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The security of the B92 protocol using single photon polarization states against an individual attack over a realistic channel is estimated. We calculated an upper bound of Eve's information and clarified the region where B92 over a realistic channel is secure against any individual attack.

An experimental scheme for preparing a polarization entangled W states from four photons emitted by parametric down-conversion is proposed. We consider two different configurations and a method of improving the yield by using single photon sources. In the proposed scheme, one uses only linear optical elements and photon detectors, so that this scheme is feasible by current technologies., 4 pages, 3 figures

Vascular injury stimulates the cytokine-growth factor network in the vascular wall, including transforming growth factor-beta (TGF-beta). Reportedly, the intracellular signaling of TGF-beta is mediated by Smad proteins. We tested the effects of the ectopic expression of inhibitory Smads in cultured rat smooth muscle cells (SMC) to identify the role of TGF-beta/Smad signaling on the phenotypic modulation of SMC. The cells exposed to human recombinant TGF-beta1 (10 ng/ml) were stimulated Smad2 phosphorylation. Infection with the replication-deficient adenovirus vector expressing Smad7, but not bacterial beta-galactosidase or Smad6, was found to inhibit TGF-beta-induced Smad2 phosphorylation in a dose-dependent manner. TGF-beta suppressed the serum-induced proliferation of SMC from 36.3% to 51.0% (p0.01), as measured by hand-counting, and this inhibition was attenuated by the ectopic expression of Smad7 (from 30.7% to 74.8% of the reduction of TGF-beta-response, p0.05), but not Smad6. A BrdU incorporation assay also showed that TGF-beta-mediated growth inhibition was attenuated by exogenous Smad7 and that this inhibition can be reversed by an additional expression of exogenous Smad2. TGF-beta increased the expression of alpha-smooth muscle actin and myosin heavy chain by 1.3-fold and 1.6-fold in comparison to the control, respectively, and these increases were attenuated by exogenous Smad7, but not Smad6. Our data indicate that Smads mediate TGF-beta responses on SMC phenotypes. Smad7, but not Smad6, may specifically act as an inhibitor of TGF-beta responses.

Caveolae in mesangial cells and caveolin expression in mesangial proliferative glomerulonephritis. Background Caveolae are plasma membrane invaginations that have a diameter of 40 to 60 nm. Recent evidences have demonstrated that caveolae contain a variety of signal transduction molecules. Caveolin is a marker protein of caveolae and has been proposed to play a negative regulatory role in signal transduction. The aim of this study was to investigate the behavior of caveolae and caveolin in experimental glomerulonephritis, the localization of both platelet-derived growth factor (PDGF) and transforming growth factor-βbgr; (TGF-βbgr;) receptors in the caveolae membrane, and the regulation of caveolin expression in cultured mesangial cells. Methods The expression of caveolin-1 was examined by immunoblotting and immunohistology using anti-caveolin antibody in anti-Thy-1 nephritis. The caveolae membrane fraction of mesangial cells was isolated by sucrose gradient method and expression of PDGF receptor and TGF-βbgr; receptor were detected by immunoblotting. The effects of mitogens such as phorbol 12-myristate 13-acetate (PMA) and PDGF on the expression of caveolin-1 protein and mRNA were also examined in cultured mesangial cells. Results Caveolin-1 was mainly expressed in glomeruli and was significantly up-regulated in anti-Thy-1 nephritis rat kidney. In cultured mesangial cells, the membrane invaginations of caveolae were revealed by electron microscopy. PDGF receptors abounded in the caveolae membrane and rapidly changed their subcellular distribution after ligand stimulation. In contrast, TGF-βbgr; receptors abounded in the non-caveolae membrane and did not change after ligand stimulation. Decreases in caveolin-1 protein, which were associated with increases in mRNA expression after the exposure of PMA or PDGF-BB, suggested an increased turnover of caveolin-1 in mesangial cells stimulated by mitogens. Conclusion To our knowledge, this electron microscopical study is the first to demonstrate the presence of caveolae in cultured mesangial cells. Caveolae integrate PDGF receptors, and caveolin-1 may play a role in the pathogenesis of the mesangial proliferative glomerular diseases through PDGF signaling.

