[COVID-19 in haemodialysis patients: result analysis of the first year of the pandemic].

BACKGROUND: Present concepts of the novel coronavirus infection prognosis in haemodialysis (HD) patients are rather controversial. There is little information on therapy efficiency and safety in such patients. We studied COVID-19 course specifics, prognostic factors associated with fatal outcomes, therapy efficiency and its transformation at different stages of the pandemic first year. MATERIALS AND METHODS: Single-centre retrospective uncontrolled study included 653 COVID-19 HD-patients treated at Moscow City Nephrology Centre from April 1 to December 31, 2020. RESULTS: This period mortality rate was 21.0%. Independent predictors of COVID-19 unfavourable outcome in HD patients were pulmonary lesion extension (CT grades 34), high comorbidity index, and mechanical ventilation. Approaches to COVID-19 treatment modified significantly at different periods. Immunomodulatory drugs (monoclonal antibodies to IL-6, corticosteroids) were used largely at later stages. With tocilizumab administration, mortality was 15.1%, tocilizumab together with dexamethasone 13.3%; without them 37.8% (р0,001). Tocilizumab administration in the first 3 days after hospitalization of patients with CT grades 12 was associated with more favourable outcomes: 1 out of 29 died vs 6 out of 20 (tocilizumab administered at later periods); p0.04. There was no significant difference in death frequency in patients with CT grades 34 depending on tocilizumab administration time. CONCLUSION: COVID-19 in HD patients can manifest in a severe course with unfavourable outcome. It is urgent to identify reliable disease outcome predictors and develop efficient treatment in this population.

4-n-butylresorcinol enhances proteolytic degradation of tyrosinase in B16F10 melanoma cells.

OBJECTIVE: 4-n-butylresorcinol is a competitive inhibitor of tyrosinase and has been used as an antimelanogenic agent. However, its inhibition mechanism in intact cells is not fully understood. To elucidate the cellular mechanism, we compared in vitro and in vivo inhibitory effects of 4-n-butylresorcinol on tyrosinase activity. METHODS: B16F10 melanoma cells were cultured in media containing α-MSH in the presence or absence of 4-n-butylresorcinol. Tyrosinase mRNA levels, protein levels and activity in B16F10 cells were compared by real-time PCR, immunostaining combined with western blot and colorimetric analysis, respectively. Melanin concentration was measured by colorimetry both in the cells and in the media. Tyrosinase glycosylation and proteolytic degradation were analysed by immunoblotting after cells were treated with Endo H/PNGase F and E64/proteasome inhibitors, respectively. RESULTS: 4-n-butylresorcinol inhibited tyrosinase activity and melanin synthesis more effectively in intact cells than in cell lysates. Western blotting and real-time RT-PCR showed that 4-n-butylresorcinol reduced protein levels, but not mRNA levels, of tyrosinase in B16F10 cells. 4-n-butylresorcinol showed no effect on the processing of tyrosinase glycosylation or on trafficking to melanosomes. However, treatment of B16F10 cells with E64 or proteasome inhibitor abrogated the 4-n-butylresorcinol-induced decrease of tyrosinase. Moreover, 4-n-butylresorcinol activated p38 MAPK, resulting in increased ubiquitination of tyrosinase. CONCLUSION: 4-n-butylresorcinol inhibits melanogenesis by enhancing proteolytic degradation of tyrosinase as well as competitive binding to tyrosinase. These findings will help to develop new, effective and safe chemicals for the treatment of hyperpigmentation disorders.

C3d-binding Donor-specific HLA Antibody Is Associated With a High Risk of Antibody-mediated Rejection and Graft Loss in Stable Kidney Transplant Recipients: A Single-center Cohort Study.

BACKGROUND: One risk factor for antibody-mediated rejection (ABMR) and poor outcome after kidney transplantation is donor-specific anti‒human leukocyte antigen (anti-HLA) antibodies (DSAs). In this study we sought to determine whether the presence of DSAs that bind complement component C3d could better predict ABMR and graft loss in stable kidney transplant recipients (KTRs). METHODS: We included 220 stable KTRs in this study and screened them for DSAs from July 2013 to July 2016. RESULTS: Of the 220 KTRs, DSAs were detected in 24 (10.9%). The incidence of ABMR was 3.6% (8 of 220) overall, and C3d-DSA‒positive KTRs had a significantly higher incidence than SA-DSA‒positive KTRs (63.3% vs 38.9%, P = .03). Most C3d-binding DSAs were anti-HLA class II antibodies (11 of 13, 84.6%). Class II C3d-binding DSA was also significantly associated with graft failure on multivariate analysis, as were ABMR, chronic ABMR, and high serum creatinine. Class II C3d-binding DSA was also significantly associated with lower graft survival after ABMR. CONCLUSION: C3d-binding DSA, especially class II, was significantly associated with the risk of ABMR and graft loss in stable KTRs. We suggest that monitoring of stable KTRs for C3d-binding DSA, followed by biopsy, could aid in early recognition of ABMR and prevention of graft loss.

