A Deep Learning Computer-Aided Diagnosis Approach for Breast Cancer.

Breast cancer is a gigantic burden on humanity, causing the loss of enormous numbers of lives and amounts of money. It is the world's leading type of cancer among women and a leading cause of mortality and morbidity. The histopathological examination of breast tissue biopsies is the gold standard for diagnosis. In this paper, a computer-aided diagnosis (CAD) system based on deep learning is developed to ease the pathologist's mission. For this target, five pre-trained convolutional neural network (CNN) models are analyzed and tested-Xception, DenseNet201, InceptionResNetV2, VGG19, and ResNet152-with the help of data augmentation techniques, and a new approach is introduced for transfer learning. These models are trained and tested with histopathological images obtained from the BreakHis dataset. Multiple experiments are performed to analyze the performance of these models through carrying out magnification-dependent and magnification-independent binary and eight-class classifications. The Xception model has shown promising performance through achieving the highest classification accuracies for all the experiments. It has achieved a range of classification accuracies from 93.32% to 98.99% for magnification-independent experiments and from 90.22% to 100% for magnification-dependent experiments.

The Course of Hepatitis C Infection and Response to Anti-viral Therapy in Patients with Thalassemia major and Hepatitis C Infection: A Longitudinal, Prospective Study.

BACKGROUND: The course of hepatitis C infection (HCV) in patients with thalassemia has not been adequately studied, and management has not been optimized. The current prospective longitudinal study assessed the clinical course, outcome, progression, and management of recently acquired HCV in patients with transfusion-dependent thalassemia major versus acute HCV without thalassemia. METHODS: A well-characterized cohort of patients with thalassemia and recent HCV infection or recent HCV without thalassemia were enrolled and prospectively followed. The blood transfusion needs and chelating agents were determined. Liver functions tests, HCV-RNA, iron, and ferritin levels were measured. Patients with chronic HCV evolution received treatment for HCV. The fibrosis progression rate was determined in chronic HCV patients with or without thalassemia by paired liver biopsies or serial transient elastography (TE), or serum markers of liver fibrosis. Liver iron content (LIC) was assessed by R2 MRI. RESULTS: Self-limited acute HCV was observed in 17% of patients with acute HCV and thalassemia versus 35% of patients without thalassemia (P=0.031). The fibrosis progression rates were significantly higher in patients with chronic HCV and thalassemia compared to those with chronic HCV alone (1.14±0.48) and (0.35±0.14) (P<0.0001), respectively. A direct linear correlation was observed between the fibrosis progression rate and each of LIC (R=+0.67; P=0.01) and ferritin (R=0.77; P<0.01). In patients with chronic HCV and thalassemia, the sustained virologic response (SVR) to pegylated interferon-based therapy and direct antiviral agents (DAAS) were 33% and 82% respectively (P<0.0001), while in chronic HCV patients without thalassemia, the SVR rates to PEG-IFN/RBV and DAAs were 51% and 92% respectively. Five patients with concomitant HCV and thalassemia died during the study due to cardiac causes (n=3) and liver cancer (n=2). CONCLUSIONS: Patients with acute HCV and thalassemia have low rates of spontaneous resolution of HCV infection, and the majority develop chronic HCV. Direct-acting antiviral combinations are associated with high SVR rates and low adverse event in treatment naïve and experienced patients with chronic HCV and thalassemia. Liver fibrosis is accelerated in thalassemia patients with chronic HCV; therefore, early diagnosis, treatment with DAAs, adequate iron chelation, and non-invasive monitoring liver status are recommended to prevent cirrhosis and hepatocellular carcinoma.

Synthesis, antimicrobial activity and molecular modeling study of 3-(5-amino-(2H)-1,2,4-triazol-3-yl]-naphthyridinones as potential DNA-gyrase inhibitors.

