Biomedical subjects
Publications and source records attributed to L Taylor.
There is a growing awareness that women who give birth prematurely have a particular need for specialist after-care and support. Jane Littlewood and Lesley Taylor report the findings of a study to examine the differing experiences of postnatal care reported by women following full-term and premature birth.
Witnessing violence can have an adverse effect on children and adults. To determine the prevalence and selected correlates of witnessing violence among young children and their mothers, we consecutively recruited 143 parents (88% of those eligible) with children 1 to 5 years of age from the pediatric primary care clinic at Boston City Hospital. The final sample of 115 mothers were English-speaking, primarily minority and poor (76% living on < $10,000/year). In response to a standardized questionnaire, 10% of children were reported to have witnessed a knifing or shooting; 18% had witnessed shoving, kicking, or punching; and 47% had heard gunshots. Thirty-six percent of the mothers reported witnessing a knifing or shooting and 9% had been victims of a knifing or shooting. Mothers of children who had witnessed violence were more likely to limit their movements (80% vs 50%, p < .003) and were more concerned about safety (67% vs 24%, p < .001) compared to mothers whose children did not witness violence. This finding needs to be replicated in other settings, and potential consequences need to be identified.
This article describes a study that tested the effectiveness of culturally sensitive educational material on hearing loss and performed mass screenings to evaluate the prevalence of hearing impairment among urban African-American and Latino seniors. Bilingual information booklets on hearing loss were mailed to households and senior centers in 45 census tracts with high concentrations of minority elderly. Seniors were invited for hearing evaluations and were screened using a handheld audioscope. Subjects with hearing impairment were referred for specialized testing and later telephoned to assess subsequent care. Four hundred thirty-three persons (3.14%) responded to three mailings, typically by presenting for a hearing evaluation. Responses to a brief questionnaire indicated a high degree of learning about hearing loss. Of the 296 seniors screened, 174 demonstrated abnormal hearing, but only 26% obtained further testing. Barriers to follow-up care included problems with finances, transportation, and illness.
Gastroendoscopic surveys have shown that horses in race training have a greater prevalence of gastric ulceration than sedentary horses. To determine if exercise affects gastric endocrine function the following experiment was performed. Four horses were fed total mixed ration of ground corn and chopped hay at 2% of their body weight, divided into 2 equal portions, daily. Horses were fasted overnight, and serum gastrin concentration was determined just before and 2 hours after feeding. The horses were then sprint trained on a high speed treadmill for 6 weeks. The response of serum gastrin to feeding was then repeated as before. Serum gastrin increased following feeding both before and after training, however the postfeeding gastrin value was higher [p = 0.035] after training (68.1 +/- 6.9 pg/ml [mean +/- 1 SEM]) than before (42.7 +/- 3.8 pg/ml). These data show that treadmill exercise has an effect upon the gastric hormonal response to a meal in the horse. The relationship of this finding to the development of gastric ulcer disease is unknown at present, but warrants further investigation.
Experiments were conducted to determine the roles of the rate limiting enzymes, cyclooxygenase 1 and 2 (COX1 and COX2) and cytoplasmic phospholipase A2 (PLA2), in transforming growth factor beta (TGF-beta) and interleukin-1 (IL-1 beta) activated prostaglandin synthesis. Results show that TGF-beta increases steady state levels of COX1 mRNA in both human embryo lung fibroblasts (IMR90) and calf pulmonary artery endothelial cells (BPAEC). Temporal experiments show that TGF-beta increases, within 2hrs, a 5.5kb COX1 in IMR90 and the 2.7kb COX1 mRNA in BPAEC. IL-1 beta increases COX1 mRNA only in IMR-90, not BPAEC. COX2 mRNA, under basal conditions, is not detected in BPAEC and is expressed only marginally in IMR90. TGF-beta or IL-1 beta have no effect on expression of COX2 gene in either cell type. IL-1 beta increases steady state levels of PLA2 mRNA in both IMR90 and BPAEC while TGF-beta increases expression of the PLA2 gene only in BPAEC. Time experiments with TGF-beta show induction of PLA2 mRNA within 1hr, peaking at 4hrs. PG synthesis in response to the cytokines was determined in IMR90 and BPAEC to further assess the significance of the above results. TGF-beta increases the synthesis of prostacyclin in BPAEC in a time related fashion peaking at 8hrs at 13 fold above basal. To focus on the action of COX1 and bypass the action of PLA2, exogenous arachidonic acid was used as substrate for PG synthesis. In these experiments IL-1 beta increases PGE2 synthesis 8 fold in IMR90 while IL-1 beta and TGF-beta added simultaneously increases PGE2 synthesis 25 fold. These results in sum illustrate that the cytokines, TGF-beta and IL-1 beta, regulate both COX1 and PLA2 mRNA levels. Furthermore, this regulation appears coordinated to bring about elevation of prostaglandin synthesis.
