Association between child marriage and institutional delivery care services use in Bangladesh: intersections between education and place of residence.

OBJECTIVES: To examine the association between child marriage and women's use of institutional delivery care services and whether education and place of residence moderate this association. STUDY DESIGN: The study used de-identified data from four rounds (2004, 2007, 2011, and 2014) of the Bangladesh Demographic and Health Survey (BDHS). The BDHS is a cross-sectional survey conducted every three years. The analysis was based on 16,099 ever-married women aged 15-49 years with at least one live birth in the three years before the survey. METHODS: The study used multivariable logistic regression models with interaction terms between age at marriage, education, and place of residence. Adjusted predicted probabilities of outcome variables were computed from interaction models. RESULTS: Child marriage is significantly associated with decreased use of institutional delivery care services. Compared to women who married at adult ages (≥18 years), women who married between ages of 12-14 years were the most disadvantaged in having delivered at a health facility (odds ratio [OR]: 0.62; 95% confidence interval [CI]: 0.51-0.74) and having a skilled attendant present (OR: 0.63; 95% CI: 0.53-0.75) at the birth of their last child. The analysis suggests that the effect of education on the use of institutional delivery care is stronger among women married at age 18 or older compared to women who married younger than age 18 years. Further, the joint effect of age at marriage and education is stronger for women living in urban than rural place of residence. CONCLUSIONS: Increasing the age at marriage and discouraging child marriage may be a fruitful way to improve mother and child health in Bangladesh. Encouraging girls to complete high school and pursue college education would also help decline the rate of child marriage and, in turn, benefit social mobility and health.

Association between maternal periapical lesions and brain inflammation in rat pups.

OBJECTIVE: The objective of this study was to determine whether the presence of maternal tooth periapical lesions was associated with foetal brain inflammation in a pregnant rat model. METHODS: Sprague-Dawley rats were divided into two groups: pregnant rats with induced periapical abscesses (E, n=8) and sham-operated control pregnant rats (S, n=8). The pulps of the first and second maxillary right molars had been exposed and the tooth left open to the oral environment for two weeks prior to initiation of the pregnancy. Following delivery of the pups (E, n=99; S, n=101), each pup was decapitated and the brain was removed and immediately frozen in liquid nitrogen. The tissues were solubilized in PBS containing a protease inhibitor, and norepinephrine (NE), IL-6, IL-1-ß, TNF-α, and myelin basic protein (MBP) were determined by ELISA. Group means were compared by factorial analysis of variance, a post hoc Tukey test, and Pearson's correlation test. p<0.05 was used to reject the null hypothesis. RESULTS: E pups were significantly heavier than S pups. Brain tissue concentrations of IL-6, IL-1-ß, and TNF-α were significantly higher and MBP and norepinephrine concentrations significantly lower in E pups than S pups. Concentrations of IL-6, TNF-α and IL-1-ß were significantly correlated between E serum, pup birthweight, and E pup brain tissue. MBP, NE and IL-6 were significantly correlated within the brain tissues of E pups. CONCLUSION: The data suggest that brain inflammation may be associated with maternal periapical inflammation. This association identifies a modifiable risk factor for adverse pregnancy outcomes.

Effects of gender on serum biomarkers of systemic inflammation coincident to experimentally-induced periapical lesions.

OBJECTIVE: The literature suggests that females have less adverse effects to infection than males, due to the protective effects of oestrogen. The purpose of our study is to compare the systemic effects of induced periapical lesions between groups of animals with various serum concentrations of oestrogen. METHODS: To induce periapical inflammation, two molar tooth pulps were exposed in ovariectomized (OVX) and normal female (F) and castrated (Cast-M) and normal male (M) Sprague-Dawley rats (Experimental group, E). Sham-operated control animals from each group were also studied (Control group, C). Twenty-eight days later, serum and maxillas were collected. Serum 17ß-oestradiol, testosterone, MMP-9, IL-18, IL-6, TNF-α, and IL-1ß concentrations were measured by ELISA. Maxillas were cleaned of residual tissue and digital radiographs were made to verify the presence of periapical lesions. Data were compared by factorial ANOVA, post hoc Tukey, and Pearson correlation tests. Groups were considered to be significantly different when p<0.05. RESULTS: The serum concentration of IL-18, TNF-α, IL-1-ß, IL-6 and MMP-9 was greatest in OVX-E animals, compared to all other groups (p<0.001). F-E rats had significantly higher serum concentrations of these cytokines, compared to F-C. The fold difference in serum concentration of the biomarkers (between E and C groups) was significantly greater in females than males, even though males had higher baseline concentrations of all these biomarkers. CONCLUSION: When females are oestrogen-deficient, their systemic response to periapical lesions is significantly greater than males, suggesting that oestrogen is essential in protecting females from the effects of this type of inflammation.

