Does the cerebellar sequential theory explain spoken language impairments? A literature review.

During the past decades, converging evidence from clinical, neuroimaging and neuroanatomical studies has demonstrated the key role of the cerebellum in the processing of non-motor aspects of language. Although more is known about the way in which the cerebellum participates in the mechanisms involved in written language, there is ambiguous information on its role in other aspects of language, such as in non-motor aspects of spoken language. Thus, to contribute additional insight into this important issue, in the present work, we review several original scientific papers focusing on the most frequent non-motor spoken language impairments evidenced in patients affected by cerebellar pathology, namely, verbal working memory, grammar processing and verbal fluency impairments. Starting from the collected data, we provide a common interpretation of the spoken language disorders in cerebellar patients, suggesting that sequential processing could be the main mechanism by which the cerebellum participates in these abilities. Indeed, according to the cerebellar sequential theory, spoken language impairments could be due to altered cerebellar function to supervise, synchronize and coordinate the activity of different functional modules, affecting the correct optimization of linguistic processing.

Functional Changes of Mentalizing Network in SCA2 Patients: Novel Insights into Understanding the Social Cerebellum.

In recent years, increasing evidence of the cerebellar role in social cognition has emerged. The cerebellum has been shown to modulate cortical activity of social brain regions serving as a regulator of function-specific mentalizing and mirroring processes. In particular, a mentalizing area in the posterior cerebellum, specifically Crus II, is preferentially recruited for more complex and abstract forms of social processing, together with mentalizing cerebral areas including the dorsal medial prefrontal cortex (dmPFC), the temporo-parietal junction (TPJ), and the precuneus. In the present study, the network-based statistics approach was used to assess functional connectivity (FC) differences within this mentalizing cerebello-cerebral network associated with a specific cerebellar damage. To this aim, patients affected by spinocerebellar ataxia type 2 (SCA2), a neurodegenerative disease specifically affecting regions of the cerebellar cortex, and age-matched healthy subjects have been enrolled. The dmPFC, left and right TPJ, the precuneus, and the cerebellar Crus II were used as regions of interest to construct the mentalizing network to be analyzed and evaluate pairwise functional relations between them. When compared with controls, SCA2 patients showed altered internodal connectivity between dmPFC, left (L-) and right (R-) TPJ, and right posterior cerebellar Crus II.The present results indicate that FC changes affect a function-specific mentalizing network in patients affected by cerebellar damage. In particular, they allow to better clarify functional alteration mechanisms driven by the cerebellar damage associated with SCA2 suggesting that selective cortico-cerebellar functional disconnections may underlie patients' social impairment in domain-specific complex and abstract forms of social functioning.

Sequential treatment with monofluorophosphate and zoledronic acid in osteoporotic rats.

OBJECTIVE: Osteoporosis is the consequence of an imbalance in bone remodeling caused by excessive resorption or inappropriate bone formation. This paper proposes a sequential treatment with monofluorophosphate (MFP) and zoledronic acid (Z), together with changes in the calcium content in the diet. METHOD: Seven-week-old female Sprague Dawley rats were divided into five groups (n = 21 per group): (1) sham-operated rats (Sham); (2) ovariectomized (OVX) rats fed with a normal calcium diet (OVX); (3) OVX rats fed with a normal calcium diet and treated sequentially with monofluorophosphate and zoledronic acid (OVX.G1); (4) OVX rats sequentially fed with a low calcium diet and then a high calcium diet, without treatment (OVX.G2); (5): OVX rats fed with a low calcium diet and then a high calcium diet, treated sequentially with monofluorophosphate and zoledronic acid (OVX.G3). RESULTS: After 150 days, the OVX.G3 group showed a similar bone volume to that of the Sham group due to an increase in trabecular number. Dual X-ray absorptiometry bone analysis showed an increase of 9.8% compared with OVX rats. Additionally, an increase in the fracture load at the cortical bone and higher fracture load, ultimate load and stiffness in the compression test were found. CONCLUSION: The sequential treatment with monofluorophosphate and zoledronic acid increases trabecular bone mass, bone mineral density and bone strength.

Interval training in men at risk for insulin resistance.

