bluuebunny/crossref_metadata_2025 huggingface dataset:
The effects of long-term total parenteral nutrition on gut mucosal immunity in children with short bowel syndrome: a systematic review
Authors: Duran Beyhan
Published: February 2005

Background

Short bowel syndrome (SBS) is defined as the malabsorptive state that often follows massive resection of the small intestine. Most cases originate in the newborn period and result from congenital anomalies. It is associated with a high morbidity, is potentially lethal and often requires months, sometimes years, in the hospital and home on total parenteral nutrition (TPN). Long-term survival without parenteral nutrition depends upon establishing enteral nutrition and the process of intestinal adaptation through which the remaining small bowel gradually increases its absorptive capacity. The purpose of this article is to perform a descriptive systematic review of the published articles on the effects of TPN on the intestinal immune system investigating whether long-term TPN induces bacterial translocation, decreases secretory immunoglobulin A (S-IgA), impairs intestinal immunity, and changes mucosal architecture in children with SBS.

Methods

The databases of OVID, such as MEDLINE and CINAHL, Cochran Library, and Evidence-Based Medicine were searched for articles published from 1990 to 2001. Search terms were total parenteral nutrition, children, bacterial translocation, small bowel syndrome, short gut syndrome, intestinal immunity, gut permeability, sepsis, hyperglycemia, immunonutrition, glutamine, enteral tube feeding, and systematic reviews. The goal was to include all clinical studies conducted in children directly addressing the effects of TPN on gut immunity.

Results

A total of 13 studies were identified. These 13 studies included a total of 414 infants and children between the ages approximately 4 months to 17 years old, and 16 healthy adults as controls; and they varied in design and were conducted in several disciplines. The results were integrated into common themes. Five themes were identified: 1) sepsis, 2) impaired immune functions: In vitro studies, 3) mortality, 4) villous atrophy, 5) duration of dependency on TPN after bowel resection.

Conclusion

Based on this exhaustive literature review, there is no direct evidence suggesting that TPN promotes bacterial overgrowth, impairs neutrophil functions, inhibits blood's bactericidal effect, causes villous atrophy, or causes to death in human model.

The hypothesis relating negative effects of TPN on gut immunity remains attractive, but unproven. Enteral nutrition is cheaper, but no safer than TPN. Based on the current evidence, TPN seems to be safe and a life saving solution.
Are ICD-10 codes appropriate for performance assessment in asthma and COPD in general practice? Results of a cross sectional observational study
Authors: Schneider Antonius , Gantner Lutz , Maag Inko , Borst Mathias M , Wensing Michel , Szecsenyi Joachim
Published: February 2005

Background

The increasing prevalence and impact of obstructive lung diseases and new insights, reflected in clinical guidelines, have led to concerns about the diagnosis and therapy of asthma and COPD in primary care. In Germany diagnoses written in medical records are used for reimbursement, which may influence physicians' documentation behaviour. For that reason it is unclear to what respect ICD-10 codes reflect the real problems of the patients in general practice. The aim of this study was to assess the appropriateness of the recorded diagnoses and to determine what diagnostic information is used to guide medical treatment.

Methods

All patients with lower airway symptoms (n = 857) who had attended six general practices between January and June 2003 were included into this cross sectional observational study. Patients were selected from the computerised medical record systems, focusing on ICD-10-codes concerning lower airway diseases (J20-J22, J40-J47, J98 and R05). The performed diagnostic procedures and actual medication for each identified patient were extracted manually. Then we examined the associations between recorded diagnoses, diagnostic procedures and prescribed treatment for asthma and COPD in general practice.

Results

Spirometry was used in 30% of the patients with a recorded diagnosis of asthma and in 58% of the patients with a recorded diagnosis of COPD. Logistic regression analysis showed an improved use of spirometry when inhaled corticosteroids were prescribed for asthma (OR = 5.2; CI 2.9–9.2) or COPD (OR = 4.7; CI 2.0–10.6). Spirometry was also used more often when sympathomimetics were prescribed (asthma: OR = 2.3; CI 1.2–4.2; COPD: OR = 4.1; CI 1.8–9.4).

Conclusions

This study revealed that spirometry was used more often when corticosteroids or sympathomimetics were prescribed. The findings suggest that treatment was based on diagnostic test results rather than on recorded diagnoses. The documented ICD-10 codes may not always reflect the real status of the patients. Thus medical care for asthma and COPD in general practice may be better than initially found on the basis of recorded diagnoses, although further improvement of practice patterns in asthma and COPD is still necessary.
Morning versus evening dosing of desloratadine in seasonal allergic rhinitis: a randomized controlled study [ISRCTN23032971].
Authors: Haye Rolf , Høye Kjetil , Berg Olof , Frønes Sissel , Ødegård Tone
Published: February 2005

Background

A circadian rhythm of symptoms has been reported in allergic rhinitis and some studies have shown the dosing time of antihistamines to be of importance for optimizing symptom relief in this disease. The objective of this study was to examine the efficacy of morning vs. evening dosing of the antihistamine desloratadine at different time points during the day.

Methods

Patients ≥ 18 years, with seasonal allergic rhinitis received desloratadine 5 mg orally once daily in the morning (AM-group) or evening (PM-group) for two weeks. Rhinorrhea, nasal congestion, sneezing and eye symptoms were scored morning and evening. Wilcoxon rank sum and 2-way ANOVA test were used.

