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Background:. Evaluation of practice patterns by American Board of Plastic Surgery (ABPS) diplomates allows for a greater understanding as to how the field is progressing. Understanding evolving procedural trends can give insight into plastic surgeons’ subspecialty focus and influence resident training to prepare them for future practice. Methods:. American Society of Plastic Surgeons member only projections for aesthetic and reconstructive procedures were reviewed from 1999 to 2018 in 5-year increments to identify shifts in frequency between the beginning (1999–2003) and end (2014–2018) of the timeframe. Tracer utilization for all four ABPS modules were also examined between 2014 and 2018. Descriptive statistics were performed to identify significant changes (P < 0.05) in subspecialty focus and procedure trends. Results:. Annual procedure incidence between 2014 and 2018 was compared with that between 1999 and 2003. The annual number of procedures more than doubled from 3,244,084 to 6,628,082. Among reconstructive procedures, there was a statistically significant increase in the number of breast reconstruction, breast implant removal, and maxillofacial surgery procedures, and a statistically significant decrease in the number of procedures focused on reconstruction of birth defects, burn injuries, and hand anomalies. In aesthetic surgery, significant increases were seen in the number of augmentation mammoplasty, abdominoplasty, and mastopexy procedures, with significant decreases in the number of blepharoplasty and rhinoplasty procedures. Conclusions:. Understanding the changing practice patterns of ABPS diplomates is essential to define the direction that our specialty is taking over time, and to guide program directors in plastic surgery on areas of focus for appropriate training of plastic surgeons.

Summary:. Asian rhinoplasty generally requires augmentation procedures rather than reduction. Alloplastic grafts are fraught with higher complication rates. Autologous cartilage grafts are safer. However, Asian patients typically do not have adequate septal cartilages, and other autologous cartilage grafts may cause surgical site morbidities, prolonged surgical time, and complications, including warping and infection. Asian rhinoplasties were performed using fresh frozen cartilage by the senior author. Patients’ demographics and medical histories were recorded. Anthropometric measurements (nasofrontal angle, nasofacial angle, nasolabial angle, and Goode ratio) were taken on two-dimensional photographs. FACE-Q scales were used to assess patient-reported outcomes. Five Asian patients underwent rhinoplasty using the fresh frozen cartilage and were followed up for an average period of 14.2 ± 3.35 months. There was no resorption, warping, or infection. Anthropometric measurements showed no significant changes 2–4 months or 8–20 months after surgery. At the time of the 1-year follow-up, mean FACE-Q Satisfaction with Nose, and Satisfaction with Nostrils scores improved from 35.2 ± 10.06 to 60 ± 15.48 (P = 0.0002), and 42.6 ± 20.31 to 59.8 ± 38.21 (P = 0.12), respectively. Fresh frozen cadaveric cartilage is a novel option for Asian rhinoplasty. Our study demonstrated its safety and satisfying surgical outcomes.

