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Background Surgical patients are at high risk of developing pressure injuries (Pls) due to anaesthesia-induced immobility as well as risk factors such as length of surgery and co-morbidities. Few Australian studies have investigated the incidence of PIs in surgical patients. This prospective cohort study assessed the incidence of post-surgical PIs and identified gaps in pressure injury prevention (PIP) for elective surgical patients. Methods Consecutive elective surgery patients at an urban tertiary referral hospital were recruited who had an expected length of stay of >48 hours. Baseline PI risk (measured by the Waterlow scale) and PIP strategies implemented at five time points were collected from medical records. Two prospective outcome assessments were conducted at 24 and 48 hours post-operatively. Data were analysed descriptively. Results One patient out of 150 (incidence rate 0.7) developed an intra-operative Stage 1 PI. Four patients developed skin tears. PIP strategies were applied inconsistently throughout the patient journey, regardless of risk status. Conclusions While the incidence of surgically acquired PIs in this study was low, ongoing staff education is needed about the importance of consistent skin and risk assessments and of implementing strategies appropriate for level of PI risk. What is already known: *PIs are widely considered to be an adverse event of hospitalisation and are largely preventable. *Surgical patients are at risk of developing a PI primarily due to immobilisation following anaesthesia, length of surgery and co-morbidities. *There are few studies on PI incidence and prevention strategies used in the post-operative period. What this manuscript contributes: Although the incidence of post-surgical PIs among elective surgical patients was low, there are gaps in PIP for this group of patients, including for those deemed at high risk of PI. There is a need for clinicians to improve documentation of risk assessment and strategies implemented to reduce the risk of PIs, throughout the surgical patient journey. [ABSTRACT FROM AUTHOR]

Aim Lower limb amputation is a serious complication of diabetic foot disease and there are unexplained ethnic variations in incidence. This study investigates the risk of amputation among different ethnic groups after adjusting for demographic, socio-economic status and clinical variables. Methods We used primary care data from a large national multi-ethnic cohort of patients with Type 2 diabetes in New Zealand and linked hospital records. The primary outcome was time from initial data collection to first lower limb amputation. Demographic variables included age of onset and duration since diabetes diagnosis, gender, ethnicity and socio-economic status. Clinical variables included smoking status, height and weight, blood pressure, HbA1c, total cholesterol/HDL ratio and albuminuria. Cox proportional hazards models were used. Results There were 892 lower limb amputations recorded among 62 002 patients (2.11 amputations per 1000 personyears), followed for a median of 7.14 years (422 357 person-years). After adjusting for demographic and socio-economic variables and compared with Europeans, Maori had the highest risk [hazard ratio (HR) 1.84 (95% CI:1.54-2.19)], whereas East Asians [HR 0.18, (0.08-0.44)] and South Asians [HR 0.39 (0.22-0.67)] had the lowest risk. Adjusting for available clinical variables reduced the differences but they remained substantial [HR 1.61 (1.35-1.93), 0.23 (0.10-0.56) and 0.48 (0.27-0.83), respectively]. Conclusions Ethnic groups had significantly different risk of lower limb amputation, even after adjusting for demographic and some major clinical risk factors. Barriers to care should be addressed and intensive prevention strategies known to reduce the incidence of lower limb amputations could be prioritized to those at greatest risk. [ABSTRACT FROM AUTHOR]

