Biomedical subjects

M Heintzelman

Publications and source records attributed to M Heintzelman.

3 recordsLinked to original sources

PubMed1992

Localization and differential expression of two isoforms of the tight junction protein ZO-1.

ZO-1 is a peripheral membrane protein of approximately 225 kDa located on the cytoplasmic side of all tight junctions. ZO-1 cDNA sequencing disclosed the presence of a 240-bp sequence in only some of the ZO-1 cDNAs studied. This 240-bp region encoded an inframe insertion of 80 amino acids, named motif-alpha. Expression of the predicted transcripts in normal rat and human tissues and in human epithelial cell lines (Caco-2, T84, Hep G2) was shown by reverse transcription of RNA and then DNA amplification. Immunoblot analysis showed both protein isoforms were present; however, in different cell lines, their amounts differed markedly relative to each other. Immunolocalization at light and ultrastructural levels, using antibodies generated against motif-alpha or shared sequences flanking it, indicated both forms localized indistinguishably to tight junctions. These observations demonstrate the existence and variable expression of ZO-1 isoforms and raise the question whether these isoforms contribute to tight junction diversity in different epithelia.

Amino Acid Sequence↗

PubMed1984

Biologic activity in a fragment of recombinant human interferon alpha.

To attempt to locate functionally important regions of the interferon (IFN) molecule, recombinant human IFN-alpha 2 was subjected to proteolytic digestion. The bacterial proteinase thermolysin produced two major complementary fragments, HuIFN-alpha 2-(1-110) and HuIFN-alpha 2-(111-153). After reduction with 2-mercaptoethanol and separation of the two major fragments on NaDodSO4/polyacrylamide gel electrophoresis, antiviral activity persisted in the larger, Mr 12,000, fragment consisting of the amino-terminal 110 amino acids.

Animals↗

PubMed1982

Exercise performance after ventilatory work.

Although increased ventilation is one of the most readily observed physiological responses to exercise, it is uncertain how severely this hyperpnea stresses the ventilatory muscles. As one approach to this question, we compared short-term maximal running performance in nine subjects with and without prior ventilatory work designed to reduce ventilatory muscle endurance. This work consisted of 150 min of sustained maximum ventilation performed isocapnically while the subjects were seated. Both the level of sustained expired minute ventilation and the O2 uptake associated with it slowly declined with time during this 150-min period. On the average, subjects were able to maintain two-thirds of their 12-s maximum voluntary ventilation (MVV) during this long-term breathing test. The test had no effect on subsequently measured vital capacity, forced expiratory volume in 1 s, or the MVV. However, in short-term maximal running, at constant speed upgrades increased 1% each minute until volitional exhaustion, performance after prior breathing work was reduced as compared with control (6.5 vs. 7.6 min; P less than 0.01). Subjects ceased work at significantly lower ventilation (117 vs. 124 1.min-1 BTPS; P less than 0.05) and heart rate (179 vs. 187 beats.min-1; P less than 0.01) and reached significantly lower peak O2 uptake (3.07 vs. 3.24 1.min-1 STPD; P less than 0.05) during maximal running after ventilatory work. We conclude that reduced ventilatory muscle endurance alone is sufficient to decrease short-term maximal running performance.

Adult↗