Hematocolpos due to lower vaginal agenesis in an adolescent girl.

Background: Hematocolpos due to imperforate hymen is an important differential diagnosis of abdominal pain in early adolescent stage. However, hematocolpos due to lower vaginal agenesis must be considered because the management differs. Case Presentation: A healthy 11-year-old girl presented with a 2-day left lower abdominal pain history. Her breast development had begun, but she had not reached menarche. Computed tomography showed high absorptive value liquid filling the upper vaginal to uterine cavity, a pale highly absorptive fluid component suggestive of hemorrhagic ascites in the abdominal cavity on both sides of the uterus, and normal bilateral ovaries. Magnetic resonance imaging diagnosed hematocolpos due to lower vaginal agenesis. The blood clot was aspirated with a transabdominal ultrasound-guided transvaginal puncture. Conclusion: History-taking, imaging tests, and appropriate collaboration with obstetrician/gynecologist with awareness of secondary sexual characteristics were crucial in this case.

Treatment of acute hypernatremia caused by sodium overload in adults: A systematic review.

BACKGROUND: Rapid-onset, acute hypernatremia caused by sodium overload is a rare, life-threatening condition. Although experts recommend rapid correction of sodium concentration [Na] based on pathophysiological theories, only a few reports have documented the specific details of sodium correction methods. The objective of this study was to systematically review the reported treatment regimens, achieved [Na] correction rates, and treatment outcomes. METHODS: PubMed, Ichushi-database, and references without language restrictions, from inception to January 2021, were searched for studies that described ≥1 adult (aged ≥18 years) patients with rapid-onset hypernatremia caused by sodium overload, whose treatment was initiated ≤12 hours from the onset. The primary outcome of interest was the [Na] correction rate associated with mortality. RESULTS: Eighteen case reports (18 patients; median [Na], 180.5 mEq/L) were included. The cause of sodium overload was self-ingestion in 8 patients and iatrogenic sodium gain in 10 patients; baseline [Na] and symptoms at presentation were comparable for both groups. Individualized rapid infusion of dextrose-based solutions was the most commonly adopted fluid therapy, whereas hemodialysis was also used for patients already treated with hemodialysis. The correction rates were more rapid in 13 successfully treated patients than in 5 fatal patients. The successfully treated patients typically achieved [Na] ≤160 within 8 hours, [Na] ≤150 within 24 hours, and [Na] ≤145 within 48 hours. Hyperglycemia was a commonly observed treatment-related adverse event. CONCLUSION: The limited empirical evidence derived from case reports appears to endorse the recommended, rapid, and aggressive sodium correction using dextrose-based hypotonic solutions.

Effectiveness of a novel semi-closed barrier device with a personalized exhaust in cough aerosol simulation according to particle counts and visualization of particles.

Oxygen therapy is an essential treatment for patients with coronavirus disease 2019, although there is a risk of aerosolization of additional viral droplets occurring during this treatment that poses a danger to healthcare professionals. High-flow oxygen through nasal cannula (HFNC) is a vital treatment bridging low-flow oxygen therapy with tracheal intubation. Although many barrier devices (including devices without negative pressure in the barrier) have been reported in the literature, few barrier devices are suitable for HFNC and aerosol infection control procedures during HFNC have not yet been established. Hence, we built a single cough simulator model to examine the effectiveness of three protective measures (a semi-closed barrier device, a personalized exhaust, and surgical masks) administered in isolation as well as in combination using particle counter measurements and laser sheet visualization. We found that the addition of a personalized exhaust to a semi-closed barrier device reduced aerosol leakage during HFNC without negative pressure. This novel combination may thus reduce aerosol exposure during oxygen therapy, enhance the protection of healthcare workers, and likely reduce nosocomial infection risk.

Rapidly progressive acute necrotizing encephalopathy associated with influenza A in an elderly adult.

BACKGROUND: Among the influenza-associated encephalopathies, acute necrotizing encephalopathy (ANE) has a particularly poor prognosis. While it usually progresses within 48 h, we encountered a rapidly evolving case with the patient falling into coma from lucidity within 10 min. CASE PRESENTATION: A 71-year-old man was found unconscious after taking a 10-min bath and brought to the emergency room. The head computed tomography (HCT) was normal, and he was diagnosed with heatstroke as a complication of influenza A. Despite effective therapy to correct his temperature, his consciousness did not improve, and within 24 h he progressed to multiple organ injury. Repeat HCT and subsequent magnetic resonance imaging revealed irreparably progressed ANE. CONCLUSION: To effectively treat ANE, early recognition and diagnosis are critical. Our case suggests that ANE should be considered and added to the differential diagnosis for adult patients with rapid cognitive deterioration.