Laparoscopic repair of traumatic intrapericardial diaphragmatic hernia.

Diaphragm rupture is associated with approximately 5% of blunt abdominal trauma. However, rupture of the central tendon of the diaphragm leading to an intrapericardial diaphragmatic hernia is very rare, with less than 100 cases reported in the world literature. All previously reported cases have been repaired via laparotomy or thoracotomy. In this paper, we present the first laparoscopic repair of a traumatic intrapericardial diaphragmatic hernia.

Comparative gender differences in local and systemic concentrations of pro-inflammatory cytokines in rats with experimental periodontitis.

BACKGROUND AND OBJECTIVE: There have been few studies of gender differences in response to periodontitis. Thus, we compared gender-specific differences in systemic cytokine concentrations in rats with and without ligature-induced periodontitis. MATERIAL AND METHODS: Experimental periodontal disease was initiated in Sprague-Dawley rats by placing a ligature around the crowns of the second right maxillary molar tooth. Sham-operated control groups were also created. Two weeks later, the right and left maxillary quadrants of teeth, liver and serum were collected from all the rats, and uterine horns were collected from the female rats. Liver and uterine samples were ground in phosphate-buffered saline (10 mg of tissue/mL of phosphate-buffered saline + protease inhibitor) containing a protease inhibitor, and cytokine concentrations were determined by enzyme-linked immunosorbent assay. Digital radiographs were made of maxillary quadrants, and the distance from cemento-enamel junction to alveolar crest was measured using image analysis software. Data were compared by factorial analysis of variance and a post-hoc Tukey test. RESULTS: Female rats with ligatures had greater, but not significantly different, alveolar bone loss than males with ligatures. However, they had higher serum concentrations of interleukin-6, tumor necrosis factor-alpha and C-reactive protein, and liver C-reactive protein (p < 0.05). These females also had higher interleukin-6, tumor necrosis factor-alpha and vascular endothelial growth factor concentrations within the uterine horn, compared to female controls (p < 0.05). Male animals with ligatures had lower serum concentrations of C-reactive protein and higher interleukin-6 and tumor necrosis factor-alpha concentrations within serum, compared to male controls (p < 0.05). CONCLUSION: Our study suggests that females with periodontal disease have a greater risk for inflammatory-based systemic diseases than males.

Effects of induced periapical abscesses on rat pregnancy outcomes.

OBJECTIVE: The objective of this study was to determine the effects of induced periapical abscesses on pregnant rats. DESIGN: In 1/2 of the animals (n=16), the pulps of the maxillary right molars were exposed to the oral environment, which resulted in a periapical abscess. The other 1/2 (n=16) were sham-operated. 1/2 of the animals of both groups became pregnant 2 weeks later. The pregnancy duration, and weight and number of pups were assessed at delivery. Serum, liver and uterine horn samples were taken from all animals at euthanasia and serum IL-6, endothelin-1, TNF-alpha, IL-10, cortisol and insulin were determined by ELISA. Liver concentrations of IL-6, CRP and IL-6 and uterine horn concentrations of IL-6, vascular endothelial growth factor (VEGF), TNF-alpha, IL-10 and IL-1-beta were assessed by ELISA. Blood glucose concentrations were determined using a glucometer. Outcome variables were compared by factorial ANOVA, a post hoc Tukey test, and Pearson's correlation test. RESULTS: Pregnant rats with periapical abscesses had a significantly longer pregnancy and delivered pups with a significantly higher birthweight (p<0.05). They had significantly higher concentrations of IL-6, VEGF, IL-1-beta, and IL-10 within the uterine horn and IL-6, CRP and TNF-alpha within the liver (p<0.01). Blood glucose and serum TNF-alpha, IL-6, endothelin-1, IL-10, and insulin concentrations were significantly higher in the pregnant animals with pulpal abscesses (p<0.01). CONCLUSION: The significant increase in serum TNF-alpha, taken together with significant increases in blood glucose and serum insulin concentrations, suggest that animals with induced periapical abscesses developed insulin resistance, which significantly affected their pregnancy outcomes.