Results

Six-hundred and sixty-three patients were randomized; 336 in the AM-group; 327 in the PM-group. No statistically significant differences were seen between the AM and PM group at any time points. In the sub-groups with higher morning or evening total symptom score no difference in treatment efficacy was seen whether the dose was taken 12 or 24 hours before the higher score time. There was a circadian variation in baseline total symptom score; highest during daytime and lowest at night. The circadian variation in symptoms was reduced during treatment. This reduction was highest for daytime symptoms.

Conclusions

A circadian rhythm was seen for most symptoms being more pronounced during daytime. This was less apparent after treatment with desloratadine. No statistically significant difference in efficacy was seen whether desloratadine was given in the morning or in the evening. This gives the patients more flexibility in choosing dosing time.
Genomic analysis of early murine mammary gland development using novel probe-level algorithms
Authors: Master Stephen R , Stoddard Alexander J , Bailey L Charles , Pan Tien-Chi , Dugan Katherine D , Chodosh Lewis A
Published: February 2005

We describe a novel algorithm (ChipStat) for detecting gene-expression changes utilizing probe-level comparisons of replicate Affymetrix oligonucleotide microarray data. A combined detection approach is shown to yield greater sensitivity than a number of widely used methodologies including SAM, dChip and logit-T. Using this approach, we identify alterations in functional pathways during murine neonatal-pubertal mammary development that include the coordinate upregulation of major urinary proteins and the downregulation of loci exhibiting reciprocal imprinting.
Port site tuberculosis following laparoscopic cholecystectomy
Authors: Chintamani  , Kumar Vikas , Singhal Vinay
Published: February 2005

Port site metastasis is being increasingly reported as a complication following laparoscopic surgery for malignant disorders. Various factors have been reported to be responsible and most are associated with either a high intra-peritoneal pressure due to pneumoperitoneum or the ‘chimney effect’ following sudden decompression of the abdomen. Direct implantation of the offending cells at the raw surface at the port has also been implicated and the use of retrieval bags is therefore recommended. We report on a rare case of port site seeding of tuberculosis in a 65-year-old woman following laparoscopic cholecystectomy.
Peptic ulcer perforation: Management of high-risk cases by percutaneous abdominal drainage
Authors: Rahman M Mizanur , Mamun A Al , Hossain M Delwar , Das M Kante
Published: February 2005

Sixty-six patients were selected as high-risk cases of duodenal ulcer perforation. After resuscitation with intravenous fluids and nasogastric suction, a wide-bore percutaneous intra-abdominal drain was put in under local anaesthesia. There were three (4.5%) deaths; 58 (87.8%) patients improved satisfactorily. High-risk peptic ulcer perforation patients can be managed by putting in an intra-abdominal drain supported by conservative treatment.
Winter peak of respiratory syncytial virus in Islamabad
Authors: Tariq Waheed-Uz-Zaman , Waqar Talal , Ali Salman , Ghani Eijaz
Published: February 2005

A study was carried out on 391 cases of bronchiolitis and pneumonia from different paediatric units in Rawalpindi/Islamabad, Pakistan. A clear winter spike of respiratory syncytial virus (RSV) was noted. It was found that there was a substantial increase of 30-50% in the positivity of RSV from December to February.
Nucleation-Dependent Polymerization Is an Essential Component of Amyloid-Mediated Neuronal Cell Death
Authors: Wogulis Mark , Wright Sarah , Cunningham Damian , Chilcote Tamie , Powell Kyle , Rydel Russell E.
Published: February 2005

Accumulating evidence suggests that amyloid protein aggregation is pathogenic in many diseases, including Alzheimer's disease. However, the mechanisms by which protein aggregation mediates cellular dysfunction and overt cell death are unknown. Recent reports have focused on the potential role of amyloid oligomers or protofibrils as a neurotoxic form of amyloid-β (Aβ) and related amyloid aggregates. Here we describe studies indicating that overt neuronal cell death mediated by Aβ1-40is critically dependent on ongoing Aβ1-40polymerization and is not mediated by a single stable species of neurotoxic aggregate. The extent and rate of neuronal cell death can be controlled by conditions that alter the rate of Aβ polymerization. The results presented here indicate that protofibrils and oligomeric forms of Aβ most likely generate neuronal cell death through a nucleation-dependent process rather than acting as direct neurotoxic ligands. These findings bring into question the use of the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide formazan assay (MTT assay) as a reporter of Aβ-mediated neuronal cell death and suggest that diffusible Aβ protofibrils and oligomers more likely mediate subtle alterations of synaptic function and long-term potentiation rather than overt neuronal cell death. These results have been extended to Aβ1-42, the non-Aβ component of Alzheimer's disease amyloid plaques, and human amylin, suggesting that nucleation-dependent polymerization is a common mechanism of amyloid-mediated neuronal cell death. Our findings indicate that ongoing amyloid fibrillogenesis may be an essential mechanistic process underlying the pathogenesis associated with protein aggregation in amyloid disorders.
Age-Dependent Enhancement of Hippocampal Long-Term Potentiation and Impairment of Spatial Learning through the Rho-Associated Kinase Pathway in Protein Tyrosine Phosphatase Receptor Type Z-Deficient Mice
Authors: Niisato Kazue , Fujikawa Akihiro , Komai Shoji , Shintani Takafumi , Watanabe Eiji , Sakaguchi Gaku , Katsuura Goro , Manabe Toshiya , Noda Masaharu
Published: February 2005

