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This study presents detailed foraminiferal, ostracod, and calcareous nannofossil analyses of five Middle Miocene sections located in the Central Paratethyan realm, namely in Poland, Romania and the Republic of Moldova. Based on foraminiferal distribution, five biostratigraphically important assemblages (labelled A-E) are distinguished. Foraminifera data combined with ostracoda and nannofossil evidence allowed correlation between the studied sections, and a comparison with the deposits of similar age from the Transylvanian, Vienna and Pannonian basins, as well as with the Transcarpathian regions. The micropaleontological record across the Badenian-Sarmatian boundary interval is also presented.

Three enzymes were immobilized onto polyionic hydrogel, ChitoXan, obtained by complexation between chitosan and xanthan. The biocatalysts used were two proteases (protease type XIX from Fungal d'Aspergillus sojae and the trypsin type II.S from Porcine Pancreas) and a lipase (lipase Type VII from Candida rugosa). The immobilization efficiencies and the relative activities were investigated for these enzymes. The immobilization efficiencies changed with each enzyme and varied between 53 and 80%. Good relative activities were found for the lipase Type VII from Candida rugosa and the protease type XIX from Fungal d'Aspergillus sojae. For the latter, the influenced of serveral factors were studied: molarity of the storage buffer, storage temperature and time of hydrogel, and the enzyme concentration. For the immobilized lipase, hydrolysis of olive oil in aqueous and organic media has been compared. This study confirmed that the lipase modified the external and internal structure of the hydrogel from fibrillar to the formation of globular structures in the presence of lipases. [ABSTRACT FROM AUTHOR]

Poly(methylmethacrylate-b-styrene) and poly(methylmetha-crylate-b-acrylonitrile) block copolymers are synthesized by means of the 4,4′-azo-bis-(4-cynovaleryl)-benzoyldiperoxide. In the first stage a polymethylme-thacrylate prepolymer is synthesized using the above mentioned initiator.The prepolymer containing peroxide end groups is employed in the second stage for the block copolymerization of styrene or acrylonitrile.The block copolymer structure was elucidated by means of IR and NMR spectral measurements. [ABSTRACT FROM AUTHOR]

A method for the preparation of hydrogels from the complexation of chitosan and xanthan is reported. Stable hydrogels capable of retaining be tween 65 and 95% weight water were prepared. The water retention and prop erties of the hydrogels were studied as a function of the degree of acetylation of chitosan and the ratio chitosan/xanthan used in the preparation of the gel. Spectroscopic FTIR was used to confirm complexation between the amine (chi tosan) and carboxylic (xanthan) groups. Electron micrographs (SEM and TEM) show the formation of a fibrillar structure with characteristic pore sizes be tween 100 and 1000 nm and fibril diameters between 50 and 100 nm. The diffu sion coefficient of 4-O-methyl-d-glucurono-D-xylan Remazol Brilliant Blue R (RBB-xylan) in the complex chitosan-xanthan was 2.02 × 10-12 m 2s-1 at 30°C. The chitosan-xanthan complex was used to immobilize two enzymes (endo-1,4- β-xylanase and protease) either as single enzymes or as a binary system. Immo bilization varied between 85 and 98%. The immobilized xylanase activity was significantly greater with respect to the free enzyme while the binary enzyme system promoted protease activity. [ABSTRACT FROM PUBLISHER]

Descoperirea genei methyl-CpG binding protein 2 (MECP2) situate pe cromozomul Xq28 ca fiind implicata in producerea Sindromului Rett (RTT) a fost urmata de asocierea unui spectru de fenotipuri cu mutatiile acestei gene. Distributia mutatiilor MECP2 a fost studiata in diverse populatii, doar recent acest studiu fiind ini- tiat in Romania. Am initiat primul studiu localizat pentru identificarea mutatiilor genei MECP2 utilizand PCR si secventiere Sanger. Am investigat 9 paciente, din zona de vest a tarii, 7 prezentand forma clasica de RTT si 2 prezentand forme atipice, provenite. Screeningul mutatiilor a relevat 3 mutatii diferite, prezente la 4 paciente si 5 variatii genetice nonpatogenice. Una dintre mutatiile detectate, deletia unei nucleotide in pozitia 225 (c.225delG) nu a mai fost descrisa anterior. Rata de detectie a mutatiilor in studiul nostru a fost de 44%. In aceast studiu ne-am centrat pe o abordare practica necesara geneticianului molecular in cadrul procesului de screening al mutatiilor genei MECP2 la pacientii cu RTT. Dezideratul nostru este de a extinde protocolul de screening al mutatiilor MECP2 la cazurile de tulburari asociate genei MECP2, de a oferi diagnostic prenatal, si de a-l completa cu alte tehnici care pot detecta rearanjamente ale genei MECP2.