Aims/hypothesis: To compare the effectiveness of low-fat high-protein and low-fat high-carbohydrate dietary advice on weight loss, using group-based interventions, among overweight people with type 2 diabetes. Study design: Multicentre parallel (1:1) design, blinded randomised controlled trial. Methods: Individuals with type 2 diabetes aged 30-75 years and a BMI >27 kg/m were randomised, by an independent statistician using sequentially numbered sealed envelopes, to be prescribed either a low-fat high-protein (30% of energy as protein, 40% as carbohydrate, 30% as fat) or a low-fat high-carbohydrate (15% of energy as protein, 55% as carbohydrate, 30% as fat) diet. Participants attended 18 group sessions over 12 months. Primary outcomes were change in weight and waist circumference assessed at baseline, 6 and 12 months. Secondary outcomes were body fatness, glycaemic control, lipid profile, blood pressure and renal function. A further assessment was undertaken 12 months after the intervention. Research assessors remained blinded to group allocation throughout. Intention-to-treat analysis was performed. Results: A total of 419 participants were enrolled (mean ± SD age 58 ± 9.5 years, BMI 36.6 ± 6.5 kg/m and HbA 8.1 ± 1.2% (65 mmol/mol)). The study was completed by 70% (294/419). No differences between groups were found in change in weight or waist circumference during the intervention phase or the 12-month follow-up. Both groups had lost weight (2-3 kg, p < 0.001) and reduced their waist circumference (2-3 cm, p < 0.001) by 12 months and largely maintained this weight loss for the following 12 months. By 6 months, the difference in self-reported dietary protein between groups was small (1.1% total energy; p < 0.001). No significant differences between groups were found in secondary outcomes: body fatness, HbA, lipids, blood pressure and renal function. There were no important adverse effects. Conclusions/interpretation: In a 'real-world' setting, prescription of an energy-reduced low-fat diet, with either increased protein or carbohydrate, results in similar modest losses in weight and waist circumference over 2 years. Trial registration:: Australia New Zealand Clinical Trials Register ACTRN12606000490572 Funding:: The Health Research Council of New Zealand (06/337). [ABSTRACT FROM AUTHOR]

ims/hypothesis: Fenofibrate caused an acute, sustained plasma creatinine increase in the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) and Action to Control Cardiovascular Risk in Diabetes (ACCORD) studies. We assessed fenofibrate's renal effects overall and in a FIELD washout sub-study. Methods: Type 2 diabetic patients ( n = 9,795) aged 50 to 75 years were randomly assigned to fenofibrate ( n = 4,895) or placebo ( n = 4,900) for 5 years, after 6 weeks fenofibrate run-in. Albuminuria (urinary albumin/creatinine ratio measured at baseline, year 2 and close-out) and estimated GFR, measured four to six monthly according to the Modification of Diet in Renal Disease Study, were pre-specified endpoints. Plasma creatinine was re-measured 8 weeks after treatment cessation at close-out (washout sub-study, n = 661). Analysis was by intention-to-treat. Results: During fenofibrate run-in, plasma creatinine increased by 10.0 μmol/l ( p < 0.001), but quickly reversed on placebo assignment. It remained higher on fenofibrate than on placebo, but the chronic rise was slower (1.62 vs 1.89 μmol/l annually, p = 0.01), with less estimated GFR loss (1.19 vs 2.03 ml min 1.73 m annually, p < 0.001). After washout, estimated GFR had fallen less from baseline on fenofibrate (1.9 ml min 1.73 m, p = 0.065) than on placebo (6.9 ml min 1.73 m, p < 0.001), sparing 5.0 ml min 1.73 m (95% CI 2.3-7.7, p < 0.001). Greater preservation of estimated GFR with fenofibrate was observed with baseline hypertriacylglycerolaemia ( n = 169 vs 491 without) alone, or combined with low HDL-cholesterol ( n = 140 vs 520 without) and reductions of ≥0.48 mmol/l in triacylglycerol over the active run-in period (pre-randomisation) ( n = 356 vs 303 without). Fenofibrate reduced urine albumin concentrations and hence albumin/creatinine ratio by 24% vs 11% ( p < 0.001; mean difference 14% [95% CI 9-18]; p < 0.001), with 14% less progression and 18% more albuminuria regression ( p < 0.001) than in participants on placebo. End-stage renal event frequency was similar ( n = 21 vs 26, p = 0.48). Conclusions/interpretation: Fenofibrate reduced albuminuria and slowed estimated GFR loss over 5 years, despite initially and reversibly increasing plasma creatinine. Fenofibrate may delay albuminuria and GFR impairment in type 2 diabetes patients. Confirmatory studies are merited. Trial registration: ISRCTN64783481 Funding: The study was funded by grants from Laboratoires Fournier SA (Dijon, France; now part of Abbott Pharmaceuticals) and the National Health and Medical Research Council, Australia [ABSTRACT FROM AUTHOR]

