Multiscale Modelling of De Novo Anaerobic Granulation.

A multiscale mathematical model is presented to describe de novo granulation, and the evolution of multispecies granular biofilms, in a continuously fed bioreactor. The granule is modelled as a spherical free boundary domain with radial symmetry. The equation governing the free boundary is derived from global mass balance considerations and takes into account the growth of sessile biomass as well as exchange fluxes with the bulk liquid. Starting from a vanishing initial value, the expansion of the free boundary is initiated by the attachment process, which depends on the microbial species concentrations within the bulk liquid and their specific attachment velocity. Nonlinear hyperbolic PDEs model the growth of the sessile microbial species, while quasi-linear parabolic PDEs govern the dynamics of substrates and invading species within the granular biofilm. Nonlinear ODEs govern the evolution of soluble substrates and planktonic biomass within the bulk liquid. The model is applied to an anaerobic, granular-based bioreactor system, and solved numerically to test its qualitative behaviour and explore the main aspects of de novo anaerobic granulation: ecology, biomass distribution, relative abundance, dimensional evolution of the granules and soluble substrates, and planktonic biomass dynamics within the bioreactor. The numerical results confirm that the model accurately describes the ecology and the concentrically layered structure of anaerobic granules observed experimentally, and that it can predict the effects on the process of significant factors, such as influent wastewater composition; granulation properties of planktonic biomass; biomass density; detachment intensity; and number of granules.

Water activity in subaerial microbial biofilms on stone monuments.

Stone monuments can be difficult environments for life, particularly with respect to liquid water access. Nevertheless, microbial communities are found on them with apparent ubiquity. A variety of strategies for access to liquid water have been proposed. Regardless of their water-retention mechanisms details, though, we argue that water activity (a key indicator for cell viability) is constrained by environmental conditions, largely independently of community structure, and is predicted by the local temperature and relative humidity. However, direct measurement of water activity in SABs, particularly those growing on stone surfaces, is difficult. A method for estimating water activity within SABs is presented that uses a minimally invasive combination of conservative sampling, weather data, confocal imaging, and mathematical modeling. Applying the methodology to measurements from the marble roofs of the Federal Hall National Memorial and of the Thomas Jefferson Memorial, estimations are made for water activity in their subaerial stone communities over the course of an approximately one year period.

Long-term follow-up of diabetes in two patients with thiamine-responsive megaloblastic anemia syndrome.

OBJECTIVE: To describe a 15-year follow-up of diabetes and to present data regarding pancreatic beta-cell function in two adolescents affected by the thiamine-responsive megaloblastic anemia (TRMA) syndrome. CASE REPORTS: The first patient (PMR) is a 17.5-year-old Italian girl who presented megaloblastic anemia at 7.5 months of age. At age 2.5 years, because of the presence of diabetes and sensorineural deafness, she was diagnosed with TRMA syndrome and started treatment with thiamine-HCl, followed very early by benzoyloxymethyl-thiamine (BOM-T). The second patient (PF) is a 16.8-year-old Italian boy born to consanguineous parents. Sensorineural deafness was diagnosed at age 1.5 years, while diabetes with ketoacidosis and megaloblastic anemia were diagnosed at age 3 years. Treatment with thiamine HCl was started immediately after diagnosis and changed to BOM-T 2 months later. Subsequent to the initiation of the vitamin, the two patients did not require insulin for approximately 7 and 10 years, respectively. Puberty was determinant in deteriorating the metabolic control in these patients, leading to treatment with an oral hypoglycemic agent and finally to a reinstitution of insulin therapy. CONCLUSIONS: The hormonal assessment in our patients (normal insulin response to oral glucose in childhood, preserved C-peptide secretion in case 2) and the good response to an oral hypoglycemic agent would indicate that the pancreatic disease may initiate as type 2 diabetes and may progress after several years to an insulin-requiring diabetes, as indicated by the exhaustion of the insulin secretory capacity.

Pubertal growth, sexual maturation, and final height in children with IDDM. Effects of age at onset and metabolic control.