We compared 3 months of eucaloric (12 kcal/kg/wk) steady state aerobic training (AER) to interval training (INT) in men at risk for insulin resistance. Primary outcomes included oral glucose tolerance testing (OGTT) and HOMA-IR 24 h and 72 h after each participants last exercise session. Secondary outcomes were VO2max, anthropometry, and metabolic syndrome expressed as a summed z-score (zMS). We also performed a sub-analysis for participants entering the trial above and below the HOMA-IR study median. Mean (95% CI) AER ( - 12.81 mg/dl; - 24.7, - 1.0) and INT ( - 14.26 mg/dl; - 24.9, - 3.6) significantly improved 24 h OGTT. HOMA-IR did not improve for AER, but did for INT 24 h and 72 h post-exercise. VO2max improved similarly for both groups. Changes in body mass for INT ( - 2.29 kg; - 3.51, - 1.14), AER, ( - 1.32 kg; - 2.62, 0.58)] and percent body fat [INT, - 0.83%; - 1.62, - 0.03), AER ( - 0.17%; - 1.07, 0.06)] were only significant for INT. When examined as a full cohort, zMS improved for both groups. Upon HOMA-IR stratification, only high HOMA-IR AER showed significant improvements, while both low and high INT HOMA-IR participants demonstrated significant reductions (P<0.05). Eucaloric AER and INT appear to affect fasting glucose, OGTT and VO2max similarly, while INT may have a greater impact on HOMA-IR and zMS.

Effect of astaxanthin on cycling time trial performance.

We examined the effect of Astaxanthin (AST) on substrate metabolism and cycling time trial (TT) performance by randomly assigning 21 competitive cyclists to 28 d of encapsulated AST (4 mg/d) or placebo (PLA) supplementation. Testing included a VO2max test and on a separate day a 2 h constant intensity pre-exhaustion ride, after a 10 h fast, at 5% below VO2max stimulated onset of 4 mmol/L lactic acid followed 5 min later by a 20 km TT. Analysis included ANOVA and post-hoc testing. Data are Mean (SD) and (95% CI) when expressed as change (pre vs. post). Fourteen participants successfully completed the trial. Overall, we observed significant improvements in 20 km TT performance in the AST group (n=7; -121 s; 95% CI, -185, -53), but not the PLA (n=7; -19 s; 95% CI, -84, 45). The AST group was significantly different vs. PLA (P<0.05). The AST group significantly increased power output (20 W; 95% CI, 1, 38), while the PLA group did not (1.6 W; 95% CI, -17, 20). The mechanism of action for these improvements remains unclear, as we observed no treatment effects for carbohydrate and fat oxidation, or blood indices indicative of fuel mobilization. While AST significantly improved TT performance the mechanism of action explaining this effect remains obscure.

Small bowel gastrointestinal stromal tumor presenting with gastrointestinal bleeding in patient with type 1 Neurofibromatosis: Management and laparoscopic treatment. Case report and review of the literature.

INTRODUCTION AND IMPORTANCE: Gastrointestinal stromal tumor (GIST) is the most common mesenchymal neoplasm of the gastrointestinal tract. It may be asymptomatic; nevertheless, gastrointestinal bleeding is the most frequent symptom, due to mucosal erosion. Its poor lymph node metastatic spread makes GIST often suitable of minimally invasive surgical approach. The importance of this study is to increase the awareness among physicians about this condition in particular scenarios as in our case and to stress the role of laparoscopic surgery. CASE PRESENTATION: A 74-year-old female patient presented to the emergency department with hematemesis, followed by haematochezia and melena. The patient had a medical history of type 1 Neurofibromatosis (NF1). She underwent, after CT scan, esophagogastroduodenoscopy, and endoscopic haemostasis. Finally, we performed a laparoscopic resection of a mass of the first jejunal loop. The postoperative period was predominantly uneventful. Pathological examination confirmed a low-risk GIST. CLINICAL DISCUSSION: Proximal jejunal GIST may cause an upper and lower gastrointestinal bleeding. A multidisciplinary team approach is mandatory for the correct management of this disease and its complications (bleeding). GISTs are indicated as the most commonly gastrointestinal NF1 associated tumours. In case of localised and resectable GIST surgical treatment is the mainstay and laparoscopic surgery is a valid alternative. CONCLUSION: In case of abdominal bleeding mass in a NF1 patient, it is important to keep in mind the well-known association between NF1 and GIST to facilitate the diagnosis and to quickly perform the appropriate treatment. Laparoscopic approach is safe and effective if the oncological radicality is respected.

16p11.2 microdeletion syndrome: a case report.