Purpose: To test the impact of professional management of soft contact lens wear on symptoms and ocular complications., Methods: Subjective symptoms and ocular complications of soft CL users who did not seek professional follow-up care (self-managed, SM), were compared to users who were prescribed CLs and their care professionally managed in optometry practices (PM), and to a control group of non-CL wearers. Habitual visual acuity, subjective dry-eye symptoms, and corneal abnormalities were assessed in all participants. CL wearers filled-out a usage habits questionnaire, and their CL fit was assessed. Outcomes were compared using Kruskal-Wallis and Chi Squared tests., Results: The SM, PM, and non-CL wearers cohorts included 127 (mean age:24.3±5.1, median:23, range:16-45 years,104 female), 132 (mean age:25.5±6.2, median:23, range:18-43 years,103 female), and 56 (mean age:22.3±3.5, median:21, range:18-39 years,36 female) participants, respectively. Meibomian gland dysfunction grade (p = 0.004, p<0.0001), limbal redness (both p = 0.04), corneal neovascularization (both p = 0.003), and papillary conjunctivitis (p<0.0001,p = 0.005) were significantly worse in SM CL wearers compared with both the non-CL wearers and PM CL wearers, respectively. Conjunctival staining was significantly worse in the SM cohort compared with the PM cohort (p = 0.01). 38.6% of the SM compared with 22.8% of the PM CL wearers, had an inappropriate refractive correction (p = 0.006). SM CL wearers wore CLs significantly more years (mean and median 1 year,p = 0.008), for more daily hours (mean and median of 2 hours,p<0.00001), and tended to nap or sleep with their CLs compared with the PM CL wearers (47 vs. 29,p = 0.02). The cohorts did not differ in their subjective symptoms., Conclusions: Complications are significantly more prevalent in SM CL wearers compared with PM CL wearers, and SM CL wearers tend to wear CLs with incorrect powers, and are less compliant with napping or sleeping with the CLs compared with PM CL wearers. These findings emphasize the importance of fitting, patient education and follow-ups in CL wearers., Competing Interests: Cooper-Vision Israel provided contact lens solutions that were provided to participants of the study. This does not alter our adherence to PLOS ONE policies on sharing data and materials. There are no patents, products in development, or marketed products associated with this research to declare., (Copyright: © 2024 Gantz et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Sulfur mustard (HD), a very potent alkylating agent and lipopolysacchride (LPS), are both well characterized inflammatory factors. We have found that concomitant exposure of murine macrophage cells (RAW264.7) to LPS and HD induced protection against HD induced cytotoxicity. Both HD and LPS induce release of inflammatory markers in RAW264.7 cells. However, there are marked differences in the repertoire of inflammatory factors released by the two toxins: While exposure to HD, induced a dose-dependant death of these cells, no significant change in survival rate was observed following LPS (1-100 ng/ml) exposure. Additionally, LPS elicited a robust nitric oxide (NO) and TNF-alpha secretion whereas HD was practically ineffective. Both toxins increased PGE(2) secretion in a concentration dependent manner. Treatment of HD-exposed RAW264.7 cells with anti-inflammatory drugs such as dexamethazone (5 muM), voltaren (diclofenac) (8 muM) or doxycycline (5 muM), decreased the release of cytokines but had no effect on cell viability. Simultaneous application of LPS (100 ng/ml) and HD (20-100 muM) resulted in an amelioration of HD cytotoxicity. Adding the NO generator S-nitrosoglutathione (GSNO) or inhibiting NO production using L-N(G)-monomethyl Arginine, had no effect on cell viability. Moreover, addition of PGE(2) (20 ng/ml) failed to induce any changes in cell viability under basal or HD-induced toxicity. In contrast, TNF-alpha (20 ng/ml) provided remarkable protection against HD-induced cell death. These findings strongly suggest that LPS exerts its protective action against HD toxicity through the generation of TNF-alpha and may provide better understanding of the mechanism of cytoprotection.

The hormonal changes associated with immobilization stress (IMO) include a swift increase in corticosterone (CORT) concentration and a decrease in circulating testosterone (T) levels. There is evidence that the production of the short-lived neuromodulator nitric oxide (NO) is increased during stress in various tissues, including the brain. NO also suppresses the biosynthesis of T. Both the inducible and the neuronal isoforms of NO synthase (iNOS and nNOS, respectively) have been implicated in this suppression, but the evidence has not been conclusive. We used adult wild-type (WT) and nNOS knockout male mice (nNOS-/-) to assess the respective roles of CORT and nNOS-derived NO in stress mediated inhibition of T production. Animals were assigned to either basal control or 3-hour IMO groups. No difference in basal plasma and testicular T levels were observed between WT and nNOS-/-, although testicular weights of mutant mice were slightly lower compared to WT animals. The plasma contents of luteinizing hormone (LH) and CORT in unstressed mice of both genotypes were similar. Exposure to 3 hours of IMO increased plasma CORT and decreased T concentrations in mice of both genotypes. However, comparable levels of plasma LH and testicular nitrite and nitrate (NOx), NO stable metabolites, were detected in control and stressed WT and nNOS-/- mice. Adrenal concentrations of NOx declined after IMO, but the reduction was not statistically significant. These findings implicate CORT rather than NO generated by nNOS in the rapid stress-induced suppression of circulating T.