ims/hypothesis: We investigated effects of renal function and albuminuria on cardiovascular outcomes in 9,795 low-risk patients with diabetes in the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study. Methods: Baseline and year 2 renal status were examined in relation to clinical and biochemical characteristics. Outcomes included total cardiovascular disease (CVD), cardiac and non-cardiac death over 5 years. Results: Lower estimated GFR (eGFR) vs eGFR ≥90 ml min 1.73 m was a risk factor for total CVD events: (HR [95% CI] 1.14 [1.01-1.29] for eGFR 60-89 ml min 1.73 m; 1.59 [1.28-1.98] for eGFR 30-59 ml min 1.73 m; p < 0.001; adjusted for other characteristics). Albuminuria increased CVD risk, with microalbuminuria and macroalbuminuria increasing total CVD (HR 1.25 [1.01-1.54] and 1.19 [0.76-1.85], respectively; p = 0.001 for trend) when eGFR ≥90 ml min 1.73 m. CVD risk was further modified by renal status changes over the first 2 years. In multivariable analysis, 77% of the effect of eGFR and 81% of the effect of albumin:creatinine ratio were accounted for by other variables, principally low HDL-cholesterol and elevated blood pressure. Conclusions/interpretation: Reduced eGFR and albuminuria are independent risk factors for cardiovascular events and mortality rates in a low-risk population of mainly European ancestry. While their independent contributions to CVD risk appear small when other risk factors are considered, they remain excellent surrogate markers in clinical practice because they capture risk related to a number of other characteristics. Therefore, both should be considered when assessing prognosis and treatment strategies in patients with diabetes, and both should be included in risk models. [ABSTRACT FROM AUTHOR]

Aims To investigate the association between ethnicity and risk of first cardiovascular (CV) event for people with Type 2 diabetes in New Zealand. Methods A prospective cohort study using routinely collected data from a national primary health care diabetes annual review programme linked to national hospital admission and mortality data. Ethnicity was recorded as European, Maori, Pacific, Indo-Asian, East-Asian or Other. A Cox proportional hazards model was used to investigate factors associated with first CV event. Data was collected from 48 444 patients with Type 2 diabetes, with first data collected between 1 January 2000 and 20 December 2005, no previous cardiovascular event at entry and with complete measurements. Risk factors included ethnicity, gender, socio-economic status, body mass index, smoking, age at diagnosis, duration of diabetes, systolic blood pressure, serum lipids, glycated haemoglobin and urine albumin : creatinine ratio. The main outcome measures were time to first fatal or non-fatal CV event. Results Median follow-up was 2.4 years. Using combined European and Other ethnicities as a reference, hazard ratios for first CV event were 1.30 for Maori (95% confidence interval 1.19–1.41), 1.04 for Pacific (0.95–1.13), 1.06 for Indo-Asian (0.91–1.24) and 0.73 for East-Asian (0.62–0.85) after controlling for all other risk factors. Conclusions Ethnicity was independently associated with time to first CV event in people with Type 2 diabetes. Maori were at 30% higher risk of first CV event and East-Asian 27% lower risk compared with European/Other, with no significant difference in risk for Pacific and Indo-Asian peoples. [ABSTRACT FROM AUTHOR]