OBJECTIVE: To evaluate growth and pubertal development in children with IDDM and the influence of the age at onset of IDDM and the degree of metabolic control on final height. RESEARCH DESIGN AND METHODS: We conducted a retrospective evaluation of 62 subjects followed longitudinally both clinically and metabolically from the onset of IDDM until final height was reached. RESULTS: Height at diagnosis was within the normal percentiles in boys (0.5 +/- 1.0 standard deviation score [SDS]) and girls (0.4 +/- 1.0 SDS), but above the genetic target height (-1.0 +/- 0.9 SDS in boys and -1.1 +/- 0.6 SDS in girls; P = 0.0001 for both comparisons). Although a lesser height gain was observed during the ensuing years, the final height reached by boys (-0.4 +/- 1.1 SDS) and girls (-0.4 +/- 0.9 SDS) was higher than the genetic target height. Blunted total pubertal growth was observed both in boys (24.5 +/- 3.6 cm) and girls (20.1 +/- 4.2 cm). The decrease in height gain was independent of the duration of IDDM, the degree of metabolic control, or the insulin requirement. The greater the height at diagnosis, with respect to the genetic target height, the lesser was the subsequent height gain to reach final adult height (r = 0.34, p < 0.01). BMI increased with age as normally occurs in healthy children, independent of the duration of disease and the degree of metabolic control. Pubertal development began and progressed normally both in boys and girls. In boys, a testicular volume of 4 ml was reached at a mean age of 12.1 +/- 0.9 years. In girls, breast enlargement occurred at a mean age of 10.4 +/- 1.2 years and the mean age of menarche was 12.8 +/- 1.4 years. Pubertal development and progression occurred independent of the age at onset of IDDM, the glycemic control, or the insulin requirement during the pubertal period. CONCLUSIONS: Children with IDDM have normal onset of puberty and normal sexual maturation. Even though final height falls within the normal percentiles, the diminished height gain after diagnosis requires further investigation.

Characterization of somatogenic and lactogenic binding sites in isolated rat hepatocytes.

Suspensions of rat hepatocytes isolated enzymatically by the method of Berry and Friend were used to study the binding of 125I-labeled human (hGH) and bovine (bGH) growth hormones and ovine prolactin (oPRL). Displacement of these labeled hormones by their unlabeled analogues was analyzed by means of Scatchard plots and affinity constants (K) and the number of binding sites per cell (q) were calculated. Specificity of binding was studied using hGH, bGH oPRL and rat growth hormone (rGH) and rat prolactin (rPRL). Rat hepatocytes contained two types of binding sites which bound hGH. The first, somatogenic, was specific for the growth-promoting hormones bGH and rGH. The second, lactogenic, was specific for lactogenic hormones, oPRL and rPRL. Human GH, which has both lactogenic and growth-promoting properties in rodents, bound to both sites. The somatogenic binding sites were present in both males and females, and the number of sites was similar in females and in males and was not affected by hypophysectomy. The lactogenic binding sites were present only in females, and the number of lactogenic and somatogenic sites was similar (40,000/cell). The affinity of hGH for the lactogenic binding sites was less than for the somatogenic (0.37 X 10(9) vs. 1 X 10(9)M-1). The lactogenic binding sites were lost when female rats were hypophysectomized and could not be restored by estrogen treatment.

Basal and stimulated serum growth hormone concentrations in inflammatory bowel disease.

Patients with inflammatory bowel disease (IBD) manifest growth failure which may antecede abdominal symptoms by some years. Eight of ten children with documented IBD had records of decreasing growth velocities. Investigation of growth hormone reserves showed excessive rather than impaired responses. Mean basal GH level was 6.2 +/- 0.75 (SEM) ng/ml. During sleep, the mean GH level rose to 26.0 +/- 4.7 ng/ml and following propranolol-glucagon stimulation, to 46.0 +/- 4.5 ng/ml. All values were significantly higher than levels obtained in a control population of 25 children investigated for short stature who were not GH deficient. The mean peak GH response following insulin in the IBD group (10.8 +/- 3.8 ng/ml), however, did not differ from the mean peak response in the control group (13.5 +/- 3.3 ng/ml). Growth failure in patients with IBD is not the result of GH deficiency and is not an irreversible phenomenon. On the contrary, judicious use of glucocorticoids aimed at the control of the disease usually produces compensatory growth acceleration ("catch-up growth").

