Softening of a flat phonon mode in the kagome ScV6Sn6.

Geometrically frustrated kagome lattices are raising as novel platforms to engineer correlated topological electron flat bands that are prominent to electronic instabilities. Here, we demonstrate a phonon softening at the kz = π plane in ScV6Sn6. The low energy longitudinal phonon collapses at ~98 K and q = [Formula: see text] due to the electron-phonon interaction, without the emergence of long-range charge order which sets in at a different propagation vector qCDW = [Formula: see text]. Theoretical calculations corroborate the experimental finding to indicate that the leading instability is located at [Formula: see text] of a rather flat mode. We relate the phonon renormalization to the orbital-resolved susceptibility of the trigonal Sn atoms and explain the approximately flat phonon dispersion. Our data report the first example of the collapse of a kagome bosonic mode and promote the 166 compounds of kagomes as primary candidates to explore correlated flat phonon-topological flat electron physics.

Gonioscopic findings in patients with acute central/hemicentral retinal vein occlusions.

OBJECTIVES: To evaluate prospectively the gonioscopic findings and their changes during a 3-year follow-up period in patients with acute central/hemicentral retinal vein occlusions (C/HRVOs). MATERIAL AND METHODS: A comprehensive ophthalmological examination of both eyes including static and dynamic gonioscopy as well as ocular biometric measurements was performed in 57 patients with acute C/HRVOs. The angle configuration and its changes, the axial length of the globe, the anterior chamber depth and the corneal thickness were assessed. RESULTS: 12 C/HRVO patients presented with narrow drainage angles (< or = 20 degrees) and 45 had normal angles (> 20 degrees). Ocular globes with narrow angles had axial length and anterior chamber depth significantly smaller as well as cornea thickness significantly greater than the eyes with normal angles. Out of the 12 patients with narrow angles, 6 cases had primary angle closure suspect (PACS), 5 cases had primary angle closure (PAC) and one case primary angle closure glaucoma (PACG). 3 of the 6 PACS patients progressed to PAC in the 6th, 10th, and 18th months of the follow-up period. From the 8 PAC cases existing during the whole study interval, one case progressed to PACG during the 24th month of the folow-up interval. CONCLUSIONS: In the context of an ocular globe having its size significantly smaller than the normal eye, narrow angle may represent a local risk factor predisposing to C/HRVO. Intermittent episodes of angle closure may contribute by increasing the intraocular pressure to the occurrence of C/HRVO as well to the progression of the gonioscopic configuration from PACS to PAC and from PAC to PACG.

[Neovascular glaucoma--etipathogeny and diagnosis]. / Glaucom neovascular: etiopatogenie si diagnostic.

Neovascular glaucoma is defined as an iris and/or anterior chamber angle neovascularization associated with increased intraocular presure. It is a secondary glaucoma most frequently determined by a severe retinal ischemia. The most common diseases responsible for the development of neovascular glaucoma are diabetic retinopathy, ischemic central retinal vein occlusion and ocular ischemic syndrome; the uncommon causes include ocular radiation, ocular tumors, uveitis and other miscellaneous conditions. Vascular endothelial growth factor is an important and probably predominant agent in the pathogenesis of both intraocular neovascularization and neovascular glaucoma. The evolution of clinical and histopathological changes from predisposing conditions to the occurrence of rubeosis iridis as well as neovacular glaucoma is divided into four grades that is prerubeotic, preglaucomatous, open-angle and angle closure glaucoma stages.

[Treatment of neovascular glaucoma]. / Tratamentul glaucomului neovascular.

Neovascular glaucoma management is divided into preventive and curative procedures.Pre vention therapy consists of the treatment of the common underlying causes of the disease (ie diabetic retinopathy, ischemic central retinal vein occlusion and ocular ischemic syndrome) as well as the less frequent causes attributed to ocular radiation, ocular tumors, uveitis and other miscellaneous condi tions.Curative therapy includes both the neovascularization treatment and the treatment of the in creased intraocular pressure.lntravitreal Bevacizumab injection enables us to block up the neovascular trigger preparing thereby the pacient to a complement of panretinal photocoagulation or surgical treatment. Since Bevacizumab injection activity is transient, the retinal ischemia treatment by panretinal photocoagulation is mandeited in order to avoid neovascular recurrence.Short term efficacy of Bevacizumab injection is obvious with a constant, marked and swift intraocular pressure lowering espe cially in less severe and/or early forms of the disorder. In more advanced stages of neovascular glaucoma after closing the chamber angle by peripheric anterior synechiae the outcomes of this treatment are inconstant, most of cases necessitating the resorting to surgery (trabeculectomy with antifi brosis drugs or glaucoma drainage implants).

[Etiology of central retinal vein occlusion]. / Etiologie a ocluziei venei centrale a retinei.

Arteriosclerosis is responsible for the majority of primitive pictures of central retinal vein occlusion occurrence. The venous occlusions appearing during the development of the already known disorders represent secondary venous occlusions. In young adults central retinal vein occlusion probably represents a general nonspecific change emerging from a number of individual causes or maybe a combination of causes e.g. multifactorial etiology. During unusual cases of central retinal vein occlusion the etiology is known but within the vast majority of patients the specific cause or even the causes that contribute the occurrence of this disease remain unknown since the ophthalmic literature is limited by a scarcity of histopathologic material.

