Post-mortem diagnosis of human rabies in SARS-CoV-2 coinfected patient with minimally invasive autopsy in northeastern Brazil.

INTRODUCTION: Human rabies (HR) is a lethal zoonotic disease caused by lyssaviruses with increase in the number of cases post-coronavirus disease 2019 (COVID-19) pandemic. METHODOLOGY: We report a case of human rabies in a patient from a rural area of Ceará, northeastern Brazil in 2023, who was bitten by a white-tufted-ear marmoset (Callithrix jacchus jacchus). The patient was co-infected with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and was diagnosed by minimally invasive autopsy (MIA). RESULTS: MIA offers many advantages related to biosafety, and speed of sample acquisition; and markedly reduces disfigurement of the body compared with complete autopsy. It is a great alternative in COVID-19 patients. CONCLUSIONS: New methods such as MIA are a promising tool for diagnosis, and have the potential to improve family cooperation and support rabies surveillance.

Ultrasonography-Derived Elasticity Estimation of Live Porcine Oral Mucosa.

OBJECTIVES: To investigate the biomechanical properties of porcine oral tissues with in vivo ultrasonography and to compare the difference between oral alveolar mucosa and gingival tissue concerning compressional and tensile mechanical strain. MATERIALS AND METHODS: Sinclair minipigs (6 females and 4 males, 6 to 18 months of age) were anesthetized for ultrasonography. In vivo high-frequency tissue harmonic ultrasound (12/24 MHz) cine-loops were obtained while inducing mechanical tissue stress (0 to 1 N). Post-processing strain analysis was performed in a cardiac speckle tracking software (EchoInsight®). Region of interest (ROI) was placed for gingival and alveolar mucosa tissues for longitudinal (compressional) and tensile strain analyses. A calibrated gel pad was employed to determine the absolute force (pressure) for the measured tissue strain response function. The resulting elasticity data was statistically analyzed using custom Matlab scripts. RESULTS: In total, 38 sonography cine-loops around the third premolars were included in the investigation. The longitudinal strain of alveolar mucosa ε AM L was found to be significantly (P < .05) larger than that of gingiva ε G L . Across the measured force range, ε AM L ~ 1.7 × Îµ G L . Significant differences between alveolar mucosa and gingiva tissues were found for all forces. The tensile strain of the alveolar mucosa ε AM T was found to be ~2 × Îµ G T (on the epithelial surface of the gingiva). Both were statistically significantly different for forces exceeding ~0.08 N. At depth, that is, 500 and 1000 µm below the epithelial surface, the gingiva was found to have less ability to stretch contrary to the alveolar mucosa. Gingival tissue at 500 µm depth has significantly less tensile strain than at its surface and more than at 1000 µm depth. In contrast, the tensile strain of alveolar mucosa is largely independent of depth. CONCLUSION: Ultrasonography can reveal significant differences in oral alveolar mucosal and gingival elastic properties, such as compressional and tensile strain. Under minute forces equivalent to 10 to 40 g, these differences can be observed. As dental ultrasound is a chairside, and noninvasive modality, obtaining real-time images might soon find clinical utility as a new diagnostic tool for the objective and quantitative assessment of periodontal and peri-implant soft tissues in clinical and research realms. As ultrasound is a safe modality with no known bioeffects, longitudinal monitoring of areas of concern would be particularly attractive.

Establishment of Reference Intervals for Renal Function Clinical Chemistry Parameters in an Indonesian Tertiary Hospital.

