Diabetes is a predictor of coronary artery stenosis in patients hospitalized with heart failure

In patients with heart failure, coronary artery disease is the most common underlying heart disease, and is associated with increased mortality. However, estimating the presence or absence of coronary artery disease in patients with heart failure is sometimes difficult without coronary imaging. We reviewed 155 consecutive patients hospitalized with heart failure who underwent coronary angiography. The patients were divided into two groups: patients with (N = 59) and without (N = 96) coronary artery stenosis. The clinical characteristics and blood sampling data were compared between the two groups. The patients with coronary artery stenosis were older than those without. The prevalence of diabetes mellitus (DM), dyslipidemia and a history of revascularization was higher in the patients with coronary artery stenosis. Patients with coronary artery stenosis tended to have wall motion asynergy more frequently than those without. On the other hand, the prevalence of atrial fibrillation (AF) was lower in patients with coronary artery stenosis. The serum hemoglobin level and estimated glomerular filtration rate were lower in patients with coronary artery stenosis than in those without. In the multivariate analysis, DM (odds ratio 3.517, 95 % CI 1.601–7.727) was found to be the only the predictor of the presence of coronary artery stenosis in patients with heart failure. In conclusion, coronary imaging is strongly recommended for heart failure patients with DM to confirm the presence of coronary artery stenosis.     

IFN-γ directly inhibits TNF-α-induced osteoclastogenesis in vitro and in vivo and induces apoptosis mediated by Fas/Fas ligand interactions

Cytokines secreted by T cells play a pivotal role in inflammatory bone destruction. Tumor necrosis factor-α (TNF-α) is a major proinflammatory cytokine produced by macrophages following T cell activation, and directly promotes osteoclast differentiation resulting in accelerated bone resorption. Interferon-γ (IFN-γ) attenuates RANKL-initiated cellular signals through osteoclast formation and counterbalances aberrant bone resorption. With respect to this crosstalk during osteoclastogenesis, the direct interruption of IFN-γ in TNF-α-induced osteoclast formation still requires elucidation. We have demonstrated that IFN-γ directly inhibits osteoclastogenesis induced by TNF-α stimulation and accelerates apoptosis mediated by Fas/Fas ligand signals. There were a decreased number of osteoclasts and reduced mRNA levels encoding Nfatc1 in cultured bone marrow macrophages. Apoptotic responses of cultured cells were observed, with accelerated nuclear fragmentation in osteoclast precursor cells and increased FasL mRNA levels in bone marrow cells stimulated with TNF-α evident. IFN-γ reduced the level of osteoclastogenesis in response to TNF-α treatment in vivo. IFN-γ inhibited TNF-α-induced osteoclastogenesis in mice with T cells that had been exposed to anti-CD4 and -CD8 antibodies. These results provide evidence that IFN-γ directly inhibits osteoclastogenesis and induces cells apoptosis by Fas/FasL signals, leading to the indirect regulation of bone resorption, which is required for protective roles in bone destruction at an inflammation site.     

Biomechanical evaluation of segmental instability in degenerative lumbar spondylolisthesis

Here we investigated the biomechanical properties of spinal segments in patients with degenerative lumbar spondylolisthesis (DLS) using a novel intraoperative measurement system. The measurement system comprised spinous process holders, a motion generator, a load cell, an optical displacement transducer, and a computer. Cyclic displacement of the holders produced flexion-extension of the segment with all ligamentous structures intact. Stiffness, absorption energy (AE), and neutral zone (NZ) were determined from the load-deformation data. Forty-one patients with DLS (M/F = 15/26, mean age 68.6 years; Group D) were studied. Adjacent segments with normal discs in six patients (M/F = 3/3, mean age 35 years) were included as a control group (Group N). Flexion stiffness was significantly lower in Group D than in Group N. The NZ, however, was significantly greater in Group D than in Group N. Thus, compared to normal segments, spinal segments with DLS had a lower flexion stiffness and a higher NZ. NZs in Group D were, however, widely distributed compared to those in Group N that showed NZ <2 mm/N in all cases, suggesting that the segment with DLS is not always unstable and that the segments with NZ >2 mm/N can be considered as unstable. A patent application for the intraoperative measurement system has been submitted.     

