Pre-emergent indaziflam can enhance forest seed germination in direct seeding?

Pre-emergent herbicides can contribute to the control of weed competition in direct seeding restoration, however it is necessary to evaluate their effects on seeds of native tropical forest species. The aim of the study was to assess the potential impact of the herbicide indaziflam on the germination of 17 forest species. For this, a dosage of 180 mL of the product in 200L of water was compared to the control without herbicide. The degree of sensitivity of each species was calculated by a ratio between the percentage of germination with herbicide (GH) and the control without herbicide (GC) classifying them as: extremely sensitive (ES= (GH/GC) <0.25), sensitive (S=0.25< (GH/GC) <0.50), low sensitivity (LS=0.50< (GH/GC) <0.75), indifferent (I=0.75< (GH/GC) <1.0) and potentiated (P= (GH/GC) >1). The herbicide promoted a significant reduction in mean germination in 35% (n=6) of the species and 59% (n = 10) were sensitive or extremely sensitive to indaziflam, and only three did not germinate. On the other hand, 29.4% (n=5) showed low sensitivity or indifference to the herbicide, while seed germination was slightly increased by indaziflam to 11.7% (n=2). Pre-emergent indaziflam can be recommended in direct seeding restoration, as only 17.6% (n=3) of the species were inhibited by pre-emergent. However, the effect of indaziflam varies by species and requires further studies to support large-scale use in direct seeding.

Effects of prenatal hypoxia-ischemia on male rat periaqueductal gray matter: Hyperalgesia, astrogliosis and nitrergic system impairment.

Prenatal hypoxic-ischemic insult (HI) may lead to a variety of neurological consequences that may persist throughout adulthood. In the most severe cases, HI is known to increase pain sensitivity which profoundly impacts quality of life. Periaqueductal gray matter (PAG) is a relevant region of the descending pain pathway and its function may be modulated by a complex network that includes nitrergic neurons and glial response, among other factors. Astrocytes, central players in pain modulation, are known to respond to HI by inducing hyperplasia, hypertrophy and increasing the number of their processes and the staining of glial fibrillary acidic protein (GFAP). In this work we investigated the effects of prenatal HI on touch and pain sensitivity, besides the distribution of the neuronal isoform of Nitric Oxide Synthase (nNOS) and GFAP in the PAG of young and adult male rats. At 18 days of gestation, rats had their uterine arteries clamped for 45 min (HI group). SHAM-operated animals were also generated (SHAM group). At post-natal day 30 (P30) or 90 (P90), the offspring was submitted to the behavioral tests of Von Frey and formalin or histological processing to perform immunohistochemistry for nNOS and GFAP. Although there was no significant difference between the groups concerning touch sensitivity, we observed an increase in pain sensitivity in HI P30 and HI P90. The number of nNOS + cells was reduced in HI adult animals in dlPAG and vlPAG. GFAP immunostaining was increased in HI P90 in dlPAG and dmPAG. Our results demonstrated for the first time an increase in pain sensitivity as a consequence of prenatal HI in an animal model. It reinforces the relevance of this model to mimic the effects of prenatal HI, as hyperalgesia.

Impact of Treatment on Host Responses in Young Individuals with Periodontitis.

Grade C periodontitis in young individuals is characterized by severe/rapid periodontal destruction, usually early onset, in systemically healthy individuals. An individual's host response, triggered by a dysbiotic subgingival biofilm, has been reported as a contributor to the tissue destruction, although mechanisms of this response and contributions to such disease remain poorly understood. Nonsurgical treatment has resulted in positive clinical responses for both localized (now molar-incisor pattern) and generalized forms of grade C periodontitis, especially when adjunctive systemic antibiotics are used. Nonsurgical treatment may also affect host responses, although mechanisms leading to significant changes in this response remain unclear. Significant effects on inflammatory response to antigens/bacteria have been described posttreatment, but evidence for long-term effects remains limited. Nonsurgical treatment in these individuals may also modulate a variety of host markers in serum/plasma and gingival crevicular fluid along with clinical parameter improvements. The impact of other adjuncts to nonsurgical treatment focusing on controlling exacerbated immunoinflammatory responses needs to be further explored in grade C periodontitis in young individuals. Recent evidence suggests that nonsurgical treatment with adjunctive laser therapy may modulate host and microbial responses in those subjects, at least in the short term. Available evidence, while very heterogeneous (including variations in disease definition and study designs), does not provide clear conclusions on this topic yet provides important insights for future studies. In this review, studies within the past decade evaluating the impact of nonsurgical treatment on systemic/local host responses in young individuals with grade C periodontitis, as well as long-term clinical responses posttreatment, will be critically appraised and discussed.