Although protein tyrosine phosphatases (PTPs) are expressed abundantly in the brain, their roles in synaptic plasticity have not been well elucidated. In this study, we have examined the physiological functions of Ptprz, which is a receptor-type PTP expressed predominantly in the brain as a chondroitin sulfate proteoglycan. We have examined phenotypes of mutant mice deficient inPtprzusing electrophysiological, pharmacological, and behavioral approaches. Mutant mice exhibit enhanced long-term potentiation (LTP) in the CA1 region of hippocampal slices and impaired spatial learning abilities in an age-dependent manner: young adult (<10 weeks old) mutant mice show normal LTP and learning abilities in the Morris water maze task, whereas adult (>13 weeks old) mutant mice exhibit enhanced LTP and impairment in the task. The enhanced LTP is specifically canceled out by pharmacological inhibition of Rho-associated kinase (ROCK), a major downstream effector of Rho. These findings suggest that the lack ofPtprzleads to aberrant activation of ROCK and resultantly to enhanced LTP in the slice and learning impairments in the animal.
Changes of Internal State Are Expressed in Coherent Shifts of Neuromuscular Activity inAplysiaFeeding Behavior
Authors: Zhurov Yuriy , Proekt Alex , Weiss Klaudiusz R. , Brezina Vladimir
Published: February 2005

The multitasking central pattern generator (CPG) that drives consummatory feeding behaviors ofAplysiacan produce ingestive, egestive, and intermediate motor programs. External stimuli trigger the programs but, remarkably, do not directly specify which type of program is produced. Rather, recent work has proposed, the type of program is determined by the internal network state of the CPG that has developed in response to the previous history of the stimulation. Here we have tested a key prediction of this network-state hypothesis. If the network state has a real existence and governs real functional behavior, changes in the state should be seen as coherent, coordinated changes along many dimensions of interneuron and motor neuron activity, muscle contraction, and ultimately movement, that underlie functional behavior. In reduced neuromuscular preparations, we elicited repetitive motor programs by continued stimulation of the esophageal nerve while recording the firing of motor neurons B8, B15, B16, B4/5, and B48, and contractions of the accessory radula closer and I7-I10 muscles that respectively close and open the animal's food-grasping organ, the radula. Using sonomicrometric techniques, we similarly recorded the movement of the radula in the complete buccal mass. Successive esophageal nerve programs indeed exhibited clear progressive changes in motor neuron firing, muscle contractions, and the phasing of radula movements within each cycle, from an initially intermediate or even ingestive character to a strongly egestive character. We conclude that theAplysiafeeding CPG really has a coherent internal network state whose dynamics are likely to be reflected in the real behavior of the animal.
Brain-Derived Neurotrophic Factor and Antidepressant Drugs Have Different But Coordinated Effects on Neuronal Turnover, Proliferation, and Survival in the Adult Dentate Gyrus
Authors: Sairanen Mikko , Lucas Guilherme , Ernfors Patrik , Castrén Maija , Castrén Eero
Published: February 2005

Antidepressants increase proliferation of neuronal progenitor cells and expression of brain-derived neurotrophic factor (BDNF) in the hippocampus. We investigated the role of BDNF signaling in antidepressant-induced neurogenesis by using transgenic mice with either reduced BDNF levels (BDNF+/-) or impaired trkB activation (trkB.T1-overexpressing mice). In both transgenic strains, chronic (21 d) imipramine treatment increased the number of bromodeoxyuridine (BrdU)-positive cells to degree similar to that seen in wild-type mice 24 h after BrdU administration, although the basal proliferation rate was increased in both transgenic strains. Three weeks after BrdU administration and the last antidepressant injection, the amount of newborn (BrdU- or TUC-4-positive) cells was significantly reduced in both BDNF+/-and trkB.T1-overexpressing mice, which suggests that normal BDNF signaling is required for the long-term survival of newborn hippocampal neurons. Moreover, the antidepressant-induced increase in the surviving BrdU-positive neurons seen in wild-type mice 3 weeks after treatment was essentially lost in mice with reduced BDNF signaling. Furthermore, we observed that chronic treatment with imipramine or fluoxetine produced a temporally similar increase in both BrdU-positive and terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end-labeled neurons in the dentate gyrus, indicating that these drugs simultaneously increase both neurogenesis and neuronal elimination. These data suggest that antidepressants increase turnover of hippocampal neurons rather than neurogenesis per se and that BDNF signaling is required for the long-term survival of newborn neurons in mouse hippocampus.
Release of ATP in the Ventral Medulla during Hypoxia in Rats: Role in Hypoxic Ventilatory Response
Authors: Gourine Alexander V. , Llaudet Enrique , Dale Nicholas , Spyer K. Michael
Published: February 2005

P2X2receptor subunits of the ATP-gated ion channels are expressed by physiologically identified respiratory neurons in the ventral respiratory column, implicating ATP in the control of respiratory activity. We now show that, during hypoxia, release of ATP in the ventrolateral medulla (VLM) plays an important role in the hypoxic ventilatory response in rats. By measuring ATP release in real time at the ventral surface of the medulla with novel amperometric biosensors, we found that hypoxia (10% O2; 5 min) induced a marked increase in the concentration of ATP (∼3 μm). This ATP release occurred after the initiation of enhanced respiratory activity but coincided with the later hypoxia-induced slowing of the respiratory rhythm. ATP was also released at the ventral surface of the medulla during hypoxia in peripherally chemodenervated animals (vagi, aortic, and carotid sinus nerve sectioned). By using horizontal slices of the rat medulla, we found that, during hypoxia, ATP is produced throughout the VLM in the locations corresponding to the ventral respiratory column. Blockade of ATP receptors in the VLM (microinjection of P2 receptor antagonist pyridoxal-5′-phosphate-6-azophenyl-2′,4′-disulphonic acid; 100 μm) augmented the hypoxia-induced secondary slowing of the respiratory rhythm. Our findings suggest that ATP released within the ventral respiratory column is involved in maintenance of the respiratory activity in conditions when hypoxia-induced slowing of respiration occurs. These data illustrate a new functional role for ATP-mediated purinergic signaling in the medullary mechanisms controlling respiratory activity.
Estrogen Influences Cocaine-Induced Blood Oxygen Level-Dependent Signal Changes in Female Rats
Authors: Febo Marcelo , Ferris Craig F. , Segarra Annabell C.
Published: February 2005