Reference intervals aid clinical decision-making for clinical chemistry values. Laboratory test results are compared to reference intervals to aid in the diagnosis, therapy, and monitoring decisions. Due to the differences in ethnicity, gender, age, and analytical methods, reference intervals (RIs) vary between populations. This study aimed to establish the reference values for renal function tests in targeted populations in Indonesia. This research was conducted with a cross-sectional observational analytic design. The research sample consisted of medical check-up data from health professionals at Dr. Mohammad Hoesin Hospital in Palembang, Indonesia. The Kolmogorov-Smirnov test was used to determine the normality of data distribution.   The RIs were computed using reference limits at the 2.5th and 97.5th percentiles (abnormal distribution) or ±two standard deviations (±2 SD) (normal distribution).  The independent t-test (parametric) or Mann-Whitney test was used to compare the RIs of males and females (non-parametric). Males and females had a significant difference (P<0.001) regarding the values of uric acid, urea, and creatinine parameters, requiring the reference intervals to be separated. The following reference intervals were established: uric acid: 230,78-526,99 mol/L for males and 179,03-415.17 mol/L for females, urea: 2,22-4,99 mmol/L for males and 1,78-4,28 mmol/L for females, and creatinine: 61,01-106,99 mol/L for males and 40,67-77,81 mol/L for females. This study defined gender-specific RIs for three renal function test parameters for the adult population of Palembang, Indonesia. The deployment of population-specific RIs may facilitate better laboratory testing.

Comparison of Liver Function Test Results between Architect C8000 and COBAS C501 Automatic Chemistry Analyzer.

Liver function tests are frequently used to screen liver function, monitor therapy, and determine the severity of liver problems. The present study aimed to assess the consistency of the results of the liver function parameters between the two analyzers, Architect c8000 and Cobas C501. This laboratory-based analytical observational study was conducted in a cross-sectional manner. Sample collection was performed through a consecutive sampling procedure from June to December 2019 in the Clinical Pathology Laboratory, Dr. Mohammad Hoesin General Hospital, Palembang, South Sumatra, Indonesia. The research sample consisted of the liver function examination results of patients, carried out using the Architect c8000 and Roche Cobas c501 chemistry analyzers. Serum albumin, alanine transaminase, aspartate aminotransferase, and total protein were the studied variables. The Spearman, Mann-Whitney, and Bland-Altman tests were used to evaluate the comparison test. In total, 100 blood samples were obtained in this study. The results revealed a highly significant correlation (r>0.90, P=0<001) among the four liver function parameters. The results of the liver function parameters inspected by the two analyzers did not differ significantly (P>0.05). In addition, there was a solid agreement on all parameters, with a near-perfect level (concordance correlation coefficient>0.90) and more than 95% of data points falling within the acceptable range. The Architect c8000 and Cobas c501 analyzers produced similar results for liver function tests; hence, these devices can be used interchangeably.

Using PDX animal models to identify and stratify adenoid cystic carcinoma patients presenting an enhanced response to HDAC inhibitors.

Adenoid cystic carcinoma (ACC) patients face a highly infiltrative and metastatic disease characterized by poor survival rates and suboptimal response to available therapies. We have previously shown that sensitization of ACC tumors to chemotherapy using histone deacetylase inhibitors (HDACi) constitutes a promising therapeutic strategy to manage tumor growth. Here, we used patient-derived xenografts (PDX) from ACC tumors to evaluate the effects of in vivo administration of the HDAC inhibitor Entinostat combined with Cisplatin over tumor growth. RNA from PDX tumor samples receiving the proposed therapy were analyzed using NanoString technology to identify molecular signatures capable of predicting ACC response to the therapy. We also used an RNAseq dataset from 68 ACC patients to validate the molecular signature identified by the NanoString platform. We found that the administration of Entinostat combined with Cisplatin resulted in a potent tumor growth inhibition (TGI) ranging from 38% to 106% of the original tumor mass. Enhanced response to therapy is consistent with the reactivation of tumor suppressor genes, including SFRP1, and the downregulation of oncogenes like FGF8 and CCR7. Nanostring data from PDX tumors identified a genetic signature capable of predicting tumor response to therapy. We further stratified 68 ACC patients containing RNAseq data accordingly to the activity levels of the identified genetic signature. We found that 23% of all patients exhibit a genetic signature consistent with a high ACC tumor response rate to Entinostat and Cisplatin. Our study provides compelling preclinical data supporting the deployment of a powerful systemic anticancer therapy crafted and explicitly tested for ACC tumors.