In vitro short-term platelet adhesion on various metals

The in vitro short-term platelet adhesion on various metals, as accelerated by the addition of Ca²⁺, was evaluated in this study. Metals used for medical devices [an austenitic stainless steel, a cobalt (Co)-chromium (Cr)-molybdenum (Mo) alloy, a titanium (Ti)-6 aluminum (Al)-4 vanadium (V) alloy, a Ti-6Al-7 niobium (Nb) alloy, a Tinickel (Ni) alloy, and commercially pure Ti] were immersed into a platelet-rich plasma solution for 5 or 20 min, and platelet adhesion and aggregation on the surfaces were observed using a scanning electron microscope. The platelet adhesion level on each metal after 5 min of immersion in a platelet-rich plasma solution was the smallest in this order: stainless steel ≤ Co-Cr-Mo alloy < Ti-6Al-4V alloy < Ti-6Al-7Nb alloy < Ti-Ni alloy = Ti. The levels after 5 min of immersion were almost the same as those after 20 min of immersion. Platelet adhesion was minimal on stainless steel and Co-Cr-Mo alloy, which have a Cr₂O₃-containing passive surface oxide film, but was accelerated on Ti and Ti alloys having a TiO₂-contanining film. A Cr₂O₃-containing oxide film has a lower relative permittivity than a TiO₂-contanining film; it thus supports a larger electrostatic force than the latter, adsorbs more albumins, which work as inhibitory proteins, and inhibits platelet aggregation. Therefore, platelet adhesion and aggregation are controlled by the composition of the surface oxide film on a metal due to the relative permittivity of the metal, which influences the amount of adsorbed proteins.     

IL-12 inhibits TNF-α induced osteoclastogenesis via a T cell-independent mechanism in vivo

It has been reported that TNF-α plays an important role in bone resorption in pathological conditions. IL-12, which is a T cell mediator, is also an important inflammatory cytokine. We previously reported that IL-12 induces apoptosis in bone marrow cells treated with TNF-α in vitro via an interaction between TNF-α-induced Fas and IL-12-induced Fas ligand (FasL), and that, as a result, osteoclastogenesis is inhibited. The purpose of this study was to investigate the effects of IL-12 on TNF-α-mediated osteoclastogenesis in vivo. We administered TNF-α with and without IL-12 into the supracalvaria in mice. The numbers of osteoclasts in the sutures in the calvaria were higher in mice administered TNF-α than in control mice not administered TNF-α. The numbers of osteoclasts in mice administered both TNF-α and IL-12 were lower than those in mice administered only TNF-α. Next, we determined the levels of mRNAs for cathepsin K and tartrate-resistant acid phosphatase (TRAP). mRNA levels were increased in mice administered TNF-α compared with control mice, but not in mice administered both TNF-α and IL-12. We also evaluated the amounts of tartrate-resistant acid phosphatase 5b (TRACP 5b) in mouse sera. The levels of TRACP 5b in mice administered TNF-α were higher than those in control mice. On the other hand, in mice administered both TNF-α and IL-12, the levels were lower than those in mice administered TNF-α alone. Fas and FasL expression levels were analyzed by real-time RT-PCR. The levels of Fas mRNA were increased in the calvaria of mice administered TNF-α compared with control mice, while those of FasL mRNAs were increased in the calvaria of mice administered IL-12. In TdT-mediated dUTP-biotin nick end-labeling (TUNEL) assays, many apoptotic cells were found in the sutures in the calvaria of mice administered both TNF-α and IL-12. IL-12 also inhibited TNF-α-induced osteoclastogenesis in mice whose T cells were blocked by anti-CD4 and anti-CD8 antibodies. These results suggest that IL-12 inhibits TNF-α-mediated osteoclastogenesis and induces apoptotic changes through an interaction between TNF-α-induced Fas and IL-12-induced FasL, in vivo, via a T cell-independent mechanism.     

