ConGPS: A Smart Container Positioning System Using Inertial Sensor and Electronic Map with Infrequent GPS.

Real-time global positioning is important for container-based logistics. However, a challenge in real-time global positioning arises from the frequency of both global positioning system (GPS) calls and GPS-denied environments during transportation. This paper proposes a novel system named ConGPS that integrates both inertial sensor and electronic map data. ConGPS estimates the speed and heading direction of a moving container based on the inertial sensor data, the container trajectory, and the speed limit information provided by an electronic map. The directional information from magnetometers, coupled with map-matching algorithms, is employed to compute container trajectories and current positions. ConGPS significantly reduces the frequency of GPS calls required to maintain an accurate current position. To evaluate the accuracy of the system, 280 min of driving data, covering a distance of 360 km, are collected. The results demonstrate that ConGPS can maintain positioning accuracy within a GPS-call interval of 15 min, even if using low-cost inertial sensors in GPS-denied environments.

Plug-and-play QKD architecture with a self-optical pulse train generator.

The commercialization of quantum key distribution (QKD), which enables secure communication even in the era of quantum computers, has acquired significant interest. In particular, plug-and-play (PnP) QKD has garnered considerable attention owing to its advantage in system stabilization. However, a PnP QKD system has limitations on miniaturization owing to a bulky storage line (SL) of tens of kilometers. And, the secure key rate is relatively low because Bob transmits the signal pulses only at the dedicated time slots to circumvent backscattering noise. This study proposes a new method that can eliminate the SL by realizing an optical pulse train generator based on an optical cavity structure. Our method allows Alice to generate optical pulse trains herself by duplicating Bob's seed pulse and excludes the need for Bob's strong signal pulses that trigger backscattering noise as much as the conventional PnP QKD. Accordingly, our method can naturally overcome the miniaturization limitation and the slow secure key rate, as the storage line is no longer necessary. We conducted a proof-of-concept experiment using our method and achieved a key generation rate of 1.6×10-3 count/pulse and quantum bit error rate ≤ 5%.

Carrying Position-Independent Ensemble Machine Learning Step-Counting Algorithm for Smartphones.

Current step-count estimation techniques use either an accelerometer or gyroscope sensors to calculate the number of steps. However, because of smartphones unfixed placement and direction, their accuracy is insufficient. It is necessary to consider the impact of the carrying position on the accuracy of the pedometer algorithm, because of people carry their smartphones in various positions. Therefore, this study proposes a carrying-position independent ensemble step-counting algorithm suitable for unconstrained smartphones in different carrying positions. The proposed ensemble algorithm comprises a classification algorithm that identifies the carrying position of the smartphone, and a regression algorithm that considers the identified carrying position and calculates the number of steps. Furthermore, a data acquisition system that collects (i) label data in the form of the number of steps estimated from the Force Sensitive Resistor (FSR) sensors, and (ii) input data in the form of the three-axis acceleration data obtained from the smartphones is also proposed. The obtained data were used to allow the machine learning algorithms to fit the signal features of the different carrying positions. The reliability of the proposed ensemble algorithms, comprising a random forest classifier and a regression model, was comparatively evaluated with a commercial pedometer application. The results indicated that the proposed ensemble algorithm provides higher accuracy, ranging from 98.1% to 98.8%, at self-paced walking speed than the commercial pedometer application, and the machine learning-based ensemble algorithms can effectively and accurately predict step counts under different smart phone carrying positions.

Chrysin Induces Apoptosis via the MAPK Pathway and Regulates ERK/mTOR-Mediated Autophagy in MC-3 Cells.

Chrysin is a flavonoid found abundantly in substances, such as honey and phytochemicals, and is known to exhibit anticancer effects against various cancer cells. Nevertheless, the anticancer effect of chrysin against oral cancer has not yet been verified. Furthermore, the mechanism underlying autophagy is yet to be clearly elucidated. Thus, this study investigated chrysin-mediated apoptosis and autophagy in human mucoepidermoid carcinoma (MC-3) cells. The change in MC-3 cell viability was examined using a 3-(4,5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide cell viability assay, as well as 40,6-diamidino-2-phenylindole, annexin V, and propidium iodide staining. Western blotting was used to analyze the proteins related to apoptosis and the mitogen-activated protein kinase (MAPK) pathway. In addition, the presence or absence of autophagy and changes in the expression of related proteins were investigated using acridine orange staining and Western blot. The results suggested that chrysin induced apoptosis and autophagy in MC-3 oral cancer cells via the MAPK/extracellular signal-regulated kinase pathway. Moreover, the induced autophagy exerted a cytoprotective effect against apoptosis. Thus, the further reduced cell viability due to autophagy as well as apoptosis induction highlight therapeutic potential of chrysin for oral cancer.

