Effect of acetazolamide on lithium reabsorption and lithium-induced GSK3ß phosphorylation in rat kidney.

Lithium promotes the phosphorylation of glycogen synthase kinase-3ß (GSK3ß), and this reaction protects against acute kidney injury mediated by renal apoptosis. Lithium is considered to be reabsorbed by sodium-phosphate cotransporters and sodium-proton exchanger NHE3. This study evaluated the relation between the lithium reabsorption and the phosphorylation of GSK3ß, by using acetazolamide, an NHE3 inhibitor. In rats infused with lithium chloride, the plasma concentration of lithium was 4.77 mEq/l, and the renal clearance of lithium and its fractional excretion were calculated to be 2.29 ml/min/kg and 0.405, respectively. Coadministration of acetazolamide decreased creatinine clearance and the reabsorption rate of lithium, increased the fractional excretion of lithium, and did not affect its plasma concentration. Western blot analysis exhibited the facilitation of GSK3ß phosphorylation in the kidney cortex by lithium infusion, and acetazolamide inhibited the lithium-induced phosphorylation of GSK3ß. Lithium did not affect GSK3ß phosphorylation in the liver and did not affect Akt in the kidney cortex and liver. These data show that lithium reabsorption contributes to GSK3ß phosphorylation in the kidney cortex.

Novel pre-therapeutic scoring system using patient and haematological data to predict facial palsy prognosis.

OBJECTIVES: We describe a novel scoring system, the facial Palsy Prognosis Prediction score (PPP score), which we test for reliability in predicting pre-therapeutic prognosis of facial palsy. We aimed to use readily available patient data that all clinicians have access to before starting treatment. DESIGN: Multicenter case series with chart review. SETTING: Three tertiary care hospitals. PARTICIPANTS: We obtained haematological and demographic data from 468 facial palsy patients who were treated between 2010 and 2014 in three tertiary care hospitals. Patients were categorised as having Bell's palsy or Ramsey Hunt's palsy. MAIN OUTCOME MEASURES: We compared the data of recovered and unrecovered patients. PPP scores consisted of combinatorial threshold values of continuous patient data (eg platelet count) and categorical variables (eg gender) that best predicted recovery. We created separate PPP scores for Bell's palsy patients (PPP-B) and for Ramsey Hunt's palsy patients (PPP-H). RESULTS: The PPP-B score included age (≥65 years), gender (male) and neutrophil-to-lymphocyte ratio (≥2.9). The PPP-H score included age (≥50 years), monocyte rate (≥6.0%), mean corpuscular volume (≥95 fl) and platelet count (≤200 000 /µL). Patient recovery rate significantly decreased with increasing PPP scores (both PPP-B and PPP-H) in a step-wise manner. PPP scores (ie PPP-B score and PPP-H score) ≥2 were associated with worse than average prognosis. CONCLUSIONS: Palsy Prognosis Prediction scores are useful for predicting prognosis of facial palsy before beginning treatment.

Isolation of Ralstonia solanacearum-infecting bacteriophages from tomato fields in Chiang Mai, Thailand, and their experimental use as biocontrol agents.

AIMS: To isolate and characterize novel bacteriophages infecting the phytopathogen, Ralstonia solanacearum, and to evaluate them as resources with potential uses in the biocontrol of bacterial wilt. METHODS AND RESULTS: Fourteen phages infecting R. solanacearum were isolated from soil samples collected in Chiang Mai, Thailand. The phages showed different host ranges when tested against 59 R. solanacearum strains isolated from Thailand and Japan. These phages were characterized as nine podoviruses and five myoviruses based on their morphology. Podovirus J2 in combination with another podovirus (φRSB2) lysed host cells very efficiently in contaminated soil. J2 treatment prevented wilting of tomato plants infected with a highly virulent R. solanacearum strain. CONCLUSIONS: Treatment with J2 effectively reduced the amount of the bacterial wilt pathogen in contaminated soil and prevented bacterial wilt of tomato in pot experiments. Myovirus J6 possessed jumbo phage features, giving a unique opportunity to study its utilization as a biocontrol agent. SIGNIFICANCE AND IMPACT OF THE STUDY: As exemplified by J2, the phages isolated in this study represent valuable resources with potential uses in biocontrol of bacterial wilt. A rare jumbo phage J6 served as a valuable subject to understand and utilize this new group of phages.