[Risk factors in central retinal vein occlusion]. / Factori de risc în ocluzia venei centrale a retinei.

Risk factors for the occurrence of central retinal vein occlusion are to a certain extent similar to those of cardiovascular diseases (e.g. arteriosclerosis, arterial systemic hypertension, diabetes mellitus, dislipidemia). Hyperhomocysteinemia is an essential risk factor for arteriosclerosis intervening also directly in the local mechanism of causing venous and arterial occlusions. Ocular hypertension and glaucoma are risk factors significantly associated with pathogenesis of central retinal vein occlusion. Therapy with anticoagulants and platelet anti-aggregating agents exposes the patient to developing central retinal vein occlusion influencing also adversely the visual outcome without having any evidence of protective or beneficial effect.

[Azarga, a new and useful fixed combination in glaucoma treatment]. / Azarga,o noua si utila combinatie medicaméntoasa fixa în tratamentul glaucomului.

Azarga is a new fixed combination product that consists of the carbonic anhydrase inhibitor brinzolamide 1% and the betablocker timolol 0,5%. Its efficacy in lowering intraocular pressure is similar to that of Cosopt, a fixed combination that combines another carbonic anhydrase inhibitor (eg dorzolamide 2%) with the betablocker timolol 0,5%. The main difference between these two ocular hypotensive agents lies in their safety profiles with Cosopt causing more ocular discomfort to appear while instilling (burning,stinging and smarting sensations) probably due to the differences between the pH of these two fixed combinations agents. Its similar efficacy and enhanced tolerability compared with Cosopt make Azarga represent a resonable alternative for the patients who do not achieve an adequate intraocular pressure control while treating with a monotherapeutic agent.

[The latest developments in glaucoma therapy using fixed combination products]. / Actualitati în tratamentul glaucomului cu combinatii fixe medicamentoase.

Modern fixed-combination products simplify medication dose regimen without sacrificing their effectiveness.Potential benefits of the therapy with fixed-combination products are enhanced tolerability increased convenience,better compliance,cost and time economy and removal of the wash out effect. Regarding intraocular pressure lowering effect, fixed-combination agents are superior to monotherapy with the two medication components, with the exception of Duotrav that is not superior to travoprost action.Fixed-combination products are noninferior to concomitant administration of the two components of medication (nonfixed-combination agents) relative to their ocular hypotensive efficacy with the exception of Ganfort that is however inferior to concurrent administration of both the bimatoprost and timolol.

[Mendelian molecular genetics in glaucoma]. / Genetica moleculara in glaucom.

Early-onset forms of glaucoma are inherited as Mendelian-dominant or Mendelian-recessive traits. They encompass primary congenital or infantile glaucoma; juvenile primary open-angle glaucoma; development glaucomas including Rieger syndrome, glaucoma associated with nail-patella syndrome, Peters' anomaly, and nanophthalmos; and glaucoma associated with pigment dispersion syndrome. Personalized gene therapy has been proposed as an alternative therapeutic strategy for ocular diseases. This approach might be applicable in families with primary congenital glaucoma and defined mutations in the CYP1B1 gene.

[Monotherapy with lipid structural derivatives in glaucoma]. / Monoterapia cu derivate structurale lipidice în glaucom.

Lipid structural derivatives (latanoprost, travoprost and bimatoprost) are ocular hypotensive agents that significantly lower ocular tension with more than 30% from baseline by once-daily dosing.Ocular tension reduction from baseline is statistically significantly greater for bimatoprost than for latanoprost at all time points measured. Compared with travoprost, ocular tension decrease was statistically greater with bimatoprost at 8AM and 12PM. This trend was also seen at 4PM and 8PM, even though the difference was not statistically significant at the former time point and borderline at the latter time point. The findings for latanoprost and travoprost indicate that these two agents are comparable in their ability to reduce ocular pressure with no statistically significant difference seen at any time point measured. There does not exist any evidence, excepting conjunctival hyperemia which has been lesser with latanoprost compared to both the bimatoprost and travoprost, that any of these 3 medications significantly differs with respect to their adverse effects.

[Multifactorial molecular genetics in glaucoma]. / Genetica moleculara multifactoriala în glaucom.

Diseases with nonmendelian, complex, polygenic or multifactorial heredity are defined as disorders that do not exhibit a classic mendelian inheritance attributable to a single gene but are determined by a number of genetic and environmental factors. Glaucoma forms having a multifactorial heredity encompass primary open-angle glaucoma, normal tension glaucoma, pseudoexfoliation glaucoma, steroid induced glaucoma and hypertensive uveitis Future directions in molecular genetics of glaucoma, admirably synthesized within The European Glaucoma Society GlaucoGENE project, comprise reviewing the genotype-phenotype correlations, identification of the new glaucoma genes, investigating gene-environment interactions and gene-gene interactions as well as developing a mutation database that can be used for diagnostic and prognostic testing.