BACKGROUND: The recurrent ∼ 600 kb 16p11.2 microdeletion is among the most commonly known genetic etiologies of autism spectrum disorder, overweightness, and related neurodevelopmental disorders. CASE PRESENTATION: Our patient is a 2-year-old white girl from the first pregnancy of a non-consanguineous healthy young white couple (father 33-years old and mother 29-years old). Our patient and her parents' DNA were analyzed by comparative genomic hybridization-array platform. Comparative genomic hybridization-array analysis highlighted a ∼ 600 kb deletion in 16p11.2 region. It has a segregant nature, since it was found in the mother and in her 2-year-old daughter. The microdeletion was confirmed by fluorescence in situ hybridization analysis. CONCLUSIONS: The presented clinical case is worthy of note since the observed microdeletion is often associated with a clinical phenotype tending to overweightness, but the proband (female) was hospitalized due to poor height and weight development, and anorexia. Moreover, the segregant nature of the observed genomic abnormality has to be noted, as well as the phenotypic variability between the mother and daughter. The case described here enriches the phenotypical spectrum linked to the 16p11.2 microdeletion. For these reasons, in the presence of a suspected genetic pathology it is fundamental to study the proband from the clinical point of view, to extend the clinical observation to the parents, and to provide a good family anamnesis. In this way, it is possible to reveal the presence of a familial genetic pathology whose phenotypical outcomes can be highly variable among the members of a family.

Structural cerebellar correlates of cognitive functions in spinocerebellar ataxia type 2.

Spinocerebellar ataxia type 2 (SCA2) is an autosomal dominant neurodegenerative disease involving the cerebellum and characterized by a typical motor syndrome. In addition, the presence of cognitive impairment is now widely acknowledged as a feature of SCA2. Given the extensive connections between the cerebellum and associative cerebral areas, it is reasonable to hypothesize that cerebellar neurodegeneration associated with SCA2 may impact on the cerebellar modulation of the cerebral cortex, thus resulting in functional impairment. The aim of the present study was to investigate and quantitatively map the pattern of cerebellar gray matter (GM) atrophy due to SCA2 neurodegeneration and to correlate that with patients' cognitive performances. Cerebellar GM maps were extracted and compared between SCA2 patients (n = 9) and controls (n = 33) by using voxel-based morphometry. Furthermore, the relationship between cerebellar GM atrophy and neuropsychological scores of the patients was assessed. Specific cerebellar GM regions were found to be affected in patients. Additionally, GM loss in cognitive posterior lobules (VI, Crus I, Crus II, VIIB, IX) correlated with visuospatial, verbal memory and executive tasks, while additional correlations with motor anterior (V) and posterior (VIIIA, VIIIB) lobules were found for the tasks engaging motor and planning components. Our results provide evidence that the SCA2 neurodegenerative process affects the cerebellar cortex and that MRI indices of atrophy in different cerebellar subregions may account for the specificity of cognitive symptomatology observed in patients, as result of a cerebello-cerebral dysregulation.

Neural substrates of motor and cognitive dysfunctions in SCA2 patients: A network based statistics analysis.

Spinocerebellar ataxia type 2 (SCA2) is an autosomal dominant neurodegenerative disease characterized by a progressive cerebellar syndrome, which can be isolated or associated with extracerebellar signs. It has been shown that patients affected by SCA2 present also cognitive impairments and psychiatric symptoms. The cerebellum is known to modulate cortical activity and to contribute to distinct functional networks related to higher-level functions beyond motor control. It is therefore conceivable that one or more networks, rather than isolated regions, may be dysfunctional in cerebellar degenerative diseases and that an abnormal connectivity within specific cerebello-cortical regions might explain the widespread deficits typically observed in patients. In the present study, the network-based statistics (NBS) approach was used to assess differences in functional connectivity between specific cerebellar and cerebral "nodes" in SCA2 patients. Altered inter-nodal connectivity was found between more posterior regions in the cerebellum and regions in the cerebral cortex clearly related to cognition and emotion. Furthermore, more anterior cerebellar lobules showed altered inter-nodal connectivity with motor and somatosensory cerebral regions. The present data suggest that in SCA2 a cerebellar dysfunction affects long-distance cerebral regions and that the clinical symptoms may be specifically related with connectivity changes between motor and non-motor cerebello-cortical nodes.

Prevention of neural tube defects and maternal gestational diabetes through the inositol supplementation: preliminary results.