Corporate social responsibility (CSR) is a progressively significant issue for organizations and governments. To benefit from a good reputation that reflects on organizational performance, organizations must ensure the balance between stakeholders' needs. This paper studies the direct and indirect effects of CSR on organizational financial performance as perceived by employees of organizations. The investigation used structural equation modeling to evaluate and describe the nature of the relationship between these two variables. The empirical study uses a perceptual approach, evaluating the perceptions of the closest stakeholders (employees). Data on the perceptions of 431 employees in Romanian organizations were collected following a questionnaire-based survey. The results indicate a strong effect of social responsibility on both direct and mediated organizational financial performance. The relationships established with the stakeholders ultimately affect organizational financial performance through variables such as the attraction and retention of employees, the attraction and loyalty of customers, more accessible access to capital, and the organization's reputation.

Social responsibility (SR) is a concept or practice by which organizations take into account the interest of society by taking responsibility for the impact of their activities on all stakeholders. The SR of organizations implies ethical behavior concerning all stakeholders and a company's commitment to the sustainable economic development of society. Organizational ethics is a set of written and unwritten codes of principles and values that govern decisions and actions within an organization. Ethics has a rather internal perspective, while social responsibility has a rather external perspective. This study examines the impact of social responsibility and organizational ethics on employees' wellbeing. To perform the empirical analysis, we conducted a survey among 423 employees from Romanian organizations. Using the structural equation modeling, we analyzed the relationships between social responsibility, organizational ethics, and employees' wellbeing, emphasizing the positive impact of ethical and responsible behavior of the organization on the employees' wellbeing. The organization's employees play a dual role: firstly, they are all internal stakeholders, and secondly, they are constituents of an external stakeholder essential for the organization-the community. The results show a significant positive influence of social responsibility and organizational ethics on employees' wellbeing as a result of a responsible and ethical behavior in relation to the organizational stakeholders.

A major challenge in validating genetic causes for patients with rare diseases (RDs) is the difficulty in identifying other RD patients with overlapping phenotypes and variants in the same candidate gene. This process, known as matchmaking, requires robust data sharing solutions to be effective. In 2014 we launched PhenomeCentral, a RD data repository capable of collecting computer-readable genotypic and phenotypic data for the purposes of RD matchmaking. Over the past 7 years PhenomeCentral's features have been expanded and its data set has consistently grown. There are currently 1615 users registered on PhenomeCentral, which have contributed over 12,000 patient cases. Most of these cases contain detailed phenotypic terms, with a significant portion also providing genomic sequence data or other forms of clinical information. Matchmaking within PhenomeCentral, and with connections to other data repositories in the Matchmaker Exchange, have collectively resulted in over 60,000 matches, which have facilitated multiple gene discoveries. The collection of deep phenotypic and genotypic data has also positioned PhenomeCentral well to support next generation of matchmaking initiatives that utilize genome sequencing data, ensuring that PhenomeCentral will remain a useful tool in solving undiagnosed RD cases in the years to come., (© 2022 Wiley Periodicals LLC.)

Background: The endocytic reabsorption of proteins in the proximal tubule requires a complex machinery and defects can lead to tubular proteinuria. The precise mechanisms of endocytosis and processing of receptors and cargo are incompletely understood. EHD1 belongs to a family of proteins presumably involved in the scission of intracellular vesicles and in ciliogenesis. However, the relevance of EHD1 in human tissues, in particular in the kidney, was unknown., Methods: Genetic techniques were used in patients with tubular proteinuria and deafness to identify the disease-causing gene. Diagnostic and functional studies were performed in patients and disease models to investigate the pathophysiology., Results: We identified six individuals (5-33 years) with proteinuria and a high-frequency hearing deficit associated with the homozygous missense variant c.1192C>T (p.R398W) in EHD1 . Proteinuria (0.7-2.1 g/d) consisted predominantly of low molecular weight proteins, reflecting impaired renal proximal tubular endocytosis of filtered proteins. Ehd1 knockout and Ehd1 R398W/R398W knockin mice also showed a high-frequency hearing deficit and impaired receptor-mediated endocytosis in proximal tubules, and a zebrafish model showed impaired ability to reabsorb low molecular weight dextran. Interestingly, ciliogenesis appeared unaffected in patients and mouse models. In silico structural analysis predicted a destabilizing effect of the R398W variant and possible inference with nucleotide binding leading to impaired EHD1 oligomerization and membrane remodeling ability., Conclusions: A homozygous missense variant of EHD1 causes a previously unrecognized autosomal recessive disorder characterized by sensorineural deafness and tubular proteinuria. Recessive EHD1 variants should be considered in individuals with hearing impairment, especially if tubular proteinuria is noted., (Copyright © 2022 by the American Society of Nephrology.)

