A somatostatin analogue decreases embryonic loss following superovulation in rats by normalizing insulin-like growth factor-I action in the uterus

This study was designed to determine whether the somatostatin analogue, octreotide, could prevent embryonic loss by normalizing increased uterine insulin-like growth factor-I (IGF-I) action related to hyperoestrogenaemia following superovulation. Superovulated immature and oestradiol-17beta-treated adult rats were infused with 100 or 300 microg/ml of octreotide respectively, or injected daily with 1 or 10 microg of octreotide from day 1 to day 3 of pregnancy. On day 3, embryos were collected from the oviducts and uteri. Uterine luminal fluid was subjected to embryo culture. The amounts of uterine IGF-I and IGF binding proteins (IGFBP) were determined by radioimmunoassay and ligand binding assay respectively. Octreotide infusion normalized uterine IGF-I action following superovulatory and oestradiol-17beta treatment, by reducing IGF-I concentrations and increasing IGFBP concentrations. Octreotide infusion increased the number of normal embryos by 2.7-fold and 1.7-fold in superovulated and oestradiol-17beta- treated rats respectively, and reversed the detrimental effects of uterine luminal fluid on embryonic development caused by superovulatory and oestradiol-17beta treatment. Daily injections with octreotide had similar but reduced effects in all parameters examined in both treatment groups. In conclusion, octreotide may reduce embryonic loss, at least in part, by normalizing IGF-I action following superovulation.      

A prospective trial of short‐fractionation radiotherapy for the palliation of liver metastases

The purpose of this study was to prospectively examine the effectiveness and tolerability of a simple radiotherapy technique for the palliation of symptomatic liver metastases. Twenty‐eight patients with symptomatic liver metastases were enrolled from seven centres, and received targeted (partial or whole) liver irradiation consisting of 10 Gy in two fractions over 2 days. Symptoms at baseline were hepatic pain (27 patients), abdominal distension (19), night sweats (12), nausea (18) and vomiting (eight). Twenty‐two patients (76%) had failed previous treatment with chemotherapy, hormonal therapy and/or high‐dose steroids. Symptoms and potential toxicities were prospectively assessed at the time of treatment, then 2, 6 and 10 weeks later. Individual symptom response rates were 53?66% at 2 weeks. Partial or complete global symptomatic responses were noted in 15 patients (54%) overall. The treatment was well tolerated with two patients (7%) experiencing grade 3 toxicity (one vomiting and one diarrhoea); however, four patients reported temporary worsening of pain shortly after treatment. This simple and well‐tolerated treatment achieves useful palliation.     

The distribution of erythrocyte phospholipids in hereditary spherocytosis demonstrates a minimal role for erythrocyte spectrin on phospholipid diffusion and asymmetry

In the human erythrocyte membrane phosphatidylcholine and sphingomyelin reside mainly in the outer leaflet, whereas the aminophospholipids, phosphatidylethanolamine and phosphatidylserine, are mainly found in the inner leaflet. Maintenance of phospholipid asymmetry has been assumed to involve interactions between the aminophospholipids and the membrane skeleton, in particular spectrin. To investigate whether spectrin contributes to maintaining the phospholipid transbilayer distribution and kinetics of redistribution, we studied erythrocytes from hereditary spherocytosis patients whose spectrin levels ranged from 34% to 82% of normal. The phospholipid composition and the accessibility of membrane phospholipids to hydrolysis by phospholipases were in the normal range. Spin-labeled phosphatidylserine and phosphatidylethanolamine analogues that had been introduced into the outer leaflet were rapidly transported at 37 degrees C to the inner leaflet, whereas the redistribution of spin-labeled phosphatidylcholine was slower. The kinetics of transbilayer movement of these spin-labeled phospholipid in all samples was in the normal range and was not affected by the level of spectrin. Although these erythrocyte membranes contained as little as 34% of the normal level of spectrin and were characterized by several physical abnormalities, the composition, distribution, and transbilayer kinetics of the phospholipids were found to be normal. We therefore conclude that spectrin plays, at best, only a minor role in maintaining the distribution of erythrocyte membrane phospholipid.     