Development of dissociative force field for all-atomistic molecular dynamics calculation of fracture of polymers.

A dissociative force field for all-atomistic molecular dynamics calculations has been developed to investigate impact fracture of polymers accompanying dissociation of chemical bonds of polymer main chain. Energy of dimer molecules was evaluated as a function of both bond-length b and bond-angle θ by CASPT2 calculations, whose quality is enough to describe dissociation of chemical bonds. Because we found that the bond dissociation energy D decreases with increasing bond-angle, we employed the Morse-type function VBond (b, θ) = {D - VAngle (θ)}[1 - exp{-α(b - b0 ) - ß(b - b0 )2 }] where a quartic function VAngle (θ) = k1 (θ - θ0 ) + k2 (θ - θ0 )2 + k3 (θ - θ0 )3 + k4 (θ - θ0 )4 . This function reproduced well the CASPT2 potential energy surface in a wide range of b and θ. The parameters have been obtained for four popular glassy polymers, polyethylene, poly(methyl methacrylate), poly(styrene), and polycarbonate. © 2019 Wiley Periodicals, Inc.

Clostridium Perfringens Infection in a Febrile Patient with Severe Hemolytic Anemia.

BACKGROUND: Clostridium perfringens (C. perfringens) can cause various infections, including gas gangrene, crepitant cellulitis, and fasciitis. While C. perfringens sepsis is uncommon, it is often rapidly fatal because the alpha toxin of this bacterium induces massive intravascular hemolysis by disrupting red blood cell membranes. CASE REPORT: We present the case of a male patient with diabetes who developed a fatal liver abscess with massive intravascular hemolysis and septic shock caused by toxigenic C. perfringens. The peripheral blood smear showed loss of central pallor, with numerous spherocytes. Multiplex PCR only detected expression of the cpa gene, indicating that the pathogen was C. perfringens type A. CONCLUSIONS: C. perfringens infection should be considered in a febrile patient who has severe hemolytic anemia with a very low MCV, hemolyzed blood sample, and negative Coombs test. The characteristic peripheral blood smear findings may facilitate rapid diagnosis.

Neutrophil extracellular traps in patients with sepsis.

BACKGROUND: Release of neutrophil extracellular traps (NETs) has been identified as an important aspect of innate immunity. We examined whether sepsis had any influence on ex vivo generation of NETs by neutrophils. MATERIALS AND METHODS: We isolated neutrophils from consecutive patients with sepsis (n = 17) and without sepsis (n = 18) admitted to the intensive care unit. Neutrophils were activated by incubation with phorbol-12-myristate-13-acetate (PMA) to induce release of NETs, and NET formation was assessed by measuring the extracellular DNA level. Immunolabeling and fluorescence imaging were also performed. Extracellular killing of bacteria by NETs was studied by co-culture of Escherichia coli and neutrophils in the presence of a phagocytosis inhibitor. To assess in vivo NET formation, plasma levels of cell-free DNA and histones were measured. RESULTS: After stimulation with PMA, neutrophils isolated from septic patients released 4.08 ± 1.02% of their total DNA, whereas neutrophils from nonseptic patients released 29.06 ± 2.94% (P = <0.0001). Immunofluorescent staining of released DNA, elastase, and myeloperoxidase also revealed similar results. Neutrophils from nonseptic patients showed effective extracellular killing of E coli through NETs, whereas neutrophils from septic patients did not (P < 0.001). Plasma levels of cell-free DNA and histones were higher in septic patients than nonseptic patients (P < 0.001). CONCLUSIONS: The ex vivo generation of NETs is downregulated in neutrophils isolated from patients with sepsis. However, it is unclear whether in vivo NET formation is also impaired during sepsis, so further investigation is necessary.

ASIC2 subunits facilitate expression at the cell surface and confer regulation by PSD-95.

