Apocrine secretion--fact or artifact?

In this review, the history of apocrine secretion and the essential categories are briefly mentioned and fused into a more generally applicable terminology. Using the coagulating gland of the male rat as a model, the mechanisms of apocrine secretion, the participation of the cytoskeleton in the formation of the apocrine blebs ("aposomes") and the structure of the secretory proteins, as well as the hormonal regulation of their biosynthesis are described. Apocrine secreted proteins share the following peculiarities: (i) Their biosynthesis and post-translational modification (including an unusual form of glycosylation) take place in the cytoplasm. (ii) Intracellular transport proceeds without participation of the endomembrane system, the Golgi apparatus and secretion granules. (iii) Blood serum derived transsudated albumin entering the secretory cells functions as a carrier of the apocrine-released proteins. Some common molecular features are specific for the apocrine-synthesized proteins studied so far by our group: (a) Their primary sequence is synthesized without a signal peptide. (b) Their N-terminus is blocked by acetylation. (c) The substituting glycanes are neither O- nor N-linked. (d) At least one of the apocrine-synthesized proteins (secretory transglutaminase) contains a glycerol-phosphoinositol (GPI-) anchor. There are a number of still open questions in apocrine secretion, pertaining to (I) the intracellular transport and targeting of the proteins, (II) the coordination of simultaneously occurring apocrine and merocrine secretion in several of the apocrine glands, (III) the biosynthesis of the apical membrane proteins surrounding the aposomes and (IV) the repair mechanisms of the apical cell pole following the release of the aposomes. In conclusion, apocrine release is not an artifact but rather an alternative extrusion mechanism of soluble and membrane-associated proteins, usually linked with sex- or reproductive-related glands, such as the prostate, the mammary glands, apocrine sweat glands or epididymis.     

Somatization or psychosomatic symptoms?

The author describes some problems emerging from the approach to and comprehension of somatization symptoms, discussing ambiguities regarding somatization seen in the current classification manuals (ICD-10 and DSM-IV). Then the author presents a case report of a man who presented with a bizarre symptom of feminization that was successfully treated with psychotherapy. The author ends with a discussion of the relationship between meaning and symptom.     

Boom or bubble? Is medical research thriving or about to crash?

A recent issue of JAMA (2005; vol. 294) presented a portrait of medical research as a booming enterprise. By contrast I have suggested that medical research is a speculative bubble due to burst. How can two such different predictions be compatible? From inside the expanding world of medical research everything seems fine and getting better. But to people outside the system, it seems like there is an awful lot of money going in, and not much coming out. Professional criteria of success (publications, impact factors, citations, grant income, large teams, etc.) are not the same as the outsider's view of success. Outsiders want the medical research system to generate therapeutic progress as efficiently as possible: the most progress for the least resources. Medical research is not the only good way of spending money and is in competition with other social systems. As funding increases, diminishing returns will set-in, opportunity costs will begin to bite, and there will be more and more social benefit to be gained from spending the extra research money on something else. Therefore, future cuts in medical research will happen because of pressure from outside the system - specifically pressure from other powerful social systems which will press their alternative claims for funding. In the short term, there will be a quantitative decline of research production. But in the longer term the medical research system will re-grow in a more efficient form. After a 'golden age of therapeutic progress in the mid-20th century, recent decades have seen a 'silver age' of scholasticism which is due to end soon. Perhaps a renaissance of medical research lies not too many years in the future.     

B-cell or T-cell immunity?

The influenza virus behaves unpredictably and can cause devastating pandemics. Nearly 50 years after its first isolation it is probably the most infectious agent known that we cannot yet control. Why? The answer lies in the virus's unique capacity to alter antigenically and in the inability of the host's immune system to respond satisfactorily to the vaccines currently available. What follows is a record, prepared exclusively for Immunology Today, of a conference held in Oxford on March 21–24 this year, to discuss problems relating to protection against influenza.