Applications of commercial biosensors in clinical,food, environmental,and biothreat/biowarfare analyses

The lack of specific, low-cost, rapid, sensitive, and easy detection of biomolecules has resulted in the development of biosensor technology. Innovations in biosensor technology have enabled many biosensors to be commercialized and have enabled biomolecules to be detected onsite. Moreover, the emerging technologies of lab-on-a-chip microdevices and nanosensors offer opportunities for the development of new biosensors with much better performance. Biosensors were first introduced into the laboratory by Clark and Lyons. They developed the first glucose biosensor for laboratory conditions. Then in 1973, a glucose biosensor was commercialized by Yellow Springs Instruments. The commercial biosensors have small size and simple construction and they are ideal for point-of-care biosensing. In addition to glucose, a wide variety of metabolites such as lactate, cholesterol, and creatinine can be detected by using commercial biosensors. Like the glucose biosensors (tests) other commercial tests such as for pregnancy (hCG), Escherichia coli O157, influenza A and B viruses, Helicobacter pylori, human immunodeficiency virus, tuberculosis, and malaria have achieved success. Apart from their use in clinical analysis, commercial tests are also used in environmental (such as biochemical oxygen demand, nitrate, pesticide), food (such as glutamate, glutamine, sucrose, lactose, alcohol, ascorbic acid), and biothreat/biowarfare (Bacillus anthracis, Salmonella, Botulinum toxin) analysis. In this review, commercial biosensors in clinical, environmental, food, and biowarfare analysis are summarized and the commercial biosensors are compared in terms of their important characteristics. This is the first review in which all the commercially available tests are compiled together.     

Mean-variance performance optimization of response time in a tandem router network with batch arrivals

The end-to-end performance of a simple wireless router network with batch arrivals is optimized in an M/G/1 queue-based, analytical model. The optimization minimizes both the mean and variance of the transmission delay (or ‘response time’), subject to an upper limit on the rate of losses and finite capacity queueing and recovery buffers. Losses may be due to either full buffers or corrupted data. The queueing model is also extended to higher order moments beyond the mean and variance of the response time. The trade-off between mean and variance of response time is assessed and the optimal ratio of arrival-buffer size to recovery-buffer size is determined, which is a critical quantity, affecting both loss rate and transmission time. Graphs illustrate performance in the near-optimal region of the critical parameters. Losses at a full buffer are inferred by a time-out whereas corrupted data is detected immediately on receipt of a packet at a router, causing a N-ACK to be sent upstream. Recovery buffers hold successfully transmitted packets so that on receiving a N-ACK, the packet, if present, can be retransmitted, avoiding an expensive resend from source. The impact of the retransmission probability is investigated similarly: too high a value leads to congestion and so higher response times, too low and packets are lost forever.

c-Jun N-terminal kinase mediates hydrogen peroxide-induced cell death via sustained poly(ADP-ribose) polymerase-1 activation

Reactive oxygen species (ROS) have been closely associated with both apoptotic and non-apoptotic/necrotic cell death. Our previous study has illustrated that c-Jun-N-terminal kinase 1 (JNK1) is the main executor in hydrogen peroxide (H(2)O(2))-induced nonapoptotic cell death. The main objective of this study is to further elucidate the molecular mechanisms downstream of JNK1 in H(2)O(2)-induced cell death. In this study, poly(ADP-ribose) polymerase-1 (PARP-1), a key DNA repair protein, was readily activated by H(2)O(2) and inhibition of PARP-1 activation by either a pharmacological or genetic approach offered significant protection against H(2)O(2)-induced cell death. More importantly, H(2)O(2)-mediated PARP-1 activation is subject to regulation by JNK1. Suppression of JNK1 activation by a chemical inhibitor or genetic deletion markedly suppressed the late-phase PARP-1 activation induced by H(2)O(2), suggesting that JNK1 contributes to the sustained activation of PARP-1. Such findings were supported by the temporal pattern of nuclear translocation of activated JNK and a direct protein-protein interaction between JNK1 and PARP-1 in H(2)O(2)-treated cells. Finally, in vitro kinase assay suggests that PARP-1 may serve as the direct phosphorylation target for JNK1. Taken together, data from our study reveal a novel underlying mechanism in H(2)O(2)-induced nonapoptotic cell death: JNK1 promotes a sustained PARP-1 activation via nuclear translocation, protein-protein interaction and PARP-1 phosphorylation.     

Differentiation of Entamoeba histolytica and Entamoeba dispar by PCR: a preliminary study in Izmir, Turkey

The causative agent of amoebiasis is currently attributed to two distinct species (E. histolytica and E. dispar). The aim of this study was to differentiate these species by PCR in stool samples. Isolated genomic DNA was amplified by PCR and band products of 101 bp (E. dispar) were obtained. All seven stool samples were found to be E. dispar, not E. histolytica. Our results demonstrated the significance of E. histolytica/dispar differentiation in the diagnosis of amoebiasis. This study is preliminary to our current research project entitled "Investigation of the prevalence of amoebiasis and Entamoeba species in Izmir and its hinterland".     