Four series of triazolylnaphthyridinone derivatives were synthesized as structural surrogates of nalidixic acid. The targeted derivatives involve: 3-(5-acylamino-2H-1,2,4-triazol-3-yl)-naphtyridin-4-ones 6(a-e); 3-(5-benzylidineamino-2H-1,2,4-triazol-3-yl)-naphthyridin-4-ones 8(a-g) and their 6-bromonaphthyridin-4-one analogs 7(a-e); 9(a-g). The synthesized compounds were evaluated In vitro for their antimicrobial activity against selected resistant strains of G+ve, G-ve, and Mycobacterium phlei. The results revealed remarkable selectivity, of the tested compounds, against Bacillus subtilis and Aggregatibacter actinomycetemcomitans, which are resistant to nalidixic acid. The growth inhibition zones were ranging from 20 to 40 mm at 10 mg/ml and the respective MIC-values ∼3.68-6.3 µM. The results illustrate that the 6-bromo derivatives 7(a-e) and 9(a-g) were more potent than the non-brominated counterparts 6(a-e) and 8(a-e) respectively. Inhibition of E. coli DNA-gyrase supercoiling activity is also evaluated. The 5-(4-methoxybanzamido)-triazolyl-6-bromonaphthyridinone (7e) exhibits IC50 = 1.94 µg/ml, which is comparable to that of nalidixic acid (IC50: 1.74 µg/ml). In addition, the most prominent IC50-values are displayed by: (7a;IC50: 2.77 µg/ml); (8g; IC50: 3.78 µg/ml); and (9d;IC50: 3.21 µg/ml). Molecular docking to the active site of DNA-gyrase cleavage complex of Acinetobacter baumannii (PDB code: 2xkk) co-crystallized with moxifloxacin revealed similar binding modes in addition to new interactions. Assessment of drug-likeness characteristics illustrate that the synthesized compounds showed agreement to Lipinski's and Veper's parameters. The study could offer an exceptional framework that may lead to the discovery of new potent antimicrobial agents.

First description of plasmid mediated quinolone resistance genes in salmonella isolates from Saudi hospitals.

OBJECTIVES: To detect resistance genes to fluoroquinolones and ß-lactams in Salmonella strains from a Saudi hospital. METHODS: From October 2015 to December 2016, a total of 149 Salmonella strains were collected from stool specimens from patients admitted to King Fahad Hospital of the University, AlKhobar, Saudi Arabia using CHROMagar Salmonella. The organism identification and antimicrobial susceptibility testing were performed using Vitek 2 system. Strain serogrouping was performed using Wellcolex color Salmonella kit. Fluoroquinolone resistance genes, extended-spectrum ß-lactamases (ESBLs), and AmpC ß-lactamase were determined using polymerase chain reaction (PCR). Enterobacterial repetitive intergenic consensus sequence-based PCR (ERIC-PCR) was used to determine clonal relatedness. RESULTS: The resistance rates to cefotaxime were 1.3% and ciprofloxacin 19.5%. Plasmid mediated quinolone resistance (PMQR) genes, qnrB and qnrS, were detected in 8 strains, qnrB (n=5) and qnrS (n=3), respectively. No ESBLs, AmpC, or mutations in the topoisomerases were detected. Salmonella isolates formed 7 clusters with similarity. CONCLUSIONS: This study reveals the emergence of fluoroquinolone resistant Salmonella in the region imposing public health concerns.

Synthesis, biological investigation and molecular docking study of N-malonyl-1,2-dihydroisoquinoline derivatives as brain specific and shelf-stable MAO inhibitors.

A group of N-malonyl-1,2-dihydroisoquinoline derivatives were synthesized and investigated as brain specific and shelf-stable MAO inhibitors. N-malonyl-1,2-dihydroisoquinoline redox carrier system was linked through amidic bond to 4-chloro and 4-nitrobenzylidenehydrazines (9a-b), as monoamine oxidase inhibitors (MAOIs), and ß-phenethylamine (14), as a model drug, to afford a novel group of N-malonyl-1,2-dihydroisoquinoline chemical delivery systems (DHIQCDSs) (13a-b and 18). These systems are expected to be stable against air oxidation due to the presence of the carbonyl group close to nitrogen of the dihydroisoquinoline. The synthesized DHIQCDS (18) was subjected to various chemical and biological investigations to evaluate its stability and prove its ability to cross the blood brain barrier and "lock-in" the brain. The in vitro chemical and enzymatic oxidation studies showed reasonable stability and adequate rate of conversion of DHIQCDS (18) to its corresponding quaternary metabolites. In vivo distribution study in rats revealed preferential concentration of the active moiety in the brain. Moreover, compounds (9a-b, 12a-b and 17) were screened for their in vitro MAO inhibitory activity compared to clorgyline as a reference compound. The inhibition profile was found to be competitive for both MAO-A and MAO-B isozymes with more selectivity toward MAO-A. Molecular docking study of compounds (9a-b, 12a-b and 17) and the suggested metabolites was carried out on both MAO-A and MAO-B isozymes. Observation of the docked poses revealed many interactions with many residues previously reported to have an effect on the inhibition of MAO enzyme.

