Ultrasound vasography evaluation of radial arterial grafts used for coronary arterial bypass surgery

OBJECTIVES: For coronary bypass surgery, radial arteries are often used as bypass grafts. Some of these arteries however, have arteriosclerotic lesions. We attempted to evaluate the relationship between arteriosclerosis and vasodilation. METHODS: Prior to bypass surgery, 20 patients underwent ultrasound vasography to determine the condition of their radial and brachial arteries. Flow-mediated dilation, which is the same as endothelium-dependent vasodilation, was measured in the brachial artery of the nondominant arm by reactive hyperemia after 5-minute forearm ischemia. Vasodilation after application of a sublingual glyceryl trinitrate spray was also measured. RESULTS: During surgery, 4 of 20 radial arteries demonstrated calcification, and 3 of the 4 could be used by removing the calcified part. However, the other artery, which had extensive calcification that could not be detected by ultrasound vasography, was discarded. The amount of vasodilation seen after the administration of sublingual glyceryl trinitrate had no correlation with calcified grafts. Calcified radial arteries demonstrated significantly poor brachial artery vasodilation by an endothelial-dependent vasodilation test. CONCLUSIONS: Calcification in radial arteries can thus only be evaluated by flow-mediated dilation.     

EFFECTS OF V2 RECEPTOR ACTIVITY ON THE PRESSOR RESPONSE TO VASOPRESSIN IN THE RAT

1. To determine the contribution of V1 and V2 receptor activity on the enhancement of reflex buffering of the pressor response to arginine-vasopressin (AVP), mean arterial pressure (MAP) and heart rate (HR) changes were examined in response to graded injections of phenylephrine, AVP, or Phe2Orn8OT, a potent, selective V1-receptor agonist in the absence and presence of Val4DArg8VP, a potent, selective V2-receptor agonist. 2. There were no significant differences in MAP responses to the V1 agonist in the absence and presence of the V2 agonist in either conscious intact or autonomic-blocked rats. 3. Autonomic blockade with methscopolamine and hexamethonium increased the pressor sensitivity to phenylephrine threefold. In contrast, the pressor sensitivities to AVP and Phe2Orn8OT were increased 14-fold and 11-fold, respectively, by autonomic blockade. 4. V2-receptor activity does not have any inherent vasocative action or synergistic vasoactive action with V1-receptor activity. 5. V2 receptors do not play a role in enhancing reflex buffering of the pressor response to AVP; V1 receptors are suggested to play the role.     

Early Gastric Lymphoma Coexisting with Reactive Lymphoreticular Hyperplasia (RLH) -A Case Report-

A 34-year-old female visited our hospital because of epigastralgia. We performed an upper gastrointestinal x-ray examination, and both conventional endoscopy and dye-spraying endoscopy (indigo-carmine contrast method). We diagnosed early gastric lymphoma which simulated Borrmann 3 type gastric cancer with IIb type early gastric cancer on the middle body and reactive lymphoreticular hyperplasia (RLH) of cobble stone-like granular pattern by endoscopic appearance on the lower body. Although dye-spraying endoscopy showed the details of the mucosa, it was very difficult to diagnose the lesions correctly by gross appearance alone. Because gastric lymphoma arises from the mucosal or submucosal layer and spreads in the mucosa diffusely, ultrasonic visualization by echo-endoscopy might be useful in the diagnostic procedure. We report a case of early gastric lymphoma coexisting with RLH; both lesions showed uncommon endoscopic features.     

Combination therapy with an angiotensin-converting enzyme (ACE) inhibitor and a calcium antagonist: beyond the renoprotective effects of ACE inhibitor monotherapy in a spontaneous hypertensive rat with renal ablation.

To assess the renal benefits of combined angiotensin-converting enzyme inhibition and calcium antagonism, we studied the antihypertensive and renoprotective effects of temocapril (TMP) alone or in combination with azelnidipine (AZN) in a spontaneously hypertensive rat (SHR) remnant kidney model of chronic renal failure. Male 5/6-nephrectomized SHR/Izumo rats were randomly assigned to receive vehicle (control group), TMP (TMP group; 10 mg x kg(-1) x day(-1)), AZN (AZN group; 3 mg x kg(-1) x day(-1)), or both (TMP+AZN group) orally for 12 weeks. Systolic blood pressure (SBP) and urinary excretion of albumin (UalbV) were measured every 2 weeks. At the end of the experiment, serum creatinine (Scr), heart weight (HW), and blood urea nitrogen (BUN) levels were measured and the remnant kidneys were examined to determine the index of glomerular sclerosis (IGS). SBP and UalbV in the control group increased progressively throughout the experimental period. TMP, AZN, and TMP+AZN blocked the development of hypertension. TMP+AZN did not enhance the antihypertensive effects of either TMP or AZN used singly. TMP, AZN, and TMP+AZN all significantly decreased the UalbV, Scr, BUN, and HW/body weight (BW) ratio. The level of UalbV and the HW/BW ratio in the TMP+AZN group were significantly lower than those in the TMP and AZN groups, and the level of Scr in the TMP+AZN group was significantly lower than that in the TMP group. TMP, AZN, and TMP+AZN all significantly protected against an increase in the IGS. The IGS in the TMP+AZN group was significantly lower than that in the TMP and AZN groups. These results indicate that both TMP and AZN have antihypertensive and renoprotective effects in this model. They also suggest that simultaneous administration of TMP and AZN provides greater renoprotective effects than TMP alone.     