Infection with Trypanosoma spp. in Platydoras armatulus (Siluriformes, Doradidae), in southwestern Amazon, Brazil.

Trypanosoma is a hemoflagellate capable of infecting a wide variety of invertebrates and vertebrates, such as Neotropical freshwater fish. The present study described and morphologically compared Trypanosoma spp., found in Platydoras armatulus, Valenciennes, 1840, in southwestern Amazon. Fish specimens were sampled in Ipixuna and Juruá rivers located in the states of Amazonas and Acre, Brazil. Fish blood samples were taken by cardiac puncture, and smears were prepared for quantification, morphometric measurements, and morphotyping (characterization of the trypanosomes according to their morphological variations) of trypanosomes found. Prevalence, mean abundance, and intensity of parasitism were estimated in the parasitized fish specimens. Five fish specimens were collected, showing a 100% prevalence of parasites in the host. We found two Trypanosoma morphotypes, A and B, in which A had the highest infection intensity in host specimens. Thus, the present study presented the first report of Trypanosoma parasitizing P. armatulus, with different morphological variations.

Effect of the intra-alveolar administration of dexamethasone on swelling, trismus, and pain after impacted lower third molar extraction: a randomized, double-blind clinical trial.

BACKGROUND: To evaluate the efficacy of intra-alveolar administration of dexamethasone 4 mg in the control of edema, trismus, and pain resulting from the extraction of impacted lower third molars and the drug permeability through the oral mucosa by in silico prediction. MATERIAL AND METHODS: The randomized, double-blind, split-mouth clinical trial included patients who had both impacted lower third molars in equivalent positions. Hemiarches were divided into control side when dexamethasone was administered orally and experimental side when dexamethasone was administered using the intra-alveolar route. Patients were evaluated considering edema, trismus, and pain. The permeability of dexamethasone through the oral mucosa was assessed by in silico prediction. Student's t-test was selected for comparative analysis of edema and trismus, and the chi-square test analyzed the distribution of postoperative pain between the sides. RESULTS: There were no significant differences between the routes of administration in measuring symptoms between the pre and postoperative times (p>0.05). In silico prediction suggested that dexamethasone molecular characteristics facilitate intra-alveolar administration. CONCLUSIONS: Intra-alveolar administration had similar efficacy to oral administration in controlling symptoms of post-surgical inflammation of impacted lower third molars.

18F-FDG PET/CT images defined the true extent of a urothelial bladder carcinoma.

A patient was referred, after neoadjuvant chemotherapy, for pre-surgical evaluation of urothelial bladder carcinoma (single lesion). Two thickenings in the left ureter wall identified on the CT scan were equivocal for malignancy. 18F-FDG PET/CT with delayed pelvic images, hyperhydration, and furosemide showed hypermetabolic ureteral metastases and multifocal bladder tumors. There were no lymph nodes or distant metastases. These 18F-FDG PET/CT findings completely altered the surgical treatment. The patient underwent left nephroureterectomy, radical cystoprostatectomy, and lymphadenectomy, followed by a urinary transit reconstruction. Histopathology confirmed multifocal high-grade urothelial carcinoma in the bladder walls and left ureter and benign lymph nodes.

Local and Plasma Biomarker Profiles in Localized Aggressive Periodontitis.