Molecular characterization of extended-spectrum beta-lactamase producing Enterobacteriaceae in a Saudi Arabian tertiary hospital.

INTRODUCTION: The aim of this study was to determine the prevalence of extended-spectrum beta-lactamase (ESBL) producing Escherichia coli (E. coli), Klebsiella pneumoniae (K. pneumoniae), and Proteus mirabilis (P. mirabilis). In addition, different methods for detection of these enzymes, including the newly introduced CHROMagar ESBL, were evaluated. METHODOLOGY: A total of 382 Enterobacteriaceae clinical isolates were obtained from King Fahad Specialist Hospital - Dammam, during 2011 and screened for production of ESBL using advanced expert system of Vitek 2, CHROMagar and ESBL-E-strips. PCR assay was used to detect blaTEM, blaSHV, and blaCTX-M genes. Susceptibility to a panel of antibiotics was determined. RESULTS: The overall proportion of ESBL-producing enterobacterial isolates was 30.6%, which was higher in E. coli (35.8%) than in K. pneumoniae (25.7%). ESBL genotypes showed remarkable increase in the CTX-M (97.4%) compared to SHV (23.1%). The predominant ESBL was CTX-M- 15 (92.1 %). No TEM ESBL was detected in this study. The Vitek2 showed the highest sensitivity (100%), and the CHROMagar had the lowest specificity (97.3%) compared to the molecular method. All isolates were susceptible to imipenem and meropenem. CONCLUSIONS: This study confirms a high level of blaCTX-M positive ESBL isolates are circulating in the Eastern Province of Saudi Arabia. The trend of a multidrug-resistant profile associated with the recovery of the blaCTX-M gene is alarming.

Characterization of carbapenem-resistant Acinetobacter baumannii clinical isolates in a tertiary care hospital in Saudi Arabia.

This study characterized the occurrence of carbapenem resistance of Acinetobacter baumannii isolates in a tertiary care hospital in Saudi Arabia. From January 2010 until February 2012, Acinetobacter spp. isolates were collected from different wards and were identified using Vitek 2 system and 16S rRNA gene sequencing. Vitek 2 system and Etest were used for susceptibility testing. PCR and Pulse field gel electrophoresis (PFGE) were used for detecting and typing genes associated with carbapenem resistance. A total of 141 isolates were identified as A. baumannii. A total of 46 (32.6%) isolates were carbapenem-resistant Acinetobacter baumannii (CRAB) isolates and had wild diversity by PFGE. Metallo ?-lactamase confirmatory test was positive for 43 isolates with negative PCR for blaIMP and blaVIM. Among the 46 CRAB strains, 37 isolates harbored blaOXA-23 which was encoded downstream of ISAba1 and 1 isolate had ISAba1 encoded upstream blaOXA-51. These data reveal that the interhospital transmission of CRAB isolates was apparently insignificant. BlaOXA-23 adjacent to ISAba1 was the main mechanism of carbapenem resistance in these isolates. To our knowledge, this is the first molecular study characterizing carbapenem resistance in A. baumannii in the Eastern Province of Saudi Arabia.

Salmonella bacilli negative image recognized on Diff-Quik stain from pleural fluid cytology.

Understanding the significance of cytopathological tests in evaluating various infectious processes have become very essential nowadays, as it is a safe, fast, and cost-effective procedure. We present a case of a 52-year-old male with Salmonella empyema where the causative organisms were initially identified on cytology, and subsequently confirmed by microbiological culture. Diff-Quik stained smears showed many colorless, slender, fat short bacilli, which were visualized against the blue-gray background of the smear. These bacilli were identified both intracellularly inside the histiocytes and neutrophils cytoplasm as well as extracellularly in the smear background. We consider that this negative image represents the organism and its capsule creating an area that did not take the Diff-Quik stain. The patient was treated accordingly with suitable antibiotics. A brief discussion of this interesting finding in such a rare infection with pertinent literature review is presented.

Biofilm-derived Legionella pneumophila evades the innate immune response in macrophages.