Smad6 and Smad7 prevent ligand-induced activation of signal-transducing Smad proteins in the transforming growth factor-beta family. Here we demonstrate that both Smad6 and Smad7 are human bone morphogenetic protein-2 (hBMP-2)-inducible antagonists of hBMP-2-induced growth arrest and apoptosis in mouse B cell hybridoma HS-72 cells. Moreover, we confirmed that the ectopic expressions of Smad6 and Smad7 inhibited the hBMP-2-induced Smad1/Smad5 phosphorylation. We previously reported that Smad7 is an activin A-inducible antagonist of activin A-induced growth arrest and apoptosis in HS-72 cells. Interestingly, although mRNA expression of Smad6 was induced by activin A in HS-72 cells, Smad6 showed no antagonistic effect on activin A-induced growth arrest and apoptosis. Moreover, we found that the ectopic expression of Smad7, but not Smad6, inhibited the activin A-induced Smad2 phosphorylation in HS-72 cells. Thus, Smad6 and Smad7 exhibit differential inhibitory effects in bone morphogenetic protein-2- and activin A-mediated signaling in B lineage cells.

Smad proteins play pivotal roles in the intracellular signaling of the multifunctional transforming growth factor-beta (TGF-beta) family members downstream of serine/threonine kinase type I and type II receptors. Smad2 and Smad3 are specific mediators of TGF-beta and activin, while Smadl and Smad5 are involved in bone morphogenetic protein-2 (BMP-2) and BMP-4 signaling. Here we report that osteogenic protein-1 (OP-1), also termed BMP-7, binds predominantly to BMPR-IB in the rat osteoprogenitor-like cell line, ROB-C26. Smad1, Smad5, and Smad8, but not Smad2 and Smad3, were found to stably interact with the kinase-deficient BMPR-IB after it was phosphorylated by the BMPR-II kinase. In ROB-C26 cells, which express Smad2, Smad3, Smad4, and Smad5, OP-1 was found to stimulate the phosphorylation of Smad5. Whereas transfection of wild-type Smad5 enhanced the OP-1-induced response, transfection of wild-type Smad2 had no effect on OP-1 signaling. A Smad5-2SA mutant, in which the two most carboxy-terminal serine residues were mutated to alanine residues, was found to act as a dominant negative inhibitor of OP-1-induced responses upon its transfection into various cell types, including ROB-C26 cells, in contrast to ectopic expression of a Smad2-2SA mutant which was without effect. Smad5, therefore, is a key component in the intracellular signaling of OP-1.

Abstract —We previously reported that the chronic inhibition of nitric oxide (NO) synthesis increases cardiac tissue angiotensin-converting enzyme expression and causes cardiac fibrosis in rats. However, the mechanisms are not known. Transforming growth factor-β (TGF-β) is a key molecule that is responsible for tissue fibrosis. The present study investigated the role of TGF-β in the pathogenesis of cardiac fibrosis. The development of cardiac fibrosis by oral administration of the NO synthesis inhibitor N ω -nitro- l -arginine methyl ester (L-NAME) to normal rats was preceded by increases in mRNA levels of cardiac TGF-β 1 and extracellular matrix (ECM) proteins. TGF-β immunoreactivity was increased in the areas of fibrosis. Treatment with a specific angiotensin II type 1 receptor antagonist, but not with hydralazine, completely prevented the L-NAME–induced increases in the gene expression of TGF-β 1 and ECM proteins and also prevented cardiac fibrosis. Intraperitoneal injection of neutralizing antibody against TGF-β did not affect the L-NAME–induced increase in TGF-β 1 mRNA levels but prevented an increase in the mRNA levels of ECM protein. These results suggest that the early induction of TGF-β 1 via the angiotensin II type 1 receptor plays a major role in the development of cardiac fibrosis in this model.

A 64-year-old male was treated continuously with rifampin, isoniazid and streptomycin for pulmonary atypical mycobacteriosis, Mycobacterium kansasii. Five weeks after beginning the treatment, the patient suddenly developed acute renal failure. A renal biopsy showed crescentic lesions characteristic of rapidly progressive glomerulonephritis with moderate interstitial changes. Serum antirifampin antibody was detected, and the cessation of rifampin treatment was followed by a rapid spontaneous recovery of the patient’s renal function. This is, to our knowledge, the first case of rapidly progressive crescentic glomerulonephritis associated with rifampin treatment where circulating antirifampin antibody is demonstrated and the renal function spontaneously improved after discontinuing rifampin treatment.

