Continuous monitoring of glucose levels in the hepatic vein and systemic circulation during the Pringle maneuver in beagles

Intraoperative continuous glucose monitoring revealed that liver ischemia/reperfusion causes a rapid and profound transition in glucose concentration. We hypothesized that the washout of the glucose stored in the liver leads to a rapid transition in blood glucose concentration. Six female beagles were studied. A portosystemic shunt was established, and the glucose levels in the jugular, hepatic, and portal veins were continuously monitored. All beagles were stabilized for 30 min, and, subsequently, the hepatic artery and portal vein were clamped (the Pringle maneuver). After 30 min of warm hepatic ischemia, the clamp was removed in order to initiate hepatic reperfusion. The endpoint of the experiment was 60 min after the onset of reperfusion. The glucose levels in the abovementioned veins were recorded continuously. The glucose level in the hepatic vein increased 10 min after the start of the Pringle maneuver and was significantly higher than that in the jugular vein and portal vein just before unclamping. The glucose level in the hepatic vein peaked at 2 min after unclamping and that in the portal and jugular veins started to increase after reperfusion. The glucose level in the hepatic vein was significantly higher than that in the jugular and portal veins between 9 min after clamping and 8 min after reperfusion. In conclusion, our study among beagles showed that glucose release from the hepatic vein and sinusoid leads to a rapid elevation in systemic blood glucose levels after liver ischemia/reperfusion. This knowledge might help in the development of new strategies for blood glucose management during hepatectomy.     

Rhabdoid tumor predisposition syndrome with renal tumor 10 years after brain tumor

We report a case of rhabdoid tumor predisposition syndrome with a renal tumor developing 10 years after a brain tumor, which demonstrated an unexpectedly favorable outcome. A 2-year-old boy underwent gross total resection of a brain tumor located in the fourth ventricle, and received adjuvant chemotherapy and radiotherapy. At the age of 11 years, a renal tumor was found and nephrectomy was performed. He is currently alive without evidence of disease over 2 years without postoperative therapy. Histologically, rhabdoid cells were observed in both brain and renal tumors. Loss of SMARCB1 (also known as INI1) expression was found in the nucleus of both tumor cells. Genetic testing revealed pathogenic variants of SMARCB1 exon 5 in the renal tumor and SMARCB1 exon 9 in the brain tumor. In addition, heterozygous deletion of 22q11.21-q11.23 containing the SMARCB1 locus was shared by both tumors and this deletion was identified in normal peripheral blood. Considering the histopathological and genetic findings, our case was considered to be rhabdoid tumor predisposition syndrome with atypical teratoid/rhabdoid tumor and late-onset rhabdoid tumor of the kidney.     

Exophytic cavernous hemangioma arising from the right ventricle: Report of a rare case

Cardiac hemangioma is relatively rare, accounting for approximately 1–3% of all primary heart tumors. This benign tumor may be an incidental lesion, but can also cause arrhythmias, pericardial effusion, congestive heart failure or outflow obstruction. We report a rare case with exophytic cardiac hemangioma arising from the right ventricle. Echocardiography showed an approximately 40 mm round protruding mass on the anterior wall of the right ventricle. Cardiovascular magnetic resonance demonstrated isointense and hyperintense signals on T1- and T2-weighted images, respectively. These imaging studies suggested a pericardial cyst. Perioperative findings indicated a globular, exophytic mass, vascular in nature, arising from the right ventricle. The lesion was resected directly, and the space left by defect in the right ventricular wall was covered with a bovine pericardial patch. Cardiac hemangiomas are generally endoluminal tumors, but we must keep in mind that the differential diagnoses include various pericardial lesions by medical images.     

Effect of Diesel Exhaust Particles on House Dust Mite–Induced Airway Eosinophilic Inflammation and Remodeling in Mice

Recent research has focused on the effects of ambient particulate pollution and much evidence has indicated that particulate pollution is associated with the onset of asthma and allergy; however, the effect of diesel exhaust particles (DEP) on the development of allergen-induced airway remodeling has not been fully investigated in vivo. In the present study, we examined the effects of DEP on Dermatophagoides farinae allergens (Der f)–induced asthma-like phenotypes in mice. Mice were administered i.t. 8 times with Der f. DEP were injected i.t. with Der f 4 times throughout the experiment or twice at the sensitization period. In both cases, DEP aggravated Der f–induced increases in airway responsiveness to acetylcholine, the number of eosinophils and neutrophils in the bronchoalveolar lavage fluid (BALF), serum Der f–specific IgG1 levels, Th2 cytokines and transforming growth factor-β 1 levels in BALF, and amount of hydroxyproline in the right lungs. Furthermore, goblet cell hyperplasia and subepithelial fibrosis were also markedly aggravated. These findings indicate that DEP can potentiate airway remodeling induced by repeated allergen challenge as well as Th2-drived airway hyperresponsiveness, eosinophilic inflammation, and IgG1 production and that DEP can exhibit adjuvant activity for airway remodeling, probably due to the enhancement of allergen sensitization and/or of Th2 polarizing pathways.     

