Biological evaluation of a new pulp capping material developed from Portland cement

This study evaluates the biological properties of a new pulp capping material developed from Portland cement. This study was conducted on 48 teeth in 4 dogs (12 teeth/dog). The dogs were classified into two equal groups (n = 24 teeth) according to the evaluation period including: group A (3 weeks) and group B (3 months). Each group was further subdivided into three equal subgroups (n = 8 teeth) according to the capping material including: subgroup 1: mineral trioxide aggregate (MTA), subgroup2: Portland cement + 10% calcium hydroxide + 20% bismuth oxide (Port Cal) and subgroup 3: Portland cement + bismuth oxide. After general anesthesia, a class V buccal cavity was prepared coronal to the gingival margin. After pulp exposure and hemostasis,the capping materials and glass ionomer filling were placed on the exposure sites. All histopathological findings, inflammatory cell count and dentin bridge formation were recorded. Data were analyzed statistically. After 3 months, the histopathological picture of the pulp in subgroup 1 showed normal pulp, continuous odontoblastic layer and complete dentin bridge formation while subgroup 2 showed partial and complete dentin bridge over a normal and necrotic pulps. Subgroup 3 showed loss of normal architecture, areas of necrosis, complete, or incomplete dentin bridge formation, attached and detached pulp stones and fatty degeneration in group B. For group A, MTA subgroup showed the least number of inflammatory cell infiltrate followed by Port Cal subgroup. While subgroup 3 showed the highest number of inflammatory cell infiltrate. For group B, the mean inflammatory cell count increased with the three tested materials with no statistical difference. Regarding dentin bridge formation at group A, no significant differences was found between subgroups, while at group B, MTA subgroup exhibited significantly higher scores than other subgroups. In conclusion, addition of calcium hydroxide to Portland cement improves the dentin bridge formation qualitatively and quantitatively.     

High Grade Gynecomastia: Surgical Correction and Potential Impact on Erectile Function

IntroductionGynecomastia denotes benign enlargement of the male breast. It is a common belief that gynecomastia is stigmatizing and may frequently cause social embarrassment and psychological stress. It is possible that this may reflect on erectile function of the afflicted. High grade gynecomastia requires radical breast tissue excision and skin reduction ending up in aesthetically unappealing scars.AimThe purpose of this study is to evaluate the reduction mammaplasty using no vertical scar technique in males with high grade gynecomastia; as regards technical refinements and outcome in the hope of providing a cosmetically appealing solution to this condition. This study also reports on the effect of high grade gynecomastia on erectile function, as well as the effect of surgery.MethodsFifteen male patients with gynecomastia underwent breast reduction using the “no vertical scar reduction mammaplasty.” Erectile function was evaluated before and after surgery.Main Outcome MeasuresSurgical outcome and erectile function.ResultsAll patients but one were satisfied with the outcome. Complications were minimal and manageable. Eleven out of 15 patients had a preoperative International Index of Erectile Function (IIEF) score less than 20 denoting erectile dysfunction. All but one (n = 10) showed improvement in their IIEF score following surgery. The difference between pre-operative IIEF (average 17.8) and postoperative (average 23.5) was statistically significant.ConclusionsThe “no vertical scar reduction mammaplasty” is a reliable technique in cases with gynecomastia and significant ptosis. It has the added benefits of avoiding the vertical scar, hiding the transverse scar in the shadow of the inferior aspect of the breast, with minimal complications. Gynecomastia as a condition causing a feminized outlook may have a negative impact on self confidence and body image. We suggest that this may have a potential negative effect on erectile function, that can be improved by adequate surgical correction. El Noamani S, Thabet AM, Enab AA, Shaeer O, and El-Sadat A. High grade gynecomastia: Surgical correction and potential impact on erectile function.     

Stent design favorably influences the vascular response in normal porcine coronary arteries

