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Biomedical subjects

S Schwarz

Publications and source records attributed to S Schwarz.

At least 163 records · Page 9Linked to original sources

The promoters for human and monkey poliovirus receptors. Requirements for basic and cell type-specific activity.

The cellular receptors for poliovirus (PVR) are glycoproteins belonging to the immunoglobulin superfamily. Functional receptors for poliovirus are only expressed by primates; known rodent homologues lack the ability to bind virus due to amino acid differences. Human poliovirus infections are targeted to the gastrointestinal tract and, rarely, to motor neurons in the central nervous system. Available evidence suggests that poliovirus uses only one cellular receptor, implying that the tissue tropism of poliovirus is likely to be related to the expression of the human PVR (hPVR). However, low levels of expression of hPVR-specific mRNAs can be detected in many human tissues other than the apparent target cells. The nonpathogenic function of hPVR is unknown. For a study of the transcriptional control of hPVR expression, we have isolated and characterized the promoter of the hPVR gene. Deletion analysis defined an approximately 280 base pair minimal promoter fragment that: 1) lacks TATA- and CAAT-like elements, 2) is distinguished by a high GC content, and 3) promotes transcription at multiple start sites. The pattern of activity caused by transfection of serial 5'- and 3'-promoter deletions is almost identical in HEp2, HeLa, COS-1, and mouse L929 cells, indicating a similar transcriptional regulation of the hPVR promoter in these cell lines. However, on transfection of Raji cells, a Burkitt's lymphoma cell line harboring a transcriptionally inactive hPVR gene, all promoter reporter constructs tested exerted only residual activity. These results suggest that the cis-element(s) governing cell type-specific hPVR expression resides in the minimal promoter region. We also report the sequences of the promoters of two monkey homologues to hPVR (AGMalpha1 and AGMalpha2). Transcripts encoding the monkey poliovirus receptors originate from a region analogous to that identified for hPVR transcripts.

Animals↗

CR1, CD35 in synovial fluid from patients with inflammatory joint diseases.

OBJECTIVE: To investigate synovial fluid (SF) for the presence of CR1 and to study its relationship to SF leukocytes and to serum levels of soluble CR1 (sCR1) in patients with rheumatic diseases. METHODS: Synovial fluids were collected from 35 patients with rheumatoid arthritis (RA) and 26 patients with other inflammatory joint diseases. Total CR1 in the SF and serum were measured with a sandwich enzyme-linked immunosorbent assay (ELISA) that recognized both soluble and transmembrane forms of CR1. The characteristics of CR1 in SF were analyzed by ultracentrifugation and by a second ELISA specific for transmembrane CR1. RESULTS: CR1 was found in all SF samples tested (range 5-281 ng/ml). SF CR1 was higher in patients with RA (mean +/- SD 81 +/- 66 ng/ml) than in those with other inflammatory joint diseases (31.8 +/- 23.8 ng/ml) (P < 0.001). Serum sCR1 was not significantly increased in the patients compared with the normal subjects. There was no correlation between serum sCR1 and SF CR1. In 44% of the patients, the SF CR1 level was higher than the serum sCR1 level. A fraction (30-80%) of SF CR1 was pelleted by ultracentrifugation and, unlike serum sCR1, it reacted in an ELISA specific for transmembrane CR1. Thus, SF contained 2 forms of CR1: a membrane-associated and a soluble form, which was confirmed by sucrose density-gradient ultracentrifugation. SF CR1 levels correlated directly with the number of SF total leukocytes and polymorphonuclear leukocytes (PMN). These 2 forms of CR1 were also found in the supernatant of in vitro-activated PMN from normal subjects. SF CR1 exhibited the capacity to act as a cofactor for the factor I degradation of C3b. CONCLUSION: CR1 is found in the SF of patients with joint inflammation. The data suggest that SF CR1 originates from the infiltrating leukocytes, which shed both a soluble and a membrane-associated form. Whether SF CR1 participates in the local regulation of complement activation remains to be examined.

Arthritis↗

Haematoma evacuation does not improve outcome in spontaneous supratentorial intracerebral haemorrhage: a case-control study.

