A case of spontaneous mesenteric hematoma successfully diagnosed and treated with aggressive imaging

Introduction: Spontaneous mesenteric hematoma is an uncommon syndrome triggered by bleeding localized in the mesenteric vascular tree of a bowel segment for no apparent underlying reason. We herein report a surgical patient with an extremely rapidly growing spontaneous mesenteric hematoma that we successfully diagnosed using careful radiologic examination. Presentation of case: A 56-year-old old male presenting sudden onset lower abdominal pain was referred to our emergency department. At the time of admission, his physical examination revealed stable vital signs without radiological abnormality. On the following day, the patient suddenly presented hypotension, tachycardia, and increased abdominal pain. Contrast-enhanced computed tomography examination showed a mass with both high- and low-density areas with a 130 mm maximum diameter bordering the transverse colon. Since interventional radiologists were not available, we decided to perform emergency exploratory laparotomy. On laparotomy, a 13 × 8 cm hematoma was found in the mesentery of the transverse colon. As bleeding was noted from the branches of the middle colic artery and gastrocolic artery, these responsible vessels were ligated. The patient was finally given the diagnosis of spontaneous mesenteric hematoma. Discussion and conclusion: The present case, initially diagnosed as enterocolitis, suddenly manifested hypovolemic shock. Close monitoring for any signs of further deterioration, as well as aggressive imaging diagnosis, enabled us to avoid delays in treatment. Early diagnosis and treatment of mesenteric hematomas are essential to prevent them from rupturing and triggering life-threatening adverse events

Glycogenic hepatopathy following attempted suicide by long-acting insulin overdose in patient with type 1 diabetes

Patients with poorly controlled insulin-dependent type 1 or type 2 diabetes rarely present with glycogenic hepatopathy, which is characterized by hepatomegaly and liver enzyme abnormalities. Glycogenic hepatopathy occurs as a consequence of excessive accumulation of glycogen in hepatocytes caused by insulin. We report a young male patient with type 1 diabetes mellitus who developed glycogenic hepatopathy following a suicide attempt by insulin overdose via subcutaneous injection. The patient's medication/nutrition compliance and adherence to insulin were poorly controlled due to comorbid schizophrenia. Our patient required a large amount of continuous glucose to maintain euglycemia for persistent intractable hypoglycemia induced by overdose of long-acting insulin. On admission day 4, the patient presented elevated transaminases, hepatomegaly, and lactic acidosis. Computed tomography revealed swollen liver parenchyma with a diffusely high absorption. The patient gradually recovered without any medical intervention except for adequate control of blood sugar and was moved to a psychiatric ward on day 8 for schizophrenia management. This report may help emergency physicians be aware of the common symptoms, clinical course, and pathophysiology of glycogenic hepatopathy. Doctors should include glycogenic hepatopathy in the differential diagnosis of abnormal liver enzymes and hepatomegaly for those with poorly controlled insulin-dependent diabetes mellitus or unstable blood sugar levels due to insulin overdose like our patient

Novel role of neuronal Ca2+ sensor-1 as a survival factor up-regulated in injured neurons

A molecular basis of survival from neuronal injury is essential for the development of therapeutic strategy to remedy neurodegenerative disorders. In this study, we demonstrate that an EF-hand Ca2+-binding protein neuronal Ca2+ sensor-1 (NCS-1), one of the key proteins for various neuronal functions, also acts as an important survival factor. Overexpression of NCS-1 rendered cultured neurons more tolerant to cell death caused by several kinds of stressors, whereas the dominant-negative mutant (E120Q) accelerated it. In addition, NCS-1 proteins increased upon treatment with glial cell line–derived neurotrophic factor (GDNF) and mediated GDNF survival signal in an Akt (but not MAPK)-dependent manner. Furthermore, NCS-1 is significantly up-regulated in response to axotomy-induced injury in the dorsal motor nucleus of the vagus neurons of adult rats in vivo, and adenoviral overexpression of E120Q resulted in a significant loss of surviving neurons, suggesting that NCS-1 is involved in an antiapoptotic mechanism in adult motor neurons. We propose that NCS-1 is a novel survival-promoting factor up-regulated in injured neurons that mediates the GDNF survival signal via the phosphatidylinositol 3-kinase–Akt pathway

応急仮設住宅居住者の集まる場と環境要素の関係性に関する研究 ‐福島県いわき市を事例として‐

Assuming that a major disaster will take place in the future, the purpose of this research is to gain design insights by considering the environment of emergency temporary housing, which provides a phase in people’s recovery in the aftermath of a major disaster. For this study, interviews of residents of temporary housing in Iwaki City, Fukushima Prefecture, Japan were conducted. Focus was especially placed on venues where communication occurred. Relationships between the characteristics of behaviors in those areas and environmental elements were analyzed and discussed

Effects of muscle cooling on kinetics of pulmonary oxygen uptake and muscle deoxygenation at the onset of exercise

