Notes: Abstract The Assessment Protocol for Excellence in Public Health (APEXPH) is a method for comprehensive public health planning that can be implemented by state and local health departments. Many local health departments have limited resources for the data analysis and synthesis needed for APEXPH. To facilitate the implementation of APEXPH in Michigan, we used the Centers for Disease Control and Prevention (CDC) Epi Info software package to develop an APEXPH information manager (CDC-AIM) for use by the 50 local health departments in that state. This report describes our methods for formatting, compressing, and presenting data. Examples of tables are provided for demographics by age and sex, numbers of deaths, years of potential life lost, crude mortality rates, and perinatal indicators such as low birthweight. Areas where additional work is needed to further improve CDC-AIM are discussed. Our experience in Michigan suggests that CDC-AIM potentially is an extremely helpful tool to assist state and local health departments in working with their communities to establish public health program plans based on mortality, morbidity, and risk-factor data.

Notes: Purpose The purpose of this investigation was to measure and describe the lingual tissues of the anterior mandible to determine the acceptable boundaries of the zone of nonmovable tissue for placement of a lingual bar and to compare these to existing numerical guidelines.Materials and Methods Eighty subjects, grouped by age and gender, with clinically normal mandibular lingual gingival tissues from second premolar to second premolar were examined. The lingual sulcular depths (AB) and the distance from the gingival crest to movable tissue of the floor of the mouth (AC) were recorded. The zone of lingual nonmovable tissue was calculated (AC − AB) for each tooth.Results For all subjects, the mean value of the probing depth (AB) ranged from 1.22 mm (±0.33 mm) for central incisors to 1.66 mm (±0.43 mm) for second premolars. The mean distance from the gingival crest to movable tissue of the floor of the mouth (AC) ranged from 7.44 mm (±1.59 mm) for central incisors to 10.28 mm (±2.55 mm) for second premolars. The mean height of the lingual nonmovable tissue (the zone available for the lingual bar; AC − AB) ranged from 6.22 mm (±1.59 mm) for central incisors to 8.63 mm (±2.57 mm) for second premolars. Most subjects presented with the minimum zone of nonmovable tissue at the central incisors, but with increasing age more subjects presented with minimum values at the posterior teeth. The multifactorial analysis of variance (ANOVA) for males' available nonmovable tissue shows significance for both tooth (p 〈 0.001) and age (p 〈 0.001) factors. The multifactorial ANOVA for females' available nonmovable tissue shows significance for both tooth (p 〈 0.001) and age (p 〈 0.001) factors. Of all subjects, 85% (88% of males, 83% of females) had 4 mm or more of nonmovable tissue, sufficient for a lingual bar. The amount of available room decreased in older females.Conclusion Within the limits of this study, the use of actual measurements of lingual tissues versus existing numerical guidelines increased the percentage of patients for which the lingual bar can be used from approximately 6% to approximately 85%.

Notes: Failed crowns and failure load data were studied to gain insights into the fracture behavior of prostheses under incisal-directed, load-to-failure testing.〈section xml:id="abs1-2"〉〈title type="main"〉Materials and MethodsIncisor crowns (n = 68) were fabricated: two all-ceramic groups (feldspathic veneer on high-strength core), differing in core design, and two metal-ceramic groups, differing in metal oxidation time (30 seconds v 3 minutes). Crowns were loaded to failure on their incisal edge. Gross visual, microscopic, and elemental microprobe analyses of failed crowns were coupled with Weibull analysis of the failure load data.〈section xml:id="abs1-3"〉〈title type="main"〉ResultsFailure loads were higher for the normal oxidation time (TN) than for the extended oxidation time (TE) metal-ceramic crowns (P 〈 .02), but both groups had indistinguishable Weibull moduli indicating the possibility of a common failure origin. Fracture behavior and Weibull results both implicated the oxide layer as being the origin of failure. The ratio of fracture loads (TE/TN) corresponded well with calculated oxide-volume ratios. Failure loads were lower for the all-ceramic than for the metal-ceramic crowns (P 〈 .001). Fifty percent of the all-ceramic crowns failed by delamination of veneering glass alone, leaving a thin layer of residual glass on the core surface. Scanning electron microscope views showed that delamination occurred 10 to 50 μm away from the core-veneer interface. Electron microprobe elemental analysis of the core-veneer interface showed that residual core infiltration glass was not present on the core surface and that chemical alterations in the veneering glass were apparently limited to less than a 2- to 3-μm thick layer.〈section xml:id="abs1-4"〉〈title type="main"〉ConclusionsFailure for both restorative systems involved interfacial stresses with crack propagation occurring at or near the core-veneer interface. The weaker interface in the metal-ceramic system probably resulted from an increase in surface oxide volume, irrespective of any change in its adherence or physical properties. For the ceramic crowns, delamination crack fronts appeared to propagate through chemically unaltered veneering porcelain. Both the Weibull moduli and characteristic strengths were indistinguishable between either of the two ceramic core designs or between groups failing from delamination with or without core cracking/failure. This is consistent with delamination being the primary fracture process during failure. Clinical implications should not be drawn from results of this study because no correlation is known to have ever been established between clinical behavior and incisal load-to-failure results.