Enamel renal syndrome (ERS) is a rare autosomal recessive disorder not fully characterized. Here we investigated ERS characteristics in 11 patients from 5 Brazilian families through clinical examination, imaging, renal ultrasonography, laboratory tests and DNA sequencing. The patients' age ranged from 6 to 25 years-old, and the presence of hypoplastic amelogenesis imperfecta, microdontia, intra-pulpal calcification, impacted posterior teeth with hyperplastic pericoronal follicles, gingival fibromatosis, ectopic calcifications on gingival and pericoronal tissues, and nephrocalcinosis were common findings to all patients. Only 4 patients showed abnormal laboratory tests (vitamin D, parathyroid hormone, phosphate, calcium). Intellectual disability and renal cysts were present in 2 patients each. Biallelic loss of function mutation in FAM20A gene, characterized by one base pair deletion in exon 11, resulting in a frameshift replacing a glutamine at codon 483 for a lysine and terminating at position 24 [NG_029809.1: c.1447delG; p.(Glu483Lysfs*24)], was detected in all patients, strongly suggesting a founder effect. Our results reinforce the distinct orofacial features of ERS, which are the clue for kidney examination and genetic testing. Early diagnosis is essential to minimize the deleterious effects related to ERS. Here we report the largest series of patients with ERS in a same population, and describe, for the first time, a founder mutation for FAM20A., (Copyright © 2018 Elsevier Masson SAS. All rights reserved.)

Background For many patients with kidney failure, the cause and underlying defect remain unknown. Here, we describe a novel mechanism of a genetic order characterized by renal Fanconi syndrome and kidney failure. Methods We clinically and genetically characterized members of five families with autosomal dominant renal Fanconi syndrome and kidney failure. We performed genome-wide linkage analysis, sequencing, and expression studies in kidney biopsy specimens and renal cells along with knockout mouse studies and evaluations of mitochondrial morphology and function. Structural studies examined the effects of recognized mutations. Results The renal disease in these patients resulted from monoallelic mutations in the gene encoding glycine amidinotransferase (GATM), a renal proximal tubular enzyme in the creatine biosynthetic pathway that is otherwise associated with a recessive disorder of creatine deficiency. In silico analysis showed that the particular GATM mutations, identified in 28 members of the five families, create an additional interaction interface within the GATM protein and likely cause the linear aggregation of GATM observed in patient biopsy specimens and cultured proximal tubule cells. GATM aggregates-containing mitochondria were elongated and associated with increased ROS production, activation of the NLRP3 inflammasome, enhanced expression of the profibrotic cytokine IL-18, and increased cell death. Conclusions In this novel genetic disorder, fully penetrant heterozygous missense mutations in GATM trigger intramitochondrial fibrillary deposition of GATM and lead to elongated and abnormal mitochondria. We speculate that this renal proximal tubular mitochondrial pathology initiates a response from the inflammasome, with subsequent development of kidney fibrosis., (Copyright © 2018 by the American Society of Nephrology.)