The present study demonstrated the elevated synthesis and gene expressions of transforming growth factor beta (TGF-beta) or latent TGF-beta binding protein (LTBP) in an irreversible glomerulosclerosis rat model induced by two consecutive injections of monoclonal antibody (MoAb) 1-22-3. The rats were intravenously injected with 500 microg of MoAb 1-22-3 either once or twice at an interval of 2 weeks. The rats were sacrificed at 24 h, 1 week, 2 weeks or 16 weeks after the last injection. At 24 h, the mesangiolytic changes in the rats with two injections of MoAb 1-22-3 were similar to those in the rats with one injection. The glomerular matrix score in the rats with two injections was significantly higher than that in the rats with one injection at weeks 1, 2 or 16. An increased LTBP localization in the glomeruli of the rats at week 1 after either one or two injections was detected in the segmentally expanded mesangial matrix. Moreover, LTBP in the glomeruli of rats at week 1 after two injections appeared to be more strongly stained in the enlarged mesangial matrix than that in the rats after one injection. A TGF-beta bioassay using mink lung epithelial cells revealed that the total TGF-beta in the glomerular culture conditioned medium in the rats at week 1 after two injections was significantly larger than that in the rats after one injection. A Northern blotting analysis of the glomeruli showed that both the expressions of TGF-beta and LTBP mRNA in the rats after two injections were higher than those in the rats after one injection. These findings suggested that the elevated TGF-beta or LTBP may thus be related to the irreversible glomerulosclerosis that was induced by two injections of MoAb 1-22-3 into rats.

Increased synthesis and gene expression of fibronectin or transforming growth factor-beta (TGF-beta) have been reported to be involved in the progressive process of doxorubicin hydrochloride (Adriamycin)-induced nephropathy. In the present study, the effects of dietary protein restriction on the synthesis and gene expression of fibronectin or TGF-beta were investigated by immunoprecipitation, Northern blotting, and TGF-beta bioassay in this model after subjects were given either short- or long-term low-protein diets. In the long-term diet experiment, either a normal protein diet (NPD, 20%) or low-protein diet (LPD, 5%) was fed to the Adriamycin rats for 8 weeks after the injection of Adriamycin. An 8-week LPD significantly ameliorated kidney destruction and remarkably reduced the fibronectin synthesis. Furthermore, the significant decreases of the latent TGF-beta secretion and the expression of TGF-beta 1 mRNA were observed in the Adriamycin rats fed an 8-week LPD. In the short-term diet experiment, an NPD or LPD was fed to the Adriamycin rats for 2 weeks at weeks 4, 8, or 16 after the injection of Adriamycin. A 2-week LPD did not ameliorate kidney damage. Although fibronectin synthesis by the renal cortex in the Adriamycin rats was remarkably reduced by a 2-week LPD, there was no significant decrease in the latent TGF-beta secretion in the Adriamycin rats. The mRNA expressions of fibronectin or TGF-beta 1 were not affected by a 2-week LPD in the Adriamycin rats at any stage. In conclusion, decreased fibronectin and TGF-beta synthesis may be one of the mechanisms by which the long-term dietary protein restriction ameliorates kidney damage. On the other hand, a 2-week LPD affected the only fibronectin synthesis, which thus suggested that an LPD might exert a quicker influence on the protein synthesis of fibronectin than on the transcriptional events of fibronectin.

The accumulation of extracellular matrix (ECM) is an important feature of most forms of progressive glomerular diseases. In order to examine the relationship between ECM synthesis and glomerulosclerosis, we evaluated fibronectin synthesis by glomeruli with the immunoprecipitation of conditioned media from isolated glomeruli in 5/6 nephrectomized spontaneously hypertensive rats (5/6N-SHR). There was no difference in blood pressure between 5/6N-SHR and control SHR throughout the experiment. Two weeks after the nephrectomy, most of the glomeruli were intact and no difference in the synthesis of fibronectin was observed between either groups. Twenty weeks after the nephrectomy, marked glomerulosclerosis associated with an increase in urinary protein was revealed in 5/6N-SHR but no glomerular lesions in control SHR. The synthesis of fibronectin by isolated glomeruli increased in 5/6N-SHR compared to control SHR. The administration of enalapril or hydralazine + reserpine + hydrochlorothiazide markedly attenuated the glomerular sclerosis and urinary protein excretion to a comparable degree, although the later therapy reduced blood pressure more effectively. These antihypertensive therapies also suppressed fibronectin synthesis in the 5/6N-SHR group at week 20. In conclusion, increased synthesis of glomerular fibronectin appeared to contribute to the glomerulosclerosis caused by subtotal nephrectomy and hypertension.

