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N Teich

Publications and source records attributed to N Teich.

35 records · Page 2Linked to original sources
PubMed1999

Screening for mutations of the cationic trypsinogen gene: are they of relevance in chronic alcoholic pancreatitis?

BACKGROUND: In hereditary pancreatitis mutations of exons 2 (N21I) and 3 (R117H) of the cationic trypsinogen gene have been described. AIMS: To investigate whether the same mutations can also be found in patients with chronic alcoholic pancreatitis. METHODS: Leucocyte DNA was prepared from 23 patients with chronic alcoholic pancreatitis, 21 with alcoholic liver cirrhosis, 34 individuals from seven independent families with hereditary pancreatitis, and 15 healthy controls. DNA was also obtained from pancreatic tissue (n=7) and from pancreatic juice (n=5) of patients suffering from chronic alcoholic pancreatitis. R117H was detected by restriction digestion with Afl III. N21I was identified by an allele specific polymerase chain reaction (PCR). RESULTS: R117H was detected in four families with hereditary pancreatitis. The N21I mutation was identified in three families. All mutations were confirmed by sequencing of the corresponding DNAs. In patients with chronic alcoholic pancreatitis neither the exon 2 nor exon 3 mutations were present in blood leucocytes, pancreatic juice, or pancreatic tissue. DNA of the patients with alcoholic liver cirrhosis as well as all controls was of wild type. CONCLUSIONS: The allele specific PCR may be used to screen for the N21I mutation of cationic trypsinogen. Both trypsinogen mutations were found in hereditary pancreatitis but do not seem to be major pathogenic factors in chronic alcoholic pancreatitis.

Adult↗
PubMed1998

Mutations of the cationic trypsinogen in hereditary pancreatitis.

Hereditary pancreatitis (OMIM 167800) is thought to be associated with a mutation of the exon 3 of cationic trypsinogen (Nature Genet (1996): 14:141-145). This paper reports sequence data of two independent families suffering from this disease. PCR amplificates from leukocyte or buccal swab DNA showed no mutation of exon 3 of cationic trypsinogen. Instead, in exon 2, an A-to-T tranversion was found that led to the substitution of Asn by Ile in the sixth amino acid of the active trypsin. In exons 4 and 5, silent mutations were found. In the other expressed trypsinogens, several homozygous alterations not associated to hereditary pancreatitis were identified. As a model of pathogenesis, we hypothesize that mutation of trypsinogen in exon 2 could lead to premature cleavage of the activation peptide of trypsinogen or to altered intracellular transport.

Base Sequence↗
PubMed1998

A comparison of lipase and amylase in the diagnosis of acute pancreatitis in patients with abdominal pain.

The clinical value of amylase and lipase measurement for the diagnosis of acute pancreatitis was evaluated in 253 patients presenting with acute abdominal pain. Acute pancreatitis was detected in 32 patients by computed tomography or ultrasound. In the serum samples collected on days 0-1 after the onset of symptoms, lipase was elevated in 100% and amylase in 95%. A 95% sensitivity/specificity was reached at a lipase cutoff near twofold above normal. The receiver-operating characteristics (ROC) showed similar curves for both enzymes, lipase being slightly superior to amylase. The ROC curves from days 2-3 demonstrated a much lower sensitivity/specificity of both enzymes. Lipase, however, was notably superior to amylase: at a sensitivity of 85% the specificity of lipase (amylase) was 82% (68%). In samples from days 4-5 the accuracy of the enzyme assays was even worse; at a sensitivity of 60% the specificity did not increase above 70%. The diagnostic value of simultaneous measurement of amylase and lipase was tested at different cutoffs in two groups: the OR group, in which one of the two parameters had to be elevated, and the AND group, in which both parameters had to be above normal. Combination of both parameters mainly improved the specificity of the assay (from 91 to 98% on days 2-3 and from 93 to 97% on day 4-5) but only when, in the OR group, twofold elevated amylase was combined with lipase. We conclude that the simultaneous determination of serum lipase and amylase marginally improved the diagnosis of acute pancreatitis in patients with acute abdominal pain, however, the sensitivity of the assay with samples collected 4-5 days after onset of the disease remained low.

Abdominal Pain↗
PubMed1997

Polyclonal pancreatic elastase assay is superior to monoclonal assay for diagnosis of acute pancreatitis.

We compared the clinical values for diagnosis of acute pancreatitis of two commercial assays for pancreatic elastase: an ELISA procedure with monoclonal antibodies and a RIA technique with polyclonal antibodies. In 14 patients with acute pancreatitis, serum concentrations of elastase determined by ELISA (ELISA-elastase) decreased much faster (half-life 0.4 days) than those of elastase determined by RIA (RIA-elastase) (2.2 days), amylase (0.8 days), or lipase (0.9 days). Serum samples from 253 additional patients with abdominal pain (32 of these with acute pancreatitis) were analyzed. In sera collected up to 48 h after the onset of disease, the ROC curves showed a slightly higher diagnostic value of RIA-elastase. In samples taken later, at a sensitivity of 90% the specificity of RIA-elastase was 95% (ELISA-elastase 40%). We conclude that serum ELISA-elastase is of much lower clinical value than RIA-elastase for diagnosis of acute pancreatitis.

Abdomen, Acute↗
PubMed1986

Postnatal development of pulmonary alveoli: modulation in rats by thyroid hormones.

