An animal experimental study on pubourethral ligament restoration with platelet rich plasma for the treatment of stress urinary incontinence.

Introduction: Minimally invasive methods for injured ligament and tendon restoration have been developed and gained popularity in recent years. Injury and relaxation of the pubourethral ligament (PUL) can lead to stress urinary incontinence (SUI). The aim of this study was to investigate the impact of injecting platelet rich plasma (PRP) into the PUL following its surgical transection resulting in SUI, confirmed by leak point pressure (LPP) measurements pre- and post-intervention in an experimental animal model. Material and methods: Twenty female adult Sprague-Dawley rats were assigned in 2 groups: 1) treatment group with transection of the PUL and application of PRP at the time of transection and at one month follow-up and 2) a control group, with transection of the PUL only. Leak point pressures (LPPs) were measured prior to transection, immediately following the transection and at 1 and 2 months in both groups. Results: The median LPPs for the control group were: LPP - preT: 35.6 (29.8-44.8) cmH2O, LPP - postT: 14.6 (5.8-19.0) cmH2O, LPP - 1 month: 27.3 (19.2-33.8) cmH2O, LPP - 2 months: 29.0 (27.0-34.0) cmH2O, whereas for the PRP group were: LPP-preT: 40.5 (33.2-46.3) cmH2O, LPP - postT: 15.7 (3.0-24.0) cmH2O, LPP - 1month: 31.6 (24.8-37.4) cmH2O, LPP - 2 months: 36.8 (32.5-45.4) cmH2O. PRP injections on transected PULs significantly increased LPPs at one month follow-up [31.6 cmH2O vs. 27.3 cmH2O, p = .043]. This effect was confirmed at two months [36.8 cmH2O vs. 29.0 cmH2O, p <.001]. Conclusions: Injection of PRP into transected PULs significantly improved LPPs at one and two months' follow-up. However, further experimental and clinical research is needed to evaluate the safety and efficacy of this treatment, in clinical practice

Effects of diet consistency on mandibular growth. A review

Το παρόν άρθρο είναι μια ανασκόπηση που διαπραγματεύεται την επίδραση της σύστασης της διατροφής στην μορφολογία της κάτω γνάθου. Πολλές δημοσιευμένες εργασίες έχουν επικεντρωθεί στη μελέτη της σχέσης της μασητικής λειτουργίας και της αύξησης της κάτω γνάθου, εξαιτίας της θεώρησης ότι η αύξηση της κάτω γνάθου εξαρτάται απο τις φορτίσεις που ασκούνται απο τους μασητήριους μύες. Επιπρόσθετα ο σύγχρονος τρόπος διατροφής με μαλακές τροφές έχει ενοχοποιηθεί για την αύξηση των ορθοδοντικών ανωμαλιών. Ακόμα και στους επίμυς η διατροφή με μαλακή τροφή θεωρείται ένας απο τους παράγοντες που συντελεί σε ανωμαλίες της σύγκλεισης. Όλες οι δημοσιευμένες εργασίες είναι πειραματικές, κυρίως σε τρωκτικά ζώα, επειδή είναι αδύνατον να εφαρμοσθούν ανάλογες μελέτες σε ανθρώπους σε σύντομο χρονικό διάστημα. Οι περισσότερες πειραματικές μελέτες συμπεραίνουν πως οι μασητικές φορτίσεις επηρεάζουν την οστική μάζα, τη ποσότητα του οστού, τη πυκνότητα του οστού, το μήκος και το πλάτος του οστού, το βαθμό της επιμετάλωσης, την γενετική έκφραση, και την ανοσοιστοχημική αντίδραση του κολλαγόνου, όπως και τη δράση των χονδροκυττάρων στο χόνδρο του κονδύλου της κάτω γνάθου. Έχει διατυπωθεί πως το βάρος και η πυκνότητα των γνάθων επίμυων που είχαν διατραφεί με μαλακή τροφή ήταν μικρότερα απο τα αντίστοιχα των ζώων που είχαν διατραφεί με σκληρή τροφή. Επίσης οι γνάθοι και οι κόνδυλοι επίμυων που έχουν διατραφεί με μαλακή τροφή ήταν μικρότεροι σε μέγεθος και παρουσιάζουν μικρότερη πυκνότητα σε σύγκριση με τις γνάθους και τους κονδύλους των ζώων ελέγχου. Επιπρόσθετα το μήκος και το πλάτος των κονδύλων των ζώων που είχαν διατραφεί με μαλακή τροφή ήταν μικρότερα απο τα αντίστοιχα των κονδύλων των ζώων που είχαν διατραφεί με σκληρή τροφή. Η μαλακή διατροφή διαπιστώθηκε ότι επηρεάζει τέλος το βαθμό επιμετάλλωσης όπως και τη δράση των χονδροκυττάρων στο χόνδρο.This article is a review that focuses on the diet consistency and how this affects mandibular morphology. Various published studies focused on the relationship between mastication and growth of the mandible because it is considered that mandibular growth is dependent on the loads exerted by the function of the masticatory muscles. Moreover it has been pointed out that the increase of orthodontic anomalies is due to the modern softer diet. Even in rats, soft diet is one of the factors causing malocclusions. All of the studies have been experimental, mainly in rodents, since this research is impossible to be applied on humans in a short period of time. Most experimental studies suggested that occlusal loading affects bone mass, bone amount, bone density, the length and the width of the bone, the degree of mineralization, the genetic expression, the collagen immunoreaction and the chondrocytes action on the cartilage. It is stated that bone volumes and thickness of the mandible of rats fed with soft diet were smaller when compared to animals fed with hard diet. Also the mandibles and condyles were smaller and less dense in the rats of soft diet as compared to controls. Furthermore the length and the width of the condyle in the soft diet group of animals were smaller as compared to the condyle of the hard diet group of animals. Soft diets affect also the degree of mineralization, and the action of the chondrocytes on the cartilage