Localized aggressive periodontitis (LAP) patients possess a systemic hyperinflammatory response after lipopolysaccharide stimulation. However, the levels of inflammatory and bone biomarkers in plasma, as well as possible associations between local and plasma biomarkers, are unknown in LAP. This cross-sectional study aimed to characterize gingival crevicular fluid (GCF) and plasma biomarker profiles in LAP patients, their healthy siblings (HS), and healthy unrelated controls (HC). Fifty-eight LAP subjects, 33 HS, and 49 HC (African Americans, aged 5 to 25 y) were included. Following collection of clinical parameters with GCF and plasma samples, levels of 16 inflammatory and bone resorption biomarkers were determined with Milliplex. Univariate and correlation analyses were performed among all clinical and laboratorial parameters. Discriminant analyses were used to investigate groups of biomarkers discriminating LAP from HS and HC in GCF and plasma. GCF levels of multiple cytokines and chemokines and RANKL:OPG ratio (receptor activator of nuclear factor kappa-B ligand:osteoprotegerin) were higher in LAP disease, most of which positively correlated with probing depth and attachment loss of sampled sites. A group of IL-12p40, IL-6, IL-12p70, IL-2, and MIP-1α discriminated LAP diseased sites from twheir healthy sites, as well as from HS and HC healthy sites. In plasma, only RANKL levels were increased in LAP versus controls, which positively correlated with the percentage of affected sites and deep/bleeding sites. A plasma inflammatory profile including MIP-1α, IL-8, IL-10, and INF-γ could significantly discriminate LAP patients from HS and HC. No correlations were found between GCF and plasma levels of biomarkers. In conclusion, an inflammatory profile including groups of specific biomarkers in GCF and plasma may significantly discriminate LAP from healthy individuals. The hyperinflammatory response previously found in the peripheral blood of LAP patients is dependent on lipopolysaccharide stimulation, apparently resulting mostly in local tissue destruction and changes in biomarker profile, with a slight influence in the systemic inflammatory profile (ClinicalTrials.gov NCT01330719). Knowledge Transfer Statement: The results of this study can be possibly used by clinicians in the future as diagnostic tools for localized aggressive periodontitis. Thus, in the future, with proper consideration of cost, patient preference, chair-side feasibility and ultimately further studies validating the role of GCF markers for disease progression and response to treatment, this information could lead to more appropriate therapeutic decisions and the development of preventive approaches for susceptible patients.

Impact of periodontal disease on quality of life: a systematic review.

The diagnosis of periodontal disease is commonly based on objective evaluations of the patient's medical/dental history as well as clinical and radiographic examinations. However, periodontal disease should also be evaluated subjectively through measures that quantify its impact on oral health-related quality of life. The aim of this study was to evaluate the impact of periodontal disease on quality of life among adolescents, adults and older adults. A systematic search of the literature was performed for scientific articles published up to July 2015 using electronic databases and a manual search. Two independent reviewers performed the selection of the studies, extracted the data and assessed the methodological quality. Thirty-four cross-sectional studies involving any age group, except children, and the use of questionnaires for the assessment of the impact of periodontal disease on quality of life were included. Twenty-five studies demonstrated that periodontal disease was associated with a negative impact on quality of life, with severe periodontitis exerting the most significant impact by compromising aspects related to function and esthetics. Unlike periodontitis, gingivitis was associated with pain as well as difficulties performing oral hygiene and wearing dentures. Gingivitis was also negatively correlated with comfort. The results indicate that periodontal disease may exert an impact on quality of life of individuals, with greater severity of the disease related to greater impact. Longitudinal studies with representative samples are needed to ensure validity of the findings.

Mutational characterization of the P3H1/CRTAP/CypB complex in recessive osteogenesis imperfecta.

Osteogenesis imperfecta (OI) is a genetic disease characterized by bone deformities and fractures. Most cases are caused by autosomal dominant mutations in the type I collagen genes COL1A1 and COL1A2; however, an increasing number of recessive mutations in other genes have been reported. The LEPRE1, CRTAP, and PPIB genes encode proteins that form the P3H1/CRTAP/CypB complex, which is responsible for posttranslational modifications of type I collagen. In general, mutations in these genes lead to severe and lethal phenotypes of recessive OI. Here, we describe sixteen genetic variations detected in LEPRE1, CRTAP, and PPIB from 25 Brazilian patients with OI. Samples were screened for mutations on single-strand conformation polymorphism gels and variants were determined by automated sequencing. Seven variants were detected in patients but were absent in control samples. LEPRE1 contained the highest number of variants, including the previously described West African allele (c.1080+1G>T) found in one patient with severe OI as well as a previously undescribed p.Trp675Leu change that is predicted to be disease causing. In CRTAP, one patient carried the c.558A>G homozygous mutation, predicted as disease causing through alteration of a splice site. Genetic variations detected in the PPIB gene are probably not pathogenic due to their localization or because of their synonymous effect. This study enhances our knowledge about the mutational pattern of the LEPRE1, CRTAP, and PPIB genes. In addition, the results strengthen the proposition that LEPRE1 should be the first gene analyzed in mutation detection studies in patients with recessive OI.

