Although fire is now rarely used in synthetic chemistry, it was not until Robert Bunsen invented the burner in 1855 that the energy from this heat source could be applied to a reaction vessel in a focused manner. The Bunsen burner was later superseded by the isomantle, oil bath, or hot plate as a source for applying heat to a chemical reaction. In the past few years, heating and driving chemical reactions by microwave energy has been an increasingly popular theme in the scientific community. This nonclassical heating technique is slowly moving from a laboratory curiosity to an established technique that is heavily used in both academia and industry. The efficiency of "microwave flash heating" in dramatically reducing reaction times (from days and hours to minutes and seconds) is just one of the many advantages. This Review highlights recent applications of controlled microwave heating in modern organic synthesis, and discusses some of the underlying phenomena and issues involved.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/anie.200400655

Controlled microwave heating in modern organic synthesis.

There is increasing concern that most current published research findings are false. The probability that a research claim is true may depend on study power and bias, the number of other studies on the same question, and, importantly, the ratio of true to no relationships among the relationships probed in each scientific field. In this framework, a research finding is less likely to be true when the studies conducted in a field are smaller; when effect sizes are smaller; when there is a greater number and lesser preselection of tested relationships; where there is greater flexibility in designs, definitions, outcomes, and analytical modes; when there is greater financial and other interest and prejudice; and when more teams are involved in a scientific field in chase of statistical significance. Simulations show that for most study designs and settings, it is more likely for a research claim to be false than true. Moreover, for many current scientific fields, claimed research findings may often be simply accurate measures of the prevailing bias. In this essay, I discuss the implications of these problems for the conduct and interpretation of research.

Why most published research findings are false

The TFOS DEWS II Pathophysiology Subcommittee reviewed the mechanisms involved in the initiation and perpetuation of dry eye disease. Its central mechanism is evaporative water loss leading to hyperosmolar tissue damage. Research in human disease and in animal models has shown that this, either directly or by inducing inflammation, causes a loss of both epithelial and goblet cells. The consequent decrease in surface wettability leads to early tear film breakup and amplifies hyperosmolarity via a Vicious Circle. Pain in dry eye is caused by tear hyperosmolarity, loss of lubrication, inflammatory mediators and neurosensory factors, while visual symptoms arise from tear and ocular surface irregularity. Increased friction targets damage to the lids and ocular surface, resulting in characteristic punctate epithelial keratitis, superior limbic keratoconjunctivitis, filamentary keratitis, lid parallel conjunctival folds, and lid wiper epitheliopathy. Hybrid dry eye disease, with features of both aqueous deficiency and increased evaporation, is common and efforts should be made to determine the relative contribution of each form to the total picture. To this end, practical methods are needed to measure tear evaporation in the clinic, and similarly, methods are needed to measure osmolarity at the tissue level across the ocular surface, to better determine the severity of dry eye. Areas for future research include the role of genetic mechanisms in non-Sjogren syndrome dry eye, the targeting of the terminal duct in meibomian gland disease and the influence of gaze dynamics and the closed eye state on tear stability and ocular surface inflammation.

TFOS DEWS II pathophysiology report

The tarsal glands of Meibom (glandulae tarsales) are large sebaceous glands located in the eyelids and, unlike those of the skin, are unassociated with hairs. According to Duke-Elder and Wyler,1 they were first mentioned by Galenus in 200 AD and later, in 1666, they were described in more detail by the German physician and anatomist Heinrich Meibom, after whom they are named.

Lipids produced by the meibomian glands are the main component of the superficial lipid layer of the tear film that protects it against evaporation of the aqueous phase and is believed also to stabilize the tear film by lowering surface tension.2 Hence, meibomian lipids are essential for the maintenance of ocular surface health and integrity.

Although they share certain principal characteristics with ordinary sebaceous glands, they have several distinct differences in anatomy, location, secretory regulation, composition of their secretory product, and function.

Functional disorders of the meibomian glands, referred to today as meibomian gland dysfunction (MGD),3 are increasingly recognized as a discrete disease entity.4–8 In patients with dry eye disease, alterations in the lipid phase that point to MGD are reportedly more frequent than isolated alterations in the aqueous phase. In a study by Heiligenhaus et al.,9 a lipid deficiency occurred in 76.7% of dry eye patients compared with only 11.1% of those with isolated alterations of the aqueous phase. This result is in line with the observations by Shimazaki et al.10 of a prevalence of MGD in the absolute majority of eyes with ocular discomfort defined as dry eye symptoms. These observations noted that 64.6% of all such eyes and 74.5% of those excluding a deficiency of aqueous tear secretion were found to have obstructive MGD, or a loss of glandular tissue, or both.10 Horwath-Winter et al.11 reported MGD in 78% of dry eye patients or, if only non-Sjogren patients are considered, in 87% compared with 13% with isolated aqueous tear deficiency. It may thus be accepted that MGD is important, conceivably underestimated, and possibly the most frequent cause of dry eye disease due to increased evaporation of the aqueous tears.5,9–12

After some excellent reviews of MGD4,7,8,13,14 in the past, many new findings have been reported in recent years, and other questions remain to be identified and resolved. A sound understanding of meibomian gland structure and function and its role in the functional anatomy of the ocular surface15 is needed, to understand the contribution of the meibomian glands to dysfunction and disease. Herein, we seek to provide a comprehensive review of physiological and pathophysiological aspects of the meibomian glands.