We investigated the effect of estrogen on cocaine-induced brain activity using blood oxygen level-dependent (BOLD) magnetic resonance imaging. Ovariectomized (Ovx) rats without estrogen and Ovx rats with estrogen (Ovx+E) were given a single saline or cocaine injection (15 mg/kg, i.p.) for 5 d. After 7 d of withdrawal from injections, rats were challenged with cocaine during functional imaging. Acute cocaine administration produced positive BOLD activation in the prefrontal cortex, nucleus accumbens, striatum, ventral tegmental area, and hippocampus, among other brain regions. Positive BOLD signal changes were lower in Ovx+E than in Ovx rats. With repeated cocaine administration, Ovx+E rats showed enhanced BOLD signal changes in the nucleus accumbens, ventral tegmental area, and hippocampus compared with acutely treated animals. Our results indicate that estrogen influences the effects of acute and repeated cocaine administration on BOLD signal changes. The data suggest that in females with estrogen, cocaine-induced neuronal activity is enhanced after repeated cocaine administration. It is possible that the actions of estrogen within the aforementioned brain regions potentiate the behavioral response to cocaine observed in female rats.
A Novel Phenylalanine-Based Targeting Signal Directs Telencephalin to Neuronal Dendrites
Authors: Mitsui Sachiko , Saito Michiko , Hayashi Ken , Mori Kensaku , Yoshihara Yoshihiro
Published: February 2005

Neurons sort out a variety of functional molecules to appropriate subcellular destinations. Telencephalin (TLCN; intercellular adhesion molecule-5) is a cell adhesion molecule specifically localized to somatodendritic membranes in the telencephalic neurons. Here, we established a newin vivostrategy to analyze neuronal sorting mechanisms by ectopic expression of molecules of interest in the cerebellar Purkinje cells of transgenic mice. By using this system, we identified a novel dendritic targeting determinant in the cytoplasmic tail region of TLCN. A full-length TLCN ectopically expressed in the Purkinje cells was localized exclusively to dendrites but not to axons. In contrast, a deletion of cytoplasmic C-terminal 12 amino acids (residues 901-912) or a point mutation of Phe905 to Ala abrogated the dendrite-specific targeting with appearance of the truncated and point-mutated TLCN in both axons and dendrites. Furthermore, an addition of the C-terminal 17 amino acids (residues 896-912) of TLCN to an unrelated molecule (CD8) was sufficient for its specific targeting to dendrites in several types of neurons. Because the C-terminal region of TLCN does not contain any canonical dendritic targeting sequences such as the tyrosine-based motif or the dileucine motif, this study suggests a novel mechanism of protein trafficking to the dendritic compartment of neurons.
Calmodulin-Dependent Kinase Kinase/Calmodulin Kinase I Activity Gates Extracellular-Regulated Kinase-Dependent Long-Term Potentiation
Authors: Schmitt John M. , Guire Eric S. , Saneyoshi Takeo , Soderling Thomas R.
Published: February 2005

Intracellular Ca2+and protein phosphorylation play pivotal roles in long-term potentiation (LTP), a cellular model of learning and memory. Ca2+regulates multiple intracellular pathways, including the calmodulin-dependent kinases (CaMKs) and the ERKs (extracellular signal-regulated kinases), both of which are required for LTP. However, the mechanism by which Ca2+activates ERK during LTP remains unknown. Here, we describe a requirement for the CaMK-kinase (CaMKK) pathway upstream of ERK in LTP induction. Both the pharmacological inhibitor of CaMKK, STO-609, and dominant-negative CaMKI (dnCaMKI), a downstream target of CaMKK, blocked neuronal NMDA receptor-dependent ERK activation. In contrast, an inhibitor of CaMKII and nuclear-localized dnCaMKIV had no effect on ERK activation. NMDA receptor-dependent LTP induction robustly activated CaMKI, the Ca2+-stimulated Ras activator Ras-GRF1 (Ras-guanyl-nucleotide releasing factor), and ERK. STO-609 blocked the activation of all three enzymes during LTP without affecting basal synaptic transmission, activation of CaMKII, or cAMP-dependent activation of ERK. LTP induction itself was suppressed ∼50% by STO-609 in a manner identical to the ERK inhibitor U0126: either inhibitor occluded the effect of the other, suggesting they are part of the same signaling pathway in LTP induction. STO-609 also suppressed regulatory phosphorylation of two downstream ERK targets during LTP, the general translation factors eIF4E (eukaryotic initiation factor 4) and its binding protein 4E-BP1 (eukaryotic initiation factor 4E-binding protein 1). These data indicate an essential role for CaMKK and CaMKI to link NMDA receptor-mediated Ca2+elevation with ERK-dependent LTP.
Association of CaV1.3 L-Type Calcium Channels with Shank
Authors: Zhang Hua , Maximov Anton , Fu Yu , Xu Fang , Tang Tie-Shan , Tkatch Tatiana , Surmeier D. James , Bezprozvanny Ilya
Published: February 2005

