Revision surgical hair restoration: repair of undesirable results

Surgical hair restoration has been performed as a treatment for male pattern hair loss for more than 40 years. Although techniques have changed dramatically over the past several years, making it possible to achieve natural-appearing results, there are still many patients with unacceptable outcomes. These patients may have had procedures performed in the past with antiquated techniques or performed recently with substandard techniques. The causes of unfavorable results can be classified into one of three categories: technical errors, poor planning, or complications. The results in these patients can be dramatically improved through a number of different reparative surgical techniques. The majority of these techniques can be performed in an office outpatient setting. More than 40 patients unsatisfied with previous surgical hair restoration have been treated with the different techniques reviewed in this article. All patients had successful outcomes with significant improvement in appearance. Despite the increased challenges when performing reparative surgery, outcomes were favorable in all patients, with small to significant improvements in appearance achieved. Some of these challenges include the limited supply of donor hairs, reduced scalp laxity, and theoretically reduced vascularity due to scarring and transected blood vessels, and patient skepticism. Furthermore, the few complications that occurred were minor and correctable, including one case each of poor hair growth associated with extensive small graft (consisting of one to four hairs) transplanting, and of scalp scarring associated with the removal and primary closure of a large number of "plug" grafts (typically grafts 3 to 4 mm in size consisting of seven or more hairs) in a single procedure.     

Hominid brain evolution: two conceptions of science.

This paper re-examines the repeatedly-offered hypothesis (Fialkowski 1978, 1986, 1987, 1988) that hominid brain expansion was largely a side effect of evolutionary response to increased heat stress under conditions of primitive hunting, and resulted in a preadaptation to enhanced cognitive abilities. Fialkowski's hypothesis, previously shown to be based on data that are seriously inaccurate, continues to be presented in a manner that precludes testing. Consequently, however interesting these ideas may be, they are beyond the conventional domain of anthropology as a legitimate subdiscipline of modern science.     

Protein affinities for small molecules: conceptions and misconceptions.

There is much confusion and error in published treatments of data for multiple binding of ligands (e.g., substrates) by proteins (e.g., enzymes). There is a widespread impression that if the equilibrium binding, r, of ligand, A, by a protein with n sites can be fitted to an equation with two hyperbolic terms, i.e., $\text{r=}\text{n}{}_{\mathrm{\alpha }}\text{k}{}_{\mathrm{\alpha }}\text{(A)}\text{1+k}{}_{\mathrm{\alpha }}\text{(A)}\text{+}\text{n}{}_{\mathrm{\beta }}\text{k}{}_{\mathrm{\beta }}\text{(A)}\text{1+k}{}_{\mathrm{\beta }}\text{(A)}\text{(n}{}_{\mathrm{\alpha }}\text{+n}{}_{\mathrm{\beta }}\text{=n)}$ then k_β and k_β are always the intrinsic binding constants for two sets of sites. Such a conclusion is often incorrect. For example, in many cases, the protein is constituted of identical protomers with initially identical sites for binding ligands, and yet graphical representations of the binding data appear to behave as if the sites are partitioned between two classes. Although the use of a linear combination of hyperbolic terms to represent binding of ligands by macromolecules always yields empirical parameters k_α, k_β … k_λ, they cannot correspond to site binding constants when there are interactions between sites. In some circumstances their values may even be imaginary, complex numbers. On the other hand, stoichiometric binding constants can be assigned unambiguously without making any assumption regarding the nature of the interactions among binding sites. These principles are illustrated concretely by analyses of binding measurements for several different proteins containing two to six sites.     

Identification of undesirable white-colony-forming yeasts appeared on the surface of Japanese kimchi

To identify yeasts involved in white-colony formation on Japanese commercial kimchi products, three types of kimchi were prepared and fermented at four different temperatures. At 4 °C, yeast colonies did not appear until 35 days, while more rapid white-colony formation occurred at higher temperatures (10, 15, and 25 °C). Combination of PCR-DGGE and direct isolation of yeasts from white colonies revealed that Kazachstania exigua and K. pseudohumilis were responsible for the white-colony formation. Inoculation of the isolated Kazachstania strains into fresh kimchi successfully reproduced white-colony formation at 15 °C but not at 4 °C. Growth experiments in liquid medium revealed that Kazachstania spp. grew fast at 15 °C even in the presence of acidulants, which are commonly added to Japanese kimchi products for prevention of yeast growth. These results suggest that white-colony formation on Japanese kimchi is caused by the genus Kazachstania, and that one of important factors determining white-colony formation is its fermentation temperature.     

Honest signals and sexual conflict: Female lizards carry undesirable indicators of quality

Sex differences in animal coloration often result from sex‐dependent regulatory mechanisms. Still, some species exhibit incomplete sexual dimorphism as females carry a rudimentary version of a costly male trait, leading to intralocus sexual conflict. The underlying physiology and condition dependence of these traits can inform why such conflicts remain unresolved. In eastern fence lizards (Sceloporus undulatus), blue iridophore badges are found in males and females, but melanin pigmentation underneath and surrounding badges is male‐exclusive. We track color saturation and area of badges across sexual maturity, and their relationship to individual quality (body condition and immunocompetence) and relevant hormones (testosterone and corticosterone). Saturation and testosterone were positively correlated in both sexes, but hormone and trait had little overlap between males and females. Saturation was correlated with body condition and immunocompetence in males but not in females. Co‐regulation by androgens may have released females from resource allocation costs of color saturation, even when in high condition. Badge area was independent of testosterone, but associated with low corticosterone in females, indicating that a nonsex hormone underlies incomplete sexual dimorphism. Given the evidence in this species for female reproductive costs associated with ornamentation, this sex‐nonspecific regulation of an honest signal may underlie intralocus sexual conflict.     

DNA damage and repair: consequences on dose-responses

Damage to DNA is considered to be the main initiating event by which genotoxins cause hereditary effects and cancer. Single or double strand breaks, bases modifications or deletions, intra- or interstrand DNA-DNA or DNA-protein cross-links constitute the major lesions formed in different proportions according to agents and to DNA sequence context. They can result in cell death or in mutational events which in turn may initiate malignant transformation. Normal cells are able to repair these lesions with fidelity or by introducing errors. Base excision (BER) and nucleotide excision (NER) repair are error-free processes acting on the simpler forms of DNA damage. A specialized form of BER involves the removal of mismatched DNA bases occurring as errors of DNA replication or from miscoding properties of damaged bases. Severe damage will be repaired according to several types of recombinational processes: homologous, illegitimate and site-specific recombination pathways. The loss of repair capacity as seen in a number of human genetic diseases and mutant cell lines leads to hypersensitivity to environmental agents. Repair-defective cells show qualitative (mutation spectrum) and quantitative alterations in dose-effect relationships. For such repair-deficient systems, direct measurements at low doses are possible and the extrapolation from large to low doses fits well with the linear or the linear-quadratic no-threshold models. Extensive debate still takes place as to the shape of the dose-response relationships in the region at which genetic effects are not directly detectable in repair-proficient normal cells. Comparison of repair mutants and wild-type organisms pragmatically suggests that, for many genotoxins and tissues, very low doses may have no effect at all in normal cells.