/pdf/the-international-workshop-on-meibomian-gland-dysfunction-1rohh1kg6i.pdf

The International Workshop on Meibomian Gland Dysfunction: Report of the Subcommittee on Anatomy, Physiology, and Pathophysiology of the Meibomian Gland

The members of the Management and Therapy Subcommittee undertook an evidence-based review of current dry eye therapies and management options. Management options reviewed in detail included treatments for tear insufficiency and lid abnormalities, as well as anti-inflammatory medications, surgical approaches, dietary modifications, environmental considerations and complementary therapies. Following this extensive review it became clear that many of the treatments available for the management of dry eye disease lack the necessary Level 1 evidence to support their recommendation, often due to a lack of appropriate masking, randomization or controls and in some cases due to issues with selection bias or inadequate sample size. Reflecting on all available evidence, a staged management algorithm was derived that presents a step-wise approach to implementing the various management and therapeutic options according to disease severity. While this exercise indicated that differentiating between aqueous-deficient and evaporative dry eye disease was critical in selecting the most appropriate management strategy, it also highlighted challenges, based on the limited evidence currently available, in predicting relative benefits of specific management options, in managing the two dry eye disease subtypes. Further evidence is required to support the introduction, and continued use, of many of the treatment options currently available to manage dry eye disease, as well as to inform appropriate treatment starting points and understand treatment specificity in relation to dry eye disease subtype.

TFOS DEWS II Management and Therapy Report

EINLEITUNG: Die Bestimmung der Viskositat von Kammerwasser bzw. Tranenflussigkeit einer einzigen Person ist mit konventionellen KPG-Ubbelohde Viskosimetern wegen der geringen Volumina nicht durchfuhrbar. Bisher war die Messung der Viskositat dieser Flussigkeiten nur durch Poolen mehrerer Proben machbar. Wir versuchten, ein Viskosimeter zu gestalten, das zur Messung kleinster Flussigkeitsmengen geeignet ist. METHODE: Ein kaufliches KPG-Ubbelohde Viskosimeter wurde von einem auf Medizintechnik spezialisierten Glasblaser modifiziert. Ein von uns angefertigter und zur Messung von Volumina unter 100 µl geeigneter Prototyp diente ihm dabei als Vorlage. ERGEBNISSE: Das so hergestellte Mini-Viskosimeter erlaubt nun die Messung der kinematischen Viskositat geringer Flussigkeitsmengen (60 µl). Damit konnen einzelne Proben von Kammerwasser, Tranenflussigkeit und anderen Korperflussigkeiten, ohne sie zu poolen, viskosimetrisch untersucht werden. SCHLUSSFOLGERUNG: Erstmals besteht die Moglichkeit, mit einem KPG-Ubbelohde Viskosimeter die Viskositat von Flussigkeitsvolumina im Mikroliterbereich zu messen. Damit war es uns moglich, die Viskositat des Kammerwassers oder der Tranenflussigkeit mittels einer einzigen Probenabnahme an einem bestimmten Auge zu messen. Mit dieser Methode kann zum Beispiel die Fragestellung bearbeitet werden, ob bei verschiedenen Glaukomarten unterschiedliche Kammerwasser-Viskositaten vorliegen. Ebenso besteht die Moglichkeit, die Rolle der Viskositat der Tranenflussigkeit beim trockenen Auge zu ermitteln.

Ein modifiziertes KPG-Ubbelohde Viskosimeter zur Bestimmung der Viskosimeter zur Bestimmung der Viskosität kleiner Volumina von Kammerwasser und Tränenflüssigkeit

Hyperhomocysteinemia and BRVO: Author reply

26 Patienten im Alter von 14 – 86 Jahren (Mittel 62,3 Jahre) mit Zentralvenenthrombosen wurden in einer retrospektiven Studie mit einem Nachbeobachtungszeitraum von 7 – 36 Monaten (Mittel 21,5 Monate) untersucht. Als Behandlung hatten die Patienten, je nach Hamatokrit, eine isobzw. hypervolamische Hamodilution mit 10% Hydroxyathylstarke 200/05, uber 8–10 Tage erhalten, wodurch eine signifikante Reduktion (p 40%) or hypervolemic (Hct ⩽ 40%) hemodilution over 8–10 days with daily infusion of 10% hydroxyethyl-starch 200/0.5. The hematocrit decreased significantly (p < 0.001) from 43.4 ± 3.7 to 37.5 ± 2.8 after this 10-day hemodilution treatment. Depending on the funduscopic features, focal or panretinal photocoagulation was done. Prior treatment the visual acuity ranged in 15% of all patients between 1.0 and 0.5, in 50% between 0.4 and 0.1 and in 35% worse than 0.1. After the longterm follow-up 11% of the patients had an improvement of the central vision by two or more lines, 58% had an deterioration, 31% remained unchanged. The visual acuity was between 0,5–1,0 in 15%, 0.4–0.1 in 19% and worse than 01. in 35%. Retinal neovascularization occurred in 31% of all patients, anterior segment neovascularization in 15%. All patients with ischemic central retinal vein occlusion developed neovascularization.

Otto Schmut

Papers

Ein modifiziertes KPG-Ubbelohde Viskosimeter zur Bestimmung der Viskosimeter zur Bestimmung der Viskosität kleiner Volumina von Kammerwasser und Tränenflüssigkeit

Hyperhomocysteinemia and BRVO: Author reply

Langzeitergebnisse von Patienten mit Zentralvenenverschlüssen nach Hämodilutionstherapie