Acid-sensing ion channels (ASICs) are Na+ channels activated by changes in pH within the peripheral and central nervous systems. Several different isoforms of ASICs combine to form trimeric channels, and their properties are determined by their subunit composition. ASIC2 subunits are widely expressed throughout the brain, where they heteromultimerize with their partnering subunit, ASIC1a. However, ASIC2 contributes little to the pH sensitivity of the channels, and so its function is not well understood. We found that ASIC2 increased cell surface levels of the channel when it is coexpressed with ASIC1a, and genetic deletion of ASIC2 reduced acid-evoked current amplitude in mouse hippocampal neurons. Additionally, ASIC2a interacted with the neuronal synaptic scaffolding protein PSD-95, and PSD-95 reduced cell surface expression and current amplitude in ASICs that contain ASIC2a. Overexpression of PSD-95 also reduced acid-evoked current amplitude in hippocampal neurons. This result was dependent upon ASIC2 since the effect of PSD-95 was abolished in ASIC2-/- neurons. These results lend support to an emerging role of ASIC2 in the targeting of ASICs to surface membranes, and allows for interaction with PSD-95 to regulate these processes.

Successful treatment of septic shock due to New Delhi metallo-ß-lactamase-1-producing Klebsiella pneumoniae in a patient transferred from India to Japan.

CASE: Here we report the fifth case of New Delhi metallo-ß-lactamase-1-producing Enterobacteriaceae infection in Japan. A 39-year-old Japanese man suffered a subarachnoid hemorrhage due to rupture of aneurysm in India. Once he was deemed stable enough, he was transferred from a hospital in India to our hospital in Japan. On day 5 after transfer, the patient suddenly developed septic shock and multidrug-resistant Klebsiella pneumoniae was isolated from a blood culture. OUTCOME: Treatment with colistin and high-dose meropenem as well as organ support were initiated, resulting in successful resolution of septic shock. This K. pneumoniae was shown to carry blaNDM-1 by polymerase chain reaction analysis. CONCLUSION: Our case suggests that New Delhi metallo-ß-lactamase-1-producing bacteria could be introduced into Japan easily. It is important to apply strict surveillance and infection control measures to prevent the spread of carbapenem resistance genes to Enterobacteriaceae in Japan.

ASIC2a and ASIC3 heteromultimerize to form pH-sensitive channels in mouse cardiac dorsal root ganglia neurons.

RATIONALE: Acid-sensing ion channels (ASICs) are Na+ channels that are activated by acidic pH. Their expression in cardiac afferents and remarkable sensitivity to small pH changes has made them leading candidates to sense cardiac ischemia. OBJECTIVE: Four genes encode six different ASIC subunits, however it is not yet clear which of the ASIC subunits contribute to the composition of ASICs in cardiac afferents. METHODS AND RESULTS: Here, we labeled cardiac afferents using a retrograde tracer dye in mice, which allowed for patch-clamp studies of murine cardiac afferents. We found that a higher percentage of cardiac sensory neurons from the dorsal root ganglia respond to acidic pH and generated larger currents compared to those from the nodose ganglia. The ASIC-like current properties of the cardiac dorsal root ganglia neurons from wild-type mice most closely matched the properties of ASIC2a/3 heteromeric channels. This was supported by studies in ASIC-null mice: acid-evoked currents from ASIC3(-/-) cardiac afferents matched the properties of ASIC2a channels, and currents from ASIC2(-/-) cardiac afferents matched the properties of ASIC3 channels. CONCLUSIONS: We conclude that ASIC2a and -3 are the major ASIC subunits in cardiac dorsal root ganglia neurons and provide potential molecular targets to attenuate chest pain and deleterious reflexes associated with cardiac disease.

Before-after study of a restricted fluid infusion strategy for management of donor hepatectomy for living-donor liver transplantation.

PURPOSE: Intraoperative fluid infusion strategy remains controversial. Many animal model studies have shown that restricted fluid infusion reduces blood loss, though reports on this topic in humans are rare. The purpose of this study was to determine the effects on volume of blood loss of a restricted fluid infusion strategy for hepatectomy in donors for living donor liver transplantation. METHODS: A before-after study design was used with prospective consecutive data collection. A total of 22 patients who underwent living-donor hepatectomy were enrolled. Eleven patients who were managed before the implementation of restricted-volume fluid administration comprised the standard-volume group, and 11 who were evaluated after the implementation of the restricted-volume infusion strategy comprised the restricted-volume group. In the standard-volume group, the donors were given 10 ml x kg(-1) x h(-1) of lactated Ringer's solution and additional plasma expander corresponding to blood loss. In the restricted-volume group, the donors received 5 ml x kg(-1) x h(-1) of lactated Ringer's solution until the resection of the hepatic graft, followed by 15 ml x kg(-1) x h(-1) of lactated Ringer's solution after the completion of resection until the end of the operation. RESULTS: Intraoperative blood loss was less in the restricted-volume group (445 +/- 193 ml) than in the standard-volume group (1331 +/- 602 ml; P < 0.01). Intraoperative fluid infusion was also less in the restricted-volume group (4130 +/- 563 ml) than in the standard-volume group (5634 +/- 1260 ml; P < 0.01). There were no differences in length of hospital stay or side effects between the two groups. CONCLUSION: Our restricted-volume strategy reduced blood loss and had no adverse effects during living-donor hepatectomy.