A series of dimethylammonium salts having two long alkyl groups were shown by electron microscopy to form in water lamellar and vesicle structures which are composed of the bilayer structure similar to that of biomembranes.

The micelle of 1-lauryl-3-carbamoylpyridinium bromide(NLaN) and poly-1-(p-vinylbenzyl)-3-carbamoylpyridinium chloride (PVCG) were shown to form charge transfer complexes with dihydronicotinamides and several aromatic compounds in aqueous media. A broad charge transfer absorption at longer wavelengths was easily detected, and the association constant of 1 : 1 complexes which was estimated from the CT band was enhanced by 6.2–220 times in the NLaN micelle and by 14–66 times in the polymeric system, compared with non-micellar, monomeric system. The enhancement of the interaction between NLaN and its reduced from (NLaNH) was similar in the CTAB micelle and in a nonionic micelle. The increased electron-acceptabilities of the pyridinium group in micellar and polymeric systems were discussed in reference to NAD coenzyme.

The present study was carried out to obtain some information about the effects of topping on the growth, the translocation and accumulation of carbohydrates in corn plants, using the variety "Shiratamamochi" as material. The effects of topping treatments by removing six leaves at each of the three stages, silking (T1), early-maturing (T2) and mid-maturing (T3), were investigated by comparing with non-topped controls. The results obtained may be summarized as follows: 1. Toppings at any of the three stages resulted in the reduction of not only the grain yield but also the dry weights of various aphotosynthetic organs, especially of stalks, and the reductions were greater in earlier treatments. 2. In the treated plots, the chlorophyll content in leaf-blades was reduced after the treatment, but the senescence of lower leaves, which received comparatively sufficient light, was slightly delayed. 3. In the control plots, the Brix readings in stalks increased until the mid-maturing stage, while in the treated plots, these decreased immediately after the treatment. 4. As regards the variations of carbohydrate contents in various organs of the treated plots, the contents of reducing, non-reducing sugars and starch proceeded generally lower than those in the control plots, except for the temporary increase of reducing sugar content in the plots treated at silking stage. 5. Judging from the results obtained, it is evident that the reduction of grain yield by topping is due to the reduction of photosynthates which are primarily due to the loss of upper leaves, and that the greatest effect of the treatment takes place during the stages from silking over to early-maturing.

AGEs activate mesangial TGF-β–Smad signaling via an angiotensin II type I receptor interaction. Background The renin-angiotensin system (RAS) and the accumulation of advanced glycation end products (AGEs) have been implicated in the pathogenesis of diabetic nephropathy. Whether there is a functional interaction between the RAS and AGEs in diabetic nephropathy is not known. In this study, we investigated whether AGEs could activate autocrine angiotensin II (Ang II) signaling and subsequently induce transforming growth factor-β (TGF-β)–Smad signaling in cultured rat mesangial cells. Methods The intracellular formation of reactive oxygen species (ROS) was detected using the fluorescent probe CM-H 2 DCFDA. Ang II was measured by radioimmunoassay. TGF-β released into media was quantitatively analyzed in an enzyme-linked immunosorbent assay (ELISA). Smad2, p27 Kip1 (p27), fibronectin, and receptor for AGEs (RAGE) protein expression were determined by Western blot analysis. TGF-β–inducible promoter activity was analyzed by a luciferase assay. DNA synthesis was evaluated by 5-bomo-2′-deoxyuridine (BrdU) incorporation and de novo protein synthesis was determined by [ 3 H]leucine incorporation. Results AGEs increased intracellular ROS generation in mesangial cells, and this effect was significantly inhibited by an antiserum against RAGE. AGEs also were found to stimulate Ang II production in a time- and dose-dependent manner, which was completely prevented by an antioxidant, N -acetylcysteine (NAC). AGE-induced TGF-β overproduction was completely blocked by candesartan, an Ang II type 1 receptor (AT 1 R) antagonist. Both candesartan and neutralizing antibody against TGF-β completely prevented AGEs-induced Smad2 phosphorylation and TGF-β–inducible promoter activity. Furthermore, AGEs were found to inhibit DNA synthesis and to stimulate de novo protein synthesis and fibronectin production in association with up-regulation of p27. All of these phenomena were completely prevented by candesartan or a polyclonal antibody against TGF-β. Conclusion The present study suggests that AGE-RAGE–mediated ROS generation activates TGF-β–Smad signaling and subsequently induces mesangial cell hypertrophy and fibronectin synthesis by autocrine production of Ang II. This pathway may provide an important link between metabolic and haemodynamic factors in promoting the development and progression of diabetic nephropathy.