Reuse of Living-Donor Liver Graft in Second Recipient with Long-Term Survival.

Brain death is a rare situation after living-donor liver transplantation. However, the recipient who suffers from brain death and has functional liver graft is a potential liver donor. We report the 1st case of successful reuse of extended right living-donor liver graft after brain death of the first recipient. The first recipient, who had acute liver failure caused by hepatitis A virus, experienced brain death on the 2nd day after the transplantation. The allograft had a favorable regeneration and functional recovery. On the 7th day, the allograft was procured with a patent hepatic artery, bile duct, portal vein, and reconstructed outflow (right hepatic vein and middle hepatic vein) and successfully implanted into the second recipient. The second recipient has experienced a long-term survival without any complications.

[Transplantation of the kidney--optimal treatment of patients suffering from diabetes mellitus type 1 with terminal chronic renal failure].

AIM: To assess long-term results of renal transplantation in patients with diabetes mellitus of type 1 (DM-1) with terminal chronic renal failure (tCRF); to detect risk factors of low survival of the patients and development of dysfunction of renal transplant. MATERIAL AND METHODS: A retrospective comparative analysis of 418 recipients of the kidney with non-diabetic nephropathies (NDN) and 113 recipients with DM-1. RESULTS: Survival of DM-1 patients with tCRF after allotransplantation of the kidney was lower than in patients with NDN. Low survival risk factors for DM-1 patients after transplantation of the kidney are: DM-1 duration up to tCRF 25 years and more, minimum 3-year history of dialysis before transplantation, age at transplantation over 45 years, persistence of anemia (hemoglobin < 110 g/l) after operation. Survival of the transplanted kidney in DM-1 and NDN patients was the same. Risk factors of dysfunction of the transplanted kidney are the following: acute crises of rejection and delayed function of the transplant, arterial hypertension > 130/80 mmHg, proteinuria > 300 mg/day. Survival of the transplanted kidney is higher in transplantation from the relative donor, does not depend on the kind and duration of previous dialysis. Causes of a decline in the function of the transplanted kidney (by the data of puncture biopsy of 34 transplants) are the following: acute rejection crises (38%), chronic transplantation nephropathy (24%), toxic nephropathy (18%), recurrent diabetic nephropathy (6%), chronic pyelonephritis (6%). Lethality in DM-1 patients after renal transplantation is 2 times higher than in patients with NDN. Death was due to cardiovascular diseases, gangrene of the lower limbs, infectious complications (in 31%, 15% and 35% cases, respectively). CONCLUSION: Transplantation of the kidney is an optimal treatment in DM-1 patients with tCRF.

[Risk factors and pathogenetic mechanisms of left ventricular hypertrophy in progressive chronic kidney disease and after transplantation of the kidney].

AIM: To specify the trend in the incidence of left ventricular hypertrophy (LVH) at a predialysis stage of chronic kidney disease (CKD) in the course of its progression from stage III to stage V and after transplantation of the kidney (TK); to study correlations between homeostatic disorders caused by CKD progression and myocardial remodeling; to define the role of some hemodynamic and nonhemodynamic factors in formation of LVH. MATERIAL AND METHODS: The study enrolled 128 patients (58 males and 70 females, age 18-55 years, mean age 42 +/- 11 years) at a predialysis stage of CKD (group 1) and 225 recipients of renal allotransplant--RRA (group 2, 140 males and 85 females, age 18-69 years, mean age 43 +/- 12 years). General clinical examination, biochemical and immunological blood tests, echocardiography were made. RESULTS: At a predialysis stage of CKD, LVH was diagnosed in 56% patients. Incidence of LVH was directly related with age of the patients (p = 0.001), blood pressure (p < 0.001), duration of arterial hypertension (p = 0.004), severity of anemia (p = 0.017), the level of C-reactive protein (p = 0.003), blood phosphorus concentration and inversely correlated with glomerular filtration rate--GFR (p = < 0.001), albumin level (p = 0.023) and blood Ca (p < 0.001). LVH was followed up for 12 months in 35 patients with predialysis CKD. Factors of LVH progression and factors hindering its regression were systolic blood pressure, Hb and Ca in the blood. In group 2 of RRA incidence of LVH was 53%. Significant factors of LVH risk after transplantation were age (p = 0.002), hypertension (p = 0.005) and anemia (p = 0.04). Moreover, LVH closely correlated with proteinuria (p < 0.03), transplant dysfunction (p = 0.002) and posttransplantation ischemic heart disease (p < 0.037). Changes in LVH were analysed in 30 RRA. Frequency of LVH decreased for 2 years after transplantation (from 56 to 32%) but 36-60 and more months after transplantation it increased (46 and 64%, respectively). Transplant dysfunction was the leading factor hindering LVH regression after transplantation. CONCLUSION: The same mechanisms are involved in LVH pathogenesis after transplantation and at a predialysis stage of CKD. The significance of initial renal lesion signs--minimal proteinuria and hypercreatininemia--was higher after renal transplantation than in patients with CKD.

