Life course dental caries determinants and predictors in children aged 12 years: a population-based birth cohort

Abstract – Objective: To investigate the main dental caries life course determinants and predictors of dental caries at age 12. Methods: This study was nested in a population‐based birth cohort started in 1993 in Pelotas, Brazil. A sample of 359 children was followed‐up. Dental examinations and interviews were performed at 6 and at 12 years old. Dental caries (DMFT) at 12 years old was the outcome. Exploratory variables included socioeconomic and demographic variables at birth, children’s nutritional and development characteristics, primary dental caries, oral health related behaviors and dental service use at age 6 and 12. Poisson regression was used in order to provide relative risk ratio estimates. Attributable risk or etiology fraction and population attributable risk for both main early life variables were calculated. Dental caries prediction (DMFT ≥ 1) at 12 years old was tested using logistic regression analyses. Results: Children who presented height‐for‐age deficit at 12 months (RR 1.50 CI: 95% = 1.03–2.18), children who showed a DMFT of 1–3 and 4–19 at 6 years (RR = 2.01; CI: 95% = 1.33–3.03, and RR = 2.66; CI: 95% = 1.81–2.53, respectively) and those children aged 12 in the highest tertile of proportion of teeth experiencing gingival bleeding (RR = 1.58; CI: 95% = 1.11–2.24) presented a higher level of dental caries at age 12. Attributable risk for dental caries at age 12 were 79.1% and 74.2% for deficit in height for age at 12 months and for primary dental caries at age 6 years respectively; population attributable risk for dental caries at age 12 were 3.1% for deficit in height for age at 12 months and 64.9% for primary dental caries at age 6. The level of accuracy in predicting dental caries at age 12 by using life course socioeconomic, behavioral and clinical data was modest. Conclusions: The results of this study support the hypothesis linking social, biological and behavioral exposures and dental caries at 12 years old. In addition, the findings reinforce the lack of accuracy of dental caries predictors therefore limiting the individuals high‐risk approach as a public health strategy.     

T1a as the Sole Selection Criterion for RFA of Renal Masses: Randomized Controlled Trials versus Surgery Should Not Be Postponed

Purpose

To evaluate the long-term effects of radiofrequency ablation (RFA) of renal masses (RM) and compare them with surgery.

Methods

A total of 203 RM (193 malignant; mean size 30 mm) in 137 patients (95 male subjects; average age 64 years) underwent RFA. Complications and technique effectiveness were evaluated. Overall survival, cancer-specific survival, and disease-free survival were calculated (mean follow-up time 39 months). Predictors for complications, technique effectiveness, and survival were investigated.

Results

Seventeen (8.4 %) adverse events were recorded (2 % major complications). Exophytic development and smaller size were protective against adverse events. Complete ablation was obtained in 87 % RM (93 % ≤3 cm, 89 % ≤4 cm). T1a threshold was a positive predictor for complete ablation and central location a negative one. Three- and 5-year overall survival were 84 and 75 %; cancer-specific survival 96 and 91 %; and disease-free survival 80 and 75 %. Considering only the 79 patients with newly diagnosed renal cell carcinoma, T1a disease stage resulted a positive predictor for both overall survival (87 and 83 % at 3 and 5 years) and cancer-specific survival (100 % at 5 years).

Conclusion

RFA of noncentral small RM is safe and effective, and it provides favorable long-term oncological outcomes. Selection criteria for RFA can also include T1a renal cell carcinoma in patients without surgical contraindications, even though randomized controlled trials are needed to establish the best treatment.     