Neurons express multiple types of voltage-gated calcium (Ca2+) channels. Two subtypes of neuronal L-type Ca2+channels are encoded by CaV1.2 and CaV1.3 pore-forming subunits. Both CaV1.2 and CaV1.3 subunits contain class I PDZ (postsynaptic density-95/Discs large/zona occludens-1) domain-binding consensus at their C termini. In yeast two-hybrid screen of rat brain cDNA library with the C-terminal bait of CaV1.3a (long C-terminal splice variant) L-type Ca2+channel subunit, we isolated multiple clones of postsynaptic adaptor protein Shank. We demonstrated a specific association of CaV1.3a C termini, but not of CaV1.2 C termini, with Shank PDZ domainin vitro. We further demonstrated that the proline-rich region present in C termini of CaV1.3a subunit binds to Shank Src homology 3 domain. We established that CaV1.3a and Shank localized to postsynaptic locations in cultured rat hippocampal neurons. By expressing epitope-tagged recombinant CaV1.3 subunits in rat hippocampal neuronal cultures, we demonstrated that the presence of Shank-binding motifs in CaV1.3a sequence is both necessary and sufficient for synaptic clustering of CaV1.3 L-type Ca2+channels. In experiments with dominant-negative peptides and dihydropyridine-resistant CaV1.3a mutants, we demonstrated an importance of Shank-binding motif in CaV1.3a sequence for phosphorylated cAMP response element-binding protein (pCREB) signaling in cultured hippocampal neurons. Our results directly link CaV1.3 neuronal L-type Ca2+channels to macromolecular signaling complex formed by Shank and other modular adaptor proteins at postsynaptic density and provide novel information about the role played by CaV1.3 L-type Ca2+channels in pCREB signaling.
Altered Thermal Selection Behavior in Mice Lacking Transient Receptor Potential Vanilloid 4
Authors: Lee Hyosang , Iida Tohko , Mizuno Atsuko , Suzuki Makoto , Caterina Michael J.
Published: February 2005

Transient receptor potential vanilloid 4 (TRPV4), a cation channel responsive to hypotonicity, can also be activated by warm temperatures. Moreover, TRPV4-/-mice reportedly exhibit deficits in inflammation-induced thermal hyperalgesia. However, it is unknown whether TRPV4 or related transient receptor potential channels account for warmth perception under injury-free conditions. We therefore investigated the contribution of TRPV4 to thermosensation and thermoregulationin vivo. On a thermal gradient, TRPV4-/-mice selected warmer floor temperatures than wild-type littermates. In addition, whereas wild-type mice failed to discriminate between floor temperatures of 30 and 34°C, TRPV4-/-mice exhibited a strong preference for 34°C. TRPV4-/-mice also exhibited prolonged withdrawal latencies during acute tail heating. TRPV4-/-and wild-type mice exhibited similar changes in behavior on a thermal gradient after paw inflammation. Circadian body temperature fluctuations and thermoregulation in a warm environment were also indistinguishable between genotypes. These results demonstrate that TRPV4 is required for normal thermal responsivenessin vivo.
Septicemia in the First Week of Life in a Norwegian National Cohort of Extremely Premature Infants
Authors: Rønnestad Arild , Abrahamsen Tore G. , Medbø Sverre , Reigstad Hallvard , Lossius Kristin , Kaaresen Per I. , Engelund Inger E. , Irgens Lorentz M. , Markestad Trond
Published: February 2005

Objectives. To investigate the incidence, causes, predictors, and outcomes of septicemia in the first week of life in a national cohort of extremely premature infants.

Methods. A prospective study of survival of all infants with gestational age of <28 weeks or birth weight of <1000 g who were born in Norway in 1999–2000 was performed. Data on the maternal prenatal history, delivery, and neonatal course, including detailed information on episodes of microbiologically verified septicemia, were collected on predefined forms. Septicemia was reported in 2 groups, ie, episodes diagnosed on the day of delivery (ie, very early-onset septicemia [VEOS]) and episodes diagnosed from day 2 to day 7 of life (ie, early-onset septicemia [EOS]). Logistic regression models were used for the selection of variables for predictor analysis in each group.

Results. Of 462 included infants, VEOS occurred for 15 (32.5 per 1000 population) and EOS for 15 (35.5 per 1000 population). The most prevalent bacteria were Escherichia coli in VEOS (n = 9) and staphylococci (coagulase-negative staphylococci and Staphylococcus aureus) (n = 15) in EOS. Case fatality rates were 40% and 13%, respectively. Independent predictive factors for VEOS were clinical chorioamnionitis (odds ratio [OR]: 10.5; 95% confidence interval [CI]: 3.3-33.4) and high maternal age (OR: 1.2; 95% CI: 1.0–1.3), whereas not receiving systemic antibiotic therapy within 2 days of age (OR: 13.6; 95% CI: 3.7–50.2) and receiving nasal continuous positive airway pressure (n-CPAP) support at 24 hours of age (OR: 9.8; 95% CI: 2.5–38.4) independently predicted septicemia after the first day of life.