Aims To investigate the association between long-term glycaemic control, measured by glycated haemoglobin (HbA1c), and time to first cardiovascular disease (CVD) event for people with Type 2 diabetes in New Zealand. Methods A prospective cohort study including people with Type 2 diabetes but no previous CVD. The primary outcome measure was time to first recorded fatal or non-fatal CVD event (ischaemic heart disease, cerebrovascular accident, transient ischaemic attack or peripheral vascular disease) as identified from linked primary care, hospital and mortality records between January 2000 and December 2005. A Cox proportional hazards model was used to examine the association between HbA1c and time to CVD event, adjusting for age at diagnosis, duration of diabetes, gender, ethnicity, socio-economic status, smoking, blood pressure (BP), serum total cholesterol : high-density lipoprotein ratio, body mass index (BMI) and urine albumin : creatinine ratio. Results Participants included 48 444 people with Type 2 diabetes. Fifty-one per cent ( n = 24 721) were women, median age 60 years. Median duration of diabetes was 3 years, median BMI 31 kg/m2, median HbA1c 7.1% and mean BP was 138/81 mmHg. During the study period (median follow-up 2.4 years), there were 5667 first CVD events (11.7% of cohort). Each 1% increase in HbA1c was associated with an increase in hazard ratio (HR) for CVD of 1.08 (95% confidence interval 1.06–1.10, P < 0.001), myocardial infarction [HR 1.08 (1.04, 1.11)] and stroke [HR 1.09 (1.04, 1.13)]. Conclusion This study has confirmed in a large prospective cohort that increased HbA1c is an independent risk factor for cardiovascular disease after controlling for traditional risk factors. [ABSTRACT FROM AUTHOR]

We report a prospective, randomized, multicenter, open-label 2-year trial of 81 postmenopausal women aged 53-79 years with at least one minimal-trauma vertebral fracture (VF) and low (T-score below - 2) lumbar bone mineral density (BMD). Group HRT received piperazine estrone sulfate (PES) 0.625 – 1.25 mg/d ± medroxyprogesterone acetate (MPA) 2.5 – 5 mg/d; group HRT/D received HRT plus calcitriol 0.25 µg bd. All with a baseline dietary calcium (Ca) of <1 g/d received Ca carbonate 0.6 g nocte. Final data were on 66 – 70 patients. On HRT/D, significant (P < 0.001) BMD increases from baseline by DXA were at total body – head, trochanter, Ward’s, total hip, intertrochanter and femoral shaft (% group mean Δ 4.2, 6.1, 9.3, 3.7, 3.3 and 3.3%, respectively). On HRT, at these 6 sites, significant Δs were restricted to the trochanter and Wards. Significant advantages of HRT/D over HRT were in BMD of total body (- head), total hip and trochanter (all P= 0.01). The differences in mean Δ at these sites were 1.3, 2.6 and 3.9%. At the following, both groups improved significantly -lumbar spine (AP and lateral), forearm shaft and ultradistal tibia/fibula. The weightbearing, site — specific benefits of the combination associated with significant suppression of parathyroid hormone—suggest a beneficial effect on cortical bone. Suppression of bone turnover was significantly greater on HRT/D (serum osteocalcin P= 0.024 and urinary hydroxyproline/creatinine ratio P= 0.035). There was no significant difference in the number of patients who developed fresh VFs during the trial (HRT 8/36, 22%; HRT/D 4/34, 12% - intention to treat); likewise in the number who developed incident nonvertebral fractures. This is the first study comparing the 2 treatments in a fracture population. The results indicate a significant benefit of calcitriol combined with HRT on total body BMD and on BMD at the hip, the major site of osteoporotic fracture. [ABSTRACT FROM AUTHOR]