A thyroxine-binding protein in human breast milk similar to serum thyroxine-binding globulin.

A thyroid hormone-binding substance (TBGw) similar to serum T4-binding globulin (TBG) has been identified in the whey fraction of human breast milk. TBGw coeluted with serum TBG, as determined by Bio-Gel P-100 chromatography, and has an isoelectric point of 4.2-4.8, similar to that of serum TBG. The affinity constant of TBGw for T4 was similar to that of serum TBG(Ka, 1.54 +/- 0.38 X 10(9) M-1). Marked inhibition of TBGw binding of [125I]T4 was achieved by the addition of 1.5 X 10(-3) M 8-anilino-1-naphthalene-sulfonic acid. An albumin-like low affinity site (Ka, greater than 10(7) M-1) was also found. RIA of whey concentrates serially diluted in TBG-depleted serum indicated nearly identical binding curves for TBGw and TBG, with slopes of 2.33 (n = 15; r = 0.947) and 2.54 (n = 7; r = 0.996), respectively. Using a specific TBG RIA, a TBGw concentration of 0.29 +/- 0.08 microgram/ml (mean +/- SD) in breast milk (n = 26) was determined. Paired serum and whey specimens from individuals between 6 and 20 weeks of lactation were analyzed by TBG RIA; in these individuals, mean serum TBG concentrations were 25.0 +/- 3.4 micrograms/ml (n = 7); corresponding TBGw levels were 0.26 +/- 0.08 micrograms/ml (n = 7), i.e. approximately 1% of serum levels. Nonetheless, linear regression analysis of the data revealed no significant correlation between serum and whey TBG concentrations in these individuals.

Differential expression of surface membrane growth hormone receptor on human peripheral blood lymphocytes detected by dual fluorochrome flow cytometry.

Although several reports indicate proliferative and functional effects of human GH (hGH) on peripheral blood lymphocytes (PBL), no information is available about hGH receptor (GHR) expression in PBL subsets. Here, the surface membrane GHR levels were investigated in different human PBL subpopulations using a fluorescein isothiocyanate (FITC)-conjugated monoclonal antibody specific for the GHR (mAb263) in dual fluorochrome flow cytometric assays. Strong GHR expression was found in B-cells (CD20+), whereas CD2+ lymphocytes, including T-cells as well as natural killer cells, exhibited considerably lower levels of receptor expression. Similarly, using FITC-labeled recombinant hGH, receptor expression on CD20+ cells was significantly higher than that on CD2+ cells. Abundant expression of GHR in B-lymphocytes was confirmed by reverse transcriptase-polymerase chain reaction analysis of GHR messenger ribonucleic acid from isolated B-cells. Accordingly, the B-cell merits greater consideration as a GH target cell. The use of FITC-labeled mAb263 and hGH is of potential use for the study of GHR levels in patients exhibiting different types of growth disorders. Because of its high specificity for GHR, FITC-labeled mAb263 is also of considerable value for specifically demonstrating the presence of GHR, because hGH may interact with and act through PRL receptor, as shown previously in human neutrophils.

Thyroxine effect on intestinal Cl-/HCO3- exchange in hypo- and hyperthyroid rats.

Changes in transepithelial water and electrolyte transport as causative or contributing factors of the diarrhoea and constipation found associated with changes in thyroid physiology were studied. Albino Wistar rats were pharmacologically made either hypothyroid or hyperthyroid. After sacrifice, the small intestine was mounted in Ussing chambers in order to measure in vitro ion net fluxes under short-circuit conditions. Hypothyroid animals showed an increase in intestinal transit time, Cl- absorption (mainly due to an increment in its mucosal to serosal component) and residual ion flux (which is believed to represent HCO3- secretion) when compared with euthyroid animals. The hyperthyroid animals showed a decrease in Cl- mucosal to serosal transport. Furthermore, a significant correlation was found between serum L-thyroxine (T4) levels and both net Cl- transport (r = -0.74, P < 0.00001) and residual ion flux (r = -0.55, P < 0.005). These results indicate that the effect of T4 is firstly to inhibit Cl-/HCO3- anion exchange thereby influencing transepithelial flux transport and secondly to affect intestinal motility. Such inhibition was not found when T4 was acutely added to rat ileum, suggesting that the effect on electrolyte transport probably requires protein synthesis. In conclusion, the phenomenon observed in vitro could explain the clinical manifestations of constipation and diarrhoea in hypo- and hyper-thyroidism respectively.