The effects of dexmedetomidine on inflammatory mediators after cardiopulmonary bypass.

Cardiac surgery with cardiopulmonary bypass is associated with the development of a systemic inflammatory response that can often lead to dysfunction of major organs. We hypothesised that the highly selective α2-adrenergic agonist, dexmedetomidine, attenuates the systemic inflammatory response. Forty-two patients were randomly assigned to receive dexmedetomidine or saline after aortic cross-clamping). The mean (SD) levels of the nuclear protein plasma high-mobility group box 1 increased significantly from 5.1 (2.2) ng ml(-1) during (16.6 (7.3) ng ml(-1) ) and after (14.3 (8.2) ng ml(-1) ) cardiopulmonary bypass in the saline group. In the dexmedetomidine group, the levels increased significantly only during cardiopulmonary bypass (4.0 (1.9) ng ml(-1) baseline vs. 10.8 (2.7) ng ml(-1) ) but not after (7.4 (3.8) ng ml(-1) ). Dexmedetomidine infusion also suppressed the rise in mean (SD) interleukin-6 levels after cardiopulmonary bypass (a rise of 124.5 (72.0) pg ml(-1) vs. 65.3 (30.9) pg ml(-1)). These suppressive effects of dexmedetomidine might be due to the inhibition of nuclear factor kappa B activation and suggest that intra-operative dexmedetomidine may beneficially inhibit inflammatory responses associated with ischaemia-reperfusion injury during cardiopulmonary bypass.

Elevation of interleukin-6 and attenuation of tumor necrosis factor-α during wheelchair half marathon in athletes with cervical spinal cord injuries.

STUDY DESIGN: Nonrandomized study. OBJECTIVES: The purpose of this study was to determine the effects of long and intensive exercise on interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in athletes with cervical spinal cord injuries (CSCI). SETTING: The 30th Oita International Wheelchair Marathon Race. METHODS: Blood samples from six athletes with CSCI and eight athletes with thoracic and lumber spinal cord injuries (SCI) participating in wheelchair half marathon race were collected before the race, immediately after the race and 2 h after the race. IL-6, TNF-α, adrenaline and blood cell counts were measured. RESULTS: Monocyte count remained stable throughout the study in the CSCI group but was significantly high at 2 h after the race in the SCI group. Plasma IL-6 concentrations were significantly elevated immediately after the race in both groups, although the levels in CSCI were significantly lower than in the SCI group. Plasma adrenaline was significantly elevated immediately after the race in the SCI group but recovered at 2 h after the race. In contrast, plasma adrenaline did not change in the CSCI group throughout the study and was significantly lower than in the SCI group. Plasma TNF-α did not change throughout the study in the SCI group compared with a significant decrease at 2 h after the race in the CSCI group. CONCLUSION: Long and intensive exercise increased IL-6 in the CSCI group despite the small muscle mass and lack of sympathetic nervous system. The post-race fall in plasma TNF-α in the CSCI group could be related to the inhibitory effect of rising IL-6 in the presence of normal monocyte count and stable adrenaline level.

Evidence for direct CP violation in B±â†’ηh± and observation of B0→ηK0.

We report measurements of the branching fractions and CP asymmetries for B(±)→ηh(±) (h=K or π) and the observation of the decay B(0)→ηK(0) from the final data sample of 772×10(6) B ̅B pairs collected with the Belle detector at the KEKB asymmetric-energy e(+)e(-) collider. The measured branching fractions are B(B(±)→ηK(±))=(2.12±0.23±0.11)×10(-6), B(B(±)→ηπ(±))=(4.07±0.26±0.21)×10(-6), and B(B(0)→ηK(0))=(1.27(-0.29)(+0.33)±0.08)×10(-6), where the last decay is observed for the first time with a significance of 5.4 standard deviations (σ). We also find evidence for CP violation in the charged B modes, A(CP)(B(±)→ηK(±))=-0.38±0.11±0.01 and A(CP)(B(±)→ηπ(±))=-0.19±0.06±0.01 with significances of 3.8 σ and 3.0 σ, respectively. For all measurements, the first and second uncertainties are statistical and systematic, respectively.

Search for CP violation in D± meson decays to ϕπ±.