Protective effect of alpha-linolenic acid on gentamicin-induced ototoxicity in mice

Alpha-linolenic acid is one of the fatty acids known as omega 3. Previous studies have shown the antioxidant and anti-inflammatory effects of alpha-linolenic acid, which prevented cell damage by inhibiting apoptotic pathway. Also, it is known that gentamicin activates apoptotic mediators and causes necrosis in the kidney. Due to this reason, we planned a study to evaluate the protective effects of alpha-linolenic acid on gentamicin induced ototoxicity by evaluating inflammation and apoptotic mediators. For this purpose, 100?mg/kg gentamicin (i.p; intraperitoneally) and 200?mg/kg alpha-linolenic acid (gavage) are administered to mice for 9?days. On 9th and 10th days, rotarod performance was assessed to test the effect of gentamicin and alpha-linolenic acid treatment on the motor coordination of mice. Gentamicin treatment decreased fall latency of mice and gentamicin treatment together with alpha-linolenic acid increased fall latency of mice. Gentamicin treatment also increased expression of phospholipase A2(plA2), cyclooxygenase-2(COX-2) and inducible nitric oxide syntheses (iNOS). Furthermore, it increased Bax and caspase-3, which are proapoptotic proteins and decreased bcl-2 that is an antiapoptotic protein. Gentamicin treatment together alpha-linolenic acid recovered the change of expression of these enzymes. In conclusion, this study showed that alpha-linolenic acid will be useful to prevent gentamicin-induced ototoxicity by inhibiting apoptosis and inflammation.     

The Association of Plasminogen Activator Inhibitor Type 1 (PAI-1) Level and PAI-1 4G/5G Gene Polymorphism with the Formation and the Grade of Endometrial Cancer

Plasminogen activator inhibitor type 1 (PAI-1) is a serine protease inhibitor (Serpine 1), and it inhibits both tissue plasminogen activator and urokinase plasminogen activator which are important in fibrinolysis. We aimed to find whether there is a possible association between PAI-1 level, PAI-1 4G/5G polymorphism, and endometrial cancer. PAI-1 levels in peripheral blood were determined in 82 patients with endometrial carcinoma and 76 female healthy controls using an enzyme-linked immunoassay (ELISA). Then, the genomic DNA was extracted and screened by reverse hybridization procedure (Strip assay) to detect PAI 1 4G/5G polymorphism. The levels of PAI-1 in the patients were higher statistically in comparison to controls (P < 0.001). The distribution of PAI-1 4G/5G polymorphism was quite different between patients and controls (P = 0.008), and 4G allelic frequency was significantly higher in the patients of endometrial cancer than in controls (P = 0.026). We found significant difference between Grade 1 and Grade 2+3 patients in terms of the PAI-1 levels (P = 0.047). There was no association between PAI-1 4G/5G polymorphism and the grades of endometrial cancer (P = 0.993). Our data suggest that the level of PAI-1 and PAI-1 4G/5G gene polymorphism are effective in the formation of endometrial cancer. PAI-1 levels are also associated with the grades of endometrial cancer.     

Typifications of Linnaean names in the genus Centaurea and Serratula (Asteraceae)

The typification of three Linnaean names in the genus Centaurea and one in Serratula (Asteraceae): C. lippii (syn. Volutaria lippii), C. muricata (Volutaria muricata), C. repens (Rhaponticum repens) and S. babylonica (Centaurea babylonica), is discussed. Designations of nomenclatural types based on the consultation of Linnaeus's original material and the literature cited in the respective protologues are proposed. Three names are lectotypified using specimens from both Linnaeus herbarium at LINN and the illustrations from Isnard and Dodoëns. Furthermore, a neotype is designated for Serratula babylonica from a specimen at LINN.     

Extensive yellow crusts below limestone overhangs: a new taxon close to a minute epiphytic lichen

A conspicuous yellow crust forming extensive covers on some dry and shaded limestone rocks in Europe is described here as Caloplaca substerilis subsp. orbicularis M. Haji Moniri, Vondrák & Malí?ek subsp. nov. Based on nuITS rDNA, 28S nuLSU rDNA and mtSSU rDNA sequence data, the new taxon is closely related to Caloplaca substerilis and C. ulcerosa. The three taxa form a supported clade in the subfamily Xanthorioideae (Teloschistaceae), but none of the recently seggregated genera are suitable for them. In the ITS phylogeny, the new taxon forms a monophylum nested within C. substerilis. However, its extensive yellow thalli and absence of vegetative diaspores clearly distinguish it from Caloplaca substerilis (subsp. substerilis). Indeed, if it had not been for the molecular evidence, we would have described it at the rank of species. We suggest that the substrate switch and accompanying processes are responsible for the striking phenotypic difference between Caloplaca substerilis subsp. substerilis and C. substerilis subsp. orbicularis.