The impact of glucocorticoids therapy on cutaneous wounds in Kawasaki disease: A meta-analysis of randomized controlled trials.

Kawasaki disease (KD) is one of the most challenging diseases that is defined as an acute vasculitis that affects the coronary arteries primarily in children. It causes complications if left untreated at early stages, ultimately leading to death. Corticosteroids have been recognized to treat and cause great impact on the patients with KD. Glucocorticoid is one of the main corticosteroids that are being used to treat KD and cutaneous wounds. However, ineffectiveness of a few glucocorticoids can limit the efficacy of this treatment. This study particularly aimed to elucidate the impact of glucocorticoids on cutaneous wounds in KD. To perform the meta-analysis, a comprehensive literature survey was conducted to unveil the studies and research conducted on Kawasaki patients that revealed different glucocorticoids in the form of specific interventions influencing KD. The literature was searched using numerous keywords, screened and data was extracted to perform the meta-analysis and then it was conducted using the metabin function of R package meta. A total of 2000 patients from both intervention and control groups were employed to carry out the meta-analysis to analyse and evaluate the impact of glucocorticoids on curing KD and cutaneous wounds in patients. The results disclosed that glucocorticoids along with other steroids, mainly IVIG (intravenous immunoglobulin), was an effective intervention to patients suffering from Kawasaki. The results depicted significant outcomes with the values (risk ratio [RR]: 1.08, 95% confidence interval [CI]: 0.58-2.00, p < 0.01) and enlightened the fact that adopting different glucocorticoids may significantly improve the efficacy of skin lesions along with KD. Hence, interventions of glucocorticoids must be utilized in the clinical practice to reduce the incidence of skin wounds and adverse effects caused due to KD.

The safety and effectiveness of clopidogrel versus aspirin in Kawasaki disease with mild-to-moderate liver injury.

Kawasaki disease can be combined with liver injury. As a mainstay treatment for Kawasaki disease, aspirin may cause liver injury. This study aimed to compare the safety and effectiveness of clopidogrel versus aspirin in Kawasaki disease with mild-to-moderate liver injury. This study retrospectively analysed 166 children with Kawasaki disease combined with mild-to-moderate liver injury. The children treated with clopidogrel were less likely to have aggravated liver injury than those treated with aspirin (n = 2/100 vs. n = 13/66, P < 0.001). The initial alanine aminotransferase value of the clopidogrel group was higher (131.5 [98.5, 167.5] vs. 96 [72, 133], P < 0.001), while the time of alanine aminotransferase recovery to normal was similar (5 [4, 7] vs. 4 [3, 7], P = 0.179). No significant fever differences observed between groups: 7.5 [6, 9] for aspirin vs. 7 [6, 8] for clopidogrel group, P = 0.064. The probability of nonresponse to intravenous immunoglobulin (n = 29/100 vs. n = 30/66, P = 0.030) and the days of hospitalization (n = 6 [4, 9] vs. n = 7 [5, 10], P = 0.007) in the clopidogrel group were less than those in the aspirin group. In conclusion, the application of clopidogrel is potentially superior to aspirin in Kawasaki disease combined with mild-to-moderate liver injury.

Clinical features of Streptococcus intermedius infection in children: a case series study.

Introduction: Streptococcus intermedius is an opportunistic pathogen associated with prolonged hospital stays and high mortality rates in adults. However, little is currently known about the clinical features of Streptococcus intermedius infection in children. Methods: This retrospective case series study included 40 children diagnosed with Streptococcus intermedius, confirmed through bacterial cultures or high-throughput sequencing. Antibiotic resistance was assessed through susceptibility testing. The site and clinical manifestations were evaluated for all patients. Results: The common infection sites were the abdominal cavity, skin and soft tissue, intracranial, and invasive pulmonary, with the abdominal cavity being the most frequently affected. The drug susceptibility test showed 100% sensitivity to ceftriaxone, levofloxacin, chloramphenicol, vancomycin, and linezolid, 92.6% sensitivity to penicillin, 73.3% resistance to erythromycin, and 76.7% resistance to clindamycin. Besides antibiotic therapy, surgical intervention or pus drainage was often necessary. Lung imaging of four patients revealed pulmonary abscesses, nodules, or encapsulated pleura. Two cases yielded positive culture results, while three were identified as positive through high-throughput nucleotide sequencing of pleural effusion. Discussion: In children with Streptococcus intermedius infection, emphasis should be placed on the risk of pus or abscess formation. In cases of pulmonary abscess and pleural effusion, especially in male children, Streptococcus intermedius should be suspected even if the culture is negative. Improvements in high-throughput nucleotide sequencing are required to reduce misdiagnosis rates.