The aim of this study has been to determine the distribution of somatic mutations in the 5' flanking regions of rearranged immunoglobulin heavy chain variable region genes (VDJ). We sequenced the 5' flanking region in 12 secondary immune response antibodies produced in C57BL/6j mice against the hapten (4-hydroxy-3-nitrophenyl)acetyl (NP) coupled to chicken-gamma-globulin. In these and previously published sequences, almost 97% of the mutations occurred in the transcribed region of the gene, and only a minority of genes (5/29) contained mutations upstream of the transcription start (cap) site. No potential germ-line donor was found for a cluster of five base changes previously found in a single heavy chain gene, 3B62. However, the uniqueness of this mutational cluster and its distance from the normally mutated region suggests that the nucleotide changes may not be due to the normal mutator mechanism. Thus, as this was the only instance of somatic mutations that far upstream of the promoter/cap site region, the reverse transcriptase model for somatic hypermutation is still a possibility. The data are consistent with a mutational mechanism that requires transcription of the rearranged target V(D)J gene which appears to result in the generation of a positively skewed asymmetrical distribution of somatic mutations. A single mode is centered near the V(D)J and a long tail extends into the 3' non-translated region of the J-C intron. Two classes of model could explain this mutation distribution pattern: those where transcription products (RNA, cDNA) are the direct mutational substrates, or those that postulate local unfolding of the chromatin around a V(D)J rearrangement directly exposing the DNA of the transcribed region to specific mutational enzymes.
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Rise in free cytosolic calcium concentrations [Ca2+]i in response to bradykinin and guanosine 5'-O-thiotriphosphate (GTP tau S) was related to the action of phospholipase A/ (arachidonic acid release). At 900 microM extracellular CaCl2, bradykinin induced a typical Ca2+ movement consisting of an initial [Ca2+]i peak at approximately 400 nM followed by a sustained increase in the steady-state cytosolic Ca2+ level at approximately 290 nM. As the extracellular CaCl2 concentration was reduced to 100 microM, the bradykinin induced initial spike was reduced followed by only a marginal increase in steady-state cytosolic Ca2+ levels. Treatment of endothelial cells with saponin (0.002% w/w) did not increase [Ca2+]i and saponin treated cells exhibited a very similar pattern of Ca2+ mobilization in response to bradykinin. However, with saponin treatment, GTP tau S (100 microM) increased [Ca2+]i at an almost identical tracing exhibited with 50 nM bradykinin stimulation (in either the presence or absence of 0.002% saponin). No additive increase in [Ca2+]i was observed in cells stimulated with both 100 microM GTP tau S and 50 nM bradykinin or in bradykinin stimulated cells subsequently exposed to GTP tau S. Pertussis toxin (PTX) did not affect the bradykinin induced Ca2+ mobilization. However, as we showed previously, PTX inhibited bradykinin stimulated arachidonic acid release. These results indicate transduction of the bradykinin signal by G-protein for both phospholipase A2 (PLA2) activation and Ca2+ mobilization but likely by different G alpha subunits, a PTX sensitive and an insensitive subunit. Furthermore, the bradykinin and GTP tau S stimulated release of arachidonic acid appears to be only partially dependent on [Ca2+]i.(ABSTRACT TRUNCATED AT 250 WORDS)
During late December 1989 and early January 1990, a cluster of six unexplained deaths occurred on a paediatric intensive care unit (PICU) among children with congenital heart disease who had undergone cardiac surgical procedures. The children were all aged three years or less. In each case death was preceded by an unexpected increase in ventilatory pressure requirement followed by the development of a similar pulmonary shadowing on chest radiography. The radiological abnormality was felt to be consistent with a pneumonitis associated with some small airway disease. The clustering of these deaths, occurring in a similar unusual manner, was felt to constitute an outbreak warranting investigation. An Incident Committee was established to plan and manage a large multidisciplinary investigation during which the unit was temporarily closed. Following extensive investigation no bacterium, virus, fungus or other pathogen, toxic agent, or any other explanation for the cluster of deaths could be found. The possibility that the cluster occurred by chance remains although this was felt to be unlikely.