Administrative Issues in Child Psychiatry

Administrative issues related to operating child and adolescent psychiatry programs or child mental health centers are substantially different than their adult counterpart programs. The increasing demands from managed care and other regulatory agencies make these programs difficult to operate. The smaller scale of these programs and the fewer existing programs make managing access to care more complicated. The administrators and clinicians in these programs have to be vigilant of legal responsibilities and reporting mandates that child practitioners and agencies that treat children need to abide by. In order to continue thriving, programs need to be efficient and fiscally viable. Issues such as building the continuum of care and finding the qualified personnel to staff these services are discussed in this article.     

The proton pumping pathway of bovine heart cytochrome c oxidase

X-ray structures of bovine heart cytochrome c oxidase have suggested that the enzyme, which reduces O(2) in a process coupled with a proton pumping process, contains a proton pumping pathway (H-pathway) composed of a hydrogen bond network and a water channel located in tandem across the enzyme. The hydrogen bond network includes the peptide bond between Tyr-440 and Ser-441, which could facilitate unidirectional proton transfer. Replacement of a possible proton-ejecting aspartate (Asp-51) at one end of the H-pathway with asparagine, using a stable bovine gene expression system, abolishes the proton pumping activity without influencing the O(2) reduction function. Blockage of either the water channel by a double mutation (Val386Leu and Met390Trp) or proton transfer through the peptide by a Ser441Pro mutation was found to abolish the proton pumping activity without impairment of the O(2) reduction activity. These results significantly strengthen the proposal that H-pathway is involved in proton pumping.     

Progressive congestive heart failure due to common iliac arteriovenous fistula: a case report

Arteriovenous shunt is one of the causes of heart failure, but heart failure caused by common iliac arteriovenous fistula is relatively rare. A 64-year-old man who developed acute heart failure due to venous perforation of a common iliac aneurysm and also had bilateral aneurysms (diameter 58 mm) was referred to our department. On admission, the patient complained of dyspnea and swollen left leg, so diuretic agent was administered to treat the heart failure. Cardiac catheterization showed a shunt rate of 80.6%, as well as 5.0 Qp/Qs and O2 step-up across perforation of the common iliac vein. Despite the therapy, pleural effusion and ascites exacerbated, and the heart failure became difficult to control, so surgical treatment was performed. The aneurysm was replaced with an artificial vessel, and the fistula was closed by direct suturing. Postoperatively, the symptoms disappeared, and the patient is in good health.     

Leakage in anesthesia circuits--a comparison between 1998 and 2005 investigations

BACKGROUND: We checked for the occurrence of any leakage in an anesthesia circuit to estimate the present situation of airtightness of an anesthesia circuit in 55 anesthesia machines at various medical institutions in Okinawa. METHODS: Leakage was detected and measured by a leak checker. RESULTS: A certain degree of leakage was found in 28 of the anesthesia machines (51%). The average and maximal amounts of leakage in the anesthesia machines were 0.26, and 1.29 l x min(-1), respectively. Thirty-eight of anesthesia machines met the standards of a low flow leak test (69%). The average and maximal amounts of leakage in the inside circuit were 0.02, and 0.20 l x min(-1), respectively. The leak points of the inside circuit were present in a unidirectional valve for an oxygen sensor (14%) and for unknown reason (7%). The average and maximal amounts of leakage in the outside circuit were 0.24, and 1.29 l x min(-1), respectively. Leak points in the inside circuit were found in the corrugated breathing tube (82%) and canister (32%). CONCLUSIONS: Most instances of leakage of the above described anesthesia circuits were identified in the corrugated breathing tube and canister. As a result of our findings, we strongly recommend that these parts be checked very carefully during pre-anesthetic leak tests.