The Impact of Mitral Stenosis on Left Atrial Function Assessed by Two‐Dimensional Speckle Tracking Echocardiography

Aims: The aim of this study is to investigate the effect of mitral stenosis (MS) on left atrial (LA) function using two‐dimensional speckle tracking echocardiography (2DSTE). Methods and Results: The study subjects consisted of 52 patients with asymptomatic MS and 52 control subjects. LA function was assessed using prototype speckle tracking software and manual tracking method. Maximal LA volume (LAVmax) and minimal LA volume (LAVmin) and LA volume before atrial contraction (LAVpre‐a) were measured. Using these volumes, LA reservoir, conduit and booster pump fuction parameters were calculated. Indexed LAVmax, LAVmin, and LAVpre‐a measurements via speckle tracking were highly correlated with manual tracing methods in both groups. Expansion index (67.8 ± 36.4 vs. 148.3 ± 44.2), diastolic emptying index (37.7 ± 12.9 vs. 58.0 ± 8.5), passive emptying (37.3 ± 14.1 vs. 70.4 ± 10.4) and passive emptying index (13.3 ± 6.3 vs. 41.3 ± 10.6) were decreased significantly in MS patients (P < 0.001). In contrast active emptying index (62.6 ± 4.1 vs. 29.5 ± 10.1) increased in MS group (P < 0.001) while active emptying (28.1 ± 13.0 vs. 28.3 ± 6.9) remained same among both groups. Conclusions: This is the first study relating LA volumes and function assessed by 2DSTE to MS. 2D speckle tracking analysis of LA volume is relatively easy and provides more detailed information regarding the changes in LA volumes during the cardiac cycle.     

Effect of topically applied charged particles on healing of colonic anastomoses

HYPOTHESIS: Various forms of electrical stimulation can improve wound healing in different tissues, but their application to gastrointestinal tract healing has not been investigated. We assumed that positively charged diethylaminoethyl cross-linked dextran bead (diethylaminoethyl Sephadex [DEAE-S]) particles would have a beneficial effect on the healing of colonic anastomoses. DESIGN: Experimental animal study. SETTING: Animal research laboratory of a university hospital. ANIMALS: Forty female Wistar albino rats. INTERVENTIONS: Right colonic transection and anastomosis was performed in 5 animal groups. The control group received no treatment; the placebo group, methylcellulose gel; and the DEAE-S group, DEAE-S in methyl cellulose gel applied topically around the anastomoses. The fecal peritonitis (FP) group underwent cecal ligation and perforation simultaneously with the anastomosis to cause FP; the FP + DEAE-S group also received DEAE-S applied around the anastomoses. MAIN OUTCOME MEASURES: After the completion of postoperative day 4, all rats were killed. Anastomotic bursting pressures and hydroxyproline concentrations in perianastomotic tissue were measured and compared. RESULTS: Mean bursting pressures were 115.1 mm Hg in the control group, 113.6 mm Hg in the placebo group, 159.4 mm Hg in the DEAE-S group, 62.8 mm Hg in the FP group, and 121.1 mm Hg in the FP + DEAE-S group (P =.001, 1-way analysis of variance [ANOVA]). The differences between the control vs DEAE-S groups, placebo vs DEAE-S groups, and FP vs FP + DEAE-S groups were significant (P<.05, t test). Mean hydroxyproline concentrations were 5.2 microg/mg in the control group, 4.9 microg/mg in the placebo group, 5.6 microg/mg in the DEAE-S group, 4.5 microg/mg in the FP group, and 5.4 microg/mg in the FP + DEAE-S group (P =.09, 1-way ANOVA). The difference between the FP and FP + DEAE-S groups was significant (P =.04, t test). CONCLUSIONS: A positively charged particle, DEAE-S, improves healing of colonic anastomoses in healthy rats and in rats with FP. This inexpensive, nontoxic material is easily applied and deserves further evaluation in gastrointestinal tract healing.     

