AlphaV beta3 (αvβ3) integrin inhibition reduces leukocyte–endothelium interaction in a pressure-induced reperfusion model

The leukocyte-endothelium interaction is known to contribute to reperfusion injury, which is considered to participate in the pathophysiology of pressure ulcers, and integrin alphaV beta3 (alphavbeta3) has been shown to mediate the processes of cellular adhesion in various types of cells. This study aims to clarify leukocyte behavior in our original microcirculatory pressure-induced reperfusion model, which can visualize the microcirculation in vivo. We also estimated the effect of alphavbeta3 integrin inhibition on the reduction of the leukocyte-endothelium interaction. Mice with dorsal skinfold chambers were divided into three groups: the baseline group (n=6), in which animals received no compression; the compression-reperfusion group (n=6), in which animals underwent 2-hour compression of the dorsal skin, followed by release, and the inhibitor-treated group (n=7), in which an alphavbeta3 inhibitor, CP4715, was administered in addition to the compression-release procedure. Staining with rhodamine 6G quantitatively visualized leukocyte behavior under the intravital fluorescent microscope. Compression-reperfusion induced a significant increase in rolling, sticking, and extravasation of the leukocytes. Treatment with the inhibitor strikingly reduced leukocyte sticking and extravasation. The present experiment has provided evidence that alphavbeta3 inhibition reduces leukocyte-endothelium interaction in our original pressure-induced reperfusion model.     

Arthroscopic Shoulder Stabilization: Is There Ever a Need to Open?

Recent studies show comparable results of arthroscopic shoulder stabilization techniques compared with the gold standard open Bankart reconstruction. Great technical advances and ever-increasing surgeon experience have rendered pathology once deemed an indication for open surgery as treatable by arthroscopic means. With this movement toward a more universal application of all-arthroscopic techniques, we might consider the following question: Is there ever a need to open? To answer this question, we must first consider normal anatomy and then appreciate the contribution of deranged pathoanatomy to recurrent instability in each individual case. The surgeon must then determine whether this is best addressed via an arthroscopic or open technique. Arthroscopy, as compared with open stabilization procedures, holds the potential benefits of decreased morbidity rates, early functional rehabilitation, and improved range of motion. Despite potential advantages, arthroscopic stabilization is clearly contraindicated when a significant pathologic lesion contributing to recurrent instability cannot be adequately addressed as a result of the limitations of current techniques or instrumentation. On the basis of this principle, we believe that sizable glenohumeral bone defects remain the only absolute contraindication to an all-arthroscopic approach. Many complicating issues, such as attenuated capsule, humeral avulsion of the glenohumeral ligament lesions, cases of revision surgery, and collision or contact athletes, exist and warrant close attention. We prefer to think of these situations as “challenges” for which both arthroscopic and open surgery should be considered, rather than as true contraindications to arthroscopic shoulder stabilization. We are, by no means, advocating arthroscopic treatment in all cases of shoulder instability, because this would represent a gross oversimplification of the issues at hand. However, we do acknowledge that the steadfast contraindications to arthroscopic shoulder stabilization are decreasing every day.     

Analysis of ischemia-reperfusion injury in a microcirculatory model of pressure ulcers

The aim of this study was to establish a pressure ulcer model that visualizes the microcirculation, and to examine the participation of ischemia-reperfusion injury in the pathophysiology of pressure ulcers. An original system composed of a new skin fold chamber and compression device allowed loading quantitative vertical stress to the skin. An intravital microscopic technique enabled direct visualization of the microcirculation in the physiological condition and in response to pressure application. To estimate the effect of ischemia-reperfusion injury, animals were divided into two groups: the compression-release group (n = 8), in which the animals received four cycles of compression-release which consisted of 2 hours of compression followed by 1 hour of pressure release; and the compression alone group (n = 8) in which the animals underwent continuous compression for 8 hours. Functional capillary density was quantified before the compression procedure and on day 1 (35 hours) after the first evaluation. The cyclic compression-release procedure significantly decreased functional capillary density as compared to continuous compression, indicating that in our experimental setting repetition of ischemia-reperfusion cycle more severely damaged the microcirculation than single prolonged ischemic insult. This finding supports the significant contribution of ischemia-reperfusion injury to the pathophysiology of pressure ulcers at the level of dynamic in vivo microcirculation.     