OBJECTIVE: Our study aims to demonstrate that the use in the preconceptional period until the 24th week of pregnancy of inositol and folic acid, first of all, preserves the product of conception from neural tube defects (NTDs) and then, thanks to inositol supplementation, it possibly counteracts and prevents the onset of maternal gestational diabetes (GDM). PATIENTS AND METHODS: We have collected data derived from pregnant women arrived at our laboratory, from January 2014 to January 2016, with no family history of type 2 diabetes and hypertension. The first group (n = 68 women) was treated from the preconceptional period until the 24th week of pregnancy with 1.75 g/day myo-inositol, 250 mg/day D-chiro-inositol, 12.5 mg/day Zinc pidolate, 100 mg/day methylsulfonylmethane, 120 mg/day Vitamin C and 400 mcg/day (6S)-5-methyltetrahydrofolic acid. The control group (n = 72) was only treated with 400 mcg/day folic acid. The main outcome measure was the prevalence of maternal GDM. Secondary outcome measures were the prevalence of NTDs and fetal macrosomia. RESULTS: A significant difference was found regarding body mass index (BMI), fasting oral glucose tolerance test (OGTT), after 1-h-glucose OGTT, 2-h-glucose OGTT, glycated hemoglobin (HbA1c) and serum folate, between the two groups. Five infants, in the control group, weighted greater than 4 kg. Moreover, we found a positive correlation between HbA1c and OGTT at the 24th week of pregnancy. CONCLUSIONS: This study shows the efficacy of preconceptional supplementation of inositol to reduce the risk of the onset of GDM and to confirm the importance of folic acid supplementation to avoid NTDs development. Moreover, the positive correlation between HbA1c and OGTT may be useful to consider the use of HbA1c as a single tool for GDM prevention and diagnosis in selected woman in pregnancy.

Microstructural MRI Basis of the Cognitive Functions in Patients with Spinocerebellar Ataxia Type 2.

Spinocerebellar ataxia type 2 (SCA2) is an autosomal dominant neurodegenerative disease involving the cerebellum. The particular atrophy pattern results in some typical clinical features mainly including motor deficits. In addition, the presence of cognitive impairments, involving language, visuospatial and executive functions, has been also shown in SCA2 patients and it is now widely accepted as a feature of the disease. The aim of the study is to investigate the microstructural patterns and the anatomo-functional substrate that could account for the cognitive symptomatology observed in SCA2 patients. In the present study, diffusion tensor imaging (DTI) based-tractography was performed to map the main cerebellar white matter (WM) bundles, such as Middle and Superior Cerebellar Peduncles, connecting cerebellum with higher order cerebral regions. Damage-related diffusivity measures were used to determine the pattern of pathological changes of cerebellar WM microstructure in patients affected by SCA2 and correlated with the patients' cognitive scores. Our results provide the first evidence that WM diffusivity is altered in the presence of the cerebellar cortical degeneration associated with SCA2 thus resulting in a cerebello-cerebral dysregulation that may account for the specificity of cognitive symptomatology observed in patients.

Obesity does not induce abnormal CSF pressure in subjects with normal cerebral MR venography.

Obesity has been shown to increase lumbar CSF pressure in healthy subjects. The authors studied lumbar CSF opening pressure in 18 obese, 33 overweight, and 49 nonoverweight subjects with normal MRI and MR venography (MRV) of the brain. No subject had a CSF pressure above 200 mm H2O. Obesity does not cause abnormal CSF pressure in subjects with normal MRV. Individuals with a CSF pressure higher than 200 mm H2O should undergo MRV to exclude cerebral venous thrombosis.

Serum ferritin levels in celiac disease.

Of the various common assayed parameters of iron metabolism, serum ferritin levels are the most discriminatory in distinguishing between non-treated celiac disease and other gastrointestinal disorders in the pediatric age group. Patients on normal diets usually have very low ferritin levels that increase at an average rate of 1 microgram/1/month when placed on a gluten-free diet. When the patient returns to a normal diet, however, ferritin levels decrease rapidly at an average rate of about 4 microgram/1/month. There is a relationship between abnormal intestinal changes and low ferritin levels in celiac disease with improvement in both when the patient is on a gluten-free diet. It is suggested that serial blood ferritin evaluations together with the leukocyte migration inhibition factor production assay should eliminate the need for invasive intestinal biopsies for the confirmation and possible follow-up to response to treatment.

Kinetics of lactate transport into rat liver in vivo.