Legionella pneumophila, the causative agent of Legionnaire's disease, replicates in human alveolar macrophages to establish infection. There is no human-to-human transmission and the main source of infection is L. pneumophila biofilms established in air conditioners, water fountains, and hospital equipments. The biofilm structure provides protection to the organism from disinfectants and antibacterial agents. L. pneumophila infection in humans is characterized by a subtle initial immune response, giving time for the organism to establish infection before the patient succumbs to pneumonia. Planktonic L. pneumophila elicits a strong immune response in murine, but not in human macrophages enabling control of the infection. Interactions between planktonic L. pneumophila and murine or human macrophages have been studied for years, yet the interface between biofilm-derived L. pneumophila and macrophages has not been explored. Here, we demonstrate that biofilm-derived L. pneumophila replicates significantly more in murine macrophages than planktonic bacteria. In contrast to planktonic L. pneumophila, biofilm-derived L. pneumophila lacks flagellin expression, do not activate caspase-1 or -7 and trigger less cell death. In addition, while planktonic L. pneumophila is promptly delivered to lysosomes for degradation, most biofilm-derived bacteria were enclosed in a vacuole that did not fuse with lysosomes in murine macrophages. This study advances our understanding of the innate immune response to biofilm-derived L. pneumophila and closely reproduces the natural mode of infection in human.

A bacterial protein promotes the recognition of the Legionella pneumophila vacuole by autophagy.

Legionella pneumophila (L. pneumophila) is an intracellular bacterium of human alveolar macrophages that causes Legionnaires' disease. In contrast to humans, most inbred mouse strains are restrictive to L. pneumophila replication. We demonstrate that autophagy targets L. pneumophila vacuoles to lysosomes and that this process requires ubiquitination of L. pneumophila vacuoles and the subsequent binding of the autophagic adaptor p62/SQSTM1 to ubiquitinated vacuoles. The L. pneumophila legA9 encodes for an ankyrin-containing protein with unknown role. We show that the legA9 mutant replicate in WT mice and their bone marrow-derived macrophages. This is the first L. pneumophila mutant to be found to replicate in WT bone marrow-derived macrophages other than the Fla mutant. Less legA9 mutant-containing vacuoles acquired ubiquitin labeling and p62/SQSTM1 staining, evading autophagy uptake and avoiding lysosomal fusion. Thus, we describe a bacterial protein that targets the L. pneumophila-containing vacuole for autophagy uptake.

Depletion of the ubiquitin-binding adaptor molecule SQSTM1/p62 from macrophages harboring cftr ΔF508 mutation improves the delivery of Burkholderia cenocepacia to the autophagic machinery.

Cystic fibrosis is the most common inherited lethal disease in Caucasians. It is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR), of which the cftr ΔF508 mutation is the most common. ΔF508 macrophages are intrinsically defective in autophagy because of the sequestration of essential autophagy molecules within unprocessed CFTR aggregates. Defective autophagy allows Burkholderia cenocepacia (B. cepacia) to survive and replicate in ΔF508 macrophages. Infection by B. cepacia poses a great risk to cystic fibrosis patients because it causes accelerated lung inflammation and, in some cases, a lethal necrotizing pneumonia. Autophagy is a cell survival mechanism whereby an autophagosome engulfs non-functional organelles and delivers them to the lysosome for degradation. The ubiquitin binding adaptor protein SQSTM1/p62 is required for the delivery of several ubiquitinated cargos to the autophagosome. In WT macrophages, p62 depletion and overexpression lead to increased and decreased bacterial intracellular survival, respectively. In contrast, depletion of p62 in ΔF508 macrophages results in decreased bacterial survival, whereas overexpression of p62 leads to increased B. cepacia intracellular growth. Interestingly, the depletion of p62 from ΔF508 macrophages results in the release of the autophagy molecule beclin1 (BECN1) from the mutant CFTR aggregates and allows its redistribution and recruitment to the B. cepacia vacuole, mediating the acquisition of the autophagy marker LC3 and bacterial clearance via autophagy. These data demonstrate that p62 differentially dictates the fate of B. cepacia infection in WT and ΔF508 macrophages.

Acinetobacter baumannii Septicemia in a Recipient of an Allogeneic Hematopoietic Stem Cell Transplantation.

Acinetobacter baumannii is a gram-negative, nonfermentative coccobacillus that causes infections in immunocompromised and chronically ill patients and is associated with multidrug resistance. Two days before receiving her nonmyeloablative stem cell allograft, a patient with acute myeloid leukemia developed Acinetobacter baumannii bacteremia that caused septic shock which was successfully treated with imipenem and removal of the central venous catheter. To our knowledge, this is the first report of Acinetobacter baumannii septicemia in a hematopietic stem cell transplantation recipient.