Surgical intervention in supratentorial intracerebral haemorrhage (ICH) is still controversial. We assessed the value of haematoma evacuation with a case-control study. 145 consecutive patients with supratentorial spontaneous ICH without tumour or vascular abnormalities were analysed. Haematoma evacuation was performed in 24 patients. Age, sex, Glasgow Coma Scale (GCS), level of consciousness, pupillary reaction on admission, localisation, aetiology and volume of the haematoma, presence of ventricular blood, and Glasgow Outcome Scale (GOS) on discharge were analysed. From statistical analysis 40 patients > 80 years and with haematoma volume < 10 ml, who were always treated conservatively, were excluded. Prognostic factors retained from a multiple regression model with the dichotomised GOS scale (GOS 1-3, 4 + 5) as response variable were GCS, haematoma volume and location. The only difference between all medically treated and "operated" patients was haematoma volume, which was larger in the "operated" patients. All 24 evacuated cases could be matched to a medically treated control regarding age, haematoma volume and location, GCS, and pupillary reaction. Significant differences between the two groups could not be detected. Outcome was not different between the two groups. After separating the sample into patients with and without ventricular haemorrhage, there was no different outcome between the two groups either. We conclude that haematoma evacuation did not improve outcome in supratentorial spontaneous ICH. Since haematomas were evacuated mainly in clinically deteriorating patients, our data suggest that the only effect of haematoma evacuation is to stop progressive deterioration rather than to improve overall clinical outcome.

Adult↗

[Infection: impaired consciousness as the initial symptom. Clinical and pathophysiologic aspects of septic encephalopathy].

Septic encephalopathy (SE) is present in up to 70% of all patients with sepsis. In some cases, SE may proceed other parameters of sepsis. Loss of consciousness to a various extent is the leading symptom. CSF findings and CCT are usually unremarkable. EEG is a sensitive parameter to monitor SE. EEG-changes deteriorate in correspondence to the degree of SE. If sepsis can be treated successfully, clinical and electrophysiological signs are completely reversible. SE has a complex etiology. Bacterial endotoxins and other microbial products trigger the release of a multitude of mediators of sepsis. Due to liver dysfunction in sepsis, the brain neurotransmitter profile may be deranged. Other etiological factors include bacteriemia, liver or renal dysfunction, fluid and electrolyte imbalance, hypoglycemia and drug effects. Due to the prognostic significance of early adequate treatment, recognition of SE as a possible initial sign may be crucial for patients with sepsis.

Aged↗

[Neurogenic disorders of heart and lung function in acute cerebral lesions].

Incidence and clinical significance of cardiopulmonary complications of acute cerebral lesions are still unclear. Neurogenic pulmonary edema (NPE) is characterized as an acute, protein-rich lung edema occurring shortly after cerebral lesions associated with an acute rise of intracranial pressure. NPE is infrequently diagnosed, usually in association with head trauma. Pathophysiological mechanisms include a rise of the pulmonary vascular hydrostatic pressure either due to sympathetic innervation with pulmonary vasoconstriction or increased left-atrial pressure following systemic arterial hypertension or an increase in pulmonary capillary permeability. In contrast to NPE, cardiac complications are frequently observed, most consistently in patients with subarachnoid hemorrhage. Typical ECG changes are repolarization abnormalities, similar to those observed in coronary heart disease, and cardiac arrhythmias. The CK-MB may be slightly elevated; echocardiographic findings show a depressed left-ventricular function. Pathological examination reveals myofibrillar necrosis. Cardiac complications are explained with overactivity of the sympathetic innervation and high levels of circulating catecholamines. For adequate treatment, close cardiac monitoring is required in all patients with acute cerebral lesions.

Arrhythmias, Cardiac↗

Influence of subchronic administration of oestradiol, ethinyloestradiol and oestradiol sulphamate on bile flow, bile acid excretion, and liver and biliary glutathione status in rats.

The cholestatic effect of the newly developed oestradiol sulphamate (J995) was compared with that of the natural oestrogen oestradiol (E) and of the cholestatic standard oestrogen ethinyloestradiol (EE). Female ovariectomized rats were orally treated for 7 days with oestrogen doses molar equivalent to 0.01, 0.1, 1, and 10 mg E/kg body wt. Bile flow, biliary bile acid and glutathione excretion as well as liver glutathione status were determined after bile duct cannulation under the influence of ketamine anaesthesia. For systemic oestrogen activity, the increase of uterine weight was measured. J995 showed the highest oestrogenic activity followed by EE and E. Impairment of bile flow and biliary glutathione excretion (GSH, GSSG) were found to be in the order E < J995 < EE. As all three oestrogens did not influence bile acid excretion, we postulate that mainly the bile acid-independent fraction of bile flow was inhibited, caused at least partly by impairment of canalicular glutathione transport. Based on the results of these studies, we conclude that a tenfold higher dose of J995 exhibited the same cholestatic effect as EE. Together with higher systemic oestrogenic activity, J995 may be used as a prodrug with reduced hepatic side-effects to replace EE in contraception strategies.

