Effects of diode low-level laser therapy on healing of tooth extraction sockets: a histopathological study in diabetic rats

Lasers in Medical Science - Diabetes mellitus is mostly interrelated to deficiency in wound healing. Low-level laser therapy has been shown to exert reliable effects on the acceleration of wound...     

Toll-like receptor-2 mediates systemic inflammation in gentamicin-induced rat nephrotoxicity

Gentamicin is an aminoglycoside antibiotic commonly administrated to patients with Gram-negative infections. Gentamicin induced nephrotoxicity by functional and structural impairment. Toll-like receptors (TLRs) as key mediators in the innate and adaptive immune system response involved in gentamicin-induced nephrotoxicity. The present study aimed to investigate the gene expression of TLR2 and pro-inflammatory cytokines in the renal tissues and buffy coat of the whole blood in gentamicin-treated rats. Twenty adult male Sprague Dawley rats weighing 180–200 were randomly divided into gentamicin (100 mg/kg, i.p) and control groups (n = 10). After 10 days, the serum creatinine (Cr) levels and blood urea nitrogen (BUN) were measured. The mRNA levels of TLR2, tumour necrosis factor (TNF)-α, interleukin (IL)-1β, and monocyte chemoattractant peptide (MCP)-1 were investigated in the renal tissue and buffy coat by qRT-PCR. Kidney histological analysis performed by hematoxylin-eosin (H&E) staining. Functional disturbance is characterized by a significant increase in the serum levels of Cr and BUN in the gentamicin group. Renal tissue slides of the gentamicin group indicated severe glomerular and tubular damage including lobulation of the glomerular tuft, Bowman's space enlargement, acute tubular necrosis, and proximal tubular destruction. The mRNA levels of IL-1β, TNF-α, MCP-1, and TLR2 increased in the buffy coat, but all of them except TLR2 decreased in the renal tissues in the gentamicin group compared with controls. Gentamicin administration induced relative systemic inflammation, which may be related to an increase in the mRNA levels of TLR2 results in gene expression of pro-inflammatory chemokines and cytokines including IL-1β, TNF-α, and MCP-1 in immune cells.     

A comparison of sodium bicarbonate infusion versus normal saline infusion and its combination with oral acetazolamide for prevention of contrast-induced nephropathy: a randomized, double-blind trial

Background  Contrast-induced nephropathy (CIN) is commonly encountered. Because the therapy of choice for prevention of CIN is controversial, in this study we compared the preventive efficacy of bicarbonate (Bi) infusion in dextrose water versus normal saline (NLS) infusion alone or in combination with oral acetazolamide (AZ). Methods  In a double-blind and randomized clinical trial, all patients undergoing coronary angiography or percutaneous coronary intervention received NLS (NLS group), its combination with AZ (AZ group) or infusion of Bi (Bi group) before the procedures. RIFLE (risk of renal failure, injury to the kidney, failure of kidney function, loss of kidney function, and end-stage renal disease) criteria were used to define CIN-associated acute kidney injury (AKI). Results  The risk of AKI in CIN was significantly lower in the Bi and AZ groups than in the NLS group (P ≤ 0.04). Comparing pre-treatment and post-treatment values in each group the following results were obtained: serum creatinine (Scr) increased and eGFR decreased significantly in the NLS group (P = 0.04) and in all patients (P = 0.001, P = 0.02, respectively). In addition, serum potassium decreased significantly in the Bi and NLS groups (P ≤ 0.02). Also, serum Bi increased significantly in the Bi group (P = 0.001) whereas it decreased significantly in the AZ group (P = 0.001). Urinary pH also increased in all groups (P ≤ 0.04) except the NLS group (P > 0.05). Conclusions  It seems that both Bi and AZ reduce the risk of CIN-related AKI, and close monitoring of serum potassium is needed during bicarbonate infusion.     

The preventive effect of pentoxifylline on contrast-induced nephropathy: a randomized clinical trial

Background

Percutaneous coronary intervention provides a high-risk condition for incidence of CIN even in patients with normal renal function. Pentoxifylline (PTX) with a variety of mechanisms may prevent CIN.

Materials and methods

Between April 5, 2011, and February 20, 2012, all consecutive eligible patients referred for elective percutaneous coronary intervention were asked to participate in the study (n = 199). Eligibility was defined as the age between 18 and 65 years and baseline serum creatinine ≤132.6 μmol/l (1.5 mg/dl). The patients were randomly allocated to two groups either receiving saline or saline plus pentoxifylline 400 mg orally three times a day for 48 h. Serum creatinine was measured 24 h prior to the procedure and 48 h thereafter. The primary endpoint was occurrence of CIN defined as 25 % rise in serum creatinine 48 h after the procedure.

Results

The overall incidence of CIN was 6 % in this study (6.2 % in the PTX group versus 5.9 % in the hydration group, P = 0.92). Absolute rise in serum creatinine was not also significantly different between the two groups (P = 0.97). In hypertensive patients, however, the incidence of CIN was lower among those receiving PTX: 5 % in the PTX group versus 8.7 % in the hydration group. Nevertheless, this difference was not statistically significant (P = 0.68).

Conclusion

Short-term prophylaxis with pentoxifylline added to optimal hydration does not seem to reduce the risk of CIN in patients with normal renal function undergoing PCI. Further clinical trials in patients with renal impairment are warranted to define its role.     

Laboratory effect of HBV infection in kidney transplant recipients and donors

Background

Viral infections are the most common cause of opportunistic infections after kidney transplantation. Among hepatotropic viruses that induce kidney graft failure and rejection, hepatitis B virus (HBV) has an important and critical role. Extrahepatic HBV-related disorders increase morbidity and mortality in kidney transplant recipients.

Objective

To analyze the molecular prevalence of HBV infection in kidney transplant recipients and donors before and after transplantation.

Patients and Methods

This cross-sectional study included 273 serum samples collected between 2005 and 2008 in 96 kidney transplant recipients and 59 donors. Detection of HBV DNA was via amplification of the S gene fragment of HBV genome using a qualitative simple polymerase chain reaction assay. Also analyzed were statistical relationships between HBV infection and laboratory and clinical demographic data in all kidney transplant donors and recipients.

Results

The HBV genome was detected in 102 of 273 serum samples. Molecular HBVinfection was demonstrated in 2 of 13 serum samples (15.4%) from recipients testedbefore transplantation. HBV DNA was detected in 42 of 96 patients (43.7%) after kidneytransplantation. The HBV genome was demonstrated in 21 of 59 donors (35.6%).Significant relationships were observed between HBV infections and hematologic andbiochemical indices after kidney transplantation.

Conclusion

Detection of a high molecular prevalence of HBV infection in kidneyrecipients enforces the importance of HBV infection in clinical outcome.