: Postmenopausal Caucasian women aged less than 80 years (n= 99) with one or more atraumatic vertebral fracture and no hip fractures, were treated by cyclical administration of enteric coated sodium fluoride (NaF) or no NaF for 27 months, with precautions to prevent excessive stimulation of bone turnover. In the first study 65 women, unexposed to estrogen (–E study), age 70.8 ± 0.8 years (mean ± SEM) were all treated with calcium (Ca) 1.0–1.2 g daily and ergocalciferol (D) 0.25 mg per 25 kg once weekly and were randomly assigned to cyclical NaF (6 months on, 3 months off, initial dose 60 mg/day; group F CaD, n= 34) or no NaF (group CaD, n= 31). In the second study 34 patients, age 65.5 ± 1.2 years, on hormone replacement therapy (E) at baseline, had this standardized, and were all treated with Ca and D and similarly randomized (FE CaD, n= 17; E CaD, n= 17) (+E study). The patients were stratified according to E status and subsequently assigned randomly to ± NaF. Seventy-five patients completed the trial. Both groups treated with NaF showed an increase in lumbar spinal density (by DXA) above baseline by 27 months: FE CaD + 16.2% and F CaD +9.3% (both p= 0.0001). In neither group CaD nor E CaD did lumbar spinal density increase. Peripheral bone loss occurred at most sites in the F CaD group at 27 months: tibia/fibula shaft –7.3% (p= 0.005); femoral shaft –7.1% (p= 0.004); distal forearm –4.0% (p = 0.004); total hip –4.1% (p = 0.003); and femoral neck –3.5% (p= 0.006). No significant loss occurred in group FE CaD. Differences between the two NaF groups were greatest at the total hip at 27 months but were not significant [p<0.05; in view of the multiple bone mineral density (BMD) sites, an alpha of 0.01 was employed to denote significance in BMD changes throughout this paper]. Using Cox’s proportional hazards model, in the –E study there were significantly more patients with first fresh vertebral fractures in those treated with NaF than in those not so treated (RR = 24.2, p= 0.008, 95% CI 2.3–255). Patients developing first fresh fractures in the first 9 months were markedly different between groups: –23% of F CaD, 0 of CaD, 29% of FE CaD and 0 of E CaD. The incidence of incomplete (stress) fractures was similar in the two NaF-treated groups. Complete nonvertebral fractures did not occur in the two +E groups; there were no differences between groups F CaD and CaD. Baseline BMD (spine and femoral neck) was related to incident vertebral fractures in the control groups (no NaF), but not in the two NaF groups. Our results and a literature review indicate that fluoride salts, if used, should be at low dosage, with pretreatment and co-treatment with a bone resorption inhibitor. [ABSTRACT FROM AUTHOR]

SUMMARY Aim To examine the effects of improved glycaemic control over 20 weeks on the type and distribution of weight change in patients with type 2 diabetes who at baseline have poor glycaemic control. Methods Forty-three patients with type 2 diabetes and HbA1c > 8.9% were randomised to either intensive glycaemic control (IC) n = 21 or usual glycaemic control (UC) n = 22 for 20 weeks. Dual energy X-ray absorptiometry was used to assess the type and distribution of weight change during the study. Results After 20 weeks HbA1c was significantly lower in patients randomised to IC than UC (HbA1c IC 8.02 ± 0.25% vs. UC 10.23 ± 0.23%, p < 0.0001). In the IC group weight increased by 3.2 ± 0.8 kg after 20 weeks (fat-free mass increased by 1.8 ± 0.3 kg) compared to 0.02 ± 0.70 kg in UC (p = 0.003). The gain in total body fat mass comprised trunk fat mass (IC 0.94 ± 0.5 kg vs. UC 0.04 ± 0.4 kg, p = 0.18) and peripheral fat mass (total body fat – trunk fat) (IC 0.71 ± 0.32 kg vs. UC -0.21 ± 0.28 kg, p = 0.04). Blood pressure and serum lipid concentrations did not change over time in either group. Conclusions Intensive glycaemic control was associated with weight gain which was distributed in similar proportions between the central and peripheral regions and consisted of similar proportions of fat and fat-free mass. Blood pressure and serum lipid concentrations were not adversely affected. [ABSTRACT FROM AUTHOR]

In view of recent investigations suggesting that the circadian rhythm of urine output is reversed in the elderly, the present study was designed to see if increased urine flow at night may be related to change in posture. Urine flow, urea and electrolyte excretion were measured 4-hourly for 6 consecutive days and nights in four catheterized female patients, mean age 83 years. Two were nursed in chairs for 8 h daily for 3 days, followed by total bed-rest for 3 days, and the other two in reverse order. None of the patients showed the morning rise of water and electrolyte excretion which has been described in young people. On full bed-rest, there was no significant day-night difference in water, sodium, potassium, urea or creatinine excretion. Chair nursing produced a negative mean day-night difference in water excretion (−321 ml: <0.001) and in sodium (−11.7 mmol: <0.002), urea (−26.6 mmol: =0.005) and creatinine excretion (−0.6 mmol: =0.008), but had no significant effect on potassium excretion. These results suggest that sitting upright may have important effects on water and electrolyte balance in elderly patients and may contribute to nocturia and nocturnal incontinence. [ABSTRACT FROM PUBLISHER]