Relationship between the gingival sulcus depth and interleukin-1 isoform concentrations within the adjacent gingival tissue.

BACKGROUND AND OBJECTIVE: While there is substantial information concerning the concentrations of interleukin-1 isoforms within gingival crevicular fluid, there is little information concerning their concentrations within either normal or diseased gingival tissues. Therefore, the aim of this study was to evaluate the relationship between the concentrations of gingival interleukin-1 isoforms and the adjacent sulcular depth. MATERIAL AND METHODS: Interdental gingival papillae were excised and grouped based on adjacent pocket depth and the presence of bleeding on probing. Gingiva adjacent to a sulcus of < or = 3 mm without bleeding on probing were classified as 'normal'; gingiva adjacent to a 3-mm sulcus with bleeding on probing were classified as 'diseased-slight'; gingiva adjacent to a 4-6-mm sulcus featuring bleeding on probing were classified as 'diseased-moderate'; and gingiva adjacent to a sulcus of > 6 mm featuring bleeding on probing were classified as 'diseased-severe'. Tissues were solublized and the concentrations of interleukin-1beta, interleukin-1alpha, interleukin-1 receptor antagonist and interleukin-6 were assessed by enzyme-linked immunosorbent assay. Data were compared by factorial analysis of variance, the post-hoc Tukey test and the Pearson's correlation test. RESULTS: Gingival concentrations of interleukin-6, interleukin-1 receptor antagonist, interleukin-1alpha- and interleukin-1beta were significantly greater at diseased-severe sites than at normal, diseased-slight, or diseased-moderate sites (p < 0.05); the gingival concentrations of interleukin-1 receptor antagonist and interleukin-1alpha were significantly greater at diseased-severe than at diseased-moderate sites (p < 0.05). Interleukin-1 receptor antagonist concentrations were significantly correlated with both interleukin-1alpha and interleukin-1beta concentrations. The ratios of concentrations of the interleukin-1 isoforms were different at the various stages of inflammation. CONCLUSION: Our data indicated a progressive increase in gingival concentrations of interleukin-1 isoforms with increased adjacent sulcular depth. However, within 'diseased' tissues, the proportional concentrations of interleukin-1alpha and -beta to interleukin-1 receptor antagonist were lowest within diseased-severe tissues.

Synergism between nifedipine and cyclosporine A on the incorporation of [35S]sulfate into human gingival fibroblast cultures in vitro.