Longitudinal growth, sexual maturation and final height in patients with congenital hypothyroidism detected by neonatal screening.

OBJECTIVE: To evaluate longitudinal growth, pubertal development and final height in patients with congenital hypothyroidism (CH) detected by a neonatal screening programme, and to identify factors potentially affecting growth outcome. PATIENTS: Fifty-five patients (41 females) detected by neonatal screening and followed longitudinally from the time of diagnosis and treatment (25+/-5 days) up to the age of 17+/-0.5 years were evaluated retrospectively. RESULTS: Pubertal development began and progressed normally in both males and females. In boys, a testicular volume of 4 ml was reached at 11.3+/-1.0 years. In girls breast enlargement (B2) occurred at a mean age of 10.3+/-1.2 years and the mean age of menarche was 12.5+/-1.2 years. The onset and the progression of puberty were independent of the aetiology, the severity of CH and the timing of the beginning of treatment. Girls treated with an initial amount of L-thyroxine (L-T4) greater than 8 microg/kg per day showed an earlier onset of puberty (B2 9.4+/-0.9 years; menarche 11.5+/-0.8 years) compared with girls treated with a lower initial dose of L-T4 (B2 10.5+/-1.2 years; menarche 12.6+/-1.2 years; P<0.02). However, both groups attained a similar final height (-0.1+/-1.0 SDS and 0.4+/-1.0 SDS, respectively), which in both cases was above the target height (P=0.03). All the patients in the study attained a mean final height (0.1+/-1.1 SDS) within the normal range for the reference population and above the target height (-0.9+/-0.9 SDS, P<0.0001). No significant relationship was found between final height and severity of CH at diagnosis, initial L-T4 dosage or aetiology of the defect. Patients with ectopic gland, thyroid aplasia or in situ gland attained a similar mean final height (0.1+/-1.1 SDS, 0.5+/-1.0 SDS and -0.5+/-1.0 SDS, respectively), which was in all cases greater than target height (-1.0+/-0.9, -0.6+/-0.8, -0.9+/-0.8 respectively; P<0.05). CONCLUSIONS: Our results suggest that conventional management of children with CH detected by neonatal screening leads to normal sexual development and normal adult height, and that the major factor determining height in these children is familial genetic growth potential.

Intellectual outcome at 12 years of age in congenital hypothyroidism.

BACKGROUND: The intellectual outcome in children with congenital hypothyroidism detected by neonatal screening is generally good; however, subtle neurological dysfunctions, subnormal IQ, or both, have been reported. OBJECTIVE: To evaluate the intellectual outcome in 12-year-old patients with congenital hypothyroidism, detected by neonatal screening, in an attempt to identify factors that may affect intellectual development. METHODS: The intelligence quotient (IQ) of 40 children with congenital hypothyroidism was evaluated at 12 years of age, using the Wechsler Intelligence Scale for Children -- Revised, and compared with the IQ of 40 healthy siblings (control group). RESULTS: The mean IQ score (88.4+/-13.1) was not significantly different from that of the control group (93.4+/-10.7). Thirteen patients showed subnormal IQ score (72.4+/-4.9) compared with their siblings (86.7+/-9.6; P<0.0001) and with the other patients (96.1+/-9.6; P<0.0001). The low IQ score was associated with lower serum concentrations of thyroxine at diagnosis, poor treatment compliance during follow-up and lower familial IQ. Interviews with parents of children with congenital hypothyroidism revealed that a refusal to acknowledge the disease was linked to poor attention to the child's emotional life and to poor treatment compliance in some cases (11%). CONCLUSION: Even though the mean IQ score in patients with congenital hypothyroidism falls within normal for the control population, low IQ scores may be present in patients with severe hypothyroidism, inadequate compliance to replacement therapy during follow-up and poor parental pedagogic attitude.