We search for CP violation in Cabibbo-suppressed charged D meson decays by measuring the difference between the CP-violating asymmetries for the Cabibbo-suppressed decays D(±)→K(+)K(-)π(±) and the Cabibbo-favored decays D(s)(±)→K(+)K(-)π(±) in the K(+)K(-) mass region of the ϕ resonance. Using 955 fb(-1) of data collected with the Belle detector, we obtain A(CP)(D+→ϕπ+)=(+0.51±0.28±0.05)%. The measurement improves the sensitivity of previous searches by more than a factor of 5. We find no evidence for direct CP violation.

Measurement of the CP-violation parameter sin2φ1 with a new tagging method at the Υ(5S) resonance.

We report a measurement of the CP-violation parameter sin2φ1 at the Υ(5S) resonance using a new tagging method, called "B-π tagging." In Υ(5S) decays containing a neutral B meson, a charged B, and a charged pion, the neutral B is reconstructed in the J/ψK(S)(0) CP-eigenstate decay channel. The initial flavor of the neutral B meson at the moment of the Υ(5S) decay is opposite to that of the charged B and may thus be inferred from the charge of the pion without reconstructing the charged B. From the asymmetry between B-π(+) and B-π(-) tagged J/ψK(S)(0) yields, we determine sin2φ1=0.57±0.58(stat)±0.06(syst). The results are based on 121 fb(-1) of data recorded by the Belle detector at the KEKB e(+)e(-) collider.

Wheelchair half-marathon race increases natural killer cell activity in persons with cervical spinal cord injury.

STUDY DESIGN: Non-randomized study. OBJECTIVE: We reported that individuals with cervical spinal cord injury (CSCI) showed no increase in natural killer cell activity (NKCA) in response to 20-min arm exercise. It could be argued that this lack of response was owing to the short duration and intensity of the exercise. SETTING: The 29th Oita International wheelchair marathon race. METHODS: The present study compared the effects of wheelchair half-marathon race on natural killer (NK) cell count, NKCA and other hematological and hormonal parameters in six subjects with CSCI and seven control subjects with spinal cord injury between T4 and L1 (SCI), before, immediately after and 2 h after recovery. RESULTS: NK cell counts increased at both time points after the race in SCI, but not in CSCI, compared with before the race. NKCA increased immediately in both groups of subjects after the race, and then returned to the pre-race level at 2 h after the race. Plasma cortisol did not change in both groups throughout the study. Plasma adrenaline increased sharply in SCI after the race, then returned to the pre-race level at 2 h after the race, whereas no change was observed in CSCI throughout the study. CONCLUSION: The present study demonstrated that wheelchair half-marathon race increases NKCA despite the lack of increase in plasma adrenaline in CSCI, suggesting the activation of NKCA by mechanisms other than circulating adrenaline level.

Folie à Deux During Self-Quarantine in the COVID-19 Pandemic: a Case Report.

Folie à deux is also known as psychosis of association or shared paranoid disorder. We describe a mother and her two daughters who experienced shared delusions and hallucinations during self-quarantine in COVID-19 pandemic. The mother was later diagnosed with schizophrenia and prescribed brexpiprazole, whereas her two daughters were diagnosed with psychosis of association affected by their mother.

Deep water pathways in the North Pacific Ocean revealed by Lagrangian particle tracking.

Lagrangian particle tracking experiments are conducted to investigate the pathways of deep water in the North Pacific Ocean. The flow field is taken from a state-of-the-art deep circulation simulation. An unprecedented number of particles are tracked to quantify the volume transport and residence time. Half of the North Pacific deep water returns to the Southern Ocean, and its principal pathway is along the western boundary current in the Southwest Pacific Basin in the deep layer. About 30% is exported to the Indian Ocean after upwelling to the shallow layer in the western North Pacific Ocean. The rest is transported to the Arctic Ocean through the Bering Strait or evaporates within the Pacific Ocean. Upwelling of deep water is confined in the western North Pacific Ocean owing to the strong vertical mixing. The mean residence time of deep water in the North Pacific Ocean is estimated to be several hundred years, which is consistent with the observed radiocarbon distribution.

Search for CP violation in τ±â†’K(S)0π±ντ decays at Belle.

