Venous velocity of the right femoral vein decreases in the right lateral decubitus position compared to the supine position: a cause of postoperative pulmonary embolism?

The right lateral decubitus position is a risk factor for postoperative pulmonary embolism. We examined postural changes of femoral vein velocity in order to elucidate the mechanism. Thirty patients scheduled for general thoracic surgery were enrolled in this study. The common femoral veins on both sides were examined by color-duplex ultrasound for venous caliber and velocity when the patients were in the right lateral, left lateral, and supine positions. The maximum diameters of the right femoral vein in the right lateral decubitus position and the left femoral vein in the left decubitus position were significantly larger than those in the other positions. The venous velocity of the right femoral vein in the right lateral decubitus position was significantly smaller than that in the supine position, while the velocity of the left femoral vein in the left lateral decubitus position was not significantly decreased. We speculate that the decreased venous velocity of the right femoral vein in the right lateral decubitus position could result in a deep venous thromboembolism in the right leg, making this position a possible risk factor for postoperative pulmonary embolism.</p

ノウコウソク ノ キュウセイキ チリョウ : Stroke Care Unit オ チュウシン トシテ

Stroke remains the second or third leading cause of the death and major cause of adultdisability in Japan. Cerebral infarction is major cause of stroke, therefore, it is very importantthat precious diagnosis and acute treatment of cerebral infarction should be done.Recently diffusion-weighted (DWI) and perfusion-weighted MRI (PWI) were clinically used andsensitivity of these stools is superior to T2-MRI in diagnosis of acute cerebral infarction.We performed acute intra-arterial thrombolysis and evaluated this efficacy by DWI andPWI. For the patients with embolic cerebral infarction, anticoagulant therapy should beperformed and tarns-esophageal heart echography in acute stage of infarction is useful fordetection of embolic source. Stroke Care Unit (SCU) was opened in our hospital since lastNovember and 8 patients per month were admitted to SCU. Over 75% of patients weretreated conservatively, and 6 patients were performed intra-arterial thrombolysis. Over80% of patients with cerebral infarction in SCU showed good clinical recovery. We needmore patients to show the superiority compared to the general medical wards

Pathophysiology and treatment of cerebral ischemia

This article describes the pathophysiology of, and treatment strategy for, cerebral ischemia. It is useful to think of an ischemic lesion as a densely ischemic core surrounded by better perfused “penumbra” tissue that is silent electrically but remains viable. Reperfusion plays an important role in the pathophysiology of cerebral ischemia. Magnetic resonance imaging (MRI) and histological studies in rat focal ischemia models using transient middle cerebral artery (MCA) occlusion indicate that reperfusion after an ischemic episode of 2- to 3-hour duration does not result in reduction of the size of the infarct. Brief occlusion of the MCA produces a characteristic, cell-type specific injury in the striatum where medium-sized spinous projection neurons are selectively lost ; this injury is accompanied by gliosis. Transient forebrain ischemia leads to delayed death of the CA1 neurons in the hippocampus. Immunohistochemical and biochemical investigations of Ca2+/calmodulin-dependent protein kinase II(CaM kinase II) and protein phosphatase (calcineurin) after transient forebrain ischemia demonstrated that the activity of CaM kinase II was decreased in the CA1 region of the hippocampus early (6- 12 hours) after ischemia. However, calcineurin was preserved in the CA1 region until 1.5 days after the ischemic insult and then lost ; a subsequent increase in the morphological degeneration of neurons was observed. We hypothesized that an imbalance of Ca2+/calmodulin dependent protein phosphorylation-dephosphorylation may be involved in delayed neuronal death after ischemia. In the treatment of acute ischemic stroke, immediate recanalization of the occluded artery, using systemic or local thrombolysis, is optimal for restoring the blood flow and rescuing the ischemic brain from complete infarction. However, the window of therapeutic effectiveness is very narrow. The development of effective neuroprotection methods and the establishment of reliable imaging modalities for an early and accurate diagnosis of the extent and degree of the ischemia are imperative

Blocking COX-2 induces apoptosis and inhibits cell proliferation via the Akt/survivin- and Akt/ID3 pathway in low-grade-glioma

Approximately half of surgically-treated patients with low-grade-glioma (LGG) suffer recurrence or metastasis. Currently there is no effective drug treatment. While the selective COX-2 inhibitor celecoxib showed anti-neoplastic activity against several malignant tumors, its effects against LGG remain to be elucidated. Ours is the first report that the expression level of COX-2 in brain tissue samples from patients with LGG and in LGG cell lines is higher than in the non-neoplastic region and in normal brain cells. We found that celecoxib attenuated LGG cell proliferation in a dose-dependent manner. It inhibited the generation of prostaglandin E2 and induced apoptosis and cell-cycle arrest. We also show that celecoxib hampered the activation of the Akt/survivin- and the Akt/ID3 pathway in LGGs. These findings suggest that celecoxib may have a promising therapeutic potential and that the early treatment of LGG patients with the drug may be beneficial

CD153/CD30 signaling promotes age-dependent tertiary lymphoid tissue expansion and kidney injury