BACKGROUND AND OBJECTIVE: We assessed the effects of cyclosporine A and nifedipine on the in vitro incorporation of [(35)S]sulfate into gingival fibroblast cell cultures derived from responder and nonresponder subjects who had received an organ transplant followed by a therapeutic regimen using a combination of those drugs. MATERIAL AND METHODS: Gingival fibroblasts were isolated from responder and nonresponder subjects and maintained in vitro. Prior to cell harvest, gingival interleukin-1beta concentrations were determined by enzyme-linked immunosorbent assay (ELISA). Cells were untreated or exposed to either 10(-7)-10(-10) m nifedipine or 100-500 ng/ml cyclosporine A. Incorporation of [(3)H]proline or [(35)S]sulfate into the cell cultures was determined by liquid scintillation analysis. In addition, the effects of 400 ng/ml cyclosporine A + 10(-7) m nifedipine and 400 ng/ml cyclosporine A + 10(-10) m nifedipine on incorporation of [(35)S]sulfate into the cell cultures was determined. Data were compared by factorial analysis of variance (anova) and a posthoc Tukey's test. RESULTS: Gingiva from responders contained significantly more interleukin-1beta than gingiva from nonresponders (p < 0.01). The cell cultures derived from responders incorporated significantly more [(35)S]sulfate than those derived from nonresponders following exposure to either cyclosporine A or 10(-7) m nifedipine. In addition, the exposure of fibroblasts derived from gingival overgrowth to either 400 ng/ml cyclosporine A + 10(-7) m nifedipine or 400 ng/ml cyclosporine A + 10(-10) m nifedipine significantly increased or decreased, respectively, the incorporation of [(35)S]sulfate into the cultures. CONCLUSION: The therapeutic combination of cyclosporine A and nifedipine could be a significant risk factor for gingival overgrowth in subjects susceptible to either agent. The mechanism for overgrowth could include edema secondary to increased sulfated-glycosaminoglycan (sGAG) synthesis by fibroblasts, but further investigation is required.

Effects of doxorubicin on human dental pulp cells in vitro.

There is substantial information concerning the effects of continuous exposure to supratherapeutic or therapeutic concentrations of doxorubicin on human molar pulpal cells; the effects of continuous exposure to subtherapeutic concentrations of this agent are undetermined. To this end, we studied the proliferation of human fibroblasts and pulpal cells and their pattern of mineralized nodule deposition in vitro. Cell proliferation was assessed at 1, 3, 5, and 7 days from populations with either no exposure (control) or exposure to 10(-6)-10(-9) mol/L doxorubicin. Mineralized nodule deposition and calcium-45 incorporation were assessed at 7 and 21 days of culture. Data were compared by factorial ANOVA and a post-hoc Tukey test. 10(-6) and 10(-7) mol/L doxorubicin significantly reduced the total number of viable pulpal cells in cultures from days 1 to 3 (p < 0.05); doxorubicin 10(-6)-10(-9) mol/L significantly inhibited cell proliferation (p < 0.05) and DNA synthesis 5 days after plating (p < 0.001). After 21 days, doxorubicin 10(-6)-10(-8) mol/L significantly decreased calcium-45 incorporation into pulpal cultures (p < 0.001); all dilutions significantly reduced the number of mineralized nodules within the 21-day pulpal cultures (p < 0.05). In addition, all dilutions of doxorubicin significantly inhibited fibroblast cell proliferation and incorporation of [(3)H]thymidine. In contrast, the fibroblast cultures did not produce mineralized nodules, suggesting that the mineralized nodules within the pulpal cell cultures did not result from dystrophic calcification. Thus, exposure to subtheraputic doxorubicin concentrations has potential adverse effects on mineralized tissue formation within the pulp, which could affect the rates of reparative dentin deposition within the tooth pulps of patients receiving this chemotherapeutic agent.

Interleukin-18 concentrations and the pathogenesis of periodontal disease.

BACKGROUND: Interleukin-18 (IL-18) is reported as an important regulatory cytokine in non-oral inflammation. Our objective was to compare the concentrations of IL-18 within diseased and healthy human gingiva with concentrations of other T(H)1 and T(H)2 cytokines to determine possible effects of IL-18 on gingival inflammation. METHODS: Gingival biopsies were obtained prior to routine tooth extraction. Gingiva was grouped by the depth of the adjacent gingival sulcus: < or =3 healthy (featuring no bleeding on probing) and > or =3 mm diseased (featuring bleeding on probing). Diseased gingiva was subdivided into 3, 4 to 6 and >6 mm groups. Gingival interleukin (IL)-2, IL-4, IL-6, IL-10, IL-12, IL-18, and interferon (IFN)-gamma concentrations were assessed by enzyme linked immunosorbent assay (ELISA). Data were compared by factorial analysis of variance and the Pearson's correlation test. RESULTS: Concentrations of IL-2, IL-4, IL-6, IL-10, IL-18, and IFN-gamma adjacent to 4 to 6 mm diseased sites were greater than adjacent to < or =3 mm healthy sites (P <0.001). IL-12 concentrations were lower within diseased than within healthy gingiva (P <0.001). IL-6 and IL-18 concentrations were greater adjacent to >6 mm sites compared to healthy sites (P <0.001); the concentrations of the other cytokines (except IL-12) were similar to healthy sites. IL-6 and IL-18 concentrations were positively correlated, and IFN-gamma and IL-12 negatively correlated, with the adjacent gingival sulcular depth. CONCLUSIONS: Periodontal inflammation may not successfully resolve because of accumulation of IL-6 and IL-18, and decreased concentrations of IL-12, within diseased gingiva. Because of the highly significant correlation between IL-18 concentration and gingival sulcular depth, IL-18 may be a useful target for either preventive or palliative therapy for periodontitis.