Animals↗

Novel "scavestrogens" and their radical scavenging effects, iron-chelating, and total antioxidative activities: delta 8,9-dehydro derivatives of 17 alpha-estradiol and 17 beta-estradiol.

Antioxidant effects of delta 8,9-dehydro derivatives of 17 alpha-estradiol and 17 beta-estradiol were investigated using four different in vitro models: rat synaptosomal lipid peroxidation induced by Fenton's reagent, Fe(II)-chelating activities, the formation of superoxide anion radicals, and total antioxidative activities. The parent molecules, 17 alpha-estradiol and 17 beta-estradiol as well as estrone and estriol inhibit iron-dependent lipid peroxidation and stimulate total antioxidant activity. In contrast, delta 8,9-dehydro estrogens such as J811, J861, J835, or J851 not only exhibit the antioxidative activities as the parent molecules do but also directly alter the iron redox chemistry and drastically inhibit the formation of superoxide anion radicals generated by a xanthine/xanthine oxidase-dependent luminescence reactions. These in vitro findings indicate that 17 alpha-estradiol as well as 17 beta-estradiol, modified with an additional double bond in the basic structure, trigger more potent antioxidant properties. These results suggest that relatively minor modifications in the chemical structure of estrogenic compounds can enhance antioxidative actions.

Acridines↗

Novel estrogens and their radical scavenging effects, iron-chelating, and total antioxidative activities: 17 alpha-substituted analogs of delta 9(11)-dehydro-17 beta-estradiol.

Antioxidant effects of N,N-dimethyl-p-toluidine, p-cresol, and p-(hydroxy)thioanisol 17 alpha-substituted analogs of 17 beta-estradiol and their delta 9(11)-dehydro homologs were investigated using four different in vitro models: rat synaptosomal lipid peroxidation induced by Fenton's reagent, Fe(II)-chelating activities, the formation of superoxide anion radicals, and total antioxidative activity. Whereas the classical estrogen 17 beta-estradiol as well as selected phenolic compounds was only moderately inhibiting iron-dependent lipid peroxidation and stimulating total antioxidative activity, besides delta 9(11)-dehydro-17 beta-estradiol (J 1213), novel estrogens such as C-17-oriented side chain analogs of 17 beta-estradiol (J 843, J 872, and J 897) and delta 9(11)-dehydro homologs (J 844, J 864, and J 898) directly altered the iron redox chemistry and diminished the formation of superoxide anion radicals generated by a xanthine/xanthine oxidase-dependent luminescence reaction to a great extent. These results suggest that definite modifications in the chemical structure of 17 beta-estradiol, e.g., the introduction of a delta 9(11)-double bond and/or p-cresol as well as p-(hydroxy)thioanisol C-17 substitution, may result in substantial changes in their antioxidant behavior. These compounds may be drug candidates for treating pathologies related to free radical formation.

Animals↗

Molecular analysis of naturally occuring ermC-encoding plasmids in staphylococci isolated from animals with and without previous contact with macrolide/lincosamide antibiotics.

A total of 16 epidemiologically unrelated macrolide-resistant staphylococcal isolates of various animal origins were investigated for the molecular basis of macrolide resistance with respect to previous contact of their host animals with macrolides and lincosamides. All isolates carried ermC-encoding plasmids of 2.3-4.0 kbp. The eight plasmids of staphylococci from animals which had not received macrolides or lincosamides showed inducible ermC gene expression and did not exhibit alterations in the ermC regulatory region. The remaining eight plasmids expressed the ermC gene constitutively. Six of these plasmids were from staphylococci from animals which had received tylosin or spiramycin as feed additives or lincomycin for therapeutic purposes. All constitutively expressed ermC genes revealed either sequence deletions or sequence duplications in their ermC regulatory region, as detected by a PCR assay and by sequence analysis. These sequence deletions and duplications found in naturally occurring plasmids corresponded closely to the mutations seen in the ermC-encoding plasmids after growth of an inducibly resistant strain in the presence of non-inducing macrolides or lincosamides under in vitro conditions.

