The effect of calcium dobesilate on venous function following saphenectomy in coronary artery bypass grafting

BACKGROUND: The aim of this study was to determine whether prophylactic use of calcium dobesilate (CD) can improve venous function after saphenous vein harvest in coronary artery bypass graft (CABG). MATERIALS AND METHODS: A total of 100 patients who underwent elective CABG were divided into four equal groups. In Group A, the greater saphenous vein (GSV) was harvested below the knee and, in Group B, through the knee till the groin. These patients remained untreated. Group C received CD in a dosage of 1500 mg po daily after the GSV was harvested below the knee. Group D received same dosage of CD after the GSV was harvested through the knee till the groin. Venous function of ipsilateral leg was evaluated clinically and by Doppler ultrasonography in the postoperative first week and second month. RESULTS: Clinical findings of venous insufficiency were observed with a similar rate between groups at both early and late periods. In Groups A and B, after 2 months, flow velocities decreased and reflux periods increased significantly. In groups C and D, treatment with CD for 2 months after saphenectomy resulted in a significant increase in flow velocities and a significant decrease in reflux periods. Patients in Groups B and D have significantly more impaired venous functions. CONCLUSION: Saphenectomy results in ipsilateral leg venous dysfunction, which seems to be unrelated to leg swelling and to be more prominent in patients with high-level saphenectomy. In addition, to be careful about the restriction of the saphenectomy procedure into the most appropriate level, prophylactic use of CD can prevent this deterioration when it was added to varice socks.     

Does the MMR vaccine and secretin or its receptor share an antigenic epitope?

In a subgroup of children with autism-spectrum like conditions symptoms seem to appear as a 'regression' (in normal development). It has been postulated that the onset of such autistic symptoms may involve an autoimmune response against the central nervous system and that the antigenic determinant could possibly be gastrointestinal in origin. It has been suggested that the presence of the measles virus and 'autistic enterocolitis' demonstrates the possibility that the MMR triple vaccine may be mediating the inflammation with possible production of antibodies against the virus containing vaccine. Such an antibody may share antigenic determinant to molecules found in the gut. We propose that this may be secretin or its receptor, found in the gut as well as in the central nervous system. The antibody response to the gut may also conceivably occur in the brain at a critical time in development. The modulation of development by secretin may be a static event possibly occurring at a specific time in early childhood development and if it involves an autoimmune response then a disruption in development may result. These hypothesized events can only occur if the MMR vaccine shares antigenic determinants that resemble secretin or any of its receptor types and remains to be studied.     

Can Ki67 immunostaining predict response to radiotherapy in oral squamous cell carcinoma?

AIMS--To determine whether immunohistochemical evaluation of the abatement of proliferating cells after a first course of radiotherapy could predict the final response to treatment in oral squamous cell carcinoma (SCC). METHODS--Frozen sections from 31 cases of histologically confirmed oral SCC were stained with the monoclonal antibody Ki67 at diagnosis and after 10 Gy of radiotherapy. The percentage difference of Ki67 positive cells among the biopsy specimens taken at the beginning and after 10 Gy was correlated with the clinical response obtained at the end of the treatment and its significance determined. RESULTS--The percentage of Ki67 positive cells at diagnosis had no significant correlation with the final therapeutic result of radiotherapy. By contrast, the 32% difference of proliferating cells after 10 Gy of radiotherapy significantly differentiated responders from non-responders (p < 0.05). Furthermore, the abatement of the growth fraction after 10 Gy of radiotherapy was significantly correlated with the complete response (p < 0.01). CONCLUSIONS--These data show that the immunohistochemical evaluation of the abatement of Ki67 positive cells after 10 Gy of radiotherapy provides an independent variable of responsiveness to radiotherapy, allowing a reliable prediction of the final therapeutic result to be made.     

Left ventricular pseudoaneurysm developing as a late complication of coronary artery bypass grafting with apicoseptal plication

Left ventricular pseudoaneurysm is a false aneurysm, which results from a left ventricle rupture contained by adherent pericardium or scar tissue. The most common etiology of left ventricular pseudoaneurysm is acute myocardial infarction but one-third of pseudoaneurysms develop following surgery. We present a case report of a patient who developed a false aneurysm of the left ventricle 2 months following surgical repair of a left ventricular aneurysm with a concomitant coronary bypass.     

