Autopsies and sudden infant death syndrome.
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Biomedical subjects
Publications and source records attributed to M Bass.
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Infection continues to be the number one cause of morbidity in terms of complications for the renal transplant patient. Overwhelming infection may lead to hypoxemia, sepsis, and cardiovascular instability, which necessitate intensive care nursing for the patient. Although the care may be similar to that of other patients with these pathophysiologic processes, the transplant patient has the added complication of iatrogenic immunosuppression. On the other hand, immunosuppressive therapy may be discontinued, if necessary, in order to save the patient's life. Therefore, if the renal transplant patient needs to be treated in the intensive care unit, it is primarily important for the nurse to monitor for signs and symptoms of the infections.
The likelihood of twin infants dying suddenly and simultaneously of SIDS, a natural disorder, defies credibility. However, injuries associated with environmental hazards provide possible mechanisms of sudden death. A search for hazards in the homes of 13 pairs of healthy twins who died together of no apparent cause formed the basis of this study. Ten of the 13 sets were certified by medical examiners as simultaneous twin SIDS. The findings in this study suggest that all 13 sets died from injuries, either unintentional or otherwise, and that these deaths could have been prevented.
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Phospholamban, the putative regulatory proteolipid of the Ca2+/Mg2+ ATPase in cardiac sarcoplasmic reticulum, was selectively phosphorylated by a Ca2+/calmodulin (CaM)-dependent protein kinase associated with a cardiac membrane preparation. This kinase also catalyzed the phosphorylation of two exogenous proteins known to be phosphorylated by the multifunctional Ca2+/CaM-dependent protein kinase II (Ca2+/CaM-kinase II), i.e., smooth muscle myosin light chains and glycogen synthase a. The latter protein was phosphorylated at sites previously shown to be phosphorylated by the purified multifunctional Ca2+/CaM-kinase II from liver and brain. The membrane-bound kinase did not phosphorylate phosphorylase b or cardiac myosin light chains, although these proteins were phosphorylated by appropriate, specific calmodulin-dependent protein kinases added exogenously. In addition to phospholamban, several other membrane-associated proteins were phosphorylated in a calmodulin-dependent manner. The principal one exhibited a Mr of approximately 56,000, a value similar to that of the major protein (57,000) in a partially purified preparation of Ca2+/CaM-kinase II from the soluble fraction of canine heart that was autophosphorylated in a calmodulin-dependent manner. These data indicate that the membrane-bound, calmodulin-dependent protein kinase that phosphorylates phospholamban in cardiac membranes is not a specific calmodulin-dependent kinase, but resembles the multifunctional Ca2+/CaM-kinase II. Our data indicate that this kinase may be present in both the particulate and soluble fractions of canine heart.
The response of known hypertensives to advice on sodium restriction was examined as part of a 5-year study on hypertension screening in family practice. The study comprised 34 family practices, pair-matched for location, activity level, and length of time in present practice. One practice in each matched pair was randomly allocated to an experimental or a control group. All hypertensive patients in each experimental practice were exposed to a management program which included dietary counseling to restrict sodium intake. A sample of hypertensive patients (N = 1,001) in both control and experimental groups was interviewed 3.5 years into the study. Although more subjects in experimental practices reported not adding salt (22.9%) compared with those in control practices (17.3%), the results of multivariate analysis showed that type of practice (experimental or control) was not significantly associated with salt use. Salt avoidance was strongly related to lower levels of education and to sex (men were less likely to use salt). Subjects who did not use salt also tended to avoid high-sodium foods. The response to nutritional advice was less favorable than expected. Difficulties in compliance with dietary recommendations are discussed.