Effects of multiple dentinal lesions on the rat pulp.

The purpose of this study was to compare the effects of single and multiple dentinal lesions on the dental pulps of rats. 3H-proline was used to measure pulpal reactionary dentin deposition, and 3H-thymidine was used to measure pulpal cell proliferation by radioautography. Data were compared by factorial analysis of variance and a post-hoc Tukey test. A significant increase in radiolabeled collagenous proteins within reactionary dentin and pulpal cell labeling indices were evident coincident to single dentinal injuries, compared with controls (p < 0.001). After double injuries, the radiolabeled collagenous proteins within reactionary dentin and the pulpal labeling indices remained significantly greater than in controls (p < 0.01); however, each was significantly less than after single injuries (p < 0.05). These data suggest that pulpal cell proliferation and collagenous protein deposition into reactionary dentin are decreased subsequent to a previous dentinal injury. Thus, the healing potential of the dental pulp could be decreased by recent tooth cavity preparation.

Effect of strain on bone nodule formation by rat osteogenic cells in vitro.

The purpose of this study was to assess in vitro bone nodule formation by cells exposed to a range of microstrain, at a sub-optimal oscillation frequency for bone formation. Fetal rat calvarial cells experienced a Flexercell regimen within either FLEX I (deformable) or FLEX II (non-deformable) substrates. Cells in FLEX I plates were exposed to growth medium only; those in FLEX II plates were exposed to either growth medium only, or growth medium + 10(-7) M IGF-1. Cell numbers were assessed from 1 to 6 days. Other cells were exposed to the Flexercell regimen (-2 kPa, 0.05 Hz) for 1-3 (Group 1), 3-6 (Group 2), 1-9 (Group 3) or 10-15 (Group 4) days and were maintained, at other times, under standard conditions. After 21 days, nodules were counted within each well and within the compression, <999, 1000-4900, 5000-9999, 10,000-14,999 and 15,000-25,000 microstrain regions of the FLEX I membrane. Cyclic deformation inhibited cell numbers from 1 to 6 days, compared to control or IGF-1 groups (P<0.001). The number of nodules in Groups 2 and 4 were greater than Groups 1 or 3 (P<0.001), but not different from control or IGF-1 groups. Compression or tensile microstrain significantly affected nodule formation in all groups, with Group 4 producing more nodules than other groups in most microstrain regions. Thus, the number of bone nodules produced by osteogenic cell cultures exposed to cyclic deformation was significantly affected by the timing of initiation and the characteristics and magnitude of the deformation regimen.

The ovariectomized sheep as a model for human bone loss.

The aim of this study was to determine the effects of ovariectomy on the trabeculae of ovine iliac bone, with a view to the further development of a model for human osteoporosis. Seven ovariectomized (OVX) and five control Dorset ewes were observed for one year. Iliac crest bone samples were obtained at the time of ovariectomy ("time 0") and again when the animals were killed 12 months later. At "time 0" and at 3-month intervals thereafter samples of blood and urine were collected for the assay of serum 17beta-oestradiol and osteocalcin (OC) and urinary deoxypyridinium (D-PYR). One year after ovariectomy, trabecular bone volume and thickness were reduced (P<0.05) and trabecular separation was increased (P<0.05) as compared with the controls. In OVX sheep, serum 17beta-oestradiol concentrations were significantly lower at the end of the experiment than at "time 0", while serum OC and urinary D-PYR concentrations were significantly higher (P<0.001). The results suggest that the OVX sheep is a valid model for changes in trabecular bone architecture associated with oestrogen deficiency, especially in women experiencing early menopause.