A novel secure communication network with quantum key distribution in a metropolitan area is reported. Different QKD schemes are integrated to demonstrate secure TV conferencing over a distance 45km, stable long-term operation, and application to secure mobile phones.

In this thesis, we analyze the security of the Bennett 1992 quantum key-distribution protocol (B92 protocol) over a realistic channel assuming that bit values are encoded in single photon polarization states. First, we study the security of the B92 protocol against individual attack. In the individual attack, eavesdropper (Eve) interacts a qubit emitted by the sender (Alice) with her probe system followed by a measurement on each probe. To make our analysis simple, we propose a modified B92 protocol. Using this protocol, Alice and the receiver (Bob) can estimate Eve's information gain as a function of a few parameters that reflect the imperfections of devices or Eve's disturbance. We find a counter-intuitive behavior of Eve's maximum information gain, i.e., it decreases as the amount of disturbances increases. We also estimate the secret key gain that is the net growth of the secret key per one pulse. We show the region where the modified B92 protocol over a realistic channel is secure against individual attack. Next, we study the unconditional security of the B92 protocol, which is the security against any attack. To prove the security, we first propose a protocol that is unconditionally secure and can be reduced to the B92 protocol. This protocol employs the entanglement distillation protocol (EDP) based on a filtering operation and the Calderbank-Shor-Steane (CSS) quantum error correcting codes. The bit errors and the phase errors, which have to be estimated for the EDP based on the CSS codes, are correlated after the filtering operation, and we can bound the amount of phase errors from the observed bit errors by an estimation method involving nonorthogonal measurements. The angle between the two states shows a trade-off between accuracy of the estimation and robustness to noises. We show a way to run the unconditionally secure B92.

We analyze real-life implementations of measurement-device-independent quantum-key-distribution (MDI-QKD): a general system model, a finite-decoy protocol and a finite-key analysis. Our work is relevant to not only QKD but also general experiments on quantum interference.

Quantum-key distribution has been studied as an ultimate method for secure communications, and now it is emerging as a technology that can be deployed in real fiber networks. Here, we present our QKD experiments based on the differential- phase-shift QKD protocol. A DPSQKD system has a simple configuration that is easy to implement with conventional optical communication components, and it is suitable for a high-clock rate system. Moreover, although the DPS-QKD system is implemented with an attenuated laser source, it is inherently secure against strong eavesdropping attacks called photon number-splitting attacks, which pose a serious threat to conventional QKD systems with attenuated laser sources. We also describe three types of single-photon detectors that are suitable for high-speed, long-distance QKD: an up-conversion detector, a superconducting single-photon detector, and a sinusoidally gated InGaAs avalanche photodiode. We present our recordsetting QKD experiments that employed those detectors.

While many studies concerning the changes in the components of sweet potatoes during storage have been investigated, the detailed distributions in the varied region of seed tuber are little understood. In the present paper, with a desire to obtain some further information on the physiological nature of seed tuber during the storage period, particular attention was paid to the variations of carbohydrate and nitrogen contents at the apex, center and tail both in the pith and cortex of seed tuber, using the variety "Gokokuimo" as material. The experimental results obtained are summarized as follows : 1. At the early stage of storage, the reducing sugar contents rose at the apex and center both in the pith and cortex, while those at the tail fell particularly in the pith. Moreover, the non-reducing sugar contents increased at all of the parts of tuber, and the starch contents declined at every part except the tail in the pith. 2. Being accompanied with the stage advanced, the reducing and non-reducing sugar contents were rich only at the tail in the pith, but poor at the other parts of tuber. And at the same time the starch contents were comparatively abundant at the apex and center, while those at the tail decreased both in the pith and cortex. 3. At the later stage of storage period, the reducing sugar consents declined at the apex, but they were considerably high at the center and tail both in the pith and cortex. Moreover, the non-reducing sugar contents were high at the apex and center, while those at the tail were low. On the other hand, the starch contents showed a striking contrast to the tendencies of non-reducing sugar contents in the pith and cortex. 4. Concerning nitrogen compounds, the soluble-N contents were generally high at the early and later stage, on the contrary the protein-N contents were abundant in the middle stage at all of the parts of tuber.

