The Influence of Site of Care on the Content of Prenatal Care for Low-Income Women

Objective: To assess whether site of prenatal care influences the content of prenatal care for low-income women. Design: Bivariate and logistic analyses of prenatal care content for low-income women provided at five different types of care sites (private offices, HMOs, publicly funded clinics, hospital clinics, and other sites of care), controlling for sociodemographic, behavioral, and maternal health characteristics. Participants: A sample of 3405 low-income women selected from a nationally representative sample of 9953 women surveyed by the National Maternal and Infant Health Survey, who had singleton live births in 1988, had some prenatal care (PNC), Medicaid participation, or a family income less than $12,000/year. Outcome Measures: Maternal report of seven initial PNC procedures (individually and combined), six areas of PNC advice (individually and combined), and participation in the Women Infant Children (WIC) nutrition program. Results: The content of PNC provided for low-income women does not meet the recommendations of the U.S. Public Health Service, and varies by site of delivery. Low-income women in publicly funded clinics (health departments and community health centers) report receiving more total initial PNC procedures and total PNC advice and have greater participation in the WIC program than similar women receiving PNC in private offices. Conclusions: Publicly funded sites of care appear to provide more comprehensive prenatal care services than private office settings. Health care systems reforms which assume equality of care across all sites, or which limit services to restricted sites, may foster unequal access to comprehensive PNC.     

Differential roles of neurokinin 1 and neurokinin 2 receptors in the development and maintenance of heat hyperalgesia induced by acute inflammation

1. Following induction of acute inflammation by intraarticular injection of kaolin and carrageenan into the knee joint in rats, there was a significant decrease in the withdrawal latency to radiant heat applied to the paw (i.e. heat hyperalgesia), an increased joint circumference and increased joint temperature.
2. A neurokinin₁ (NK₁) receptor antagonist (CP-99,994, 10 mM) had no effect on the paw withdrawal latency when it was administered spinally through a microdialysis fibre before the induction of inflammation. Pretreatment with a NK₂ receptor antagonist (SR48968, 1 mM) administered spinally through the microdialysis fibre prevented the heat hyperalgesia from developing in the early stages of the inflammation.
3. Post-treatment through the microdialysis fibre with the NK₁ receptor antagonist (0.0110 mM) was effective in reversing the heat hyperalgesia. In contrast, post-treatment spinally with the NK₂ receptor antagonist (0.011 mM) had no effect on the heat hyperalgesia. The inactive stereoisomers of the NK₁ receptor antagonist, CP100,263, or the NK₂ receptor antagonist, SR48965, administered at the same doses, had no effect on the joint inflammation or the heat hyperalgesia.
4. Pretreatment systemically with the NK₁ receptor antagonist (30 mg kg⁻¹) had no effect on the heat hyperalgesia or pain-related behaviour ratings where 0 is none and 5 is non weight bearing and complete avoidance of limb contact. Pretreatment with a NK₂ receptor antagonist (10 mg kg⁻¹) systemically prevented the heat hyperalgesia and pain-related behaviour ratings from developing in the early stages of the inflammation. The inactive stereoisomers of NK₁ receptor antagonist, CP100,263, or the NK₂ receptor antagonist, SR48965, administered at the same doses, had no effect on the joint inflammation or the heat hyperalgesia.
5. Post-treatment systemically with either the NK₁ (0.130 mg kg⁻¹) or the NK₂ (0.110 mg kg⁻¹) receptor antagonist resulted in a dose-dependent reversal of the heat hyperalgesia. Pain-related behaviour ratings were reduced by post-treatment only with the NK₁ receptor antagonist. The inactive stereoisomers of the NK₁ receptor antagonist, CP100,263, or the NK₂ receptor antagonist, SR48965, administered at the same doses, had no effect on the behavioural responses.
6. Direct pretreatment of the knee joint with either the NK₁ (30 mg) or the NK₂ (10 mg) receptor antagonist prevented the heat hyperalgesia from developing without affecting joint swelling. The inactive stereoisomers of the NK₁ receptor antagonist, CP100,263, or the NK₂ receptor antagonist, SR48965, administered at the same doses, had no effect on the joint inflammation or the heat hyperalgesia.
7. There appears to be a differential role for the spinal tachykinin receptors in the development and maintenance of the heat hyperalgesia associated with acute joint inflammation. The NK₂ receptors appear to be activated early in the development of the heat hyperalgesia and NK₁ receptors are involved in the maintenance of the heat hyperalgesia.
8. Peripherally, both NK₁ and NK₂ receptors are involved in the development of heat hyperalgesia and pain-related behaviour ratings induced by acute inflammation.