Interleukin-11 and IL-17 and the pathogenesis of periodontal disease.

BACKGROUND: Interleukin (IL)-11 and IL-17 are cytokines that modulate the inflammatory process and have not been assessed within normal or inflamed gingival tissues. Our purpose was to compare concentrations of human IL-11 and IL-17 within healthy and diseased human gingiva to determine their possible role in the initiation or progression of periodontal diseases. METHODS: Biopsies from healthy (non-hemorrhagic gingiva adjacent to a < or = 3 mm gingival sulcus) and diseased gingiva (hemorrhagic gingiva adjacent to a > or = 3 mm periodontal pocket) were studied. IL-11, IL-17, RANTES, and IL-6 concentrations were assessed within solubilized gingival biopsies by enzyme-linked immunosorbent assay. Data were compared by factorial analysis of variance and a post-hoc Tukey honestly significant difference (HSD) test. Regression analysis and partial correlation analysis (adjusted for sample weight) were also used to determine correlations between the variables. RESULTS: Interleukin-11 concentrations were highest within gingiva adjacent to 3 mm diseased pockets (P < 0.001), and IL-17 concentrations were highest at 4 to 5 mm sites compared to other sites (P < 0.001). Gingival concentrations of both cytokines were significantly lower in gingiva adjacent to a > or = 6 mm pocket. RANTES concentrations were significantly greater in gingiva adjacent to > or = 6 mm pockets than in tissues derived from other sites (P < 0.001). IL-11, IL-6, and RANTES concentrations were significantly correlated with sulcular depth. CONCLUSIONS: Gingival concentrations of IL-11 and IL-17 are different in diseased gingiva adjacent to 3, 4 to 5, and > or = 6 mm pockets, suggesting that their concentrations change as a consequence of the progression of gingivitis to periodontitis and that both cytokines could have a significant role in this progression. These data may be useful for the design of procedures for prevention of periodontal disease.

Sensitivity, specificity and accuracy of stress SPECT myocardial perfusion imaging for detection of coronary artery disease in the distribution of first-order branch vessels, using an anatomical matching of angiographic and perfusion data.

We sought to investigate the utility of stress single-photon emission computed tomography (SPECT) myocardial perfusion imaging (MPI) for the identification of coronary artery disease (CAD) in the distribution of first-order branch vessels. We evaluated 135 consecutive patients with coronary angiography and stress SPECT MPI. We anatomically matched angiography and SPECT to assess the sensitivity, specificity and accuracy of SPECT MPI for the detection of CAD in the distribution of first-order branches. Subgroup analysis for stress test performance and previous coronary artery bypass grafting (CABG) was also performed. The sensitivity, specificity and accuracy of stress SPECT MPI for the detection of CAD in the distribution of first-order branch vessels were all 67%. For isolated branch vessel CAD, stress SPECT MPI had a sensitivity of 44%. In patients without CABG, the sensitivity, specificity and accuracy for the detection of CAD in the distribution of first-order branch vessels were 71%, 67% and 68%, compared with 60%, 67% and 64% for patients with CABG. The sensitivity for isolated branch vessel CAD was 50% for patients without CABG, but only 29% for patients with CABG. The sensitivity and specificity for CAD in the distribution of branch vessels were similar for all patients for all stress test modalities and heart rate response (sensitivity, 64-69%; specificity, 61-69%). Stress SPECT MPI offers intermediate sensitivity, specificity and accuracy for the detection of CAD in the distribution of first-order coronary artery branch vessels. However, for isolated branch vessel CAD, stress SPECT has a lower sensitivity, particularly in patients with previous CABG.

Effect of estrogen deficiency on skeletal and alveolar bone density in sheep.