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Pregnant Swiss-Webster mice were vaginally inoculated with 10(5) virulent and avirulent serotype III Streptococcus agalactiae and treated 4 days later with topical vaginal inhibitor solutions. Preparations containing lipoteichoic acid (LTA) or glycerophosphate (GP), the repeating linear backbone of LTA, significantly reduced neonatal colonization and bacteremia by the virulent isolate and colonization by the avirulent strain. Similar results were obtained if bacteria were preincubated with LTA or GP at 37 degrees C for 30 min before vaginal inoculation. Human serum albumin (HSA), a known inhibitor of binding of LTA to human fetal epithelial cells, also resulted in reduction in colonization and bacteremia of neonatal mice. However, maternal treatment with a combination of HSA (2%) and GP (1%) completely prevented neonatal colonization and bacteremia without altering the normal aerobic bacterial vaginal flora. These results provide impetus to the development of an alternative means of preventing neonatal group B streptococcal infections in humans without requiring maternal immunization or chemoprophylaxis.
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Interleukin-8 (IL-8) is a key mediator in the migration of neutrophils from the circulation to the site of inflammation in the tissue. IL-8 is secreted by many cell types in response to proinflammatory stimuli such as interleukin 1, tumor necrosis factor, and lipopolysaccharide and is a potent chemoattractant and activator of neutrophils. Neutrophil activating peptide-2 (NAP-2) and melanoma growth-stimulatory activity (MGSA/GRO) are structurally and functionally related to IL-8 and, like IL-8, bind to specific G protein-coupled receptors on neutrophils. In the present study two closely related cloned IL-8 receptor subtypes are characterized by expression of the cDNA clones in monkey kidney cells (COS-7) or chinese hamster ovary cells and analysis of their ligand binding profiles. Both receptor subtypes bind 125I-labeled IL-8 with similar high affinity, however, the F3R receptor binds IL-8 exclusively, while the 4Ab receptor binds both IL-8 and MGSA/GRO with high affinity and NAP-2 with lesser affinity. Furthermore, we demonstrate with the use of intersubtype chimeric receptors that the specificity of ligand binding to both IL-8 receptor subtypes is dictated by the heterogeneous NH2-terminal domain. The F3R receptor is representative of a restricted IL-8 receptor subtype, and 4Ab represents a nonrestricted receptor subtype. It is proposed that these subtypes be named IL-8 receptors alpha and beta, respectively.