Alexander disease with mild dorsal brainstem atrophy and infantile spasms

We present the case of a Japanese male infant with Alexander disease who developed infantile spasms at 8 months of age. The patient had a cluster of partial seizures at 4 months of age. He presented with mild general hypotonia and developmental delay. Macrocephaly was not observed. Brain magnetic resonance imaging (MRI) findings fulfilled all MRI-based criteria for the diagnosis of Alexander disease and revealed mild atrophy of the dorsal pons and medulla oblongata with abnormal intensities. DNA analysis disclosed a novel heterozygous missense mutation (c.1154 C>T, p.S385F) in the glial fibrillary acidic protein gene. At 8 months of age, tonic spasms occurred, and electroencephalography (EEG) revealed hypsarrhythmia. Lamotrigine effectively controlled the infantile spasms and improved the abnormal EEG findings. Although most patients with infantile Alexander disease have epilepsy, infantile spasms are rare. This comorbid condition may be associated with the distribution of the brain lesions and the age at onset of Alexander disease.     

Presynaptic protein synaptotagmin1 regulates the activity‐induced remodeling of synaptic structures in cultured hippocampal neurons

Activity‐dependent reorganizations of central neuronal synapses are thought to play important roles in learning and memory. Although the precise mechanisms of how neuronal activities modify synaptic connections in neurons remain to be clarified, the activity‐induced neuronal presynaptic proteins such as synaptotagmin1 may contribute to the onset of synaptic remodeling. To understand better the physiological roles of synaptotagmin1, we first examined the prolonged effects of neuronal stimulation capable of inducing synaptotagmin1 on the distribution of a postsynaptic proteins (PSD) protein Homer1c by immunostaining. Previously we found that glutamate stimulation induced other postsynaptic proteins, such as postsynaptic density‐95 (PSD95), a biphasic change with an initially diffuse distribution after 30 min to 1 hr, followed by reassembly to more than the original level after 4–8 hr, suggesting that glutamate stimulation induces a global biphasic alteration in synaptic structures. To dissect further the functions of synaptotagmin1 in the activity‐induced synaptic remodeling, short hairpin RNA (shRNA) vectors that specifically block the expression of endogenous synaptotagmin1 were constructed. When the shRNA of synaptotagmin1 was introduced to the neurons, the activity‐induced changes were almost completely suppressed. We found that synaptotagmin1 contributes to the postsynaptic remodeling in a retrograde manner. Our data indicate that synaptotagmin1 regulates the activity‐induced biphasic changes of post‐ and presynaptic sites. © 2013 Wiley Periodicals, Inc.     

Stimulus duration and pain in nerve conduction studies

Introduction: It is generally believed that a shorter stimulus duration is less painful in nerve conduction studies (NCS). We investigated whether a shorter duration stimulus is actually less painful when the same physiological effect, such as supramaximal stimulation, is achieved in motor NCS. Methods: The tibial nerve was stimulated at the ankle in 14 control subjects and the median nerve at the wrist in 20 subjects. Two stimulations of different durations were given blindly, and each subject was asked to report which was more painful. Results: A 0.2‐ms‐duration stimulus was significantly less painful than those with longer or shorter durations for the tibial nerve. For the median nerve, the 0.05‐ and 0.2‐ms durations were equally less painful than a 1‐ms‐duration stimulus. Conclusions: As a common duration for motor NCS, 0.2 ms seems appropriate, because the tibial nerve stimulation was more painful than the median nerve stimulation. Muscle Nerve, 2013     

Progress in biological reconstruction and enhanced bone revitalization for bone defects

Bone defect reconstruction with artificial materials may produce good functional recovery in the short term. Over time, the durability of artificial materials becomes an issue, and therefore, artificial materials cannot be considered a permanent solution to reconstruction. For long-term outcomes, the goal is to regain function, permanence, and form that are as close to normal as possible. Thus, physiological materials are desirable for use in reconstruction.Biological reconstruction involves the use of materials that are modified in vivo following reconstruction of bone defects. The goal is to achieve bone union, bone revival and remodeling, with biointegration of soft tissue and bone. Allograft use has been the mainstay of bone defect reconstruction in most parts of the world, although in some countries like Japan, allogeneic bone is difficult to obtain due to socio-religious concerns. Therefore, we developed new biological reconstruction techniques to overcome this problem.Bone derived from distraction osteogenesis is autologous bone, which must be an ideal reconstruction material for its biological affinity, strength, resilience, and immunity to infection. When applying this method to patients with malignant disease however, it is important to preserve as much of the local soft tissue as possible, and the clinician must be especially careful of infection and callus formation. Liquid nitrogen treatment of tumor-bearing bone produces equal, if not better, bone revitalization compared to other forms of treatment to date. Reconstruction with liquid nitrogen-treated bone involves resecting the diseased bone and returning it to the body following liquid nitrogen treatment (free-freezing method). Another method involves dislocating the joint proximal to the tumor, or cutting the bone while the distal side remains attached to the body and the limb inverted and treated with liquid nitrogen (pedicle freezing method). When both methods are possible, the pedicle freezing method is preferable since it is performed with minimal osteotomy.Our recent research has looked into the possible role of adipose-derived stem cells in promoting bone fusion and revitalization. This method has produced promising results for the future of biological reconstruction.