Intramuscular distribution of nerves supplying the soleus muscle in the chimpanzee

The human soleus muscle is considered a specialized muscle in terms of its origin, insertion and muscle fibre architecture (especially with regard to the existence of the bipenniform part). Its peculiarities have been understood as results of erect posture and bipedal walking (Frey, 1913). Sekiya (1991) pointed out that another feature of the human soleus muscle the nerve supply, i.e. the muscle received two kinds of nerves, the anterior branch (R. anterior) and the posterior branch (R. posterior); the former supplied the bipenniform part at the anterior surface of the muscle and communicated with the R. posterior within the muscle. In nonhuman primates, the soleus muscle has no bipenniform part and the nerve, identical with the R. anterior to the human soleus muscle, is unknown. The purpose of the present study is to clarify the pattern of the nerve supply to the soleus muscle in the chimpanzee, with special reference to the intramuscular distribution of the nerves and to discuss the origin of the R. anterior to the human soleus muscle from a comparative anatomical point of view. Six soleus muscles from three chimpanzees (Pan troglodytes) were examined under a stereomicroscope to clarify the intramuscular distribution of nerves supplying these muscles. The nerves supplying the soleus muscle were classified into three types according to the sites of their entry into the muscle. The first group nerve was the thickest of all nerves innervating the muscle, entered the muscle at the posterior surface of the proximal third and was considered as homologous with the R. posterior in the human.(ABSTRACT TRUNCATED AT 250 WORDS)     

Serum immunoreactive beta-glucuronidase determined by an enzyme-linked immunosorbent assay in patients with hepatic diseases.

An enzyme-linked immunosorbent assay (ELISA) was developed for human beta-glucuronidase, using a specific polyclonal antibody raised against the purified enzyme. beta-Glucuronidase from human liver consisted of three subunits with molecular mass of 76, 64 and 18 kDa. The assay offered a specific, sensitive and convenient means of measuring immunoreactive beta-glucuronidase in human sera. beta-Glucuronidase activity determined by the conventional method appeared to be extremely low, indicating that in human sera beta-glucuronidase exists in an enzymatically inactive form. The sensitivity of the assay permitted the detection of 1-100 ng of purified beta-glucuronidase. A mean serum level in normal subjects was 108 +/- 25 ng/ml (mean +/- S.D.). A high level of beta-glucuronidase was found in sera of patients with severe hepatocellular necrosis, including liver cirrhosis (152 +/- 130 ng/ml) and chronic active hepatitis (220 +/- 99 ng/ml), whereas no significant increase of the enzyme protein was observed in chronic persistent hepatitis (102 +/- 42 ng/ml). beta-Glucuronidase was also increased in sera of patients with primary hepatoma (156 +/- 125 ng/ml). The immunoreactive beta-glucuronidase determined in this assay was thought to be a supplementary serological indicator for hepatocellular necrosis.     

Five cases of intracranial lipoma; CT and magnetic resonance images]

We encountered five cases of intracranial lipoma after introduction of MRI. They were located in the quadrigeminal plate, interpeduncular fossa, pineal region and two of them were found in the cerebellopontine angle, (although intracranial lipoma in this location has been reported to be extremely rare). MRI can precisely locate a small lesion that would be overlooked by CT scans. Operative treatment was performed in two symptomatic cases (CP angle and pineal lesions) and the tumors were subtotally resected. The symptoms of the patients disappeared postoperatively. This indicated that even subtotal removal can alleviate the symptoms of intracranial lipomas and that favorable results can be obtained.     

The effect of IL-6 on the des-gamma-carboxy prothrombin synthesis in human hepatoma cells.

Effects of several cytokines on des-gamma-carboxy prothrombin (PIVKA II) synthesis in human hepatoma cells were investigated to know the process of PIVKA II production during a liver allograft rejection. Human recombinant interleukin-6 (IL-6) significantly stimulated the PIVKA II synthesis without any influence on the cell proliferation. The effect was almost completely neutralized by the specific anti-IL-6 antibody. Neither tumor necrosis factor (TNF), interleukin-1 (IL-1) nor interferon-gamma (IFN-gamma) had such a stimulative effect. IL-6 appears to stimulate PIVKA II production, and would be a candidate of factors that enhance the production of PIVKA II during a liver allograft rejection.