Hyperinsulinemic hypoglycemia (HI) and congenital polycystic kidney disease (PKD) are rare, genetically heterogeneous disorders. The co-occurrence of these disorders (HIPKD) in 17 children from 11 unrelated families suggested an unrecognized genetic disorder. Whole-genome linkage analysis in five informative families identified a single significant locus on chromosome 16p13.2 (logarithm of odds score 6.5). Sequencing of the coding regions of all linked genes failed to identify biallelic mutations. Instead, we found in all patients a promoter mutation (c.-167G>T) in the phosphomannomutase 2 gene ( PMM2 ), either homozygous or in trans with PMM2 coding mutations. PMM2 encodes a key enzyme in N-glycosylation. Abnormal glycosylation has been associated with PKD, and we found that deglycosylation in cultured pancreatic β cells altered insulin secretion. Recessive coding mutations in PMM2 cause congenital disorder of glycosylation type 1a (CDG1A), a devastating multisystem disorder with prominent neurologic involvement. Yet our patients did not exhibit the typical clinical or diagnostic features of CDG1A. In vitro, the PMM2 promoter mutation associated with decreased transcriptional activity in patient kidney cells and impaired binding of the transcription factor ZNF143. In silico analysis suggested an important role of ZNF143 for the formation of a chromatin loop including PMM2 We propose that the PMM2 promoter mutation alters tissue-specific chromatin loop formation, with consequent organ-specific deficiency of PMM2 leading to the restricted phenotype of HIPKD. Our findings extend the spectrum of genetic causes for both HI and PKD and provide insights into gene regulation and PMM2 pleiotropy., (Copyright © 2017 by the American Society of Nephrology.)

Enamel-renal syndrome (OMIM #204690) is an uncommon disorder characterized by amelogenesis imperfecta and nephrocalcinosis and is caused by mutations in FAM20 A. We report 2 patients with enamel-renal syndrome who exhibited the typical features of this syndrome and a homozygous nonsense mutation in the FAM20 A gene (c.406 C>T), genetically confirming the diagnosis. They also exhibited 2 undescribed clinical features, hypertrichosis and hearing loss. Alterations in genes frequently associated with nonsyndromic hearing loss in the Brazilian population, including connexin 26 (GJB2), connexin 30 (GJB6) and mitochondrial 12 S rRNA (m.A1555 G mutation), were not found. These results suggest a putative function of FAM20 A in the development of the inner ear and in the formation of hair. The presence of nephrocalcinosis is a risk factor for renal impairment, and it is important to perform regular renal monitoring in order to avoid renal failure., (Copyright © 2016 Elsevier Inc. All rights reserved.)

The National Institutes of Health Undiagnosed Diseases Program (NIH UDP) applies translational research systematically to diagnose patients with undiagnosed diseases. The challenge is to implement an information system enabling scalable translational research. The authors hypothesized that similar complex problems are resolvable through process management and the distributed cognition of communities. The team, therefore, built the NIH UDP integrated collaboration system (UDPICS) to form virtual collaborative multidisciplinary research networks or communities. UDPICS supports these communities through integrated process management, ontology-based phenotyping, biospecimen management, cloud-based genomic analysis, and an electronic laboratory notebook. UDPICS provided a mechanism for efficient, transparent, and scalable translational research and thereby addressed many of the complex and diverse research and logistical problems of the NIH UDP. Full definition of the strengths and deficiencies of UDPICS will require formal qualitative and quantitative usability and process improvement measurement.

Despite the increasing prevalence of clinical sequencing, the difficulty of identifying additional affected families is a key obstacle to solving many rare diseases. There may only be a handful of similar patients worldwide, and their data may be stored in diverse clinical and research databases. Computational methods are necessary to enable finding similar patients across the growing number of patient repositories and registries. We present the Matchmaker Exchange Application Programming Interface (MME API), a protocol and data format for exchanging phenotype and genotype profiles to enable matchmaking among patient databases, facilitate the identification of additional cohorts, and increase the rate with which rare diseases can be researched and diagnosed. We designed the API to be straightforward and flexible in order to simplify its adoption on a large number of data types and workflows. We also provide a public test data set, curated from the literature, to facilitate implementation of the API and development of new matching algorithms. The initial version of the API has been successfully implemented by three members of the Matchmaker Exchange and was immediately able to reproduce previously identified matches and generate several new leads currently being validated. The API is available at https://github.com/ga4gh/mme-apis., (© 2015 WILEY PERIODICALS, INC.)

There are few better examples of the need for data sharing than in the rare disease community, where patients, physicians, and researchers must search for "the needle in a haystack" to uncover rare, novel causes of disease within the genome. Impeding the pace of discovery has been the existence of many small siloed datasets within individual research or clinical laboratory databases and/or disease-specific organizations, hoping for serendipitous occasions when two distant investigators happen to learn they have a rare phenotype in common and can "match" these cases to build evidence for causality. However, serendipity has never proven to be a reliable or scalable approach in science. As such, the Matchmaker Exchange (MME) was launched to provide a robust and systematic approach to rare disease gene discovery through the creation of a federated network connecting databases of genotypes and rare phenotypes using a common application programming interface (API). The core building blocks of the MME have been defined and assembled. Three MME services have now been connected through the API and are available for community use. Additional databases that support internal matching are anticipated to join the MME network as it continues to grow., (© 2015 WILEY PERIODICALS, INC.)