Amino Acid Sequence↗

Acute and critical care in neurology.

The diagnostic and therapeutic management of selected neurological diseases requiring intensive treatment is summarized with special regard for current standards and new developments in therapy. Ischemic stroke is an emergency since the outcome can be improved by immediate and adequate general supporting as well as specific (thrombolytic) therapy in specialized stroke units. Surgical evacuation of supratentorial intracerebral hemorrhage is still controversial. We give an overview of conditions in which surgical therapy such as cerebellar hemorrhage and large, nondominant ganglionic hemorrhage might be advisable. Cerebral venous thrombosis is treated with full-dose intravenous heparin even if hemorrhage is present. In acute bacterial meningitis, early treatment of foci and empiric antibiotic therapy is crucial in order to prevent complications. The outcome of herpes simplex encephalitis can be favorably influenced by treatment with aciclovir and aggressive therapy of elevated ICP and seizures. Acute Guillain-Barré syndrome requires daily monitoring of vital functions in order to recognize the need for intensive care; intravenous immunoglobulins and plasmapheresis are equally recommended for clinical and financial reasons.

Acute Disease↗

Barbiturate coma in severe hemispheric stroke: useful or obsolete?

Barbiturates are administered in a variety of clinical conditions to control elevated intracranial pressure (ICP). However, their routine use to treat elevated ICP has been questioned because it may cause severe side effects. We therefore investigated the effect of high-dose barbiturate therapy on ICP and outcome in patients with severe brain edema after severe middle cerebral artery (MCA) or hemispheric infarction. Barbiturate coma was induced with thiopental infusion in 60 patients with critically increased ICP due to large hemispheric or MCA territory infarction, defined by CT. ICP was monitored in all patients during barbiturate therapy. Barbiturate coma was induced after a standardized treatment protocol for increased ICP after failure of osmotherapy and mild hyperventilation. During barbiturate administration, cerebral perfusion pressure (CPP) and mean arterial pressure were recorded. Clinical outcome of these patients and the individual effect on ICP were analyzed. Only five of 60 patients who were treated with barbiturate coma survived (8%). All other patients died after transtentorial herniation with subsequent brain death. Barbiturate infusion was followed by a drop in ICP in 50 patients and showed no effect on ICP values in 10 patients. CPP decreased with a mean of 9 mm Hg (range, 5 to 20 mm Hg). Although barbiturates were initially effective, only in some patients was ICP control sustained. Severe side effects of barbiturate therapy, besides arterial hypotension, were seen in 15 patients (25%). Barbiturate coma in the therapy of increased ICP after severe ischemic hemispheric stroke can lower critically elevated ICP levels. However, it seems to have no positive effect on neurologic outcome.

Adult↗

Basilar artery embolism. Clinical syndrome and neuroradiologic patterns in patients without permanent occlusion of the basilar artery.

The objective of this study was to clarify the clinical and radiologic features, risk factors, and prognosis of basilar embolism without permanent basilar artery occlusion. Forty-five patients (mean age, 59 years) with basilar artery embolism participated in the study. Patients with basilar artery occlusion were excluded. The Glasgow Coma Scale (GCS) score on admission was < 7 in five patients, 7 to 12 in 11 patients, and > 12 in 29 patients. Etiologic factors were cardiac arrhythmia (17 patients), vertebral artery occlusion (12 patients), cervical spine trauma (4 patients), embolism following angiography (2 patients), and surgery (1 patient). MRI was performed in 17 patients and CT in 39 patients. Radiologic examinations were initially normal in 14 patients and remained normal in three patients. Final infarct localization was the thalamus (36 patients), cerebellum (20 patients), posterior cerebral artery territory (21 patients), midbrain (12 patients), and pons (8 patients). Eight to 12 weeks after stroke 12 patients were without clinical signs (Glasgow Outcome Scale [GOS] 1), 15 patients had minor neurologic deficits (GOS 2), 10 were severely disabled (GOS 3), and eight patients had died (GOS 5). Outcome correlated with GCS on admission (p < 0.0001) and with the number of ischemic lesions (p = 0.0001). The typical syndrome is an acute loss of consciousness followed by multiple brainstem symptoms. Usually, clinical symptoms improve rapidly and, in some patients, completely. Compared with basilar occlusion, basilar embolism has a relatively low mortality and outcome is frequently excellent.