Detection of SARS-CoV-2 in different human biofluids using the loop-mediated isothermal amplification assay: A prospective diagnostic study in Fortaleza, Brazil.

We adopted the reverse-transcriptase-loop-mediated isothermal amplification (RT-LAMP) to detect severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) in patient samples. Two primer sets for genes N and Orf1ab were designed to detect SARS-CoV-2, and one primer set was designed to detect the human gene Actin. We collected prospective 138 nasopharyngeal swabs, 70 oropharyngeal swabs, 69 salivae, and 68 mouth saline wash samples from patients suspected to have severe acute respiratory syndrome (SARS) caused by SARS-CoV-2 to test the RT-LAMP in comparison with the gold standard technique reverse-transcription quantitative polymerase chain reaction  (RT-qPCR). The accuracy of diagnosis using both primers, N5 and Orf9, was evaluated. Sensitivity and specificity for diagnosis were 96% (95% confidence interval [CI]: 87-99) and 85% (95% CI: 76-91) in 138 samples, respectively. Accurate diagnosis results were obtained only in nasopharyngeal swabs processed via extraction kit. Accurate and rapid diagnosis could aid coronavirus disease 2019 (COVID-19) pandemic management by identifying, isolating, and treating patients rapidly.

Curcuma longa L. Effects on Akt/mTOR Pathway and NF-κB Expression During Skin Wound Healing: An Immunohistochemical Study.

Skin ulcers, wounds, or burns represent a burden for health care worldwide. Our aim was to explore the effects of mucoadhesive formulation with Curcuma longa L. extract mucoadhesive formulation containing curcumin (MFC) on skin healing in Wistar rats. Fifty-four rats were randomly allocated into 3 groups: control, vehicle, and MFC. A full-thickness circular wound was induced on the back of each animal. Two daily applications of the products were performed according to the experimental group. On days 3, 10, and 21, 6 animals in each group were euthanized. Clinical analysis was based on wound area. Histologic analysis was performed in hematoxylin and eosin-stained sections, with re-epithelization and inflammation being assessed by means of semiquantitative scores. To analyze the Akt/mTOR pathway, immunohistochemistry for phospho Akt (pAkt) and phospho ribosomal protein S6 were investigated. In addition, nuclear factor kappa-light-chain-enhancer of activated B cells immunolabeling was performed. Clinical analysis revealed wounds with a smaller area on days 3 and 10 in curcumin-treated animals. Histologically, MFC had a significant impact on inflammatory events on days 3 and 10 and promoted faster re-epithelization, which was evidenced on day 10. MFC-treated wounds exhibited pAkt upregulation on day 10 and both pAkt and phospho ribosomal protein S6 downregulation on day 21. Nuclear factor kappa-light-chain-enhancer of activated B cells expression varied through the evaluation periods; however, no significant difference was observed between groups. Collectively, our results indicate that MFC is efficient in accelerating cutaneous wound repair through modulation of the inflammatory process and stimulus of re-epithelization by an Akt/mTOR-dependent mechanism.

Pharmacological PTEN inhibition: potential clinical applications and effects in tissue regeneration.

Although the human body can heal, it takes time, and slow healing and chronic wounds often occur. Thus, identifying novel therapies to aid regeneration is needed. Here, we conducted a systematic review following the Preferred Reporting Items for Systematic Reviews guidelines and assessed preclinical studies on phosphatase and tensin homolog (PTEN) inhibitors and their effects on tissue repair and regeneration. In conditions associated with neurodegeneration, tissue injury and ischemia, the PTEN-regulated PI3K/AKT signaling pathway is activated. The use of PTEN inhibitors resulted in better tissue response by reducing the healing time and lesion sizes or inducing neuronal regeneration. Notably, all studies included in this systematic review indicated that pharmacological inhibition of PTEN enhanced the repair process of the eye, lung, muscle and nervous system.