[Recent research on platelet-leukocyte aggregates and their role in the pathogenesis of Kawasaki disease]. / 血小板-ç™½ç»†èƒžèšé›†ä½“åŠå ¶åœ¨å·å´Žç— å‘ç— ä¸­çš„ç ”ç©¶è¿›å±•.

Activated platelets may interact with various types of leukocytes such as monocytes, neutrophils, dendritic cells, and lymphocytes, trigger intercellular signal transduction, and thus lead to thrombosis and synthesis of massive inflammatory mediators. Elevated levels of circulating platelet-leukocyte aggregates have been found in patients with thrombotic or inflammatory diseases. This article reviews the latest research on the formation, function, and detection methods of platelet-leukocyte aggregates and their role in the onset of Kawasaki disease, so as to provide new ideas for studying the pathogenesis of Kawasaki disease.

Identification of Key LncRNAs and Pathways in Prediabetes and Type 2 Diabetes Mellitus for Hypertriglyceridemia Patients Based on Weighted Gene Co-Expression Network Analysis.

Aims: Prevalence of prediabetes and type 2 diabetes mellitus(T2DM) are increasing worldwide. Key lncRNAs were detected to provide a reference for searching potential biomarkers of prediabetes and T2DM in hypertriglyceridemia patients. Methods: The study included 18 hypertriglyceridemia patients: 6 newly diagnosed type 2 diabetes patients, 6 samples with prediabetes and 6 samples with normal blood glucose. Weighted gene co-expression network analysis (WGCNA) was conducted to construct co-expression network and obtain modules related to blood glucose, thus detecting key lncRNAs. Results: The green, yellow and yellow module was significantly related to blood glucose in T2DM versus normal controls, T2DM versus prediabetes, prediabetes versus normal controls, respectively. ENST00000503273, ENST00000462720, ENST00000480633 and ENST00000485392 were detected as key lncRNAs for the above three groups, respectively. Conclusions: For hypertriglyceridemia patients with different blood glucose levels, ENST00000503273, ENST00000462720 and ENST00000480633 could be potential biomarkers of T2DM.

The role of the BMP4/Smad1 signaling pathway in mesangial cell proliferation: A possible mechanism of diabetic nephropathy.

AIMS: This study explored the role of the BMP4/Smad1 signaling pathway in mesangial matrix expansion during the process of diabetic nephropathy. MAIN METHODS: Diabetic rats were induced by high-fat feeding followed by an intraperitoneal injection of streptozotocin. Glomerular lesions were examined. Immunohistochemical analysis was performed in order to identify BMP4/Smad1 signaling proteins (BMP4, ALK3, and Smad1) and mesangial ECM proteins (Col1 and Col4) in kidney tissue. Cell proliferation and the expression of BMP4, Smad1 and Col4 were determined in cultured mesangial cells exposed to high glucose. The specific regulatory role of BMP4 was evaluated by detecting BMP4/Smad1 signaling pathway proteins and mesangial ECM proteins after blocking BMP4 both at the gene and protein levels. KEY FINDINGS: Rats with DN exhibited mesangial expansion and a thickened glomerular basement membrane. Immunohistochemical analysis of glomeruli showed increased expression of BMP4, Smad1, ALK3, Col1, and Col4 but less expression of MMP9 than observed in controls. High glucose induced slight proliferation of cultured rat mesangial cells after 48 h of incubation but there was no significant different from the control (p > 0.05). High glucose activated the BMP4/Smad1 signaling pathway and stimulated Col4 expression in mesangial cells. Both silencing of the bmp4 gene (with siRNA) and blocking BMP4 protein signaling (with the BMP4 protein antagonist Noggin) reduced the expression of ALK3, Smad1, Col4, and Col1 in high glucose-stimulated mesangial cells. SIGNIFICANCE: The BMP4/Smad1 signaling pathway is crucial to the progression of mesangial expansion, and suppressing this signaling pathway may present a novel therapeutic strategy for DN.

[Aliskiren inhibits angiotensin II/angiotensin 1-7(Ang II/Ang1-7) signal pathway in rats with diabetic nephropathy].