     

Modulation of retinal pigment epithelial cell behavior by Agaricus bisporus lectin.

PURPOSE: To determine whether Agaricus bisporus lectin (ABL) binds retinal pigment epithelial cells (RPEs), to conduct a preliminary viability study of RPEs exposed to ABL, and to evaluate the effects of ABL on RPE proliferation and RPE-mediated matrix contraction in vitro. METHODS: Using cultured bovine RPEs, immunohistochemistry was used to study ABL binding. Morphologic and trypan blue exclusion techniques were used for toxicity studies. The effect of ABL on RPE proliferation was investigated by [methyl-3H]-thymidine incorporation. The effect of ABL on RPE-mediated matrix contraction was evaluated with RPE-populated three-dimensional collagen matrices. RESULTS: ABL bound to RPE cells. This binding was inhibited by asialomucin. No change in RPE morphology or trypan blue exclusion compared with controls was observed in RPEs incubated with 5 to 60 microg/ml ABL for 3 days. Twenty-four-hour incubations of RPEs with ABL significantly inhibited RPE proliferation in a dose-dependent way, 40 microg/ml ABL inhibited proliferation by 83% (SE 14, P<0.05). ABL showed a dose-dependent significant inhibition of RPE-mediated collagen matrix contraction over 3 days, with 93% inhibition compared with controls by 40 microg/ml lectin (P<0.05). The inhibitory effect of ABL on proliferation and gel contraction was partly reversible after eliminating ABL from the culture medium. CONCLUSIONS: Bovine RPE cells bind ABL, and preliminary evaluations suggest that levels of ABL that are nontoxic to the cells potently inhibit RPE proliferation and RPE-mediated matrix contraction. ABL deserves further investigation as a potential inhibitor of RPE proliferation and cell-mediated matrix contraction in anomalous reparative processes such as proliferative vitreoretinopathy and as a laboratory tool for RPE behavioral studies.     

Diode laser thermokeratoplasty – first clinical experience

Purpose: Pulsed holmium lasers are currently used to correct hyperopia by means of laser thermokeratoplasty (LTK). Series of μs laser pulses are applied with a high repetition rate to induce shrinkage of corneal collagen fibers. The pulsed energy application results in intrastromal temperature peaks of up to 200 °C. A continuously emitting laser diode can – as we demonstrated recently in an invivo study on minipigs – be used for LTK and may be of advantage because the temperature rise is more steady. The aim of this study was to examine the safety, amount, and stability of hyperopic correction of diode LTK on blind human eyes. Methods: We used a laserdiode that was set to continuously emit light at λ = 1.854 μm/μ_a = 1.04 mm^–1(group I, n = 4) or 1.87 μm/μ_a = 1.92 mm^–1 (group II, n = 4). Radiation energy was 100 to 150 mW for 10 s per coagulation. Eight coagulations on a single ring (group I) and 16 coagulations on a double ring (group II) diameter were applied in the cornea concentric to the entrance pupil by means of a vacuum-fixed application mask (group I = conjunctival fixation; group II = corneal fixation) and a handpiece with a focusing optic. Preoperatively as well as 1 week, 1, 2, 3, 6 12 and 18 months postoperative ophthalmologic controls were performed and the corneal refractive power was measured. Results: In group I initial refractive changes of up to + 4.9 D were achieved (1 week postoperative). However, due to the great penetration depth of the laser irradiation, large endothelial defects resulted beneath the stromal coagulations. In group II an initial refractive change of up to + 6.8 D was achieved and as a result of the reduced penetration depth, the endothelial cell damage was much reduced. Partial regression of the refractive effect occured in all subjects, which continued in higher refractive changes during the 2^nd postoperative year. The refractive effect at 12 months was + 0.6 to + 1.5 D in group I and + 0.9 to + 5.7 D in group II. At 12 months the induced astigmatism was 0.5 to 2.2 D in group I and 0.3 to 1.6 D in group II. No serious adverse effects were noticed. Conclusion: A continously emitting laser diode working at a wavelength of 1.87 μm can be used to correct hyperopia by means of LTK safely and effectively. Regression occurs predominantly in the first 6 postoperative months. Further studies must be conducted to determine the importance of patient inherent parameters such as age in establishing a nomogram.      