Acid-sensing ion channel 3 (ASIC3) cell surface expression is modulated by PSD-95 within lipid rafts.

Acid-sensing ion channel 3 (ASIC3) is a H(+)-gated cation channel primarily found in sensory neurons, where it may function as a pH sensor in response to metabolic disturbances or painful conditions. We previously found that ASIC3 interacts with the postsynaptic density protein PSD-95 through its COOH terminus, which leads to a decrease in ASIC3 cell surface expression and H(+)-gated current. PSD-95 has been implicated in recruiting proteins to lipid rafts, which are membrane microdomains rich in cholesterol and sphingolipids that organize receptor/signaling complexes. We found ASIC3 and PSD-95 coimmunoprecipitated within detergent-resistant membrane fractions. When cells were exposed to methyl-beta-cyclodextrin to deplete membrane cholesterol and disrupt lipid rafts, PSD-95 localization to lipid raft fractions was abolished and no longer inhibited ASIC3 current. Likewise, mutation of two cysteine residues in PSD-95 that undergo palmitoylation (a lipid modification that targets PSD-95 to lipid rafts) prevented its inhibition of ASIC3 current and cell surface expression. In addition, we found that cell surface ASIC3 is enriched in the lipid raft fraction. These data suggest that PSD-95 and ASIC3 interact within lipid rafts and that this raft interaction is required for PSD-95 to modulate ASIC3.

Inadvertent intrathecal cannulation in an infant, demonstrated by three-dimensional computed tomography: a rare complication of internal jugular vein catheterization.

We describe a case of inadvertent intrathecal cannulation with a central venous catheter in an infant, confirmed by three-dimensional computed tomography, which clearly demonstrated the track of the catheter. We believe that this complication could have been related to two major factors: depth of needle insertion and penetration of the vein by a straight-tip guidewire. To avoid this complication, the depth of needle insertion must be carefully checked, a "J"-tipped rather than a straight-tipped guidewire should be used, and puncture should be guided by ultrasound.

BINAP/1,4-diamine-ruthenium(II) complexes for efficient asymmetric hydrogenation of 1-tetralones and analogues.

A combined system of a RuCl(2)(binap)(1,4-diamine) complex and t-C(4)H(9)OK in i-C(3)H(7)OH catalyzes enantioselective hydrogenation of various 1-tetralone derivatives and some methylated 2-cyclohexenones. Hydrogenation of 2-methyl-1-tetralone under dynamic kinetic resolution gives the cis alcohol with high ee. [reaction: see text]

Involvement of H2O2 in superoxide-dismutase-induced enhancement of endothelium-dependent relaxation in rabbit mesenteric resistance artery.

1 The mechanism underlying the enhancement by superoxide dismutase (SOD) of endothelium-dependent relaxation was investigated in rabbit mesenteric resistance arteries. 2 SOD (200 U ml(-1)) increased the production of H(2)O(2) in smooth muscle cells (as indicated by the use of an H(2)O(2)-sensitive fluorescent dye). 3 Neither SOD nor catalase (400 U ml(-1)) modified either the resting membrane potential or the hyperpolarization induced by acetylcholine (ACh, 1 micro M) in smooth muscle cells. 4 In arteries constricted with noradrenaline, the endothelium-dependent relaxation induced by ACh (0.01-1 micro M) was enhanced by SOD (200 U ml(-1)) (P<0.01). This action of SOD was inhibited by L-N(G)-nitroarginine (nitric oxide (NO)-synthase inhibitor) but not by either charybdotoxin+apamin (Ca(2+)-activated-K(+)-channel blockers) or diclofenac (cyclooxygenase inhibitor). 5 Neither ascorbate (50 micro M) nor tiron (0.3 mM), superoxide scavengers, had any effect on the ACh-induced relaxation, but each attenuated the enhancing effect of SOD on the ACh-induced relaxation. Similarly, catalase (400 U ml(-1)) inhibited the effect of SOD without changing the ACh-induced relaxation. 6 In endothelium-denuded strips constricted with noradrenaline, SOD enhanced the relaxation induced by the NO donor 1-hydroxy-2-oxo-3-(N-methyl-3-aminopropyl)-3-methyl-1-triazene (NOC-7) (P<0.05). Ascorbate and catalase each attenuated this effect of SOD. 7 H(2)O(2) (1 micro M) enhanced the relaxation on the noradrenaline contraction induced by NOC-7 and that induced by 8-bromo-cGMP, a membrane-permeable analogue of guanosine 3',5' cyclic monophosphate (cGMP). 8 SOD had no effect on cGMP production, whether measured in endothelium-intact strips following an application of ACh (0.1 micro M) or in endothelium-denuded strips following an application of NOC-7 (0.1 micro M). 9 It is suggested that in rabbit mesenteric resistance arteries, SOD increases the ACh-induced, endothelium-dependent relaxation by enhancing the action of NO in the smooth muscle via its H(2)O(2)-producing action (rather than via a superoxide-scavenging action).