High-performance reconfigurable coincidence counting unit based on a field programmable gate array.

We present a high-performance reconfigurable coincidence counting unit (CCU) using a low-end field programmable gate array (FPGA) and peripheral circuits. Because of the flexibility guaranteed by the FPGA program, we can easily change system parameters, such as internal input delays, coincidence configurations, and the coincidence time window. In spite of a low-cost implementation, the proposed CCU architecture outperforms previous ones in many aspects: it has 8 logic inputs and 4 coincidence outputs that can measure up to eight-fold coincidences. The minimum coincidence time window and the maximum input frequency are 0.47 ns and 163 MHz, respectively. The CCU will be useful in various experimental research areas, including the field of quantum optics and quantum information.

Kaempferol Inhibits Cervical Cancer Cells by Inducing Apoptosis and Autophagy via Inactivation of the PI3K/AKT/mTOR Signaling Pathway.

BACKGROUND/AIM: Kaempferol, a natural flavonoid, occurs abundantly in fruits and vegetables. It has various bioactivities, with antioxidant, anti-inflammatory, and other beneficial properties. The aim of this study was to investigate the in vitro effects of kaempferol on the proliferation, apoptosis, and autophagy of KB cells, a human cervical cancer cell line, and the corresponding action mechanisms. MATERIALS AND METHODS: The inhibitory efficacy of kaempferol on KB cervical cancer cells was investigated through 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, migration assay, 4',6-diamidino-2-phenylindole staining, flow cytometry, acridine orange staining and western blotting. RESULTS: Kaempferol reduced KB cell viability and migration in a dose-dependent manner. Additionally, kaempferol-induced apoptosis was confirmed, and kaempferol treatment influenced levels of apoptotic proteins. Autophagy was detected upon visualization of characteristic autophagic vacuoles and acidic vesicular organelles, and verified using western blotting, which revealed elevated levels of autophagy-related proteins. Kaempferol-mediated apoptosis and autophagy were evidently attributable to reduced phosphorylation in the phosphoinositide 3-kinase (PI3K)/serine/threonine kinase 1 (AKT)/mammalian target of rapamycin (mTOR) pathway. This finding was validated using a pharmacological inhibition assay with the PI3K pathway inhibitor LY294002, which promoted KB cell apoptosis and autophagy. CONCLUSION: Our results suggest that kaempferol induces apoptosis and autophagy by inhibiting the PI3K/AKT/mTOR pathway in human cervical cancer cells, empirically showing the anticancer effects of kaempferol, and thereby presenting it as a potential anticancer therapeutic agent.

Platycodin D induces apoptosis via regulating MAPK pathway and promotes autophagy in colon cancer cell.

Platycodin D (PD) is the main component of triterpene saponins found in Platycodi radix. In this study, we observed a decrease in cell viability, an increase in apoptotic bodies, and an increase in the rate of apoptosis. Also, we observed an increase in cleaved PARP and Bax, a decrease in Bcl-2, and p-ERK, and an increase in p-p38 and p-JNK. Furthermore, a change in cell viability and the expression of p-p38, Bax, and Bcl-2 using the p38 inhibitor revealed a decrease in p-p38 and Bax and an increase in Bcl-2 in the inhibitor treatment group. In addition, we observed an increase in vacuole formation through morphological changes and an increase in acidic vesicular organelles (AVOs). We also observed an increase in the expression of beclin 1, LC 3-I, and -II. There was no significant decrease in cell viability in the group treated with 3-MA, but a decrease in cell viability was noted in the group treated with HCQ. HCQ treatment resulted in an increase in Bax and a decrease in Bcl-2. These findings reveal that in HT-29 colon cancer cells, PD induces apoptosis through the MAPK pathway, thereby exerting anticancer effects. Moreover, autophagy caused by PD inhibits apoptosis by protecting the cells.