水溶性药物的疏水性修饰及其重组型脂质体的研究

脂质体载水溶性药物出现的共同问题是药物的包封量低、稳定性差。本文以甲硝唑(Ⅰ)为水溶性药物模型,进行疏水性结构修饰,得其肉豆蔻酸酯(Ⅱ)前体药物,分别进行Ⅰ和Ⅱ的脂质体研究,结果表明Ⅱ在脂质体中的包封率较Ⅰ提高10倍以上,渗漏速率降至十分之一,制成含Ⅱ的脂质干膜,经超声分散,可得合乎要求的重组型脂质体,为解决脂质体载药的稳定性问题提供有效途径。体外抗阿米巴原虫试验,镜检观察到载药脂质体进入阿米巴原虫的细胞内,且100%抑制原虫所需剂量Ⅱ脂质体是Ⅰ游离药的二分之一。因此药物疏水化修饰是解决脂质体载水溶性药物稳定性问题的理想途径。     

Protein C deficiency in a controlled series of unselected outpatients: an infrequent but clear risk factor for venous thrombosis (Leiden Thrombophilia Study) [see comments]

A deficiency of protein C (PC), antithrombin, or protein S is strongly associated with deep-vein thrombosis in selected patients and their families. However, the strength of the association with venous thrombosis in the general population is unknown. This study was a population-based, patient-control study of 474 consecutive outpatients, aged less than 70 years, with a first, objectively diagnosed, episode of venous thrombosis and without an underlying malignant disease, and 474 healthy controls who matched for age and sex. Relative risks were estimated as matched odds ratios. Based on a single measurement, there were 22 (4.6%) patients with a PC deficiency (PC activity, less than 0.67 U/mL or PC antigen, less than 0.33 U/mL when using coumarins). Among the controls, the frequency was 1.5% (seven subjects). Thus, there is a threefold increase in risk of thrombosis in subjects with PC levels below 0.67 or 0.33 U/mL [matched odds ratio, 3.1; 95% confidence interval (CI), 1.4 to 7.0]. When a PC deficiency was based on two repeated measurements, the relative risk for thrombosis increased to 3.8 (95% CI, 1.3 to 10); when it was based on DNA-confirmation, the relative risk increased further to 6.5 (95% CI, 1.8 to 24). In addition, there was a gradient in thrombosis risk, according to PC levels. The results for antithrombin are similar to those for PC, although less pronounced (relative risk, 2.2; 95% CI, 1.0 to 4.7). We could not find an association between reduced total protein S (relative risk, 0.7; 95% CI, 0.3 to 1.8) or free protein S levels (relative risk, 1.6; 95% CI, 0.6 to 4.0) and thrombosis risk. Although not very frequent, PC and antithrombin deficiency are clearly associated with an increase in thrombosis risk.     

Emerging and changing viral diseases in the new millennium

Most viral infections encountered in resource‐rich countries are relatively trivial and transient with perhaps fever, malaise, myalgia, rash (exanthema) and sometimes mucosal manifestations (enanthema), including oral in some. However, the apparent benignity may be illusory as some viral infections have unexpected consequences – such as the oncogenicity of some herpesviruses and human papillomaviruses. Infections are transmitted from various human or animal vectors, especially by close proximity, and the increasing movements of peoples across the globe, mean that infections hitherto confined largely to the tropics now appear worldwide. Global warming also increases the range of movement of vectors such as mosquitoes. Thus recent decades have seen a most dramatic change with the emergence globally also of new viral infections – notably human immunodeficiency viruses (HIV) – and the appearance of some other dangerous and sometimes lethal infections formerly seen mainly in, and reported from, resource‐poor areas especially in parts of Asia, Latin America and Africa. This study offers a brief update of the most salient new aspects of the important viral infections, especially those with known orofacial manifestations or other implications for oral health care.     