So far as the writers are aware, few accounts seem to have been given to the physiological behavior of sweet potato roots by the root tuber formation. The present investigation was undertaken to see whether the carbohydrate contents, amylase and phosphorylase activities in the sweet potato roots may relate to the differentiation of root tuber and to the determination of the thickened part of tuberous roots. Sweet potato of the variety "Okinawa No. 100" was used as material. The experimental results obtained may be summarized as follows: 1. By the 10 day after planting, the carbohydrate contents in the tuberous roots showed no remarkable difference from those in the fibrous roots. While by the 20 day after planting, the accumulations of non-reducing sugar and starch were observed in the slightly thickened part of tuberous roots. By the 30 day after planting, it was recognized that the contents of reducing and non-reducing sugars and starch were high in the distinctly thickened part of tuberous roots and also that the non-reducing sugar and starch contents were pretty abundant in the upper part of tuberous roots. Judging from these results, the carbohydrate contents in the tuberous roots may-be assumed to proceed parallel to the progress of root tuber formation. 2. As the characteristic features of the root tuber formation throughout the whole stage, the carbohydrate contents in the lower part of tuberous roots were almost similar to those in the fibrous roots, and the interrelation of carbohydrate contents between the thickened, upper and lower parts of tuberous roots added further confirmatory support to the previous results (1958, a). 3. Concomitant with the behavior of carbohydrate contents, the amylase and phosphorylase activities in the tuberous and fibrous roots differed from each other. Moreover, the variations of these enzyme activities in the tuberous roots were closely related to the root tuber formation.

In order to obtain some informations on the variations of the carbohydrate and nitrogen contents of potato plants by applying 0.02 % 2, 4, 5-T (sodium salt) foliage sprays. the present investigation was undertaken, using potatoes of variety "Norin No. 1" as material. The results obtained may be summarized as follows : 1. In 12 hours after treatment wilting of leaves, curling of petioles and stalks were caused. The retarded growth of tops and tubers in the sprayed plots was recovered in 10 days and thenceforth surpassed their growth in the control plots. 2. In the control plots, the sugar contents stored temporarily in the tops at rhe flowering stage decreased rapidly, as tubers developed. In the sprayed plots, however, these processes were delayed. 3. In the control plots, the nitrogen contents in the tops and the tubers were high at the early stage, then decreased gradually in the later stage. In the sprayed plots, however, they decreased rapidly towards the blooming stage and thenceforth decreasing rate became loose. 4. Judging from the results it seems that the physiological role of the tops as a temporally storing organ of the assimilates was put off and intensified by treating potato plants with the 2, 4, 5-T foliage sprays.

The present investigation was undertaken to obtain some informations concerning the relations between the variations of carbohydrate and nitrogen contents in the tops and roots of broad bean plants during the entire growing period, using the variety "Sanuki-Nagasaya" as material. The results obtained may be summarized as follows : 1. In winter, the top growth was not remarkable and the root growth was considerably vigorous. But in spring, the former which was accompanied with flowering surpassed the latter, moreover, the root nodules began to collapse at the flowering stage. 2. In the tops, the carbohydrate and nitrogen contents was high at the early stage of growth, then decreased as the growth advanced, finally increased at the maturing stage. 3. In the roots, high sugar contents at the early stage related to the subsequent growth of the tops, roots and root nodules, besides, high starch contents at the maturing stage owed to the assimilates of the tops. On the other hand, high nitrogen contents especially high protein-N contents at almost all of the growing period related to the action of bacteroid and the collapse of the root nodules.

Several quantum key distribution (QKD) protocols employ iterative sifting. After each quantum transmission round, Alice and Bob disclose part of their setting information (including their basis choices) for the detected signals. The quantum phase of the protocol then ends when the numbers of detected signals per basis exceed certain pre-agreed threshold values. Recently, however, Pfister et al. [New J. Phys. 18 053001 (2016)] showed that iterative sifting makes QKD insecure, especially in the finite key regime, if the parameter estimation for privacy amplification uses the random sampling theory. This implies that a number of existing finite key security proofs could be flawed and cannot guarantee security. Here, we solve this serious problem by showing that the use of Azuma's inequality for parameter estimation makes QKD with iterative sifting secure again. This means that the existing protocols whose security proof employs this inequality remain secure even if they employ iterative sifting. Also, our results highlight a fundamental difference between the random sampling theorem and Azuma's inequality in proving security., Comment: 9 pages. We have found a flaw in the first version, which we have corrected in the revised version