Differential Effects of Two Isoenergetic Meals Rich in Saturated or Monounsaturated Fat on Endothelial Function in Subjects With Type 2 Diabetes

OBJECTIVE—To examine the acute effects of consumption of monounsaturated (MUFAs) and saturated fatty acids (SAFAs) on endothelial function in subjects with type 2 diabetes

Immunomodulatory intervention in sepsis by multidrug-resistant Pseudomonas aeruginosa with thalidomide: an experimental study

BACKGROUND: Thalidomide is an inhibitor of tumour necrosis factor-alpha (TNFα) that has been proven effective for the treatment of experimental sepsis by Escherichia coli. It was tested whether it might behave as an effective immunomodulator in experimental sepsis by multidrug-resistant (MDR) Pseudomonas aeruginosa. METHODS: Sepsis was induced by the intraperitoneal injection of 1 × 10(8 )cfu/kg inoculum of the test isolate in a total of 109 Wistar rats divided in three groups as follows: group A controls; group B administered seed oil 30 minutes before bacterial challenge; and group C administered 50 mg/kg of thalidomide diluted in seed oil 30 minutes before bacterial challenge. Blood was sampled for estimation of endotoxins (LPS), TNFα, interferon-gamma (IFNγ), nitric oxide (NO) and malondialdehyde (MDA). LPS was measured by the QCL-1000 LAL assay, TNFα and IFNγ by ELISA, NO by a colorimetric assay and MDA by the thiobarbiturate assay. RESULTS: Mean (± SE) survival of groups A, B and C were 18.60 ± 1.84, 12.60 ± 0.60 and 30.50 ± 6.62 hours (p of comparisons A to C equal to 0.043 and B to C equal to 0.002). Decreased TNFα and NO levels were found in sera of animals of group C compared to group A. Plasma levels of LPS, MDA and IFNγ did not differ between groups. CONCLUSION: Intake of thalidomide considerably prolonged survival in experimental sepsis by MDR P.aeruginosa an effect probably attributed to decrease of serum TNFα