We report on a search for CP violation in τ(±)→K(S)(0)π(±)ν(τ) decays using a data sample of 699 fb(-1) collected by the Belle experiment at the KEKB electron-positron asymmetric-energy collider. The CP asymmetry is measured in four bins of the invariant mass of the K(S)(0)π(±) system and found to be compatible with zero with a precision of O(10(-3)) in each mass bin. Limits for the CP violation parameter Im(η(S)) are given at the 90% confidence level. These limits are |Im(η(S))| < 0.026 or better, depending on the parametrization used to describe the hadronic form factors, and improve upon previous limits by 1 order of magnitude.

Observation of X(3872)→J/ψγ and search for X(3872)→ψ'γ in B decays.

We report a study of B→(J/ψγ)K and B→(ψ'γ)K decay modes using 772×106 B ̅B events collected at the Υ(4S) resonance with the Belle detector at the KEKB energy-asymmetric e(+)e(-) collider. We observe X(3872)→J/ψγ and report the first evidence for χ(c2)→J/ψγ in B→(X_{c ̅cγ)K decays, while in a search for X(3872)→ψ'γ no significant signal is found. We measure the branching fractions, B(B(±)→X(3872)K(±))B(X(3872)→J/ψγ)=(1.78(-0.44)(+0.48)±0.12)×10(-6), B(B(±)→χ(c2)K(±))=(1.11(-0.34)(+0.36)±0.09)×10(-5), B(B(±)→X(3872)K(±))B(X(3872)→ψ'γ)<3.45×106 (upper limit at 90% C.L.), and also provide upper limits for other searches.

Search for CP violation in the decays D(0)→K(S)(0)P(0).

We have searched for CP violation in the decays D(0)→K(S)(0)P(0) where P(0) denotes a neutral pseudoscalar meson that is either a π(0), η, or η' using KEKB asymmetric-energy e(+)e(-) collision data corresponding to an integrated luminosity of 791 fb(-1) collected with the Belle detector. No evidence of significant CP violation is observed. We report the most precise CP asymmetry measurement in the decay D(0)→K(S)(0)π(0) to date: A(CP)(D(0)→K(S)(0)π(0))=(-0.28±0.19±0.10)%. We also report the first measurements of CP asymmetries in the decays D(0)→K(S)(0)η and D(0)→K(S)(0)η': A(CP)(D(0)→K(S)(0)η)=(+0.54±0.51±0.16)% and A(CP)(D(0)→K(S)(0)η')=(+0.98±0.67±0.14)%, respectively.

Evidence for the suppressed decay B(-)→DK(-), D→K(+)π(-).

The suppressed decay chain B(-)→DK(-), D→K(+)π(-), where D indicates a D(¯)(0) or D(0) state, provides important information on the CP-violating angle ϕ(3). We measure the ratio R(DK) of the decay rates to the favored mode B(-)→DK(-), D→K(-)π(+) to be R(DK)=[1.63(-0.41)(+0.44)(stat)(-0.13)(+0.07)(syst)]×10(-2), which indicates the first evidence of the signal with a significance of 4.1σ. We also measure the asymmetry A(DK) between the charge-conjugate decays to be A(DK)=-0.39(-0.28)(+0.26)(stat)(-0.03)(+0.04)(syst). The results are based on the full 772×10(6) BB(¯) pair data sample collected at the Υ(4S) resonance with the Belle detector.

Neuroendocrine ductal carcinoma in situ of the breast: cytological features in 32 cases.

OBJECTIVE: The purpose of this study was to clarify the cytological features of neuroendocrine ductal carcinoma in situ (NE-DCIS) of the breast. METHODS: We analysed the cytopathological findings in 22 fine needle aspiration (FNA) smears and 17 nipple discharge smears obtained from 32 Japanese patients with NE-DCIS. RESULTS: The background of the FNA smears was clear (59%), mucoid (23%), haemorrhagic (14%) or necrotic (5%). Most of the FNA smears (95%) showed high cellularity. Characteristically, NE-DCIS cells were loosely arranged in three-dimensional solid clusters or singly dispersed. Well-developed vascular cores with or without malignant cells were occasionally recognized. The tumour cells were polygonal or spindle-shaped with a fine granular, abundant cytoplasm. Nuclei with finely granular chromatin were round or oval and often eccentrically located (plasmacytoid appearance). Mitotic figures were infrequent. Nuclear grade was estimated to be low in 86%. Most nipple discharge smears had fairly low cellularity with poorly preserved cell clusters in a markedly haemorrhagic background, although two (12%) were extremely cellular with cytological characteristics similar to those of the FNA smears. Pre-operative cytological malignant diagnoses were made in 42% of FNA smears and 0% of nipple discharge smears. Immunohistochemistry for neuroendocrine markers (chromogranin A and synaptophysin) confirmed the neuroendocrine nature of this tumour in adequate cytological specimens. CONCLUSIONS: NE-DCIS has distinctive cytological features and can therefore be diagnosed as a neuroendocrine tumour in most FNAs and some nipple discharge smears by cytological examination employing immunohistochemical techniques. We emphasize that a breast lesion with these features may be in situ and not invasive, and also that there is a risk of under-diagnosis.