Conclusions. Whereas vertically transmitted septicemia was dominated by Gram-negative bacteria, with predictors being exclusively of maternal origin, EOS was dominated by typically nosocomial flora, with n-CPAP treatment at 24 hours of age being a powerful predictor. Early n-CPAP treatment, as opposed to mechanical ventilation, as a powerful predictor of septicemia in the early neonatal period, even with adjustment for early systemic antibiotic treatment, is a new observation among extremely premature infants that warrants additional study.
Utility of Rapid B-Type Natriuretic Peptide Assay for Diagnosis of Symptomatic Patent Ductus Arteriosus in Preterm Infants
Authors: Choi Byung Min , Lee Kee Hyoung , Eun Baik Lin , Yoo Kee Hwan , Hong Young Sook , Son Chang Sung , Lee Joo Won
Published: February 2005

Objective. In preterm infants, the rapid and accurate determination of the presence of a hemodynamically significant patent ductus arteriosus (PDA) is extremely important, but this is often difficult. Plasma B-type natriuretic peptide (BNP) measurement has been reported to be a helpful aid in the diagnosis of hemodynamically significant PDA in preterm infants. The aim of our study was to investigate the usefulness of a rapid BNP assay as a diagnostic marker of symptomatic PDA (sPDA) in preterm infants.

Methods. Sixty-six preterm infants, ranging from 25 to 34 gestational weeks of age, underwent clinical and echocardiographic examinations for PDA every other day from the third day of life until the disappearance of ductal flow. Blood samples were collected and plasma BNP concentrations were measured simultaneously using a commercial kit, (Triage BNP test kit; Biosite Diagnositics, San Diego, CA). When ≥2 clinically significant features of PDA were noted, and a large ductal flow was confirmed by color Doppler echocardiography, sPDA was diagnosed and treated with indomethacin.

Results. On the third day after birth, the mean BNP concentration in the sPDA group (n = 23) was significantly higher than in the control group (n = 43) (2896 ± 1627 vs 208 ± 313 pg/mL). Seventeen infants (74%) in the sPDA group became asymptomatic after an initial course of indomethacin and their BNP levels concomitantly decreased. Moreover, BNP concentrations were significantly correlated with the magnitudes of the ductal shunt, such as the ratio of left atrial to aortic root diameter and the diastolic flow velocity of the left pulmonary artery (r = 0.726 and 0.877). The area under the receiver operator characteristic curve for the detection of sPDA was high: 0.997 (95% confidence interval: 0.991–1.004). The best cutoff of BNP concentration for the diagnosis of sPDA was determined to be 1110 pg/mL (sensitivity: 100%; specificity: 95.3%).

Conclusion. In preterm infants, the circulating BNP levels correlated well with the clinical and echocardiographic assessments of PDA. Although not a stand-alone test, the rapid BNP assay provides valuable information for the detection of infants with sPDA that require treatment. Moreover, serial BNP measurements may be of value in determining the clinical course of PDA in preterm infants.
Periodontitis
Authors: Flemmig Thomas F.
Published: February 2005

The purpose of this review was to assess the scientific and clinical bases for the proposed classification of periodontitis. The clinical and histopathological signs and the etiology of periodontitis were described. Cross‐sectional studies were analyzed to determine when onset of periodontitis most frequently occurs in adults. In addition, the progression rates of periodontitis have been assessed from longitudinal studies. No clinical, histopathological, or microbiological features could be identified that would characterize different disease entities of chronic periodontitis. The prevalence, extent, and severity of periodontitis were found to increase continually with higher age and there was no age when onset of disease would most likely occur. The rate of periodontitis progression varies largely between patients and there is no natural threshold for distinguishing various rates of disease progression. The incidence of periodontitis unresponsive to treatment depends on pretreatment progression rate, extent and severity of disease, tooth type, smoking, high levels of putative periodontal pathogens, a deficient immune response, and the type of therapy provided. There is no scientific basis for the classification “adult periodontitis” and “refractory adult periodontitis.” Extensive clinical examinations are required for the diagnosis of “rapidly progressive adult periodontitis.” It appears unrealistic that these examinations can be performed routinely in clinical practice. Therefore, the classification proposed by the Organizing Committee to define adult, rapidly progressive, and refractory periodontitis as specific disease entities was replaced with a simplified classification of periodontitis based on the scientific data available. Ann Periodontol 1999;4:32‐37.
Periodontic‐Endodontic Lesions
Authors: Meng Huan Xin
Published: February 2005

Lesions of the periodontal ligament and adjacent alveolar bone may originate from infections of the periodontium or tissues of the dental pulp. This review focuses on the relationship of lesions of endodontic origin with lesions of periodontal origin and their classification. Ann Periodontol 1999;4:84‐89.
Mucogingival Deformities
Authors: Prato Giovan Paolo Pini
Published: February 2005

The presence of mucogingival deformities often have an impact on patients in terms of esthetics and function. The variety of the conditions makes it difficult to place gingival and alveolar mucosa deformities under a single definition. Mucogingival deformities, as defined in this paper, may be congenital, developmental, or acquired defects. These may occur around natural teeth or implants and in edentulous ridges. They may be localized to soft tissues or be associated with defects in the underlying bone. They may show different degrees of severity and extension. A classification of mucogingival deformities should provide a method for identifying the different conditions in order to improve diagnosis, etiologic identification, research, treatment, and insurance evaluation. Ann Periodontol 1999;4:98‐100.
The Influence of Bone Thickness on Facial Marginal Bone Response: Stage 1 Placement Through Stage 2 Uncovering
Authors: Spray J. Robert , Black C. Gary , Morris Harold F. , Ochi Shigeru
Published: February 2005

Background: Various causes of facial bone loss around dental implants are reported in the literature; however, reports on the influence of residual facial bone thickness on the facial bone response (loss or gain) have not been published. This study measured changes in vertical dimension of facial bone between implant insertion and uncovering and compared these changes to facial bone thickness for more than 3,000 hydroxyapatite (HA)‐coated and non–HA‐coated root‐form dental implants.