Objective To investigate the role of aliskiren (AL) in the angiotensinII/ angiotensin 1-7 (AngII/Ang1-7) signal pathway in renal tissue of diabetic nephropathy (DN) rats. Methods 40 male SD rats were randomly divided into 4 groups including normal group, diabetes group, AL group and valsartan (Val) group. Animal models of diabetes were induced by high fat diet combined with small dose of streptozotocin injection. Rats in AL group were administered 50 mg/(kg.d) AL by gavage, and rats in Val group were administered 30 mg/(kg.d)Val by gavage. 24-hour urine protein (24 h-UP) were observed by Coomassie blue colorimetry at 2, 4 and 6 weeks after modeling, serum creatinine was detected by automatic biochemical analyser, kidney index [kidneys mass(g)/body mass (kg)] was measured. HE and PAS staining were used to observe renal pathological changes. Immunohistochemistry was used to detect the expression of ACE2, MAS receptor, AT1R and AT2R in the kidney. Results After 6 weeks of modeling, there was no significant difference in creatinine level among groups. The levels of glucose, 24 h-UP and kidney index in diabetes group, AL group and Val group significantly increased. Compared with diabetes group, the levels of 24 h-UP and kidney index were lower in AL group and Val group. Immunohistochemistry showed that the expression of AT2R and ACE2 was lower and the expression of MAS receptor was higher in AL group than diabetes group and Val group. Compared to normal group and Val group, AT1R expression was significantly up-regulated in AL group, without significant difference between diabetes group and AL group. Conclusion AL down-regulates the expression of AT2R and ACE2, thus inhibits the AngII/ Ang1-7 signal axis and improves/alleviates the symptoms in diabetic rats.

Male asymptomatic hyperuricemia patients display a lower number of NKG2D+ NK cells before and after a low-purine diet.

BACKGROUND: Aberrant activation of the immune system has been reported in asymptomatic hyperuricemia (HUA) patients. However, very few studies have elucidated the role of natural killer (NK) cells in this disease. METHODS: In this study, we evaluated the relationship between NK cells and HUA in 16 control subjects and 20 patients, who were all on a low-purine diet. We analyzed the number of circulating NK cells, its subsets, interferon-γ, and CD107 NK cells, by flow cytometry, before and after 4 and 24 weeks of diet control. We also assessed the potential association of the NK cells with clinical measures. RESULTS: The patients consistently had a lower number of NKG2D NK cells before and after low-purine diet, even the serum uric acid (SUA) levels <7 mg/dL after diet control. Moreover, a lower number of NK cells and a higher number of CD107a NK cells were observed on recruitment. Low-purine diet was benefit on the improvement of the SUA levels, body mass index (BMI), and the number and functions of NK cells. Furthermore, the number of CD3CD56 NK cells and NKG2D NK cells negatively correlated with the BMI before and after diet control. CONCLUSION: The consistent lower number of NKG2D NK cells and correlated with BMI before and after low-purine diet may be involved in the occurrence and development of HUA.

DUT-58 (Co) Derived Synthesis of Co Clusters as Efficient Oxygen Reduction Electrocatalyst for Zinc-Air Battery.

To meet the requirement of fuel cells and metal-air batteries, non-noble metal catalysts have to be developed to replace precious platinum-based catalysts. Herein, Co nanoclusters (≈2 nm) are anchored on nitrogen-doped reduced graphene oxide (Co/N-r-GO) by using DUT-58 (Co) metal-organic framework and GO as precursors. Compared with single-atom catalysts usually with ultralow concentration (<0.5 wt%), Co nanoclusters are more beneficial to break the O-O bond to ensure four electronic way for oxygen reduction reaction (ORR), since they can provide more adsorption centers for reactants. Therefore, as expected, the sample with 6.67 wt% Co content (Co/N-r-GO-5%-850) exhibits better ORR activity with a higher half-wave potential of 0.831 V, a more positive onset potential of 0.921 V than Pt/C, and a comparable limiting current density in alkaline medium. The Co nanoclusters enhance the catalytic performance for ORR in three aspects: quantum size effects, metal-support interactions, and low-coordination environment of metal centers. Furthermore, the sample is assembled into a zinc-air battery as the outstanding durable ORR catalyst. It displays a higher specific capacity (795 mAh g-1 at the current density 50 mA cm-2) and power density (175 mW cm-2) than Pt/C (731 mAh g-1 and 164 mW cm-2, respectively).

Notch4 signaling pathway in a Kawasaki disease mouse model induced by Lactobacillus casei cell wall extract.