Evaluation of pleural fluid human epididymis 4 (HE4) as a marker of malignant pleural effusion.

Pleural effusion is a commonly encountered problem in clinical practice, and pleural fluid analysis is usually the first step towards identifying the underlying etiology. Numerous studies have been published analyzing the potential utility of measuring biomarkers in pleural fluid as possible indicators of a malignant effusion; however, there are no studies that have examined the presence of human epididymis 4 (HE4) in pleural effusions. The aims of this study were to assess pleural effusion and serum concentrations of HE4 in patients with different types of pleural effusions and to evaluate the diagnostic performance of HE4 in detecting malignant pleural effusion. A prospective cohort study was carried out of 88 consecutive patients presenting with pleural effusions. The patients were divided into three groups: 22 patients with transudative effusions, 32 patients with non-malignant exudative effusions, and 34 patients with malignant pleural effusions. Blood and pleural fluid HE4 levels were measured using immunoassay. Both serum HE4 levels and pleural effusion HE4 levels were significantly higher in patients with malignant effusions than in patients with transudative or non-malignant exudative effusions. A pleural fluid HE4 cutoff value of 1,675 pmol/L was found to predict malignant pleural effusions with a diagnostic sensitivity of 85.3 % and specificity of 90.7 %. The current study reports a novel finding of increased serum and pleural fluid HE4 levels in patients with malignant effusions compared to non-malignant effusions. This finding has the potential to strengthen the diagnostic performance of tumor markers in detecting malignant pleural effusions.

Caspase-11 promotes the fusion of phagosomes harboring pathogenic bacteria with lysosomes by modulating actin polymerization.

Inflammasomes are multiprotein complexes that include members of the NLR (nucleotide-binding domain leucine-rich repeat containing) family and caspase-1. Once bacterial molecules are sensed within the macrophage, the inflammasome is assembled, mediating the activation of caspase-1. Caspase-11 mediates caspase-1 activation in response to lipopolysaccharide and bacterial toxins, and yet its role during bacterial infection is unknown. Here, we demonstrated that caspase-11 was dispensable for caspase-1 activation in response to Legionella, Salmonella, Francisella, and Listeria. We also determined that active mouse caspase-11 was required for restriction of L. pneumophila infection. Similarly, human caspase-4 and caspase-5, homologs of mouse caspase-11, cooperated to restrict L. pneumophila infection in human macrophages. Caspase-11 promoted the fusion of the L. pneumophila vacuole with lysosomes by modulating actin polymerization through cofilin. However, caspase-11 was dispensable for the fusion of lysosomes with phagosomes containing nonpathogenic bacteria, uncovering a fundamental difference in the trafficking of phagosomes according to their cargo.

Cell intrinsic roles of apoptosis-associated speck-like protein in regulating innate and adaptive immune responses.

The role of apoptosis-associated speck-Like protein (ASC) in the assembly of the inflammasome complex within macrophages has been elucidated in several studies. In this particular role, ASC functions as an adaptor protein by linking nod-like receptors (NLRs) and procaspase-1, thereby leading to the activation of caspase-1 to cleave inflammatory cytokines IL-1ß and IL-18 and inducing pyroptosis. It has been noted that ASC maintains inflammasome-independent roles, including but not limited to controlling the expression of Dock2 and mitogen-activated protein kinases (MAPK/ERK2) and regulating the NF-κB pathway. This paper will emphasize the major roles of ASC during pathogen infection, the mechanisms by which it mediates inflammation, and discuss its more recently discovered functions.

Pharmacophoric model building for antitubercular activity of the individual Schiff bases of small combinatorial library.

Synthesis and evaluation of anti-TB activity of individual compounds of Schiff bases combinatorial library were done against Mycobacterium tuberculosis H(37)Rv at a single concentration of 6.25mug/mL according to the protocol of TAACF. Compounds 2C and 3D produced 99% inhibitory activity on the investigated organism, while the other tested compounds showed lower activity ranging from 35 to 84%. It was found that there are no relation between the anti-TB activity of the tested compounds and their lipophilicity expressed by ClogP of these compounds. A 3D pharmacophoric model has been generated by Molecular Operating Environment (MOE) using a training set of 10 reported anti-TB compounds and testing the synthesized compounds (1A, 1B, 1D, 1E, 2C, 3A, 3C, 3D, 3E and 4A-4E). The generated pharmacophoric features include, F1: hydrogen bond donors (Don), F2: aromatic rings (Aro), F3: hydrogen bond acceptors (Acc)/metal ligator (ML), F4: Aro/hydrophobic (Hyd). In all hit set, it was found that the amidic nitrogen CONH-NC fitted the region of the Don, F1, while the amidic carbonyl group fitted the region of the Acc/ML, F3. The distances bridging F1 to F2, F3 and F4 were essential for anti-TB activity in the developed pharmacophore model, as it was confirmed from model validation procedure.