Immobilization stress (IMO) induces a rapid increase in glucocorticoid secretion [in rodents, corticosterone CORT)] and this is associated with decreased circulating testosterone (T) levels. Nitric oxide (NO), a reactive free radical and neurotransmitter, has been reported to be produced at higher rates in tissues such as brain during stress. The biosynthesis of T is also known to be dramatically suppressed by NO. Specifically, the inducible isoform of nitric oxide synthase (iNOS) was directly implicated in this suppression. To assess the respective roles of CORT and NO in stress-mediated inhibition of T production, adult wild-type (WT) and inducible nitric oxide synthase knockout (iNOS(-/-)) male mice were evaluated. Animals of each genotype were assigned to either basal control or 3-h IMO groups. Basal plasma and testicular T levels were equivalent in both genotypes, whereas testicular weights of mutant mice were significantly higher compared with WT animals. Exposure to 3-h IMO increased plasma CORT and decreased T concentrations in mice of both genotypes. Testicular T levels were also affected by stress in WT and mutant males, being sharply reduced in both genotypes. However, the concentrations of nitrite and nitrate, the stable metabolites of NO measured in testicular extracts, did not differ between control and stressed WT and iNOS(-/-) mice. These results support the hypothesis that CORT, but not NO, is a plausible candidate to mediate rapid stress-induced suppression of Leydig cell steroidogenesis.

The free radical nitric oxide (NO), generated through the oxidation of L-arginine to L-citrulline by NO synthases (NOSs), has been shown to inhibit steroidogenic pathways. NOS isoforms are known to be present in rat and human testes. Our study examined the sensitivity of Leydig cells to NO and determined whether NOS activity resides in Leydig cells or in another cell type such as the testicular macrophage. The results showed a low level of L-[14C]arginine conversion in purified rat Leydig cell homogenates. Administration of the NOS inhibitor L-N(G)-nitro-arginine methyl ester (L-NAME), or the calcium chelator ethylenebis (oxyethylenenitrilo)tetraacetic acid (EGTA), had no effect on L-[14C]citrulline accumulation. Increased intracellular Ca2+ concentrations that were induced by a calcium ionophore, or the addition of luteinizing hormone (LH), failed to affect NO formation in intact cells that were cultured in vitro. Introduction of a high concentration of the NO precursor L-arginine did not decrease testosterone (T) production, and NOS inhibitors did not increase T biosynthesis. However, exposing Leydig cells to low concentrations of the NO donor S-nitrosoglutathione (GSNO) induced a dramatic blockade of T production under basal and LH-stimulated conditions. DNA array assays showed a low level of expression of endothelial NOS (eNOS), while the neuronal and inducible isoforms of NOS (nNOS and iNOS) were below detection levels. Reverse transcriptase-polymerase chain reaction (RT-PCR) analyses confirmed these findings and demonstrated the presence of high iNOS messenger RNA (mRNA) levels in activated testicular macrophages that produced large amounts of NO. These data suggest that, while T production in rat Leydig cells is highly sensitive to NO and an endogenous NO-generating system is not present in these cells, NOS activity is more likely to reside in activated testicular macrophages.

Nitric oxide synthases (NOSs) are classified functionally, based on whether calmodulin binding is Ca2+-dependent (cNOS) or Ca2+-independent (iNOS). This key dichotomy has not been defined at the molecular level. Here we show that cNOS isoforms contain a unique polypeptide insert in their FMN binding domains which is not shared with iNOS or other related flavoproteins. Previously identified autoinhibitory domains in calmodulin-regulated enzymes raise the possibility that the polypeptide insert is the autoinhibitory domain of cNOSs. Consistent with this possibility, three-dimensional molecular modeling suggested that the insert originates from a site immediately adjacent to the calmodulin binding sequence. Synthetic peptides derived from the 45-amino acid insert of endothelial NOS were found to potently inhibit binding of calmodulin and activation of cNOS isoforms. This inhibition was associated with peptide binding to NOS, rather than free calmodulin, and inhibition could be reversed by increasing calmodulin concentration. In contrast, insert-derived peptides did not interfere with the arginine site of cNOS, as assessed from [3H]NG-nitro-L-arginine binding, nor did they potently effect iNOS activity. Limited proteolysis studies showed that calmodulin's ability to gate electron flow through cNOSs is associated with displacement of the insert polypeptide; this is the first specific calmodulin-induced change in NOS conformation to be identified. Together, our findings strongly suggest that the insert is an autoinhibitory control element, docking with a site on cNOSs which impedes calmodulin binding and enzymatic activation. The autoinhibitory control element molecularly defines cNOSs and offers a unique target for developing novel NOS activators and inhibitors.