The present study aimed to explore the role of the Notch4 signaling pathway in a mouse model of Kawasaki disease (KD) induced by Lactobacillus casei cell wall extract (LCWE). BALB/c male mice (4-6 weeks old) were intraperitoneally injected with 500 µg LCWE in phosphate-buffered saline (PBS) or PBS alone (control group). At days 3, 7, 14 and 28, the numbers of circulating endothelial progenitor cells (EPCs) in the peripheral blood and the expression of Notch4 on the surface of EPCs were detected. In addition, the levels of vascular cell adhesion molecule 1 (VCAM-1) and P-selectin in the roots of coronary arteries were evaluated. The results demonstrated that the level of circulating EPCs increased significantly at day 3, decreased progressively from day 3 onwards, and recovered to the normal level at day 28. Furthermore, the expression of Notch4 on the surface of EPCs was evidently higher in the KD model compared with that in the control group at day 7. In the endothelial cells of the coronary artery root, the protein levels of VCAM-1 and P-selectin protein increased in the KD model. In conclusion, the Notch4 signaling pathway participated in the coronary artery lesions in the KD animal model induced by LCWE.

Decreased percentage of NKG2D+NK cells in patients with incident onset of Type 1 Diabetes.

Type 1 diabetes mellitus (T1DM) is characterized by absolute insulin deficiency owing to autoimmune destruction of the pancreatic ß cells. A significant decrease in natural killer (NK) cells in peripheral blood has been observed in patients with untreated T1DM. In the present study, we aimed to explore the role of NK cells and their subsets in young T1DM patients. A total of 30 children and adolescents with untreated T1DM and 27 healthy controls (HC) were recruited in this study. Flow cytometry analysis indicated that the percentage of peripheral blood CD3-CD56+ NK cells and NK cells subsets (CD56bright, CD56dim and CD56neg), were significantly decreased in the T1DM patients compared to healthy controls. In addition, the percentage of inducible CD107a+ and IFN-γ-secreting NK cells was significantly decreased compared to HC. Interestingly, the percentage of NKG2D+ NK cells negatively correlated with the level of serum TCHOL and TG in T1DM patients. Our data indicate that decreased number and impaired function of NK cells may have a role in the pathogenesis of T1DM.

Predictive value of red blood cell distribution width for coronary artery lesions in patients with Kawasaki disease.

Recent studies have shown that elevated red blood cell distribution width is associated with poor outcome in cardiovascular diseases. In order to assess the predictive value of red blood cell distribution width, before treatment with intravenous immunoglobulins, for coronary artery lesions in patient with Kawasaki disease, we compared 83 patients with coronary artery lesions and 339 patients without coronary artery lesions before treatment with intravenous immunoglobulin. Clinical, echocardiographic, and biochemical values were evaluated along with red blood cell distribution width. A total of 422 consecutive patients with Kawasaki disease were enrolled into our study. According to receiver operating characteristic curve analysis, the optimal red blood cell distribution width cut-off value for predicting coronary artery lesions was 14.55% (area under the curve was 0.721; p=0.000); eighty-three patients (19.7%) had coronary artery lesions, and 70% of the patients with coronary artery lesions had red blood cell distribution width level >14.55%. Logistic regression analysis revealed that fever duration >14 days (odds ratio was 3.42, 95% confidence interval was 1.27-9.22; p=0.015), intravenous immunoglobulin resistance (odds ratio was 2.33, 95% confidence interval was 1.02-5.29; p=0.04), and red blood cell distribution width >14.55% (odds ratio was 3.49, 95% confidence interval was 2.01-6.05; p=0.000) were independent predictors of coronary artery lesions in patients with Kawasaki disease. In Conclusion, red blood cell distribution width may be helpful for predicting coronary artery lesions in patients with Kawasaki disease.

Receptor for advanced glycation end products involved in circulating endothelial cells release from human coronary endothelial cells induced by C-reactive protein.