Methods: Subjects were predominantly white males, 18 to 80+ years of age (mean 62.9 years), who were patients at 30 Department of Veterans Affairs Medical Centers and two university dental clinics. Alveolar ridges ranged from normal to resorbed with intact basal bone. Following preparation of the osteotomy site, direct measurements with calipers were made of the residual facial bone thickness, approximately 0.5 mm below the crest of the bone. The distance from the top of the implants to the crest of the facial bone was also measured using periodontal probes. Implants were uncovered between 3 to 4 months in the mandible and 6 to 8 months in the maxilla after insertion. Facial bone response was the difference between the height of facial bone at Stage 1 (insertion) and Stage 2 (uncovering).

Results:The mean facial bone thickness after osteotomies were made was 1.7 ± 1.13 mm. When a mean facial bone thickness of 1.8 ± 1.41 mm or larger remained after site preparation, bone apposition was more likely to occur. The mean facial bone response for 2,685 implants was −0.7 ± 1.70 mm. For implants integrated at uncovering, the mean bone response was −0.7 ± 1.69 mm, and −2.8 ± 1.57 mm for implants mobile at uncovering. Bone quality‐4 had the least facial bone response, −0.5 ± 2.11 mm. Bone responses were similar for both HA‐coated and non—HA‐coated implants.

Conclusions: Significantly greater amounts of facial bone loss were associated with implants that failed to integrate. As the bone thickness approached 1.8 to 2 mm, bone loss decreased significantly and some evidence of bone gain was seen. There was no statistically or clinically significant difference in bone response between HA‐coated and non—HA‐coated implants. Ann Periodontol 2000;5:119‐128.
Survival and Stability (PTVs) of Six Implant Designs From Placement to 36 Months
Authors: Morris Harold F. , Ochi Shigeru
Published: February 2005

Background: Numerous new implant designs and materials have become available over the last decade, each with special claims of superiority in restoring complex cases. Differences in existing clinical databases, study designs, and methods of determining failures/survival are seldom standardized, which complicates comparisons of clinical performance of these new designs. Little information is available concerning the changes in stability of various designs and materials following clinical loading.

Methods: A total of 30 VA medical centers and 2 dental schools combined to form the Dental Implant Clinical Research Group (DICRG). More than 2,900 implants were placed, restored and data gathered from the time of placement to 36 months. Implant stability from uncovering to 36 months and survival from placement to 36 months were determined. Survival was determined using two different approaches—considering all implants removed at any time, regardless of the reason (DICRG approach), and considering only those that were removed following loading of the prosthesis (post‐loading approach). Survival was also determined for each of the three phases of implant treatment—phase 1, from the time of placement to uncovering and abutment connection; phase 2, from uncovering to placement and loading of the prosthesis; and phase 3, from loading of the prosthesis to 36 months.

Results: The two approaches to determining survival for each implant design and/or material included in the study showed differences in reported numbers ranging from 1.1% to 21.7%. The largest difference in survival was for the commerically pure titanium screw (used in this study only in the maxillary completely edentulous applications), which showed a 21.7% greater survival rate. With the DICRG approach, the hydroxyapatite (HA)‐cylinder had the highest survival (97.5%). When considering the post‐loading approach, the titanium‐alloy screw had the highest survival (99.4%), with the HA‐cylinder having the next highest survival (98.6%). The HA‐cylinder did not show increased stability from uncovering to 36 months, and the HA‐grooved implant became less stable.

Conclusions: HA‐coated implants demonstrated the highest survival rate; 2) the post‐loading analysis approach inflated survival; 3) non‐HA implants showed increased stability following loading; 4) HA‐coated implants showed a slight decrease or no change in stability; and 5) the clinical significance of the changes in implant stability must be determined for the long term. Ann Periodontol 2000;5:15‐21.
Implant Survival to 36 Months as Related to Length and Diameter
Authors: Winkler Sheldon , Morris Harold F. , Ochi Shigeru
Published: February 2005

Background: It is generally accepted that diameter and length of an endosseous dental implant and its stability at placement are critical factors in achieving and maintaining osseointegration. In the event of slight implant mobility at placement, the conventional or accepted treatment is to place a longer implant and/or one of wider diameter. This manuscript presents stability and survival/failure data for implants of different diameters and lengths following 36 months post‐placement, as well as crestal bone loss data between placement and uncovering.

Methods: A subset of the Dental Implant Clinical Research Group's database was used to study the 3‐ year survival and stability of various implant lengths (7 mm, 8 mm, 10 mm, 13 mm, and 16 mm) and diameters (3 mm+ and 4 mm+). Placement to uncovering crestal bone loss was also determined. The implants were generally representative of those available for clinical use (screws, basket, grooved, hydroxy‐apatitecoated, CP‐Ti, Ti‐alloy). The study protocol specified that the implants be randomized to various jaw regions to accomplish the primary goals of the study—the comparison of each implant design's overall survival. A total of 2,917 implants were placed, restored, and followed. Data for all 3 mm to 3.9 mm diameter implants were pooled into a “3+” group, and the 4 mm to 4.9 mm diameter implants into a “4+” mm group. No attempt was made to look at the influence of any other variables on survival outcomes. The possible influence of clustering on survival was taken into consideration.