Deletion of claudin-10 (Cldn10) in the thick ascending limb impairs paracellular sodium permeability and leads to hypermagnesemia and nephrocalcinosis

In the kidney, tight junction proteins contribute to segment specific selectivity and permeability of paracellular ion transport. In the thick ascending limb (TAL) of Henle's loop, chloride is reabsorbed transcellularly, whereas sodium reabsorption takes transcellular and paracellular routes. TAL salt transport maintains the concentrating ability of the kidney and generates a transepithelial voltage that drives the reabsorption of calcium and magnesium. Thus, functionality of TAL ion transport depends strongly on the properties of the paracellular pathway. To elucidate the role of the tight junction protein claudin-10 in TAL function, we generated mice with a deletion of Cldn10 in this segment. We show that claudin-10 determines paracellular sodium permeability, and that its loss leads to hypermagnesemia and nephrocalcinosis. In isolated perfused TAL tubules of claudin-10-deficient mice, paracellular permeability of sodium is decreased, and the relative permeability of calcium and magnesium is increased. Moreover, furosemide-inhibitable transepithelial voltage is increased, leading to a shift from paracellular sodium transport to paracellular hyperabsorption of calcium and magnesium. These data identify claudin-10 as a key factor in control of cation selectivity and transport in the TAL, and deficiency in this pathway as a cause of nephrocalcinosis.     

SPAK Differentially Mediates Vasopressin Effects on Sodium Cotransporters

Activation of the Na⁺-K⁺-2Cl⁻-cotransporter (NKCC2) and the Na⁺-Cl⁻-cotransporter (NCC) by vasopressin includes their phosphorylation at defined, conserved N-terminal threonine and serine residues, but the kinase pathways that mediate this action of vasopressin are not well understood. Two homologous Ste20-like kinases, SPS-related proline/alanine-rich kinase (SPAK) and oxidative stress responsive kinase (OSR1), can phosphorylate the cotransporters directly. In this process, a full-length SPAK variant and OSR1 interact with a truncated SPAK variant, which has inhibitory effects. Here, we tested whether SPAK is an essential component of the vasopressin stimulatory pathway. We administered desmopressin, a V2 receptor–specific agonist, to wild-type mice, SPAK-deficient mice, and vasopressin-deficient rats. Desmopressin induced regulatory changes in SPAK variants, but not in OSR1 to the same degree, and activated NKCC2 and NCC. Furthermore, desmopressin modulated both the full-length and truncated SPAK variants to interact with and phosphorylate NKCC2, whereas only full-length SPAK promoted the activation of NCC. In summary, these results suggest that SPAK mediates the effect of vasopressin on sodium reabsorption along the distal nephron.The furosemide-sensitive Na⁺-K⁺-2Cl⁻-cotransporter (NKCC2) of the thick ascending limb (TAL) and the thiazide-sensitive Na⁺-Cl⁻-cotransporter (NCC) of the distal convoluted tubule (DCT) are key regulators of renal salt handling and therefore participate importantly in BP and extracellular fluid volume homeostasis.¹ Loss-of-function mutants in the SLC12A1/ A3 genes encoding NKCC2 and NCC cause salt-losing hypotension and hypokalemic alkalosis in Bartter’s and Gitelman’s syndromes,^2,3 whereas their overactivity may contribute to essential hypertension.^4,5 Recently, attention has been focused on the two closely related STE20-like kinases, SPS-related proline/alanine-rich kinase (SPAK) and oxidative stress responsive kinase 1 (OSR1), which can phosphorylate NKCC2 and NCC at their N-terminal conserved threonine or serine residues (T96, T101, and T114 of mouse NKCC2 and T53, T58, and S71 of mouse NCC) and thereby activate the transporters.^6–8 Despite the high homology between SPAK and OSR1 and their overlapping renal expression patterns, distinct roles along the nephron have been suggested based on data from SPAK-deficient and kidney-specific OSR1-deficient mice: deletion of SPAK primarily impairs the function of NCC, whereas deletion of OSR1 negatively affects NKCC2.^9–11 The complex functional properties of a WNK-SPAK/OSR1-N(K)CC interaction cascade are currently being defined.¹² Recently, arginine vasopressin (AVP), signaling via the V2 receptor (V2R), has been identified as an efficient activator of both cotransporters, affecting their luminal trafficking and phosphorylation.^13–18 Because plasma AVP levels may vary not only with the sleep-wake cycle or long-term physiologic challenges, but also with pulsatile changes over the short term, distinct, time-dependent responses may occur.¹⁹ SPAK and OSR1 are well placed to regulate distal NaCl reabsorption in response to AVP. Here we tested the role of SPAK in AVP-induced activation of NKCC2 and NCC, acutely and during long-term treatment. The results suggest that SPAK is an essential kinase that modulates distal nephron function in response to AVP stimulation.     