Myricetin induces apoptosis through the MAPK pathway and regulates JNK­mediated autophagy in SK­BR­3 cells.

Myricetin, a flavonoid found in fruits and vegetables, is known to have antioxidant and anticancer effects. However, the anticancer effects of myricetin on SK­BR­3 human breast cancer cells have not been elucidated. In the present study, the anticancer effects of myricetin were confirmed in human breast cancer SK­BR­3 cells. As the concentration of myricetin increased, the cell viability decreased. DAPI (4',6­diamidino­2­phenylindole) and Annexin V/PI staining also revealed a significant increase in apoptotic bodies and apoptosis. Western blot analysis was performed to confirm the myricetin­induced expression of apoptosis­related proteins. The levels of cleaved PARP and Bax proteins were increased, and that of Bcl­2 was decreased. The levels of proteins in the mitogen­activated protein kinase (MAPK) pathway were examined to confirm the mechanism of myricetin­induced apoptosis, and it was found that the expression levels of phosphorylated c­Jun N­terminal kinase (p­JNK) and phosphorylated mitogen­activated protein kinases (p­p38) were increased, whereas that of phosphorylated extracellular­regulated kinase (p­ERK) was decreased. It was also demonstrated that myricetin induced autophagy by promoting autophagy­related proteins such as microtubule­associated protein 1A/1B­light chain 3 (LC 3) and beclin 1. In addition, 3­methyladenine (3­MA) was used to evaluate the association between cell viability and autophagy in cells treated with myricetin. The results showed that simultaneous treatment with 3­MA and myricetin promoted the apoptosis of breast cancer cells. Furthermore, treatment with a JNK inhibitor reduced cell viability, promoted Bax expression, and reduced the expression of p­JNK, Bcl­2, and LC 3­II/I. These results suggest that myricetin induces apoptosis via the MAPK pathway and regulates JNK­mediated autophagy in SK­BR­3 cells. In conclusion, myricetin shows potential as a natural anticancer agent in SK­BR­3 cells.

Pharmacokinetics of toltrazuril and its metabolites, toltrazuril sulfoxide and toltrazuril sulfone, after a single oral administration to pigs.

Toltrazuril (TZR) is a triazine-based antiprotozoal agent. Following a single oral administration of TZR at 10 and 20 mg/kg to male pigs, the mean TZR concentration in plasma peaked at 4.24 and 8.18 microg/ml at 15.0 and 12.0 hr post-dose, respectively. TZR absorbed was rapidly converted to the short-lived intermediary metabolite toltrazuril sulfoxide (TZR-SO), and then metabolized to the reactive toltrazuril sulfone (TZR-SO2). TZR-SO2 was actually more slowly eliminated, with average half-lives of 231 and 245 hr, compared with TZR (48.7 and 68.9 hr) or TZR-SO (51.9 and 53.2 hr) in the 10 and 20 mg/kg groups, respectively. This study demonstrates that TZR metabolizes to TZR-SO2 having a long-terminal half-life, enabling the persistent clinical efficacy in the treatment of I. suis infection. In contrast, special consideration should be given to the residual of TZR-SO2.

Apigenin induces apoptosis by regulating Akt and MAPK pathways in human melanoma cell A375SM.

Apigenin, an aromatic compound, exhibits antioxidant, anti­inflammatory and anti­viral effects. The present study aimed to investigate the effects of apigenin on cell proliferation and apoptosis of human melanoma cells A375P and A375SM. Therefore, melanoma cells were treated with apigenin to determine its anti­proliferative and survival effects, using wound healing and MTT assays. The results revealed that melanoma cell viability was decreased in a dose­dependent manner. Furthermore, chromatin condensation, indicating apoptosis, was significantly increased in a dose­dependent manner, as demonstrated by DAPI staining. In addition, increased apoptosis rate following treatment with apigenin was confirmed by Annexin V­propidium iodide staining. The changes in the expression levels of apoptosis­related proteins in A375P and A375SM melanoma cells were subsequently detected using western blot analysis. The results demonstrated that the protein expression levels of Bcl­2 were decreased, whereas those of Bax, cleaved poly ADP­ribose polymerase, cleaved caspase­9 and p53 were upregulated in a dose­dependent manner in apigenin­treated cells compared with those noted in untreated cells. In addition, in apigenin­treated A375P cells, phosphorylated (p)­p38 was upregulated and p­extracellular signal­regulated kinase (ERK), p­c­Jun N­terminal kinase (JNK) and p­protein kinase B (Akt) were downregulated. However, in A375SM cells, apigenin treatment increased p­ERK and p­JNK and decreased p­p38 and p­Akt protein expression levels. Subsequently, the inhibitory effect of apigenin on tumor growth was investigated in vivo. Tumor volume was significantly reduced in the 25 and 50 mg/kg apigenin­treated groups compared with the control group. Additionally, a TUNEL assay was performed to detect apoptotic cells. Immunohistochemical staining also revealed elevated p­ERK expression in the apigenin­treated group compared with the control group. Overall, the findings of the present study indicated that apigenin attenuated the growth of A375SM melanoma cells by inducing apoptosis via regulating the Akt and mitogen­activated protein kinase signaling pathways.