Phospholipase A2 levels in acute chest syndrome of sickle cell disease

Acute chest syndrome (ACS) is associated with significant morbidity and is the leading cause of death in patients with sickle cell disease (SCD). Recent reports suggest that bone marrow fat embolism can be detected in many cases of severe ACS. Secretory phospholipase A2 (sPLA2) is an important inflammatory mediator and liberates free fatty acids, which are felt to be responsible for the acute lung injury of the fat embolism syndrome. We measured SPLA2 levels in 35 SCD patients during 20 admissions for ACS, 10 admissions for vaso-occlusive crisis, and during 12 clinic visits when patients were at the steady state. Eleven non-SCD patients with pneumonia were also evaluated. To determine if there was a relationship between sPLA2 and the severity of ACS we correlated SPLA2 levels with the clinical course of the patient. In comparison with normal controls (mean = 3.1 +/- 1.1 ng/mL), the non- SCD patients with pneumonia (mean = 68.6 +/- 82.9 ng/mL) and all three SCD patient groups had an elevation of SPLA2 (steady state mean = 10.0 +/- 8.4 ng/mL; vaso-occlusive crisis mean = 23.7 +/- 40.5 ng/mL; ACS mean = 336 +/- 209 ng/mL). In patients with ACS sPLA2 levels were 100- fold greater than normal control values, 35 times greater than values in SCD patients at baseline, and five times greater than non-SCD patients with pneumonia. The degree of SPLA2 elevation in ACS correlated with three different measures of clinical severity and, in patients followed sequentially, the rise in SPLA2 coincided with the onset of ACS. The dramatic elevation of SPLA2 in patients with ACS but not in patients with vaso-occlusive crisis or non-SCD patients with pneumonia and the correlation between levels of SPLA2 and clinical severity suggest a role for SPLA2 in the diagnosis and, perhaps, in the pathophysiology of patients with ACS.     

Exacerbation of left ventricular ischemic diastolic dysfunction by pressure-overload hypertrophy. Modification by specific inhibition of cardiac angiotensin converting enzyme.

Hearts with compensatory pressure-overload hypertrophy show an increased intracardiac activation of angiotensin II that may contribute to ischemic diastolic dysfunction. We studied whether pressure-overload hypertrophy in response to aortic banding would result in exaggerated diastolic dysfunction during low-flow ischemia and whether the specific inhibition of the cardiac angiotensin converting enzyme by enalaprilat would modify systolic and diastolic function during ischemia and reperfusion in either hypertrophied or nonhypertrophied hearts. Isolated, red blood cell-perfused isovolumic nonhypertrophied and hypertrophied rat hearts were subjected to enalaprilat (2.5 x 10(-7) M final concentration) infusion during 20 minutes of baseline perfusion and during 30 minutes of low-flow ischemia and 30 minutes of reperfusion. Coronary flow per gram was similar in nonhypertrophied and hypertrophied hearts during baseline perfusion, ischemia, and reperfusion. At baseline, left ventricular developed pressure was higher in hypertrophied than nonhypertrophied hearts in untreated groups (224 +/- 8 versus 150 +/- 9 mm Hg; p less than 0.01) and in enalaprilat-treated groups (223 +/- 9 versus 145 +/- 8 mm Hg; p less than 0.01). During low-flow ischemia, left ventricular developed pressure was depressed but similar in all groups. All groups showed deterioration of diastolic function; however, left ventricular end-diastolic pressure increased to a significantly higher level in untreated hypertrophied than in nonhypertrophied hearts (65 +/- 7 versus 33 +/- 3 mm Hg; p less than 0.001). Enalaprilat had no effect in nonhypertrophied hearts, but it significantly attenuated the greater increase in left ventricular end-diastolic pressure in hypertrophied hearts treated with enalaprilat compared with no drug (65 +/- 7 versus 50 +/- 5 mm Hg; p less than 0.01). The beneficial effect could not be explained by differences in coronary blood flow per gram left ventricular weight, glycolytic flux as reported by lactate production, myocardial water content, oxygen consumption, and tissue levels of glycogen and high energy phosphate compounds. During reperfusion, all hearts showed a partial recovery of developed pressure to 70-74% of initial values. No effect of enalaprilat could be detected during reperfusion on systolic and diastolic function or restoration of tissue levels of high energy compounds. In conclusion, our experiments show that hypertrophied red blood cell-perfused hearts manifest a severe impairment of left ventricular diastolic relaxation in response to low-flow ischemia in comparison with control hearts. Further, our experiments support the hypothesis that the enhanced conversion of angiotensin I to angiotensin II in rats with pressure-overload hypertrophy contributes to the enhanced sensitivity of hypertrophied hearts to diastolic dysfunction during low-flow ischemia.     

Retrospective Analysis of Ponticulus Posticus in Indian Orthodontic Patients-A Lateral Cephalometric Study

Background

The lateral cephalogram is the most common diagnostic radiograph used in clinical orthodontics. Significant cervical spine pathology can be detected on the routine lateral cephalogram. The aim of this study is to sensitize clinicians for examining the cervical area of lateral cephalogram carefully and thus record anatomical variations.

Materials and Methods

The presence and types of ponticuli posticus were investigated on 650 lateral cephalograms which were randomly selected from archived records at AECS Maaruti College of Dental Sciences & Research Centre, Bangalore

Results

The prevalence rate of Ponticulus Posticus in our study was found to be 11.1%. Though there was slight female predominance of 11.7% as compared to 10.4% in males, difference was not statistically significant.

Conclusion

Ponticulus posticus is a common anomaly in the Indian population. If any such anomaly is detected or suspected, it must be documented in the patient''s health record and specialist consultation must be sought. The lateral cephalogram must thus be considered as one of the baseline screening tool for detecting anomalies and pathology in the cervical spine region.     