Lactate clearance by liver plays an important role in lactate homeostasis and in the development of lactic acidosis. The role of lactate delivery to liver as a limiting factor in hepatic uptake of lactate is unclear. Lactate delivery of mechanisms could be important if rates of lactate transport approximate rates of lactate metabolism by liver. The rates of lactate transport into liver have been determined in vitro with isolated liver cells and the results have been conflicting. Therefore, the present studies measure the rate of transport of [14C]-L-lactate, and its poorly metabolizeable stereoisomer, [14C]-D-lactate, into rat liver in vivo using a portal vein injection technique. The transport of [3H]-water and of [14C]-sucrose, an extracellular reference compound, were also studied. Portal blood flow was determined from the kinetics of [3H]-water efflux in liver and was 1.93 +/- 0.22 mL/min/g. The volumes of distribution of [14C]-L-lactate, and [14C]-sucrose were 1.31 +/- 0.22, 0.71 +/- 0.07, and 0.22 +/- 0.07 mL/g, respectively. The extraction of unidirectional influx of [14C]-L-lactate and [14C]-D-lactate by rat liver was 93% +/- 10% and 91% +/- 9%, respectively. The rate of lactate transport into rat liver in vivo, 1.8 mumols.min-1.g-1, is approximately twofold greater than the rate of lactate metabolism by rat liver reported in the literature. Therefore, lactate uptake by liver may not be limited by transport under normal conditions. However, conditions such as decreased portal blood flow, which slow lactate delivery to liver by 50% or more, could cause lactate uptake by liver to be limited by transport of circulating lactate.

Sleep disturbances in children with atopic dermatitis.

OBJECTIVES: To test hypotheses based on clinical impressions that children with atopic dermatitis (AD) have frequent sleep-related problems, including difficulty falling asleep, night waking due to itching and scratching, and daytime symptoms of tiredness and irritability. DESIGN: Sleep habits and behaviors were assessed using the Child Sleep Behavior Scale (a 22-item Likert-type questionnaire for parents) in children with AD compared with normative data for age. Twelve questions were added to the questionnaire to address sleep-related habits relevant to night time pruritus, and to assess daytime behavioral symptoms of inadequate sleep. SETTING: Tertiary care center. PATIENTS: Fifty-nine children between ages 5 and 12 years meeting criteria for AD representing a referral population to a regional center. RESULTS: Compared with normative data, children with AD showed notable differences for nine of the 22 items on the sleep questionnaire, including the following: greater difficulty falling asleep, frequent night waking, less total sleep, and greater difficulty awakening for school. The children with AD also reported frequent daytime tiredness and irritability, and the severity of AD symptoms showed moderate correlations with sleep problems and with daytime behaviors suggestive of inadequate sleep. Difficulty falling asleep and night waking correlated with daytime behavior and discipline problems. CONCLUSIONS: Children with AD often have disrupted sleep and daytime behavioral difficulties associated with insufficient sleep. Improved sleep may be an important treatment focus in the clinical management of children with AD.

Epithelioid sarcoma. Report of a case.

Epithelioid sarcoma is familiar to orthopedic surgeons but not to dermatologists. Because this malignant neoplasm presents as a subcutaneous mass, often with overlying epidermal changes, the patient may be seen by a dermatologist for evaluation. The differential diagnosis often includes nodular fasciitis and tenosynovitis. The histopathologic interpretation of the biopsy specimen may be difficult, so it is helpful for the physician to suspect and consider epithelioid sarcoma in the differential diagnosis given to the pathologist. Early, accurate diagnosis can be achieved and can thus spare the patient significant morbidity or even death.

Antimicrobial therapy of Broviac catheter infections in pediatric hematology oncology patients.

Long-term therapy of pediatric oncology patients has been facilitated by permanent indwelling venous catheters. Over a 3-year period, 54 Broviac catheters were placed in 43 oncology patients and two hemophiliacs. There were 20 episodes of sepsis in 14 patients and the most common bacteria were S epidermidis (4), S aureus (4), and K pneumoniae (3). Catheter exit site infections occurred ten times in six patients; S aureus eight of ten. Antibiotic therapy without catheter removal was successful in 18 of 20 children with catheter sepsis and 8 of 10 patients with exit site infections. These data strongly suggest that although catheter-related infections are common, removal of Broviac catheters is not required for successful treatment of the infection.

Matrix metalloproteinases. Their role in degenerative chronic diseases of abdominal aorta.