Inhibition of colony formation in agarose of metastatic human breast carcinoma and melanoma cells by synthetic glycoamine analogs

We studied the influence of 10 synthetic glycoamine analogs on colony formation in 0.3 and 0.9% agarose by metastatic human breast carcinoma (MDA-MB-435) and melanoma (TXM-13) cells. Nine synthetic analogs significantly inhibited the colony formation in 0.9% agarose of MDA-MB-435 human breast carcinoma cells; five compounds caused a 73–83% reduction of colony formation. Seven synthetic glycoamines caused a significant inhibition of colony formation in 0.9% agarose by TXM-13 melanoma cells with the inhibitory effect ranging from 71 to 87%. The 50% inhibition (I₅₀) doses and relative activity rank of the compounds were similar for both breast carcinoma and melanoma cell lines. The murine B16 melanoma cell aggregation assay was employed to elucidate the potential mechanism(s) of the inhibitory activity of synthetic glycoamines. The relative activity ranks of the compounds based on the independently determined I₅₀ doses for both cell aggregation and clonogenic growth assays were very similar for the four most active synthetic analogs and clearly indicated the importance of hydrophobic amino acid in mediating the bioactivity of synthetic glycoamines. In both experimental systems (clonogenic growth in agarose and cell aggregation assay) the leading compound was N-(1-deoxy-d-fructos-1-y1)-d-leucine (Fru-d-Leu) and the least active analog was N-(1-deoxy-d-fructos-1-yl)-glycine (Fru-Gly). These results show that synthetic glycoamines may act by competing for specific carbohydrate-lectin interactions, particularly those involving -galactoside-specific lectins expressed on metastatic cells.     

Razabrasion: An alternative approach to perioral rhytides

Persistence of perioral rhytides is a frequent source of patient concern following standard rhytidectomy. Dissatisfaction with the limited results and occasional complications that result from mechanical, manual, and chemical abrasive methods of management prompted application of the steel blade dermal shave technique to this problem. Manual oscillation of a sterile commercial razor blade with depth and width controlled by digital pressure eradicates all but the deepest perioral wrinkles. Eleven patients have undergone razabrasion within the past 19 months without complication. Local anesthesia is sufficient. Topographically distant but synchronous facial operations may be performed safely, but undermining of the shaved facial skin should be avoided for 6 months after razabrasion. Later results will be studied to define the longevity of the effect, but we are encouraged that the method offers the most gentle, most rapid, and best controlled (as to level of dermal shave) current method of tangential dermal splitting. The paper describes the technique of razabrasion of perioral rhytides and reports our early results.     

Screening for hypertension

A strategy for the control of hypertension in communities is presented as a staged program. Stage I consists of the evaluation and improvement of hypertension management in health care facilities. State II entails case-finding in health care facilities. Finally, Stage III involves targeted screening in the community. While isolated screening programs have been justly labeled irrational, such a sequential strategy represents a highly rational approach to the community control of hypertension.Dr. Gillum is with the Laboratory of Physiological Hygiene, University of Minnesota School of Public Health, Minneapolis, Minnesota 55455. Dr. Stason is with the Center for the Analysis of Health Practices, Harvard School of Public Health, Boston, Massachusetts 02115. Dr. Weinstein is with the John F. Kennedy School of Government, Harvard University, Cambridge, Massachusetts 02138. This work was supported in part by grant F32HL5018 from the National Institutes of Health. The Hypertension Screening Group of the 1974–75 Harvard School of Public Health Faculty Seminar on the Analysis of Health and Medical Practices provided an ongoing forum for the development of this work.     

The clinical utility of provocative radionuclide oesophageal transit in the evaluation of non-cardiac chest pain

We combined edrophonium provocative testing with the technique of radionuclide oesophageal transit (RET) in 30 consecutive patients with non-cardiac chest pain (NCCP) and 12 controls. The oesophageal transit time of aqueous technetium-99m sulfur colloid was determined before and after intravenous infusion of 80 g/kg edrophonium chloride (ED). Patient symptoms during provocative RET (P-RET) were recorded. Thirteen (43%) of the patients had abnormal study results, whereas all control subjects had normal results. Three groups considered abnormal were observed: (a) in two patients (6%), the pain was reproduced and transit pre- and post-ED administration was prolonged (>15 s); (b) in six patients (20%), the pain was reproduced, but transit was normal pre- and post-ED; (c) in five patients (17%), transit pre- and post-ED was prolonged, but no pain was reproduced. In five patients (17%), ED prolonged the transit time > 15 s without pain, but the baseline transit was normal. Transit time was measurable in 23 patients. Mean pre-ED transit time was 10.2 ± 7.4 s (mean ± SD) and post-ED, 12.4 ± 8.0 s (P=0.3). We conclude that ED has no significant effect on transit time, and the pain induced by ED rarely correlates with an abnormal transit; P-RET provides additional information to baseline RET, increasing sensitivity, and may be a useful screening method in the evaluation of patients with NCCP.