Notes: The medical records of 209 dogs receivingtotal parenteral nutrition (TPN) over a 84-month period were examined retrospectively to determine patient profiles, frequency and type of complications, and prognostic factors affecting clinical outcome. TPN administration accounted for 895 patient days. Dogs with diarrhea or vomiting associated with gastrointestinal disease, pancreatitis, or renal failure constituted the largest proportion of patient receiving TPN. The median duration of TPN administration was 3.5 days (range 0.05 to 25 days). The median length of hospitalization before initiation of TPN was 1.5 days (range 0.05 days to 15 days). and this durationwas not associated with survival. Metabolic complications were frequent (329 of 473 complications observed) and were due predominantly to hyperglycemia. Mechanical (118 of 473) and septic (26 of 473) complications occurred less commonly. The overall mortality rate for dogs receiving TPN was 48.8%. Our conclusion: TPN can be a beneficial mode of therapy for carefully selected dogs that have impaired gastrointestinal function (parvovirus, pancreatitis, or inflammatory bowel disease) and are expected to be anorectic for morethan 5 days.

Notes: Abstract: Plasma membrane proteolipid protein (PMPLP) synthesis was examined in embryonic rat neurons and neonatal rat glial cells during differentiation in culture. Glial cultures were treated with 1 mM N6,O2, dibutyryl cyclic adenosine monophosphate (dbcAMP) following confluency to induce differentiation, which resulted in the elaboration of long cellular processes. However, no changes in the biosynthetic level of PMPLP was observed during the differentiation of these cells. Neurons differentiated spontaneously in culture, forming cellular aggregates immediately following plating and elaborating a network of neurites over 7 days. The differentiation of neurons was accompanied by a sevenfold increase in PM-PLP synthesis with increases in biosynthetic rate observed betvyeen days 1 and 3 and between days 3 and 7 in culture. Ultrastructural examination of neurons indicated that the Golgi apparatus was also developing during this period of time, with an increase in both the number of lamellae and generation of vesicles. The transport of PM-PLP to the plasma membrane was therefore examined in neurons at day 7 in culture by pulse labeling experiments with monensin and colchicine. Monensin (1 μM) was found to inhibit the appearance of radiolabeled PM-PLP in the plasma membrane by 63%, indicating that a functional Golgi apparatus is required for transport of PM-PLP to its target membrane. Colchicine (125 μM) also inhibited the appearance of newly synthesized PM-PLP in the plasma membrane by 〉40%, suggesting that microtubules may also be required for PM-PLP transport to the plasma membrane.

Notes: Abstract: A decrease in protein kinase C activity caused either by treatment with inhibitors, such as staurosporine or H-7, or by prolonged exposure to phorbol diesters has been proposed to be involved in the early events of SH-SY5Y neuroblastoma cell differentiation. Because eight distinct isoforms of protein kinase C with discrete subcellular and tissue distributions have been described, we determined which isoforms are present in SH-SY5Y cells and studied their modifications during differentiation. The α, β, δ, and ɛ isoforms were present in SH-SY5Y cells, as well as in rat brain. Protein kinase C-α and -β1 were the most abundant isoforms in SH-SY5Y cells, and immunoreactive protein kinase C-δ and -ɛ were present in much smaller amounts than in rat brain. Subcellular fractionation and immunocytochemistry demonstrated that all four isoforms are distributed bimodally in the cytoplasm and the membranes. Immunocytochemical analysis showed that the α isoform is associated predominantly with the plasma membrane and the processes extended during treatment with 12-tetradecanoyl-13-acetyl-β-phorbol or staurosporine, and that protein kinase C-ɛ is predominantly membrane-bound. Its localization did not change during differentiation. Western blots of total SH-SY5Y cell extracts and of subcellular fractions probed with isoform-specific polyclonal antibodies showed that when SH-SY5Y cells acquired a morphologically differentiated phenotype, protein kinase C-α and -ɛ decreased, and protein kinase C-β1, did not change. These data suggest distinct roles for the different protein kinase C isoforms during neuronal differentiation, as well as possible involvement of protein kinase α and ɛ in neuritogenesis.