Hanging Hepato-Atrial Anastomosis in Deceased-Donor Liver Transplantation for Budd-Chiari Syndrome With Extensive Vena Cava Obliteration: A Case Report.

INTRODUCTION: Although outcomes of liver transplantation (LT) have improved as the result of progress in surgical procedures, a failure to restore sufficient graft outflow may yield fatal consequences including graft dysfunction and even graft loss to date. In particular, patients with pre-existing obliterated venous drainage, such as those with Budd-Chiari syndrome (BCS), are at high risk of having venous complications followed by conventional LT. In selected cases, the transplant surgeons are compelled to modify the surgical procedures of LT from the conventional procedure. METHODS: We describe an LT performed in a BCS patient with complete inferior vena cava (IVC) obstruction. A procedure that we named "hanging hepato-atrial anastomosis" was performed, in which 2 major modifications were made. One modification was the dissection of the lower inlet of the right atrium by use of a trans-abdominal approach and hepato-atrial anastomosis. This was performed by exposing the thoracic IVC through a trans-abdominal approach. The other modification was the manufacture of a blind pouch from the graft's infra-hepatic IVC without anastomosis. RESULTS: Modifications were made possible as the result of meticulous examination of the patient's vascular anatomy before the operation. Fortunately, the patient had a heavy network of pre-vertebral veins that drained blood from the lower extremity and both kidneys to the azygos-hemi-azygos veins. CONCLUSIONS: We learned that a meticulous assessment of vascular anatomy and complete understanding of hemodynamics are the keys to the successful LT for BCS in patients with extensive IVC abnormality. Thoracotomy may not be necessary to explore thoracic IVC when performing hepato-atrial anastomosis in LT for BCS.

[Coronary artery disease after renal transplantation: epidemiology, risk factors, and surgical approaches to treatment].

Coronary artery disease (CAD) is the main cause of death in renal transplant recipients. The aim of the present study was to determine the frequency and risk factors of post-transplantation CAD and its influence on the long-term results of surgery, as well as to evaluate the efficiency of myocardial revascularization in patients with severe CAD. Analysis of the observation of 479 renal recipients (332 men and 147 women) aged 38.69 +/- 11.2 was performed. The mean follow-up period was 64.56 +/- 37.44 months. Sixty-eight patients had diabetes mellitus. CAD was diagnosed in 14.8% (71 out of 479) renal recipients; in 12.7% of patients it developed de novo and was revealed 32.4 +/- 18.6 months after the surgery. Ten-year survival of renal recipients with CAD was only 39%, while in the group of non-CAD patients it was 75% (p < 0.0001). Age more than 45, male gender, diabetes mellitus, hypercholesterolemia, infections, pre-existing left ventricular myocardial hypertrophy, and renal transplant dysfunction were defined as significant risk factors of CAD de novo. Multi-factor Cox model found only age more than 45 (p < 0.009), male gender (p < 0.00001), and hyperlipidemia (p < 0.0058) to be independent risk factors of CAD. Myocardial revascularization was performed in 29 patients with coronary lesions: 27 patients underwent percutaneous transluminal coronary angioplasty with stenting and 2 patients underwent coronary artery bypass grafting (5 and 52 months after renal transplantation). However, angioplasty had to be repeated in 6 out of 27 (22%) patients within 3 to 6 months. The average follow-up duration was 23 months (2 to 74 months) after revascularization. Prolonged effect (more than 12 months) was achieved in 17 out of 29 (58.6%) patients. None of the patients developed myocardial infarction after revascularization. Two patients died 28 and 35 months after angioplasty due to extracardial complications (hepatic cirrhosis and an oncological disease); one patient died 78 months after repeated revascularization from progressive cardiac insufficiency while receiving dialysis due to a relapse of renal transplant insufficiency. Thus, CAD develops in 14.8% of renal transplant recipients; in 12.7 of patients it develops de novo. There are conventional and nonconventional post-transplantation CAD risk factors, which include renal transplant dysfunction and post-transplantation infections. Association with myocardial hypertrophy, observed in a significant number of patients, is a feature of post-transplantation CAD. Coronary revascularization, angioplasty with stenting in particular, may be considered to be an effective method of CAD treatment in renal transplant recipients.