OBJECTIVES: This study was designed to investigate the effect of receptor for advanced glycation end products (RAGE), S100A12 and C-reactive protein (CRP) on the release of circulating endothelial cells (CECs) from human coronary artery endothelial cells (HCAECs). MATERIALS AND METHODS: HCAECs were cultured in increasing concentration of CRP (0, 12.5, 25, 50µg/ml) or S100A12 protein (0, 4, 10, 25µg/ml) for 24 hr. CECs were measured by flow cytometry. Small interfering RNA (siRNA) was designed to decrease RAGE level. Fluorescence microscopy and real-time quantitative polymerase chain reaction were used to assess the efficiency of siRNA silencing RAGE. The release of CECs from HCAECs was further evaluated by flow cytometry. RESULTS: CRP caused a significant increase in the release of CECs from HCAECs. The number of CECs increased by about 2-fold in 25 µg/ml CRP-treated group compared to the control group (12.22% compared to 6.82%, P=0.032). But S100A12 failed to increase the release of CECs from HCAECs. Blockade of RAGE by siRNA significantly decreased the release of CECs induced by CRP (13.22% of CRP group compared to 8.77% of CRP+siRNA group, P=0.017). CONCLUSION: RAGE is involved in the release of CECs induced by CRP, and the effect can be attenuated by silencing RAGE. RAGE may play an important role in endothelial dysfunction in cardiovascular disease. Inhibition of RAGE may be a therapeutic target for coronary artery lesions in Kawasaki disease.

Effect and mechanisms of zinc supplementation in protecting against diabetic cardiomyopathy in a rat model of type 2 diabetes.

Diabetic cardiomyopathy is a prominent cause of heart failure in patients with diabetes mellitus. Currently, there is no specific treatment for diabetic cardiomyopathy. This study aimed to investigate the effect and underlying mechanisms of Zinc (Zn) supplementation in the protection against diabetic cardiomyopathy in a rat model of type 2 diabetes mellitus (T2DM). T2DM-like lesions in male Wistar rats were induced by introducing the high-fat diet and by administration of streptozocin (STZ). After STZ induction, animals with fasting plasma glucose level ≥16.7 mM were considered as diabetic, and randomly assigned to the group receiving physiological saline (control) or ZnSO4 for 56 days. On days 0, 7, 28 and 56 of treatment, animals were weighed, and their blood samples were analyzed. On day 56, hemodynamic assessment was performed right before the sacrifice of animals. Cardiac tissue specimens were collected and subjected to pathologic assessment, metallothionein (MT) concentration measurement and Western blot analysis of microtubule-associated protein light chain 3 (LC3), the marker of autophagy, and glucose-regulated protein-78 (GRP78), an oxidative stress marker. High-fat diet feeding followed by STZ administration resulted in weight loss, hyperglycemia, polydipsia, polyphagia, hemodynamic anomalies and a significant increase in the myocardial content of LC3 and GRP78 proteins, but not in MT protein. Zn supplementation effectively attenuated all these aberrations induced by high-fat diet and STZ. These findings suggest that Zn might be a protective factor in diabetic cardiomyopathy, acting in two ways: at least partially, through inhibiting autophagy and by endoplasmic reticulum stress.

A successfully treated case of hypopituitarism complicated with hyperosmolar hyperglycaemic state and rhabdomyolysis.

INTRODUCTION: This study aimed to report a rare case of hypopituitarism complicated with hyperosmolar hyperglycaemic state and rhabdomyolysis. CASE PRESENTATION: Hypopituitarism is a clinical syndrome in which there is a deficiency in hormone production by the pituitary gland. It often leads to hypoglycaemia, but in this case the patient was complicated with hyperosmolar hyperglycaemic state. The patient received prompt medical treatment, which effectively prevented the occurrence of possible acute kidney failure and other complications. CONCLUSION: This is a complicated and rare case. Our report provides some indications for the timely diagnosis and the standardised treatments for a patient who has hypopituitarism complicated with hyperosmolar hyperglycaemic state and rhabdomyolysis.

Advances in the relationship between perauorinated compounds and thyroid function.

The influence of perauorinated compounds (PFCs) on human health has increasingly been recognized. Recent studies have shown that PFCs are associated with the incidences of tumors, neurotoxicities, reproductive toxicity, and metabolic syndrome. However, the relationship between PFCs and thyroid diseases remains unclear. While some foreign studies have explored their potential correlations, the findings were still controversial due to different methodologies and populations. This article reviews the recent advances in the research on the relationship between PFCs and thyroid function.

A new method for evaluating tricuspid valve displacement in children with Ebstein's anomaly: using the annulus and coronary sinus as a reference point.