A model of in vivo purging with Rituximab and high-dose AraC in follicular and mantle cell lymphoma.

We studied a model of in vivo purging with Rituximab and high-dose (HD) cytarabine in 14 patients with relapsed/refractory follicular lymphoma and two with refractory mantle cell lymphoma enrolled in a program of HD chemotherapy and autotransplant. After two courses of debulking immunochemotherapy with Rituximab, Vincristine and Cyclophosphamide, we used a combination of Rituximab, HD cytarabine and granulocyte colony-stimulating factor for peripheral blood stem cells (PBSC) mobilization. The median number of CD34+ cells collected was 14.69 x 10(6)/kg (range 5.74-73.2). Monitoring of peripheral CD19+ and CD20+ B cells prior to and throughout the purging period showed that a treatment with Rituximab, Vincristine and Cyclophosphamide results in a profound depletion of B cells in peripheral blood. B-cell depletion persists during mobilization with Rituximab and HD cytarabine allowing a collection of PBSC free of B cells (median CD19+ and CD20+ cells counts 0%). Of nine patients PCR positive for bcl-2 or bcl-1 in blood and marrow at the start of immunochemotherapy, all showed PCR-negative PBSC. In conclusion, in patients with indolent lymphoma, the concurrent administration of Rituximab and HD cytarabine is a safe and efficient method to obtain in vivo purged PBSC. Immunochemotherapy prior to mobilization produces B-cell depletion and seems to be a useful preparative step.

Changes in serum N-acetyl-beta-hexosaminidase levels after treatment of hypothyroid and hyperthyroid individuals with L-thyroxine and propylthiouracil.

Multiple serum samples were obtained from six hypothyroid and six hyperthyroid females, 11--17 years of age, over the course of their corrective treatment with L-thyroxine (LT4) and propylthiouracil (PTU), respectively. Sera were assayed for total N-acetyl-beta-hexosaminidase (HEX), the A (heat-labile) and B (heat-stable) isozymes, and total T4. HEX activity (total HEX A) in sera from hypothyroid (< 4 micrograms/dl T4) patients (total HEX: 518 +/- 66 nmol/60 min/ml, mean +/- S.D.; HEX A: 325 +/- 55; n = 5) was significantly lower than that of the euthyroid control group (total HEX: 638 +/- 77 (p < 0.005); HEX A: 420 +/- 76 ( p < 0.01); n = 23); no difference in HEX B levels was noted. Serum samples from patients successfully treated for hypothyroidism via oral administration of LT4 (n = 12) displayed levels of total HEX (722 +/- 113) and HEX A (491 +/- 91) significantly higher than those of the control group (p < 0.01 in both cases); again, no change in levels of HEX B was observed. HEX activity in sera from hyperthyroid (> 13 micrograms/dl T4) individuals (total HEX: 839 +/- 96; HEX A: 540 +/- 74; HEX B: 299 +/- 52; n =20) was significantly higher than that of the control group (p < 0.005 in all cases). The depression of hormone activity to the euthyroid range by PTU was accompanied ay a decrease in enzyme activity to control levels (total HEX: 632 +/- 92; HEX A: 400 +/- 55; HEX B: 232 +/- 52; n = 16). Non-parametric analysis of the data shows highly significance differences between pre- and post-treatment enzyme levels (alpha < 0.001) in both hyper- and hypothyroid groups. Alteration of thyroid status, and specifically T4 level is, therefore, indicated to be a contributing factor in the regulation of serum HEX activity in humans, as evidenced by individual responsiveness to oral administration of this hormone, or inhibitors of its peripheral metabolism.

Relationship of thyroid status and serum N-acetyl-beta-glucosaminidase isoenzyme activities in humans.

