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Limited data are available on the serum levels of different sphingomyelin (CerPCho) and ceramide (CER) species in sickle-cell disease (SCD). This study was aimed at identifying the levels of C16-C24 CerPCho and C16-C24 CER in serum obtained from SCD patients and controls. Circulating levels of neutral sphingomyelinase (N-SMase) activity, ceramide-1-phosphate (C1P), and sphingosine-1-phosphate (S1P) were also determined. Blood was collected from 35 hemoglobin (Hb)A volunteers and 45 homozygous HbSS patients. Serum levels of C16-C24 CerPCho and C16-C24 CER were determined by an optimized multiple reaction monitoring (MRM) method using ultrafast liquid chromatography (UFLC) coupled with tandem mass spectrometry (MS/MS). Serum activity of N-SMase was assayed by standard kit methods, and C1P and S1P levels were determined by enzyme-linked immunosorbent assay. A significant decrease was observed in the serum levels of C18-C24 CerPCho in patients with SCD compared to controls. No significant difference was found in C16 CerPCho levels between the two groups. Very-long-chain C22-C24 CER were significantly decreased in SCD, while long-chain C16-C20 CER levels showed no significant difference between SCD patients and controls. Significant positive correlation was found between the serum total cholesterol levels and C18-C24 CerPCho and C22-C24 CER in SCD patients. Patients with SCD had significantly elevated serum activity of N-SMase as well as increased circulating levels of C1P and S1P compared to controls. The decrease in serum levels of C18-C24 CerPCho in patients with SCD was accompanied by decreased levels of C22-C24 CER. Future studies are needed to understand the role of decreased CerPCho and CER in the pathophysiology of SCD.

BackgroundThis study aimed to determine early postoperative changes of serum sphingomyelin (SM) and ceramide (CER) species following laparoscopic sleeve gastrectomy (LSG).MethodsTwenty obese patients [mean body mass index (BMI) 45,64 ± 6,10 kg/m2] underwent LSG and normal weight control patients (mean BMI 31,51 ± 6,21 kg/m2) underwent laparoscopic cholecystectomy. Fasting blood samples were collected prior to surgery, at day 1 and day 30 after surgery. Circulating levels of C16-C24 SMs, C16-C24 CERs and sphingosine-1-phosphate (S1P) were determined by an optimized multiple reaction monitoring (MRM) method using ultra fast-liquid chromatography (UFLC) coupled with tandem mass spectrometry (MS/MS). Serum activity of neutral sphingomyelinase (N-SMase) was assayed by standard kit methods, and ceramide-1-phosphate (C1P) levels were determined by enzyme-linked immunosorbent assay (ELISA). Lipid profile, routine biochemical and hormone parameters were assayed by standard kit methods. Insulin sensitivity was evaluated using homeostatic model assessment for insulin resistance (HOMA IR).ResultsA significant decrease was observed in serum levels of very-long-chain C24 SM, very-long-chain C22-C24 CERs, HOMA-IR, N-SMase and C1P in LSG patients after postoperation day 1 and day 30 compared to preoperation levels. At 30 days postsurgery, BMI was reduced by 11%, fasting triglycerides were significantly decreased, and insulin sensitivity was increased compared to presurgery values. A significant positive correlation was found between HOMA-IR and serum levels of C22-C24 CERs in LSG patients.ConclusionWe conclude that very long chain CERs may mediate improved insulin sensitivity after LSG.

Exposure to a high‐fat diet (HFD) has been reported to impair central autonomic and enteric neurocircuitries, however, the relevant mechanisms and their time course are inadequately clarified. This study aimed to investigate the effects of HFD consumption through the period of adolescence on gastric motor functions in adulthood. Male Sprague‐Dawley rats consumed a regular diet or HFD (60% kcal by fat) from 4 to 12 weeks of age. Body weight and food intake were monitored weekly. In adult rats, gastric emptying (GE) was measured. Additionally, using in‐vitro organ bath, contractile and relaxant responses of antral and fundic strips were assessed with bethanechol and sodium nitroprusside (SNP), respectively. The expressions of choline acetyltransferase (ChAT), neuronal nitric oxide synthase (nNOS) and vasoactive intestinal polypeptide (VIP) were detected by immunofluorescence, whereas, the number of myenteric neurons were evaluated by staining with cuprolinic blue and enteric neuronal marker PGP 9.5. In adulthood, the HFD did not alter food intake, while significantly increasing the body weight. In HFD‐fed adult rats, increased visceral fat mass was accompanied by delayed GE. Moreover, bethanechol‐ and SNP‐induced responses were attenuated in antral and fundic tissues. HFD remarkably decreased the number of myenteric neurons and NOS immunoreactivity both in fundus and antrum. HFD remarkably decreased ChAT expression, while increasing the immunoreactivity for VIP in antrum. In conclusion, consumption of HFD between early adolescence and adulthood results in obesity and impairment of gastric motor functions. Particularly, HFD‐induced gastric dysmotility appears to be predominantly dependent on the modifications in the non‐adrenergic non‐cholinergic inhibitory neurotransmission.

Amaç: Bu çalışmada, pulmoner embolili hastalarda oksidatif stres ürünleri olan iskemi modifiye albumin (IMA), ileri oksidasyon protein ürünü (AOPP) ve malondialdehit (MDA) düzeylerini belirleyerek pulmoner embolideki oksidatif stresin gösterilmesi amaçlanmıştır. Gereç ve Results:There was no significant difference between the two groups in terms of age, height, and weight. The difference in the AOPP levels of the two groups was not significant. The difference in the serum albumin levels of the two groups was found significant (p<0.001). The difference in levels of IMA after being corrected according to the albumin levels of the two groups was not significant. MDA levels of the two groups showed a significant difference (p=0.032). Conclusion:AOPP levels in patients with pulmonary embolism were not found different but, the increases of MDA levels were significant. We suggest using albumin-adjusted IMA levels to interpret IMA levels more correctly. We need more studies about using IMA levels as an indicator for diagnosis of pulmonary embolism. ( TANI YÖNTEMLERİ DIAGNOSTIC METHODS Pulmoner Embolide Oksidatif Stres Ürünlerinin Tanısal DeğeriThe GİRİŞPulmoner embolizm (PE), etkin tedavisi olmasına rağ-men mortalitesi yüksek seyreden bir hastalıktır [1].Oksidatif stres aralarında PE, akut myokard enfarktü-sü, geçici iskemik atak, inme ve akut mezenterik iskemi gibi tromboembolik hadiselerin de bulunduğu organizmadaki bir çok patolojik süreçte rol almaktadır [2]. Pulmoner emboli nedeniyle ortaya çıkan pulmoner dolaşım yetmezliğinin sonucunda dolaşımda instabilite, hipoperfüzyon, hipoksi ve iskemi meydana gelir. Tüm bu durumlar organizmada oksidatif stres yaratır [3]. Oksidanantioksidan sistemler arasındaki dengenin bozulması olarak tanımlanan oksidatif stres, protein oksidasyonu ve lipid peroksidasyonu gibi mekanizmalarla doku hasarına neden olmaktadır [4,5].Protein oksidasyonu, proteinlerin reaktif oksijen türev-leri veya oksidatif stres ürünleri ile kovalent modifikasyonu sonucu meydana gelir. Proteinlerde yapısal değişikliğe yol