高齢者腎臓病を悪化させる原因細胞・分子の同定に成功. 京都大学プレスリリース. 2021-11-30.A new drug target for kidney disease. 京都大学プレスリリース. 2021-11-30.Tertiary lymphoid tissues (TLTs) facilitate local T- and B-cell interactions in chronically inflamed organs. However, the cells and molecular pathways that govern TLT formation are poorly defined. Here we identify TNF superfamily CD153-CD30 signaling between two unique age-dependent lymphocyte subpopulations, CD153⁺PD-1⁺CD4⁺ senescence-associated T (SAT) cells and CD30+T-bet+ age-associated B cells (ABCs), as a driver for TLT expansion. SAT cells, which produced ABC-inducing factors IL21 and IFNγ, and ABCs progressively accumulated within TLTs in aged kidneys after injury. Notably, in kidney injury models, CD153 or CD30 deficiency impaired functional SAT cell induction, which resulted in reduced ABC numbers and attenuated TLT formation with improved inflammation, fibrosis and renal function. Attenuated TLT formation after transplantation of CD153-deficient bone marrow further supported the importance of CD153 in immune cells. Clonal analysis revealed that SAT cells and ABCs in the kidneys arose from both local differentiation and recruitment from the spleen. In the synovium of aged rheumatoid arthritis patients, T peripheral helper/T follicular helper cells and ABCs also expressed CD153 and CD30, respectively. Together, our data reveal a previously unappreciated function of CD153-CD30 signaling in TLT formation and propose targeting CD153-CD30 signaling pathway as a therapeutic target for slowing kidney disease progression

Heterogeneous fibroblasts underlie age-dependent tertiary lymphoid tissues in the kidney

Acute kidney injury (AKI) is a common clinical condition defined as a rapid decline in kidney function. AKI is a global health burden, estimated to cause 2 million deaths annually worldwide. Unlike AKI in the young, which is reversible, AKI in the elderly often leads to end-stage renal disease, and the mechanism that prevents kidney repair in the elderly is unclear. Here we demonstrate that aged but not young mice developed multiple tertiary lymphoid tissues (TLTs) in the kidney after AKI. TLT size was associated with impaired renal function and increased expression of proinflammatory cytokines and homeostatic chemokines, indicating a possible contribution of TLTs to sustained inflammation after injury. Notably, resident fibroblasts from a single lineage diversified into p75 neurotrophin receptor(+) (p75NTR(+)) fibroblasts and homeostatic chemokine-producing fibroblasts inside TLTs, and retinoic acid-producing fibroblasts around TLTs. Deletion of CD4(+) cells as well as late administration of dexamethasone abolished TLTs and improved renal outcomes. Importantly, aged but not young human kidneys also formed TLTs that had cellular and molecular components similar to those of mouse TLTs. Therefore, the inhibition of TLT formation may offer a novel therapeutic strategy for AKI in the elderly.</p

Isospin Properties of (K−K^-, NN) Reactions for the Formation of Deeply-bound Antikaonic Nuclei

The formation of deeply-bound antikaonic $K^-/\bar{K}^0$ nuclear states by nuclear ($K^-$, $N$) reactions is investigated theoretically within a distorted-wave impulse approximation (DWIA), considering the isospin properties of the Fermi-averaged $K^-+ N \to N + \bar{K}$ elementary amplitudes. We calculate the formation cross sections of the deeply-bound $\bar{K}$ states by the ($K^-$, $N$) reactions on the nuclear targets, $^{12}$C and $^{28}$Si, at incident $K^-$ lab momentum $p_{K^-}$ = 1.0 GeV/c and $\theta_{\rm lab} = 0^{\circ}$, introducing a complex effective nucleon number $N_{\rm eff}$ for unstable bound states in the DWIA. The results show that the deeply-bound $\bar{K}$ states can be populated dominantly by the ($K^-$, $n$) reaction via the total isoscalar $\Delta T=0$ transition owing to the isospin nature of the $K^-+ N \to N + \bar{K}$ amplitudes, and that the cross sections described by ${\rm Re}N_{\rm eff}$ and ${\rm Arg}N_{\rm eff}$ enable to deduce the structure of the $\bar{K}$ nuclear states; the calculated inclusive nucleon spectra for a deep $\bar{K}$-nucleus potential do not show distinct peak structure in the bound region. The few-body $\bar{K}\otimes [NN]$ and $\bar{K}\otimes [NNN]$ states formed in ($K^-$, $N$) reactions on $s$-shell nuclear targets, $^3$He, $^3$H and $^4$He, are also discussed.Comment: 61 pages, 17 figures, proofread version to be published in Nucl. Phys.

Minimally invasive approach for cancer of the esophagogastric junction

The incidence of esophagogastric junction (EGJ) cancer is increasing in the world. EGJ cancer is traditionally classified by the Siewert classification, despite its limitations. The definition and classification of EGJ cancer is a controversial topic. Thus, the best available strategy for the surgical treatment of EGJ cancer remains controversial. This chapter reviews a minimally invasive approaches for EGJ cancer. Most operations for EGJ cancer that are performed by open surgery can be performed minimally invasively. A minimally invasive transthoracic approach (Ivor-Lewis or McKeown esophagectomy) is the optimal surgical approach for Siewert type I cancer. Mediastinoscope-assisted transhiatal esophagectomy, which was recently reported, may be a suitable surgical option, especially for frail patients with Siewert type I cancer. Generally, laparoscopic total or proximal gastrectomy is regarded as the standard for surgerical method for Siewert type III cancer, while both laparoscopic gastrectomy (with lower esophagectomy) or a minimally invasive Ivor-Lewis approach are recommended for Siewert type II cancer. Minimally invasive surgery (MIS) has the potential to shorten the length of hospitalization, reduce the risk of postoperative pulmonary complications, and improve quality of life with a similar margin status, nodal harvest, and survival rate to open techniques. However, as the existing literature is still limited, the choice of surgical method should be judged by the experienced surgeons, especially in MIS. This review reveals that further large clinical stuidies are need to deepen our understanding of MIS for EGJ cancer