Observation of B(s)(0) → D(s)(*)+ D(s)(*)- using e+ e- collisions and a determination of the B(s)-B(s) width difference ΔΓ(s).

We have made the first observation of B(s)(0)→D(s)(*)+ D(s)(*)- decays using 23.6 fb(-1) of data recorded by the Belle experiment running on the Υ(5S) resonance. The branching fractions are measured to be B(B(s)(0)→D(s)+ D(s)-)=(1.03(-0.32-0.25)(+0.39+0.26))%, B(B(s)(0)→D(s)(*±) D(s)(∓))=(2.75(-0.71)(+0.83)±0.69)%, and B(B(s)(0)→D(s)*+ D(s)*-)=(3.08(-1.04-0.86)(+1.22+0.85))%; the sum is B[B(s)(0)→D(s)(*)+ D(s)(*)-]=(6.85(-1.30-1.80)(+1.53+1.79))%. Assuming B(s)(0)→D(s)(*)+ D(s)(*)- saturates decays to CP-even final states, the branching fraction determines the ratio ΔΓ(s)/cosφ, where ΔΓ(s) is the difference in widths between the two B(s)-B(s) mass eigenstates, and φ is a CP-violating weak phase. Taking CP violation to be negligibly small, we obtain ΔΓ(s)/Γ(s)=0.147(-0.030)(+0.036)(stat)(-0.041)(+0.042)(syst), where Γ(s) is the mean decay width.

Observation of B(s)(0) → D(s)(*-) π+ and B(s)(0) → D(s)(*-) ρ+ and measurement of the B(s)(0) → D(s)(*-) ρ+ longitudinal polarization fraction.

First observations of the B(s)(0) → D(s)(*-) π+, B(s)(0) → D(s)(-) ρ+ and B(s)(0) → D(s)(*-) ρ+ decays are reported together with measurements of their branching fractions: B(B(s)(0) → D(s)(*-) π+) = [2.4(-0.4)(+0.5)(stat) ± 0.3(syst) ± 0.4(f(s))]×10(-3), B(B(s)(0) → D(s)(-) ρ+) = [8.5(-1.2)(+1.3)(stat) ± 1.1(syst) ± 1.3(f(s))]×10(-3) and B(B(s)(0) → D(s)(*-) ρ+) = [11.9(-2.0)(+2.2)(stat) ± 1.7(syst) ± 1.8(f(s))]×10(-3) (f(s) = N(B(s)(*) B(s)(*))/N(bb)). From helicity-angle distributions, we measured the longitudinal polarization fraction in B(s)(0) → D(s)(*-) ρ+ decays to be f(L)(B(s)(0) → D(s)(*-) ρ+) = 1.05(-0.10)(+0.08)(stat)(-0.04)(+0.03)(syst). These results are based on a 23.6 fb(-1) data sample collected at the Υ(5S) resonance with the Belle detector at the KEKB e+ e- collider.

Search for a low mass particle decaying into µ+ µ- in B0 → K*0 X and B0 → ρ0 X at Belle.

We search for dimuon decays of a low mass particle in the decays B0→K*0 X and B0→ρ0 X using a data sample of 657×10(6)BB events collected with the Belle detector at the KEKB asymmetric-energy e+ e- collider. We find no evidence for such a particle in the mass range from 212 MeV/c2 to 300 MeV/c2 for lifetimes below 10(-12) s, and set upper limits on its branching fractions. In particular, we search for a particle with a mass of 214.3 MeV/c2 reported by the HyperCP experiment, and obtain upper limits on the products B(B0→K*0 X)×B(X→µ+ µ- )<2.26(2.27)×10(-8) and B(B0→ρ0 X)×B(X→µ+ µ-)<1.73(1.73)×10(-8) at 90% C.L. for a scalar (vector) X particle.