Anti-inflammatory effects of talosin A via inhibition of NF-kappaB activation in lipopolysaccharide-stimulated RAW264.7 cells.

Aim of work To determine whether talosin A inhibits production of pro-inflammatory cytokines and nitric oxide (NO) in lipopolysaccharide (1 mug/ml)-stimulated RAW 264.7 macrophages. Talosin A (10 and 50 mug/ml) significantly reduced LPS-induced overproduction of tumor necrosis factor-alpha, interleukin IL-1beta, -6 and NO in a dose-dependent manner (P < 0.01). Talosin A had a direct NO-scavenging activity in the cell-free system. In RT-PCR analysis, gene expressions were inhibited at a transcriptional level. Moreover, the activation of nuclear factor-kappa B (NF-kappaB) was significantly suppressed by talosin A in LPS-stimulated macrophage cells (P < 0.05). Therefore, we confirmed anti-inflammatory activity of talosin A was via suppression of pro-inflammatory cytokines, NO production and NF-kappaB activation, suggesting a therapeutic candidate for inflammatory disorders.

Antitumor and Apoptosis-inducing Effects of Piperine on Human Melanoma Cells.

BACKGROUND/AIM: Piperine is a major pungent alkaloid present in black pepper (Piper nigrum L). This study investigated the potential anticancer effects of piperine on human melanoma cells and explored the potential pharmacological mechanisms in vitro and in vivo. MATERIALS AND METHODS: Studies were performed using the MTT assay, 4',6-diamidino-2-phenylindole (DAPI) staining, western blotting, a xenograft model, the terminal deoxynucleotidyl transferase dUTP nick end labeling assay, and immunohistochemistry. RESULTS: Piperine inhibited the growth of melanoma cells. Several apoptotic events were observed following treatment, as revealed by DAPI staining. Piperine increased the expression of BCL2-associated X, apoptosis regulator (BAX), cleaved poly(ADP-ribose)polymerase, cleaved caspase-9, phospho-c-Jun N-terminal kinase and phospho-p38, and reduced that of B-cell lymphoma 2 (BCL2), X-chromosome-linked inhibitor of apoptosis, and phospho-extracellular signal-regulated protein kinase (ERK1/2) in a concentration-dependent manner. Treatment of mice for 4 weeks with piperine inhibited tumor growth without apparent toxicity. Piperine increased the expression of apoptotic cells and cleaved-caspase-3 protein and reduced the expression of phospho-ERK1/2 protein in melanoma tumors. CONCLUSION: Piperine suppressed the growth of human melanoma cells by the induction of apoptosis via the inhibition of tumor growth of human melanoma cells and tumor xenograft models.

Pharmacokinetics of florfenicol and its metabolite, florfenicol amine, in dogs.

A study on the bioavailability and pharmacokinetics of florfenicol was conducted in six healthy dogs following a single intravenous (i.v.) or oral (p.o.) dose of 20 mg kg(-1) body weight (b.w.). Florfenicol concentrations in serum were determined by a high-performance liquid chromatography/mass spectrometry. Plasma concentration-time data after p.o. or i.v. administration were analyzed by a non-compartmental analysis. Following i.v. injection, the total body clearance was 1.03 (0.49) L kg(-1)h(-1) and the volume of distribution at steady-state was 1.45 (0.82) L kg(-1). Florfenicol was rapidly distributed and eliminated following i.v. injection with 1.11 (0.94)h of the elimination half-life. After oral administration, the calculated mean C(max) values (6.18 microg ml(-1)) were reached at 0.94 h in dogs. The elimination half-life of florfenicol was 1.24 (0.64) h and the absolute bioavailability (F) was achieved 95.43 (11.60)% after oral administration of florfenicol. Florfenicol amine, the major metabolite of florfenicol, was detected in all dogs after i.v. and p.o. administrations.

