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The diatomic collisional intermediate responsible for the formation of an electronically excited molecule by teratomic recombination has been observed in both the spectral and temporal domains by laser spectroscopy. We report experiments demonstrating thermal Xe(6s[3/2]2)-Xe(5p6 1S0) atomic collision pairs to be the immediate precursor to the formation of Xe*2(a³Σ+u, A¹Σ+u) by the three body process: Xe*(6s)+2Xe → Xe*2 + Xe, where the asterisk denotes an excited electronic state. Photoassociating Xe(6s)-Xe atomic pairs by free ← free transitions of the collision complex interrupts the production of the electronically excited Xe dimer, thereby suppressing Xe2 spontaneous emission in the vacuum ultraviolet (VUV, λ ~ 172 nm, A¹Σ+u → X¹Σ+g). Intercepting Xe(6s)-Xe pairs before the complex is stabilized by the arrival of the third atom in the teratomic collision process selectively depletes the pair population in a specific Franck-Condon region determined by the probe laser wavelength (λ). Measurements of the variation of VUV emission suppression with λ provide a spectral signature of the [Xe(6s[3/2]2) - Xe(¹S0)]* complex and map the probe laser wavelength onto the thermal energy (∊″) of the incoming collision pairs. [ABSTRACT FROM AUTHOR]

Bound←bound transitions of the Xe dimer at small internuclear separation (R < 4.0 Å) have been observed in the 545-555 nm and 675-800 nm spectral regions by laser spectroscopy in the afterglow of a pulsed Xe microplasma with a volume of ∼160 nl. Transient suppression of Xe2 A¹Σu+ (Ou+) → X¹Σg+ (Og+) emission in the vacuum ultraviolet (∼172 nm), induced by laser excitation of Ωg ← a³Σu+ (1u,Ou-) [Rydberg←Rydberg] transitions of the molecule, has confirmed the existence of structure between 720 and 770 nm (reported by Killeen and Eden [J. Chem. Phys. 84, 6048 (1986)]) but also reveals red-degraded vibrational bands extending to wavelengths beyond 800 nm. Spectral simulations based on calculations of Franck-Condon factors for assumed Ωg ← a³Σu+ transitions involving Ω = 0±,1 gerade Rydberg states suggest that the upper level primarily responsible for the observed spectrum is an Ω = 1 state correlated, in the separated atom limit, with Xe(5p6 ¹S0) + Xe(5p5 6p) and built on a predominantly A²Π3/2g molecular ion core. Specifically, the spectroscopic constants for the upper state of the 1g ← 1u,Ou± absorptive transitions are determined to be Te = 13 000 ± 150 cm-1, ωe′ = 120 ± 10 cm-1, ωexe′ = 1.1 ± 0.4 cm-1, De = 3300 ± 300 cm-1, and ΔRe = Re′- Re″ = 0.3 ± 0.1 Å which are in general agreement with the theoretical predictions of the pseudopotential hole-particle formalism, developed by Jonin and Spiegelmann [J. Chem. Phys. 117, 3059 (2002)], for both the (5)1g and (3)Og+ states of Xe2. These spectra exhibit the most extensive vibrational development, and provide evidence for the first molecular coreswitching transition, observed to date for any of the rare gas dimers at small R (<4 Å). Experiments in the green (545-555 nm) also provide improved absorption spectra, relative to data reported in 1986 and 1999, associated with Xe2 Rydberg states derived from the Xe(7p) orbital. [ABSTRACT FROM AUTHOR]

Introduction: Attention Deficit Hyperactivity Disorder (ADHD) is the main neurobehavioral disorder affecting children and adolescents between six and seventeen years of age; It is a neurodevelopmental disorder of chronic and hereditary characteristics, with behavioral patterns of inattention, impulsivity, and hyperactivity1,4. ADHD affects 5% of school-age children and 2.5% of adults.² In addition, 60-80% of patients remain with symptoms in adulthood.? Among the etiologies involved in ADHD, the main one is heritability, whichmay reach 75%2,3. Regarding the prognosis, there is a relationship between ADHD and substance abuse and other psychiatric disorders, academic and professional failure, difficulty in interpersonal relationships3. It is recommended that the treatment be multimodal, involving drug therapy, psychological and psychoeducation5. The drugs of choice are methylphenidate and dexamphetamine4. Objectives: To present a multidisciplinary university extension project that works in the diagnosis and treatment of children with ADHD. Methods: The project operates in a multidisciplinary way, involving the medical, psychological and psycho-pedagogical areas. Patients undergo initial medical evaluation, followed by neuropsychological evaluation to confirm or exclude the diagnosis. When associated with learning disorders, psychopedagogic intervention is performed. Results: In 2019, the project provided over 130 consultations, covering more than 60 patients. Conclusions: The project performance is justified, being ADHD a prevalent disease in the population and with developmental damage; thus, it is of utmost importance to correctly diagnose and treat patients with a specialized and multidisciplinary team. [ABSTRACT FROM AUTHOR]

