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N Chang

Publications and source records attributed to N Chang.

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Methylation of the ribosomal proteins in Escherichia coli. Nature and stoichiometry of the methylated amino acids in 50S ribosomal proteins.

Methylated ribosomal proteins from Escherichia coli 50S subunit are localized by growing cells in a medium containing (1-14C)methionine and (3H-methyl)-methionine and comparing the 3H/14C ratio for each of the 50S ribosomal proteins. The following proteins are methylated: L11, L1, L3, L5, L7, L8, L9, L12, L18, and L33. The nature and stoichiometry of the methylated amino acid(s) in each of the methylated proteins are determined. Protein L11 is the most heavily methylated of all the 50S subunit proteins. This protein has previously been implicated in the peptidyl transferase reaction during protein synthesis (K. H. Nierhaus and V. Montejo (1973), Proc. Nat. Acad. Sci. U. S. 47, 1588-1602). Three proteins (L1, L3, and L5) have intermediate levels of methylation and contain about 0.4-0.6 methyl groups each per molecule of protein. Five other proteins (L7, L8, L9, L12, and L18) are also methylated to a slight extent (-0.1 methyl group/molecule of protein). One unknown methylated neutral amino acid was detected in protein L11 and at least one and possibly two other unidentified methylated amino acids appeared to be present in protein L33.

Amino Acids↗

Ovarian steroids directly alter luteinizing hormone (LH) release by pituitary homografts.

The direct role of estradiol and progesterone in sensitizing the adenohypophysis to the releasing action of LHRH (luteinizing hormone-releasing hormone) has been examined in rats bearing pituitary homografts. Groups (10-14/group) of virgin female rats (CDF) strain) were hypophysectomized, ovariectomized, and pituitaries obtained from long-term ovariectomized donors were implanted under the kidney capsule. The animals were treated on the sixth day after transplantation with sesame oil vehicle, estradiol (1.6 mug/100 g BW), progesterone (0.6 mg/100 g BW), or estradiol plus progesterone. This injection regimen was repeated 12 h later. Ninety minutes after the steroid injection on day 7 half of the animals in each group received LHRH (ip) and half received saline. Basal levels of LH in the steroid-treated groups not injected with LHRH were, in general, elevated as compared to the oil-injected group. Following LHRH, blood samples were collected by cardiac puncture under light ether anesthesia at 5, 15, 30, 60, and 90 min postinjection. Animals receiving LHRH responded with significant elevations of LH both in the presence and absence of steroids while saline was without effect. However, the magnitude of the LH peak was found to be significantly blunted by estrogen treatment. Moreover, the peak LH response to LHRH occurred 30 min following injection in all groups except the progesterone primed animals. In this group the peak LH was delayed by 30 min. These results suggest that estradiol directly inhibits the release of LH at the level of the pituitary and that the ovarian steroids, estradiol and progesterone probably interact to determine the time of optimal pituitary sensitivity to LHRH.

Animals↗

Use of hypothermic circulatory arrest for cerebral protection during aortic surgery.

Optimal use of hypothermic circulatory arrest during aortic surgery requires understanding of its physiology. Research in laboratory animals and clinical observations have now documented that considerable residual cerebral metabolism remains with cooling to levels of 15-18 degrees C, especially if cooling intervals are short, reflected by persistent jugular venous desaturation. Cooling should be continued to below 15 degrees C if the duration of HCA is expected to exceed 20 minutes, and continued until jugular venous saturations exceed 95%. There is considerable laboratory evidence that even short durations of HCA are followed by a prolonged interval of increased cerebral vascular resistance during which cerebral metabolism is maintained at normal levels by markedly increased oxygen extraction. Clinical observations have now confirmed that considerable jugular venous desaturation is present in patients following HCA: it is more pronounced with prolonged HCA, and is still present as late as six hours after the start of rewarming. This reinforces the concept of a prolonged postoperative vulnerable interval following HCA, during which any compromise in oxygen delivery has the potential for producing cerebral injury. Several adjunctive measures have been shown to improve outcome following HCA. The simplest and most important is topical hypothermia: packing the head in ice during the interval of HCA. Retrograde cerebral perfusion (RCP) has also been shown to improve EEG recovery as well as histological and behavioral outcome in laboratory animals following prolonged HCA, but some of its effect may be secondary to its efficacy in keeping the brain cold, since RCP provides very low rates of flow and supports metabolism at a much lower level than antegrade perfusion at the same temperature. But despite the clear superiority of antegrade perfusion, and the documentation of some benefits of RCP in laboratory measures of cerebral protection, clinical results using RCP and ACP have not yet demonstrated the superiority of these methods over use of HCA alone, perhaps because these modalities are usually employed in patients with unusually high risk of neurological injury: those with dissection or with clot or atheroma in the aorta. Nevertheless, recent years have seen considerable reduction in mortality following aortic surgery, especially in older patients, and a trend toward a lower incidence of permanent neurologic dysfunction. The presence of preoperative rupture or hemodynamic compromise, and of clot or atheroma in the aorta, remain the most significant risk factors both for death and occurrence of stroke.

Animals↗