BMAL1 Modulates Epidermal Healing in a Process Involving the Antioxidative Defense Mechanism.

The circadian rhythm regulates the physiology and behavior of living organisms in a time-dependent manner. Clock genes have distinct roles including the control over gene expression mediated by the transcriptional activators CLOCK and BMAL1, and the suppression of gene expression mediated by the transcriptional repressors PER1/2 and CRY1/2. The balance between gene expression and repression is key to the maintenance of tissue homeostasis that is disrupted in the event of an injury. In the skin, a compromised epithelial barrier triggers a cascade of events that culminate in the mobilization of epithelial cells and stem cells. Recruited epithelial cells migrate towards the wound and reestablish the protective epithelial layer of the skin. Although we have recently demonstrated the involvement of BMAL and the PI3K signaling in wound healing, the role of the circadian clock genes in tissue repair remains poorly understood. Here, we sought to understand the role of BMAL1 on skin healing in response to injury. We found that genetic depletion of BMAL1 resulted in delayed healing of the skin as compared to wild-type control mice. Furthermore, we found that loss of Bmal1 was associated with the accumulation of Reactive Oxygen Species Modulator 1 (ROMO1), a protein responsible for inducing the production of intracellular reactive oxygen species (ROS). The slow healing was associated with ROS and superoxide dismutase (SOD) production, and pharmacological inhibition of the oxidative stress signaling (ROS/SOD) led to cellular proliferation, upregulation of Sirtuin 1 (SIRT1), and rescued the skin healing phenotype of Bmal1-/- mice. Overall, our study points to BMAL1 as a key player in tissue regeneration and as a critical regulator of ROMO1 and oxidative stress in the skin.

Improvement of human pancreatic islet quality after co-culture with human adipose-derived stem cells.

The aim of this study was to investigate whether co-culture of human islets with adipose-derived stem cells (ASCs) can improve islet quality and to evaluate which factors play a role in the protective effect of ASCs against islet dysfunction. Islets and ASCs were cultured in three experimental groups for 24 h, 48 h, and 72 h: 1) indirect co-culture of islets with ASC monolayer (Islets/ASCs); 2) islets alone; and 3) ASCs alone. Co-culture with ASCs improved islet viability and function in all culture time-points analyzed. VEGFA, HGF, IL6, IL8, IL10, CCL2, IL1B, and TNF protein levels were increased in supernatants of islet/ASC group compared to islets alone, mainly after 24 h. Moreover, VEGFA, IL6, CCL2, HIF1A, XIAP, CHOP, and NFKBIA genes were differentially expressed in islets from the co-culture condition compared to islets alone. In conclusion, co-culture of islets with ASCs promotes improvements in islet quality.

Kidney size in relation to ageing, gender, renal function, birthweight and chronic kidney disease risk factors in a general population.

BACKGROUND: The relationship of kidney size to ageing, kidney function and kidney disease risk factors is not fully understood. METHODS: Ultrasound length and parenchymal kidney volume were determined from a population-based sample of 3972 Sardinians (age range 18-100 years). We then identified the subset of 2256 'healthy' subjects to define age- and sex-specific reference ranges (2.5-97.5 percentile) of kidney volume. Logistic regression (accounting for family clustering) was used to identify the clinical characteristics associated with abnormally large kidneys or abnormally small kidneys. RESULTS: In the healthy subset, kidney volume and length increased up to the fourth to fifth decade of life followed by a progressive decrease in men, whereas there was a gradual kidney volume decrease throughout the lifespan of women. In the whole sample, independent predictors of lower kidney volume (<2.5 percentile for age and sex) were male sex, low body mass index, short height, low waist:hip ratio and high serum creatinine (SCr); the independent predictors of larger kidney volume (>97.5 percentile for age and sex) were younger age, female sex, diabetes, obesity, high height, high waist:hip ratio and lower SCr. Estimated heritability for kidney volume was 15%, and for length 27%; kidney volume correlated strongly with birthweight. CONCLUSIONS: Overall, in a general healthy population, kidney measures declined with age differently in men and women. The determinants of kidney parenchymal volume include genetic factors and modifiable clinical factors.