Lasing on the 62P1/2→62S1/2 (D1) resonance transition of atomic Cs at 894.3 nm has been realised in mixtures of Ar, ethane, and Cs vapour by the photoexcitation of ground state Cs–Ar collision pairs and subsequent dissociation of diatomic, electronically-excited CsAr molecules (excimers). The blue satellites of the alkali D2 lines provide a pathway for optically pumping atomic alkali lasers on the principal series (resonance) transitions with broad linewidth (>=2 nm) semiconductor diode lasers. [ABSTRACT FROM AUTHOR]

The breakdown voltage (Vs) for a discharge in Ar at pressures between 35 and 300 torr has been reduced significantly with an array of cylindrical microdischarge devices mounted behind the tungsten cathode. For PAr = 50 torr, Vs drops by approximately a factor of two, relative to that for a conventional discharge, when the microdischarge array is in operation. The injection of electron-ion pairs into the anode-cathode gap region by the array also decreases the formative and statistical time lags associated with the startup of a cold lamp. [ABSTRACT FROM AUTHOR]

Objective: Changes in exhaled nitric oxide levels often accompany conditions associated with elevated pulmonary vascular resistance and altered lung mechanics. However, it is unclear whether changes in exhaled nitric oxide reflect altered vascular or bronchial nitric oxide production. This study determined the effects of acute hypoxia and reoxygenation on pulmonary mechanics, plasma nitrite levels, and exhaled nitric oxide production., Methods: Ten piglets underwent 90 minutes of hypoxia (fraction of inspired oxygen = 12%), 1 hour of reoxygenation on cardiopulmonary bypass, and 2 hours of recovery. Five additional animals underwent bypass without hypoxia. Exhaled nitric oxide, plasma nitrite levels, and pulmonary mechanics were measured., Results: Exhaled nitric oxide decreased to 36% of baseline by end hypoxia (34 +/- 14 vs 12 +/- 9 ppb, P =.005) and declined further to 20% of baseline at end recovery (7 +/- 6 ppb). Aortic nitrite levels decreased from baseline during hypoxia (from 102 +/- 13 to 49 +/- 7 micromol/L, P =.05) but returned to baseline during recovery. Pulmonary arterial nitrite also decreased during hypoxia (from 31.4 +/- 7.8 to 22.9 +/- 9.5 micromol/L, P =.04) and returned to baseline at end recovery. Decreased production of exhaled nitric oxide was associated with impaired gas exchange (alveolar-arterial gradient = 32 mm Hg at baseline and 84 mm Hg at end recovery), decreased pulmonary compliance (6.6 +/- 0.9 mL/cm H(2)O at baseline, 5.0 +/- 0.7 mL/cm H(2)O at end hypoxia, and 5.4 +/- 0.7 mL/cm H(2)O at end recovery), and increased inspiratory airway resistance (41 +/- 4 cm H(2)O. L(-1). s(-1) at baseline, 56 +/- 4.9 cm H(2)O. L(-1). s(-1) at end hypoxia, and 50 +/- 5 cm H(2)O. L(-1). s(-1) at end recovery)., Conclusions: A decrease in exhaled nitric oxide persisted after hypoxia, and plasma nitrite levels returned to baseline on reoxygenation, indicating that alterations in exhaled nitric oxide during hypoxia-reoxygenation might be unrelated to plasma nitrite levels. Furthermore, decreased exhaled nitric oxide corresponded with altered pulmonary mechanics and gas exchange. Reduced exhaled nitric oxide after hypoxia-reoxygenation might reflect bronchial epithelial dysfunction associated with acute lung injury.