The discovery of disease-causing mutations typically requires confirmation of the variant or gene in multiple unrelated individuals, and a large number of rare genetic diseases remain unsolved due to difficulty identifying second families. To enable the secure sharing of case records by clinicians and rare disease scientists, we have developed the PhenomeCentral portal (https://phenomecentral.org). Each record includes a phenotypic description and relevant genetic information (exome or candidate genes). PhenomeCentral identifies similar patients in the database based on semantic similarity between clinical features, automatically prioritized genes from whole-exome data, and candidate genes entered by the users, enabling both hypothesis-free and hypothesis-driven matchmaking. Users can then contact other submitters to follow up on promising matches. PhenomeCentral incorporates data for over 1,000 patients with rare genetic diseases, contributed by the FORGE and Care4Rare Canada projects, the US NIH Undiagnosed Diseases Program, the EU Neuromics and ANDDIrare projects, as well as numerous independent clinicians and scientists. Though the majority of these records have associated exome data, most lack a molecular diagnosis. PhenomeCentral has already been used to identify causative mutations for several patients, and its ability to find matching patients and diagnose these diseases will grow with each additional patient that is entered., (© 2015 WILEY PERIODICALS, INC.)

We have developed PhenoTips: open source software for collecting and analyzing phenotypic information for patients with genetic disorders. Our software combines an easy-to-use interface, compatible with any device that runs a Web browser, with a standardized database back end. The PhenoTips' user interface closely mirrors clinician workflows so as to facilitate the recording of observations made during the patient encounter. Collected data include demographics, medical history, family history, physical and laboratory measurements, physical findings, and additional notes. Phenotypic information is represented using the Human Phenotype Ontology; however, the complexity of the ontology is hidden behind a user interface, which combines simple selection of common phenotypes with error-tolerant, predictive search of the entire ontology. PhenoTips supports accurate diagnosis by analyzing the entered data, then suggesting additional clinical investigations and providing Online Mendelian Inheritance in Man (OMIM) links to likely disorders. By collecting, classifying, and analyzing phenotypic information during the patient encounter, PhenoTips allows for streamlining of clinic workflow, efficient data entry, improved diagnosis, standardization of collected patient phenotypes, and sharing of anonymized patient phenotype data for the study of rare disorders. Our source code and a demo version of PhenoTips are available at http://phenotips.org., (© 2013 WILEY PERIODICALS, INC.)

Mucopolysaccharidosis II (Hunter syndrome) is a rare x-linked disorder caused by a deficiency in the lysosomal enzyme iduronate-2-sulphatase, leading to an accumulation of the glycosaminoglycans (GAGs) dermatansulphate and heparan sulphate. The consequence of GAGs accumulation is progressive, multiorgan disease. Enzyme-replacement therapy is hypothesised to result in disease stabilisation and improved prognosis. We present a severe case of Hunter syndrome diagnosed at age 2 years and 4 months, who started enzyme-replacement therapy at the age of 3 years and 3 months. We report his evolution after 1 year of treatment. The treatment response was good and there was significant improvement in the quality of life. Owing to the rarity of Hunter syndrome, the multisystem nature and the heterogeneity of disease progression, patient care implies interdisciplinary consultations with a wide range of specialists. The best management can be provided in reference centres for metabolic diseases.

Background/aims: Mutations in the inwardly-rectifying K(+)-channel KCNJ10/Kir4.1 cause autosomal recessive EAST syndrome (epilepsy, ataxia, sensorineural deafness and tubulopathy). KCNJ10 is expressed in the distal convoluted tubule of the kidney, stria vascularis of the inner ear and brain glial cells. Patients diagnosed clinically with EAST syndrome were genotyped and mutations in KCNJ10 were studied functionally., Methods: Patient DNA was amplified and sequenced, and new mutations were identified. Mutant and wild-type KCNJ10 constructs were cloned and heterologously expressed in Xenopus oocytes. Whole-cell K(+) currents were measured by 2-electrode voltage clamping and channel expression was analysed by Western blotting., Results: We identified 3 homozygous mutations in KCNJ10 (p.F75C, p.A167V and p.V91fs197X), with mutation p.A167V previously reported in a compound heterozygous state. Oocytes expressing wild-type human KCNJ10 showed inwardly rectified currents, which were significantly reduced in all of the mutants (p < 0.001). Specific inhibition of KCNJ10 currents by Ba(2+) demonstrated a large residual function in p.A167V only, which was not compatible with causing disease. However, co-expression with KCNJ16 abolished function in these heteromeric channels almost completely., Conclusion: This study provides an explanation for the pathophysiology of the p.A167V KCNJ10 mutation, which had previously not been considered pathogenic on its own. These findings provide evidence for the functional cooperation of KCNJ10 and KCNJ16. Thus, in vitro ascertainment of KCNJ10 function may necessitate co-expression with KCNJ16., (© 2013 S. Karger AG, Basel.)