Adult↗

Induction of apoptosis in Kaposi's sarcoma spindle cell cultures by the subunits of human chorionic gonadotropin.

OBJECTIVES: Elucidation of the mechanisms of the previously shown growth-inhibitory action of human chorionic gonadotropin (hCG) on Kaposi's sarcoma (KS) cells and the role of the luteinizing hormone/hCG receptor (hCGR). DESIGN AND METHODS: Analysis of KS tissues and cultured spindle-type KS cells for the presence of the hCGR using 125I-hCG binding and reverse transcriptase-polymerase chain reaction; analysis of several hCG preparations (urinary, recombinant, isolated alpha and beta subunits); analysis of apoptosis mechanisms by several assays including using z-Val-Ala-Asp-fluoromethylketone (zVAD-FMK), a known apoptosis-inhibitory drug. RESULTS: First, we found that some urinary preparations of hCG (e.g., CG-10, Steris Profasi) were indeed KS-killing but others (such as Pregnyl, Choragon, Serono Profasi) were not. Secondly, recombinant subunits (alpha as well as beta) of hCG were KS cell-killing but recombinant intact hCG was not. Thirdly, the hCGR message and protein were undetectable in KS. Fourthly, CG10-induced cell death occurred by apoptosis and KS cells could be rescued by preincubation with zVAD-FMK. Finally, we also found that normal peripheral blood lymphocytes (PBL) were killed by CG-10. CONCLUSION: It is proposed that the action of subunits or subunit fragments of hCG, mediated by a putative orphan receptor (as opposed to the hCGR) and executed by interleukin-1-converting enzyme (ICE)-like protease(s), constitutes a novel apoptosis mechanism effective towards KS cells, but PBLs and possibly other cells as well. These results provide a basis for testing in vitro the therapeutic efficacy of hCG preparations which, in turn, should improve current clinical trials with 'hCG' in patients who have KS.

Amino Acid Chloromethyl Ketones↗

Inflammatory bowel disease and immune thrombocytopenic purpura: is there a correlation?

Different hematologic abnormalities are often encountered in patients with inflammatory bowel disease. Among them anemia, leukocytosis, and thrombocytosis are commonly seen. Leukopenia and thrombocytopenia are observed mostly as a side effect of therapy, particularly with use of immunosuppressive drugs. Immune thrombocytopenic purpura is rarely reported in association with inflammatory bowel disease. We present two cases with combination of these entities along with a literature review and treatment options. Immune thrombocytopenic purpura in these patients presented as an extraintestinal manifestation of inflammatory bowel disease mediated by a disturbance of the immune system.

Adolescent↗

[Resistance to protein biosynthesis inhibitors in Staphylococci: resistance genes and their spread--a review].

The rapid spread of antibiotic resistances in a wide variety of bacteria is mainly due to the location of antibiotic resistance genes on mobile genetic elements such as plasmids and transposons. Principal ways of transfer of plasmid- and transposon-encoded resistance genes are presented using examples of the predominant genes mediating resistances to protein biosynthesis inhibitors such as tetracyclines, aminoglycosides, macrolide-lincosamide-streptogramin B antibiotics, and chloramphenicol in staphylococci. Transfer between different staphylococcal cells is substantially based on transduction, transformation, conjugation and mobilization while transfer of resistance genes within the same bacterial cell often includes interplasmidic recombination events and chromosomal integration of resistance plasmids or transposons. The abilities of the transferred resistance plasmids or transposons to integrate or to be integrated into DNA molecules, plasmids or chromosomal DNA, of the new host cell are of major importance to circumvent strain-, species- or genusspecific barriers such as restriction/modification systems, plasmid incompatibilities or deficiencies of plasmid replication which may limit efficient resistance gene transfer.

Anti-Bacterial Agents↗

Immunochemical mapping of gonadotropins.