Background: Acute hypoxia results in increased pulmonary vascular resistance. Despite reoxygenation, pulmonary vascular resistance remains elevated and pulmonary function is altered. Endothelin-1 might contribute to hypoxia-reoxygenation-induced pulmonary hypertension and to reoxygenation injury by stimulating leukocytes. This study was carried out using an established model of hypoxia and reoxygenation to determine whether endothelin-1 blockade with Bosentan could prevent hypoxia-reoxygenation-induced pulmonary hypertension and reoxygenation injury., Methods: Twenty neonatal piglets underwent 90 minutes of hypoxia, 60 minutes of reoxygenation on cardiopulmonary bypass, and 2 hours of recovery. Control animals (n = 12) received no drug treatment, whereas the treatment group (n = 8) received the endothelin-1 receptor antagonist, Bosentan, throughout hypoxia., Results: In controls, pulmonary vascular resistance increased during hypoxia to 491% of baseline and remained elevated after reoxygenation; however in the Bosentan group, it increased to only 160% of baseline by end-hypoxia, then decreased to 76% at end-recovery. Arterial endothelin-1 levels in controls increased to 591% of baseline after reoxygenation. Arterial nitrite levels decreased during hypoxia in controls but were maintained in the Bosentan group. Consequently, animals in the Bosentan group had better postreoxygenation pulmonary vascular resistance, A-a gradient, and airway resistance along with lower myeloperoxidase levels than controls., Conclusions: Acute hypoxia and postreoxygenation pulmonary hypertension was attenuated by Bosentan, which maintained nitric oxide levels during hypoxia, decreased leukocyte-mediated injury, and improved pulmonary function.

A highly purified protein from lysates of human umbilical vein endothelial cells (HUVECs) inhibited the activation of factor XII [Hageman factor (HF)] and removed factor XIIa from an activating surface, thus impairing HF-dependent coagulation and kinin-releasing activities. Two tryptic peptides from this protein had 100% identity with amino acids 31-44 and 89-101 of a nonhistone DNA-binding protein known as high-mobility group protein (HMG-I). In specific antibody experiments, the clot-inhibiting property in purified lysate protein from HUVECs was associated with HMG-I. The molecular weight of the protein that inhibited clotting was consistent with that predicted for HMG-I. Protein that inhibited contact activation and had antigenic properties of HMG-I and HUVEC lysate protein also was found in conditioned media from unchallenged cultured HUVECs. After HUVECs were incubated with 14C lysine, conditioned media contained immunoprecipitable radiolabeled protein with the same molecular weight as that recovered from cell lysates, suggesting that this high-mobility group protein (HMG-I) may be secreted. Purified factor XII antigens were displaced from a glass surface by HMG-I from lysates in proportion to the amount of HMG-I protein that was added. This HMG-I probably inhibits factor XII functions because its high positive charge favors competitive binding to an activating substance.

A patient with severe acquired angioneurotic edema had essentially no C1- inhibitor activity in his serum and nearly died of cardiopulmonary arrest during an acute episode of facial, oral, and pharyngeal edema. This patient had an antibody directed against C1- inhibitor and C1- inhibitor-anti-C1- inhibitor complexes in his serum. The antibody required a normal residue (Arg) in the reactive center of the inhibitor for its optimal interaction with the inhibitor. Plasmapheresis with 5% human serum albumin replacement relieved him of his antibody load and the edema; additional treatment with pulsed cyclophosphamide has provided a sustained remission. The 5% albumin solution that was used contained functional C1- inhibitor; other lots that were tested contained only traces or none. No underlying disease has yet been identified. During this acute episode of edema, the C1- inhibitor in the patient's plasma was a 92 kd component, and on recovery, a 105 kd component reappeared. C1- inhibitor isolated from the patient's plasma, which was obtained before pheresis, was mainly in lower molecular weight forms (56 kd and 45 kd). The antibody in the patient's serum appeared to render C1- inhibitor susceptible to proteolysis, for when purified antibody was added to normal serum, a cleaved form of C1- inhibitor was generated.

The long-term immunologic changes with allergy injection therapy have been widely studied. There are few data, however, on the immunologic response to a single injection during the course of this therapy. Ten patients who had attained maintenance (1:100 w/v) within six months and 13 patients who had been on maintenance longer than three years were compared. Following baseline studies patients received their standard ragweed injections and were followed without further injections for 30 days. Titrated prick tests to short ragweed, specific IgE to short ragweed and IgG antibody to ragweed AgE were determined at intervals during the 30 days. Baseline values of skin tests, specific IgE and specific IgG did not differ significantly for the two groups. Values for all three parameters did not fluctuate significantly during the study. This study suggests that blocking antibody levels are stable soon after reaching maintenance and that allergy injections can be safely administered at monthly intervals beginning at that time.