Blood pressure has been measured by a single observer using a standardised technique in 163 Type 1 (insulin-dependent) diabetic patients aged 4 to 32 years, 232 of their non-diabetic siblings in the same age range and in 292 of their natural parents. Results for each sex were examined separately by analysis of variance. Systolic pressures were not significantly different overall nor in any single 4-year age band. In contrast, phase IV diastolic pressure was slightly but significantly higher in the diabetic males than in their sibling group overall (increment= +2.8 mmHg; p<0.03), a difference also shown individually within the 16-20 year age band (81.3 versus 76.5 mmHg, p<0.025). There were no significant differences in diastolic pressure between the female groups, and no effect of duration of diabetes on blood pressure was shown in either sex. Eighteen of 97 male diabetic patients (19%) had mean blood pressures above the 90th centile for age, derived from the sibling data, compared with 12 of 137 siblings (9%, p=0.05). The higher blood pressures among the diabetic males could not be explained solely by early nephropathy; familial factors appeared to be important in the determination of elevated blood pressure in this group as well as in the siblings. Alone, these small differences in blood pressure are unlikely to make a major contribution to the incidence of diabetic vascular disease, but the isolated increase in diastolic pressure may indicate altered vascular regulation in Type 1 diabetes. [ABSTRACT FROM AUTHOR]

The blood pressure response to infused angiotensin II (0.3 to 3 ng · kg · min ) was investigated in six normotensive patients with Type 1 (insulin-dependent) diabetes free of complications and in six healthy subjects matched for age, sex and weight. Basal blood pressures (111/68 and 114/72 mmHg) and basal plasma angiotensin II levels (18.0±5.2 and 14.1±2.4 pmol/l; mean + SD) were similar in the diabetic and control groups as were 24 h urinary excretions of sodium (157±88 and 154±84 mmol/24h). Equal increments in plasma angiotensin II were produced during the infusions in the two groups. Increases in both diastolic and systolic blood pressure were significantly greater in the diabetic patients throughout the infusion. Mean diastolic increments were: 6.7 versus 1.3 mmHg (0.3 ng dose), 11.0 versus 6.9 mmHg (1 ng dose) and 16.7 versus 12.3 mmHg (3 ng dose) ( p<0.001). Corresponding figures for systolic pressure were: 8.7 versus 1.3mmHg, 10.3 versus 3.7mmHg and 15.3 versus 8.7mmHg ( p<0.001). Vasopressor responsiveness to angiotensin II is thus increased in Type 1 diabetic patients without complications; it may, therefore, be a consequence of the diabetes rather than of the presence of microvascular disease or hypertension. [ABSTRACT FROM AUTHOR]

The epidemiology, pathogenesis, significance and management of hypertension in diabetic subjects are discussed. In Type 1 diabetes the presence of diastolic hypertension is closely related to the presence of diabetic nephropathy, from the stage of persistent proteinuria onwards. There may also be some elevation of systolic pressure. The apparent increased prevalence of hypertension in Type 2 diabetes is largely explicable, directly or indirectly, by obesity but there may be an excess of systolic hypertension among elderly patients. Hypertension in the diabetic population is associated with an increased incidence of both microvascular and macrovascular complications, but whether the high blood pressure is causal is not clear. The possible roles of sodium and insulin, the renin-angiotensin system, catecholamines and physical factors are explored. All current antihypertensive agents have additional limitations and disadvantages when used in diabetic patients: diuretics and beta-blockers are probably the initial drugs of choice. Only in the case of diabetic nephropathy is there yet reasonable evidence of antihypertensive treatment reducing the rate of progression of the disease. [ABSTRACT FROM AUTHOR]