Results: The 3+ mm group had a mean stability (PTV) of −3.8 (SD = 2.9), and the 4+ group had a mean PTV of −4.4 (SD = 2.7) (P <0.05). The PTVs for implant lengths ranged from −2.9 (SD = 2.8) for 7 mm lengths to −3.9 (SD = 2.9) for 16 mm lengths (P <0.05). Survival to 36 months was 90.7% for the 3+ diameter and 94.6% for the 4+ group (P = 0.01). Survival ranged from 66.7% for the 7 mm implants to 96.4% for 16 mm implants (P = 0.001). Outcomes did not change when clustering was considered, although the P value decreased slightly.

Conclusions: The results indicate that: 1) shorter implants had statistically lower survival rates as compared with longer implants; 2) 3+ mm diameter implants had a lower survival rate as compared with 4+ mm implants; 3) 3+ mm diameter implants are less stable (more positive PTVs) than 4+ mm implants; and 4) there was no significant difference in crestal bone loss for the two different implant diameters between placement and uncovering.Ann Periodontol 2000;5:22‐31.
The Influence of Smoking on 3‐Year Clinical Success of Osseointegrated Dental Implants
Authors: Lambert Paul M. , Morris Harold F. , Ochi Shigeru
Published: February 2005

Background: Health risks associated with smoking have been exhaustively documented and include increased incidence of periodontal disease, greater risk of osteitis following oral surgery, and compromised wound healing due to hypoxia. Information related directly to dental implants, although limited, points to higher rates of implant failures among smokers than non‐smokers. This paper reports on long‐term clinical outcomes of osseointegrated dental implants placed in smokers and non‐smokers in a longitudinal clinical study of endosseous dental implants.

Methods: In 1990, the Dental Implant Clinical Research Group (DICRG) of the Department of Veterans Affairs (DVA) launched an 8‐year, randomized, prospective clinical study of more than 2,900 endosseous dental implants in more than 800 patients at 32 study centers. Confounding variables, including smoking patterns, were recorded. For this report, new follow‐up data were analyzed for two groups: 1) current smokers and 2) those who never smoked combined with those who quit. Most of the variables recorded for each implant were screened on a univariate basis as possible predictors associated with implant survival/failure. Those with P values less than 0.15 and those likely to be a factor of clinical importance were placed in a logistic regression equation and analyzed for a simultaneous effect on survival. A step‐wise procedure was used to eliminate those variables that showed the least significance, until only those variables with a Wald chi‐square of significance in the presence of others remained. The effects of clustering within patients and of unbalanced distribution within hospitals were standardized to facilitate analysis of influence of demographic variables. The GEE analysis was performed with the patient as the primary cluster.

Results:Current data do not support earlier findings that smoking contributes to early implant failure (placement to uncovering). A trend of greater failures in smokers appeared between the time after uncovering and before insertion of the prosthesis. Hydroxyapatite (HA)‐coated implants had significantly lower failure rates. For the entire 3‐year period, overall failures were significantly higher for smokers than non‐smokers.

Conclusions: Results suggest that increased implant failures in smokers are not the result of poor healing or osseointegration, but of exposure of peri‐implant tissues to tobacco smoke. Data also suggest that detrimental effects may be reduced by: 1) cessation of smoking; 2) the use of preoperative antibiotics; and 3) the use of HA‐coated implants.Ann Periodontol 2000;5:79‐89.
The Relationship Between Infection, Inflammation, and Cardiovascular Disease: An Overview
Authors: Lowe Gordon D.O.
Published: February 2005

Atherosclerotic plaques were likened histologically to healing inflammatory lesions by Russell Ross, who proposed a “response to injury” hypothesis for their formation. More recently, intraplaque inflammation has been postulated to play a role in thinning of the fibrous cap, plaque rupture, and superadded thrombosis. Potential causes for vascular injury include mechanical stress, smoke exposure, hypercholesterolemia, hyperhomocysteinemia, and chronic infection (direct, or indirect). Blood levels of inflammatory markers (e.g., C‐reactive protein [CRP]; serum amyloid A [SAA]; fibrinogen; plasma viscosity; erythrocyte sedimentation rate [ESR]; leukocyte count, low serum albumin) have been associated with vascular risk factors and with prevalent and incident atherothrombotic cardiovascular disease (CVD) (coronary heart disease, [CHD]; stroke; and peripheral arterial disease). More recently, cytokines (e.g., interleukin‐6 [IL‐6]) and soluble adhesion molecules (e.g., intercellular adhesion molecule‐1, vascular cell adhesion molecule‐1) have been associated with both risk factors and disease; and offer potential therapeutic targets for nonspecific “anti‐inflammatory” treatment of arterial disease. Infections associated with arterial disease include specific infections (Chlamydia pneumoniae, Helicobacter pylori) and nonspecific infections (periodontal infections, respiratory tract infections). Recent meta‐analyses have shown that associations of serum markers of C. pneumoniae and H. pylori with arterial disease, risk factors, or potential intermediary mechanisms for disease are weaker than was first suggested by early reports. Likewise, further studies and metaanalyses are required to evaluate the epidemiologic relationships of CVD to periodontal infection and disease and to chronic pulmonary infections and disease. The weaker the associations between chronic infections and CVD, the larger is the size of randomized controlled trials required to establish (or exclude) a preventive effect of infection treatment. While control of chronic infection in the mouth, stomach or lungs is appropriate for its local effects, proving its efficacy in prevention of CVD presents a continuing challenge to medical science. Ann Periodontol 2001;6:1‐8.