OBJECTIVES: The purpose of this study was to compare the arterial response following implantation of a stainless-steel, balloon-expandable, tubular slotted stent with that of a novel computer-designed, multi-cellular stent in normal porcine coronary arteries. BACKGROUND: Intracoronary stent placement has evolved into the primary strategy for percutaneous revascularization of symptomatic coronary arterial lesions. Presently there is intense interest in developing new stent designs to improve stent delivery and biocompatability. METHODS: Computer-assisted design was utilized to develop a balloon-expandable stent with symmetric expansion properties, uniform arterial wall coverage, longitudinal flexibility and radial strength. Quantitative coronary angiography and histological assessment of the stented arteries was used to evaluate the acute and chronic vascular responses to a stainless-steel, balloon-expandable, tubular slotted stent as compared to the computer-designed BX stent in the normolipemic swine. RESULTS: Forty stents (24 BX, 16 tubular slotted) were implanted in 19 miniature swine at a mean inflation pressure of 9 atm using identical delivery systems. Eight of the BX and none of the tubular slotted stents were post-dilated with a non-compliant balloon at 12-14 atm. The mean stent-to-artery ratio was similar for the BX (1.03 +/- 0.06) and tubular slotted (1.04 +/- 0.11; p = 0.59) designs. Protrusion or asymmetric radial flaring of a strut at the stent margin was present in 1 of 23 BX stents (4.3%) and 10 of 15 tubular slotted stents (66.7%; p < 0.0001). The mean arterial injury score was significantly less for the BX stent (0.2 +/- 0.2) as compared with the tubular slotted stents (0.4 +/- 0.4; p = 0.025). At 3 days, thrombus area was similar for the BX and tubular slotted designs (0.42 +/- 0.16 mm2 versus 0.44 +/- 0.18 mm2, respectively; p = 0.88). The mean neointimal area was significantly less for the BX at 2 months (1.09 +/- 0.25 mm2 versus 2.93 +/- 2.26 mm2 in the tubular slotted stent) and at 6 months (1.10 +/- 0.26 mm2 versus 2.07 +/- 0.65 mm2 in the tubular slotted stent; p = 0.01), resulting in approximately 50% less in-stent stenosis. CONCLUSIONS: The arterial response to a balloon-expandable stent can be favorably influenced by computer-assisted modification of design in an experimental model. Further study is warranted to determine the impact of stent design upon clinical in-stent restenosis.     

Histologic,ultrastructural, and enzymatic measurements of infarct size following coronary artery stenosis and occlusion

Coronary artery narrowing (CAN), which reduced resting coronary blood flow (BF) by 50%, was induced in 10 conscious dogs and was maintained for 4 hours. Five additional dogs (group 1) with complete coronary artery occlusion were compared to the dogs with CAN. serum isoenzymes of creatine phosphokinase (CK) and latate dehydrogenase (LD) were monitored hourly in all groups. After 36 hours, samples were obtained for regional myocardial BF, quantitative histology, and quantitative ultrastructural (EM) morphology. Six dogs with CAN had small infarcts (MI) of less than 1 gm and persistent myocardial cell injury (group 2). The other four dogs with CAN had only persistent myocardial cell injury by ultrastructural criteria (group 3). Peak serum CK activities in groups 2 and 3 were similar, as were MI sizes calculated from serum CK and myocardial depletion. MB CK was of diagnostic value in group 1 but not in groups 2 and 3. The ratio of $\text{LD}\text{1}\text{LD 2}$ had diagnostic value in all three groups. MI size by enzyme estimates was consistently higher than planimetered MI size at autopsy in both groups 1 and 2. All three groups had significant amounts of ultrastructural damage outside of histologically demonstrated MI. These findings suggest that (1) gross and histologic MI size determination of 36 hours after ischemia underestimate extent of damage, and (2) ultrastructural cell changes cause significant release of CK and LD in coronary disease (CAD).     

Linear growth in relation to the circulating concentrations of insulin-like growth factor I, parathyroid hormone, and 25-hydroxy vitamin D in children with nutritional rickets before and after treatment: endocrine adaptation to vitamin D deficiency

The objective of the study was to determine the degree of linear growth retardation of patients with vitamin D deficiency rickets at presentation and the magnitude of catch-up growth in relation to their calcium (Ca) homeostasis and hormones affecting it before and after treatment. This prospective study recorded the anthropometric data and measured the circulating 25-hydroxy vitamin D (25-OH-D), insulin-like growth factor I (IGF-I), parathyroid hormone, Ca, phosphate, and alkaline phosphatase concentrations in 46 infants and children with nutritional (vitamin D deficiency) rickets before and 6 months or more after treatment with one intramuscular injection of vitamin D3 megadose (300000 IU). Forty normal age- and sex-matched children were included as controls for the auxological data. At presentation, patients' mean age = 13.1 +/- 1.1 months, length standard deviation scores (LSDS) = -1.5 +/- 0.2, and body mass index = 16.3 +/- 0.85. They were significantly shorter and had markedly lower growth velocity standard deviation scores (GVSDS) compared with normal controls (LSDS = 0.25 +/- 0.18 and 0.31 +/- 0.22, respectively). Six months after treatment, the LSDS increased significantly in patients to -0.45 +/- 0.13, with a significantly increased GVSDS (2.76 +/- 0.45) and body mass index (16.9 +/- 0.65). They were still shorter but with significantly higher GVSDS compared with normal controls. Serum Ca and phosphate concentrations increased from 2.07 +/- 0.25 and 1.23 +/- 0.24 mmol/L, respectively, before treatment to 2.44 +/- 0.2 and 1.94 +/- 0.2 mmol/L, respectively, after treatment. Serum alkaline phosphatase and parathyroid hormone concentrations decreased from 1183 +/- 219 U/L and 294 +/- 87 pg/mL, respectively, before treatment to 334 +/- 75 U/L and 35.2 +/- 15.2 pg/mL, respectively, after treatment. The 25-OH-D level increased from 4.5 +/- 0.56 ng/mL before treatment to 44.5 +/- 3.7 ng/mL after treatment. Circulating concentrations of IGF-I increased significantly after treatment (52.2 +/- 18.9 ng/mL) vs before treatment (26.6 +/- 12.8 ng/mL). The 25-OH-D concentrations were correlated significantly with the IGF-I levels before and after treatment (r = 0.603 and r = 0.59, respectively; P < .001). The GVSDS after treatment was correlated with the increase of IGF-I and 25-OH-D levels (r = 0.325 and r= 0.314, respectively; P < .01). These data denote that the accelerated linear growth after treatment of nutritional vitamin D deficiency is mediated through activation of the growth hormone/IGF-I system and suggests an important role of vitamin D as a link between the proliferating cartilage cells of the growth plate and growth hormone/IGF-I secretion. Three different sequential stages of vitamin D deficiency can be recognized according to the clinical/radiological, biochemical, and hormonal data of patients at presentation.     