Anti­inflammatory effect of quercetin and galangin in LPS­stimulated RAW264.7 macrophages and DNCB­induced atopic dermatitis animal models.

Flavonols are compounds that have been shown to possess potent anti­inflammatory effects in cellular and animal models of inflammation. In the present study, the anti­inflammatory effects and mechanisms of two natural flavonols, quercetin and galangin, in lipopolysaccharide (LPS)­stimulated RAW264.7 macrophages were investigated. It was identified that quercetin and galangin markedly reduced the production of nitric oxide (NO), inducible NO synthase and interleukin­6, and the nuclear translocation of nuclear factor­κB (NF­κB). In addition, LPS­induced activation of extracellular signal­regulated kinase 1/2 (Erk1/2) and c­Jun N­terminal kinase (JNK) was suppressed by quercetin and galangin. Taken together, these data implied that NF­κB, Erk1/2 and JNK may be potential molecular targets of quercetin and galangin in an LPS­induced inflammatory response. Subsequently, the effects of oral administration of quercetin or galangin, either alone or in combination, in a 2,4­dinitrochlorobenzene­induced atopic dermatitis (AD) mouse model were investigated. As a result, measurements of ear thickness and the levels of serum immunoglobulin E, and histological analysis revealed that the two flavonols led to a decrease in inflammation, whereas, in combination, they were even more effective. These results suggested that quercetin and galangin may be promising therapeutic agents for AD. Additionally, their combination may be a novel therapeutic strategy for the prevention of AD.

TNF-alpha upregulates PTEN via NF-kappaB signaling pathways in human leukemic cells.

TNF-alpha plays a variety of biological functions such as apoptosis, inflammation and immunity. PTEN also has various cellular function including cell growth, proliferation, migration and differentiation. Thus, possible relationships between the two molecules are suggested. TNF-alpha has been known to downregulate PTEN via NF-kappaB pathway in the human colon cell line, HT-29. However, here we show the opposite finding that TNF-alpha upregulates PTEN via activation of NF-kappaB in human leukemic cells. TNF-alpha increased PTEN expression at HL-60 cells in a time- and dose-dependent manner, but the response was abolished by disruption of NF-kappaB with p65 antisense phosphorothioate oligonucleotide or pyrrolidine dithiocarbamate. We found that TNF-alpha activated the NF-kappaB pathways, evidenced by the translocation of p65 to the nucleus in TNF-alpha-treated cells. We conclude that TNF-alpha induces upregulation of PTEN expression through NF-kappaB activation in human leukemic cells.

Lipopolysaccharide-binding and neutralizing activities of surfactin C in experimental models of septic shock.

To evaluate the anti-endotoxin activity of surfactin C, we studied its lipopolysaccharide-binding activity in vitro and therapeutic efficacy in experimental models of gram-negative septic shock. The ability of surfactin C to bind LPS from Escherichia coli O111:B4 was determined using a limulus chromogenic assay. Male ICR mice and Sprague-Dawley rats were given intraperitoneal administration of 1x10(9) colony forming units of E. coli ATCC 25922. After bacterial challenge, all animals were randomized to receive intraperitoneally saline, polymyxin B or surfactin C. Surfactin C not only completely bound to the LPS (its median effective concentration being 13.75 microM) but also improved the survival and reduced of the number of inoculated bacteria in the mouse model of septic shock. Surfactin C reduced the plasma endotoxin, tumor necrosis factor-alpha and nitric oxide levels in response to septic shock in rats.

Increase in carbon emissions from forest fires after intensive reforestation and forest management programs.