Serum from 28 hyperthyroid, hypothyroid, and euthyroid pre- or early puberty females was examined for N-acetyl-beta-glucosaminidase (HEX) activity. Total, isoenzyme A (labile), and isoenzyme B (stable) levels were determined for this enzyme. A high degree of correlation (r = 0.76; p less than 0.001) exists between total hexosaminidase activity and thyroid hormone levels (as reflected by the Free Thyroxine Index). Examining each isoenzyme individually, A is selectively enhanced (r = 0.84; p less than 0.0005) whereas B displays no significant change regardless of thyroid activity. In hyperthyroid individuals, levels of total hexosaminidase (730 +/- 67 units) (mean +/- S.D.) and isoenzyme A (516 +/- 46) were significantly higher than levels found in either the hypothyroid (total: 547 +/- 30; isoenzyme A: 352 +/- 31) or euthyroid (total: 620 +/- 81; isoenzyme A: 423 +/- 45) groups. However, no change was observed in levels of isoenzyme B among hypothyroid (195 +/- 19), euthyroid (197 +/- 43) and hyperthyroid (215 +/- 32) groups. These data substantiate our earlier findings in the rat, wherein thyroxine administration evoked a similar response in the liver. They are of particular interest in light of the deficiency of HEX A in variants of GM2 gangliosidosis.

Impairment of T-cell growth-promoting lymphokines in human insulin-dependent diabetes mellitus.

T-cell growth factor (TCGF) activity was studied in phytohemagglutinin (PHA)-stimulated peripheral blood mononuclear cells (PBMC) from 10 type-1 diabetic patients who had been diagnosed within the previous 12 months (group A), from 9 diabetic patients in whom the duration of disease was more than 1 year (group B) and from 12 healthy controls (group C). The effects of indomethacin on PHA-induced TCGF activity and the effects of adherent cells (macrophages) from group A and group C on TCGF production of normal group-matched non-adherent cells (lymphocytes) were also studied. TCGF activity was assayed on TCGF-dependent blast cells and calculated as a stimulation index (SI). TCGF activity in group A (SI 0.86 +/- 0.8) was significantly different from that in group B (SI 1.75 +/- 1.02; P = 0.037) and in group C (SI 1.91 +/- 1.29; P = 0.023). Following the addition of indomethacin, TCGF SI was 1.35 +/- 0.74 in group A, 1.85 +/- 0.73 in group B and 2.06 +/- 1.19 in group C. The responses to indomethacin were found to correlate with the basal TCGF activity in all subjects (r = -0.48; P = 0.006) independently of the disease process studied or its duration. No correlation was found between TCGF activity and parameters of metabolic control (HBA1c and fructosamine). Interestingly, a significant inverse correlation was found between TCGF activity and the required dose of insulin only in group A (r = -0.66; P < 0.05). Adherent cells from diabetic patients were found not to inhibit TCGF production.(ABSTRACT TRUNCATED AT 250 WORDS)

Lipophilic thiamine treatment in long-standing insulin-dependent diabetes mellitus.

Thiamine plays an important role in the regulation of glucose metabolism and pancreatic beta-cell functioning. A role for this vitamin in cellular glucose transport has been indicated in the literature. The aim of this study was to determine whether a lipophilic form of thiamine (benzoyloxymethyl-thiamine, BOM) was able to improve metabolic control in patients with long-standing insulin-dependent diabetes mellitus (type 1). A total of 10 children with type 1 diabetes of long duration (age 11.4 +/- 1.2 years, duration of the disease 4.5 +/- 0.7 years, means +/- SEM) were studied before and after treatment with BOM in a randomized double-blind and placebo-controlled study. Five patients were assigned to the BOM-treated group and five to the placebo-group. In all patients basal and glucagon-stimulated C-peptide secretion was undetectable. Thiamine status was assayed by measuring the plasma content of thiamine and its monophosphate form at entry and after 3 months of treatment. The blood HbA(1C) levels and the daily dose of insulin per kg body weight were assessed in both groups before treatment, after 1 month and 3 months of treatment, then 3 months following its suspension. The plasma content of thiamine + thiamine monophosphate in type 1 diabetic patients (35.3 +/- 3.6 pmol/mL) was significantly lower when compared with that measured in six age-matched normal subjects (53.2 +/- 2.3 pmol/mL, P < 0.05).

