A hypothesized need to form and maintain strong, stable interpersonal relationships is evaluated in light of the empirical literature. The need is for frequent, nonaversive interactions within an ongoing relational bond. Consistent with the belongingness hypothesis, people form social attachments readily under most conditions and resist the dissolution of existing bonds. Belongingness appears to have multiple and strong effects on emotional patterns and on cognitive processes. Lack of attachments is linked to a variety of ill effects on health, adjustment, and well-being. Other evidence, such as that concerning satiation, substitution, and behavioral consequences, is likewise consistent with the hypothesized motivation. Several seeming counterexamples turned out not to disconfirm the hypothesis. Existing evidence supports the hypothesis that the need to belong is a powerful, fundamental, and extremely pervasive motivation.

The need to belong: Desire for interpersonal attachments as a fundamental human motivation.

Collagen and elastin networks make up the majority of the extracellular matrix in many organs, such as the skin. The mechanisms which are involved in the maintenance of homeostatic equilibrium of these networks are numerous, involving the regulation of genetic expression, growth factor secretion, signalling pathways, secondary messaging systems, and ion channel activity. However, many factors are capable of disrupting these pathways, which leads to an imbalance of homeostatic equilibrium. Ultimately, this leads to changes in the physical nature of skin, both functionally and cosmetically. Although various factors have been identified, including carcinogenesis, ultraviolet exposure, and mechanical stretching of skin, it was discovered that many of them affect similar components of regulatory pathways, such as fibroblasts, lysyl oxidase, and fibronectin. Additionally, it was discovered that the various regulatory pathways intersect with each other at various stages instead of working independently of each other. This review paper proposes a model which elucidates how these molecular pathways intersect with one another, and how various internal and external factors can disrupt these pathways, ultimately leading to a disruption in collagen and elastin networks.

/pdf/molecular-mechanisms-of-stress-responsive-changes-in-27n4lb5raa.pdf

Molecular Mechanisms of Stress-Responsive Changes in Collagen and Elastin Networks in Skin

The measurement of meaning

Interest in the role of the microbiome in human health has burgeoned over the past decade with the advent of new technologies for interrogating complex microbial communities. The large-scale dynamics of the microbiome can be described by many of the tools and observations used in the study of population ecology. Deciphering the metagenome and its aggregate genetic information can also be used to understand the functional properties of the microbial community. Both the microbiome and metagenome probably have important functions in health and disease; their exploration is a frontier in human genetics.

/pdf/the-human-microbiome-at-the-interface-of-health-and-disease-8umvuebp9h.pdf

The human microbiome: at the interface of health and disease

The skin is the human body's largest organ, colonized by a diverse milieu of microorganisms, most of which are harmless or even beneficial to their host. Colonization is driven by the ecology of the skin surface, which is highly variable depending on topographical location, endogenous host factors and exogenous environmental factors. The cutaneous innate and adaptive immune responses can modulate the skin microbiota, but the microbiota also functions in educating the immune system. The development of molecular methods to identify microorganisms has led to an emerging view of the resident skin bacteria as highly diverse and variable. An enhanced understanding of the skin microbiome is necessary to gain insight into microbial involvement in human skin disorders and to enable novel promicrobial and antimicrobial therapeutic approaches for their treatment.