Advanced remediation of uranium-contaminated soil.

The existing decontamination method using electrokinetic equipment after acidic washing for uranium-contaminated soil requires a long decontamination time and a significant amount of electric power. However, after soil washing, with a sulfuric acid solution and an oxidant at 65 °C, the removal of the muddy solution using a 100 mesh sieve can decrease the radioactivity of the remaining coarse soil to the clearance level. Therefore, only a small amount of fine soil collected from the muddy solution requires the electrokinetic process for its decontamination. Furthermore, it is found that the selective removal of uranium from the sulfuric washing solution is not obtained using an anion exchanger but rather using a cation exchanger, unexpectedly. More than 90% of the uranium in the soil washing solutions is adsorbed on the S-950 resin, and 87% of the uranium adsorbed on S-950 is desorbed by washing with a 0.5 M Na2CO3 solution at 60 °C.

Cloning and expression of human mitotic centromere-associated kinesin gene.

The human homologue of the hamster mitotic centromere-associated kinesin (HsMCAK) gene containing a central type motor domain was isolated from a Jurkat T-cell derived cDNA library. The HsMCAK gene has a predicted 723 amino acid open reading frame, encoding a 81 kDa protein that shares 79.2% homology with hamster MCAK. Unstimulated T lymphocytes contained no detectable HsMCAK-specific mRNA. Activation of resting T-cells by immobilized anti-CD3 resulted in the expression of a 2.9-kb transcript during the S phase of the cell cycle. The TPA-induced monocytic differentiation of U937 which also results in growth-arrest abruptly downregulates the expression of HsMCAK. Removal of TPA restored the growth of the cell through the retrodifferentiation process and the subsequent expression of HsMCAK. HsMCAK is expressed in tissues containing dividing cells, such as thymus, testis, small intestine, colon (mucosal lining), and placenta. These results suggest that the expression of HsMCAK is first detected in early S phase to support the proliferative response and is strictly regulated at the transcriptional level.

The Study of Optical Properties as Glass Composition of Bi2O3-Based Glass/Phosphor Mixed Paste.

Recently, White light emitting diodes (WLEDs) have been studied because of many advantages such as lower energy consumption, fast response, high brightness. Glass frit has been interested in LED packages due to their superior properties such as long-term stability and permeability. To maximize the LED light emission characteristic, the glass frit was required a low firing temperature and high refractive index. We selected the bismuth-based glass due to their low melting and high refractive index. This study was investigated characteristics of glass according to the influence of the glass within Bi2O3 content and this glass characteristic change was studied the effects on the optical properties of LED package structure. The properties changes of the glass frit affect the optical property of the mixed paste. With higher contents of Bi203 glass composition, the transmittance and emission intensity of the mixed paste was increased. These results suggest that the difference in refractive index between the phosphor and glass frit is minimized, the loss of light is minimized.

PKCδ maintains phenotypes of tumor initiating cells through cytokine-mediated autocrine loop with positive feedback.

The existence of tumor initiating cells (TICs) has been emerged as a good therapeutic target for treatment of glioblastoma that is the most aggressive brain tumor with poor prognosis. However, the molecular mechanisms that regulate the phenotypes of TICs still remain obscure. In this study, we found that PKCδ, among PKC isoforms, is preferentially activated in TICs and acts as a critical regulator for the maintenance of TICs in glioblastoma. By modulating the expression levels or activity of PKCδ, we demonstrated that PKCδ promotes self-renewal and tumorigenic potentials of TICs. Importantly, we found that the activation of PKCδ persists in TICs through an autocrine loop with positive feedback that was driven by PKCδ/STAT3/IL-23/JAK signaling axis. Moreover, for phenotypes of TICs, we showed that PKCδ activates AKT signaling component by phosphorylation specifically on Ser473. Taken together, we proposed that TICs regulate their own population in glioblastoma through an autocrine loop with positive feedback that is driven by PKCδ-dependent secretion of cytokines.