Purpose: Repeated administration of low-dose silver nitrate (SN) has been shown to be effective in creating pleurodesis. This study aimed to determine the effectiveness of a SN-eluting pleural catheter for pleurodesis., Methods: Catheters with a chitosan-SN-hyaluronic acid hydrogel coating designed to release SN over 14 days, or placebo uncoated catheters, were inserted in rabbit and lamb pleurodesis models. Pleurodesis was assessed at 28 days according to a 1-8 point scoring system and pleural fibrosis and inflammation assessed histologically on a 0-4 point scale., Results: In the rabbit model, pleurodesis scores were significantly increased in both the 24 mg and 50 mg SN catheters versus control animals as well as compared to the contralateral untreated pleural space (median-treated side scores were 5, 8, and 1, respectively, median score for contralateral side was 1 in all groups). In the lamb model, pleurodesis scores were significantly increased in both the 750 mg and 1000 mg catheter groups versus control animals as well as compared to the contralateral untreated pleural space (median-treated side scores were 7, 7, and 1, respectively, median score for contralateral pleural space was 1 in all groups). Catheters appeared well tolerated, although higher than expected mortality was seen in the 50 mg catheter rabbit group., Conclusions: A catheter designed to deliver SN to the pleural space over 14 days appears to be effective in creating pleurodesis. Further investigations to determine in-vivo catheter pharmacokinetics, toxicity, dose and optimal coating methods are warranted.

The relationship between different species of oral Treponemas and inflammation in periodontal disease progression is complex. The purpose of this study was to analyze and compare the subgingival plaque samples collected from periodontally healthy subjects and from chronic gingivitis and periodontitis patients in order to detect the presence of T. denticola, T. pectinovorum, T. socranskii and T. vincentii using nested-PCR technology. After DNA extraction from the samples using QIAmp DNA Mini Kit (QIAGEN, the four Treponema species were determined with nested-polymerase chain reaction which requires two sets of primers to amplify a specific DNA fragment in two separate runs of PCR. Pearson chi-square was implemented to compare the three groups as to the presence of four Treponema species. Results of this investigation showed significant differences between groups regarding subject proportion of T. denticola, T. socranskii, T. pectinovorum, T. vincentii, with a higher percentage of patients from associated-disease groups of patients harboring these four species than healthy subjects. These differences were more pronounced in presence of Treponema denticola and Treponema socranskii. Our findings suggest that Treponema denticola and Treponema socranskii concurrent presence indicate more accurately the association with chronic gingivitis and periodontitis.

The aim of this study was to identify at species level and to investigate the antibiotic susceptibility of oral streptococcal strains isolated from 100 pus samples collected from Romanian patients with different odontogenic infections. The isolates were identified at species level using the Rapid ID 32 STREP system and their susceptibility was testing by the Etest, against: penicillin G, ampicillin, erythromycin, clindamycin and tetracycline. For the investigation of erythromycin resistance phenotype the disk diffusion test was used. The isolates belonged to several species, with Streptococcus anginosus and Streptococcus oralis predominating. Reduced susceptibility to beta-lactam antibiotics was found only among the isolates belonging to S. mitis and S. sanguinis groups. Resistance to erythromycin was detected among all species, except for: S. constellatus, S. intermedius and S. gordonii, and the M phenotype was established, while resistance to tetracycline was detected within all species but S. gordonii. In contrast, clindamycin was fully active. As most odontogenic infections are mixed infections, often involving strictly anaerobic bacteria, which are frequently beta-lactamase producers, the association of a penicillin and a beta-lactamase inhibitor, like Amoxiclav, is recommended when the antimicrobial treatment is necessary.