This paper shows an example of substantial increase in carbon emissions from forest fires after reforestation on a national scale. It is the first estimation of historical carbon emissions from forest fires in Korea during the last 40 years. Investigation was focused on the recent increase in large forest fires and its closely related factors. A simple modeling approach to estimate carbon emission was applied. The direct carbon emission from forest fires in 2000, ranging from 115 to 300 Gg C, corresponds to 1-3% of the annual carbon uptake by forests. The influence of forest fires on the carbon cycle in Korea is not so significant, but Korean forests have a large potential for generating severe local fires due to increasing forest carbon density and a high forest area ratio (forest area/total land area) of 65%. The carbon emission per area burned (Mg C ha(-1)) clearly reflects the trend toward increases in the number of severe fires. Statistical analyses and the trends of annual temperature and precipitation show that the recent large increase in carbon emissions may be the negative consequences of intensive forest regrowth that is the product of successful reforestation and forest management programs rather than the effect of climate change. These results imply a need for further studies in other countries, where large-scale plantation has been conducted, to evaluate the role of plantation and forest fires on the global carbon cycle.

Anticancer effects of Ixeris dentata (Thunb. ex Thunb.) nakai extract on human melanoma cells A375P and A375SM.

ETHNOPHARMACOLOGICAL RELEVANCE: The plant species Taraxacum coreanum (TC), Youngia sonchifolia (YS), and Ixeris dentata (ID) belong to the family Compositae and are used for medicinal purposes in traditional medicine. However, the anticancer effects of TC, YS, and ID extracts and the underlying molecular mechanisms in melanoma cells have not been elucidated. AIM OF THE STUDY: To investigate the potential anticancer effects of TC, YS, and ID extracts on human melanoma cells and explore the potential pharmacological mechanisms in vitro and in vivo. MATERIALS AND METHODS: In this comparative study, we investigated the effects of TC, YS, and ID extracts on cell proliferation in human melanoma A375P and A375SM cells using MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assays. Apoptotic cells were detected by 4',6-diamidino-2-phenylinodole (DAPI) staining. We also investigated whether the growth-inhibitory effects were associated with the induction of apoptosis and whether the mechanisms of cell death were the result of signaling molecules such as p53, Bax, Bcl-2, caspase-9, Poly-ADP ribose polymerase (PARP), and Erk (Extracellular signal-regulated protein kinase) 1/2. The in vivo antitumor effects were evaluated by measuring the tumor volume and weight and performing Terminal deoxynucleotidyl transferase (TdT) dUTP Nick End Labeling (TUNEL) assay and immunohistochemistry (IHC) in tumor xenograft models. RESULTS: TC, YS, and ID extracts effectively inhibited the growth of A375P and A375SM cells. In addition, several apoptotic events were observed following treatment, including DNA fragmentation and chromatin condensation by DAPI staining. The extracts increased p53, Bax, cleaved-caspase-9 and cleaved-PARP expression, whereas the expression of Bcl-2 was decreased in both cell lines. Furthermore, ID extract significantly inhibited the activation of Erk1/2 in both cell lines. Among the three extracts, ID had the strongest apoptotic effects. The administration of ID extract to mice inhibited tumor growth without any toxicity following 4 weeks of treatment. This extract increased the expression of apoptotic cells and p53 protein and decreased phospho-Erk1/2 protein. CONCLUSION: TC, YS, and ID extracts suppress the growth of human melanoma cells through apoptosis. Among these extracts, ID has the strongest anticancer and apoptotic effects. It induces apoptosis through the inhibition of Erk1/2 in A375P and A375SM human melanoma cells and in tumor xenograft models and may be a potential chemotherapeutic agent against melanoma.

The anti-thrombotic activity of surfactins.

Platelet aggregation was inhibited and the density of platelet-rich plasma (PRP) clots was decreased by the preincubation of PRP with surfactins, an acidic lipopeptide of Bacillus subtilis complex BC1212 isolated from soybean paste, in dose-dependent manner. Our findings suggest that surfactins are able to prevent a platelet aggregation leading to an inhibition of additional fibrin clot formation, and to enhance fibrinolysis with facilitated diffusion of fibrinolytic agents.

Combination effects of cephalexin and gentamicin on Edwardsiella tarda and Streptococcus iniae.

The objective of this study was to determine the in vitro activity of cephalexin-gentamicin combination by a microbroth chequerboard technique against clinical isolates of Edwardsiella tarda and Streptococcus iniae. Gentamicin was shown more susceptible than cephalexin against both bacteria. The effect of cephalexin-gentamicin combination against both bacteria represented additive interaction. The combination even showed synergic interaction (22%) against E. tarda, with a FIC index of <0.5 as a borderline. No antagonism for cephalexin-gentamicin combination was observed for any bacterial strain.