Hypoxic niches are endowed with a protumorigenic mechanism that supersedes the protective function of PTEN.

Head and neck squamous cell carcinoma (HNSCC) is the sixth most common malignancy worldwide and is characterized by a fast-paced growth. Like other solid tumors, the HNSCC growth rate results in the development of hypoxic regions identified by the expression of hypoxia-inducible factor 1α (HIF-1α). Interestingly, clinical data have shown that pharmacological induction of intratumoral hypoxia caused an unexpected rise in tumor metastasis and the accumulation of cancer stem cells (CSCs). However, little is known on the molecular circuitries involved in the presence of intratumoral hypoxia and the augmented population of CSCs. Here we explore the impact of hypoxia on the behavior of HNSCC and define that the controlling function of phosphatase and tensin homolog (PTEN) over HIF-1α expression and CSC accumulation are de-regulated during hypoxic events. Our findings indicate that hypoxic niches are poised to accumulate CSCs in a molecular process driven by the loss of PTEN activity. Furthermore, our data suggest that targeted therapies aiming at the PTEN/PI3K signaling may constitute an effective strategy to counteract the development of intratumoral hypoxia and the accumulation of CSCs.-Nascimento-Filho, C. H. V., Webber, L. P., Borgato, G. B., Goloni-Bertollo, E. M., Squarize, C. H., Castilho, R. M. Hypoxic niches are endowed with a protumorigenic mechanism that supersedes the protective function of PTEN.

Interference with the bromodomain epigenome readers drives p21 expression and tumor senescence.

Head and neck cancer (HNSCC) are one of the most common solid malignancies of the world, being responsible for over 350,000 deaths every year. Much of the complications in managing and treating HNSCC advent from the complex genetic and epigenetic landscape of the disease. Emerging information has shown promising results in targeting BRD4, an epigenetic regulator bromodomain that functions as a scaffold for transcription factors at promoters and super-enhancers. Here we show that by disrupting the interaction between BRD4 and histones using the bromodomain inhibitor JQ1, HNSCC cells undergo cell growth arrest followed by cellular senescence. Mechanistically, JQ1 negatively impacted the phosphorylation levels of SIRT1 along with the acetylation levels of mutant p53 (active). In vivo administration of JQ1 resulted in disruption of HNSCC growth along with the activation of cellular senescence, observed by the accumulation of DNA double-strand breaks, p16ink4, accumulation of senescence-associated beta-galactosidase, and loss of phosphorylated Sirt1ser47. Furthermore, we also demonstrate that JQ1 was efficient in reducing the population of cancer stem cells from HNSCC xenografts.

Interfering with bromodomain epigenome readers as therapeutic option in mucoepidermoid carcinoma.