Notes: Abstract: Exposure of each of the three neurofilament proteins (NFPs) to AlCl3 resulted in their failure to migrate into sodium dodecyl sulfate (SDS)-containing gels. This effect was dependent on length of incubation (minimum, 2 h) and AlCl3 concentrations (minimum, 50 μM) and was not reversed by 20% SDS, 6 M urea, freeze-thawing, boiling, or extensive dialysis. The migration of vimentin and glial fibrillary acidic protein was not affected by AlCl3. The high-molecular-weight neurofilament subunit (NF-H) entered SDS-containing gels after exposure to aluminum lactate but migrated aberrantly as a long high-molecular-weight streak. Migration of the 160-kDa α-chymotryptic cleavage product of NF-H, which contains the higher phosphorylated tail domain, was also prevented from migrating into SDS-containing gels by AlCl3. Dephosphorylation of NF-H and the middle-molecular-weight neurofilament subunit (NF-M) eliminated these effects on gel migration. EDTA, EGTA, MgCl2, CaCl2, or FeCl3 had no effect on NF-H or NF-M migration; furthermore, preincubation with, or simultaneous exposure to, CaCl2 or FeCl3 did not alter the effect of AlCl3. One interpretation of these results is that Al3+ interacts with phosphate groups on extensively phosphorylated C-terminal sidearms of NFPs, resulting in intermolecular cross-linking. These findings demonstrate a direct effect of aluminum on NFPs and provide a possible mechanism for neurofilament accumulation in perikarya during aluminum intoxication.

Notes: Abstract: Certain biological actions of phorbol esters cannot be duplicated by diacylglycerol (DAG). Thus, the human neuroblastoma cell line SH-SY5Y differentiates when exposed to 12-tetradecanoyl-13-acetyl-β-phorbol (TPA) and protein kinase C (PKC) inhibitors, but not when exposed to DAG. To investigate the specific features of the phorbol diester molecule that might be responsible for these effects, we examined the extension of neurites, expression of neuron-specific enolase, and appearance and localization of phosphorylated high molecular weight neurofilament subunits (NF-H). TPA, 12-deoxy-13-tetradecanoyl-β-phorbol, and staurosporine, but not DAG or 4-O-methyl-TPA, caused neurite outgrowth. Neuron-specific enolase was expressed in cells treated with TPA and 12-deoxy-13-tetradecanoyl-β-phorbol but not with DAG, staurosporine, or 4-O-methyl-TPA. NF-H increased in the perikarya of cells treated with DAG and 4-O-methyl-TPA, in processes and to varying degrees in perikarya of TPA- and 12-deoxy-13-tetradecanoyl-β-phorbol-treated cells, but much more in the processes than in the perikarya of staurosporine-differentiated cells. These findings and additional differences between the differentiation induced by TPA (a PKC activator) and staurosporine (a PKC inhibitor), including distinct morphology of the cell body and processes and time of appearance of the morphological phenotype, suggest that activators and inhibitors of PKC induce differentiation of SH-SY5Y cells by different mechanisms, and that the five-membered/seven-membered terpene ring region present in TPA must be intact for the induction of morphological differentiation.

Notes: Abstract: Mouse NB2a/dl neuroblastoma cells elaborate axonal neurites in response to various chemical treatments including dibutyryl cyclic AMP and serum deprivation. Hi-rudin, a specific inhibitor of thrombin, initiated neurite outgrowth in NB2a/dl cells cultured in the presence of serum; however, these neurites typically retracted within 24 h. The cysteine protease inhibitors leupeptin and N-acetyl-leucyl-leucyl-norleucinal (CI; preferential inhibitor of micromolar calpain but also inhibits millimolar calpain) at 10-6M considerably enhanced neurite outgrowth induced by serum deprivation, but could not induce neuritogenesis in the presence of serum. A third cysteine protease inhibitor, N-acetyl-leucyl-leucyl-methional (CII; preferential inhibitor of millimolar calpain but also inhibits micromolar calpain), had no detectable effects by itself. Cells treated simultaneously with hirudin and either leupeptin, CI, or CII elaborated stable neurites in the presence of serum. Cell-free enzyme assays demonstrated that hirudin inhibited thrombin but not calpain, CI and CII inhibited calpain but not thrombin, and leupeptin inhibited both proteases. These results imply that distinct proteolytic events, possibly involving more than one protease, regulate the initiation and subsequent elongation and stabilization of axonal neurites. Since the addition of exogenous thrombin or calpain to serum-free medium did not modify neurite outgrowth, the proteolytic events affected by these inhibitors may be intracellular or involve proteases distinct from thrombin or calpain.