The oxygen permeability (Dk) of ten 24-hr collagen shields was measured directly by polarographic methodology at approximately 2 hr of hydration. Edge and boundary effects were included in the calculations. Dk was found to be approximately 26 x 10(-11) cm ml O2/sec ml mmHg at 35 degrees C. Mean water content of the shields was 65.7% (SD = 1.0%) as measured by a hand refractometer. Therefore, the projected oxygen transmissibility of collagen shields is expected to be compatible with normal corneal metabolism.

Nitrogen oxide-containing compounds displaced the peripheral benzodiazepine ligand [3H]Ro5-4864 from guinea pig membrane preparations. Sodium nitroprusside (SNP) was the most potent (IC50 = 5.61 +/- 1.72 x 10(-5) M). Moreover, its ability to bind to these receptors showed marked tissue variability (heart greater than kidney much greater than cerebral cortex). When tested on rat atrium, SNP by itself had no effect on basal inotropy or the increase in inotropy induced by (-)-S-BAY K 8644. In contrast, Ro5-4864 potentiated the marked increase in inotropy induced by (-)-S-Bay K 8644, and SNP completely abolished the potentiation of inotropy observed with Ro5-4864. Since peripheral benzodiazepine receptors are associated with calcium mobilization in the heart, these findings may indicate that some of the clinical effects of nitric oxide-generating drugs could be mediated by these receptors.

No oxygen was detected on the corneal surface of human subjects breathing air or almost pure oxygen. These results suggest that the epithelium obtains all its oxygen fro the air or the palpebral conjunctiva and that the endothelium is supplied with oxygen solely by the aqueous humor.

Aqueous humor oxygen tension of the in vivo rabbit eye was estimated by a relatively atraumatic procedure. The anterior corneal surface of the eye was first scraped free of its epithelial layer. A polarographic oxygen electrode was then used to measure the oxygen tension at the bare stromal surface. Aqueous humor oxygen tension can be estimated from this measured steady-state stromal surface oxygen tension by correcting the measured oxygen tension for the tension drop across the stroma and endothelium. When animals breathed room air (155 mm Hg oxygen tension), the oxygen tension of the aqueous humor was 13 mm Hg; this rose to 150 mm Hg when the inspired oxygen tension was 713 mm Hg.

1. The effects of intracarotid administration of Bay K 8644 on the ECG pattern along with their reversal by antianginal drugs were investigated in anaesthetized rats. 2. Intracarotid injections of Bay K 8644 (0.5-50.0 micrograms kg-1) produced a dose-related transient increase in systemic blood pressure. 3. The pressor response was accompanied by ST segment elevation (0.5-10.0 micrograms kg-1), ST segment depression concomitant with the occurrence of arrhythmias (20.0 micrograms kg-1), or A-V block (50.0 micrograms kg-1). 4. ST segment elevation reached its maximal value within 15 s and could be observed for 30-240 s. 5. The increase in blood pressure was immediate (within 5 s) and short lasting (30-120 s). After the initial increase it returned to control levels (0.5-20.0 micrograms kg-1) or dropped below (50.0 micrograms kg-1). 6. The ST segment elevation caused by 5.0 micrograms kg-1 Bay K 8644 (submaximal dose) was blocked by antianginal drugs (e.g. nitroglycerin, nifedipine and diltiazem) and by the peripheral benzodiazepine receptor antagonist PK 11195. However, the pressor response was not blocked by any of the drugs used. 7. ST segment elevation (or depression) induced by intracarotid administration of Bay K 8644 provides a useful tool for the evaluation of potential antianginal drugs.

Buspirone, MJ-13805 and MJ-13653 did not produce a '5-hydroxytryptamine (5-HT) syndrome' in rats at doses up to 20 mg kg-1. These drugs were very weak 5-HT uptake blockers (IC50 much greater than 10 microM) compared to drugs such as chlorimipramine. These drugs did not inhibit either monoamine oxidase (MAO)-A or MAO-B. The Ki values for these agents as inhibitors of [3H]-5-HT and [3H]-ketanserin binding to rat frontal cortex or hippocampal membranes were in the microM range, well above the brain concentrations achieved after an oral dose of 25 mg kg-1. Parenterally administered buspirone blocked apomorphine-induced stereotypy, inhibited the 5-HT syndrome elicited by 5-methoxy-N,N-dimethyltryptamine, and delayed the onset of p-chloroamphetamine induced behaviours.