Antimicrobial activity of Rheedia brasiliensis and 7-epiclusianone against Streptococcus mutans.

This in vitro study evaluated the antimicrobial activity of extracts obtained from Rheedia brasiliensis fruit (bacupari) and its bioactive compound against Streptococcus mutans. Hexane, ethyl-acetate and ethanolic extracts obtained (concentrations ranging from 6.25 to 800 microg/ml) were tested against S. mutans UA159 through MIC/MBC assays. S. mutans 5-days-old biofilms were treated with the active extracts (100 x MIC) for 0, 1, 2, 3 and 4h (time-kill) and plated for colony counting (CFU/ml). Active extracts were submitted to exploratory chemical analyses so as to isolate and identify the bioactive compound using spectroscopic methods. The bioactive compound (concentrations ranging from 0.625 to 80 microg/ml) was then tested through MIC/MBC assays. Peel and seed hexane extracts showed antimicrobial activity against planktonic cells at low concentrations and were thus selected for the time kill test. These hexane extracts reduced S. mutans biofilm viability after 4h, certifying of the bioactive compound presence. The bioactive compound identified was the polyprenylated benzophenone 7-epiclusianone, which showed a good antimicrobial activity at low concentrations (MIC: 1.25-2.5 microg/ml; MBC: 10-20 microg/ml). The results indicated that 7-epiclusianone may be used as a new agent to control S. mutans biofilms; however, more studies are needed to further elucidate the mechanisms of action and the anticariogenic potential of such compound found in R. brasiliensis.

A prevalent pathogenic GAMT mutation (c.59G>C) in Portugal.

Guanidinoacetate methyltransferase (GAMT) deficiency (MIM 601240), an autosomal recessive disorder of creatine biosynthesis, presents with mental retardation, extrapyramidal symptoms, autistic-like behavior and epilepsy. Other hallmarks are cerebral creatine deficiency, increased levels of guanidinoacetate in body fluids and mutations in the GAMT gene. Creatine supplementation partially restores cerebral creatine content. Worldwide, 29 patients have been identified and 15 different mutations have been reported in the GAMT gene. Ten out of these 29 patients are of Portuguese origin. Likely, a founder effect and a high carrier rate in Portugal exist, since in 17 out of the 20 Portuguese alleles the c.59G>C; p.Trp20Ser mutation was found. We investigated the carrier rate of the c.59G>C; p.Trp20Ser mutation in different regions of Portugal and confirmed the pathogenic nature of this missense mutation by transient transfections. Anonymous bloodspots (1002) were screened for the presence of the c.59G>C; p.Trp20Ser mutation by SNaPshot (Single Nucleotide Polymorphism Multiplex Kit). Eight carriers of c.59G>C; p.Trp20Ser were detected of which four are derived from the Archipelagos. This suggests that the carrier rate of the c.59G>C; p.Trp20Ser mutation is relatively high in these islands, as well as in other parts of Portugal. It also implies that newborn screening in these regions is warranted for this treatable disorder.

Overexpression of GAMT restores GAMT activity in primary GAMT-deficient fibroblasts.

Guanidinoacetate methyltransferase deficiency (MIM 601240) is an autosomal recessive disorder of creatine biosynthesis. Patients present with mental retardation, extrapyramidal symptoms, autistic-like behavior, epilepsy, cerebral creatine deficiency and increased levels of guanidinoacetate. So far 15 mutations have been reported, including six missense variants that are highly likely to be pathogenic mutations. To prove that mutations in the GAMT gene are responsible for GAMT deficiency we overexpressed the GAMT open reading frame in GAMT-deficient fibroblasts by stable transfection. In addition, HeLa cells were transiently transfected with the same expression vector. In contrast to mock transfectants transfection of primary GAMT-deficient fibroblasts with wild-type GAMT results in the restoration of GAMT activity as measured by GC-MS using stable isotope labeled substrates. Moreover, the expression of the GAMT-EGFP fusion protein was analyzed by Western blot, confirming the presence of GAMT fusion protein, both in the stable as well as in the transient transfectants. Here, we prove that mutations in the GAMT gene are responsible for GAMT deficiency, since overexpression of the GAMT open reading frame restores GAMT activity in GAMT-deficient fibroblasts. Furthermore, the transient transfection of HeLa cells will be important for functional analysis of variants of unknown consequence (i.e., missense mutations).