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.

[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.

[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.

[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.

[Steroid induced ocular hypertension and glaucoma]. / Hipertensiune oculara si glaucom induse steroidic.

Steroid induced ocular hypertension and glaucoma represent iatrogenic changes of pharmacogenic nature. They are mainly due to exogenous steroids following ocular periocular, intravitreal and systemic administration. Elevated ocular pressure is brought about by structural trabecular changes as well as obstruction of the outflow ways of the aqueous humor localized within the trabecular juxtacanalicular area. Although mostly raised ocular pressure spontaneously descends to basal values after ceasing the steroid therapy, progressive optic nerve damages and glaucomatous visual field defects may occur. Therapy of steroid induced ocular hypertension and glaucoma is similar to that of ocular hypertension and primary open-angle glaucoma.

[Bimatoprost therapy in glaucoma]. / Terapia cu bimatoprost în glaucom.

Bimatoprost is a neutral lipid, a fatty acid amide that pharmacologically acts in both its paternal amide form and through its hydrolysis product (active free fatty acid of bimatoprost). Hypotensive ocular efficacy of bimatoprost is significantly superior to that of timolol and latanoprost. Mean ocular pressure decreases as well as percentages of reaching and sustaining the low targeting ocular pressures are higher comparing with travoprost. Conjunctival hyperemia produced by bimatoprost is statistically greater than that caused by timolol, latanoprost and travoprost; nevertheless it is well tolerated and mild in severity. Bimatoprost prostamide lowers ocular tension significantly and clinically relevant in patients uncontrolled with latanoprost; that is why bimatoprost can be used as additive or replacement therapy in patients who already receive maximal tolerated dose of latanoprost.

[The role of Cosopt in glaucoma treatment]. / Locul cosoptului in tratamentul glaucomului.

The fixed combination of dorzolamide and timolol (Cosopt) represents a high effective therapy and is generally well tolerated. It produces a baro-protection similarly to that caused by both the prostaglandin analogs and the other topically fixed combinations. Cosopt is the only hypotensive medication that produces a direct vasoprotection by increasing retrobulbar, choroidal, retinal and optic nerve head blood flow. Its major indication is as second line therapy e.g. after the failure of a previously given monotherapy Cosopt is also indicated as an initial therapy (first line therapy) in ocular hypertensions associated with high risk factors of conversion, in some well chosen cases of primary open-angle glaucoma (e.g. glaucomas with untreated intraocular pressure of greater than 30 mmHg), in exfoliation glaucoma as well as in the majority forms of secondary glaucoma.

[Tendencies in the etiopathogenesis of glaucoma--present and future]. / Tendinte în etiopatogenia glaucomului: prezent si viitor.

Today, glaucoma is accepted within the family of the progressive neurodegenerative diseases caused by a multifactorial stress. The arguments that plead for the fact that glaucoma is a progressive neurodegenerative disease are (1) similarities between the glaucoma and the systemic neurodegenerative diseases, (2) similarity between the normal biological degenerative processes of the aging and the glaucoma and (3) the neurodegeneration of the optic nerve head. The factors that lead to the neurodegeneration of the retinal ganglion cells are mechanical (e.g. by an increase in intraocular pressure), ischemic/reperfusion, oxidative, autoimmune and genetic stresses.

[Fixed combinations of glaucoma medications]. / Combinatii fixe medicamintoase topice în tratamentul glaucomului.

Fixed combinations represent a combination of two ocular hypotensive agents into one single ophthalmic solution. Current commercially available fixed combinations used in glaucoma treatment include Combigan, Cosopt, Xalcom, Duotrav and Ganfort. Statistically significant superiority of the ocular hipotensive efficacy of the fixed combinations vs monotherapy with the two individual constituents is present connected with Cosopt and Xalcom. It also exists vs timolol ophthalmic solution relative to Combigan, Duotrav and Ganfort but is missing within these fixed combinations vs brimonidine, travatan and bimatoprost respectively. A slight reduction, that is clinically and statistically insignificant relative to fixed combination efficacy vs the nonfixed combinations (e.g. concomitant but separate administration of the two individual components) is acceptable when this is balanced by potential benefits of the fixed combinations therapy (improved tolerability and convenience,increased compliance,cost and time economies,decreased washout effect and reduced exposure to preservatives).

[Acute multifocal placoid pigment epiteliopathy]. / Epiteliopatia pigmentara placoida acuta multifocala.

Acute multifocal placoid pigment epitheliopathy is a fairly rare disease with unknown etiology and pathogenesis, possibly a focal response to a systemic inflammatory process. We present the case of a young patient who developed bilateral placoid retinal lesions, in different stages of evolution - cicatriceal lesions of the right eye and mixed cicatriceal and active lesions of the left eye. Investigations showed old immunity to cytomegalovirus and toxoplasma. Fluorescein angiography showed the typical fluorescein pattern (hypoflurecence in early phases and hyperfluorescence in late phases). The case is unique because of the atypical findings: choroidal neovascularization in the left eye (rarely occurs in acute multifocal placoid pigment epitheliopathy but more commonly in serpiginous choroidopathy), recurrences, asymmetry between the two eyes (at the time of investigations visual acuity is markedly depressed in the right eye - 1/10 and the left macula is threatened by the choroidal neovascularization).

[Clinical and fluorescein angiographic aspects in retinal angiomatosis (von Hippel)]. / Aspecte clinice si angiofluorografice în angiomatoza retiniana (von Hippel).

Retinal angiomas represent a rare condition consisting of hamartomas isolated or associated with a systemic disease (Von Hippel-Lindau Disease). We present a patient with multiple retinal angiomas, with atypical fluorescein angiography possible due to vascular thrombotic phenomena. Visual acuity was slightly diminished because of hemorrhagic complications. Systemic involvement was excluded with imaging studies.

[Does the ocular hypertension need treatment]. / Necesita hipertensiunea oculara tratament?

The authors review the risk factors that influence conversion of ocular hypertension into primary open-angle glaucoma. They are represented mainly by advanced age and higher intraocular pressure, central corneal thickness as well as greater values of vertical and horizontal cup/disc ratios. Therapy must be immediately performed if there is a moderate or high conversion risk (e.g. elderly age, greater intraocular pressure, central corneal thinnness, greater cup/disc ratio) (10% of cases). Should these factors be missing (more than 90% of the patients) then the treatment is not necessary, the only thing that has to be done is thorough monitoring of these patients.

[Optic nerve disc drusen]. / Drusen al papilei nervului optic.

Optic nerve head drusen represents a frequent condition, with unknown pathogenesis, mostly asymptomatic. Here, we present a patient with visual impairment, who has reacted well to anti-inflammatory and vasodilator treatment.

[Macular pigmentary epiteliopathy]. / Epiteliopatie pigmentara maculara.

This issue presents the case of a patient which present bilateral macular pigmentary epitheliopathy.