The skin microbiome

It is the prevailing doctrine that the rays of the sun that are deleterious to the skin lie in the ultraviolet (UV) region (Hausser & Vahle, 1927; Cleaver, 1970). Experimental photobiologists like Blum (1959), Magnus (1976) and Forbes (1978) have established that sunburning rays, 280-315 nm (UV-B), are photocarcinogenic. UV-A (315-400 nm), although requiring vastly higher doses than UV-B, can produce similar changes. It can induce erythema (Kaidbey & Kligman, 1979) and damage blood vessels (Kumakiri, Hashimoto & Willis, 1977; Gilchrest et al, 1982), and in murine skin it has induced elastosis (Berger, Tsambaos & Kaase, 1980). UV-A also produces papillomas which may progress to squamous cell cancers (Forbes, Davies & Cole, 1982). Finally, UV-A augments the sunburning (Willis, Kligman & Epstein, 1973) and carcinogenic effects of UV-B (Willis, Menter & Whyte, 1981). However, terrestrial sunlight is polychromatic, extending beyond the UV region into the visible (400-700 nm), infra-red (700-1,000,000 nm) and ultimately radiowaves. The latter can probably be ignored with regard to skin but visible radiation (i.e. light), seemingly innocuous, cannot. Deleterious effects ranging from phototoxic reactions (Kaidbey & Kligman, 1978) to DNA crosslinks (Gantt et al, 1979) and tumour enhancement (Griffin et al, 1955) have been reported. Light also causes solar urticaria in susceptible persons (Harber & Bickers, 1981). The effect of light in preventing or augmenting the injurious skin effects of UV-B and UV-A has yet to be investigated. Curiously infra-red radiation (IR), which comprises about 40",, of the irradiance reaching the earth's surface (Koller, 1965), has been largely ignored by experimental photobiologists. This neglect may stem from theoretical considerations which deter experimentation. It is a basic tenet that photochemical reactions are not heat dependent. Temperature is of no importance in the production of excited states. However, this ignores the fact that biochemical reactions are strongly heat dependent. Products of photochemical reactions might readily be amplified by heat. It is in this sense that the effects of heat could produce a marked effect on ultraviolet injury.

Reflections on heat.

The purpose of this paper is to define further a little-known tumor of hair follicles and to show how it illuminates the origin of the nevoid class of tumors. By our criteria we have been able to find only two previous reports of one case each, first by Prinz 1 and recently by Hyman and Clayman. 2 These were titled hair-follicle nevi, a designation which we deem inappropriate. We shall add ten additional cases, only two of which were personally observed. The remainder were gathered from the consultant histopathology practice of one of us (H. P.). The cases will be presented as a group rather than in detail, for the histologic picture is strikingly pathognomonic and Hyman and Clayman's description cannot be exceeded for clarity. Besides our main concern is to fix the position of this tumor in the galaxy of benign adnexal neoplasms. Clinical Picture The tumor is not

The histogenesis of nevoid tumors of the skin. The folliculoma--a hair-follicle tumor.

Antibacterial Effects of Dimethyl Sulfoxide The minimal inhibitory concentration (MIC) of dimethyl sulfoxide to the nearest 10% in nutrient broth was determined for two isolates each of Staphylococcus aureus, S aureus variety albus , β -hemolytic streptococci, Corynebacterium acnes, Corynebacterium species (normal skin residents), Alcaligenes faecalis, Escherichia coli , and Proteus species. Twenty percent dimethyl sufoxide was found to be bacteriostatic to all of these. The bactericidal concentrations were established by subculturing after 24 hours. For S aureus , the bactericidal concentration (50%) was 2.5 times that of the MIC; for the remainder, it ranged from 30% to 40%, with the gram-negative bacteria being somewhat more susceptible. Dimethyl sulfoxide, by modern standards, is only weakly antibacterial. It is roughly comparable to many other solvents and far inferior to alcohol. The concentration required to kill all of the above organisms after one-hour exposures to aqueous solutions of dimethyl sulfoxide ranged from 65% to 75%.

Dimethyl Sulfoxide—Part 2

The Identification of Contact Allergens by Human Assay: I. A Critique of Standard Methods

• The role of melanin pigment in sunburn protection was investigated. Deep tans were induced over the backs of volunteers with repeated exposures to longwave ultraviolet radiation (UV-A). Melanogenesis was stimulated without an appreciable thickening of the stratum corneum. Two to three times the minimal erythema dose was required to produce redness in UV-A-tanned skin. Transmission studies through isolated corneum sheets revealed that specimens from tanned skin were about twice as efficient in filtering sunburn rays as stratum corneum from untanned skin. Tanning with UV-A does not provide a substantial resistance against sunburn. ( Arch Dermatol 114:46-48, 1978)

Sunburn protection by longwave ultraviolet radiation-induced pigmentation.

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