Thrombocytopenia associated with pregnancy in a patient with type IIB von Willebrand's disease

Thrombocytopenia may accompany variant (type IIB) von Willebrand's disease (vWD) and is thought to result from binding of the abnormal von Willebrand factor (vWF) to the patient's platelets with subsequent platelet aggregate formation and clearance. We have studied a patient with type IIB vWD who became thrombocytopenic during two pregnancies. During the third trimester of pregnancy, her platelet counts dropped to 20,000 to 30,000/microL, and an increase in the intermediate-sized vWF multimers was seen on agarose gel electrophoresis. During this time her platelet-rich plasma showed spontaneous platelet aggregation, and her plasma caused spontaneous aggregation of normal washed platelets. Antibody to platelet glycoprotein Ib completely blocked the spontaneous platelet aggregation, while antibody to platelet glycoprotein IIb/IIIa did not block the response at the concentrations used. Inhibitors of platelet function that elevate platelet cyclic AMP also blocked the response, but aspirin had no effect on the spontaneous platelet aggregation. The patient illustrates that the platelet counts in one individual can vary greatly in type IIB vWD and that the thrombocytopenia that occurs can appear under physiologic conditions that stimulate the endogenous production of the patient's abnormal vWF. The mechanisms leading to spontaneous platelet aggregation and thrombocytopenia appear to be similar to those described for other patients with type IIB vWD.     

Clinical and epidemiological predictors of transmission in Severe Acute Respiratory Syndrome (SARS)

Background  

Only a minority of probable SARS cases caused transmission. We assess if any epidemiological or clinical factors in SARS index patients were associated with increased probability of transmission.     

<Emphasis Type="Italic">Kocuria kristinae</Emphasis> infection associated with acute cholecystitis

Background  

Kocuria, previously classified into the genus of Micrococcus, is commonly found on human skin. Two species, K. rosea and K. kristinae, are etiologically associated with catheter-related bacteremia.     

Cytosolic inactivation of translocated neutrophil plasma membrane protein tyrosine phosphatase

Phosphotyrosine phosphatases (PTPases) regulate cellular metabolic activation by reversing the effects of tyrosine kinases activated earlier in intracellular signaling pathways. We coupled fluorescence- activated cell sorter analysis using anti-CD45 monoclonal antibody with direct measurements of enzyme activity in resolved subcellular fractions to define mechanisms that potentially regulate the availability and activity of CD45-PTPase on neutrophil plasma membranes. Neutrophils in freshly obtained blood as well as neutrophils freshly isolated from blood were found to possess detectable levels of plasma membrane CD45 as assessed by immunofluorescence. However, plasma membranes from these cells were essentially devoid of PTPase catalytic activity, which was largely confined to the specific granules. Granulocyte-macrophage colony-stimulating factor (GM-CSF) upregulated both the catalytic and antigenic components of CD45-PTPase on the plasma membrane of these cells. Upregulation was associated with a shift in the particulate subcellular PTPase catalytic activity from the specific granule fraction to the plasma membrane fraction. The tyrosine kinase inhibitor genistein abrogated GM-CSF-promoted upregulation of plasma membrane CD45 PTPase but did not prevent the GM-CSF-dependent decrease in specific granule catalytic activity. Anti-CD45 antibody immunoprecipitated PTPase activity from both specific granules of resting cells and plasma membranes of GM-CSF-treated cells. However, antiphosphotyrosine immunoprecipitated only activity that had translocated to the plasma membrane, suggesting a role for CD45 phosphorylation in translocation. Western analysis confirmed the tyrosine phosphorylation of CD45 in plasma membranes of GM-CSF-treated neutrophils. Preincubation of plasma membranes of GM-CSF-stimulated neutrophils with cytosol from resting cells resulted in a time- and temperature-dependent loss in membrane PTPase as a consequence of the effects of a cytosolic inactivator. Cytosol obtained from stimulated neutrophils possessed substantially reduced levels of this PTPase inactivator. We conclude that activity of the catalytic component of membrane PTPase in circulating neutrophils is regulated by a cytosolic inactivator. Upon stimulation, intact CD45 PTPase is incorporated into the plasma membrane by a process that requires tyrosine phosphorylation. As a result of inhibition of the cytosolic inactivator, the translocated PTPase expresses full activity, thereby amplifying the potential regulatory influence of the enzyme on the cells' functional response.