BACKGROUND: The main chronic degenerative diseases of the abdominal aorta, namely aneurysmatic and steno-obstructive pathologies, have a common denominator: atherosclerosis. Both pathologies are characterised by the destruction of the structural integrity of the extracellular protein matrix (ME). A number of studies have shown the presence and involvement of a group of enzymes with proteolytic activity towards one or more ME components, the matrix metalloproteinases (MMPs), in the pathogenesis of aneurysms of the abdominal aorta. Other authors have underlined the role of MMPs in the proliferation and migration process of smooth muscle cells into the intima in the pathogenesis of atheromasic plaque. The aim of this study was to evaluate the possible role of these enzymes in the pathogenesis of chronic degenerative diseases of the aorta. METHODS: Fragments of aortic wall were removed from patients undergoing elective aortic surgery for aneurysms (14 patients) or aortic steno-obstruction (4 patients). The samples obtained were treated appropriately and then subject to immunohistochemical analysis. The preparations were incubated with specific anti-MMP antibodies and were also incubated with substrate and chromogen, forming a pigmented precipitate on the site of the antigen, before being observed using an optic microscopic at an enlargement of 250x. Nuclear positivity linked to the presence of the antigen testified the validity of staining. Lastly, the MMP INDEX, or in other words the number of positive cells out of 100, was stained in the adventitia and in the tunica media in each preparation. RESULTS: MMPs were divided into three main groups: interstitial collagenase (MMP1) which degrade type I and III native collagen; gelatinases (MMP9, MMP2) which act on elastin and type IV collagen; stromelysins (MMP3) with specific proteolytic action towards proteoglycans, fibronectin and laminine. In our experience, those preparations obtained from aorta affected by steno-obstructive pathologies (4 patients) revealed the presence of MMPs with a preferential localisation on the intimal side of the tunica media. In particular, the increased activity of gelatinases MMP9 in atherosclerotic aorta might be responsible for destroying the internal elastic lamina and fostering the proliferation and migration of smooth muscle cells and the formation of atheromasic plaque. On the other hand, preparations obtained from aneurysmatic aorta (14 patients) showed an opposite situation with a preferential localisation within the adventitia and on the adventitial side of the media. Above all, the loss of elastin represents an essential stage in the formation of aortic aneurysms. CONCLUSIONS: This study concords with numerous authors who have demonstrated the involvement of proteinase MMPs in the development of aortic aneurysms and their possible role in the pathogenesis of atheromasic plaque. The different origin of these enzymes (inflammatory cells and macrophages or endothelial cells) may be the result of different pathogenetic mechanisms. Although they present different pathogenetic features, aortic aneurysms and steno-obstructions have a common denominator in atherosclerosis. The mechanisms responsible for their evolution towards one or other form are not known. The different expression of MMPs in the context of the aortic wall represents a field for future research.

[Clinical approach in hypertensive elderly patients]. / Considerazioni sull'approccio clinico di pazienti anziani ipertesi.

Hypertension in the elderly represents a cardiovascular risk factor which increases due to ageing and to the raise of blood pressure (BP) values. The occurrence of hypertension depends on an interaction between genes and environment. An available antihypertensive therapy causes a reduction in the incidence of cardiovascular events. An antihypertensive therapy in the elderly must take into account: in these subjects BP might be spontaneously lower over 30 mmHg in 24 hours; people normally have a postprandial BP reduction; sudden raises or falls of pressure cause cerebral hypoperfusion; some adverse vents of hypertensive drugs worsen their quality of life, not reducing myocardial hypertrophy; possible electrolytic troubles might worsen a congestive heart failure; drastic diets cause a raise in the incidence of colorectal tumours; a high heart rate increases the risk of sudden death; a chronic NSAID intake might cause or aggravate a hypertensive state; a reduction of natrium chlorure and lipides in the diet might cause a BP fall. In short, the BP reduction should be gradual in the hypertensive elderly in order to avoid the occurrence of cardiovascular events, diets should be balanced, rich in fibres and vitamins to avoid colorectal tumours. Besides, NSAID must be used by these patients for a short time and all therapeutic interventions should improve their quality of life.

An overview of foot disease associated with diabetes mellitus.

The pathologic mechanisms by which diabetes creates alterations in the neural, vascular, and immunologic systems are complex. Thanks to increased knowledge, clinicians can intercede and prevent disease and disability. Appropriate glycemic control for all patients with diabetes can prevent neuropathy and vascular changes. Early detection and appropriate intervention for patients at risk for ulceration must be a part of every nurse's practice. Education of the patient or significant other must be included as part of instruction provided to those with diabetes. In contrast to the devastating results of the pathology of diabetes, these interventions seem "painfully" simple.