kg/m2. The average duration of dialysis was 14.9±4.9 months. The most assumed cause of native kidney disease was chronic glomerular nephritis, however one patient had chronic interstitial nephritis and another had Autosomal dominant polycystic kidney disease. The mean pre transplantation leptin concentration was 9.96±3.48 ng/ml and this decreased to 4.07±1.7 ng/ml (P<0.0001) within six days of transplantation. Plasma Creatinine level declined dramatically from 7.5±1.6 mg/dl to 1.1±0.7 mg/dl (P<0.0001) within one week Fig. 1. There was no graft rejection in any of these patients. In our study, there was no concomitant change in BMI (P>0.05). Neither pre (r=0.03, p>0.05) nor post transplant (r= - 0.01, p>0.05) plasma Leptinlevels correlated significantly with BMI.
The 164 patients with angiographically proven CAD were included in the ac- tual study group and they were followed up for a period of mean 48 months from 2012-2016 for MACE. MACE (death, non-fatal MI, coronary revasculari- zation, re-hospitalization for any cardiac reason) were recorded. Follow up data was collected from in/outpatient records. When no data was available from medical records, information was obtained through phone calls (either directly from the patient or a first degree relative).
The current study addressed the reduction of adipocytokines levels in association with de novo AML together with negativecorrelationbetween bone marrow blasts and adiponectin .These finding suggest the implication of both leptin and adiponectin in AML pathogenesis which might be useful as prognostic markers of AML , however These findings necessitate additional studies of leptin and adiponectin in AML patients and to be related to other risk factors as severe illness, altered energy balance and disease complications on large scale of cases.
Abstract: Objective: This study aimed to investigate the relationship between antibiotic resistance and serum resis- tance in clinical isolates of Acinetobacter baumannii (A. baumannii). Methods: The tested 67 clinical isolates were collected from several hospitals in China. Antibiotic resistance to 21 antibiotics from 9 antimicrobial categories was assessed by Kirby-Bauer disc diffusion or broth microdilution methods. Multilocus sequence typing (MLST) was used to group the A. baumannii isolates. At last, the in vivo mice model was used to detect the relationship between drug resistance and mortality from inoculation with A. baumannii. Results: Among all 67 isolates, 16 were defined as multidrug-resistant (MDR), and 46 were extensively drug-resistant (XDR). MLST grouped the A. baumannii iso- lates into 9 existing sequence types (STs). ST208 accounted for 44.8% (30/67) of the isolates, which belonged to clonal complex (CC) 92. The serum resistance testing showed that 53 out of 68 strains of A. baumannii (67 clinical isolates and reference strain ATCC19606) were highly resistant to killing by complement system in normal human serum (NHS). The comparison of the antibiotic resistance and serum resistant strains showed that antibiotic resis- tant isolates had stronger serum resistance than susceptible strains. Furthermore, mice infected by XDR isolates had higher mortality rate. Conclusion: Drug-resistant A. baumannii strains have stronger serum resistance. These results sounds alarming and should be considered in the clinical treatment of drug-resistant A. baumannii.
inflammatory cytokine levels, even though the results are con- flicting: in our D⫹ HUS patient group, interleukin 10 (IL-10) levels were found to be decreased in patients with EHEC infections in comparison to those in patients with bacterial gastroenteritis of other origins. Consequently, the TNF-␣/ IL-10 ratio for the HUS group was increased when the levels of the two cytokines were compared, reflecting an imbalance to- ward inflammation. This may result in the expression of an altered immunity in patients with this rare disease. Neverthe- less, measurement of systemic cytokine levels is not likely to reflect the whole picture of immune activation, as cytokines mainly act in a paracrine fashion and have short half-lives in plasma (11). Therefore, we raised the question whether the cytokine profiles observed in vivo can be reproduced by ex vivo LPS stimulation of whole blood from patients who had expe- rienced and who were recovering from an acute HUS episode. As the results of studies with animal models suggest compro- mised immune activity secondary to Stx exposure (17), we decided to study the immune response to superantigen in order to characterize T-cell immunity. Finally, the results were cor- related with clinical parameters like the glomerular filtration rate (GFR), blood pressure, protein and erythrocyte levels in urine, and others.
Abstract: Little is known about the association between the muscle Ras (MRAS) gene rs6782181 polymorphism and serum lipid levels. The aim of the present study was to investigate the association between the MRAS rs6782181 polymorphism and serum lipid levels in the Mulao and Han populations. A total of 632 subjects of Han and 629 unrelated subjects of Mulao nationalities were randomly selected from our previous stratified randomized samples. Genotypes of the MARS rs6782181 polymorphism were determined via polymerase chain reaction and restriction fragment length polymorphism. The subjects with GG genotype had higher serum total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and apolipoprotein (Apo) B levels in Han, and higher serum TC and LDL-C levels in Mulao than the subjects with AA/AG genotypes (P < 0.05-0.01). Subgroup analyses showed that the subjects with GG genotype had higher TC, TG, high-density lipoprotein cholesterol (HDL-C), LDL-C, ApoAI and ApoB in Han males, lower ApoAI and the ratio of ApoAI to ApoB in Han females; and higher LDL-C levels in Mulao males but not in Mulao females than the subjects with AG/AA genotypes. The association of the MARS rs6782181 polymor- phism and serum lipid levels is different between the Mulao and Han populations, or between males and females in the both ethnic groups. There may be an ethnic- and/or sex-specific association between the MRAS rs6782181 polymorphism and serum lipid levels in our study populations.
markers during steady and unsteady states of SCD [1,2,10]. Nevertheless, there may be a need to investigate other more specific inflammatory markers such as b 2- macroglobulin and C-reactive protein in our SCA cohort in subsequent studies to build more confidence of reli- ance on the less expensive and easy to implement ESR assay. Larger sample size is also needed to ascertaining the fitness of poor reticulocyte response as a determi- nant of low leptin level in SCA. The fact that the lean mass data in this study was obtained by calculation is itself a limitation as it may bias fat mass data of some patients. However, similar calculation was used for all the patients as previously carried out by Owa and Ade- juyigbe  in the study area to improve the credibility of the corresponding anthropometric data obtained in this study as much as possible. Future studies on the micronutrient variables such as zinc and vitamin E that have been associated with growth and immunity in SCD patients in relation to serumleptin are also advocated.
Our in vivo study showed that insulin-stimulated leptin synthesis may be mediated through increased glucose uptake by the adipose tissue in S. heathi. The in vitro study further supports this relationship. Both GLUT4 and GLUT8 are utilized to transport glucose to adipose tissue during adipogenesis in S. heathi. It is well demonstrated that GLUT4 expression in adipocytes is under insulin control and is the major transporter of glucose during adipogenesis (Sivitz et al., 1989). In our in vitro study, insulin increased its own receptors and upregulated GLUT4 expression in WAT in a dose- dependent manner. However, our in vivo data indicated that IR is downregulated during the winter despite increased insulin level. The reason for the discrepancy between the in vivo and in vitro data could be due to lack of certain factors in the in vitro study (such as neural input, feedback regulation from markers in circulation, etc). This study also demonstrates expression of novel glucose transporter GLUT8 in adipose tissue. Expression of GLUT4 and GLUT8 in adipose tissue varied significantly (P<0.05) during different stage of adipogenesis.