Low level of Nesfatin-1 is associated with gestational diabetes mellitus

Introduction: Gestational diabetes mellitus (GDM) occurs in ～10–25% of pregnancies. Nesfatin-1, plays a role in carbohydrate metabolism by inhibiting glucagon secretion, besides has a glucose-dependent insulinotropic effect. Explanation of the GDM pathogenesis is important due to preventing gestational complications. We aimed to investigate relationship between GDM and Nesfatin-1.

Material and methods: Seventy-nine pregnant subjects were randomly allocated to either GDM group (GDG, n?=?38) or control group (CG, n?=?41). For GDM diagnosis, 50 and 100?g oral glucose tolerance test (OGTT) were used. Nesfatin-1, insulin and other parameters were measured for all subjects. The homeostasis model assessment-insulin resistance (HOMA-IR) was calculated.

Results: Nesfatin-1 was found lower and insulin was found higher in GDG than CG. Negative correlation has been founded between Nesfatin-1 with weight, BMI, fasting glucose, serum glucose level at first hour of the 50?g OGTT and HOMA-IR.

Conclusion: In this study, patients with GDM had lower Nesfatin-1 levels than without GDM. Therefore, when the Nesfatin-1 effects on the GDM pathogenesis is clear, it may be contributed to diagnosis and treatment of the GDM.     

The prosthodontic restoration of a self-inflicted gunshot maxillofacial defect: a short-term follow-up case report

A self-inflicted gunshot maxillofacial defect was restored with dental implants and various attachments. Following mandibular surgical reconstruction, a fixed full-arch implant-supported prosthesis was fabricated. The maxillary defect was restored with an obturator retained with bar-clip and ball attachments. Crowns with an unfavorable crown-to-root ratio were used to rectify a compromised unilateral interocclusal space. Functional rehabilitation was achieved without any pathologic sequelae and maintained over a 1-year observation period. Provision of a fixed implant-retained mandibular prosthesis opposing a specific design for a maxillary obturator provided short-term and optimistic prognosis in the management of a serious traumatic injury.     

Histomorphometrical analysis of new bone obtained by distraction osteogenesis and osteogenesis by periosteal distraction in rabbits

The aim of this study was to compare histomorphometrically the new bone tissue obtained using two different distraction methods, and evaluate these two methods in terms of their advantages and disadvantages. In 36 New Zealand adult male rabbits, divided into two groups, a gradual distraction was performed using a device placed on the lateral surface of the mandibular corpus. In one group osteotomy was not performed and osteogenesis by periosteal distraction (OPD) only was used. In the other group, conventional distraction osteogenesis (DO) was performed. After a 7-day latent phase, the same distraction protocol was applied to both groups. Each group of rabbits was further divided into three sub-groups killed on the 15th, 30th and 60th days of the consolidation period, and histological analysis was performed. The mean extent of newly formed bone tissue was 14.4 mm2 in the OPD groups and 25.4 mm2 in the DO groups. When compared statistically, there were significant differences between all the DO and OPD sub-groups. The newly formed bone tissue obtained by OPD was rich in interstitial fatty tissue. These results indicate that bone tissue newly formed by OPD is not suitable for occlusal forces.