PURPOSE: Emerging evidence indicates that bromodomains comprise a conserved class of epigenome readers involved in cancer development and inflammation. Bromodomains are associated with epigenetic modifications of gene transcription through interactions with lysine residues of histone tails. Particularly, the bromodomain and extra-terminal domain (BET) family member BRD4 has been found to be involved in the control over oncogenes, including c-MYC, and in the maintenance of downstream inflammatory processes. The objective of this study was to evaluate the effect of pharmacologically displacing BRD4 in mucoepidermoid carcinoma (MEC) cells. METHODS: We assessed the presence of BRD4 levels in a panel of human MEC tissue samples in conjunction with histological grading and clinical information. In vitro studies were carried out using human MEC-derived cell lines. The BET inhibitor iBET762 was administered to MEC cells to assess the impact of disrupted BRD4 signaling on colony forming capacities and cell cycle status. The activation of cellular senescence induced by iBET762 was determined by immunohistochemical staining for p16ink4. Flow cytometry was used to identify populations of cancer stem cells in MEC-derived cell lines. RESULTS: We found that primary human MECs and MEC-derived cell lines are endowed with high BRD4 expression levels compared to those in normal salivary glands. We also found that, by displacing BRD4 from chromatin using the BET inhibitor iBET762, MEC cells lose their colony forming capacities and undergo G1 cell cycle arrest and senescence. Finally, we found that targeted displacement of BRD4 from chromatin results in depletion of cancer stem cells from the overall MEC cell populations. CONCLUSIONS: Our findings indicate that bromodomain-mediated gene regulation constitutes an epigenetic mechanism that is deregulated in MEC cells and that the use of BET inhibitors may serve as a feasible therapeutic strategy to manage MECs.

Hypoacetylation of acetyl-histone H3 (H3K9ac) as marker of poor prognosis in oral cancer.

AIMS: Epigenetics refers to changes in cell characteristics that occur independently of modifications to the DNA sequence. Oral carcinogenesis is influenced by modifications in epigenetic mechanisms, including changes in histones, which are proteins that support chromatin remodelling for the dynamic regulation of gene expression and silencing. The dysregulation of histone acetylation can lead to the uncontrolled activity of different genes, thereby triggering events associated with malignant transformation. The aim of this study was to analyse the expression of acetyl-histone H3 at lys9 (H3K9ac) in oral leucoplakia (OL) and oral squamous cell carcinoma (OSCC) in addition to its association with cell proliferation, epithelial-mesenchymal transition (EMT) and clinical-pathological findings. METHODS AND RESULTS: Samples of normal oral mucosa (NOM), OL and OSCC were submitted to immunohistochemical analysis using anti-H3K9ac, Ki67 and vimentin. Slides were submitted to quantitative analysis regarding the percentage of positive cells. OSCC presented less expression of H3K9ac in comparison to OL (P < 0.01), whereas Ki67 and vimentin levels increased from OL to OSCC (P < 0.001 and P = 0.03, respectively). OSCC patients with poor prognosis had less H3K9ac expression (P = 0.04). The Kaplan-Meier cumulative survival curves also revealed lower survival rates in patients with less H3K9ac expression (P < 0.01). CONCLUSIONS: The present findings suggest that changes in H3K9ac occur during the process of oral carcinogenesis along with an increase in cell proliferation and EMT. The results demonstrate that H3K9ac may be a useful novel prognostic marker for OSCC.

Overcoming adaptive resistance in mucoepidermoid carcinoma through inhibition of the IKK-ß/IκBα/NFκB axis.

Patients with mucoepidermoid carcinoma (MEC) experience low survival rates and high morbidity following treatment, yet the intrinsic resistance of MEC cells to ionizing radiation (IR) and the mechanisms underlying acquired resistance remain unexplored. Herein, we demonstrated that low doses of IR intrinsically activated NFκB in resistant MEC cell lines. Moreover, resistance was significantly enhanced in IR-sensitive cell lines when NFκB pathway was stimulated. Pharmacological inhibition of the IKK-ß/IκBα/NFκB axis, using a single dose of FDA-approved Emetine, led to a striking sensitization of MEC cells to IR and a reduction in cancer stem cells. We achieved a major step towards better understanding the basic mechanisms involved in IR-adaptive resistance in MEC cell lines and how to efficiently overcome this critical problem.

Thrombotic microangiopathy and poor renal outcome in lupus patients with or without antiphospholipid syndrome.