This study investigated effects of skeletal muscle cooling on the metabolic response and kinetics of pulmonary oxygen uptake (urn:x-wiley:2051817X:media:phy213910:phy213910-math-0001O2) and skeletal muscle deoxygenation during submaximal exercise. In the cooling condition (C), after immersion of the lower body into 12°C water for 30 min, eight healthy males performed 30‐min cycling exercise at the lactate threshold while undergoing thigh cooling by a water‐circulating pad. In the normal condition (N) as control, they conducted the same exercise protocol without cooling. Blood lactate concentration was significantly higher in C than N at 10 min after onset of exercise (4.0 ± 1.7 and 2.4 ± 1.2 mmol/L in C and N, P < 0.05). The percent change in the tissue oxygen saturation of the vastus lateralis, measured by a near‐infrared spectroscopy, was significantly lower in C at 2, 8, 10, and 20 min after the exercise onset compared with N (P < 0.05). The percent change in deoxy hemoglobin+myoglobin concentration (Deoxy[Hb+Mb]) showed a transient peak at the onset of exercise and significantly higher value in C at 10, 20, and 30 min after the exercise onset (P < 0.05). Compared to N, slower urn:x-wiley:2051817X:media:phy213910:phy213910-math-0002O2 kinetics (mean response time) was observed in C (45.6 ± 7.8 and 36.1 ± 7.7 sec in C and N, P < 0.05). The mean response time in C relative to N was significantly correlated with the transient peak of Deoxy[Hb+Mb] in C (r = 0.84, P < 0.05). These results suggest that lower oxygen delivery to the hypothermic skeletal muscle might induce greater glycolytic metabolism during exercise and slower urn:x-wiley:2051817X:media:phy213910:phy213910-math-0003O2 kinetics at the onset of exercise

Development of Kupffer cell targeting type-I interferon for the treatment of hepatitis via inducing anti-inflammatory and immunomodulatory actions

Because of its multifaceted anti-inflammatory and immunomodulatory effects, delivering type-I interferon to Kupffer cells has the potential to function as a novel type of therapy for the treatment of various types of hepatitis. We report herein on the preparation of a Kupffer cell targeting type-I interferon, an albumin-IFNα2b fusion protein that contains highly mannosylated N-linked oligosaccharide chains, Man-HSA(D494N)-IFNα2b, attached by combining albumin fusion technology and site-directed mutagenesis. The presence of this unique oligosaccharide permits the protein to be efficiently, rapidly and preferentially distributed to Kupffer cells. Likewise IFNα2b, Man-HSA(D494N)-IFNα2b caused a significant induction in the mRNA levels of IL-10, IL-1Ra, PD-L1 in RAW264.7 cells and mouse isolated Kupffer cells, and these inductions were largely inhibited by blocking the interferon receptor. These data indicate that Man-HSA(D494N)-IFNα2b retained the biological activities of type-I interferon. Man-HSA(D494N)-IFNα2b significantly inhibited liver injury in Concanavalin A (Con-A)-induced hepatitis model mice, and consequently improved their survival rate. Moreover, the post-administration of Man-HSA(D494N)-IFNα2b at 2 h after the Con-A challenge also exerted hepato-protective effects. In conclusion, this proof-of-concept study demonstrates the therapeutic effectiveness and utility of Kupffer cell targeting type-I interferon against hepatitis via its anti-inflammatory and immunomodulatory actions

Increased Circulating T Cell Reactivity to GM1 Ganglioside in Patients with Guillain-Barre Syndrome

This study was performed to determine whether increased ganglioside-specific T cell reactivity can be detected in the peripheral blood of patients with Guillain-Barre syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). T cell responsiveness to the gangliosides GM1, GM3, GD1a, GD1b, GD3, GT1b, GQ1b and sulphatide was assessed in peripheral blood mononuclear cells from untreated GBS patients (57), CIDP patients (43), patients with other peripheral neuropathies (55) and healthy control subjects (74) in a standard 6-day proliferation assay. Increased T cell reactivity to GM1 occurred in GBS patients compared to healthy controls and patients with other neuropathies. There was increased reactivity to GM3 in GBS patients compared to patients with other neuropathies but not compared to healthy controls. The frequencies of increased T cell reactivity to GM1 and GM3 in CIDP patients were intermediate between those of GBS patients and controls. We suggest that T cell reactivity to gangliosides might play a contributory role in the pathogenesis of GBS and perhaps CIDP

The ability of contemporary cardiologists to judge the ischemic impact of a coronary lesion visually

Background: Landmark trials showed that invasive pressure measurement (Fractional Flow Reserve, FFR) was a better guide to coronary stenting than visual assessment. However, present-day interventionists have benefited from extensive research and personal experience of mapping anatomy to hemodynamics. Aims: To determine if visual assessment of the angiogram performs as well as invasive measurement of coronary physiology. Methods: 25 interventional cardiologists independently visually assessed the single vessel coronary disease of 200 randomized participants in The Objective Randomized Blinded Investigation with optimal medical Therapy of Angioplasty in stable angina trial (ORBITA). They gave a visual prediction of the FFR and Instantaneous Wave-free Ratio (iFR), denoted vFFR and viFR respectively. Each judged each lesion on 2 occasions, so that every lesion had 50 vFFR, and 50 viFR assessments. The group consensus visual estimates (vFFR-group and viFR-group) and individual cardiologists' visual estimates (vFFR-individual and viFR-individual) were tested alongside invasively measured FFR and iFR for their ability to predict the placebo-controlled reduction in stress echo ischemia with stenting. Results: Placebo-controlled ischemia improvement with stenting was predicted by vFFR-group (p < 0.0001) and viFR-group (p < 0.0001), vFFR-individual (p < 0.0001) and viFR-individual (p < 0.0001). There were no significant differences between the predictive performance of the group visual estimates and their invasive counterparts: p = 0.53 for vFFR vs FFR and p = 0.56 for viFR vs iFR. Conclusion: Visual assessment of the angiogram by contemporary experts, provides significant additional information on the amount of ischaemia which can be relieved by placebo-controlled stenting in single vessel coronary artery disease