Treatment modalities and outcome of the renal victims of the Marmara earthquake

BACKGROUND/AIMS: Circulating CD14+CD16+ monocytes, a potent phagocytosing and antigen-presenting monocyte population, have been reported to be expanded in patients on hemodialysis (HD). In this study, changes in the population of CD14+CD16+ monocytes were analyzed during a single session of HD therapy, and the influence of dialyzer membrane materials on these monocytes was investigated. METHODS: Nine patients were hemodialyzed using regenerated cellulose (RC) membranes and thereafter polysulfone (PS) membranes. Peripheral blood cells were taken from these subjects, and these cells were stained with anti-CD14 and anti-CD16 antibodies. The percentages of CD14- and CD16-expressing monocytes were analyzed by two-color flow cytometric analysis. Moreover, the serum soluble CD14 (sCD14) levels were measured with an ELISA kit. RESULTS: It was found that CD14+CD16+ monocytes before HD were significantly increased in patients on HD as compared to healthy controls. In the RC group, CD14+CD16+ monocytes were decreased at both 30 and 240 min after the initiation of HD. The reduction rate of CD14+CD16+ monocytes in the RC group was higher than that in the PS group. There was no significant difference in sCD14 levels between the two groups. CONCLUSION: Monocytes are activated in patients on HD. Furthermore, the population of CD14+CD16+ monocytes was stimulated to a greater extent during HD in the RC group than in the PS group. The significant reduction in CD14+CD16+ monocytes by RC membranes indicated that the level of CD14+CD16+ monocytes is a sensitive marker for the biocompatibility of HD membranes.     

Surgical treatment of intrathoracic hydatid disease: A 5-year experience in an endemic region

Purpose  

To present our recent surgical experience in treating patients with intrathoracic hydatidosis.     

Neuroprotective effects of alpha-lipoic acid in experimental spinal cord injury in rats

Background:

Oxidative stress is a mediator of secondary injury to the spinal cord following trauma.

Objective:

To investigate the putative neuroprotective effect of α-lipoic acid (LA), a powerful antioxidant, in a rat model of spinal cord injury (SCI).

Methods:

Wistar albino rats were divided as control, vehicle-treated SCI, and LA-treated SCI groups. To induce SCI, a standard weight-drop method that induced a moderately severe injury (100 g/cm force) at T10 was used. Injured animals were given either 50 mg/kg LA or saline at 30 minutes postinjury by intraperitoneal injection. At 7 days postinjury, neurologic examination was performed, and rats were decapitated. Spinal cord samples were taken for histologic examination or determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and DNA fragmentation. Formation of reactive oxygen species in spinal cord tissue samples was monitored by using a chemiluminescence (CL) technique.

Results:

SCI caused a significant decrease in spinal cord GSH content, which was accompanied with significant increases in luminol CL and MDA levels, MPO activity, and DNA damage. Furthermore, LA treatment reversed all these biochemical parameters as well as SCI-induced histopathologic alterations. Conversely, impairment of the neurologic function caused by SCI remained unchanged.

Conclusion:

The present study suggests that LA reduces SCI-induced oxidative stress and exerts neuroprotection by inhibiting lipid peroxidation, glutathione depletion, and DNA fragmentation.     

Loss of primary cilia upregulates renal hypertrophic signaling and promotes cystogenesis

Primary cilia dysfunction alters renal tubular cell proliferation and differentiation and associates with accelerated cyst formation in polycystic kidney disease. However, the mechanism leading from primary ciliary dysfunction to renal cyst formation is unknown. We hypothesize that primary cilia prevent renal cyst formation by suppressing pathologic tubular cell hypertrophy and proliferation. Unilateral nephrectomy initiates tubular cell hypertrophy and proliferation in the contralateral kidney and provides a tool to examine primary cilia regulation of renal hypertrophy. Conditional knockout of the primary cilia ift88 gene leads to delayed, adult-onset renal cystic disease, which provides a window of opportunity to conduct unilateral nephrectomy and examine downstream kinetics of renal hypertrophy and cyst formation. In wild-type animals, unilateral nephrectomy activated the mTOR pathway and produced appropriate structural and functional hypertrophy without renal cyst formation. However, in ift88 conditional knockout animals, unilateral nephrectomy triggered increased renal hypertrophy and accelerated renal cyst formation, leading to renal dysfunction. mTOR signaling also increased compared with wild-type animals, suggesting a mechanistic cascade starting with primary ciliary dysfunction, leading to excessive mTOR signaling and renal hypertrophic signaling and culminating in cyst formation. These data suggest that events initiating hypertrophic signaling, such as structural or functional loss of renal mass, may accelerate progression of adult polycystic kidney disease toward end-stage renal disease.