Vitamin D receptor polymorphism is associated with psoriasis.

Vitamin D receptor is a trans-acting transcriptional factor that mediates 1alpha,25-dihydroxyvitamin D3 action in the regulation of target gene expression. Recent studies have shown that clinical response of psoriasis to 1alpha,25-dihydroxyvitamin D3 is correlated with the vitamin D receptor mRNA expression level, which may be influenced by the genotype of the vitamin D receptor. In this study, we have explored a possible association between psoriasis and the polymorphism in the gene encoding the vitamin D receptor. We examined the allelic frequencies of the vitamin D receptor in psoriasis patients (n = 104) and in healthy controls (n = 104) by analyzing the restriction pattern of the polymerase chain reaction products. A significant increase in the frequency of the A allele (absence of the restriction site at intron 8) by ApaI restriction fragment length polymorphism was observed in psoriasis patients compared with that of the control group, and the tendency was more accentuated in early onset psoriasis. Odds ratios (95% confidence interval) for psoriasis of AA and Aa genotypes were 5.0 (1.3-19.1) and 2.4 (1.3-4.3), and odds ratios for early onset of AA and Aa genotypes were 6.4 (1.6-25.0) and 3.1 (1.7-5.9), respectively. Allele frequencies for A and a alleles were 0.317 and 0.683 in the psoriasis group and 0.168 and 0.832 in the control group (p = 0.001). A significant association between vitamin D receptor genotypes and the mean age at onset was observed (p < 0.05). Our findings suggest that allelic variance in the vitamin D receptor gene itself or other genes in linkage disequilibrium with this gene, could predispose to the development of psoriasis.

Human trichohyalin gene is clustered with the genes for other epidermal structural proteins and calcium-binding proteins at chromosomal locus 1q21.

Trichohyalin is a major differentiation product of hard keratinizing tissues such as the inner root sheath and medullary cells of the hair follicle and the filiform papillae of the tongue, as well as terminally differentiating epidermal cells. It consists largely of quasi-repeating peptide repeats and functions primarily as an intermediate filament-associated protein in these tissues. By mapping with human-rodent somatic cell hybrids and fluorescent in situ hybridization, we demonstrate that its gene maps to chromosomal region 1q21. Interestingly, genes encoding several other structural proteins expressed during terminal differentiation in the epidermis map to this region, as do also several members of the S-100 class of small calcium-binding proteins.

Structure and organization of the human transglutaminase 3 gene: evolutionary relationship to the transglutaminase family.

The human haploid genome contains a family of at least five different transglutaminases that are differentially expressed in time- and tissue-specific ways. Of these, transglutaminase 3 (TGase3) is unusual in that it is a pro-enzyme requiring activation by proteolysis. To date it is known to be expressed only in terminally differentiating epidermal and hair follicle keratinocytes. In this paper we show that it is encoded by a gene (TGM3) of 42.8 kbp containing 13 exons. In the course of isolation of genomic clones for the TGM3 gene, we also found clones encoding the widely expressed tissue or TGase2 enzyme, perhaps due to high degrees of sequence homology. The structure of the TGM2 gene has not yet been reported. Our incomplete data suggest its exon/intron organization is very similar to that of TGM3. Although the common intron splice points of all members of the transglutaminase gene family have been conserved, the TGM3 and TGM2 genes, and the gene for the subplasma membrane transglutaminase-like protein band 4.2, lack two introns found in the TGM1 and factor XIIIa genes, and the exact intron splice point of another intron is shifted with respect to that of the TGM1 and factor XIIIa genes. Based on sequence homologies and gene structures, the data support a phylogenic tree in which the TGM2 and TGM3 genes belong on a branch distinct from other transglutaminases.

Requirement of intact human ceruloplasmin for the glutathione-linked peroxidase activity.

Structural integrity may be needed for the glutathione-linked peroxidase activity of human ceruloplasmin. Intact human ceruloplasmin has a potent peroxidase property to decompose H2O2 in the presence of reduced glutathione. However, the fragment of approximately 116000 Da produced by proteolytic degradation had less than one-third of the glutathione-linked peroxidase activity of intact ceruloplasmin. When further proteolysis occurred, glutathione-linked peroxidase activity of human ceruloplasmin disappeared. In contrast, ceruloplasmin (116000 Da and <96000 Da) fragmented by proteolysis significantly removed H2O2 irrespective of the presence of reduced glutathione. Although proteolytic fragmentation of ceruloplasmin occurs, the antioxidant activity of ceruloplasmin that prevents DNA strand breaks in a metal-catalyzed reaction system was significantly maintained.