BACKGROUND: This study provides a longitudinal assessment of changes in alveolar and skeletal bone mineral density (BMD) in ovariectomized animals. METHODS: Following ovariectomy (OVX) (n = 6) or sham-operation (n = 6) intraoral radiographs were made at 4-month intervals and serum 17-beta-estradiol, osteocalcin, and interleukin (IL)-6, urinary deoxypyridinium, and salivary IL-6, deoxypyridinium, and osteocalcin concentrations were evaluated. Twelve months after surgery, animals were sacrificed and the mandible and radius/ulna removed. Bones were sectioned and radiographed. Mean BMD and cortical thicknesses were calculated from each region. RESULTS: OVX animals had a progressive decrease in serum 17-beta-estradiol, increased serum osteocalcin and IL-6, urinary deoxypyridinium and salivary IL-6, osteocalcin and deoxypyridinium (P < 0.001), suggesting that they were becoming osteoporotic. The BMD of the radius/ulna and mandibular alveolar bone was significantly reduced in OVX animals (P < 0.05 and P < 0.001, respectively). Reduced alveolar bone BMD became evident in OVX animals 6 months after surgery and became more severe during the subsequent 6 months. Alveolar crestal height was also significantly reduced in OVX animals (P < 0.001). These biochemical and density changes preceded a significant reduction in serum 17-beta-estradiol, which occurred between 4 and 8 months following surgery. CONCLUSIONS: Serial measurements of alveolar BMD predicts loss of skeletal BMD in OVX sheep. Changes in alveolar BMD precede estrogen deficiency, suggesting that early signs of reduced BMD may be detected in peri-menopausal women. The presence of biomarkers of bone metabolism within saliva and their correlation with reduced BMD suggests that saliva could be used as an adjunct screening method for assessment of skeletal bone density.

Validation of a model of left ventricular segmentation for interpretation of SPET myocardial perfusion images.

Several models of left ventricular segmentation have been developed that assume a standard coronary artery distribution, and are currently used for interpretation of single-photon emission tomography (SPET) myocardial perfusion imaging. This approach has the potential for incorrect assignment of myocardial segments to vascular territories, possibly over- or underestimating the number of vessels with significant coronary artery disease (CAD). We therefore sought to validate a 17-segment model of myocardial perfusion by comparing the predefined coronary territory assignment with the actual angiographically derived coronary distribution. We examined 135 patients who underwent both coronary angiography and stress SPET imaging within 30 days. Individualized coronary distribution was determined by review of the coronary angiograms and used to identify the coronary artery supplying each of the 17 myocardial segments of the model. The actual coronary distribution was used to assess the accuracy of the assumed coronary distribution of the model. The sensitivities and specificities of stress SPET for detection of CAD in individual coronary arteries and the classification regarding perceived number of diseased coronary arteries were also compared between the two coronary distributions (actual and assumed). The assumed coronary distribution corresponded to the actual coronary anatomy in all but one segment (#3). The majority of patients (80%) had 14 or more concordant segments. Sensitivities and specificities of stress SPET for detection of CAD in the coronary territories were similar, with the exception of the RCA territory, for which specificity for detection of CAD was better for the angiographically derived coronary artery distribution than for the model. There was 95% agreement between assumed and angiographically derived coronary distributions in classification to single- versus multi-vessel CAD. Reassignment of a single segment (segment #3) from the LCX to the LAD territory further improved the model's fit with the anatomic data. It is concluded that left ventricular segmentation using a model with assumed coronary artery distribution is valid for interpretation of SPET myocardial perfusion imaging.

Leptin within healthy and diseased human gingiva.