Effect of smoking status on mortality and morbidity following coronary artery bypass surgery

BACKGROUND: We aimed to examine the effect of smoking on outcomes following coronary artery bypass grafting (CABG). METHODS: We retrospectively analysed 6 367 consecutive patients who underwent CABG between April 1997 and March 2003. Logistic regression was used to risk adjust in-hospital outcomes, while Cox proportional hazards analysis was used to risk adjust Kaplan-Meier survival curves. Outcomes were adjusted for variables suggested by the American Heart Association and American College of Cardiology. RESULTS: 947 (14.9 %) patients were current smokers (smoking within 1 month of surgery), while 3857 (60.6 %) were ex-smokers and 1 563 (24.5 %) were non-smokers. After adjusting for differences in case-mix, current smokers were more likely to develop chest infections ( p < 0.001), atelectasis ( p < 0.001), and require ventilation longer than 48 hours ( p = 0.003). Current smokers were also more likely to stay in intensive care for more than 3 days ( p < 0.001). Ex-smokers were not associated with excess mortality ( p = 0.11), while current smokers had significantly increased mortality during follow-up ( p = 0.029). CONCLUSIONS: Patients should be encouraged to stop smoking to maximise the long-term benefits of CABG.     

Short-term intravenous eptifibatide infusion combined with reduced dose recombinant tissue plasminogen activator inhibits platelet recruitment at sites of coronary artery injury

OBJECTIVES: This study was designed to determine in a dog model of coronary thrombosis whether short-term eptifibatide (Ep) combined with low-dose plasminogen activator (rt-PA) inhibits platelet recruitment at sites of endothelial damage after normalization of platelet function. BACKGROUND: Ep plus reduced-dose rt-PA has not previously been shown to render a recanalized coronary artery resistant to platelet recruitment after normalization of platelet function. METHOD: Inhibition of platelet recruitment was studied by scanning electron microscopy (SEM) in a canine model of left anterior descending (LAD) thrombosis. In phase I treatment groups were: 1) Ep (n = 6); 2) Ep + rt-PA (n = 6); 3) rt-PA (n = 6); and 4) placebo (n = 4). Coronary blood flow was monitored and LAD segments excised for SEM after 90-min infusion of study drug. In phase II, dogs were randomized to Ep alone (n = 5) or to Ep + rt-PA (n = 5). Coronary blood flow was monitored during and 120 min after cessation of drug when platelet function had returned to normal and LAD segments were excised. RESULTS: All animals except placebo showed reflow. In phase I, SEM showed an absence of platelet aggregates with Ep alone and with Ep + rt-PA, but not with rt-PA alone. In phase II, SEM showed an intimal surface devoid of mural thrombus and platelet aggregates only in Ep + rt-PA treated arteries. Ep-alone treated arteries showed new platelet aggregates at sites of residual mural thrombus. CONCLUSIONS: Short-term infusion Ep plus low-dose rt-PA acutely neutralizes the ability of damaged endothelial surfaces to recruit new platelets by inhibiting platelet aggregation and eliminating residual mural thrombus.     

Microvessels in Chronic Total Occlusions: Pathways for Successful Guidewire Crossing?

Arterial chronic total occlusions (CTO) are a common and clinically relevant problem in patients with coronary artery disease. Percutaneous coronary intervention (PCI) success rates in a wide range of CTO are low, primarily due to inability of guidewire crossing. The pathophysiology of CTO is poorly understood and limits our ability to introduce innovative therapies. Recent studies from our laboratory have suggested that microvessel formation within arterial CTO is a complex process with temporal and regional differences. Moreover, there is evidence from pilot studies that the presence of either microvessels or the particular extracellular matrix environment in the adjacent perivascular tissue can facilitate guidewire crossing and successful PCI. Currently, studies are underway in our experimental CTO model to delineate the pathophysiology of microvessel formation in CTO and its potential role in PCI.