Canagliflozin attenuates the progression of atherosclerosis and inflammation process in APOE knockout mice

Background: Sodium glucose co-transporter2 inhibitors reduce the incidence of cardiovascular events in patients with type 2 diabetes mellitus based on the results of recent cardiovascular outcome studies. Herein, we investigated the efects of long-term treatment with canaglifozin on biochemical and immunohistochemical markers related to atherosclerosis and atherosclerosis development in the aorta of apolipoprotein E knockout (Apo-E(−/−) ) mice. Methods: At the age of 5 weeks, mice were switched from normal to a high-fat diet. After 5 weeks, Apo-E(−/−) mice were divided into control-group (6 mice) treated with 0.5% hydroxypropyl methylcellulose and Cana-group (7 mice) treated with canaglifozin (10 mg/kg per day) per os. After 5 weeks of intervention, animals were sacrifced, and heart and aorta were removed. Sections stained with hematoxylin–eosin (H&E) were used for histomorphometry whereas Masson’s stained tissues were used to quantify the collagen content. Immunohistochemistry to assess MCP-1, CD68, a-smooth muscle actin, MMP-2, MMP-9, TIMP-1 and TIMP-2 expression was carried out and q-PCR experiments were performed to quantify mRNA expression. Results: Canaglifozin-group mice had lower total-cholesterol, triglycerides and glucose levels (P<0.01), while heart rate was signifcantly lower (P<0.05). Histomorphometry revealed that one in seven Cana-group mice versus four in six control mice developed atheromatosis, while aortic root plaque was signifcantly less, and collagen was 1.6 times more intense in canaglifozin-group suggesting increased plaque stability. Immunohistochemistry revealed that MCP-1 was signifcantly less expressed (P<0.05) in the aortic root of canaglifozin-group while reduced expression of a-actin and CD68 was not reaching signifcance (P=0.15). VCAM-1 and MCP-1 mRNA levels were lower (P=0.02 and P=0.07, respectively), while TIMP-1/MMP-2 ratio expression was higher in canaglifozin-group approaching statistical signifcance (P=0.07). Conclusions: Canaglifozin attenuates the progression of atherosclerosis, reducing (1) hyperlipidemia and hyper‑ glycemia, and (2) infammatory process, by lowering the expression of infammatory molecules such as MCP-1 and VCAM-1. Moreover, canaglifozin was found to increase the atherosclerotic plaque stability via increasing TIMP-1/ MMP-2 ratio expression

Syndromes of impaired ion handling in the distal nephron: Pseudohypoaldosteronism and familial hyperkalemic hypertension

The distal nephron, which is the site of the micro-regulation of water absorption and ion handling in the kidneys, is under the control of aldosterone. Impairment of the mineralocorticoid signal transduction pathway results in resistance to the action of aldosterone and of mineralocorticoids in general. Herein, we review two syndromes in which ion handling in the distal nephron is impaired: pseudohypoaldosteronism (PHA) and familial hyperkalemic hypertension (FHH). PHA is a rare inherited syndrome characterized by mineralocorticoid resistance, which leads to salt loss, hypotension, hyperkalemia and metabolic acidosis. There are two types of this syndrome: a renal (autosomal dominant) type due to mutations of the mineralocorticoid receptor (MR), and a systemic (autosomal recessive) type due to mutations of the epithelial sodium channel (ENaC). There is also a transient form of PHA, which may be due to urinary tract infections, obstructive uropathy or several medications. FHH is a rare autosomal dominant syndrome, characterized by salt retention, hypertension, hyperkalemia and metabolic acidosis. In FHH, mutations of WNK (with-no-lysine kinase) 4 and 1 alter the activity of several ion transportation systems in the distal nephron. The study of the pathophysiology of PHA and FHH greatly elucidated our understanding of the renin-angiotensin-aldosterone system function and ion handling in the distal nephron. The physiological role of the distal nephron and the pathophysiology of diseases in which the renal tubule is implicated may hence be better understood and, based on this understanding, new drugs can be developed