温热治疗肿瘤的基础研究进展

在肿瘤治疗学中,温热治疗是指运用不同方法对恶性肿瘤进行热治疗,他常与放疗、化疗联用,肿瘤的温度常在40-43℃．现综述温热治疗的细胞死亡、体内温热治疗的特征以及温热治疗的效应器等方面的研究进展．     

Multiple sclerosis: serial study of gadolinium-enhanced MR imaging

Thirteen patients with definite multiple sclerosis (MS), studied 16-24 months previously with magnetic resonance (MR) imaging with and without enhancement by intravenously administered gadolinium diethylenetriaminepentaacetic acid (DTPA) dimeglumine, were reexamined with a similar protocol. Assessment of enhancement and clinical activity in both studies revealed that enhancement was observed in 13 of 14 cases in which clinical activity had changed within 4 weeks of the study and thus appeared more sensitive than clinical examination in determining active disease. The 3-minute postinjection, short repetition time image (TR) was the most efficient for depicting enhancement. Enhancing lesions (active plaques) arose from previously hyper- or isointense regions on long TR images. Previously active lesions reverted to areas of iso- or hyperintensity on long TR images. Serial comparison of long TR images in this population reveals a decrease in high-intensity lesions on long TR images in some cases and an increase in others. The findings of high-intensity regions on long TR images and previously enhancing lesions both becoming isointense suggests that transient inflammatory changes with concomitant edema without demyelination and/or with significant remyelination may occur in some MS lesions. MS lesions are dynamic; both active and inactive lesions may show dramatic change on longitudinal MR imaging studies.     

Dynamic changes in sarcoplasmic reticulum function in cardiac hypertrophy and failure

Previous studies have demonstrated that cardiac function changes with development of pressure overload-induced hypertrophy. The present study was undertaken to discover the basis for the changes in sarcoplasmic reticulum (SR) functions: uptake, (as related to the SR Ca2+ pump properties) and release in isolated, perfused hypertrophied rat hearts. Our results demonstrated significant prolongation of the time-to-90%-relaxation, both during the period of compensation (8 weeks after banding the ascending aorta, group HR1), when systolic function was preserved, and later with progressive hypertrophy (20 weeks after banding, group HR2) and contractile failure (20-22 weeks after banding, group F). The initial rates of the oxalate-supported SR Ca2+ uptake and the maximum transport rate (Vmax) of the SR Ca2+ pump, measured in the left ventricular homogenates, during blockade of the SR Ca2+ release channels with ruthenium red, were preserved in group HR1. To correlate early relaxation abnormalities with SR function, the [Ca2+] required for half-maximal pump activation (EC50) was examined and increased significantly in HRI vs. Sham1 (0.95+/-0.06 vs. 0.81+/-0.04 microM, P<0.05) indicating that the affinity of the SR Ca2+ pump for Ca2+ was reduced. The same tendency was demonstrated in groups HR2 (0.94+/-0.06 vs. 0.79+/-0.05) and F (0.89+/-0.05 vs. 0.78+/-0.05). In addition, with progression of hypertrophy we observed a significant decline in the amount of SR Ca2+ pump, as assessed by the Vmax, from 31.22+/-1.20 (Sham2) to 26.47+/-1.58 HR2) nmol/mg protein per min (P<0.05), and from 33.81+/-1.23 (Sham3) to 25.15+/-1.57 (F) nmol/mg protein per min, (P<0.01). This decrease was accompanied by a parallel reduction in the number of SR Ca2+ release channels by 14% (HR2) and 23% (F), as determined by maximum [3H] ryanodine binding (Bmax). These results suggest that pressure overload-induced changes in SR Ca2+ uptake (as reflected by Vmax and EC50) and SR Ca2+ release (as reflected by Bmax), both leading to diminished Ca2+ sequestration, may contribute to impaired cardiac relaxation with compensatory hypertrophy and failure.     

Blood donation-related neurologic needle injury: evaluation of 2 years' worth of data from a large blood center

BACKGROUND: There is little information in the medical literature on t he clinical spectrum of blood donation-related neurologic needle injury and on its frequency in a blood donor population. STUDY DESIGN AND METHODS: Sixty-six cases of blood donation-related neurologic needle injury were identified from nursing reports made during a 2-year collection period involving 419,000 whole blood donations. Telephone follow-up was completed on 56 of the 66 cases to better define clinical symptoms, the donor's desire for physician consultation, recovery times, and residual effects. RESULTS: Symptoms in 66 donors included numbness or tingling (n = 54), excessive or radiating pain (n = 43), and loss of arm or hand strength (n = 8). Of the 56 donors with complete follow-up, 17 (30%) consulted a physician one or more times. Recovery times in these 56 donors were <3 days (n = 22), 4 to 29 days (n = 17), 1 to 3 months (n = 13) 3 to 6 months (n = 2), and >6 months (n = 2). Fifty-two of 56 donors achieved a full recovery, and 4 other donors had only a mild, localized, residual numbness. The incidence of blood donation-related neurologic needle injury was 1 of every 6300 donations. CONCLUSION: While donor recovery may in some cases require a great deal of time and/or physician consultation(s), total recovery appears to be the rule. The incidence of blood donation-related neurologic needle injury is relatively low.