Disturbances of Haemostasis in Diabetes Mellitus

Diabetes mellitus is associated with disturbances in haemostasis that could contribute to the development of thrombotic complications.The present study was undertaken to determine the behavior of coagulation variables and fibrinolytic system in diabetes mellitus. Forty five diabetic patients and forty five matched controls were evaluated by doing the following haemostatic parameter, prothrombin time, partial thromboplastin time, thrombin time, coagulation factors assay II, VII, IX, & plasma fibrinogen, ADP-induced platelet aggregation, protein C, a₂- antiplasmin, PAI and FDPs. Generally diabetic patients have high levels of fibrinogen, a₂- antiplasmin, & PAI and lower level of protein C. Other haemostatic parameters did not show statistically significant difference between diabetic patients and control group. Significantally elevated levels of PAI, a₂- antiplasmin together with low protein C level in diabetic patients may result in the disturbance of haemostatic balance favoring thrombotic events. Conclusion: High levels of plasma fibrinogen, a₂A- antiplasmin with low plasma protein C activity could lead to a prothrombotic tendency in insulin dependent diabetic patients. Moreover, in non-insulin dependent diabetic patients, the above mentioned parameters together with high levels of ADP-induced platelet aggregation and plasminogen activator inhibitor may increase the risk of thrombotic complications. Obesity can be considered as an additional risk factor for development of thrombosis in diabetic patients.     

Superior quality chemically reduced graphene oxide for high performance EMI shielding materials

The chemical reduction process of graphene oxide combined with a mild and controllable thermal treatment under vacuum at 200 °C for 4 hours provided a cost-effective, scalable, and high-yield route for Reduced Graphene Oxide (RGO) industrial production and became a potential candidate for producing electromagnetic interference (EMI) shielding. We investigated graphite, and RGO using l-ascorbic acid and Sodium borohydride before and after thermal treatment by carefully evaluating the chemical and morphological structures. The thermally treated l-ascorbic Acid reduction route (TCRGOL) conductivity was 2.14 × 10³ S m⁻¹ and total shielding efficiency (SET) based on mass loadings per area of shielding was 94 dB with about one-tenth less graphite weight and surpassing other graphene reduction mechanisms in the frequency range of 8.2–12.4 GHz, i.e., X-band, at room temperature while being tested using the waveguide line technique. The developed treatment represents valuable progress in the path to chemical reduction using a safe reducing agent and offering superior quality RGO rarely achieved with the top-down technique, providing a high EMI shielding performance.

The developed two-step protocol offers a superior reduced graphene oxide TCRGOL quality (7 layers), and its SET was 94 dB over the X-band.     

Role of inducible nitric oxide synthase in induction of RhoA expression in hearts from diabetic rats

AIMS: Recent studies from our laboratory demonstrated that increased expression of the small GTP-binding protein RhoA and activation of the RhoA/rho kinase (ROCK) pathway play an important role in the contractile dysfunction associated with diabetic cardiomyopathy in hearts from streptozotocin (STZ)-induced diabetic rats. Nitric oxide (NO) has been reported to be a positive regulator of RhoA expression in vascular smooth muscle, and we have previously found that the expression of inducible NO synthase (iNOS) is increased in hearts from STZ-diabetic rats. Therefore, in this study, we investigated the hypothesis that induction of iNOS positively regulates RhoA expression in diabetic rat hearts. METHODS AND RESULTS: To determine whether NO and iNOS could increase RhoA expression in the heart, cardiomyocytes from non-diabetic rats were cultured in the presence of the NO donor sodium nitroprusside (SNP) or lipopolysaccharide (LPS) in the absence and presence of the selective iNOS inhibitor, N(6)-(1-iminoethyl)-l-lysine dihydrochloride (L-NIL). In a second study, 1 week after induction of diabetes with STZ, rats were treated with L-NIL (3 mg/kg/day) for 8 more weeks to determine the effect of iNOS inhibition in vivo on RhoA expression and cardiac contractile function. Expression of iNOS was elevated in cardiomyocytes isolated from diabetic rat hearts. Both SNP and LPS increased RhoA expression in non-diabetic cardiomyocytes. The LPS-induced elevation in RhoA expression was accompanied by an increase in iNOS expression and prevented by L-NIL. Treatment of diabetic rats with L-NIL led to a significant improvement in left ventricular developed pressure and rates of contraction and relaxation concomitant with normalization of total cardiac nitrite levels, RhoA expression, and phosphorylation of the ROCK targets LIM (Lin-11, Isl-1, Mec-3) kinase and ezrin/radixin/moesin. CONCLUSION: These data suggest that iNOS is involved in the increased expression of RhoA in diabetic hearts and that one of the mechanisms by which iNOS inhibition improves cardiac function is by preventing the upregulation of RhoA and its availability for activation.     