BACKGROUND: Plasma leptin concentrations are reported to be elevated in patients with inflammatory diseases. There is no consensus concerning the biological mechanism for this phenomenon. To date, tissue leptin concentrations have not been assessed within normal or inflamed gingiva. The purpose of this study was to assess concentrations of human leptin within healthy and diseased gingiva to define its possible role in periodontal disease progression. METHODS: Healthy (non-hemorrhagic gingiva adjacent to a < or =3 mm gingival sulcus) and inflamed gingiva (hemorrhagic gingiva adjacent to a > or =3 mm periodontal pocket) were studied. Leptin, vascular endothelial growth factor (VEGF; to assess potential vascular expansion), and interleukin-6 (IL-6; to assess periodontal disease activity and severity) concentrations were assessed within solubilized gingival biopsies by enzyme-linked immunosorbent assay. Data were grouped by sulcular depth and compared by factorial analysis of variance, regression analysis, and Scheffé comparisons. RESULTS: Leptin concentrations were highest within gingiva adjacent to a < or =3 mm sulcus and progressively declined within gingiva adjacent to a > or =3 mm sulcus. VEGF concentrations were highest within gingiva adjacent to 4 to 6 mm pockets and nearly equivalent in healthy (< or =3 mm sulcus) and severely diseased gingiva (>6 mm sulcus). IL-6 was positively correlated and leptin negatively correlated with adjacent probing depth; IL-6 concentration was significantly higher and leptin significantly lower in gingiva adjacent to >6 mm pockets compared to sites adjacent to <6 mm pockets (P<0.001). CONCLUSIONS: Human leptin is present within healthy and marginally inflamed gingiva and decreases in concentration as the adjacent probing depth increases. When leptin concentrations decreased (> or =3 mm sulcus), VEGF concentrations increased, suggesting that leptin could be released from gingiva coincident to vascular expansion. Thus, gingiva, in addition to adipose tissue, could be a source of circulating leptin in patients with periodontal disease. This possibility requires further investigation.

Identification and characterization of a monofunctional glycosyltransferase from Staphylococcus aureus.

A gene (mgt) encoding a monofunctional glycosyltransferase (MGT) from Staphylococcus aureus has been identified. This first reported gram-positive MGT shared significant homology with several MGTs from gram-negative bacteria and the N-terminal glycosyltransferase domain of class A high-molecular-mass penicillin-binding proteins from different species. S. aureus MGT contained an N-terminal hydrophobic domain perhaps involved with membrane association. It was expressed in Escherichia coli cells as a truncated protein lacking the hydrophobic domain and purified to homogeneity. Analysis by circular dichroism revealed that secondary structural elements of purified truncated S. aureus MGT were consistent with predicted structural elements, indicating that the protein might exhibit the expected folding. In addition, purified S. aureus MGT catalyzed incorporation of UDP-N-acetylglucosamine into peptidoglycan, proving that it was enzymatically active. MGT activity was inhibited by moenomycin A, and the reaction product was sensitive to lysozyme treatment. Moreover, a protein matching the calculated molecular weight of S. aureus MGT was identified from an S. aureus cell lysate using antibodies developed against purified MGT. Taken together, our results suggest that this enzyme is natively present in S. aureus cells and that it may play a role in bacterial cell wall biosynthesis.

Survival of rotavirus antibody activity derived from bovine colostrum after passage through the human gastrointestinal tract.

BACKGROUND: Rotavirus is a major cause of infectious diarrhea in infants and young children. Several studies have shown that hyperimmune bovine colostrum, derived from cows immunized with rotavirus, can prevent rotavirus diarrhea when given passively. The objective of this study was to determine whether colostral antibody activity survived transit through the gut by measuring the level of rotavirus antibody activity in the feces. METHODS: Hyperimmune colostrum containing different levels of rotavirus antibody was administered to 105 children attending nine Adelaide childcare centres. Subjects were asked to drink 100 ml of whole milk supplemented with colostrum 3 times a day, for a period of 6 days. Stool samples were collected from the subjects before, during, and after consumption of the study product. Rotavirus activity was determined using a novel virus reduction enzyme-linked immunosorbent assay (ELISA) and a virus neutralization assay. RESULTS: Rotavirus antibody activity was detected in 521 (86%) of 602 fecal specimens obtained during the study using the virus reduction ELISA. The antibody activity was detected as early as 8 hours after ingestion of hyperimmune colostrum and up to 72 hours after consumption had ceased. There was a strong relation (r = 0.81) between the titer of rotavirus antibody administered to subjects and the level of antibody activity detected in the feces. CONCLUSIONS: The results show that antirotavirus activity survived passage through the gut. Therefore, passive immunotherapy may be used to prevent or treat infectious diseases that affect the entire length of the gastrointestinal tract.