Thiol-linked peroxidase activity of human ceruloplasmin.

Human ceruloplasmin exhibited different antioxidant effects according to the electron donors in a metal-catalyzed oxidation system. Purified ceruloplasmin did not play a significant role in the protection of DNA strand breaks in the ascorbate/Fe3+/O2 system. However, when ascorbates were replaced with a thiol-reducing equivalent such as dithiothreitol, DNA strand breaks were significantly prevented by the same amount of ceruloplasmin. Ceruloplasmin did not catalyze the decomposition of H2O2 in the absence of reduced glutathione. On the contrary, ceruloplasmin showed a potent peroxidase ability to destroy H2O2 in the presence of reduced glutathione. In conclusion, the removal of H2O2 by human ceruloplasmin is not simply stoichiometric but thiol-dependent.

Isolation and characterization of brain-specific transglutaminases from rat.

The relevance of transglutaminases with neural function and several disorders has been emphasized recently. Especially, many polypeptides associated with neurodegenerative diseases are suggested to be putative transglutaminase substrates such as beta amyloid protein of Alzheimer's disease, microtubule-associated proteins and neurofilaments, etc. In addition, the CAG repeated gene products with probable polyglutamine tract, putative transglutaminase substrates, were identified in several neurodegenerative disorders. However, the identity of the brain transglutaminase has not been confirmed, because of enzymic stability and low activity. In the present experiment, we have isolated brain-specific transglutaminases, designated as TGase NI and TGase NII, which are different from other types of transglutaminases in respects of molecular weights (mw. 45 kDa, 29 kDa respectively), substrate affinity, elution profile on ion-exchange chromatography, sensitivity to proteases and ethanol, and immunological properties. The enzymes were localized specifically in the brain tissues but not in the liver tissue. And neural cells such as pheochromocytoma cell, glioma cell, primary neuronal and glial cells were shown to be enriched with TGase NI and TGase NII. The possible biological roles of the enzymes were discussed not only on the aspect of crosslinking activity but also of signal transducing capacity of the enzyme in the brain.

Aging process is accompanied by increase of transglutaminase C.

Crosslinking has been suggested as one of the mechanisms involved in the aging process. Among the various random or enzyme-mediated crosslinking reactions, transglutaminase (TGase)-catalyzed crosslinking activity has been proposed for its possible involvement in cell proliferation, differentiation, carcinogenesis, programmed death, and aging. Moreover, recent findings of TGase C as a putative signal transducer and cell cycle regulator has renewed interest in the study of TGase C in relation to aging phenomena. The ubiquitous presence of TGase C compared to the organ-specific localization of other types of TGases has attracted special attention as a cellular aging device. In the present investigation for in vitro studies, we have compared the pattern of TGase C in young and old human red blood cells, separated by density differentiation, and in early and late-passage or hydrogen peroxide-treated human primary fibroblasts. For in vivo study, we monitored the age-dependent changes of TGase C in the liver and brain tissues of 4, 12, 18, and 24-month-old Sprague-Dawley rats. We obtained evidence that both the activity and protein levels of TGase C were high in old RBC and late-passage or hydrogen peroxide-treated fibroblasts. Similar findings were seen in liver and brain tissue such as age-dependent increases in TGase activity and protein level in an organ-specific pattern. These data suggest that TGase C might play an active role in the cellular process with age.

Identification of genetic factors altering the SOS induction of DNA damage-inducible yebG gene in Escherichia coli.

The yebG gene of Escherichia coli is a novel SOS regulon gene, but details of its regulation mechanism and biological function are not yet known. To characterize the regulation of yebG gene as a SOS gene, we identified the genetic factors affecting the SOS induction of yebG gene using yebG-lacZ operon fusion plasmid. We found that the SOS induction of yebG occurs as the cells enter into the stationary growth phase, but its induction is not observed in LB medium in the presence of 1% glucose. A stationary phase SOS induction of the yebG gene does not require the global regulator of stationary phase-specific genes, rpoS, or gyrA functions, but requires cya encoding the adenylate cyclase and hns encoding the histone-like protein H-NS functions. Our results demonstrated that the induction of a DNA damage-inducible yebG gene of E. coli is dependent on cyclic AMP and H-NS.