Effects of H2O2 on membrane potential of smooth muscle cells in rabbit mesenteric resistance artery.

The effects of H(2)O(2) on the membrane potential of smooth muscle cells of rabbit mesenteric resistance arteries were investigated. H(2)O(2) (3-30 microM) concentration-dependently hyperpolarized the membrane; this was inhibited by catalase but not by superoxide dismutase or the hydroxyl-radical scavenger dimethylthiourea. The cyclooxygenase inhibitor diclofenac partly inhibited the responses; the subsequent addition of the 5-lipoxygenase inhibitor 2-(12-hydroxydodeca-5,10-diynyl)-3,5,6-trimethyl-p-benzoquinone (AA-861) (but not the cytochrome P(450) inhibitor 17-octadecynoic acid) further attenuated H(2)O(2)-induced hyperpolarizations. The sarcolemmal ATP-sensitive K(+) (K(ATP)) channel inhibitor 1-[5-[2-(5-chloro-o-anisamido)ethyl]-2-methoxyphenylsulfonyl]-3-methylthiourea, sodium salt (HMR-1098), blocked the H(2)O(2)-induced hyperpolarization in the absence and presence of diclofenac. H(2)O(2) increased the production of prostaglandin E(2) and prostacyclin (estimated from its stable metabolite 6-keto-prostaglandin F(1alpha)), both of which produce a HMR-1098-sensitive hyperpolarization in the smooth muscle cells. It is concluded that, in smooth muscle cells of rabbit mesenteric artery, H(2)O(2) increases the synthesis of vasodilator prostaglandins and possibly 5-lipoxygenase products, which produce a hyperpolarization by activating sarcolemmal K(ATP) channels.

Reduced function of endothelial prostacyclin in human omental resistance arteries in pre-eclampsia.

It remains unclear in pre-eclampsia whether or not a functional change occurs in the role played by prostacyclin in endothelium-dependent relaxation in resistance arteries. We examined this using human omental resistance arteries (obtained from pre-eclamptic or normotensive pregnant women) in the presence of N(G)-nitro-L-arginine (L-NNA, an inhibitor of nitric oxide synthase). In endothelium-intact strips from both groups, 9,11-epithio-11,12-methano-thromboxane A(2) (STA(2), a thromboxane A(2) mimetic) produced a contraction. Diclofenac (an inhibitor of cyclooxygenase) enhanced the STA(2) contraction only in the normotensive pregnant group (1.4 times control, P < 0.01). In the presence of STA(2), bradykinin (0.1 microM) produced an endothelium-dependent relaxation in both groups, the relaxation being significantly smaller for the pre-eclamptic group (P < 0.002). Diclofenac significantly attenuated the bradykinin-induced relaxation only for the normotensive pregnant group (31 % inhibition, P < 0.001). The bradykinin-induced membrane hyperpolarization consisted of diclofenac-sensitive and -insensitive components. The former, but not the latter, was significantly smaller in pre-eclampsia (-4.3 vs. -2.6 mV, P < 0.05). The concentrations of 6-keto-PGF(1alpha) (a stable metabolite of prostacyclin) in these arteries were significantly lower in pre-eclampsia in both the absence and presence of bradykinin (about 0.2-0.4 times the normotensive pregnant value in each case, P < 0.01). By contrast, both the relaxation and the membrane hyperpolarization in response to beraprost (10 nM, a stable analogue of prostacyclin) were similar between the two groups. We conclude that, in pre-eclampsia, a reduced part is played by prostaglandins in the endothelium-dependent relaxation seen in resistance arteries and that this may be due to a reduced production of prostacyclin by the endothelium.