This study aimed to investigate the reference point for the downward displacement of the posterior and anterior leaflets of the tricuspid valve using echocardiography in children with Ebstein's anomaly. This study enrolled 25 patients with Ebstein's anomaly. The extent of downward displacement of the posterior and anterior leaflets of the tricuspid valve was evaluated by echocardiography using the tricuspid annulus and the coronary sinus as reference points. These results were compared with the surgical findings. The findings showed displacement of the simple septal leaflet in 1 patient, displacement of both the septal and posterior leaflets in 22 patients, displacement of both the anterior and posterior leaflets in 1 patient, and displacement of all the leaflets in 1 patient. Because the septal and posterior leaflets were close to the apex or because the posterior leaflet was nearly absent, the displacement distance of the septal and posterior leaflets could not be measured accurately in two patients. The displacement distance of the septal and posterior leaflets in the remaining 22 patients were 2.08 ± 1.15 and 2.58 ± 1.06 cm, respectively. The displacement distances of the anterior leaflet in two patients were respectively 1.0 and 2.2 cm. These results were similar to those measured during surgery. The direction of the valvular regurgitation flow was anterolateral in the apical four-chamber and apical right heart two-chamber views in patients with the downward displacement of the anterior leaflet. The tricuspid valve annulus and the coronary sinus are ideal reference points for evaluating the downward displacement of the posterior and anterior leaflets of the tricuspid valve. It is critical to evaluate the downward displacement of the anterior leaflet that the direction of the tricuspid regurgitation flow is changed.

Cardioprotection of H2S by downregulating iNOS and upregulating HO-1 expression in mice with CVB3-induced myocarditis.

AIMS: To explore the effects and potential mechanisms of hydrogen sulfide (H2S) in CVB3-induced mice with myocarditis. MAIN METHODS: A total of 75 six-week-old inbred male Balb/c mice were divided randomly into four groups (N, C, P and S). Group N was the negative control. The others were inoculated intraperitoneally (i.p.) with CVB3. Subsequently, groups P and S were injected i.p. once a day with DL-Proparglygylcine (PAG) and NaHS respectively. Group C was the positive control. Inducible nitric oxide synthase (iNOS) and heme oxygenase-1(HO-1) expression on cardiac tissues were evaluated by histopathological examination, immunohistochemistry, RT-PCR and Western blot. KEY FINDINGS: The heart-weight to body-weight (HW/BW) ratio, the histologic scores and the iNOS mRNA and protein expression levels were higher, and the HO-1 mRNA and protein expression levels were lower in mice treated with PAG than those mice solely inoculated with CVB3. Mice in group S had a significant decreased in the HW/BW ratio, the histologic scores and the iNOS mRNA and protein expression levels, and had a significant increased in the HO-1 mRNA and protein expression levels compared to the mice in group C. H2S can attenuate inflammatory cell infiltration, alleviate cardiac edema, and limit myocardial lesions. SIGNIFICANCE: Our data support that H2S can inhibit iNOS overexpression and induce HO-1 expression, both of which contribute to the cardioprotection of H2S in CVB3-induced mice myocarditis.

High frequency of activated natural killer and natural killer T-cells in patients with new onset of type 2 diabetes mellitus.

Chronic low-grade inflammation is crucial for the development of insulin resistance and type 2 diabetes mellitus (T2DM), and immunocompetent cells, such as T-cells, B-cells, mast cells and macrophages, regulate the pathogenesis of T2DM. However, little is known about the role of natural killer (NK) and natural killer T (NKT) cells in the pathogenic process of T2DM. A total of 16 patients with new onset T2DM and nine healthy subjects were recruited, and the frequency of peripheral blood activated and inhibitory NK and NKT cells in individual subjects was determined by flow cytometry. The frequency of spontaneous and inducible interferon gamma (IFN-γ) and CD107a(+) NK cells was further examined, and the potential association of the frequency of NK cells with clinical measures was analyzed. While there was no significant difference in the frequency of peripheral blood NK and NKT cells between patients and controls, the frequency of NKG2D(+) NK and NKT cells in patients was significantly higher than those in the controls (P = 0.011). In contrast, the frequency of NKG2A(+) and KIR2DL3(+) inhibitory NK and NKT cells in patients was significantly lower than those in the controls (P = 0.002, P < 0.0001, respectively). Furthermore, the frequencies of NKG2D(+) NK cells were correlated significantly with the values of body mass index in patients. Moreover, the frequencies of spontaneous and inducible CD107a(+), but not IFN-γ-secreting, NK cells in patients were significantly higher than those in the controls (P < 0.004, P < 0.0001). Our data indicated that a higher frequency of activated NK cells may participate in the obesity-related chronic inflammation involved in the pathogenesis of T2DM.