OBJECTIVES: To assess the presence of acute thrombotic microangiopathy (aTMA) and chronic vascular lesions (cTMA) in lupus nephropathy, and to evaluate their association with extrarrenal lupus features, aPL positivity, antiphospholipid syndrome (APS) and renal survival. METHODS: We studied lupus patients with renal biopsy, ≥1 year of post-biopsy follow-up and at least two aCL (IgG-IgM), anti-ß2GP-I (IgG-IgM) and/or lupus anticoagulant (LAC) determinations. A blinded nephropathologist evaluated all biopsies. We retrospectively collected clinical, serological, treatment and renal survival data. We plotted survival curves and used Cox regression analysis. RESULTS: A total of 90 biopsies were included with a median disease duration 5.9 years and median follow-up 2.4 years. Eleven patients (12.2%) had cTMA and 3 (3%) aTMA. There was no difference in age, lupus duration, hypertension, drugs, APS, non-renal lupus features, low C3 or C4 aCL IgG, anti-ß2GP1-IgG or IgM and LAC between cTMA and non-cTMA groups. The cTMA group had aCL-IgM less frequently (27% vs. 66%, p=0.02), more class IV nephropathy (100% vs. 40%, p=0.01), higher activity index scores (7.5 vs. 2, p=0.03) and a tendency to need chronic dialysis (54.5% vs. 24% p=0.06). At four years of follow-up, 28% of the cTMA group and 62% of the non-cTMA group were free of dialysis (log rank p=0.03). cTMA was associated with chronic dialysis (RR 2.9, CI 95% 1.1-8.1, p=0.03). CONCLUSIONS: cTMA conferred a poor renal outcome. We found a low frequency of TMA that was not associated with with APL positivity or APS, suggesting that other factors hitherto not studied are involved in its pathogenesis.

Repercussions of surgically assisted maxillary expansion on nose width and position of septum and inferior nasal conchae.

The aim of the present study was to assess the clinical and radiographic repercussions of surgically assisted maxillary expansion on the septum, nasal cavity and nasal conchae. The sample was made up of 15 patients with skeletal maturity (9 females and 6 males between 16 and 45 years of age) and maxillary transverse deficiency. Assessments were performed through anterior rhinoscopy and frontal cephalometric radiographs on three occasions: (T0) preoperative period, (T1) locking of the expander and (T2) six months following the locking procedure. An increase was observed in the basal portion of the pyriform aperture and distances between the lateral wall of the basal portion of the pyriform aperture and the septum. The radiographic exam revealed that the nasal septum did not undergo any statistically significant change in its position. Moreover, no significant changes in the position of the nasal septum or nasal conchae were detected throughout the three evaluation times. The results suggest that surgically assisted maxillary expansion is capable of widening the basal portion of the pyriform aperture, with little repercussion on the anterior position of the nasal septum and inferior nasal conchae.

Etiology of childhood diarrhea in the northeast of Brazil: significant emergent diarrheal pathogens.

In a study conducted in João Pessoa, northeast of Brazil, 2344 Escherichia coli isolated from 290 infants with diarrhea and 290 healthy matched controls were analyzed for virulence traits. Enteroaggregative E. coli (EAEC) was the most prevalent pathogen associated to acute diarrhea. Based on the results of colony blot hybridization, serotyping, and HEp-2 cell adherence assays, strains were separated in categories as typical enteropathogenic E. coli (EPEC) (1.7%), atypical EPEC (a-EPEC) (9.3%), EAEC (25%), enterotoxigenic E. coli (10%), and enteroinvasive E. coli (EIEC) (1.4%). No enterohemorrhagic E. coli strains were isolated. Other enteropathogens were found, including Salmonella (7.9%), Shigella spp. (4.1%), thermophilic Campylobacter spp. (2.4%), Giardia lamblia (9.3%), and Entamoeba histolytica (5.8%). All enteropathogens were associated with diarrhea (P < 0.01). However, the association was lower for EPEC and EIEC (P < 0.03). Different pathogens associated with diarrhea may have been changing in Brazil where EAEC and a-EPEC seem to be the most prevalent pathogens among them.