The bradykinin (BK) B2 receptor cDNA was synthesized by rt-PCR and transfected into the Chinese hamster lung fibroblasts, CCL39. The CCL39 do not contain the mRNA for this receptor and do not bind BK. Clones of transfected cells were screened for BK receptor mRNA, binding of BK, and for [Ca2+]i response to BK. The clones showed various levels of receptor mRNA. Scatchard analysis of three clones, B6, B5 and B1, each gave a Kd of approximately 1.0nM while the Bmax for each clone differed at 320, 38.7, and 5.39 fmoles per 10(6) cells respectively. The [Ca2+]i response of the three clones to BK decreased with the receptor number/cell. Thus, levels of mRNA, BK binding and [Ca2+]i response proved proportionally related in the transfected clones. The actions of BK and alpha-thrombin, which has an endogenous receptor in these cells, were assessed in clone B6. BK proved active but also distinct from thrombin. BK at 10nM and thrombin at 2units/ml both effectively increased cytosolic [Ca2+]i. BK at 10nM stimulated PGE2 production three fold over basal, while thrombin only marginally elevated PGE2 levels. Alone, BK stimulated a small increase in 3H-thymidine incorporation into DNA. However, in combination with insulin, BK stimulated DNA synthesis to 76% of thrombin, a potent mitogen in these cells. These results illustrate that the BK-B2 receptor cDNA can be stably transfected into a mammalian cell and can activate transmembrane signalling pathways.
Everyone is familiar with that paralyzing state of dread known as anxiety. Although it is unpleasant, the experience of anxiety has adaptive aspects: it can serve as an impetus to effect beneficial life change and can facilitate psychological development. Anxiety becomes of clinical concern, however, when it interferes with intellectual function, or arrests normal social or vocational pursuits. Anxiety disorders are chronic illnesses. Treatment can eliminate many of the disease's debilitating features, but the underlying disorder is not usually cured. Discontinuation of treatment-pharmacological, behavioral, or both-often results in the recurrence of symptoms. The focus of treatment, therefore, generally centers on striking a balance between the goal of alleviating the patient's symptoms, and the need to avoid the deleterious effects which result from long-term treatment (1). The intention of this paper is to review theoretical and therapeutic considerations for four types of anxiety disorder: panic disorder, generalized anxiety disorder, social phobia, and obsessive-compulsive disorder. In doing this, emphasis will be placed on the physiological concomitants and, when possible, neuropsychological bases of these illnesses. Furthermore, pharmacological treatment will be related to the underlying substrata of the disorder whenever possible.
SK-HEP-1 is an immortal, human cell line derived from the ascitic fluid of a patient with adenocarcinoma of the liver. We have determined that these cells are of endothelial origin. Despite the location of the tumor from which SK HEP-1 was derived, the cell line does not have properties of hepatocytes. Northern blot analysis of total cellular RNA shows no messenger RNA for the hepatic-specific proteins albumin, alpha-fibrinogen, or gamma-fibrinogen. Endothelial characteristics are seen by transmission electron microscopy. These features include numerous pinocytotic vesicles, electron dense granules consistent with Weibel-Palade bodies, and abundant intermediate filaments, identified immunocytochemically as vimentin. Cultures grown on plastic dishes grow in bundles of polygonal to spindle-shaped cells. Proteins characteristic for endothelial cells are identified by immunocytochemistry. Addition of basement membrane material (Matrigel) or type I collagen to the cultures induces these cells to organize into a tubular network.
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To study the incidence and types of infection among severely traumatized children, we reviewed the medical charts of 212 children, hospitalized following traumatic injury, who received antibiotics at sometime during their hospitalization. Infection occurred in 19%. Eleven children had trauma-related infections, whereas 29 (71% of those infected) had 36 nosocomial infections. Tracheitis, sepsis, and urinary tract infections were the most common nosocomial infections and were diagnosed in the second week (10 +/- 3 days) following injury. Nosocomial infections were more likely to develop in children who were more severely injured and who had a greater number of invasive procedures. Severe head injury (cerebral edema or subarachnoid hemorrhage) was more common in those with nosocomial infection (P < .0002, odds ratio 6.8, 95% confidence interval 2.2 to 21.3). Those without these injuries were much less likely to develop nosocomial infections (specificity 97% and negative predictive value 86%). Finally, the development of any nosocomial infection prolonged the hospitalization by a mean of 16 +/- 6 days when comparing children with the same degree of traumatic injury. Prevention of nosocomial infection in children with severe trauma will significantly reduce length of hospitalization.