The Ca2+/calmodulin (CaM)-dependent protein kinase II system in squid nervous tissue was investigated. The Ca2+/CaM-dependent protein kinase II was found to be very active in the synaptosome preparation from optic lobe, where it was associated with the high-speed particulate fraction. Incubation of the synaptosomal homogenate with calcium, calmodulin, magnesium, and ATP resulted in partial and reversible conversion of the Ca2+/CaM-dependent protein kinase II from its calcium-dependent form to a calcium-independent species. The magnitude of this conversion reaction could be increased by inclusion of the protein phosphatase inhibitor NaF or by substitution of adenosine 5'-O-(3-thiotriphosphate) for ATP. When [gamma-32P]ATP was used, proteins of 54 and 58 kilodaltons (kDa) as well as proteins greater than 100 kDa were rapidly 32P-labeled in a calcium-dependent manner. Major 125I-CaM binding proteins in the synaptosome membrane fraction were 38 and 54 kDa. The Ca2+/CaM-dependent protein kinase II was purified from the squid synaptosome and was shown to consist of 54- and 58-60-kDa subunits. The purified kinase, like Ca2+/CaM-dependent protein kinase II from rat brain, catalyzed autophosphorylation associated with formation of the calcium-independent form. These studies, characterizing the Ca2+/CaM-dependent protein kinase II in squid neural tissue, are supportive of the putative role of this kinase in regulating calcium-dependent synaptic functions.
Data from a program for hypertension screening and follow-up were used to study the relationship between age at onset of hypertension and the risk of cardiovascular complications. The risk for hypertensive subjects, compared with normotensive subjects of similar age, declined significantly as age of onset increased from 40 to 69 years. This pattern was not explained by differences in initial severity of hypertension, control of hypertension, obesity, smoking, or alcohol consumption. A sex-specific analysis showed that the pattern was confined to male subjects, but it is argued that it might be seen in female subjects if data for women of more advanced age were available. Further lines of investigation of this interesting phenomenon are proposed.
We conducted death-scene investigations in 26 consecutive cases in which a presumptive diagnosis of sudden infant death syndrome (SIDS) was made and the infants were brought to the emergency room of the Kings County Hospital Center between October 1983 and January 1985. In six cases, we observed strong circumstantial evidence of accidental death. In 18 other cases, we discovered various possible causes of death other than SIDS, including accidental asphyxiation by an object in the crib or bassinet, smothering by overlying while sharing a bed, hyperthermia, and shaken baby syndrome. This study suggests that many sudden deaths of infants have a definable cause that can be revealed by careful investigation of the death scene and that the extremely high rate of SIDS (4.2 per 1000 live births) reported in the population of low socioeconomic status served by Kings County Hospital Center should be questioned.
During the last quarter century the use of directed energy from lasers has become very important in medicine. Directed energy from lasers has been used to cut tissue, to cauterize bleeding, to drill small pressure relief holes and to selectively destroy tissue growths. In this paper lasers of interest in such applications are described and compared.
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Phosphorylation site stoichiometries were determined for skeletal muscle glycogen synthase purified from control, alloxan-diabetic, and epinephrine-treated rabbits. One method of analysis was direct determination of the total in vivo phosphate content of each site after reverse phase high performance liquid chromatography separation of a complete tryptic digest of the purified synthase. The second method of analysis, in vitro phosphorylation, was based on the premise that in vitro 32P incorporation into each site would be inversely related to the in vivo phosphate content of that site. Glycogen synthase from control rabbits had the following distribution of in vivo phosphate (mole of phosphate/mol of site): site 1a, 0.29 +/- 0.08; site 5, 0.62 +/- 0.07; site 3, 0.46 +/- 0.06; site 1b, 0.23 +/- 0.03; and site 2, 0.43 +/- 0.07. Synthase from diabetic rabbits had 2-fold elevations of in vivo phosphate contents of sites 2 and 3. Epinephrine resulted in increased phosphorylation in vivo of site 1b (2.0-fold), site 2 (2.0-fold), and site 3 (1.5-fold). The in vitro phosphorylation analysis showed decreased 32P incorporation in vitro (indicative of increased in vivo phosphorylation) as follows: epinephrine, site 1a, site 3, site 1b, site 2; diabetic, site 3, site 2. The effect of diabetes on the in vitro phosphorylation of sites 2 and 3 was reversed by insulin treatment. We conclude that the major effect of epinephrine, phosphorylation of sites 1a, 1b, and 2, is mediated by the activation of the cAMP-dependent kinase. The mechanisms accounting for the phosphorylation of site 3 in response to epinephrine and phosphorylation of sites 2 and 3 in the diabetic state are under investigation.