The perangiographic rupture of a posterior inferior cerebellar artery aneurysm is described and discussed. Only 2 other cases of perangiographic rupture of posterior fossa aneurysms have been found in the literature, and there are fewer than 60 reports of ruptures of aneurysms at all intracranial sites. [ABSTRACT FROM AUTHOR]

Left ventricular diastolic function was assessed by pulsed Doppler echocardiography in non-diabetic controls (n = 11) and in patients with type 1 diabetes without microvascular disease (n = 16; diabetic controls), with microalbuminuria (n = 9), or with early persistent proteinuria (n = 11). The peak filling velocities during the early and atrial phases of left ventricular diastole and their ratio (E:A ratio) were measured. All patients with diabetes had a normal serum concentration of creatinine and exercise electrocardiogram. The mean E:A ratio was significantly lower in those with proteinuria than in the diabetic controls because of an increase in peak atrial filling velocity; most patients with proteinuria had an abnormal E:A ratio of less than 1.0. Multiple regression analysis showed that systolic blood pressure was the major determinant of both the peak filling velocity during the atrial phase of diastole and also left ventricular mass. Blood pressures were significantly higher in the proteinuria group than in the diabetic controls. Glycaemic control and autonomic function did not influence diastolic filling. The slightly raised blood pressures at the earliest stages of diabetic nephropathy are sufficient to alter left ventricular diastolic compliance--this may reflect early hypertensive heart disease. These data do not preclude a specific heart muscle disease related to diabetes, but suggest that these slightly raised blood pressures contribute significantly to left ventricular dysfunction in these patients, in whom the risk of cardiovascular disease is already greatly increased. [ABSTRACT FROM PUBLISHER]

The article offers a discussion on the acceptance of prosthetic counterparts as replacement for malfunctioning heart valves in the routine of clinical procedure for the period of 25 years in Great Britain. An outline of the major developments of heart valve replacement from its inception is discussed. Recently, there was still no agreed standard data presentation on the size of valves.

Daily measurements of finger joint size, grip strength, and body weight have been made throughout 2 complete menstrual cycles in 7 female patients with rheumatoid arthritis and 6 healthy female controls. Sine wave analysis showed significant individual cyclical rhythms (p less than 0.05) for finger joint size (5 patients, 4 controls), nude weight (5 patients, 3 controls), and grip strength (4 patients, 3 controls). In addition analysis of group data, on the assumption of a 28-day cycle, showed a significant cycle for grip strength in the rheumatoid patients, with a nadir at 28 days. In the normal subjects much of the cyclical variation in finger joint size could be explained by changes in weight (median 49.5%), but this was not so in patients with rheumatoid arthritis (median 2.8%). These findings suggest the existence of a cyclical variation in disease activity in rheumatoid arthritis. [ABSTRACT FROM AUTHOR]

The article offers archaeological information on the establishment of the inner structures of the Colchester Castle in Essex, England in the 13th and 14th centuries. A 1977 excavation in the castle showed that the reconstruction of the north and west walls of the chapel in the castle was done in the 13th century. The Period VIIA hall walls and building were also believed to have been extended westward during the 13th century. The author revealed that considerable efforts were launched to strengthen the castle in 1214 and 1215. Excavations in the castle also revealed that minor repairs to the buildings and bailey earthworks within the castle were continuously done between the 13th and 14 centuries.

The article describes the forebuildings and barbican in the Colchester Castle in Essex, England. The architectural history of the castle is divided into three periods. During Period VIIA, a rubble wall with an outer face lined with the vertical foundation of the gateway was identified. The nature of this foundation is said to depict the intention to support light timber superstructure. The contemporary ground level was marked by a second structure found in Period VIIB, which is described with tile-built wall faces. During the VIIIB period, the addition of large forebuilding or barbican strengthened the entrance of the castle, which in turn replaced the VIIB structure.