Fluorinated 1,2,4-Triazolo[1,5-a]pyrimidine-6-carboxylic acid derivatives as antimycobacterial agents.

A series of fluorinated 1,2,4-triazolo[1,5-a]pyrimidine-6-carboxylic acid derivatives was designed and synthesized as fluoroquinolone analogues. The synthesized compounds were screened against Mycobacterium tuberculosis H(37)R(v) strain at 6.25 microg/mL concentration. Compound 4, the 7-oxo-2-(trifluoromethyl)-4,7-dihydro-1,2,4-triazolo[5,1-a]pyrimidine-6-carboxylic acid was found to be a very potent inhibitor, being able to inhibit 92% growth of M. tuberculosis H(37)R(v )at 6.25 microg/mL concentration. At the same time, it proofed to be nontoxic to mammalian cells (IC(50) > 62.5 microg/mL in VERO cells).

Osteopontin and C-reactive protein in Egyptian patients affected with tuberculous and malignant pleural effusion.

BACKGROUND: The first step in the evaluation of patients with pleural effusion is to determine whether the effusion is a transudate or an exudate. Osteopontin (OPN) is a pleiotropic integrin-binding protein with many functions. We assessed pleural effusion and serum concentrations of OPN and C-reactive protein (CRP) in patients with different types of pleural effusions. METHODS: The current study comprised three groups: 20 patients with transudative effusion, 30 patients with malignant effusion and 30 patients with tuberculous effusion. OPN was analysed using a commercially available enzyme-linked immunosorbent assay kit. RESULTS: OPN effusion values were significantly higher in exudates (both malignant and tuberculous effusion cases) compared with transudative effusion. Also when compared separately, patients with tuberculous effusion and those with malignant effusion had a significantly higher fluid and OPN effusion/serum ratio than those with transudative effusion. Patients with tuberculous effusion had a significantly higher serum CRP effusion and effusion/serum ratio of CRP than those with malignant or transudative effusion. CONCLUSION: OPN is significantly increased in exudative effusion compared with transudative ones. However, serum OPN and effusion/serum OPN ratio were not significantly different in patients with malignant from those with tuberculous effusions. The lack of difference in serum OPN and effusion/serum OPN ratio between patients with malignant and those with tuberculous effusion may be attributed to the heterogeneity of the malignant effusion group. Receiver-operating characteristic (ROC) curve analysis has shown that effusion/serum CRP ratio outperformed effusion/serum OPN ratio as a diagnostic marker for tuberculous pleural effusion.

Synthesis of 5-phenyl-1-(3-pyridyl)-1H-1,2,4-triazole-3-carboxylic acid derivatives of potential anti-inflammatory activity.

A series of 5-phenyl-1-(3-pyridyl)-1H-1,2,4-triazole-3-carboxylic acid derivatives 4-10 were synthesized by rearrangement of 4-(3-pyridyl)-hydrazono-2-phenyl-2-oxazolin-5-one 3 in the presence of different nucleophiles to afford derivatives 4, 7, and 8, while hydroxamic acid derivative 6 was prepared from reaction of methyl ester 4 with hydroxylamine hydrochloride. Semicarbazide 9 and thiosemicarbazide 10, derivatives of the 5-phenyl-1-(3-pyridyl)-1H-1,2,4-triazole-3-carboxylic acid, were synthesized via hydrazide 8 with potassium cyanate and appropriate isothiocyanate, respectively. The structures of the synthesized compounds were confirmed by elemental analyses, IR, (1)H-NMR, and mass spectra. The results of the anti-inflammatory activity of the synthesized derivatives showed that most of the tested compounds 4-10 showed significant inhibition against carrageenan-induced rat paw edema in albino rats. Derivatives 4 and 8 showed promising results and were found to be equipotent or more potent than Indomethacin and Celecoxib as reference drugs at two dose levels, 5 and 10 mg/kg, and they have no ulcerogenic activity.