We studied the effect of thyroid hormones on the postnatal development of the gas exchange region of rat lungs. Treatment with triiodothyronine (T3, 0.1 microgram . g body wt-1 . day-1) accelerated the increase of the surface-to-volume ratio (S/V) and surface area (Sa) and decrease of the mean chord length (Lm) of the gas exchange structures of pups killed at age 7 days. Propylthiouracil (PTU, 100 micrograms twice daily) from age 1 to 13 days, with death at age 14 days, diminished the rise of S/V and Sa and the fall of Lm compared with diluent-injected pups. Providing drinking water with 0.01% PTU to dams from gestation day 20 (term 22 days) to postnatal day 14 also diminished the rise of S/V and fall of Lm. Treatment of pups nursed by dams drinking 0.01% PTU with thyroxine (0.1 microgram/g body wt) every other day from age 1 to 13 days significantly diminished the effect of PTU on S/V, Sa, and Lm. We conclude thyroid hormones can modulate the postnatal architectural development of the gas exchange region of the rat lung.

Animals↗
PubMed1985

Postnatal development of alveoli. Regulation and evidence for a critical period in rats.

In many species, including humans, pulmonary alveoli are formed after birth by septal subdivision of the large gas-exchange saccules present at birth. In rats septation occurs mainly between the 4th and 14th postnatal days (Burri, P. H. 1974. Anat. Rec. 180:77-98), but little is known about the regulation of this process. We found that dexamethasone (0.1 micrograms daily) given to rats from age 4 to 13 d markedly impaired saccule septation to at least age 60 d and also diminished the extent of the increase of alveolar surface area (Sa). Underfeeding from birth to age 14 d did not diminish saccule septation but did result in diminished Sa. We conclude dexamethasone-treated rats have a critical period during which the gas-exchange saccules present at birth must be subdivided. Since Sa increased in dexamethasone-treated rats without a change in alveolar size, and, the enlargement of Sa was diminished in underfed rat pups without a deficit of saccule septation, we postulate new alveoli were formed by means other than septation of the large gas-exchange saccules present at birth. Furthermore, these various means of forming alveoli, and hence of increasing Sa, were differently regulated: dexamethasone decreased the enlargement of Sa brought about by both septation of the gas-exchange saccules present at birth and by other, as yet unidentified, means of forming alveoli; underfeeding did not diminish Sa increases produced by saccule septation but did decrease the extent of Sa enlargement due to the other means of forming alveoli.

Animals↗
PubMed1981

Expression of resistance to Friend virus-stimulated erythropoiesis in bone marrow chimeras containing Fv-2rr and Fv-2ss bone marrow.

Bone marrow chimeras were formed containing mixtures of DBA/2 (Fv-2ss, Hbbdd) and B10.D2 (Fv-2rr, Hbbss) bone marrow. When these mice were infected with the polycythemia-inducing strain of Friend virus, erythropoiesis was stimulated, but the proportion of B10.D2 hemoglobin fell rapidly and newly synthesized hemoglobin was essentially all of the DBA/2 type. The treatment of infected polycythemic chimeras with phenylhydrazine lowered the hematocrit and restored the synthesis of B10.D2 hemoglobin. These results imply that B10.D2 erythroid precursors are intrinsically resistant to Friend virus-stimulated erythropoiesis. The experiments also suggest that virus-stimulated erythropoiesis is not mediated by a factor or cell-cell interactions, unless such factors or interactions do not act across strain barriers.

Alleles↗
PubMed1981

Partial maturation and light chain restriction of Abelson virus-transformed B cell precursors.

The induction of partial maturation in an in vitro derived Abelson virus-transformed murine lymphoid cell subline (ABC-1/AT1) is described. Pre-B (cytoplasmic, mu chain-positive) lymphocytes were induced from presumptive B cell precursors by prostaglandin E1, butyric acid, lipopolysaccharide and interferon. Maturation was independent of alterations in cellular growth rate and could be achieved in the absence of cell division. The AT1 subline was found to be restricted to the expression of a single light chain type (lambda) indicating a possible B cell lineage-committed precursor as the target for viral transformation.

Abelson murine leukemia virus↗
PubMed1972

Some implications of the activation of murine leukemia virus by halogenated pyrimidines.

Genetic information of murine leukemia viruses is known to be present in essentially all mice. Delineation of the biological effects of the expression of this genetic information is complicated by the difficulty in determining whether the presence of a viral antigen in a tissue is the result of gene activation that occurs independently in a large number of cells, proliferation of antigen-positive cells, or of spread of infectious virus from a few cells. This problem is further complicated by the difficulty in determining whether activation of virus genetic material is the cause or result of a biological phenomenon, such as malignancy. Further understanding of the activation of virus genes in normal cells is of great importance in answering these questions. In vitro techniques were used for the study of induction of virus. Virus-negative cell lines were established from embryos of AKR mice, which in vivo produce high titers of infectious murine leukemia virus. It was found that 5-iododeoxyuridine and 5-bromodeoxyuridine were potent inducers of virus synthesis in all clones and subclones of the AKR cells tested. In addition to establishing that the complete viral genome is a heritable component of all cells of the AKR mouse, these studies of virus activation provide novel approaches to a number of important problems in the biology of leukemia viruses.

Animals↗
PubMed1971

Murine leukemia virus: high-frequency activation in vitro by 5-iododeoxyuridine and 5-bromodeoxyuridine.

Cells of embryos of the high leukemic mouse strain AKR can be grown in culture as virus-negative cell lines. However, these lines and clonal sublines uniformly have the capacity to initiate synthesis of murine leukemia virus. Exposure of the cells to 5-iododeoxyuridine or 5-bromodeoxyuridine induced synthesis of virus in as high as 0.1 to 0.5 percent of the cells; many of the cells were producing virus as soon as 3 days after initiation of treatment. Induction of virus by these drugs is several orders of magnitude greater than that obtained with any other treatment tested. These studies indicate that the full genome of murine leukemia virus is present in an unexpressed form in all AKR cells and provide a potentially powerful technique for activating leukemia virus genomes in other cell systems.

Animals↗