The building history of Colchester Castle is reconsidered in the light of previously unpublished evidence from excavations, 1931 to 1977. The Norman castle is seen as a development from a late Saxon villa regalis, constructed in two phases, the first beginning c. 1074 x 1076 (by the crown) arid the second c. 1101 (by Eudo Dapifer). It was strengthened in the mid-thirteenth century and maintained into the early fourteenth but thereafter declined, its main function being as a prison. The upper storey of the keep and the southern bailey defences were demolished late in the seventeenth century. [ABSTRACT FROM AUTHOR]

Porcine aortic valves stored in various concentrations of sucrose (50-80%) for up to 52 weeks were examined both histologically and by electron microscopy. The valves were compared with porcine aortic valves stored in a nutrient and antibiotic medium for 12 weeks. Overall preservation was better in those porcine valves stored in sucrose solution than in nutrient and antibiotic medium, the best preservation being in 50% sucrose. Despite wide separation of collagen at that concentration seen on electron microscopy (not noted histologically), tissue preservation was good after storage in sucrose solutions at concentrations up to 80%, at which clumping of collagen and distortion of fibroblasts occurred. It is suggested that sucrose solution is acceptable for the long-term preservation of biological valves. [ABSTRACT FROM AUTHOR]

A bicuspid mitral bioprosthesis was prepared by mounting glutaraldehyde-processed porcine pericardium onto commercially available Brownlee-Yates stents. The bioprostheses were inserted into 17 dogs. Haemodynamic performance and long-term function of the valve was assessed. Of the 11 animals in the survival group, eight died within the 24-72 hour postoperative period. The clinical picture of these animals revealed progressive left ventricular failure although the bioprostheses were tested and found competent both at insertion and at necropsy. The causes of the late deaths were deterioration of the porcine pericardium in two, and cerebral embolism in another. The acute haemodynamic studies showed a significantly high closing reflux from within the tubular bioprosthesis, and this reflux was found to be inherent in the design. It was concluded that any stented bicuspid valve where the stent assumes the function of the papillary muscles, has to be tailored so that parts of the tissue can assume the function of the chordae tendineae to minimise the closing reflux. [ABSTRACT FROM AUTHOR]

Gall bladder motor function is impaired in some patients with diabetes. It has been suggested that the abnormalities of gall bladder motility are confined to those patients with autonomic neuropathy. Erythromycin, a motilin receptor agonist, causes gall bladder contraction in both normal subjects and patients with gall stones with impaired gall bladder emptying. The effect of erythromycin on gall bladder motility in seven patients with diabetes with an autonomic neuropathy, six patients with diabetes without autonomic neuropathy, and 17 normal subjects was studied using ultrasound. There was no significant difference in gall bladder fasting volume between the three groups, but the patients with diabetes with autonomic neuropathy had impaired postprandial gall bladder emptying compared with normal subjects (percentage emptied (SEM) 40 (10.3)% v 64 (2.8)%, p < 0.01) and those with autonomic neuropathy (48 (7.7)%, NS). Erythromycin produced a dramatic reduction in gall bladder fasting volume in patients with diabetes with an autonomic neuropathy, compared with either normal subjects or patients with diabetes without autonomic neuropathy (percentage reduction 62 (4.6)% in patients with autonomic neuropathy, v 37 (17.6)% in those without autonomic neuropathy, and 26 (7.3)% in the normal subjects, (p < 0.02) and returned gall bladder emptying to normal in all patients with impaired emptying. The pronounced effect of erythromycin in diabetic autonomic neuropathy suggests denervation supersensitivity and that the action of erythromycin on the gall bladder is neurally modulated. [ABSTRACT FROM PUBLISHER]

Striking differences were found in the compartmentalization of fatty acids into liver lipid fractions. The saturated fatty acids-lauric, myristic, palmitic and stearic-were incorporated into phosphoglycerides at faster rates with increasing chain lengths, while triglyceride incorporation was almost uniform. The degree of incorporation of the unsaturated fatty acids into phosphoglycerides (structural) compared to triglyceride (storage and energy) was the converse of their oxidation rates. The incorporation of oleic, linoleic and α-linolenic acids was mainly into triglyceride, whereas dihomo-γ-linolenic acid and arachidonic acid were preferentially incorporated into phosphoglycerides. The data suggest that distribution of each fatty acid is different depending on its destination for structural or energy function. [ABSTRACT FROM AUTHOR]