Sex differences in serum levels of N-acetyl-beta-hexosaminidase in infancy: correlation of enzyme activity with testosterone levels.

Serum levels of N-acetyl-beta-hexosaminidase (HEX) (EC 3.2.1.30) activity in infants display a sexual dimorphism. Total HEX activity in males between 1 and 3 months of age is significantly elevated over female levels (male (M), 1535 +/- 300 nmol/60 min/ml; female (F), 1150 +/- 203, P < 0.0005), and the A (labile) isozyme constitutes a significantly lower proportion of the total activity present (M, 56.0 +/- 4.2, N = 24; F, 64.3 +/- 4.6, N = 21, P < 0.0005). These findings led us to investigate the relationship between testosterone concentration and HEX activity in serum. Samples from male (N = 36) and female (N = 33) infants between 1 and 6 months of age were included. In both sexes, a high degree of correlation (P < 0.0005) was observed between testosterone and total HEX (M, r = 0.71; F, r = 0.73), HEX A (M, r = 0.68; F, r = 0.56) and HEX B (M, r = 0.68; F, r = 0.72). An inverse relationship exists between testosterone levels and % A: M, r = -0.56; F, r = -0.38 (P < 0.0025 and 0.025, respectively). In contrast, no correlation between HEX levels and testosterone was evident in either male or female adults (r = 0.20 and 0.18, respectively). These data implicate testosterone in the regulation of HEX activity during the early months of human development.

Periodontal status and selected cultivable anaerobic microflora of insulin-dependent juvenile diabetics.

The periodontal status and subgingival microflora of insulin-dependent juvenile diabetic (JD) patients (n = 16, mean age = 11.3) were compared with that of their non-diabetic cohabiting healthy siblings (HS, n = 16, mean age = 13.2). JD patients were monitored every 3 months for levels of glycosylated hemoglobin (HbA1c) and clinical and microbial parameters were measured 6 weeks before drawing blood for levels of HbA1c (M% = 8.76). Clinical indices, measured for the entire permanent dentition, included: probing depth (PD), attachment level (AL), sulcus bleeding index (SBI), and plaque index (PI). Subgingival plaque samples were obtained at 2 sites from each subject; whenever possible, the site with the deepest probing depth and the mesial aspect of the maxillary right first molar were used. Microbial analyses were determined by cultural characteristics and biochemical tests. No significant differences were detected in any of the clinical indices for the entire dentition. The mean AL for JD sites was 2.32 +/- 0.83 mm and for HS sites was 2.2 +/- 0.85 mm. Mean percentage of total cultivable anaerobic microflora included Capnocytophaga spp. (JD, 13.21%; HS, 11%) and Porphyromonas gingivalis (JD, 5.1%; HS, 7.9%). Differences between the two groups were not statistically significant. When cluster analysis was performed on sampled sites, one cluster group in JD patients showed significantly elevated P. gingivalis and lower Capnocytophaga spp. levels as compared to the overall mean. The clinical parameters of this cluster were characterized by statistically significant greater loss of attachment and probing depth. These data would suggest few differences between JD patients and their HS in this population.

Spontaneous uterine rupture with amniotic sac protrusion at 28 weeks subsequent to previous hysteroscopic metroplasty.

BACKGROUND: Hysteroscopic metroplasty improves pregnancy outcome in case of uterine septum. Uterine rupture during a pregnancy following this procedure may occur. CASE: A patient with a history of hysteroscopic resection of a uterine septum complicated by fundal perforation, presented at 28 weeks a spontaneous uterine rupture with amniotic sac protrusion through the uterine wall disruption. CONCLUSION: Uterine rupture during pregnancy following a hysteroscopic metroplasty may occur even though it appears to be a very uncommon event. Patients who have had this procedure should be aware of this potential risk in case of future pregnancies. How to avoid such complication is still unclear.