Kinin-generating Cascade in Advanced Cancer Patients and in vitro Study

The role of the bradykinin-generating system in the pathogenesis of cancer was explored by simultaneously measuring plasma prekallikrein (PK), the precursor of kallikrein, which is the major enzyme responsible for kinin generation, and plasma kininogens (KNG), which are precursors of kinin, in patients with various cancers. The mean value of plasma PK in healthy volunteers was 2.5 ± 0.5 (mean ± SD) units/mg plasma protein and that in cancer patients (all stage IV) was 1.7 ± 0.7 units/ mg plasma protein. The mean value of plasma KNG in healthy volunteers was 12.5 ± 2.0 ng kinin equivalents/mg plasma protein and that in cancer patients was 10.9 ± 2,8 ng. These data showed that plasma PK and plasma KNG values were significantly lower in cancer patients compared with healthy volunteers ( P < 0.0005 for PK; 0.0005 < P < 0.005 for KNG; n = 28 for healthy subjects; n = 29 for cancer patients). These data appear to indicate that conversion of PK to kallikrein would probably occur with concomitant consumption of KNG by newly generated kallikrein for kinin generation in cancer patients. Early stage cancer patients showed little difference from healthy volunteers. For the in vitro study, activation of purified Hageman factor (HP) and PK was examined by using cancer cell lines and virus-transformed cells that produced plasminogen activator (PA) at a high rate. Both HF and PK were activated in the presence of plasminogen. Diploid cell lines and primary fibroblasts, which did not produce PA, activated neither HF nor PK. Taking all these data together, we conclude that kinin generation does occur in the plasma of patients with advanced cancer, and that one of the initiation mechanisms of the kinin-generating cascade appears to be mediated by plasmin and to depend on cancer cell-derived PA activity.     

Antigen-specific immunotherapy for autoimmune diseases

The status of autoimmune disease therapies is not satisfactory. Antigen-specific immunotherapy has potential as a future therapy that could deliver maximal efficacy with minimal adverse effects. Several trials of antigen-specific immunotherapy have been performed, but so far no clear directions have been established. With regard to antigen-specificity in the immune system, T cells are essential components. However, at present, we do not have a sufficient range of strategies for manipulating antigen-specific T cells. In this review, the authors propose that T cell receptor gene transfer could be used for antigen-specific immunotherapy. In the proposed technique, important disease-related and, thus, antigen-specific T cells in patients would first be identified, and then a pair of cDNAs encoding alpha and beta T cell receptors would be isolated from these single T cells. These genes would then be transferred into self lymphocytes. These engineered antigen-specific cells can also be manipulated to express appropriate functional genes that could then be applied to specific immunotherapy.     

Diagnosis and treatment of slipped capital femoral epiphysis: Recent trends to note

Slipped capital femoral epiphysis (SCFE) is not frequently encountered during routine practice and diagnosis and treatment are often delayed. It is important to understand symptoms and imaging features to avoid delayed diagnosis. After the diagnosis is made correct classification of the disease is required. The classification should be based on the physeal stability in order to choose safe and effective treatment. However, surgeons should bear in mind that the assessment is challenging and actual physeal stability is not always consistent with the stability predicted by a clinical classification method.

A case of an epithelioid glioblastoma with the BRAF V600E mutation colocalized with BRAF intact low‐grade diffuse astrocytoma

Epithelioid glioblastomas are one of the rarest histological variants of glioblastomas, which are not formally recognized by the World Health Organization (WHO) classification. Epithelioid glioblastomas usually occur as primary lesions, but there have been several reports of secondary epithelioid glioblastomas or epithelioid glioblastomas with pre‐ or co‐existing lesions to date. The serine/threonine‐protein kinase B‐Raf (BRAF) V600E mutation has been found at a high frequency of 54% in epithelioid glioblastomas. We present a case of a 26‐year‐old female patient with an epithelioid glioblastoma with the BRAF V600E mutation in her right frontal lobe. In the present case, a low‐grade diffuse astrocytoma component had colocalized with the epithelioid glioblastoma. The component presented prominent calcification on neuroimages as well as by histology, and low‐grade diffuse astrocytoma was considered to be a precursor lesion of an epithelioid glioblastoma. However, the BRAF V600E mutation was detected only in epithelioid glioblastoma but not in low‐grade diffuse astrocytoma. To the best of our knowledge, this is the first report demonstrating a discrepancy in the BRAF V600E mutation states between epithelioid glioblastoma and colocalized low‐grade astrocytoma.