As a glycoprotein hormone, human chorionic gonadotropic (hCG) is not a single molecular entity but this term rather comprises an array of molecular variants such as hCG, hCG beta, hCGn, hCG beta n, hCG beta cf, -CTPhCG, hCG beta CTP, deglyhCG, asialohCG, hCGav and the closely related molecules hLH, hLH beta and hLH beta ef. The advent of monoclonal antibodies (MCA), the availability of ultrasensitive detection systems and the recent determination of the crystal structure of hCG, made it possible to design special purpose diagnostic and clinical research immunoassays for hCG-like molecules. For more than a decade we and others have tried to refine epitope maps for hCG and related molecules by means of a large panel of MCA, naturally occurring metabolic variants of hCG (hCGn, hCG beta, hCG alpha, hCG beta cf, hCG beta CTP), homologous hormones and subunits of various species (e.g. hLH, hLH beta, hFSH, hTSH, oLH, rLH beta), chemically modified molecules (deglyhCG, asialohCG, tryptic and chymotryptic hCG beta and hCG alpha fragments) and synthetic peptides (octapeptides and longer). It appeared that all epitopes on molecular hCG-variants recognized by our MCA are determined by the protein backbone. Except for the two major epitopes on hCG beta CTP and parts of two antigenic domains on hCG alpha, epitopes on hCG-derived molecules are determined by the tertiary and quarternary structure. Operationally useful descriptive epitope maps were designed including information on assay suitability of antigenic determinants. On this basis we established ultrasensitive time-resolved fluoroimmuno-assays for hCG, hCG and hCGn, hCG beta and hCG beta n and hCG beta cf, hCG alpha and additional assays recognizing different spectra of hCG-variants. Such assay have been applied by us and others to the detection of pregnancy, early pregnancy loss, choriocarcinoma, testicular cancer, other cancers and prenatal diagnosis. However, as the molecular structure of many epitopes utilized in immunoassays of different laboratories was not resolved, comparability of results was not satisfactory. Consequently, attempts were made to compare schematic epitope maps from different research institutions. The situation has been much improved by solving the three-dimensional (3D) structure of hCG. It has been shown that hCG is a member of the structural superfamily of cystine knot growth factors like NGF, PDGF-B and TGF-beta. Each of its subunits is stabilized in its topology by three disulfide bonds forming a cystine knot. Moreover, it turned out that the disulfide bridges in their majority have previously been wrongly assigned. Computer molecular modeling of crystallographic coordinates of hCG and subsequent selective combined--PCR-based and immunological--mutational analyses of hCG beta expressed via the transmembrane region of a MHC molecule made it possible to more precisely localize epitopes on hCG-derived molecules. Although the entire surface of hCG has to be regarded as potentially immunogenic there seems to be hot spots where epitopes are clustered in antigenic domains. These are located on the first and third loops protuding from the cystine knots of both subunits and are possibly centered around the knot itself. Ultimate answers on epitope localizations will be given by the crystal structure determination of hCG complexed with different Fabs.

Amino Acid Sequence↗

Cloning of human ubiquitin-conjugating enzymes UbcH6 and UbcH7 (E2-F1) and characterization of their interaction with E6-AP and RSP5.

E6-AP, a 100-kDa cellular protein, was originally identified through its interaction with the E6 protein of the oncogenic human papillomavirus types 16 and 18. The complex of E6-AP and E6 specifically interacts with p53 and mediates ubiquitination of p53 in concert with the E1 ubiquitin-activating enzyme and the E2 ubiquitin-conjugating enzyme UbcH5. Recent results suggest that E6-AP is representative of a family of putative ubiquitin-protein ligases. Members of this family are characterized by a conserved C-terminal region, termed hect domain. In this paper, we describe the isolation of two human E2s, designated as UbcH6 and UbcH7, that in addition to UbcH5 can interact with E6-AP. UbcH6 is a novel member of an evolutionally conserved subfamily of E2s that includes UbcH5 and Saccharomyces cerevisiae UBC4. Although UbcH7 does not appear to be a member of this subfamily, UbcH7 efficiently substitutes for UbcH5 in E6-AP-dependent ubiquitination. Surprisingly, UbcH6 was only weakly active in this particular assay. In addition, UbcH5 but not UbcH6 or UbcH7 efficiently interacts with the heet protein RSP5. These results indicate that E6-AP can interact with at least two species of E2 and that different hect proteins may interact with different E2s.

Amino Acid Sequence↗