Kawasaki disease with Glucose-6-Phosphate Dehydrogenase deficiency,case report

Kawasaki disease (KD) is an acute, self-limited vasculitis of unknown etiology that occurs predominantly in infants and children younger than 5 years of age. Coronary artery abnormalities are the most serious complication.Based on the literatures infusion of Intravenous Immunoglobulin of 2 g/kg and a high dose of oral aspirin up to 100 mg/kg/day are the standard treatment for Kawasaki disease in the acute stage, and should be followed by antiplatelet dose of aspirin for thrombocytosis. Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is an inherited X-linked hereditary disorder, and aspirin can induce hemolysis in patients with G6PD deficiency. We report a case of a 5 year and 8 month old male with KD and G6PD deficiency.     

New Innovations in the Treatment of PJI and Biofilms—Clinical and Preclinical Topics

Purpose of Review

Periprosthetic joint infection (PJI) is a devastating complication after total joint replacement. A main source for antibiotic tolerance and treatment failure is bacterial production of biofilm—a resilient barrier against antibiotics, immune system, and mechanical debridement. The purpose of this review is to explore some novel approaches to treat PJI and biofilm-related infections.

Recent Findings

Innovative treatment strategies of bacterial and biofilm infections revolve around (a) augmenting current therapies, such as improving the delivery and efficiency of conventional antibiotics and enhancing the efficacy of antiseptics and (b) administrating completely new therapeutic modalities, such as using immunotherapy, nanoparticles, lytic bacteriophages, photodynamic therapy, novel antibiotics, and antimicrobial peptides.

Summary

Several promising treatment strategies for PJI are available to be tested further. The next requirement for most of the novel treatments is reproducing their effects in clinically representative animal models of PJI against clinical isolates of relevant bacteria.

     

Tumor necrosis factor-alpha and neuropsychiatric lupus erythematosus: relation to single photon emission computed tomography findings

This study was designed to highlight the relation of tumor necrosis factor- (TNF-) to neuropsychiatric lupus (NPLE) manifestations. The relation of TNF- to the type of single photon emission computed tomography (SPECT) findings in this context was also studied. Twenty-one systemic lupus erythematosus (SLE) females, mean age 27.57 ± 9.89 years, and twenty age-matched normal females (controls), were subjected to TNF- assessment. Different clinical and neuropsychiatric manifestations were evaluated. SPECT was carried out for all patients. The results showed that the mean TNF- level (pg/ml) was significantly raised in patients compared with controls (167.8 ± 102.5 versus 64 ± 50.2, respectively, P 0.005). Thirteen patients (69.1%) had NPLE manifestations. NPLE patients had a significantly higher mean TNF- than patients without NPLE (203 ± 102.8 versus 109 ± 47.3, respectively, P 0.03). Positive SPECT findings were found in 18 lupus patients (85.7%), including all 13 patients with NPLE (100% sensitivity), with a multiple focal pattern of hypoperfusion being the most frequent type (9/13), followed by diffuse (3/13), and then single focal pattern (1/13). The mean TNF- was significantly higher in patients with multiple focal pattern (P 0.001). In conclusion, results of this work support the hypothesis that TNF- could be involved in the pathogenesis of NPLE, and hence, it could be speculated that the evolving anti-TNF therapy can play a potential role in the management of this disease.