'Peripheral' binding sites for benzodiazepines are under neural or homonal control in the pineal gland, olfactory bulb, and kidney. These observations prompted a search for an endogenous substance which could modulate these sites under physiological conditions. Acidified methanol extracts from several tissues (e.g. stomach, kidney, lung) were found to inhibit the binding of [3H]Ro 5-4864 to 'peripheral' binding sites, but did not significantly affect the binding of [3H]diazepam to 'brain' benzodiazepine receptors. Fractionation of a crude extract prepared from antral stomach by either ultrafiltration or gel filtration chromatography yielded high (Mr greater than 10 000) and low (Mr less than 1000) Mr fractions which competitively inhibited [3H]Ro 5-4864 binding to 'peripheral' sites. These observations suggest the presence of endogenous substances in several rat tissues which may represent physiologically important ligands for 'peripheral' binding sites for benzodiazepines.

Oxygen permeability (Dk) of 15 rabbit and 19 human cornea stromal samples was measured by conventional polarographic means at 36 C. Hydration and thickness were also measured. Rabbit stromal permeability was found to be about 26 X 10(-11) ml O2 cm2/sec ml mmHg at normal in vivo hydration; in vivo human cornea stromal permeability is probably less than 29 X 10(-11) ml O2 cm2/sec ml mmHg.

Rats made dependent on heroin and morphine exhibit both qualitative and quantitative differences in the characteristics of radioligand binding to mu-opioid receptors in the central nervous system. In brain membranes prepared from control animals, [3H]dihydromorphine (DHM) binding was best described by a two-site model, while in morphine-dependent rats, [3H]DHM binding was best described by a single-site model. In contrast, [3H]DHM binding to membranes from heroin-dependent animals was best described by a two-site model, with an increased density of the high-affinity, and no change in the low-affinity population compared to controls. Furthermore, both the number of binding sites for [3H]DAGO (a ligand that selectively labels a population of high-affinity mu-opiate receptors) and the sensitivity of [3H]DHM to sodium ions was increased in heroin; but not in morphine-dependent rats. These studies demonstrate that opiate receptors are differentially regulated in heroin- and morphine-dependent animals. Such neurochemical changes in mu-opiate receptors may underlie differences in the behavioral and pharmacological profiles of heroin and morphine reported in man.

An extensive clonal differentiation into mast cells from primitive blast cell precursors occurred when lymph node cells obtained from mice immunized with horse serum were cultured on mouse embryonic skin monolayers. Horse serum was always present in the culture as a constituent of the nutritional medium. Mast cells developed to lesser extent also in cultures prepared from non-immunized mice. However, a clear difference in mast cell-granule ultrastructure and in histamine content was noted between the two. In cultures of lymph nodes cells from non-immunized mice the granules were tiny and uniform in size and in staining density; whereas granules in the immune cultures were larger and non-uniform in size and in staining density, and the intragranular organization manifested alterations of various forms. The content of intracellular histamine per 10(6) mast cells was about equal in both cultures. However, much more free histamine (per 10(6) mast cells) gradually accumulated in cultures of the immune lymph node cells, indicating higher rates of synthesis and release of histamine. The mast cells were readily degranulated by heat-inactivated (IgG1) sera of the mice used as donors of the lymph node cells. 92% of the mast cells were degranulated and as much as 80% of the histamine was released. The degranulation was accompanied by an immediate (albeit reversible) response of the fibroblast cells in the monolayer. A shift of the well-stretched cytoplasm of the fibroblasts opened numerous 'window' over the whole monolayer. The degranulated mast cells survived the process and could be maintained further in the cultures. Moreover, they were capable of repeated degranulation, releasing 50% of their histamine, even after four degranulation cycles performed over a 7 days' period of culture. No cytotoxic effect on the mast cells was noted and the histamine content in culture, 3 days after degranulation, seemed to be higher than in the undergranulated control cultures--suggesting an intensified rate of histamine synthesis.